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NUTRITION and IMMUNONUTRITION in the ICU Marcia McDougall October 2007.

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Presentation on theme: "NUTRITION and IMMUNONUTRITION in the ICU Marcia McDougall October 2007."— Presentation transcript:

1 NUTRITION and IMMUNONUTRITION in the ICU Marcia McDougall October 2007

2 A slender and restricted diet is always dangerous in chronic and in acute diseases Hippocrates 400 B.C.

3

4 Critical Illness Heterogeneous patients Extreme physiological stress/organ failure Acute phase response: TNF, IL-6, IL-1β Immuno-suppression: monocytes, MØ, NK cells, T and B lymphocytes Insulin resistance: hyperglycaemia Protein loss and fat gain in muscle Impaired gut function

5 Consequences of malnutrition Increased morbidity and mortality Prolonged hospital stay Impaired tissue function and wound healing Defective muscle function, reduced respiratory and cardiac function Immuno-suppression, increased risk of infection CIPs lose around 2%/day muscle protein

6 Scale of the problem McWhirter and Pennington 1994: McWhirter and Pennington 1994: >40% of hospital patients malnourished on admission >40% of hospital patients malnourished on admission Recent Scottish data 35% Recent Scottish data 35% Estimated cost to hospitals: £3.8bn/yr Estimated cost to hospitals: £3.8bn/yr Many ICU patients malnourished or at risk on ICU admission Many ICU patients malnourished or at risk on ICU admission

7 ICU Nutrition in the 1970s

8 ICU Nutrition through the ages Overfeeding 1980s

9 1970s: TPN - separate CH, AAs and Lipids 1970s: TPN - separate CH, AAs and Lipids 2500-3000kcals/day: Lactic acidosis, high glucose loads, fatty livers, high insulin reqt 2500-3000kcals/day: Lactic acidosis, high glucose loads, fatty livers, high insulin reqt Single lumen C/Lines, no pumps Single lumen C/Lines, no pumps Urinary urea measured, N calculated Urinary urea measured, N calculated 1980s: Scientific studies of metabolism: recognition of overfeeding 1980s: Scientific studies of metabolism: recognition of overfeeding 1990s: nitrogen limitation: 0.2g/kg/24hr, start of immunonutrition trials 1990s: nitrogen limitation: 0.2g/kg/24hr, start of immunonutrition trials 2000s: glucose control, specific nutrients 2000s: glucose control, specific nutrients

10 Nutrition trials in ICU Small, underpowered Small, underpowered Heterogeneous and complex patients Heterogeneous and complex patients Mixed nutritional status Mixed nutritional status Different feeding regimens Different feeding regimens Underfeeding – failure to deliver nutrients Underfeeding – failure to deliver nutrients Overfeeding – adverse metabolic effects Overfeeding – adverse metabolic effects Hyperglycaemia Hyperglycaemia Scientific basis essential Scientific basis essential

11 What is the evidence in ICU? Early enteral feeding is best Early enteral feeding is best Hyperglycaemia/overfeeding are bad Hyperglycaemia/overfeeding are bad PN meta-analyses controversial PN meta-analyses controversial Nutritional deficit a/w worse outcome Nutritional deficit a/w worse outcome EN a/w aspiration and VAP, PN infection EN a/w aspiration and VAP, PN infection EN and PN can be used to achieve goals EN and PN can be used to achieve goals Protocols improve delivery of feed Protocols improve delivery of feed Some nutrients show promising results Some nutrients show promising results

12 Unanswered questions Should we aim for full calorific delivery ASAP using EN + PN? Should we aim for full calorific delivery ASAP using EN + PN? What are the best lipids to use in PN? What are the best lipids to use in PN? What is the role of small bowel feeding? What is the role of small bowel feeding? Are probiotics helpful? Are probiotics helpful? Which patients will benefit from immuno- nutrition? Which patients will benefit from immuno- nutrition? The future: targeted Nutrition Therapy? The future: targeted Nutrition Therapy?

