Nutrition Updated April 2010.pdf - PACT - ESICM

AN ESICM MULTIDISCIPLINARY DISTANCE LEARNING PROGRAMMEFOR INTENSIVE CARE TRAININGNutritionSkills and techniquesUpdate April 2010Module Authors (Update 2010)RONAN THIBAULTCLAUDE PICHARDBRUNO RAYNARDPIERRE SINGERDepartment of Gastroenterology and NutritionalSupport, University Hospital (CHU) of Nantes,University of Nantes, Nantes, FranceClinical Nutrition, Geneva University Hospital,Geneva, SwitzerlandAnaesthesia, Intensive Care and Infectious Diseases.Institut Gustave Roussy, Villejuif, FranceGeneral Intensive Care Department, Rabin MedicalCenter, Beilinson Hospital, Tikva, IsraelModule Authors (first edition)Claude Pichard, Gerard Nitenberg, Philippe Jolliet, Peter SoetersModule ReviewersSection EditorGerard Nitenberg, Janice Zimmerman,Lia FluitCharles Hinds

NutritionUpdate April 2010Editor-in-ChiefDeputy Editor-in-ChiefMedical Copy-editorEditorial ManagerBusiness ManagerChair of Education and TrainingCommitteeDermot PHELAN Intensive Care Dept MaterHospital /University College Dublin, IrelandFrancesca Rubulotta, Imperial College, St Mary'sHospital, London, UKCharles Hinds, Barts and The London School ofMedicine and DentistryKathleen Brown, Triwords Limited, Tayport, UKEstelle Flament, ESICM, Brussels, BelgiumHans Flaatten, Bergen, NorwayPACT Editorial BoardEditor-in-ChiefDeputy Editor-in-ChiefAcute respiratory failureCardiovascular dynamicsNeuro-intensive care and EmergencymedicineHSRO / TAHIEnvironmental hazardsSystemic inflammation and Sepsis /InfectionMetabolism, endocrinology,nephrology, nutritionDermot PhelanFrancesca RubulottaAnders LarssonJan Poelaert/Marco MaggioriniGiuseppe CiterioCarl WaldmannJanice ZimmermanJohan GroeneveldCharles HindsPerioperative ICM and surgery Vacant (April 2010)ETC / EthicsEducation and assessmentConsultant to the PACT BoardGavin LaveryLia FluitGraham RamsayCopyright© 2010. European Society of Intensive Care Medicine. All rights reserved.

ContentsContentsIntroduction..................................................................................................................................................................... 11. Stress-related metabolic disturbances and rationale for feeding ..............................................................................2Metabolic alterations in ICU patients.........................................................................................................................2Rationale for feeding ...................................................................................................................................................42. Nutritional Assessment and Requirements................................................................................................................7Nutritional assessment................................................................................................................................................7Nutritional indices.......................................................................................................................................................8Nitrogen (N) balance...................................................................................................................................................8Measurement of body composition ............................................................................................................................9Electrolytes ..................................................................................................................................................................9Trace elements, vitamins, hormones, enzymes..........................................................................................................9Practical assessment of nutritional status..................................................................................................................9Nutritional requirements ...........................................................................................................................................11Energy and macronutrient requirements..................................................................................................................11Micronutrient requirements ..................................................................................................................................... 133. Enteral and Parenteral Nutrition.............................................................................................................................. 15Indications and contraindications............................................................................................................................ 15Enteral nutrition: routes and formulas .................................................................................................................... 21Nasogastric route .................................................................................................................................................. 21Percutaneous route ...............................................................................................................................................22Enteral nutrition formulas....................................................................................................................................23Prescription of enteral nutrition...........................................................................................................................24Early enteral nutrition ..........................................................................................................................................26Pharmacomodulation............................................................................................................................................26Parenteral nutrition: routes and formulas .............................................................................................................. 28Route of access ..................................................................................................................................................... 28Nutrients............................................................................................................................................................... 30All-in-one PN solution .......................................................................................................................................... 31Immunonutrients.................................................................................................................................................. 31Combination of EN and PN.......................................................................................................................................334. Monitoring and Complications .................................................................................................................................34Monitoring enteral nutrition.....................................................................................................................................34Tube misplacement and bronchial aspiration .....................................................................................................34Gastrointestinal dysfunction.................................................................................................................................34Monitoring of parenteral nutrition...........................................................................................................................35Catheter-related sepsis (CRS)...............................................................................................................................35Non-septic complications due to the catheters....................................................................................................36Metabolic complications of parenteral nutrition .................................................................................................36Liver abnormalities ...............................................................................................................................................37Pancreatic disorders..............................................................................................................................................37Refeeding syndrome..............................................................................................................................................385. Nutritional Support for Specific Situations ..............................................................................................................39Liver failure................................................................................................................................................................39ARDS and acute respiratory failure..........................................................................................................................39Renal dysfunction..................................................................................................................................................... 40Sepsis ........................................................................................................................................................................ 40Burns.......................................................................................................................................................................... 41Neurotrauma ............................................................................................................................................................. 41Catabolic states.......................................................................................................................................................... 41Obesity .......................................................................................................................................................................42Perioperative nutrition..............................................................................................................................................43Conclusion .....................................................................................................................................................................44Self-assessment..............................................................................................................................................................45Patient Challenges……………………………………………………………………………………………………………………………………..49Learning ObjectivesAfter studying this module on Nutrition, you should be able to:1. Determine stress-related metabolic disturbances and rationale for feeding2. Assess nutritional status and determine nutritional requirements for patients3. Appropriately order enteral and parenteral nutrition4. Review monitoring and complications5. Assess nutritional support for specific situations

IntroductionINTRODUCTIONSevere protein-calorie malnutrition (PCM) is a major problem in manyintensive care unit (ICU) patients – in part due to increased catabolism andin part to the high incidence of concomitant chronic wasting conditions.Nutritional and metabolic support, i.e. enteral (EN) and parenteral (PN)nutrition, is an important component of intensive care management.Clinicians caring for ICU patients are often faced withdiscrepant data and difficult decision-making as to optimaltiming and modalities of nutrient administration, estimation ofpatients' requirements, choice of parenteral or enteral nutritionsolutions and feeding formulas, and method of monitoring. Thepurpose of this module is to provide practical guidelines onthese issues.Nutritional care of theICU patient presentschallenges and choicesThe international guidelines regarding the use of enteral and parenteralnutrition in ICU patients are summarised in the following references:Kreymann KG, Berger MM, Deutz NE, Hiesmayr M, Jolliet P, Kazandjiev G,Nitenberg G, van den Berghe G, Wernerman J; DGEM (German Societyfor Nutritional Medicine), Ebner C, Hartl W, Heymann C, Spies C; ESPEN(European Society for Parenteral and Enteral Nutrition). ESPENGuidelines on Enteral Nutrition: Intensive care Clin Nutr. 2006;25(2):210-23. PMID 16697087Singer P, Berger MM, Van den Berghe G, Biolo G, Calder P, Forbes A, Griffiths R,Kreyman G, Leverve X, Pichard C, ESPEN. ESPEN Guidelines onParenteral Nutrition: intensive care Clin Nutr. 2009;28(4): 387-400.PMID 19505748Heyland DK, Dhaliwal R, Drover JW, Gramlich L, Dodek P; Canadian CriticalCare Clinical Practice Guidelines Committee. Canadian clinical practiceguidelines for nutrition support in mechanically ventilated, critically illadult patients JPEN J Parenter Enteral Nutr. 2003;27(5): 355-73. PMID12971736Martindale RG, McClave SA, Vanek VW, McCarthy M, Roberts P, Taylor B, OchoaJB, Napolitano L, Cresci G; American College of Critical Care Medicine;A.S.P.E.N. Board of Directors. Guidelines for the provision andassessment of nutrition support therapy in the adult critically ill patient:Society of Critical Care Medicine and American Society for Parenteral andEnteral Nutrition: Executive Summary Crit Care Med. 2009;37(5): 1757-61. Review. No abstract available. PMID 19373044In this module five key tasks are presented.1. Stress-Related Metabolic Disturbances And Rationale For Feeding2. Nutritional Assessment and Requirements3. Enteral And Parenteral Nutrition4. Monitoring And Complications5. Nutritional Support For Specific Situations

Task 1. Stress-related metabolic disturbances and rationale for feeding p21. STRESS-RELATED METABOLIC DISTURBANCES ANDRATIONALE FOR FEEDINGThe underlying nutritional status of the patient and the complexity of themetabolic response to injury/critical illness provide the basis for nutritionaltherapy. They are addressed under the headings ‘metabolic alterations in ICUpatients’ and ‘rationale for feeding’.Metabolic alterations in ICU patientsThe metabolic response to injury/sepsis is theoretically characterised by aninitial ‘ebb phase’ followed rapidly (< 24h) by a secondary ‘flow phase’.The metabolic disturbances are characterised by moderate tosevere hypermetabolism, increased gluconeogenesis with insulin resistance, alarge increase in endogenous lipolysis, and net loss of the lean body mass.Cytokines act synergistically with the stress hormones in mediating much of themetabolic disturbances seen after injury, trauma or sepsis. The major mediatorsinvolved in the Systemic Inflammatory Response are summarised in the listbelow, and the details reviewed in the following references.Plank LD, Hill GL. Sequential metabolic changes following induction of systemicinflammatory response in patients with severe sepsis or major blunttrauma World J Surg 2000; 24(6): 630-638. Review. PMID 10773114Lin E, Calvano SE, Lowry SF. Inflammatory cytokines and cell response insurgery Surgery 2000; 127(2): 117-126. Review. PMID 10686974Cytokines• Pro-inflammatory. Antiinflammatory• Tumour Necrosis FactorLipid Mediators• Platelet ActivatingFactor• Prostaglandins• Thromboxanes (TxA2)• Leukotrienes (LTB4)Opioids andNeuromediators• Enkephalins• β-endorphin• Nitric OxideHormones• Thyroxine• Catecholamines• Glucocorticoids• Insulin• Glucagon• Growth Hormone• Insulin-like growthfactor 1• Growth FactorsFibronectinComplement (C3a,C5a, C1q)Enzymes• Proteases• Other lysosomalenzymesPeptidesOxygen RadicalsThe body's reaction to stress is associated with an elevation inbody temperature, in cardiac output and in substrate turnoverICU care mayprofoundly influencethe metabolicresponse

Task 1. Stress-related metabolic disturbances and rationale for feeding p3rate, all of which should lead to an increase in energy demand.The elevation in energy expenditure (EE), primarily controlledby the counter-regulatory hormones, is directly related to theextent and type of injury/sepsis.For example, minor or localised infections generally have little effect on EE andincreases above 5-15% are rarely observed. Elevations of 10-15% are frequentlyseen in patients presenting with severe infection or multiple trauma. Thegreatest increases in EE are documented in patients with uncontrolled sepsis,with or without the Acute Respiratory Distress Syndrome (ARDS), and in burnpatients. On the other hand, prolonged starvation, severe PCM, physicalimmobilisation, sedation and/or muscle relaxation associated with criticalillness decrease EE by 15-20% and counter the hypermetabolic effects of theunderlying injury. Data on EE after severe injury are available in the followingreference.Nitenberg G. Nutritional support in sepsis: still skeptical? Curr Opin Crit Care2000; 6(4): 253-266. PMID 11329509In the following table, examples are given of adequate energy supply in differentclinical situations in the ICU, set against an arbitrary Resting EnergyExpenditure of 20 kcal/kg/day. In the table, overweight is defined as a bodymass index (BMI) between 25 and 29.9, and obesity as a BMI equal or higherthan 30.Weight should be the actual weight of the patients, i.e. before admission tothe unit, and mainly before fluid administration. If actual weight is unavailable, use theideal body weight.

