Nutritional Support in Critical Care

Nutritional Support in Critical Care
Dr. Gwynne Jones University of Ottawa and the Ottawa Hospital.

Nutrition: Metabolic Profiles

Objectives Evidence for Feeding
Metabolic Alterations in Critical Illness Hypermetabolism/Hypercatabolism. Energy expenditure/Fuel Requirements. Carbohydrate and Sugar Control. Lipids and Free Fatty Acids. The Gut. Immunonutrition. Refeeding syndrome

A 55 yr old man with Group A Streptococcal Septic Shock and Necrotising Fasciitis of the thigh is sedated and fully ventilated. He is receiving much fluid, pressors and stress dose steroids. His Lactate level is 10mMol/L.

A 55 yr old man with Group A Streptococcal Septic Shock and Necrotising Fasciitis of the thigh is sedated and fully ventilated. He is receiving much fluid, pressors and stress dose steroids. His Lactate level is 10mMol/L. Would you feed this man now?

Nutrition: Metabolic Profiles Caloric need during illness
How many Calories would you feed this man?

How many Calories would you feed this man? 1. 15 K.cal/Kg/Day 2. 20 K.cal/Kg/Day 3. 25 K.cal/Kg/Day 4. 30 K.cal/Kg/Day 5. 40 K.cal/Kg/Day

How many Calories would you feed this man? In 1997 the American College of Chest Physicians (ACCP) issued a set of nutritional guidelines to reduce the variation in practice. Cerra and colleagues recommended in these guidelines that administering 25 total kilocalories per kilogram usual body weight per day appears to be adequate for most patients.

A 55 yr old man with Group A Streptococcal Septic Shock and Necrotising Fasciitis of the thigh is sedated and fully ventilated. He is receiving much fluid, pressors and stress dose steroids. His Lactate level is 10mMol/L. How much Protein would you feed this man?

A 55 yr old man with Group A Streptococcal Septic Shock and Necrotising Fasciitis of the thigh is sedated and fully ventilated. He is receiving much fluid, pressors and stress dose steroids. His Lactate level is 10mMol/L. How much Protein would you feed this man? Gm Protein?Kg./Day Gm Protein?Kg./Day Gm Protein?Kg./Day Gm Protein?Kg./Day Gm Protein?Kg./Day

Protein Requirements in Critical Illness. A 55 yr old man with Group A Streptococcal Septic Shock and Necrotising Fasciitis of the thigh is sedated and fully ventilated. He is receiving much fluid, pressors and stress dose steroids. His Lactate level is 10mMol/L. 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. Streat et al. (J.Trauma1987;27: )

Protein Requirements in Critical Illness. A 55 yr old man with Group A Streptococcal Septic Shock and Necrotising Fasciitis of the thigh is sedated and fully ventilated. He is receiving much fluid, pressors and stress dose steroids. His Lactate level is 10mMol/L. Graham Hill and his group measured body composition by in-vivo electron analysis. 1.2G to 1.5Gm Amino Acids/Kg/day (of pre-illness body weight) seemed adequate during the first two weeks of critical illness. This amount was best at reducing protein loss (not an increase in protein anabolism). Ishibashi N et al. Crit care Med 1998;26: )

A 55 yr old man with Group A Streptococcal Septic Shock and Necrotising Fasciitis of the thigh is sedated and fully ventilated. He is receiving much fluid, pressors and stress dose steroids. His Lactate level is 10mMol/L. Should you feed this man enterally or parenterally?

Does enteral nutrition compared to parenteral nutrition result in better outcomes in the critically ill adult patient? Conclusions: 1) The use of EN compared to PN is not associated with a reduction in mortality in critically ill patients. 2) The use of EN compared to PN is associated with a significant reduction in the number of infectious complications in the critically ill. 3) No difference found in ventilator days or LOS between groups receiving EN or PN. 4) Insufficient data to comment on other complications; hyperglycemia or higher calories not found to result in higher mortality of infections /criticalcarenutrition.com

Does enteral nutrition compared to parenteral nutrition result in better outcomes in the critically ill adult patient? /criticalcarenutrition.com

A 55 yr old man with Group A Streptococcal Septic Shock and Necrotising Fasciitis of the thigh is sedated and fully ventilated. He is receiving much fluid, pressors and stress dose steroids. His Lactate level is 10mMol/L. Should you feed this man immediately or delay feeding?