13 Current practice - Scotland SICS Nutrition Survey 2005-2006 SICS Nutrition Survey 2005-2006 Wide variation in PN and NJ feeding use Wide variation in PN and NJ feeding use Wide variation in opinions about nutrition Wide variation in opinions about nutrition Lack of education about nutrition Lack of education about nutrition Lack of interest from clinicians Lack of interest from clinicians Nutrition teams in 11/24 hospitals (QIS) Nutrition teams in 11/24 hospitals (QIS) Discussion between dietitians and doctors limited Discussion between dietitians and doctors limited

14 % patients receiving PN/year

15 NJ feed: patient use per year

16 What is the maximum amount of time an ICU patient should go without nutrition?

17 Nutrition QI Study Canadian Critical Care Network Canadian Critical Care Network 156 units cf CCCN guidelines 156 units cf CCCN guidelines 8 Scotland, 22 UK 8 Scotland, 22 UK Adequacy of EN Adequacy of EN Use of PN Use of PN Use of Immunonutrition Use of Immunonutrition Protocols/Glycaemic control/Bed elevation Protocols/Glycaemic control/Bed elevation

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19 Guidelines

20 systematically developed statements to assist practitioner and patient decisions about appropriate health care for specific clinical circumstances U.S. Institute of Medicine EBM - the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients Sackett DL et al. BMJ 1996

21 What Guidelines are available? Canadian Critical Care Network 2003/2007: Clinical Practice Guidelines Canadian Critical Care Network 2003/2007: Clinical Practice Guidelines ICS: Practical Management of Parenteral Nutrition in Critically Ill Patients 2005 ICS: Practical Management of Parenteral Nutrition in Critically Ill Patients 2005 ESPEN: Enteral Nutrition 2006 ESPEN: Enteral Nutrition 2006 NICE: Nutrition Support in Adults 2006 NICE: Nutrition Support in Adults 2006

22 Organisation of Nutrition Support 3. NICE Guidelines for Nutrition Support in Adults 2006

23 Screen Various nutritional screening tools Various nutritional screening tools NRS 2002, SGA, MNA Malnutrition Universal Screening Tool from the Malnutrition Advisory Group of BAPEN Low risk: routine clinical care, Medium risk: observe High risk: treat- refer to dietitian/local protocols

24 Screening in ICU MUST not very helpful in guiding decisions Almost all patients require artificial nutrition- cannot observe Almost all patients require artificial nutrition- cannot observe What about refeeding syndrome? What about refeeding syndrome? Needs adaptation using NICE Guidelines Needs adaptation using NICE Guidelines Adapted MUST for ICU: Uses BMI/weight loss/food intake + refeeding risk assessment; linked to feeding flowchart Adapted MUST for ICU: Uses BMI/weight loss/food intake + refeeding risk assessment; linked to feeding flowchart

25 Step 3 Treat: Enteral use the most appropriate route of access and mode of delivery has a functional and accessible gastrointestinal tract if patient malnourished/at risk of malnutrition despite the use of oral interventions and 3. NICE Guidelines for Nutrition Support in Adults 2006

26 Step 3 Treat: PN and has either introduce progressively and monitor closely if patient malnourished/at risk of malnutrition a non-functional, inaccessible or perforated gastrointestinal tract inadequate or unsafe oral or enteral nutritional intake use the most appropriate route of access and mode of delivery 3. NICE Guidelines for Nutrition Support in Adults 2006

27 Routes Of feeding

28 REDUCED ENTERAL STIMULATION DECREASED: Peyers patch leukotrienes + MAdCAM-1 T & B cells in Peyers patches, Lamina propria & epithelium Reduced secretory IgA and altered cytokines Mucosal atrophy Altered flora Decreased gastric acid Bacterial translocation

29 Enteral Preserves intestinal mucosal structure and function More physiological Relatively non-invasive Reduced risk of infectious complications cf PN (?) Relatively cheap