Task 1. Stress-related metabolic disturbances and rationale for feeding p4Kreymann KG, Berger MM, Deutz NE, Hiesmayr M, Jolliet P, Kazandjiev G, et al;DGEM (German Society for Nutritional Medicine), Ebner C, Hartl W,Heymann C, Spies C; ESPEN (European Society for Parenteral andEnteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Intensive careClin Nutr 2006; 25(2): 210-223. PMID 16697087Singer P, Berger MM, Van den Berghe G, Biolo G, Calder P, Forbes A, et al,ESPEN. ESPEN Guidelines on Parenteral Nutrition: intensive care ClinNutr 2009; 28(4): 387-400. PMID 19505748Thibault R, Pichard C. Nutrition and clinical outcome in intensive care patientsCurr Opin Clin Nutr Metab Care. 2010; 13(2): 177-183. PMID 19996743Martindale RG, McClave SA, Vanek VW, McCarthy M, Roberts P, Taylor B, et al;American College of Critical Care Medicine; A.S.P.E.N. Board of Directors.Guidelines for the provision and assessment of nutrition support therapyin the adult critically ill patient: Society of Critical Care Medicine andAmerican Society for Parenteral and Enteral Nutrition: ExecutiveSummary Crit Care Med 2009; 37(5): 1757-1761. Review. No abstractavailable. PMID 19373044Q Explain why not all ICU patients are severely hypermetabolic?A. The elevation in EE is directly related to the extent and type of injury.Uncomplicated surgery or minor infections generally do not increase EE, or increaseEE by no more than 10–15%. Elevations of up to 50% are seen in patients presentingwith severe infection or multiple trauma. The greatest increases in EE occur in patientswith uncontrolled sepsis, with or without ARDS, and in burn patients. Priormalnutrition and sedation significantly reduce EE.Q Is the degree of hypermetabolism for all patients stable during theICU stay? Explain your answerA. The course of an ICU patient is rarely uniform, and EE varies according to thesecondary insults, infectious or not, complicating the ICU stay. On the other hand, ithas been suggested that total EE (i.e. energy intake minus energy balance)progressively increases in surgical patients with severe sepsis (mainly after peritonitis),and is 70% to 80% higher than resting EE after one week, as a result of progressiveactive mobilisation.Q In what way do fever and sedation modify the EE?A. EE increases with fever, and it is generally assumed that EE is increased by 10% foreach 1 degree ° Celsius above 37 °. Conversely, profound sedation, with or withoutmuscular paralysis, is able to totally counteract injury-induced hypermetabolism.Rationale for feedingProgress in intensive care has allowed prolonged survival of patientssuffering from protracted catabolic disease such as sustained sepsis andmultiple organ dysfunction. This situation has prompted heightenedawareness of the importance of optimal nutritional support. Theconsequences of this support go beyond the supply of energy and proteins to

Task 1. Stress-related metabolic disturbances and rationale for feeding p5the body. Modulation of the host's immune response and the integrity of thegastrointestinal (GI) tract are also beneficially influenced.During the initial ICU period, priority is given to management Feeding duringof the patient's cardiovascular and respiratory requirements resuscitation isand control of infection. Nutritional support, however, shouldinappropriate andmay be detrimentalbe started before the onset of severe metabolic disorders and/ornew events (second hits) which can precipitate irreversibleMultiple Organ Failure (MOF).In the absence of cardio-respiratory instability, and especially when PCM haspreceded ICU admission, nutritional intervention may be started 12-48 hoursafter admission to ICU if the patient is not expected to cover his/her energyneeds by oral intake during the next 72 hours. For the rationale of earlynutritional intervention in the ICU patient, see Heyland DK.Heyland DK. Nutritional support in the critically ill patients. A critical review ofthe evidence Crit Care Clin 1998; 14(3): 423-440. PMID 9700440Marik PE, Zaloga GP. Early enteral nutrition in acutely ill patients: a systematicreview. Crit Care Med 2001; 29(12): 2264-2270. Review. PMID 11801821When the initial injury does not rapidly lead to death, the patient enters aperiod of relative stability characterised by hypermetabolism and majormuscle catabolism. A state of post-injury wasting sets in, unless countered bynutritional and metabolic support. This state is worsened by bed rest that canlead to the loss of 20% of muscle mass without nutritional support.Nitrogen excretion can reach more than 20 g/day, which representsapproximately 600 g of muscle. The duration of this phase varies between a few daysand several weeks, according to the severity of the initial injury.Although a universal definition of PCM does not exist, it hasbeen repeatedly reported that 30-50% of hospitalised patientssuffer from various levels of PCM due to the adverse effects ofchronic and acute illnesses. Nutritional status, in turn, is amajor determinant of the response to illness; in particularresistance to infection, maintenance of gut and lung function,wound healing. Nutritional support is aimed at limiting thedegree of PCM and its consequences, particularly on theimmune system and healing processes.It contributes to ‘buying the time’ necessary to restore adequateIllness and PCMinfluence each otherand can initiate avicious cyclemicrocirculation and treat the underlying cause. The approach to metabolic andnutritional support in ICU patients depends on specific circumstances andshould be flexible. A general outline of the metabolic alterations of injury and ofa ‘phasic’ approach of nutritional support can be found in the followingreference.

Task 1. Stress-related metabolic disturbances and rationale for feeding p6Biolo G, Grimble G, Preiser JC, Leverve X, Jolliet P, Planas M, et al; EuropeanSociety of Intensive Care Medicine Working Group on Nutrition andMetabolism. Position paper of the ESICM Working Group on Nutritionand Metabolism. Metabolic basis of nutrition in intensive care unitpatients: ten critical questions Intensive Care Med 2002; 28(11): 1512-1520. PMID 12415440Biolo G, Ciocchi B, Stulle M, Bosutti A, Barazzoni R, Zanetti M, et al. Calorierestriction accelerates the catabolism of lean body mass during 2 wk ofbed rest Am J Clin Nutr 2007; 86(2): 366-372. PMID 17684207Nutritional intervention in critically ill patients is unlikely to produce‘magical’ effects, in terms of morbidity or mortality. Recovery results from thecombined effects of optimal therapeutic measures.

Task 2. Nutritional Assessment and Requirements p72. NUTRITIONAL ASSESSMENT AND REQUIREMENTSThe clinical assessment, supplemented by laboratory investigations, guidesinitial and ongoing nutritional therapy. These considerations are addressedunder the headings ‘nutritional assessment’ and ‘nutritional requirements’.Nutritional assessmentNutritional assessment is performed with two goals in mind – to detect signs ofPCM (or patients at risk of PCM) and to monitor and modify nutritional supportaccording to need. PCM potentially limits recovery and, in addition, PCMrelatedcomplications are believed to increase medical costs.Nutritional support should, therefore, be monitored with thegoal of optimising risk-benefit and cost-efficacy ratios. An idealclinical marker of nutritional status should be widely available,easily reproducible, highly specific to nutritional state andsensitive to its modifications. Unfortunately, no such marker isavailable.An ideal marker ofnutritional statusdoes not existPhysical signsSeveral signs may reflect nutritional deficiency, such as oedema, cachexia,muscle atrophy and mucosal lesions (glossitis, aphtosis).Body weight and body weight changes are difficult to interpret from anutritional point of view because of obesity, fluid movements due to stress, diureticadministration, oedema and ascites. Stable body weight can result from over hydrationwhich masks a loss of body cell mass. Nevertheless, sequential body weightdetermination offers an integrated picture of all fluid intake and loss that computationof traditional ‘fluid balance’ cannot match.Examine the next ten ICU patients for features of PCM and relate suchchanges to eventual clinical outcome.Biological markersBiological markers of PCM suffer from various shortcomings in Serum proteinICU patients. Plasma albumin, transthyretin, transferrin,levels have littleretinol-binding protein, fibronectin and insulin-like growthvalue in initialfactor-1 have been used to assess nutritional status. However, nutritionalthe intravascular concentration of these factors mostly reflectsassessment.Changes in levels,the net balance between hepatic synthesis, distribution andhowever, may bedegradation. Stress and trauma-related hormones or infectionrelatedcytokines interact with amino acids and micronutrientsimportantto regulate the levels of the above-mentioned anabolic proteinstogether with acute phase proteins, such as C-reactive proteinand alpha-1 glycoprotein acid.Low serum albumin is often correlated with a poor prognosis in hospitalisedpatients, but it is a weak short-term marker of the evolution of nutritional status

Task 2. Nutritional Assessment and Requirements p8because of its long half-life (20 days). Transferrin, transthyretin, andfibronectin, on the other hand, are sensitive to rapid changes of nutritional stateand have shorter half-lives (7 days, 2 days and approximately 4 hours,respectively), but their serum levels are also markedly influenced by acutestress, transcapillary escape and the inflammatory response.Measurements of body composition by determination of skinfold thickness andarm muscle circumference, or by bioelectrical impedance analysis suffer fromvarious shortcomings in ICU patients and are generally not relevant.Nutritional indicesSince no single parameter adequately identifies PCM, nutritional indicesintegrating a number of parameters have been developed. These include theInstant Nutritional Assessment and the Prognostic Inflammatory andNutritional Index. These examples are actually risk indices and should only beapplied to patients in whom all items are applicable. Globally, the complexityand cost of these indices have rendered them obsolete except for researchprojects. For more information on nutritional indices, refer to the followingreferences.Sungurtekin H, Sungurtekin U, Oner O, Okke D. Nutrition assessment incritically ill patients Nutr Clin Pract. 2008;23(6): 635-41. PMID 19033223Downs JH, Haffejee A. Nutritional assessment in the critically ill Curr Opin ClinNutr Metab Care. 1998;1(3): 275-9. Review. PMID 10565360Nitrogen (N) balanceIn ICU patients, major non-urinary N losses may result from protein-losingbowel disease, extensive burns, renal replacement therapy, or high-outputabdominal drains. Nitrogen balance becomes negative (–5-30 g/day), reflectingmajor protein catabolism. In practice, calculation of N balance is mainly aimedat monitoring nutritional support.Nitrogen (N) balance is calculated as follows: Nitrogen balance (g N/day) =Nitrogen intake – Nitrogen excreted. N balance = [protein intake (g)/ day/6.25]- [urinary nitrogen (g/day) + skin and stool losses (usually about 2-4 g N is lostin skin and stool per day)]. Urinary N is usually directly measured bychemiluminescence or derived from routinely measured urinary urea using thefollowing formula: Urinary N = [urinary urea (g/ 24h) / 2.14] + 2 to 4 g. Thelatter constant is an estimation of non-urea urinary losses of nitrogen (in theabsence of nephrotic syndrome), and should not be confounded with lossesfrom skin/stool.Urinary N should be measured in a 24-hour urine collection butin emergency a four hour collection may suffice. Exactdetermination of the duration and volume of the urinecollection is crucial for accurate calculation of N balance.Mmol of urea maybe converted to gusing the followingformula: Urea(g)=urea(mmol)/20.36 and6.25 g of proteinequals 1 g of N.

Task 2. Nutritional Assessment and Requirements p9Measure nitrogen balance in five of your patients and relate yourfindings to the nutritional support provided.Measurement of body compositionBioimpedance analysis (BIA) is a widely used method of body compositionassessment, but its accuracy is limited in ICU patients due to rapid changes inelectrolyte and fluid balance, themselves related to the severity of the disease.Therefore the measurement of body composition with this method is notrecommended during the acute phase of critical illness.However, during the post-acute phase and the recovery phase, BIA cancontribute to the assessment and the follow-up of nutritional status if thehydration status remains stable.Kyle UG, Bosaeus I, De Lorenzo AD, Deurenberg P, Elia M, Manuel Gómez J, etal. ESPEN Bioelectrical impedance analysis-part II: utilization in clinicalpractice. Clin Nutr 2004; 23: 1430-1453. PMID 15556267ElectrolytesPCM is associated with substantial gains of extra-cellular water and sodiumgains, as well as changes in potassium, magnesium, calcium and phosphorusconcentrations. These parameters should be initially assessed, and thencorrected according to the severity of the observed changes. Special attentionshould be paid to the risk of early deficiencies in intracellular phosphorus,magnesium and potassium, even though plasma concentrations of theseelements may remain normal.Trace elements, vitamins, hormones, enzymesPlasma concentrations of trace elements, vitamins, hormones and enzymespoorly reflect tissue concentrations. Determination of these parameters is onlyuseful for metabolic research purposes or to confirm a clinical diagnosis (e.g.suspicion of Addison's disease, or B and C vitamin deficiencies in severealcoholism).Practical assessment of nutritional statusA practical approach to detecting PCM in critically ill patients isas follows:Patient history and clinical setting• Diseases associated with increased risk of malnutrition (e.g. chronicdebilitating disease)• History of chronic low food intake, drug abuse, alcoholism, chronicpsychiatric disorders

Task 2. Nutritional Assessment and Requirements p10• Diseases associated with hypermetabolism and prolonged catabolicactivity (e.g. polytrauma, burns, persistent fever, sepsis, multipleorgan failure)Clinical and anthropometric assessment• Signs of malnutrition on physical examination (e.g. cachexia, muscleatrophy, oedema)• Recent severe body weight loss (≥5% of usual body weight in onemonth or ≥ 10% in three months)• Body mass index (body weight in kg/(height in m 2 )) < 18.5 kg/m 2Biochemical parameters• Hypoalbuminemia < 35g/L• Plasma electrolytes levels (K, Mg, P, Ca)• Nitrogen balance (negative) values:≤5 g (low stress)5 to 15 g (moderate stress)≥15 g (severe stress)(Adapted from Jolliet P, et al. Enteral nutrition in intensive care patients: apractical approach. A position paper. Clin Nutr 1999; 18: 47-56). ESPENAssess nutritional status in five of your patients at least two of whom shouldhave PCM.Q Which factors of the clinical history will point to the risk, or thereality, of malnutrition?A.History of chronic low food intakeAlcoholismSignificant recent weight loss (≥ 5% of usual body weight in one month or ≥ 10% inthree months)Chronic diarrhoeal or debilitating diseaseDrug abuseQ List two signs on physical examination indicating probablemalnutrition.A.Muscular atrophyLoss of subcutaneous fatOedema (in the absence of cardiovascular or renal disease)Mucosal lesions, including glossitis and skin rashesTHINK A skilled doctor can perform a nutritional assessment in just a few minutes.Think how you perform this assessment. The Jolliet article can be of help (seeabove).

