Nutrition in icu


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Nutrition in icu

  2. 2. OUTLINES History The Basis of Nutritional Support Physiologic Effect of malnourish Nutritional Requirement Supplimented nutrition Routes of administration ( Enteral, parenteral)
  3. 3. SIX SIMPLE QUESTIONS Why do we feed ICU patients? Which patients should we feed? When should we start to feed them? Which route should we feed by? How much feed should we give? What should the feed contain?
  4. 4. ICU Nutrition in the 1970s
  5. 5. ICU NUTRITION THROUGH THE AGES Overfeeding 1980s
  6. 6. THE BASIS OF NUTRITIONAL SUPPORT Most patients in ICU are unable to tolerate normal diet many of them are malnourished on admission nutrients can be delivered directly to the GIT by feeding tubes( enteral feeding) or by intravenous ( parentral feeding) nutrition is provided against a bakground of a continously changing physical status
  7. 7. THE BASIS OF NUTRITIONAL SUPPORT few data directly compare feeding with no feeding in critical patients and it suggest worse outcomes in underfed patients catabolism of critical illness causes malnutrition malnutrition closely associated with poor outcomes
  8. 8. THE BASIS OF NUTRITIONAL SUPPORT Stress, acute illness, surgery or trauma produce major changes in the metabolic milieu of the body  changes in substrate utilization  altered substance synthesis rates  hypermetabolism  catabolism
  9. 9. Hypermetabolism Poor intake Surgery malnutrition Immobility FACTORS FAVOURING THE DEVELOPMENT OF Stress in MALNUTRITION IN THE CRITICALLY ILL the critically ill Changes in Exogeneous steroids Prolonged bed rest substrate utilisation
  10. 10. CONSEQUENCES OF MALNUTRITION Increased morbidity and mortality Prolonged length of stay in ICU Impaired tissue function and wound healing Defective muscle function, reduced respiratory and cardiac function Immuno-suppression, increased risk of infection
  11. 11.  Malnutrition causes widespread organ dysfunction, ass. with poor healing, reduce immune competence & poor weaning from ventilator. Stress & sepsis further increase metabolic rate & if the energy required is not met with adequate dietary intake, it will results in catabolism. Goal of nutritional support : to improve patients outcome and reduce the morbidity and mortality.
  12. 12. NUTRITIONAL SUPPORT IS NOT CRUCIAL IN “GUT FAILURE” Is that the right statement?
  14. 14. NUTRITIONAL CARE PLAN Functional GI tract Yes No Enteral nutrition Parenteral nutritionStandard nutrients Speciality formulas Peripheral PN Central PN
  15. 15. PHYSIOLOGIC EFFECTS OFMALNUTRITION Pulmonary  Decreased diaphragmatic contractility  Depressed hypoxic drive & ventilatory drive to CO2 Cardiac  Decreased contractility/response to inotrope  Ventricular dilatation Renal  Decreased GFR  Impaired Na+ excretion
  16. 16. Hepatic • Altered CHO, protein & fat metabolism • Decreased protein synthesis • Decreased drug metabolism • Impaired bilirubin excretion Hematology • Anaemia & coagulopathy Immune • Depressed T-cell functions • Impaired chemotaxis and phagocytosis GIT • Decreased gut motility • Gut atrophy • Increase gut permeability to intestinal bacteria•
  18. 18. 1.Fluid 30-40 ml/kg BW2. Energy 1. Total Energy expenditure 2. Calorie/weight : 25-35 kcal/kg/day 3. Indirect calorimetry3. Protein Normal prot : 0.8 g/kg/d HD. CVVHD : 1.1 – 1.4 g/kg/d Sepsis/trauma : 1.2 – 2.0 g/kg/d Severe burns : 2.5 – 4.0 g/kg/d
  19. 19. NUTRITIONAL REQUIREMENTS Total Energy Expenditure ( TEE) = BEE x Injury Factor The BEE is the amount of energy required to perform metabolic functions at rest, and is influenced by both body size and illness BEE classically is estimated by the Harris- Benedict equation:  For men, BEE = 66.5 + (13.75 x kg) + (5.003 x cm) - (6.775 x age)  For women, B.E.E. = 655.1 + (9.563 x kg) + (1.850 x cm) - (4.676 x age)** BEE - Basal Energy Expenditure