30 NG problems Risk of microaspiration in ICU Risk of microaspiration in ICU Risk of displacement Risk of displacement High gastric aspirates with opioids, sepsis, electrolyte imbalances High gastric aspirates with opioids, sepsis, electrolyte imbalances Reaching goals uncommon Reaching goals uncommon PEG/gastrostomy feeding for long- term >4 weeks PEG/gastrostomy feeding for long- term >4 weeks

31 Jejunal Feeding Insertion Surgical jejunostomy: at laparotomy May reduce incidence of aspiration Sometimes increases dose of EN given over NG Indications

32 Parenteral Nutrition GI tract not functional GI tract not functional GI tract cannot be accessed GI tract cannot be accessed Inadequate enteral nutrition <80% 3 days Inadequate enteral nutrition <80% 3 days Do not delay nutrition in malnourished Do not delay nutrition in malnourished Keep 10ml/hr EN if possible Keep 10ml/hr EN if possible

33 Supplemental PN Optimize EN first if possible (??) Optimize EN first if possible (??) Villet: Clin Nutr 24, 2005: Caloric debt a/w increased LOS, vent days and complications Villet: Clin Nutr 24, 2005: Caloric debt a/w increased LOS, vent days and complications Need trial to compare early supplemental PN and early EN with early EN only Need trial to compare early supplemental PN and early EN with early EN only North America/Europe split over use of PN North America/Europe split over use of PN Unanswered questions Unanswered questions

34 How much to give in ICU? Schofield equation/Harris Benedict Schofield equation/Harris Benedict e.g. for 65 year old woman: BMR = (9.2x weight in kg) + 687, = requirement in Kcal/24hr e.g. for 65 year old woman: BMR = (9.2x weight in kg) + 687, = requirement in Kcal/24hr Add Activity and Stress factors e.g. 10% for bedbound + 20-60% for sepsis/burns Add Activity and Stress factors e.g. 10% for bedbound + 20-60% for sepsis/burns For 65kg woman ventilated woman with sepsis: 1670 Kcal = approx 25 Kcal/kg/24hr For 65kg woman ventilated woman with sepsis: 1670 Kcal = approx 25 Kcal/kg/24hr No dietitian? Rough guide: 25 Kcal/kg/day total energy. Increase to 30 as patient improves No dietitian? Rough guide: 25 Kcal/kg/day total energy. Increase to 30 as patient improves

35 How much to give? 0.2g/Kg/day of Nitrogen (1.25g/kg/day protein) 0.2g/Kg/day of Nitrogen (1.25g/kg/day protein) 30 – 35ml fluid/kg/24 hours baseline 30 – 35ml fluid/kg/24 hours baseline Add 2-2.5ml/kg/day of fluid for each degree of temperature Add 2-2.5ml/kg/day of fluid for each degree of temperature Account for excess fluid losses Account for excess fluid losses Adequate electrolytes, micronutrients, vitamins Adequate electrolytes, micronutrients, vitamins Avoid overfeeding Avoid overfeeding Obesity: feed to BMR, add stress factor only if severe i.e. burns/trauma Obesity: feed to BMR, add stress factor only if severe i.e. burns/trauma

36 Refeeding Syndrome Prisoners of war 1944-5, 1944: conscientious objectors in USA studied Prisoners of war 1944-5, 1944: conscientious objectors in USA studied Starvation: early use of glycogen stores for AAs - gluconeogenesis; 72 hrs: FFA oxidation; use of FFAs and ketones for energy source, low insulin Starvation: early use of glycogen stores for AAs - gluconeogenesis; 72 hrs: FFA oxidation; use of FFAs and ketones for energy source, low insulin Atrophy of organs, reduced lean body mass Atrophy of organs, reduced lean body mass