Task 2. Nutritional Assessment and Requirements p11Q What formula allows conversion of urea to nitrogen in order tocalculate nitrogen balance?A.N balance (g N/day) = [protein intake (g)/6.25] - [urinary N (g)]Urinary nitrogen is usually derived from urinary urea using the following formula:Urinary N = [Urinary urea (g/24h) / 2.14] + 2 to 4 g.Grams of urea may be converted to mmol using the following formula: Urea (mmol) =Urea (g) x 20.36 and 6.25 g of protein equals 1 g of N.Nutritional requirementsOptimal calorie and nitrogen requirements from nutritional support are difficultto define accurately. In addition, this approach is often complicated in criticallyill patients by glucose and protein intolerance as well as the risk of fluidoverload.Energy and macronutrient requirementsA variety of techniques are available for evaluating energy needs but all havedrawbacks in the critically ill patient. The reference method to evaluate energyneeds consists of the measurement of energy expenditure by indirectcalorimetry, which requires costly equipment and technical skills not widelyavailable. The method is time-consuming, and is limited in patients undermechanical ventilation to those with an inspired oxygen concentration (F iO2)lower than 0.6-0.7.Some ventilators are currently sold with the ability to directly measure energyexpenditure. However it is important to note that this method has never beenvalidated and is therefore not recommended.Basal EE may also be derived from the Harris-Benedict formulae:• Men: EE (kcal/day) = 66 + (13.7 x W) + (5 x H) - (6.8 x A)• Women: EE (kcal/day) = 655 + (9.6 x W) + (1.7 x H) - (4.7 x A)W = weight in kg, H = height in cm, A = age in years.In ventilated critically ill patients, the Faisy equation may be more accurate:• EE (kJ/day) = 8 x W + 15 x H + 32 x MV + 94 x BT -4834MV = minute ventilation in L/min, BT = body temperature in ⁰C 1kcal=4.184kJ.The Harris-Benedict may be inaccurate in ICU patients forreasons discussed in detail in the following references.Walker RN, Heuberger RA. Predictive equations for energy needs for the criticallyill. Respir Care 2009;54:509-21. PMID 19327188

Task 2. Nutritional Assessment and Requirements p12McEvoy CT, Cran GW, Cooke SR, Young IS. Resting energy expenditure in nonventilated,non-sedated patients recovering from serious traumatic braininjury: Comparison of prediction equations with indirect calorimetryvalues. Clin Nutr 2009; 28: 526-32. PMID 19423202Faisy C, Guerot E, Diehl JL, Labrousse J, Fagon JY. Assessment of resting energyexpenditure in mechanically ventilated patients. Am J Clin Nutr 2003; 78:241-9. PMID 12885704Flancbaum L, Choban PS, Sambucco S, Verducci J, Burge JC. Comparison ofindirect calorimetry, the Fick method, and prediction equations inestimating the energy requirements of critically ill patients. Am J ClinNutr 1999; 69 : 461-466. PMID 10075331In practice, a pragmatic estimate of total energy requirements is 25-35 (20-30non-protein) kcal/kg/day in males and females, respectively. 10% should beadded to energy needs for every degree of body temperature >37˚ C.Link to ESICM Flash Conference: Pierre Singer, ‘How do I evaluate energyrequirements?’ ESICM congress, Vienna 2009The main goal of nitrogen supply is to limit muscle catabolism, whilemaintaining an adequate nutrient supply to the liver. The body weight used forthis computation should be the mean between ideal and measured weights inseverely malnourished patients, and 20% higher than ideal weight in obesepatients. It must be stressed that, in this context, equilibrium or positivity ofnitrogen balance is not an end in itself and can even be detrimental if it leads toan accumulation of urea.It is generally accepted that protein intake should varybetween 1.2 and 1.5 g/kg/day, and should certainly not exceed 2.0 g/kg/dayexcept in patients with substantial losses (e.g. extensive burns, GI and/orurinary losses, etc.). For EN, standard polymeric diets, and for TPN,conventional crystalline amino acid solutions can be used. The requirements aremodified according to the level of catabolism as assessed by blood urea nitrogen(BUN) or nitrogen balance.Glucose intakes through artificial nutrition should be less than 6 g/kg/day andlipid intakes between 0.5 to ≤ 2 g/kg/day. When oral or enteral intakes arepossible, the lipid and carbohydrate requirements are the same as for healthysubjects, i.e. 30-35 % of total calorie intakes as lipids and 50-55% ascarbohydrates.Identify all patients requiring nutritional support in your ICU for aweek and determine appropriate initial prescription and the pathway to achievingcaloric goal.Q Estimate the energy expenditure of a febrile (38.5 °C) 60-year-oldman admitted to the ICU with a diagnosis of pneumonia; treatmentincludes mechanical ventilation. His body weight and height are 76kg and 173 cm respectively.

Task 2. Nutritional Assessment and Requirements p13A. Resting energy expenditure (REE) can be calculated using the Harris-Benedictformula: REE = 66 + (13.75 x 76) + (5 x 173) - (6.76 x 60) = 1571 kcal/day (otherformulae are available, and give approximately the same result).10% increase in EE per ° Celsius above 37 °C = 1571 x 0.15 = 235 kcalMechanical ventilation partially offsets the increase in EE due to fever, so that EE forthis patient is about 1700 kcal/day.Note that this result is close to the proposed simple calculation: 76 (kg) x 25(kcal/kg/day) = 1900 kcal/day.Q How many grams of protein per kg of body weight arerecommended for a 60-year-old woman (weight and height 56 kgand 162 cm respectively), with a chronic proteinuria of 25 g/day?A.Basal requirements = 1.5 x 56 = 84 g protein/dayReplacement of renal losses is recommended (as is replacement of protein lossesduring haemodialysis or continuous venovenous haemofiltration (CVVH)Total protein requirements = 84 + 25 = 109 g/dayMicronutrient requirementsTrace elements and vitamins, also known as micronutrients,play an important role in various enzyme-catalysed keyreactions, many of which exhibit increased activity during theinflammatory response associated with critical illness.Concomitantly, some critical conditions such as prolongeddiarrhoea and extensive burns or treatments such ashaemodialysis are accompanied by increased losses of traceelements, such as zinc and selenium. Requirements forvitamins B1 and B6 are considerably increased by sepsis and byPN, particularly in malnourished patients, and Vitamin B1(about 100 mg/day) is essential to avoid lactic acidosis andother complications such as beri-beri, Korsakoff syndrome andWernicke’s encephalopathy. Some vitamins, such as vitamins C,E and A are likely to prevent or counteract the cell damagecaused by free radicals, which are generated duringischemia/reperfusion.When daily caloric intake of less than 1000kcals lasts for several days, or insevere conditions combining increased needs and large losses of trace elements,intravenous administration of vitamins B1, B6, C, E and A may be beneficial (seeTask 2 sub-heading Practical assessment of nutritional status).Micronutrient requirements in critically patients are outlined in the followinglist.VitaminsStandard balanced formulas• Vitamin K (10 mg/day)• Vitamin B1 and vitamin B6 (100 mg/day)• Vitamins A-C-E (3500 IU-125 mg-10 IU)Trace elements (provided renal function normal)Complete standard solutions containing Cr, Cu, Fe, Mn, Mo, Se, Zn, F and IMinimal dailyrequirements ofmicronutrients should beroutinely administered bymeans of commerciallyavailable, preparations.Supplementation isunnecessary when intakeoccurs with ≥ 1000 kcal ofcommercial enteralformulas already enrichedwith micronutrients.

• Zn (15-20 mg/day plus 10 mg/l of liquid stool)• Se (120 mg/day)Task 2. Nutritional Assessment and Requirements p14ElectrolytesBased on clinical assessment of the patient’s volume, acid-base status and ondaily plasma concentration (Na + , K + , Ca ++ )• P 2- (>16 mmol/day)• Mg 2- (>200 mg/day; 8.3 mmol) of specific nutritional needsBerger MM, Shenkin A. Update on clinical micronutrient supplementationstudies in the critically ill. Curr Opin Clin Nutr Metab Care 2006;9:711-6.PMID 17053424Berger MM, Chioléro RL. Antioxidant supplementation in sepsis and systemicinflammatory response syndrome. Crit Care Med. 2007;35(9 Suppl):S584-90. PMID 17713413By contrast, the administration of vitamin A and manganese should be avoidedin those with severe liver insufficiency or unexplained liver enzymeabnormalities.Q Which vitamin is essential to avoid lactic acidosis due to PN in ICUpatients? Please explain your answer.A. Vitamin B1 (about 100 mg/day) is essential to avoid lactic acidosis and othercomplications such as beri-beri, Korsakoff syndrome and Wernicke's encephalopathy.Particular attention should be paid when starting glucose administration to severelymalnourished patients and patients with chronic alcoholism.Q All critically ill patients should receive vitamins and traceelements. Name two conditions when additional supplementarymicronutrients should be considered in critically ill patients.A.High output intestinal fistulaeSevere burnsSevere inflammatory and septic diseasesMultiple traumaARDSQ Name two micronutrients with proven antioxidant properties.A.Vitamin A and β-caroteneVitamin EVitamin CSelenium

Task 3. Enteral and Parenteral Nutrition p16• Promotes gut motility, thus paving the way for oral feeding• Reduces bacterial translocation from the gut (proven only in animalsbut not clearly relevant in humans)• Avoids infectious complications associated with parenteral nutrition• Reduces the risk of metabolic complications associated withparenteral nutrition: hyperglycaemia, insulin resistance,hypertriglyceridemia, fatty liver• Less costly than parenteral nutritionAdvantages of parenteral nutrition:• Easy to perform at the initial phase of injury• Ensures full delivery of specific nutritional needs• Avoids risks of gastrooesophageal reflux, aspiration pneumonia,enteral-feeding associated diarrhoea and GI intolerance (vomiting,...)Q Is bacterial translocation directly responsible for the developmentof MOF and overwhelming sepsis in ICU patients?A. This question is highly controversial. There is often confusion between increasedintestinal permeability for sugar probes – a common finding in the critically ill – andbacterial translocation, which has been shown to occur in a variety of clinicalconditions. There is no correlation between bacteria in the mesenteric lymph nodes andMOF. To date no evidence exists for a cause and effect relationship between gut failureand generalised sepsis, MOF or death, especially in the absence of an identifiablesource of infection.Hinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. SaundersLtd; 2008. ISBN: 978-0-7020259-6-9. p. 301-302 (Enteral Nutrition)A detailed discussion of the advantages of EN over PN will be found in thereferences below.Jeejeebhoy KN. Enteral and parenteral nutrition: evidence-based approach ProcNutr Soc 2001; 60(3): 399-402. Review. PMID 11681815Thibault R, Pichard C. Nutrition and clinical outcome in intensive care patientsCurr Opin Clin Nutr Metab Care 2010; 13(2): 177-183. PMID 19996743The contraindications to enteral and parenteral nutrition are detailed below:Contraindications to enteral nutritionAbsolute• Adequate oral intakes (more than 80% of the energy target)• Non-functional gut: anastomotic disruption, lower GI obstruction,gut ischaemia/necrosis• Generalised peritonitis• Uncontrolled severe shock statesAbsolute contraindications tonutritional support are rare,except during the initial phase ofresuscitation in severe illness

Task 3. Enteral and Parenteral Nutrition p17Relative• Expected period of fast ≤5 days, except in severely injured patients• Abdominal distension/severe protracted diarrhoea• Localised peritonitis, intra-abdominal abscess, active upper GI tracthaemorrhage• Coma with risk of aspiration (especially gastric feeding)• Very short bowel (less than 70 cm) or high output fistulae• Electrolytes or fluid or substrate intolerance (kidney, heart, liverfailure)• Terminal disease• Dementia, agitation, confusionContraindications to parenteral nutritionAbsolute• Adequate oral intake• Enteral nutrition feasible and covering more than 60% of the energytarget within the three days following admission• Uncontrolled severe shock statesRelative• Absence of central venous access (because of severe risk of bleeding,intrathoracic injury, infection and/or thrombosis of great veins). NB:parenteral nutrition via peripheral veins may be considered• Electrolyte or fluid or substrate intolerance (kidney, heart, liverfailure)• Incompatibility between intravenous drugs and parenteral nutritionsolution in the absence of multiple port catheters• Dementia, agitation, confusionAdapted from:Kreymann KG, Berger MM, Deutz NE, Hiesmayr M, Jolliet P, Kazandjiev G,Nitenberg G, van den Berghe G, Wernerman J; DGEM (German Societyfor Nutritional Medicine), Ebner C, Hartl W, Heymann C, Spies C; ESPEN(European Society for Parenteral and Enteral Nutrition). ESPENGuidelines on Enteral Nutrition: Intensive care Clin Nutr. 2006;25(2):210-23. PMID 16697087Singer P, Berger MM, Van den Berghe G, Biolo G, Calder P, Forbes A, Griffiths R,Kreyman G, Leverve X, Pichard C, ESPEN. ESPEN Guidelines onParenteral Nutrition: intensive care Clin Nutr. 2009;28(4): 387-400.PMID 19505748Jolliet P, Pichard C, Biolo G, Chioléro R, Grimble G, Leverve X, et al.Enteralnutrition in intensive care patients: a practical approach. Clin Nutr. 1999;18(1): 47-56.PMID 10459065Nevertheless, problems linked to EN in ICU patients, such asfunctional ileus, gut failure, bacterial overgrowth, risk ofnosocomial pneumonia, and technical problems with jejunalfeeding, must be kept in mind. In patients with poor intestinalperfusion, due to prolonged or severe shock states, and unableto sustain digestion and nutrient absorption, EN should bePN should replaceEN if patientsdevelop majorintolerance orothercontraindication

administered with caution, and supplemented with or, ifnecessary, substituted by PN, to allow nutritional requirementsto be met and to minimise excessive muscle wasting.Task 3. Enteral and Parenteral Nutrition p18Varga P, Griffiths R, Chiolero R, Nitenberg G, Leverve X, Pertkiewicz M, et al. Isparenteral nutrition guilty? Intensive Care Med 2003; 29(11): 1861-1864.PMID 14669752Although animal studies indicate that the association betweenmucosal atrophy and an increase in gut permeability can inducetranslocation of bacteria from the gut lumen to the circulation, no proof existsthat bacterial translocation, which does exist in some instances in ICU patients,is clinically relevant.The figure below proposes the management of enteral nutrition according to thegastric residual volumes.