  20. 20. NUTRITIONAL REQUIREMENTSBasal Energy Expenditure:Harris-Benedict Equation Estimate basal energy expenditure using the Harris-Benedict equations. m f Ma Female le 172 cm in Input Height cm in 60 kg lb Input Weight kg lb 40 yr mo Input Age yrs mos Infection, severe Stress Factor br am Activity Factor Bedrest Ambulating Calculate Clear 1481 B.E.E. = 2444 kcal/d Caloric Requirement = kcal/d
  21. 21.  Injury Factor  Mild illness 1 – 1.25 eg. minor op 1.2  Moderate illness 1.25 – 1.5 eg skeletal trauma 1.35  Severe illness 1.5 – 1.75 eg major sepsis 1.60 Estimated Total Energy Requirement = BEE x Activity Factor x Injury Factor
  22. 22. INDIRECT CALORIMETRY Most accurate. Portable bedside system measuring of EE and resp quotient by measuring and analysing the O2 consumed ( VO2) and the CO2 expired ( VCO2) Respiratory Quotient = CO2 production/O2consumptionRQ Interpretation> 1.00 overfeeding0.9 – 1.00 CHO oxidation0.8 – 0.9 Mixed nutrients oxidation0.7 – 0.8 Fat and protein oxidation
  23. 23. SOURCES OF ENERGY Carbohydrate, CHO  Main source of energy, 60% of total energy requirement.  2-3 g/Kg/day  1 g CHO = 4 KCal Fat  30-40% of caloric intake.  1.5-2 g/Kg/day  1 g Fat = 9 KCal Protein  Not a major energy source. Provide essential & non essential amino acids for protein synthesis. Use as energy substrate (CHO @ Fat precursor) in excess.  1-1.5 g/Kg/day  1 g Protein = 4 Kcal. 1 g N2 = 6.25 g Protein.  Non Protein Calories (CHO & Fat) : Nitrogen ratio = 80-200 : 1
  24. 24. ESSENTIAL NUTRIENTS NUTRIENTS THAT CANNOT BE SYNTHESIZED FROM OTHERS. Essential Amino Acid  Isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, valine.  Cysteine, tyrosine, histidine (in children).  Arginine, glutamine (in critical ill state). Fatty Acid Linoleic & Linolenic acid. Vitamins  A, B, C, D, E, K. Minerals  Electrolyte : Na+, K+, Ca2+, Mg2+, Cl-  Trace Element : Copper, Zinc, Selenium, Iron, Manganase
  25. 25. DAILY ALLOWANCES OF MINERALS, /KG/DAY Na+ 1-2 mmol K+ 0.7 - 1 mmol Ca2+ 0.1 mmol Mg2+ 0.1 mmol Phosphorus 0.4 mmol
  27. 27.  early feeding usually defined as starting within the first 24-48 hours of admission meta-analysis suggests reduced infections if patients are fed within 48 hours
  28. 28. BENEFIT OF ENTERAL FEEDING prevents gut mucosal atrophy by preserves intestinal mucosal structure and function More physiological Relatively non-invasive, cheap, easier it reduces bacterial translocation and multi-organ failure Reduced risk of infectious complications of PN
  29. 29. Delivery method Common indications PrecautionsNasogastric/ -Unable to consume oral nutrition -Tube must be securedorogastric ( eg. Intubated, sedated, - Verify placement of tube by blue neurologically impaired) litmus method or by x-ray - Hypermetabolism in the presence of functional GIT ( e.g. burns)Nasoduodenal/ -inadequate gastric motility -Tube must be securedNasojejunal (e.g.gastroparesis) -Verify placement of tube by X-ray -Partial gastric outlet obstruction or endoscopically - Severe aspiration risk -Potential dumping syndrome - Oesophageal reflex - After upper GI surgeryGastrotomy -Anyone who requires medium to -Caution in patients with severe-Percutaneous endoscopic (PEG) long term NG tube feeding ( > 1 GE reflux or gastroparesis-Radiological mnth) - Contraindicated in patients with-Surgical -Head and neck injury/surgery ascites and coagulopathies.Jejunostomy - Injury, obstruction or fistula - Potential dumping syndrome-PEJ proximal to jejunum-Surgical
  30. 30. Reactions Possible causesDiarrhoea +/- nausea and vomiting Medications/C. difficile/lack of dietary fibre/hyperosmolar formula/bacterial contamination/improper administration/fat malabsorptionConstipation Inadequate fluid intake/insufficient fibre/GI obstructionAspiration of tube feeding/high gastric Regurgitation of stomachresiduals ( > 150 to 200 ml) contents/feeding while supine/delayed gastric emptying/tube dislodgement/ gastro-oesophageal refluxHyperglycaemia Diabetes/stress/trauma/corticosteroid/se psis/refeeding syndromeHypoglycaemia Sudden cessation of tube feeding in patients on oral hypoglycaemic agents/insulinHypophosphataemia/hypokalaemia Refeeding syndrome / excessive losses
  31. 31. CONTRA-INDICATIONS TO ENTERAL FEEDING Bowel obstruction Ileus Intestinal ischaemia Clinical shock