37 Refeeding syndrome CH Feeding: shift to CH metabolism: insulin release CH Feeding: shift to CH metabolism: insulin release Stimulates PO 4 2- and K + shift into cells. PO 4 2- drops lower (ATP, 2-3DPG). Mg 2+ loss in urine 2 o low PO 4 2- (Na+K + ATPase) Stimulates PO 4 2- and K + shift into cells. PO 4 2- drops lower (ATP, 2-3DPG). Mg 2+ loss in urine 2 o low PO 4 2- (Na+K + ATPase) May get Lactic acidosis 2 o May get Lactic acidosis 2 o conversion of pyruvate to lactate Na + and H 2 O shift out of cells – oedema; ECF expansion 2 o reduced excretion of Na + and H 2 O; Na + and H 2 O shift out of cells – oedema; ECF expansion 2 o reduced excretion of Na + and H 2 O; Hyperinsulinaemia is antinatriuretic Hyperinsulinaemia is antinatriuretic Protein synthesis increases cellr demand for PO 4 2- and K + Protein synthesis increases cellr demand for PO 4 2- and K + Thiamine deficiency occurs (co-factor in CH metabolism): encephalopathy Thiamine deficiency occurs (co-factor in CH metabolism): encephalopathy

38 Refeeding Syndrome in ICU Unlikely to be a clear diagnosis Unlikely to be a clear diagnosis Many deleterious effects: oedema, arrhythmias, pulmonary oedema, cardiac decompensation, respiratory weakness, fits, hypotension, leukocyte dysfunction, diarrhoea, coma, rhabdomyolysis, sudden death Many deleterious effects: oedema, arrhythmias, pulmonary oedema, cardiac decompensation, respiratory weakness, fits, hypotension, leukocyte dysfunction, diarrhoea, coma, rhabdomyolysis, sudden death Screen: nutritional history and electrolytes Screen: nutritional history and electrolytes Remember in HDU patients/malnourished ward patients Remember in HDU patients/malnourished ward patients Poor awareness among doctors! Poor awareness among doctors!

39 Risk of re-feeding syndrome Two or more of the following: BMI less than 18.5 kg/m 2 (<16) BMI less than 18.5 kg/m 2 (<16) unintentional weight loss greater than 10% within the last 3-6 months (>15%) unintentional weight loss greater than 10% within the last 3-6 months (>15%) little or no nutritional intake for more than 5 days (>10) little or no nutritional intake for more than 5 days (>10) Hx alcohol abuse or drugs including insulin, chemotherapy, antacids or diuretics Hx alcohol abuse or drugs including insulin, chemotherapy, antacids or diuretics (Critically low levels of PO 4 2-, K + and Mg 2+) (Critically low levels of PO 4 2-, K + and Mg 2+)

40 Managing refeeding problems provide Thiamine/multivitamin/trace element supplementation provide Thiamine/multivitamin/trace element supplementation start nutrition support at 5-10 kcal/kg/day start nutrition support at 5-10 kcal/kg/day increase levels slowly increase levels slowly restore circulatory volume restore circulatory volume monitor fluid balance and clinical status monitor fluid balance and clinical status replace PO 4 2-, K + and Mg 2+ replace PO 4 2-, K + and Mg 2+ Reduce feeding rate if problems arise Reduce feeding rate if problems arise NICE Guidelines for Nutrition Support in Adults 2006

41 IMMUNONUTRITION Human Evolution No ambulances/hospitals First 72 hours after severe illness or injury crucial Little hope of survival past this; not desirable Significant stores of stress substrates not necessary e.g. glutamine

42 The Immune System A complex and interactive biological system that coordinates the detection, destruction and elimination of any foreign material or organism entering the body. Oxidants: cytokines, NFkB, genes, inflam n Oxidants: cytokines, NFkB, genes, inflam n Nutrients: glutamine, FFAs, protein Nutrients: glutamine, FFAs, protein Glutathione: oxidant defence Glutathione: oxidant defence Anti-inflammatory molecules: attenuation Anti-inflammatory molecules: attenuation