Task 3. Enteral and Parenteral Nutrition p19All around the world, cisapride has been taken off the market, dueto concerns about side effects and drug interactions.There is no consensus about the amount of gastric residual volume thatshould be considered abnormal. The authors suggest 500 ml as a working figure. Again,no solid data exist to indicate how many times a day gastric residual volume should bechecked, but once a day makes sense.

Task 3. Enteral and Parenteral Nutrition p20Poulard F, Dimet J, Martin-Lefevre L, Bontemps F, Fiancette M, Clementi E,Lebert C, Renard B, Reignier J. Impact of not measuring residual gastricvolume in mechanically ventilated patients receiving early enteral feeding:a prospective before-after study. JPEN J Parenter Enteral Nutr 2010;34(2): 125-130. PMID 19861528Moreira TV, McQuiggan M. Methods for the assessment of gastric emptying incritically ill, enterally fed adults Nutr Clin Pract 2009; 24(2): 261-273.Review. PMID 19321900Optimalcombination ofenteral andparenteralnutritionQ What is the only (temporary) contraindication to nutritionalsupport?A.Severe shock prior to haemodynamic and respiratory stabilisation.Q Specify at least three reasons why patients should be fed enterallyrather than parenterally? Explain your answer.A.Maintenance of gut integrityPrevention of bacterial (or endotoxin) translocation (not proven)Maintenance of adequate splanchnic blood flowMaintenance of adequate immune functions of the gutAvoidance of catheter-related sepsisCost-savingsQ Specify one situation in which PN is preferable to EN. Explain youranswer.A.Bowel obstructionMesenteric infarction and/or complete gut failureVery short bowel (

Task 3. Enteral and Parenteral Nutrition p21Enteral nutrition: routes and formulasEnteral nutrition may be administered through a nasogastric or nasojejunaltube, or through percutaneous routes such as gastrostomy or jejunostomy.Hinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. SaundersLtd; 2008. ISBN: 978-0-7020259-6-9. p.302 (Administration followed byChoice of Feed p.303)Schmidt H, Martindale R. The gastrointestinal tract in critical illness: nutritionalimplications. Curr Opin Clin Nutr Metab Care 2003; 6(5): 587-591.PMID12913678Nasogastric routeGastric feeding provides the most normal route for enteral nutrition, but poortolerance of gastric feeding in the critically ill patient is common. Tolerance isessentially limited by the severity of disease. In these circumstances, it may bedifficult to maintain an infusion rate higher than 1000 ml/24 hours and a globalenergy load higher than 1500 kcal/day. Use of prokinetics decreases (but doesnot eliminate) the incidence of aspiration in the presence of a competent pyloricsphincter. Gastrostomy or post-pyloric positioning of the feeding tube does notdecrease the risk of aspiration.The nasogastric route is used for the majority of enteralnutrition in ICU patients, for short (

Task 3. Enteral and Parenteral Nutrition p22Wiegand N, Bauerfeind P, Delco F, Fried M, Wildi SM. Endoscopic positioncontrol of nasoenteral feeding tubes by transnasal re-endoscopy: aprospective study in intensive care patients Am J Gastroenterol. 2009;104(5): 1271-1276. PMID 19319127Although frequently advised, the clinical benefits of duodenal placement of thenasogastric tube have never been clearly demonstrated.Hsu CW, Sun SF, Lin SL, Kang SP, Chu KA, Lin CH, Huang HH. Duodenal versusgastric feeding in medical intensive care unit patients: a prospective,randomized, clinical study Crit Care Med 2009; 37(6): 1866-1872. PMID19384225An abdominal radiograph is strongly recommended after placement of anasogastric tube. In US, it is only required for the smaller bore feeding tubes. X-rayshould be regularly repeated at least once a week. Malpositioning is not unusual –intracranial in patients with a skull fracture, looping in the oral cavity or in the loweroesophagus, and silent intrabronchial or tracheal placement have all been recorded.To reduce the risk of bronchoaspiration, tolerance to gastric feeding should bemonitored e.g. by measuring gastric residual volume at least once per day (seefigure p.19), especially in unintubated, comatose or sedated patients.Percutaneous routePercutaneous endoscopic gastrostomy (PEG) tube placement has becomecommon for ICU patients requiring prolonged EN support (≥4-6 weeks)especially when there is intolerance or complications of NG tubes. Tubes in therange of 9 to 24 F are available. This procedure should be considered in patientswho have normal gastric emptying and no sign of gastrointestinal intoleranceand can be performed at the bedside in the ICU.The methods and clinical utility for measuring of gastric emptying are discussedin the following reference.Moreira TV, McQuiggan M. Methods for the assessment of gastric emptying incritically ill, enterally fed adults Nutr Clin Pract. 2009; 24(2): 261-273.Review. PMID 19321900If postpyloric feeding is necessary in such patients, percutaneous endoscopy(PEJ) or radiology-guided jejunostomy may be performed.

Task 3. Enteral and Parenteral Nutrition p23PEJ utilises the same approach as for PEG but after tube insertion into thestomach the tube is guided into the duodenum under endoscopic control.Surgical placement of a gastrostomy or jejunostomy is usually performed as thelast phase of gastrointestinal surgery (gastrectomy, pancreatectomy), the goalbeing to administer perioperative nutritional support.Selection of gastrostomy, needle-catheter jejunostomy or transgastricjejunostomy depends on the primary diagnosis, the status of the patient, andhospital facilities and skills.The insertion of a percutaneous gastrostomy or a jejunostomy must be avoidedin those with uncontrolled hyperthermia or infections. A delay of 7 days withoutany fever is warranted to limit the risk of abdominal abcess. The procedure ofpercutaneous gastrostomy or jejunostomy is covered by an antibioticprophylaxis.Relative contraindications for gastrostomy or jejunostomy are: ascites, portalhypertension, local abdominal infectious problems, gastroparesis, poor gastricemptying, gastric cancer, gastric ulcer, previous laparotomy and coagulation disorders.All the issues relating to the technical aspects of EN are extensively discussedin the following reference.Gopalan S, Khanna S. Enteral nutrition delivery technique Curr Opin Clin NutrMetab Care 2003; 6(3): 313-317. Review. PMID 12690265Q Name two conditions contraindicating percutaneous gastricpositioning of enteral feeding tube.A.AscitesGastric cancer/ulcerSevere coagulation disordersPoor gastric emptying or gastroparesisQ List three criteria prompting the performance of a gastrostomy inan ICU patient.A.Enteral nutrition planned for longer than 4–6 weeksMechanical obstruction or severe mucosal oesophageal lesionsPatient intolerance of nasogastric tube.Enteral nutrition formulasStandardised, commercially produced formulas arerecommended, in the form of iso-osmotic (approximately 300Fibre-enrichedpolymeric solutionsare theoreticallymore physiological.Elemental formulasare not indicated inadult patients

Task 3. Enteral and Parenteral Nutrition p24mosm/l) polymeric solutions containing 1-1.5 kcal/ml, 45-60%of which should be in the form of carbohydrates, 20-35% aslipids, and 15-20% as proteins. Solutions are gluten and lactosefree.Polymeric EN solutions contain homogenised substratessimilar to those found in normal nutrition. The type of feedingpreparations available for enteral nutrition are listed below.These preparations generally contain between 500-1000 kcal/500 ml and 23-45g protein/500 ml. There are no available data to recommend the use of semielementalsolution in ICU patients, even in those with severe malabsorption orgut dysfunction. However, in a situation of proven or suspected intestinalmalabsorption, a semi-elemental EN solution may be introduced in patientswith severe and persistent diarrhoea associated with the administration of apolymeric solution.Elemental*Nitrogen Carbohydrate Lipid Fibrefree amino-acids glucose ormediumchainnoneoligosaccharidestriglyceridPeptides(hydrolisedproteins)oligosaccharidesSemielementalesmediumchaintriglyceridesPolymeric Whole protein polysaccharides long-chaintriglycerides*not available in all European countriesnoneavailableMore details on the composition of enteral diets can be found in the followingreference.Kreymann KG, Berger MM, Deutz NE, Hiesmayr M, Jolliet P, Kazandjiev G,Nitenberg G, van den Berghe G, Wernerman J; DGEM (German Societyfor Nutritional Medicine), Ebner C, Hartl W, Heymann C, Spies C; ESPEN(European Society for Parenteral and Enteral Nutrition). ESPENGuidelines on Enteral Nutrition: Intensive care Clin Nutr. 2006;25(2):210-23. PMID 16697087Modified formulas containing increased proportions of lipidsand less carbohydrate (to reduce CO 2 production in acuteSemi-elemental solutionsmay facilitate digestionrespiratory failure), or reduced protein content or increasedand absorption in abranched-chain amino-acids (for patients with acute renal orminority of patients withhepatic failure) have been developed. No convincing data, severe gut dysfunctionhowever, support their use.Prescription of enteral nutritionVarious techniques for administration of EN are available. We recommend theuse of 500 mL bottles/cans: this option facilitates storage, manipulation andorganisation at the bedside. Furthermore, the use of 1-2 L containers leads to awaste of feeding solution if only part of the solution can be administered due tochanges in the rate of administration or relative intolerance. There is also anincreased risk of bacterial contamination if large containers are left connected to

Task 3. Enteral and Parenteral Nutrition p25the patient for prolonged periods (>24h), unless a closed system is used, at anincreased cost.Finally, the tubing connecting the container to the patient's feeding tube shouldbe specific to EN (not interchangeable with an IV connection) and changed oncea day, to minimise the risk of bacterial contamination.Tolerance to EN can be improved by progressive increase of the feed volumeprescription (e.g. 25-50 ml/h during the first 24h, then 25 ml/h or 500 ml dailystep by step increase), by providing sufficient intraluminal sodium (above 80mmol/L of diet) and by prokinetic drug administration such as metoclopramideor erythromycin. For more information about the respective advantages of theseprokinetics, see the following reference.Röhm KD, Boldt J, Piper SN. Motility disorders in the ICU: recent therapeuticoptions and clinical practice Curr Opin Clin Nutr Metab Care. 2009;12(2):161-7. Review. PMID 19202387There is no advantage to instituting a ‘starter regimen’ at reduced osmolarity.Gastric residual volume may be checked once a day (see above and figure p19),subsequently reinstilled and the rate of administration adapted to the toleranceto EN. Thus, a quality assurance programme can be implemented and has beenshown to improve the risk-benefit ratio of EN in the critically ill.Design an EN regimen for five of your newly admitted patients and compareyour suggested formulation with that prescribed.Overly enthusiastic EN prescription may result in aspiration, aggravated gutischemia, dangerous intestinal distension and diarrhoea, especially when the infusionrate is greater than 100 ml/h.Q Why should polymeric enteral feeds be preferred to semielementalfeeds?A. Polymeric products mimic standard food, stimulate the gut mucosa and GI tractfunctions, can be enriched with fibre, are less expensive and tend to be better toleratedthan semi-elemental diet (less diarrhoea).Q When is semi-elemental enteral feeding indicated?A. Short bowel syndrome to improve nutrient absorption (but may be associated with areduction in gut mucosa stimulation).Gut allergy to macromolecules such as protein (because semi-elemental diet containshydrolysed peptides).Q What is an abnormal gastric residual volume during EN?