  32. 32. PROTOCOL FOR ENTERAL FEEDING Guidelines in Enteral_feeding.pdf
  34. 34. TYPES OF TPN1) Peripheral parenteral nutrition- Temporary access ( up to 2 weeks)- Limited caloric density- High incidence of thrombophlebitis- High-volume infusion may lead to fluid overload- Osmolarity should not exceed 900 mOsm/l- Access : peripheral veins
  35. 35.  Central parenteral nutrition- Able to provide large nutrient, fluid and electrolyte needs- Recommended for prolonged IV nutritional support- Access : - central line : via subclavian, internal or external jugular and femoral veins
  36. 36. INDICATIONS Indications ( usually) Indications ( sometimes) Inability to absorb Major surgery/stress when EN adequate nutrients via GIT not expected to resume Severe acute pancreatitis within 7-10 days. Severe Enterocutaneous fistula malnutrition/catabolism with Partial small bowel non functioning GIT obstruction Complete small bowel Intractable vomiting obstruction Severe inflammatory Inability to feed enterally bowel disease not responding to medical therapy
  37. 37.  Whenever possible, TPN should be instituted simultaneously with enteral feeding. Partial feeding via enteral route preserves intestinal mucosa viability and may prevent bacterial translocation through the gut wall.
  38. 38. SUBSTRATES IN TPN CHO- Dextrose solution are available in concentration ranging from 5-70%. Solutions greater than 10% must be administered into the central vein.- Consequences of excess CHO administration : hyperglycaemia, glucosuria, synthesis and storage of fat, hepatic steatosis, increase CO2 production. Protein- Amino acids solutions are available in concentration of 3-15%.- In critical illness, ensure that enough non protein calories are administered for the optimal utilisation of protein: approximately 100 kcal are needed for 1 g of nitrogen ( 6.25 g of protein)
  39. 39.  Fat- Lipid emulsion available in concentrations of 10% and 20%.- Consequences of excess fat administration : fat overload syndrome, impaired immune response.
  40. 40. MACRONUTRIENTS Nutrients Substrate Usual Amount Maximum units of substrate CHO Dextrose 40-60% of total 7 g/kg/day monohydrate = kcal 3.4 kcal/g Protein Amino acid = 4 0.9 to 2.0 2.5 g/kg/d kcal/g g/kg/d Fat Lipids = 9 20-40% of total < 1 g/kg/d in kcal/g ( 20% kcal high stress emulsion provides 2 kcal/ml)
  41. 41. HOW TO CALCULATE TPN ? Steps Example: A 56 y.o, 1.75 m tall, 70 kg man 1. Determine the protein 70 kg x 1.5g/kg/d = 105 g/d ( = requirement 16.8g N) 2. Determine the total caloric Using Harris Benedict equation: requirement BEE = 66 + ( 13.7 x 70kg) + ( 15 x 175cm) – (6.8 x 56 yr) = 1519 kcal/day ( round off to 1500 kcal/day) TEE = BEE x IF = 1500 x 1.3 = 1950 kcal/day 3. Divide the total caloric If ratio 60:40 requirement between two energy 1950 x 0.6 : 1950 x 0.4 = 1170 : substrate, CHO : fat ( 60:40 or 780 70:30)
  42. 42. HOW TO CALCULATE TPN..4. Determine calorie : nitrogen ratio 1950 : 16.8 = 116 : 15. Calculate amount of CHO needed If using 70% dextrose solution ( 100 ml provide 70 g CHO x 3.4 kcal/g = 238 kcal) 1170 kcal / 238 kcal x 100 mls = 492 mls ~ 500 mls6. Calculate amount of fat emulsion If using 20% intralipid ( provides 2needed kcal/ml) 780 kcal divide into 2 kcal/ml = 390 ml7. Estimate fluid requirement 40 ml/kg/day x 70 kg = 2800 ml/d Therefore : 2800 – ( 500 + 390) = 1910 ml ( of water to be added to meet fluid requirement)
  43. 43. 8. Order electrolytes: Na+, K+,Mg2+, Ca, phosphorus, acetateand chloride9. Order multivitamin, traceminerals and vitamin K if needed10. Determine flow rates : volume / 2800 ml / 24H = 117 ml/h24H
  44. 44. COMPLICATIONS OF TPN Catheter related sepsis - 3.5% increase in CRBSI in a meta-analysis compared to EN Catheter Malposition  pneumothorax  hydrothorax  Arterial puncture Metabolic  Hyperglycaemia  Hypoglycemia if TPN is abruptly stopped  Increased CO2 production & increased O2 consumption if infusion rates beyond 4 ml/kg/mt.  Hypomagnesemia, hypophosphatemia if not supplemented Fatty liver