Does enteral nutrition compared to parenteral nutrition result in better outcomes in the critically ill adult patient? Conclusions: 1) Early enteral nutrition, when compared to delayed nutrient intake is associated with a trend towards a reduction in mortality in critically ill patients. 2) Early enteral nutrition, when compared to delayed nutrient intake is associated with a significant reduction in infectious complications. 3) Early enteral nutrition, when compared to delayed nutrient intake has no effect on ICU or hospital length of stay. 4) Early enteral nutrition, when compared to delayed nutrient intake improves nutritional intake. /criticalcarenutrition.com

Does early enteral nutrition compared to delayed enteral nutrition result in better outcomes in the critically ill adult patient? /criticalcarenutrition.com

Does Early Enteral Nutrition compared to Delayed Enteral Nutrition result in better outcomes in the critically ill adult patient? /criticalcarenutrition.com

Determining Energy Expenditure
indirect calorimetry: measurement of resting energy expenditure measurement of O2 consumption and CO2 production use of Weir equation: energy expenditure = (3.94 VO2) + (1.11 VCO2) sources of error: requires stable ventilation/’steady state’/stable feeding Beware high FIO2 and system leaks -direct calorimetry: measurement of heat production as caloric expenditure -indirect calorimetry: measurement of inspired/expired oxygen and carbon dioxide to determine VO2 and VCO2 -Weir equation: requires UN to represent protein metabolism, otherwise constant introduced into equation -assumes gas volume (l) for 1 gm of substrate for both O2 and CO2 and caloric value in kcal/g -note that including protein (urea nitrogen) not required -steady state – no rapid changes in MV (ie. VCO2 would be artificially high if pt. suddenly hyperventilates), similarly changes in CO, and if shivering etc. will be temporary increase in REE of 200% or more -error with high FIO2 due to assumption that insp and exp volumes the same however not quite, and with high FIO2 this error increases -leaks in system would also include chest tube leak for example -sometimes adjustment added as ‘correction factor’ but caution that this may lead to overfeeding 21

Indirect Calorimetry VS. Predictive Equations Recommendation: There are insufficient data to make a recommendation on the use of indirect calorimetry vs. predictive equations for determining energy needs for enteral nutrition in critically ill patients. Discussion: The committee noted the paucity of data and given the lack of treatment effect and the high costs associated with the use of indirect calorimetry (metabolic carts), despite no safety concerns, no recommendation was put forward. /criticalcarenutrition.com

How Aggressively should we be in starting Feeding? 3.2 Nutritional Prescription of Enteral Nutrition: Achieving target dose of enteral nutrition Recommendation: Based on 2 level 2 studies and 2 cluster randomized controlled trials , when starting enteral nutrition in critically ill patients, strategies to optimize delivery of nutrients (starting at target rate, higher threshold of gastric residual volumes, use of prokinetics and small bowel feedings) should be considered. Large improvements in calorie/protein intake/calorie deficit, decreased complications and reduced mortality with the use of enhanced enteral nutrition. Cost and feasibility concerns were also favourable. /criticalcarenutrition.com

Feeding protocols and Prokinetics Based on 1 level 2 study and 2 cluster randomized controlled trials, an evidence based feeding protocol that incorporates prokinetics at initiation and a higher gastric residual volume (250 mls) and the use of post pyloric feeding tubes, should be considered as a strategy to optimize delivery of enteral nutrition in critically ill adult patients. /criticalcarenutrition.com

Prebiotics/Probiotocs/Synbiotics There are inconsistent effect of Prebiotics/Probiotocs/Synbiotics on mortality. There is a lack of a treatment effect on other clinical outcomes. Their use may be associated with a trend towards a reduction in diarrhea in the critically ill population. /criticalcarenutrition.com

Gastrostomy vs. Nasogastric feeding There are insufficient data to make a recommendation on gastrostomy feeding vs. nasogastric feeding in the critically ill. /criticalcarenutrition.com

Combination Parenteral Nutrition and Enteral Nutrition Based on 5 level 2 studies, for critically ill patients starting on enteral nutrition we recommend that parenteral nutrition not be started at the same time as enteral nutrition. In the patient who is not tolerating adequate enteral nutrition, there are insufficient data to put forward a recommendation about when parenteral nutrition should be initiated. We recommend that PN not be started in critically ill patients until all strategies to maximize EN delivery (such as small bowel feeding tubes, motility agents) have been attempted. /criticalcarenutrition.com

Parenteral Nutrition and Enteral Nutrition Advice! Start Early Enteral Nutrition using a small feeding tube. If it goes post-pylorically-great/fine. If it’s in the stomach and it works-fine. If the patient has huge gastric residuals or vomits-use prokinetics. Just start! Gwynne Jones-very late May 2011.