Task 3. Enteral and Parenteral Nutrition p26A. Volumes exceeding 500 mL. However this figure remains controversial in theliterature.Q What are the recommended dosages of metoclopramide anderythromycin as prokinetic drugs?A.6 mg erythromycin/kg/day (IV route)10 mg metoclopramide TID (IV route)Early enteral nutritionEarly EN may decrease mortality, infectious morbidity and reduce both lengthof stay and overall costs – all highly favourable effects. Thanks to thesebeneficial effects, EN has been proven superior to PN particularly in patientswith major trauma and in GI surgery – mainly in relation to the increasedinfection rate in severe and septic ICU patients.The institution of EN is frequently and erroneously delayed byradiologic or endoscopic examinations, GI intolerance(prolonged gastric emptying, regurgitation of enteral feeds,diarrhoea). Under these circumstances EN and PN appear togive similar results. Indeed, the timing of the initiation of thenutritional support seems to be more critical than the root ofadministration. Early PN is associated with reduced infectionrates and mortality in comparison with delayed EN.Even small amounts(250-500 ml/day) ofEN started early can bebeneficialThibault R, Pichard C. Nutrition and clinical outcome in intensive care patientsCurr Opin Clin Nutr Metab Care 2010; 13(2): 177-183. PMID 19996743Biffl WL, Moore EE, Haenel JB. Nutrition support of the trauma patient.Nutrition 2002; 18(11-12): 960-965. PMID 12431718Bisgaard T, Kehlet H. Early oral feeding after elective abdominal surgery--whatare the issues? Nutrition 2002; 18(11-12): 944-948. Review. PMID12431715Q. List three clinical conditions in which enteral nutrition carries ahigh risk of complications.A.Vomiting (risk of bronchoaspiration).Sphenoidal fracture (risk of nasogastric tube malposition). Clearly patients with thesefractures should not undergo blind placement of nasoenteric tubes to avoidmalposition, but many of these patients can be fed enterally as long as their GI tract canbe accessed safely.Severe ileus (risk of intestinal distension and/or intestinal rupture).PharmacomodulationHinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. SaundersLtd; 2008. ISBN: 978-0-7020259-6-9. p.303-305 Immunonutrition

Task 3. Enteral and Parenteral Nutrition p27On the assumption that modification of EN might reverse theimmunosuppression and modulate the inflammatory statusrelated to PCM and/or injury, the innovative concept ofpharmaconutrition has been introduced. Enrichment ofconventional nutritive mixtures with arginine, glutamine,omega-3 fatty acids, nucleotides, antioxidants, etc., has beenproposed over the last two decades. Six currently availableproducts are listed below.Pharmaconutrition isthe use of nutrients fortheir abilities tomodulateinflammatory and/orimmune response,healing or endocrinefunction,independently fromtheir nutritionalproperties.High-risk patients after major elective abdominal surgery,patients with multiple trauma, burns >30% of body surface areaand possibly some medical ICU patients on mechanicalventilation may benefit from pharmaconutrition, if patients arewithout severe sepsis and if pharmaconutrition is initiatedimmediately after ICU admission.Current evidencedoes not supportroutineimmunonutrition inall ICU patientsSeveral randomised trials suggest that supplementation of EN solutions withomega 3 fatty acids improved clinical outcome (reduced mortality, reducedlength of ICU and hospital stay, reduced duration of mechanical ventilation) f ofcritically ill patients with ARDS. A grade A recommendation has been given byESPEN for the use of EN or PN supplemented with omega 3 polyunsaturatedfatty acids in this group of patients.Link to ESICM Flash Conference: Pierre Singer, ‘Are omega 3 fatty acids safe forcritically ill patients?’ ESICM congress, Vienna 2009

Task 3. Enteral and Parenteral Nutrition p28There is not enough data to recommend the systematic use of antioxidantmicronutrient in the setting of ICU, except in severe burns – see specificparagraph in the last Task (5).Kreymann KG, Berger MM, Deutz NE, Hiesmayr M, Jolliet P, Kazandjiev G, et al;DGEM (German Society for Nutritional Medicine), Ebner C, Hartl W,Heymann C, Spies C; ESPEN (European Society for Parenteral andEnteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Intensive careClin Nutr 2006; 25(2): 210-223. PMID 16697087Singer P, Berger MM, Van den Berghe G, Biolo G, Calder P, Forbes A, Griffiths R,Kreyman G, Leverve X, Pichard C, ESPEN. ESPEN Guidelines onParenteral Nutrition: intensive care Clin Nutr 2009; 28(4): 387-400.PMID 19505748Heyland DK, Novak F, Drover JW, Jain M, Su X, Suchner U. Shouldimmunonutrition become routine in critically ill patients? A systematicreview of the evidence. JAMA 2001; 286(8): 944-953. Review. PMID11509059Montejo JC, Zarazaga A, López-Martínez J, Urrútia G, Roqué M, Blesa AL, et al;Spanish Society of Intensive Care Medicine and Coronary Units.Immunonutrition in the intensive care unit. A systematic review andconsensus statement Clin Nutr. 2003;22(3): 221-33. Review. PMID12765660Singer P, Shapiro H.Enteral omega-3 in acute respiratory distress syndrome. CurrOpin Clin Nutr Metab Care 2009; 12(2): 123-128. Review. PMID19202383[No authors listed]. Consensus recommendations from the US summit onimmune-enhancing enteral therapy. JPEN J Parenter Enteral Nutr 2001;25(2 Suppl): S61-63. PMID 11288926Parenteral nutrition: routes and formulasTwo large meta-analyses involving 19 randomised or quasi-randomised trialssuggest that PN is associated with slightly increased morbidity and is mainlybeneficial in those surgical patients who are malnourished prior to ICUadmission, but does not contribute to reduced morbidity or mortality in ‘true’critically ill patients. On this basis, PN should only by used when EN iscontraindicated (see p.10-11), not feasible, unsuccessful or insufficient.THINK. Parenteral nutrition can be indicated in the following clinical situations:Non functional gut: intestinal rupture, obstruction, gut ischemia/necrosisGeneralised peritonitisSevere shock statesPatient unable to eat adequate amounts of foodRoute of accessHinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. SaundersLtd; 2008. ISBN: 978-0-7020259-6-9. p .306 Administration

Task 3. Enteral and Parenteral Nutrition p29The vast majority of PN solutions are hyperosmotic andnecessitate central venous administration. Central catheterinsertion and maintenance require strict adherence to asepticand antiseptic protocols in order to reduce the risk of catheterrelatedinfection, which has become in the recent years a lessimportant problem of PN in critically ill patients.Subclavian veinaccess isrecommended.Subcutaneoustunnelling ofinternal jugular andfemoral cathetersreduces infectionPronovost P, Needham D, Berenholtz S, Sinopoli D, Chu H, Cosgrove S, et al. Anintervention to decrease catheter-related bloodstream infections in theICU. N Engl J Med 2006; 355: 2725-2732. PMID 17192537In particular, the tubing connecting the PN bag to the patient's catheter shouldbe changed once per day to avoid bacterial contamination.O'Grady NP, Alexander M, Dellinger EP, Gerberding JL, Heard SO, Maki DG, etal; Healthcare Infection Control Practices Advisory Committee. Guidelinesfor the prevention of intravascular catheter-related infections. Am J InfectControl 2002; 30(8): 476-489. PMID 12461511PN may also be given by peripherally inserted venous catheters, midline fineborecatheters (for PN expected to exceed six days) and by standard shortcannulae. For peripheral PN, a Teflon or polyurethane catheter should beselected, placed in an upper extremity site preferably, and changed every 3 or 4days to minimise the risk of phlebitis and infection. With peripherally insertedcatheters, full provision of nutritional needs is only possible if 2.5 to 3.5 litres ofiso- to slightly hyperosmotic (≤900 mosm/l) solutions can be tolerated.Use of a single lumen polyurethane or silicone catheter ispreferable, unless one port of a multi-lumen catheter is exclusively assignedto PN administration. The risk of drug incompatibility is thereby reduced.Routine replacement of central catheters in a new site or by guide wire exchangeincreases the risk of mechanical complications. Contrary to previous studies, theguide-wire catheter replacement did not increase the risk of infection.Randolph AG, Cook DJ, Gonzales CA, Brun-Buisson C. Tunneling short-termcentral venous catheters to prevent catheter-related infection: a metaanalysisof randomized, controlled trials. Crit Care Med 1998; 26: 1452-1457. PMID 9710109

Task 3. Enteral and Parenteral Nutrition p30NutrientsNitrogen is provided by a balanced mixture of amino acids (AA). There are noconvincing arguments to recommend the use of branched-chain AA (BCAA)instead of the various balanced AA solutions currently available. More recently,peptides have become available as immunomodulating or pharmacologicalagents (see below).Because of the relatively poor tolerance of carbohydrates together with the wellknown risks of excessive glucose administration (hyperglycaemia,hypertriglyceridemia, infections, liver steatosis), the recommended dailyquantity of glucose is ≤ 6g/kg/day (cf p.6) and should not be administered atrates exceeding 5 mg/kg/min in critically ill patients.Excessive (>23 mg/kg/min or 60% of total energy input) lipid supply can alsocause hepatic steatosis.Lipid emulsions contain energy in a small volume (9 kcal/g) reduce theosmolarity of nutritional mixtures and provide essential fatty acids necessary forcell membrane structure and stability, and for synthesis and action of theprostaglandin system. An initial supply of 0.5 to 1 g/kg/day of long chaintriglycerides (LCT) seems to be best; this can be increased up to a maximum of 2g/kg/day as long as plasma lipid clearance is regularly monitored(triglyceridemia, serum lactescence), and the infusion is given continuously overa 24h period. There is still no consensus, however, regarding the ideal quantityof lipid for critically ill patients. Whether supplementation with more than theminimum LCT requirement is of benefit during severe stress also remainsdebatable. As the severity of injury/sepsis increases, lipid oxidation andclearance from the blood decrease rapidly, which suggests poor utilisation. Therelative advantages and risks of glucose and lipid-based PN regimens have beenexamined by Tappy L et al in the reference below.Some ICU patients receive high doses of propofol which contains longchain triglycerides. The lipid emulsion administration has to be adapted to takeaccount of the quantity of lipid contained in propofol.Tappy L, Schwarz JM, Schneiter P, Cayeux C, Revelly JP, Fagerquist CK, et al.Effects of isoenergetic glucose-based or lipid-based parenteral nutritionon glucose metabolism, de novo lipogenesis, and respiratory gasexchanges in critically ill patients. Crit Care Med 1998; 26 (5): 860-867.PMID 9590315In addition, stimulation of alveolar macrophages could partially explain theabnormal pulmonary vascular tone and transient episodes of arterialdesaturation seen during intermittent infusion of lipid emulsions. Suchdeleterious effects, however, are unlikely as long as the infusion rate is notexcessive; it is therefore preferable to administer a continuous 24h infusion.

Task 3. Enteral and Parenteral Nutrition p31Controversy remains about the possible immunosuppressive effect of standardlipid emulsions in the acutely ill patient.It seems reasonable within the context of severe trauma/sepsis to limit the lipidsupply to about 40-50% of the non-protein calorie input, or even less (≤ 30%) inpatients who are severely septic.All-in-one PN solutionAll-in-one (ternary) PN bags, containing protein, carbohydrate, Uninterruptedlipid, or binary bags containing carbohydrate and protein, administration of PNreduces the risk ofsupplemented with trace elements, vitamins and electrolytes,metabolic complicationsare generally recommended for their convenience and goodmetabolic tolerance. Binary bags are less expensive and allowmodification of lipid administration.THINK In which kind of patients might use of binary PN bags be important?Patient with liver steatosisElevated blood liver enzymes or triglyceridesPatients receiving high doses of propofolPichard C, Schwarz G, Frei A, Kyle U, Jolliet P, Morel P, et al. Economicinvestigation of the use of three-compartment total parenteral nutritionbag: prospective randomized unblinded controlled study. Clin Nutr 2000;19: 245-251. PMID 10952795Convenient and simplified administration protocols are possible, andadjustment of infusion rate, when indicated, is easier.ImmunonutrientsParenterally administered immunonutrients include glutamine, omega-3 fattyacids, trace elements and vitamins. In inflammatory conditions such as injuryand sepsis, glutamine becomes a conditionally essential aminoacid and thepreferred fuel for rapidly dividing cells such as lymphocytes, macrophages andenterocytes (see figure below which illustrates immunonutrients in trauma,sepsis and inflammation). These cells in turn secrete polyunsaturated fatty acids(PUFAs) and arginine which affect gut failure, trauma, sepsis and inflammation.The optimal dosage and timing of administration of glutamine is not known.GlutamineSeveral randomised controlled trials indicate that the supplementation of PNsolutions with glutamine improves the clinical outcome (reduced mortality,reduced length of ICU and hospital stay, reduced duration of mechanicalventilation) of abdominal surgery and critically ill trauma patients. A grade Arecommendation is given by ESPEN for the use of PN supplementation withglutamine in these groups of patients.