43 Critical Illness Sepsis: Battle between inflammatory response and microbes/toxins Sepsis: Battle between inflammatory response and microbes/toxins Trauma: SIRS to non-infectious insult Trauma: SIRS to non-infectious insult Minor insult: inflammatory response wins Minor insult: inflammatory response wins Major insult: with support (antibiotics, fluids) body may be able to fight insult but in severe insult inflammatory response continues and causes organ damage, f/b immune paresis and 2° infection; death Major insult: with support (antibiotics, fluids) body may be able to fight insult but in severe insult inflammatory response continues and causes organ damage, f/b immune paresis and 2° infection; death

44 Inflammation, organ failure Inflammation and resolution THE ICU GAMBLE How to tip the scales? DEATH LIFE DISABILITY

45 Critical Illness Small reductions in mortality over years Small reductions in mortality over years Increasing problems with infection Increasing problems with infection Advances in treatment have limited effects Advances in treatment have limited effects Pathophysiology complex Pathophysiology complex The future: replacement of the bodys own stress substrates Could immunonutrition be the most important area in critical care development? Could immunonutrition be the most important area in critical care development?

46 Failed ICU strategies Anti-TNF antibodies Anti-TNF antibodies Steroids in sepsis – recent work suggests little effect Steroids in sepsis – recent work suggests little effect NO synthetase inhibitor: increased mortality NO synthetase inhibitor: increased mortality ??? Activated protein C - controversial ??? Activated protein C - controversial

47 Immuno/Pharmaconutrition Disease-modulating nutrients Attenuate metabolic response Prevent oxidant stress Favourably modulate immune response Probiotics to alter gut environment Glycaemic control: keep blood glucose <8mmol/l: reduces infections and organ failures

48 Glutamine Non-essential amino acid – conditionally essential in sepsis/major trauma Non-essential amino acid – conditionally essential in sepsis/major trauma Vital to gut, immune cells, and kidney Serves as metabolic fuel; precursor to DNA synthesis BUT Levels drop after injury, exercise and stress. Very low in critical illness first 72 hours BUT Levels drop after injury, exercise and stress. Very low in critical illness first 72 hours Glutamine deficiency at onset of critical illness/sepsis correlated with increased mortality

49 Potential Beneficial Effects of Glutamine Fuel for Enterocytes Lymphocytes NuclotideSynthesis Maintenance of Intestinal Mucosal Barrier Maintenance of LymphocyteFunction Preservation of TCA Function Decreased Free Radical availability (Anti-inflammatory action) GlutathioneSynthesis GLNpool Glutamine Therapy Enhanced Heat Shock Protein Shock Protein Anti-catabolic effect Preservation of Muscle mass ReducedTranslocation Enteric Bacteria or Endotoxins Reduction of Infectious complications Inflammatory Cytokine Inflammatory CytokineAttenuation NF-kB NF-kB? Preserved Cellular Energetics- ATP content GLNPool Critical Illness Enhanced insulin sensitivity Wischmeyer PE, Curr Opin Clin Nutr Metab Care 6: 217-222, 2003

50 Glutamine trials Modest reduction in mortality/infections in 9 studies of glutamine-supplemented PN Modest reduction in mortality/infections in 9 studies of glutamine-supplemented PN Improvement in morbidity and mortality in 2 studies of enteral glutamine in burns and trauma patients Improvement in morbidity and mortality in 2 studies of enteral glutamine in burns and trauma patients CCCN recommend enteral glutamine for burns and trauma and IV glutamine to be given with parenteral nutrition CCCN recommend enteral glutamine for burns and trauma and IV glutamine to be given with parenteral nutrition SIGNET and REDOXs awaited SIGNET and REDOXs awaited

51 PROBIOTICS Live micro-organisms which when administered in adequate amounts confer a health benefit on the host Bioecological control: Supply viable beneficial bacteria, or a substrate which enhances specific beneficial bacteria, instead of trying to eliminate the pathogen