Parenteral Nutrition and Enteral Nutrition Advice! Have a feeding protocol. Any high protein to calorie ratio Enteral Nutrition formula. Escalate to maximum predicted by pre-illness weight/predictive equation. If the patient has huge gastric residuals or vomits-use prokinetics. Just start! Gwynne Jones-very late May 2011.

Resuscitation and Nutrition The goal of resuscitation is to maintain ATP turnover. Fluids, Pressors and Inotropes are given to maintain “DO2” Oxygen needs fuel (Carbohydrate, Fat or Protein) to burn to maintain ATP turnover. Glycolysis does not need Oxygen Gwynne Jones-very late May 2011.

A 55 yr old man with Group A Streptococcal Septic Shock and Necrotising Fasciitis of the thigh is sedated and fully ventilated. He is receiving much fluid, pressors and stress dose steroids. His Lactate level is 10mMol/L.

His metabolic Rate is 1. At his resting level. 2. 120% of resting level. 3. 150% of resting level. 4. 200% of resting level. 5. 300% of resting level.

Starvation Catabolic Disease Metabolic rate to Severely ill patients (septic, major trauma or post-operative) are hypermetabolic and hypercatabolic. Oxygen consumption may be increased %. This metabolic activity is needed to maintain high cardiac output and ventilatory needs, liver acute phase response and increased immunological activity for healing.

His Body composition has changed. 1. There is an increase of lean body mass. 2. There is an increase of Body Fat. 3. There is an increase in Total Body Water.

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.

Body Composition Normal Critical Illness Weight %

His Carbohydrate Metabolism has changed has changed. 1. Insulin levels are high. 2. Glucagon levels are high. 3. Catecholamines and Cortisol are high. 4. Sugar levels are high. 5. Ketone levels are low. 6. All of the above.

Blood Sugar Insulin level Glucagon level Starvation Catabolic Disease or to to to This is the stress glucose response. There is insulin resistance both at receptor and post-receptor level. Hyperglycemia is immuno-depressive.

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

His Carbohydrate Metabolism has changed has changed. Sugar levels are high. 1. Tight control of sugar levels is beneficial. 2. Tight control of sugar levels is not beneficial.

His Fat Metabolism has changed 1. Lipolysis has increased. 2. Lipolysis has decreased. 3. Free Fatty levels are low.

Starvation Catabolic Disease Lipolysis Triglygeride recycling Lipids are well used in the stress state. Lipolysis may be so activated that free fatty acid provision exceeds requirements.

Starvation Catabolic Disease Lipolysis Triglygeride recycling Fatty Acids are elevated. FFAs are toxic for cell membranes and for the Mitochondria. Fatty Acids are re-esterified often producing hyperlipidemia. This is especially so with high lipid intakes. Hyperlipidemia is immuno-depressive.

What is our Septic Patient’s Respiratory Quotient?
0.7 0.8. 0.9. 1.0. 1.2. >1.25 suggests nonsteady state condition, hypoventilation

Q2 Respiratory Quotient A respiratory quotient of > 1 indicates which type of substrate utilization?: fat oxidation protein oxidation carbohydrate oxidation ethanol lipogenesis 10

Respiratory Quotient A respiratory quotient of > 1 indicates which type of substrate utilization?: RQ = VCO2 /VO2 fat oxidation (~ 0.7) protein oxidation (~ 0.8) carbohydrate oxidation C6H12O6 + 6O2 = 6H2O + 6 CO2 RQ = 1 ethanol (~ 0.67) lipogenesis (~ 1.2) < 0.65 suggests error (although under 7 is oxidation of ketones, ethanol, lipolysis >1.25 suggests nonsteady state condition, hyperventilation will acutely increase VCO2 and increase RQ above 1 -caution low specificity, error therefore be careful in interpretation physiologic range is ~ 0.65 to 1.3