Immunonutrients in trauma,sepsis and inflammationTask 3. Enteral and Parenteral Nutrition p32LymphocyteMacrophageEnterocytePUFA: polyunsaturated fatty acidsOKG: ornithine alpha-ketoglutarateSCFA: short chain fatty acidsOmega-3 PUFAs, derived from fish oils, give rise to 10 to 100-fold less platelet activation and thrombogenesis compared with omega-6PUFA (derived from vegetable oils), the usual component of standard lipidemulsions. Therefore, omega-3 PUFAs are less liable to induce an inflammatoryresponse to the activation of target cells by cytokines. The following fourreferences describe in more detail the impact of immunonutrients on theclinical course of ICU patients.Sacks GS, Genton L, Kudsk KA. Controversy of immunonutrition for surgicalcritical-illness patients Curr Opin Crit Care 2003; 9(4): 300-305. Review.PMID 12883285McCowen KC, Bistrian BR. Immunonutrition: problematic or problem solving?Am J Clin Nutr. 2003; 77(4): 764-770. Review. PMID 12663270Marik PE, Zaloga GP. Immunonutrition in critically ill patients: a systematicreview and analysis of the literature. Intensive Care Med 2008; 34(11):1980-1990. Review. PMID 18626628Dupertuis YM, Meguid MM, Pichard C. Advancing from immunonutrition to apharmaconutrition: a gigantic challenge Curr Opin Clin Nutr Metab Care2009; 12(4): 398-403. Review. PMID 19474715Link to ESICM Flash Conference: Pierre Singer, ‘Immunonutrition in traumapatients’ ESICM congress, Vienna 2009

Task 3. Enteral and Parenteral Nutrition p33Design a PN regimen for five of your newly admitted ICU patients andcompare your suggested formulation with that prescribed.Combination of EN and PNIt is clear that PN does not support mucosal structure and/orfunction of the gastrointestinal tract. In fact, except in cases offrank intestinal occlusion, partial EN is almost always feasible,even following major abdominal surgery. The only frequentannoying complication of EN in the ICU patient is the onset ofsevere diarrhoea. However, EN is not a dogma, and the keywordshould be flexibility: the two methods are complementary. Thedecision to use one and/or the other will depend on theexpertise, experience and training of the dieticians, medical andnursing staff, as well as the individual patient’s tolerance of EN.The type of nutritional support provided must be continuouslyadapted to the clinical situation (see p. 19).EN is preferable. PN ismore expensive,bypasses thealimentary tract andthe entero-pancreaticaxis, thus potentiallyfacilitating intestinalhyperpermeabilityand bacterialtranslocation.The indications for combined EN and PN are expected to increase in the future.Several studies have shown that the protein-energy deficit frequently observedwith the use of EN alone is associated with increased morbidity and mortality.Thus, avoiding nutritional deficiencies is a key objective of nutritional therapyin intensive care. As EN is often difficult to fully optimise in the first three daysfollowing ICU admission, supplementing EN with PN could allow a bettercoverage to help achieve the energy target and limit the protein-energy deficit.This concept is particularly important given the expected changes in thecharacteristics of the intensive care population, over the coming years. Indeed,the ageing population increased prevalence of chronic disorders (cancer,impaired organ function) and sedentary lifestyle will result in an increase in thenumber of ICU patients with loss of lean body mass and pre-existing nutritionaldeficiencies or undernutrition. The early optimisation of nutritional support willbe necessary to improve their clinical outcome and enhance their chances ofrapid recovery.Q Name at least one clinical situation in which the combination ofEN and PN is likely to be favourable. Give arguments.A.Prolonged PN and initiation of EN to 'open the intestinal route'Extensive small bowel resection (PN is indicated to cover the patient's nutritional needsand EN to promote gut adaptation)

4. MONITORING AND COMPLICATIONSAssessment and monitoring of nutritional support is mandatoryin critically ill patients; nutritional and metabolic disorders arefrequent and are important determinants of patient outcome.This process should be integrated with other aspects of ICUpatient care, as discussed in the two following reviews.Task 4 Monitoring and Complications p34Monitoring ofnutrition is anintegral part ofoverall ICU patientmonitoringHinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. SaundersLtd; 2008. ISBN: 978-0-7020259-6-9. p. 305 Complications and p.308-310 Complications and monitoring patients receiving TPNDowns JH, Haffejee A. Nutritional assessment in the critically ill Curr Opin ClinNutr Metab Care 1998;1(3): 275-279. Review. PMID 10565360Jolliet P, Pichard C, Biolo G, Chiolero R, Grimble G, Leverve X, et al. Enteralnutrition in intensive care patients: a practical approach. Working Groupon Nutrition and Metabolism, ESICM. Intensive Care Med 1998; 24 (8):848-859. PMID 9757932Monitoring enteral nutritionA number of practical clinical considerations are inherent to the safe andsmooth provision of enteral nutrition. They are addressed under the headings‘tube misplacement and bronchial aspiration’ and ‘gastrointestinal dysfunction’.Tube misplacement and bronchial aspirationX-rays are generally recommended after the placement of anasogastric tube and are repeated at least every week, especiallywith fine bore tubes in comatose patients.Malpositioning of(particularly) finebore tubes isfrequentSerious complications can occur when nutrients are infused outside thegastrointestinal tract, particularly into the airways. Bronchial aspiration may occur inpatients with swallowing disturbances even if they are intubated; the risk is partiallyreduced by raising the head 30 to 45° above the supine position during ENadministration.Gastrointestinal dysfunctionIf gastric feeding is used, monitoring of residual volume can decrease the risk ofpulmonary aspiration. If the volume is greater than 500 ml, the infusion rateshould be decreased by half for four hours and prokinetic agents used. If theresidual volume is less than 200 ml, the collected fluid should be reinstilled andfeeding resumed at the previous rate (see figure p.19).Abdominal cramps, nausea, vomiting and diarrhoea may occur when an enteralsolution is infused at a high rate (greater than 80-100 ml/h). Cramps andnausea may also result when a cold (refrigerated) nutrient solution is infused.Bacterial contamination of the nutrient solution is a rare but possible cause of

Task 4 Monitoring and Complications p35diarrhoea. In those with gastrointestinal symptoms, daily examination forabdominal distension is performed to detect a possible mesenteric ischaemia asearly as possible.In patients receiving antibiotics, pseudomembranous enterocolitis due to thetoxin of Clostridium difficile should be considered as a cause of diarrhoea. Stoolcultures (with stool Clostridium toxin assays) are indicated when diarrhoeapersists for more than three days after exclusion of other common causes. ASpanish study (see below) has reviewed the incidence of the complications ofEN in critically ill patients.Montejo JC. Enteral nutrition-related gastrointestinal complications in criticallyill patients: a multicenter study. The Nutritional and Metabolic WorkingGroup of the Spanish Society of Intensive Care Medicine and CoronaryUnits. Crit Care Med 1999; 27 : 1447-1453. PMID 10470748Monitoring of parenteral nutritionThe adverse effects of parenteral nutrition are a major limitation to its clinicaluse. These are addressed as catheter related (including septic) and asmetabolic/organ-specific complications.Catheter-related sepsis (CRS)Body temperature and insertion sites of intravenous cathetersmust be carefully monitored. A low-grade fever, in the absenceof an obvious source of infection, or a dirty, inflamed orpurulent insertion site may be a sign of catheter infection.Rigorous infectioncontrol measures aremandatory in allpatients receiving PNIf CRS is suspected to be the cause of severe sepsis or septic shock, the cathetermust be removed immediately, PN temporarily interrupted, central andperipheral blood and catheter cultures obtained.In the case of mild infection, to avoid unjustified central venouscatheter removal and the risks associated with the placement ofa new catheter in a new site, the physician has two options –either guide wire exchange for quantitative culture of thecatheter tip, or taking cultures ‘in situ’. The pros and cons ofthese options are discussed in the following references.In the absence of localor systemic signs ofsepsis, routine linechanges do notdecrease the incidenceof infectionBlot F, Nitenberg G, Chachaty E, Raynard B, Germann N, Antoun S, Laplanche A,Brun-Buisson C, Tancrède C. Diagnosis of catheter-related bacteraemia: aprospective comparison of the time to positivity of hub-blood versusperipheral-blood cultures Lancet 1999; 354(9184): 1071-1077. PMID10509498Brun-Buisson C. Suspected central venous catheter-associated infection: can thecatheter be safely retained? Intensive Care Med 2004; 30(6): 1005-1007.No abstract available. PMID 14991086

Non-septic complications due to the cathetersTask 4 Monitoring and Complications p36Complications associated with catheter insertion, such as air embolism, injuryto thoracic structures (lung, pleura, arteries) and cardiac arrhythmias, are notuncommon. General safety guidelines, not specific to PN, should be strictlyapplied. Catheter thrombosis can occur any time after insertion and is oftenassociated with catheter infection. Heparinisation of PN bags or solutions hasbeen advocated.Metabolic complications of parenteral nutritionHyperglycaemia is frequently observed in the critically ill, especially in patientswith infection, liver or pancreatic dysfunction, diabetes mellitus, and thosereceiving diabetogenic drugs such as corticosteroids and cephalosporins.Therefore blood glucose values should be checked at least daily. The monitoringof urine glucose could be used to guide insulin therapy in an ICU patient, sinceit can detect ketonuria. The association between hyperglycaemia and adverseoutcome in postoperative (mainly post cardiac surgery) patients has beendocumented.Blood glucose control lower than 10 mmol/L (1.8 mg/dL) with insulin candramatically improve morbidity and/or mortality of surgical/medical ICUpatients.Indeed, the NICE-SUGAR multicentre randomised study has recently indicatedthat the maintenance of a blood glucose lower than 10 mmol/L is associatedwith a reduced mortality rate as compared with “tight” glycaemic control (4.5-6mmol/L (0.8-1.1 mg/dL). Thus, the glycaemic control is necessary in medicalcritically ill patients treated with PN, but not as “tight” as previously indicatedby van den Berghe et al. However, it remains to be seen whether tight glycaemiccontrol should be used in specific subsets of ICU patients, such as surgicalpatients.Hypoglycaemia is much less common, and may be caused by the suddencessation of a hypertonic glucose infusion (e.g. due to kinking of the perfusiontubing), excessive insulin administration or the onset of severe sepsis.Hyperlipidaemia may be attributable to excessive administration,overproduction, or underutilisation of fat. Overproduction of lipid can resultwhen carbohydrates are given in excess of needs, and can result in hepaticsteatosis.NICE-SUGAR Study Investigators, Finfer S, Chittock DR, Su SY, Blair D, FosterD, Dhingra V, et al. Intensive versus conventional glucose control incritically ill patients. N Engl J Med 2009; 360(13): 1283-1297. PMID19318384van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M,Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R. Intensive insulintherapy in the critically ill patients. N Engl J Med 2001; 345(19): 1359-1367.PMID 11794168

Task 4 Monitoring and Complications p37Liver abnormalitiesLevels of aspartate aminotransferase, alanine aminotransferaseand bilirubin should be checked regularly e.g. every second day.The differential diagnosis of ICU-jaundice is often difficult dueto the numerous possible aetiologies such as sepsis,hypoxaemia, ischaemia, mechanical ventilation, drugs, andnutrition that can damage hepatocytes. Sludge in the biliarytract and stasis in the biliary ducts causing chronic acalculouscholecystitis may be associated with prolonged PN and may beprevented by small volume EN (100–200 ml/day). Gangrenouscholecystitis is a rare but often severe, life-threateningcomplication of total parenteral nutrition in mechanicallyventilated patients that has been described in patients with liverdysfunction.More than 60% of ICUpatients receiving PNfor more than two weekshave abnormal liverfunction tests.These mulitfactorialabnormalities areusually benign but mayherald the onset of MOF.Cabré E, Gassull MA.Nutritional issues in cirrhosis and liver transplantation.Curr Opin Clin Nutr Metab Care 1999; 2(5): 373-380. Review. PMID10589378Ziegler TR. Parenteral nutrition in the critically ill patient. N Engl J Med 2009;361(11): 1088-1097. Review. No abstract available. PMID 19741230Pancreatic disordersPancreatitis in the ICU most often results from drug toxicity. In view of therather high incidence of drug-induced pancreatitis in critically ill patients,plasma amylase and/or lipase should be checked every other day. Nowadays,EN is widely recommended for nutritional support of pancreatitis, and theresults appear to be better than in the case of PN (see the following reference fordetails).The rate and quantity of intravenous lipid infusion do not need to be modified,except if plasma triglycerides exceed 4 mmol/L (0.72 mg/dL).In acute pancreatitis with severe sepsis or shock, whether EN should beinterrupted and PN initiated is an unsolved question.Gianotti L, Meier R, Lobo DN, Bassi C, Dejong CH, Ockenga J, Irtun O, MacFie J;ESPEN. ESPEN Guidelines on Parenteral Nutrition: pancreas Clin Nutr2009; 28(4): 428-435. PMID 19464771Marik PE. What is the best way to feed patients with pancreatitis? Curr Opin CritCare 2009; 15(2): 131-138. Review. PMID 19300086