52 Probiotics Critical illness causes virulence of gut bacteria; treatment worsens gut function Critical illness causes virulence of gut bacteria; treatment worsens gut function Probiotics inhibit growth of pathogenic enteric bacteria Probiotics inhibit growth of pathogenic enteric bacteria block epithelial invasion by pathogens block epithelial invasion by pathogens eliminate pathogenic toxins eliminate pathogenic toxins improve mucosal barrier function improve mucosal barrier function enhance T-cell and macrophage function enhance T-cell and macrophage function reduce production of TNF and NFkB reduce production of TNF and NFkB

53 Probiotics Potential to cut VAP and C. diff Potential to cut VAP and C. diff BUT: safety concerns BUT: safety concerns dosage dosage which bacteria to use which bacteria to use viability in the gut viability in the gut storage issues storage issues unforeseen effects unforeseen effects More research required More research required

54 Arginine Conditionally essential amino acid derived from glutamine and citrulline Conditionally essential amino acid derived from glutamine and citrulline For protein synthesis, cell division, NO, urea cycle, creatine phosphate (ATP) For protein synthesis, cell division, NO, urea cycle, creatine phosphate (ATP) Stimulates hormone release Stimulates hormone release Deficiency: Deficiency: Immune suppression, TH2 cell function, free radical formation Abnormal microperfusion Abnormal wound healing

55 Sepsis Sepsis: iNOS, dendritic cells, IL-1, IL-6 Sepsis: iNOS, dendritic cells, IL-1, IL-6 TH1 cytokine profile: IL-2,TNF,interferon-ү TH1 cytokine profile: IL-2,TNF,interferon-ү Arginine deficiency not severe in sepsis Little drop in plasma arginine levels CCCN: not recommended (harm?)

56 Trauma Trauma: IL-10, poor antigen presentation, TH2 cytokine profile: IL-4, IL-13 Trauma: IL-10, poor antigen presentation, TH2 cytokine profile: IL-4, IL-13 Pathologic release of arginase from myeloid suppressor cells, hepatocytes, RBCs Pathologic release of arginase from myeloid suppressor cells, hepatocytes, RBCs Significant drop in arginine levels in trauma CCCN: not recommended – future role? Pre-operative patients, cancer, sickle cell, haemolytic anaemia, PIH

57 PUFAs Arachidonic Acid: COX and LOX precursor: Omega-6 ү-Linoleic acid (GLA) – borage oil Fish oils: Eicosapentanoic acid (EPA) and Docosahexanoic acid (DHA): Omega-3 FAs

58 Dietary Lipids Ratios in paleolithic diet ω-6:ω-3 1:1 Current Western diet 16.7:1 Current Western diet 16.7:1 Current UK PN Soybean oil base 7:1 (LCT) Current UK PN Soybean oil base 7:1 (LCT) New PN (SMOF) 2.5:1 (LCT/MCT) New PN (SMOF) 2.5:1 (LCT/MCT) Membrane composition depends on diet Membrane composition depends on diet AA arises from GLA AA arises from GLA AA, DHA and EPA are present in inflammatory cell membrane phospholipids AA, DHA and EPA are present in inflammatory cell membrane phospholipids Hydrolysis of FAs by phospholipase to mediators Hydrolysis of FAs by phospholipase to mediators

59 Mechanisms of Action ω-3s EPA/DHA are incorporated quickly into cell membrane: inhibit ω-6 activity ω-3s EPA/DHA are incorporated quickly into cell membrane: inhibit ω-6 activity Promote synthesis of low activity PGs and LTs Promote synthesis of low activity PGs and LTs Decrease expression of adhesion molecules Decrease expression of adhesion molecules Inhibits monocyte prod n of pro-inflamm cytokines Inhibits monocyte prod n of pro-inflamm cytokines Decreases NFkB, increases lymphocyte apoptosis Decreases NFkB, increases lymphocyte apoptosis Decreases pro-inflammatory gene expression Decreases pro-inflammatory gene expression Lipoxins, resolvins and protectins Lipoxins, resolvins and protectins