  45. 45. ENTERAL VS. PARENTERAL NUTRITIONEnteral ParenteralAdvantages Advantages-Physiological -Independent of GIT functions-Simpler-Cheaper-No CVL required-Less monitoring-Less complicationDisadvantages Disadvantages-Dependent on GIT functions -Non physiological-Diarrhea -Requires venous access-Feed intolerance -Higher risk of systemic infection-NG tube – malposition, sinusitis -Expensive-Pulmonary aspiration -More complication
  46. 46. Enteral ParenteralComplications Complications1. Mechanical 1. CVL related complication-GEReflux 2. Fluid overload-NG complication – oesophageal 3. Hyperosmolar dehydration perforation, throat injuries, syndrome – tracheal placement, hyperglycaemia, osmotic blockage, rupture diuresis oesophageal varices 4. Electrolytes imbalance2. Infection 5. Metabolic acidosis-Sinusitis, otitis 6. Hyperammonaemia-Pulmonary aspiration 7. Deficiency Syndromes-Feed contamination 8. Rebound hypoglycaemia – if3. GIT – nausea, vomit, diarrhea TPN stopped suddenly due4. Metabolic to high level endogenous-dehydration, hyperglycaemia insulin-electrolyte abnormality 9. Overfeeding syndrome.-acid base imbalance
  48. 48. GLUTAMINE 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 Glutamine deficiency at onset of critical illness/sepsis correlated with increased mortality
  49. 49. Immune enhanced diets Glutamine  can prevent or ameliorate the gastrointestinal mucosal atrophy seen during prolonged parenteral nutrition and may help the gastrointestinal mucosa heal more promptly after damage by either radiotherapy or chemotherapy  Insufficient data to support the use of glutamine in the critically ill, enteral glutamine supplementation may be of benefit in trauma and burns patients
  50. 50. Potential Beneficial Effects of Glutamine Enhanced Heat Enhanced insulin Decreased Free Shock Protein sensitivity Radical availability NF-kB (Anti-inflammatory action) Inflammatory Cytokine ? Attenuation Glutathione Glutamine Synthesis Reduced Fuel for Maintenance of Therapy Translocation Intestinal Enteric Bacteria Enterocytes Mucosal Barrier or EndotoxinsCritical Illness GLN GLN Pool pool Nuclotide Synthesis Preservation Reduction of of TCA Function Fuel for Maintenance of Infectious Anti-catabolic Lymphocyte complications effect Lymphocytes Function Preserved Cellular Preservation of Energetics- Muscle mass ATP content
  51. 51. Immune enhanced diets Arginine  Arginine-supplemented parenteral nutrition show an increased ability to synthesize acute phase proteins when challenged with sepsis.  No effect on mortality or infectious complications
  52. 52.  Omega – 3 Fatty Acids The polyunsaturated fatty acids in artificial feeding solutions are mostly omega -6 fatty acids. Replacing these with omega- 3 fatty acids has anti-inflammatory effects: 1. production of less inflammatory eicosanoid derivatives 2. reduced cytokine productionEarly clinical work in patients with ARDS using enteral feed enriched in omega-3 fatty acids found a reduction in length of ventilation and ICU stay.
  53. 53. Which Nutrient for Which Population? Elective Critically Ill Surgery General Septic Trauma Burns Acute Lung InjuryArginine Benefit No benefit (?) (Possible No No benefit) benefit benefitGlutamine Possible PN … EN EN … Benefit Beneficial Possibly Possibly Beneficial: Beneficial: Recom- Consider Consider mendOmega 3 … … … … … Recom-FFA mendAnti- … Consider … … … …oxidantsCanadian Clinical Practice Guidelines JPEN 2003;27:355
  54. 54. CONCLUSION
  55. 55.  Nutritional support is important in critically ill patients because : Improves wound healing Decreases catabolic response to injury Improves GI function and structure, Reduces complications and length of stay. Reduces morbidity and mortality Feeding must be commenced as early as possible ( within 24H) Enteral feeding is always superior than parenteral feeding
  56. 56. REFERENCES Oh’s Intensive Care Manual Bedside ICU handbook, 2nd edition, Dessmon YH Tai , Thomas WK Lew & Loo Shi, Intensive Care Units of Tan Tock Seng Hospital Basic Assessment & Support in Intensive Care F_PARENTERAL_NUTRITION.pdf