Task 4 Monitoring and Complications p38Q List at least five laboratory parameters reflecting metabolicdisturbances correctable by nutritional support.A.Hypoglycaemia and/or high acetonaemiaHypokalaemiaHypocalcaemiaHypomagnesaemiaHypophosphoraemiaHypovitaminosisQ What should be checked or corrected when hypertriglyceridaemiaexceeds 6 mmol/L (540 mg/dL)?A.Look for sepsis, hyperglycaemia, acute pancreatitis are common; familialhypertriglyceraemia (e.g. type IV) is rareCorrect excessive total energy and/or lipid administrationQ In hyperglycaemia ≥12 mmol/L (218 mg/dL), what nutritionregimen should be chosen?A. Excessive carbohydrate load (≥ 3–5 mg/kg body weight/min) should be avoided.Insulin should be titrated as needed to prevent blood glucose exceeding 10 mmol/L(180 mg/dL) and to avoid polyuria and electolyte losses. Simultaneously, screening forinfection should be initiated.Refeeding syndromePatients with severe PCM (body weight loss ≥20%) have major metabolicdisturbances. Prevention of lactic acidosis, beri-beri and/or Wernicke’sencephalopathy is achieved by high vitamin B1 levels when (or even before)hypertonic glucose is started. Reversal of acidaemia following the establishmentof mechanical ventilation may result in hypophosphataemia due to a shift ofphosphate from the extracellular to the intracellular compartment. In addition,when nutritional support is started in a malnourished patient, the intracellulardemands for phosphate and potassium are increased due to enhanced glycolysisand stimulation of the Na/K-pump. In practice, the rate of phosphate andpotassium infusion should increase from 15-30 to 30-60 mmol PO4 /day andfrom 80-120 to 120-200 mmol KCl /day. Phosphate, potassium, calcium andmagnesium should be closely monitored, and replaced as necessary. Furtherdetails on the management of the refeeding syndrome can be found in thefollowing reference.Q What are the two major risks related to rapid initiation of feedingof a severely malnourished patient?A.Severe hypokalaemia and hypophosphataemiaCardiac arrhythmiaMehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how toprevent and treat it. BMJ 2008; 336(7659): 1495-1498. PMID 1858368

Task 5. Nutritional Support for Specific Situations p395. NUTRITIONAL SUPPORT FOR SPECIFIC SITUATIONSLiver failureEnergy and protein intakes should not be modified, except in the case of severeencephalopathy clearly due to liver failure. In this case, protein intake can betransiently decreased to 0.6 g/kg/day to avoid the worsening of porto-cavalencephalopathy. Intravenous manganese and molybdenum administration shouldbe limited to three standard doses per week, instead of one daily if the patient isreceiving PN. Finally, the use of a modified nutrient profile, such as increasedbranched-chain amino acids for patients with acute hepatic failure, has never beenshown to prevent or control encephalopathy. No data support the concept of lowcalorie or low lipid PN in ICU patients with liver failure.ARDS and acute respiratory failureIn the presence of significant respiratory muscle weakness, and/or when weaningfrom the ventilator is proving difficult, the added ventilatory demand mayexacerbate respiratory muscle fatigue and jeopardise extubation. Generally, theexcess in total caloric load and the rate of administration, rather than theproportion of glucose and lipids, are responsible for these undesirable effects.Accordingly, the use of modified-feeds containing increased proportions of lipidsand less carbohydrate to reduce carbon dioxide production is not recommended.Recent data suggest that the enrichment of feeding with omega-3fatty acids can improve respiratory function in ARDS patients, and even reducethe length of stay in the ICU..Singer P, Theilla M, Fisher H, Gibstein L, Grozovski E, Cohen J. Benefit of an enteraldiet enriched with eicosapentaenoic acid and gamma-linolenic acid inventilated patients with acute lung injury. Crit Care Med 2006; 34(4): 1033-1038. PMID 16484911Singer P, Berger MM, van den Berghe G, Biolo G, Calder P, Forbes A, Griffiths R,Kreyman G, Leverve X, Pichard C, ESPEN. ESPEN Guidelines on ParenteralNutrition: intensive care Clin Nutr 2009; 28(4): 387-400. PMID 19505748For patients on EN, interruption of flow rate 3-6 hours before nasotrachealextubation after prolonged mechanical ventilation is frequently advocated toreduce the risk of aspiration. This procedure could potentially worsen respiratorymuscle dysfunction at a time when energy needs are increased to supportspontaneous breathing. We advocate continuation of EN until fifteen minutesbefore extubation when the nasogastric tube should be switched to gentle suctionto empty the stomach.

Task 5. Nutritional Support for Specific Situations p40Q To facilitate weaning of ARDS patients from MV, is it better to reducetotal energy input, glucose loading and/or lipid supply?A. Weaning from mechanical ventilation increases respiratory muscle work. Thenutritional support strategy needs to be carefully considered. Excessive glucoseloading may increase carbon dioxide production and respiratory work. Excessivelipid load may result in impaired gas exchange. It is recommended that a balancednutritional intake be maintained at a level representing 80 to 100% of the patient'senergy needs.Renal dysfunctionThe value ofNutritional therapy in patients with acute renal failure (ARF) branched-chainshould not be tailored to the impairment of renal function but to amino acids forthe severity of MOF. Renal failure occurring in ICU patients usually patients with acuterequires treatment with continuous or intermittent renalrenal failure hasreplacement therapy, which allows administration of nutrition as never been provendictated by the individual patient’s needs.Hence, the usual protein intake restrictions for non-dialysed end-stage renaldisease patients are unnecessary. The optimal composition of protein intake is notknown, but a mixture of balanced standard solution of amino acids for PN and astandard polymeric diet for EN seems sensible. Finally, the losses of glucose andamino acids in the dialysate (lipids are not dialysable) should be taken intoaccount. The metabolic features of both haemodialysis and continuoushaemofiltration are detailed in the following reference.Chan LN. Nutritional support in acute renal failure Curr Opin Clin Nutr Metab Care2004; 7(2): 207-212. Review. PMID 15075713Q In a patient on continuous haemodialysis, is it necessary to reducethe quantity of electrolytes and protein given by enteral or parenteralroutes? Explain your answer and consider whether intermittenthaemodialysis (IHD) is different.A. Continuous haemodialysis allows for full provision of nutritional needs, whileintermittent haemodialysis may necessitate reduced administration of fluid, electrolytesand protein.SepsisThere is no specific nutritional or metabolic support for critically ill septic patients.All our efforts must be concentrated on the immediate treatment of the underlyingcause and careful symptomatic, goal-directed management of the patient. Earlymetabolic (nutritional) support is required, however, once haemodynamic stabilityhas been achieved.

Task 5. Nutritional Support for Specific Situations p41Some simple guidelines can facilitate optimal nutritional management of thesepatients: restriction of energy supply (both carbohydrates and lipids) or evenhypocaloric support (

Task 5. Nutritional Support for Specific Situations p42However, insulin administration in ICU patients is limited to the control ofglycaemia, while recombinant human growth hormone (rhGH), recombinanthuman insulin-like growth factor-1 (rhIGF-1), and anabolic steroids have beeninvestigated but their use cannot be recommended.Anabolic factorscan promote leanbody massReid CL, Campbell IT, Little RA. Muscle wasting and energy balance in critical illnessClin Nutr 2004; 23(2): 273-280. PMID 15030968ObesityExcessive fat stores do not preclude the need for an external source of energy andother substrates. Indeed, ICU stay is not a favourable period for weight lossmanagement, except if weight loss is the critical issue for improving lung/cardiacfunctions. Energy needs of obese patients can be estimated (see paragraph onenergy and protein requirements), from ideal body weight increased by 20% toadjust for extra lean body mass related to obesity. The energy requirements couldbe estimated as 15 kcal/kg actual BW/day or 20 kcal/kg ideal BW/day. Dailyprotein needs vary between 1.2 and 1.5 g/kg adjusted body weight, specific lossesnot included. More details about this poorly recognised problem can be found inthe following reference.

Task 5. Nutritional Support for Specific Situations p43Kreymann KG, Berger MM, Deutz NE, Hiesmayr M, Jolliet P, Kazandjiev G, et al;DGEM (German Society for Nutritional Medicine), Ebner C, Hartl W,Heymann C, Spies C; ESPEN (European Society for Parenteral and EnteralNutrition). ESPEN Guidelines on Enteral Nutrition: Intensive care Clin Nutr2006; 25(2): 210-223. PMID 16697087Thibault R, Pichard C. Nutrition and clinical outcome in intensive care patients CurrOpin Clin Nutr Metab Care 2010; 13(2): 177-183. PMID 19996743Martindale RG, McClave SA, Vanek VW, McCarthy M, Roberts P, Taylor B, et al;American College of Critical Care Medicine; A.S.P.E.N. Board of Directors.Guidelines for the provision and assessment of nutrition support therapy inthe adult critically ill patient: Society of Critical Care Medicine and AmericanSociety for Parenteral and Enteral Nutrition: Executive Summary Crit CareMed 2009; 37(5): 1757-1761. Review. No abstract available. PMID 19373044Perioperative nutritionMalnourished patients undergoing surgery, mainly for gastrointestinal tumours,are at a higher risk of morbidity and mortality. A number of studies have shownthat nutritional support has beneficial metabolic effects, reduces morbidity(including that due to infection) and decreases mortality. See guidelines and reviewbelow.Braga M, Ljungqvist O, Soeters P, Fearon K, Weimann A, Bozzetti F; ESPEN. ESPENGuidelines on Parenteral Nutrition: surgery. Clin Nutr 2009; 28(4): 378-386.PMID 19464088Fearon KC, Luff R.The nutritional management of surgical patients: enhancedrecovery after surgery. Proc Nutr Soc 2003; 62(4): 807-811. PMID 15018479The small bowel recovers its ability to absorb nutrients almost immediatelyfollowing surgery, even in the absence of peristalsis. In abdominal surgery,placement of a nasoenteric tube or the creation of a feeding jejunostomy is clearlyappropriate to ensure nutrient delivery and to avoid the inconvenience and cost ofPN.The French and North-American consensus conferences held in 1995 and 1997concluded that 7 to 10-day preoperative PN nutrition was of value only inmalnourished gastrointestinal cancer patients, and that these patients shouldcontinue with nutritional support postoperatively for at least five days.Postoperative complications may be reduced by 10%. Preoperative PN is notrecommended in other cases, as it could increase the risk of complications.

Task 5. Nutritional Support for Specific Situations p44Recent (European Society of Parenteral and Enteral Nutrition) ESPEN guidelineson PN in Surgery concur.Braga M, Ljungqvist O, Soeters P, Fearon K, Weimann A, Bozzetti F; ESPEN. ESPENGuidelines on Parenteral Nutrition: surgery. Clin Nutr 2009; 28(4): 378-386.PMID 19464088It is suggested that postoperative nutritional support should be given to patientswho cannot resume around 60% of their calculated nutritional intake within fivedays following the operation. Enteral nutrition is the preferred route in thisindication.Perioperative EN or PN can be made more effective by the use ofpharmaconutrients. The following two references review the evidence.Martindale RG, Maerz LL. Management of perioperative nutrition support Curr OpinCrit Care 2006; 12(4): 290-294. Review. PMID 16810037Calder PC. Immunonutrition in surgical and critically ill patients Br J Nutr. 2007; 98Suppl 1: S133-S139. Review. PMID 17922951CONCLUSIONIt is relatively easy to maintain adequate nutritional status, but a more difficult andprolonged task to cure PCM.‘PCM is a sign of poverty in the Third World but of ignorance in hospitals ofindustrialised countries’ (Sir A. Wretlind 1981).Enteral nutrition is always the first choice. Parenteral nutrition should be restrictedto those situations in which there are contraindications to enteral nutrition. Thevalue of immunonutrition remains uncertain.