Overfeeding more isn’t always better CHO hyperglycemia, fatty liver carbon dioxide production protein increased urea fat increased TG, hepatic steatosis, cholestasis, pancreatitis easy with PN hypocaloric feeding ‘metabolic support’ with calories ~ 50 – 60% for 3 – 5 days and then increase over 3 – 5 days to 100% during ‘stress’ phase of illness aka permissive underfeeding support metabolic pathways but not give excess fuel less glucose less hyperglycemia lower calcium, iron and zinc may decrease inflammatory response less carbon dioxide production yet provide nutritional support for enteric function anabolic phase – repletion of mass and nutritional support may be increased

Q3 Refeeding Syndrome Which of the following is NOT part of refeeding syndrome? hypophosphatemia hypokalemia hypomagnesemia salt wasting encephalopathy

Inflammatory bowel disease; Christie&HillGastroenterology1990;99: Grip strength 100 % Vital capacity Normal Value Why Does Strength Improve So Quickly? 50 0 7 14 200 Days of Feeding

Refeeding Syndrome refeeding: sudden shift back to glucose as fuel source hypophosphatemia hypokalemia hypomagnesemia

Nutrition: Metabolic Profiles Refeeding Syndrome
management: thiamine replacement ??? avoid by initiating feeds slowly (~ 25% of estimated needs on day 1) ??? gradual increase over 3 – 5 days monitoring and replacement of electrolytes

Nutrition: Metabolic Profiles; Protein
What percentage of Protein do we Oxidise (ie Use as an energy source) in Sepsis/Stressed States. 1. 5% 2. 10% 3. 15% 4. 25% 5. 40% more than ~ 1.5 gm/kg/day doesn’t seem to increase benefit 52

What percentage of Protein do we Oxidise (ie Use as an energy source) in Sepsis/Stressed States. 1. 5% 2. 10% 3. 15% 4. 25% 5. 40% The catabolism dictates that around 25% of energy needs are supplied by protein breakdown. This can be blunted by carbohydrate and fat but not totally suppressed. more than ~ 1.5 gm/kg/day doesn’t seem to increase benefit 53

What percentage of Protein do we Oxidise (ie Use as an energy source) in Sepsis/Stressed States. The catabolism dictates that around 25% of energy needs are supplied by protein breakdown. This can be blunted by food but not totally suppressed. This is the reason that normal protein intake (± 0.7 Gm/Kg/day) is increased to between 1.3 and 1.7 Gm/Kg/Day (Usually 1.5) in very sick patients. This is why the cans of ICU TUBE FEED have a Calorie/nitrogen ratio of 150 to 1 not the regular 100 to 1 more than ~ 1.5 gm/kg/day doesn’t seem to increase benefit 54

Protein Catabolism (losses/day) N2/day Protein/day Minor surgery: Major surgery: Multiple trauma/burns: Head injury: 3-5g G 4-10G G 15-20G G 20-25G G

Starvation Catabolic Disease Nitrogen balance Protein turnover Muscle catabolism Visceral catabolism Urea production Negative Very Negative to to or or

Nutritional Metabolic Profiles: Gut Colonisation
If the Stomach has 102 organisms/ml. How many Organisms/ml are there in the large Intestine? 1. 105

If the Stomach has 102 organisms/ml. How many Organisms/ml are there in the large Intestine? 1010 TO 1015 How does the Stomach keep so clean? 1. Acid 2. Peristalsis 3. Both

Stomach: 102 organisms/ml. Small Intestine: intermediate numbers increasing distally. Large Bowel: organisms/ml. Gut Colonisation is the progressive movement of gut organisms proximally. This process is impeded by: Peristalsis Stomach acidity Normal gut ecology and food

1. The Gut contains 15% of the body’s immune system. 2. Malnutrition is more dangerous than a gut that has received no food for 3 days. 3. TPN reduces gut translocation. 4. The primary fuel source of the gut enterocytes and colonocytes is sugar. 5. All of the above 6. None of the above

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

Nutritional Metabolic Profiles : TEN VS TPN
Fong et al. Ann. Surg.1989;210: 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. TPN Stress hormone level TEN TNF

Aim of early enteral feeding
Nutrition: Metabolic Profiles Aim of early enteral feeding Purported benefit of EN Direct provision of energy(glutamine, SCFA) Enterocyte trophic hormone stimulation Increased biliary and pancreatic secretion Increased mucosal blood flow Local autonomic stimulation Influence on gut permeability, translocation, metabolism

NUTRITION:Gut hypothesis of multi-organ failure
Capillary system of Gut Mucosa Arteriolar Vaso-constriction produces movement of oxygen between arteriole and venule. This leaves the villi tips ischemic. Gut Mucosa Prolonged shut-down produces necrosis of the tips of the villi. This is a precedent to translocation.