60 Borage Oil DGLA PGE 1 and fewer Inflammatory Eicosanoids Substitution of AA By DGLA resulting in: Fish Oil GLAEPA Fewer Inflammatory Eicosanoids (TXA 3, PGE 3, LTB 5 ) Substitution of AA By EPA Resulting in: Arachidonic Acid Cyclooxygenase Lipoxygenase Pro-Inflammatory Eicosanoids (LTB 4, TXA 2, PGE 2 ) Decrease in X Mechanisms of Action

61 3 Studies: OXEPA Patients with ARDS fed with GLA, EPA and antioxidants had a reduction in pulmonary neutrophils Improvement in oxygenation Decrease in ventilator days Decrease in ICU and hospital days Gadek, Singer, Pontes-Arruda (sepsis)

62 Omega-3 Fatty Acids BUT BUT Control group had high fat diet – bad? Control group had high fat diet – bad? Was it the FAs or the antioxidants or both? Was it the FAs or the antioxidants or both? CCCN – consider in ARDS i.e. OXEPA mix CCCN – consider in ARDS i.e. OXEPA mix Other researchers: not enough evidence Other researchers: not enough evidence Science makes sense; works in IHD, PVD Science makes sense; works in IHD, PVD

63 Anti-oxidants Normal state: reduction > oxidation Normal state: reduction > oxidation Acute stress: injury/sepsis causes acute dysregulation: ROS/RNOS formed Acute stress: injury/sepsis causes acute dysregulation: ROS/RNOS formed Mitochondria are both sources and targets Mitochondria are both sources and targets Observational studies: anti-oxidant capacity inversely correlated with disease severity due to depletion during oxidative stress Observational studies: anti-oxidant capacity inversely correlated with disease severity due to depletion during oxidative stress REDUCTION OXIDATION

64 Reactive Oxygen Species O -, NO - Positive actions: Bactericidal Regulation of vascular tone Cell signalling But mostly detrimental: Cell injury (ischaemia /reperfusion) DNA, Lipids, Proteins Organ dysfunction Lungs, Heart, Kidney Liver, Blood, Brain OXIDATION REDUCTION

65 ACUTE INSULT Exacerbation of cell and tissue injury Inflammatory mediators ROS/RNOS Healing/repair/ defence

66 Antioxidants Glutathione, Vitamins A, C and E Glutathione, Vitamins A, C and E Zinc, copper, manganese, iron, selenium Zinc, copper, manganese, iron, selenium Already added to feeds Already added to feeds Should we give extra CCCN – consider Should we give extra CCCN – consider Results of SIGNET and REDOXs awaited Results of SIGNET and REDOXs awaited Oxidative stress in critically ill patients contributes to organ damage / malignant inflammation

67 Elective Surgery Critically Ill GeneralSepticTraumaBurns Acute Lung Injury Arginine Benefit No benefit Harm(?) (Possible benefit) No benefit GlutaminePossible Benefit PN Beneficial Recom- mend … EN Possibly Beneficial: Consider EN Possibly Beneficial: Consider … Omega 3 FFA …………… Recom- mend Anti- oxidants … Consider ………… Which Nutrient for Which Population? Canadian Clinical Practice Guidelines JPEN 2003;27:355

68 Immunonutrition- the future? The right nutrient or combination Correct dose The appropriate timing The right patient and circumstance The appropriate assessment of efficacy Balance between harm and benefit of the immune response ?? Nutrient-gene interactions

69 Now More & better trials of Immunonutrition More & better trials of Immunonutrition Early PN supplementation trial Early PN supplementation trial Meanwhile: the basics- screening, reaching goals, protocols, refeeding Meanwhile: the basics- screening, reaching goals, protocols, refeeding HDU feeding HDU feeding Profile of Nutrition: Education, dialogue Profile of Nutrition: Education, dialogue Funding Funding

70 MaintainsStimulates the environmentdefences FEEDING FEEDING Provides energy


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