Factors Aggravating Paralytic Ileus: The propulsive peristaltic activity and its underlying myo-electrical activity need sustained activity to maintain their function. Absence of food Electrolytes/Opiods/Shock

Elective abdominal surgery depresses muscle protein synthesis and increases fatigue B Peterson et al. Br.J.Surg1990; 77: Fatigue 5 Post-operative day 30 25

Immune Enhancing Feeds.
Nutrition: Metabolic Profiles Immune Enhancing Feeds. 10 good studies: 9 showed benefit Bower et al.(Crit.Care .Med.1995;23: ) randomised 326 ICU pts. to standard or enhanced enteral formulae. Decreased infection rate and length of stay with enhanced formula (Impact)

Immune Enhancing Feeds. CCPG – figure is meta-analysis of arginine supplementation (EN), mortality endpoint recommendations from CCPG: arginine supplementation not be used in critically ill patients 69

Glutamine Conditionally essential Most abundant amino acid Fuel for dividing cells enterocytes, lymphocytes, macrophages Released from muscle with stress, sepsis Low plasma and intracellular concentration with stress (correlates with mortality) glutamine: conditionally essential amino acid with critical illness with stress serum concentrations of glutamine decrease, and becomes essential aa also nitrogen shuttle and precursor of antioxidant glutathione glutamine is also required for purine (ATP, adenosine) synthesis rationale for use of supplemental glutamine: provide fuel for rapidly proliferating cells (incl. gut) help with integrity of intestinal mucosa synthesis of antioxidant glutathione anticatabolic, help preserve muscle mass in enteral feeds glutamine will tend to degrade packaged dry and reconstituted 70

It is an essential precursor of nucleotide synthesis
NUTRITION: Human outcome of immune enhancing enteral feeding protocols. Glutamine It is an essential precursor of nucleotide synthesis It serves as a primary substrate for renal ammoniagenesis and arginine synthesis Glutamine + Cysteine + Glycine = Glutathione. Combined with Selenium, this is a major intra-cellular anti-oxidant.

Circulating glutamine pool LYMPHOCYTE MACROPHAGE PMN
NUTRITION:Glutamine Gln. in FOOD Circulating glutamine pool LYMPHOCYTE MACROPHAGE PMN GUT MUSCLE KIDNEY Gln. ACID/BASE Glutamate LUNGS LIVER NH4

Glutamine note supplemental glutamine added (but caloric value, protein equivalent as supplement and not part of calculations) Glutamine supplementation in serious illness: a systematic review of the literature. Crit Care Med 2002;30: CCPG 2007 ‘based on 2 level 1 and 5 level 2 studies EN glutamine should be considered in burn and trauma patients. There are insufficient data to support routine use in other critically ill patients’ note some evidence for glutamine supplementation of parenteral nutrition, however not available in Canada (and $$) 73

NUTRITION: Human outcome of immune enhancing enteral feeding protocols
NUTRITION: Human outcome of immune enhancing enteral feeding protocols. The role of Glutamine. The position of the Canadian Critical Care Trials Group. Based on meta-analysis of randomised controlled trials. Glutamine supplementation demonstrated a significant reduction in mortality (Risk Ratio,0.76, 95% confidence interval ). Glutamine supplementation demonstrated a significant reduction in length of stay (Weighted mean difference in days -4.50, 95% CI to -0.72).

Arginine ‘conditionally essential’ amino acid endogenous synthesis limited with illness also arginase upregulated in critical illness precursor for proline, glutamate, NH3 detoxification role in nitric oxide synthesis L-arginine NO + citrulline normally nonessential amino acid because it can be synthesized from citrulline in urea cycle also involved in creatine synthesis arginase is the enzyme that breaks down arginine to ornithine (and then metabolized to proline (wound healing), glutamate) with critical illness increased catabolism to nitric oxide and urea therefore conditionally essential note that nitric oxide is a double edged sword: excessive NO may damage not only microbes but also host cells too much NO may also contribute to vasodilation/hypotension

Arginine arginine supplementation rationale: sepsis associated with low serum arginine levels low levels may correlate with worse outcome needed for normal T-cell function increased NO may improve microcirculatory flow and immune function however: no good evidence of benefit possibility of harm in septic patients normally nonessential amino acid because it can be synthesized from citrulline in urea cycle also involved in creatine synthesis arginase is the enzyme that breaks down arginine to ornithine (and then metabolized to proline (wound healing), glutamate) with critical illness increased catabolism to nitric oxide and urea therefore conditionally essential note that nitric oxide is a double edged sword: excessive NO may damage not only microbes but also host cells too much NO may also contribute to vasodilation/hypotension 76

Selenium recommended as supplement in PN (trace element) patients with shock have low Se levels Se is cofactor in glutathione function and also immune effect additional supplementation may improve outcome normally nonessential amino acid because it can be synthesized from citrulline in urea cycle also involved in creatine synthesis arginase is the enzyme that breaks down arginine to ornithine (and then metabolized to proline (wound healing), glutamate) with critical illness increased catabolism to nitric oxide and urea therefore conditionally essential note that nitric oxide is a double edged sword: excessive NO may damage not only microbes but also host cells too much NO may also contribute to vasodilation/hypotension 77

NUTRITION: Human outcome of immune enhancing enteral feeding protocols
NUTRITION: Human outcome of immune enhancing enteral feeding protocols. Selenium and Anti-oxidants. The position of the Canadian Critical Care Trials Group. Based on meta-analysis of randomised controlled trials. Selenium supplementation (>500ug) demonstrated a significant reduction in mortality (Risk Ratio,0.52, 95% confidence interval ). Zinc + Vits. A,C, E supplementation demonstrated a mild reduction in mortality of 0.65 (95% CI ).

essential FA: EN supplemented with
NUTRITION: Human outcome of immune enhancing enteral feeding protocols. Fatty Acids essential FA: EN supplemented with EPA (fish oil) GLA (borage oil) antioxidant vitamins: E, C Changes cell membrane flexibility and signalling. modulation of leukotriene and cyclooxygenase pathways omega-3 (alpha linoleic acid) precursor for eisonanoids omega-6 (linoleic acid) precursor for arachidonic acid potentially proinflammatory (TNF, interleukin) vasoconstriction, platelet aggregation fatty acids: aka ‘fish oils’ nomenclature refers to where the double bond is in the molecule,omega3 and 6 FA are polyunsatruated (PUFA) because they have 2 or more double bonds FA important in cell membranes as well as metabolic precursors of eicosanoids (20 carbons – from Greek) omega 3: metabolized to 3-series of prostanoids and 5- series of leukotrienes anti-inflammatory effects (for example TXA2 vasoconstrictive, platelet aggregation and TXA3 little effect on vasoconstriction, no effect on platelets) competitive inhibitors of 2- and 4- series eicosnaoids dietary sources include canola oil, flax, fish omega 6: precursor of 2- and 4- series of prostanoids (PGE2, TXA2 (thromboxane A2), leukotriene B4…) which are proinflammatory, vasoconstrictive, increase platelet aggregation, immunosuppressive (impair RES function, leukocyte migration) in addtion use of GLA increases PG1 (vasodilator) and EPA moves metabolic pathway away from the production of arachidonic acid 79

Fish Oils Enriched EN improved survival in patients with ARDS/ALI
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

Take Home Messages Food is Part of a Normal Diet

Take Home Messages An Empty Gut is a Dangerous Gut

Take Home Messages An Empty Gut is a Dangerous Gut. You are the Parasite-there are more bugs in your gut than human cells

Take Home Messages An Empty Gut is a Dangerous Gut. Pre-operative fasting is getting shorter and shorter. See NHS website

Take Home Messages An Empty Gut is a Dangerous Gut. Post-operative fasting is getting shorter and shorter. Start on POD1 See NHS website

Take Home Messages An Empty Gut is a Dangerous Gut. Post-operative fasting is getting shorter and shorter. Give Food not clear fluids. Warren et al. Nutrn in Clin Practice 2011;26:

Take Home Messages An Empty Gut is a Dangerous Gut. Posture and Deportment See NHS website

Take Home Messages An Empty Gut is a Dangerous Gut. Posture and Deportment. Eating Sitting is Easier. 45° necessary in the Ill. See NHS website

Take Home Messages For Critical Care Nutritional information see: criticalcarenutrition.com

CARBON DIOXIDE A Second Class Molecule

Nutritional Support in Critical Care

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