Self-assessment p45SELF-ASSESSMENTEDIC-style Type K1. Type K. Resting energy expenditure (REE) is defined as the energyexpenditure (EE) of the body in the resting state. Which of the followingstatements of REE is true:A. REE is always less than or equal to EEB. REE is not affected by body temperatureC. REE, measured in terms of body mass, is equal in males and femalesD. REE is often in the range of 20-30 kcal/kg body weight in ICU patients2. Type K. What is the ideal marker of protein-calorie malnutrition?A. Body mass indexB. Serum albuminC. Nitrogen balanceD. Bio-impedance analysis3. Type K. A 54-year-old female patient with chronic pancreatitis because ofalcohol abuse during several years is admitted to the ICU with a severepneumonia. She is 173 cm high and weights 43 kg. Regarding the energyrequirements in this patient:A. The goal of total energy delivery is around 2200 kcal/24hB. 50-55% of her energy intake should be carbohydrates.C. Lipid intake should not exceed 2 g/kg/dayD. Glucose requirement is usually 6-10 g /kg/day4. Type K. Contraindications to start enteral nutrition include:A. Uncontrolled acute circulatory failureB. Gastric atonia (Gastroparesis)C. PeritonitisD. Absent bowel sounds

Self-assessment p465. Type K. A 57-year-old male, body weight 72 kg, with COPD is treated withnon-invasive ventilation (NIV) applied with a mask. He is given full enteralnutrition (1750 ml, approximately 75 ml/hour) on day 3 after admission. Heis awake and cooperative. On the morning of day 4, the ICU nurse reports agastric residual volume of 650 ml. Which of the following options related tothe nutritional management this day is appropriate?A. Reduce infusion rate to 50% 4-6 hours then progressively increase over the next1-2 daysB. Permanently reduce the amount to 1250 ml/day because the present amount istoo much in COPDC. Stop all EN and give him parenteral nutrition for 1-2 days, then progressivelyincrease over the next 1-2 daysD. Consider giving i.v. erythromycin6. Type K. After a successful placement of a fine-bore nasogastric (NG) tubethe following actions is/are indicated:A. An X-ray of the upper abdomen to demonstrate proper placement of the NG tube.B. Aspiration through the NG tube to confirm the presence of gastric positionC. Installation of air through the NG and listen for characteristic sounds (bubble) inthe epigastric regionD. Gastroscopy to confirm correct position of the NG tube7. Type K. Metabolic complications of parenteral nutrition (PN) include:A. HyperglycaemiaB. HypertriglyceridaemiaC. HypoglycaemiaD. Hypophosphataemia

Self-assessment p47EDIC-style Type A8. Type A. The ‘low-phase’ of the metabolic response to injury and severeinfections is characterised by the following disturbances EXCEPT:A. Increased energy expenditureB. Decreased gluconeogenesisC. Increased endogenous lipolysisD. Loss of lean body massE. Increased insulin resistance9. Type A. The advantages of enteral nutrition include all the followingEXCEPT:A. Maintains normal IgA secretion in the gut mucosaB. Reduces the risk of hyperglycaemiaC. Reduces intestinal motilityD. Less costly than parenteral nutrition (PN)E. Decrease infectious complications compared to PN10. Type A. Regarding enteral nutrition formulas, the following statementsare true with the EXCEPTION of:A. A standard EN solution contains 1 kcal/mlB. Additional vitamins and trace elements should be added when the volume of EN

Self-assessment p48Self-assessment Answers1.2.3.4.5.6.7.A. TB. FC. FD. TA. FB. FC. FD. FA. FB. TC. TD. FA. TB. FC. TD. FA. TB. FC. FD. TA. TB. FC. TD. FA. TB. TC. TD. T8. Answer B is correct9. Answer C is correct10. Answer C is correct11. Answer A is correct

PATCH page 49NutritionPATIENT CHALLENGESMrs B., a 54-year-old, previously healthy, woman presented with acuteabdominal pain. She had a 10 year history of abdominal discomfort and nausea afterfatty meals and ingestion of coffee. Stools and urine were said to be normal. She didnot consume excessive amounts of alcohol, which was confirmed by her family. Shehas been obese since the birth of her children and at present has a stable weight of 82kg and is 1.62 m tall. She suffered from moderate hypertension but otherwise herhistory was unremarkable. The pain was located in the mid upper abdomen andradiated to the left and to the back. The pain was more severe during movement,which caused her to lie still in her bed.On examination, she looked moderately ill and experienced tenderness on palpationof the upper abdomen. There was no referred discomfort and bowel sounds wereaudible. Core temperature was 38.3° C.Abnormal findings on investigation: ultrasound upper abdomen; stone shadows inthe gallbladder and suspicion of hepatic steatosis. Intrahepatic bile ducts slightlydilated, no stone shadows visible in bile ducts. Pancreas difficult to evaluate due togas in stomach and colon.Plank LD, Hill GL. Sequential metabolic changes following induction of systemicinflammatory response in patients with severe sepsis or major blunttrauma World J Surg 2000; 24(6): 630-638. Review. PMID 10773114Venneman NG, van Brummelen SE, van Berge-Henegouwen GP, van ErpecumKJ. Microlithiasis: an important cause of "idiopathic" acute pancreatitis?Ann Hepatol 2003; 2(1): 30-35. Review. PMID 15094703Napoléon B, Lefort C, Gincoul R. State of the art lecture: lithiasis andpancreatitis. Endoscopy 2006; 38 Suppl 1: S35-40. Review. No abstractavailable. PMID 16802221Laboratory tests:Hb 8.2 g/dLLeukocytes 21.4 /fLESR 18 mm/hAlbumin 32 g/LCRP 60 mg/LUrinary Amylase 1800 IUγGT 124 IUAlk Phosph 217 IUASAT 55 IUALAT 40 IU

PATCH page 50Amylase 748 IUBilirubin - total 41 µmol/LCreat 75 µmol/L - direct 80%Blood Urea 8.3 mmol/LGluc 8.9 mmol/LMrs B. was diagnosed as having biliary pancreatitis of moderate severity.Glucose/saline 2.5 l/24h was commenced via a peripheral venous line.Haemodynamic parameters and hourly urinary output were monitored. Nasogastricsuction was started.Q. Does Mrs B. need artificial nutrition at this stage?A. Probably not. The severity of disease is moderate and it is not certain that anecrotising pancreatitis is present. In patients with interstitial pancreatitis, no benefitof artificial nutrition has been demonstrated.Indications for artificial nutrition in acute disease of short duration, and in acutepancreatitisGianotti L, Meier R, Lobo DN, Bassi C, Dejong CH, Ockenga J, Irtun O, MacFie J;ESPEN. ESPEN Guidelines on Parenteral Nutrition: pancreas Clin Nutr2009; 28(4): 428-435. PMID 19464771Meier R, Ockenga J, Pertkiewicz M, Pap A, Milinic N, Macfie J; DGEM (GermanSociety for Nutritional Medicine), Löser C, Keim V; ESPEN (EuropeanSociety for Parenteral and Enteral Nutrition). ESPEN Guidelines onEnteral Nutrition: Pancreas Clin Nutr. 2006; 25(2): 275-284. PMID16678943Marik PE. What is the best way to feed patients with pancreatitis? Curr Opin CritCare 2009; 15(2): 131-138. Review. PMID 19300086Indications for artificial nutrition in patients with normal body compositionPACT module on PancreatitisQ. Presuming your answer was no, would you have instituted artificial nutrition if sheweighed 54 kg?A. Only if the 54 kg is the result of recent substantial weight loss (e.g. about 5-6 kg inthe past 3 months) might one consider early artificial nutrition. Since 54 kg is close toideal body weight for 1.62 m there is no indication for artificial nutrition.

PATCH page 51After 2 days Mrs B's clinical state deteriorates. Urine output diminishes to 25ml/h prompting additional fluid support. She is slightly confused and has a slighttachycardia (110 b/min). Arterial blood pressure is maintained.Additional investigation. Plain abdominal and chest X-ray: still gas in transversecolon, little gas in small intestine, some pleural effusion in the left hemi-thorax.Laboratory tests:Hb 6.2 g/dLLeukocytes 21/fLThrombocytes 580 /fLAlb 21 g/LCRP 180 mg/LLiver enzymes no changesGluc 12.9 mmol/LCreat 121 µmol/LAmylase 1200 IUUrinary Amylase 23000 IUTriglycerides 2.1 mmol/LBilirubin 18 µmol/lNecrotising pancreatitis is suspected and a prolonged clinical course isexpected. With appropriate fluid support, her haemodynamic parameters remainstable.Symptomatology of severe acute disease. See PACT module on Oliguria and anuria.Werner J, Hartwig W, Uhl W, Müller C, Büchler MW. Useful markers forpredicting severity and monitoring progression of acute pancreatitisPancreatology 2003; 3(2): 115-127. Review. PMID 12748420Lempinen M, Stenman UH, Puolakkainen P, Hietaranta A, Haapiainen R,Kemppainen E. Sequential changes in pancreatic markers in acutepancreatitis Scand J Gastroenterol 2003; 38(6): 666-675. PMID 12825877Aoun E, Chen J, Reighard D, Gleeson FC, Whitcomb DC, Papachristou GI.Diagnostic Accuracy of Interleukin-6 and Interleukin-8 in PredictingSevere Acute Pancreatitis: A Meta-Analysis Pancreatology 2010; 9(6): 777-785. PMID 20110745Q. Does Mrs B. need artificial nutrition at this stage?A. A CRP above 120 mg/l is one of the most sensitive indicators for the presence ofnecrotising pancreatitis in this context. Also the low haemoglobin, albumin, the highleukocytes, thrombocytes, glucose and creatinine are indicators of severeinflammation and disease. Therefore a long clinical course is rightfully expected.Artificial nutrition should be instituted on the basis of these considerations. Mrs B'sobesity does not alter this indication.Prediction of severity of illness and consequently indications for artificial nutrition

PATCH page 52Q. Why is there a substantial drop in haemoglobin?A. The drop in haemoglobin is mainly the result of haemodilution. The drop is stillmoderate, which makes it unlikely to be due to haemorrhagic necrotisingpancreatitis.Nutritional requirements in obesityQ. What is (are) the cause(s) of the substantial drop in albumin?A. The drop in albumin is the result of several factors. The distribution has increasedboth intravascularly but also extravascularly because of the vascular expansioncaused by fluid support. In addition the transcapillary escape rate of albumin hasincreased. Furthermore the synthesis rate of albumin is generally not decreased butbreakdown most probably is increased.Kinetics of albumin. See the PACT module on High risk surgical patientQ. If you start artificial nutrition now, how and what?A. Although it is important to initiate enteral nutrition it is unlikely that this will meetthe patient's full requirements at this stage. Therefore PN is appropriate until oral orenteral nutrition can be resolved.Does enteral nutrition worsen the severity of pancreatitis by stimulation of thepancreas?Outcome of acute pancreatitis: nasogastric versus nasojejunal feeding?O'Keefe SJ.Physiological response of the human pancreas to enteral andparenteral feeding.Curr Opin Clin Nutr Metab Care 2006; 9(5): 622-628.PMID 16912561Kaushik N, Pietraszewski M, Holst JJ, O'Keefe SJ.Enteral feeding withoutpancreatic stimulation. Pancreas. 2005; 31(4): 353-359. PMID 16258370Eatock FC, Chong P, Menezes N, Murray L, McKay CJ, Carter CR, et al. Arandomized study of early nasogastric versus nasojejunal feeding in severeacute pancreatitis. Am J Gastroenterol 2005; 100(2): 432-439. PMID15667504Kumar A, Singh N, Prakash S, Saraya A, Joshi YK. Early enteral nutrition insevere acute pancreatitis: a prospective randomized controlled trialcomparing nasojejunal and nasogastric routes J Clin Gastroenterol 2006;40(5): 431-434. PMID 16721226

PATCH page 53Enteral nutritionParenteral nutritionAlthough the efficacy of antibiotic prophylaxis for the prevention ofinfections is not established and remains controversial in acutepancreatitis (see ESICM-SCCM consensus statement and references below), IVimipenem® is commenced together with enteral nutrition via a nasojejunaltube. 500 ml of a nutrition formula of polymeric composition is administeredas a continuous 24h pump driven enteral infusion.Three days later (5d after admission to the ICU) Mrs B. still requires large volumeloads and is in positive fluid balance. She is confused, is suffering from acuterespiratory insufficiency, necessitating oxygen administration. Mechanical ventilationis considered. The volume of enteral nutrition has been increased to 1000 mL/d. Onexamination Mrs B. is hyperventilating, her abdomen is distended with occasionalhigh-pitched bowel sounds, and her upper abdomen is tender on palpation. She hasnot passed a motion, and 800 ml of clear slightly brownish fluid have been aspiratedvia her stomach tube.Additional investigation.Laboratory tests:Hb 5.4 mmol/LCreat 213 µmol/LBlood Urea 21.0 mmol/LAlb 14 g/LGluc repeatedly above 10 mmol/LPersistent leukocytosisTriglycerides 3.2 mmol/LCRP 250 mg/LNathens AB, Curtis JR, Beale RJ, Cook DJ, Moreno RP, Romand JA, Skerrett SJ,Stapleton RD, Ware LB, Waldmann CS. Management of the critically illpatient with severe acute pancreatitis. Crit Care Med 2004; 32(12): 2524-2536. Review. PMID 15599161Maraví-Poma E, Gener J, Alvarez-Lerma F, Olaechea P, Blanco A, Dominguez-Muñoz JE; Spanish Group for the Study of Septic Complications in SevereAcute Pancreatitis. Early antibiotic treatment (prophylaxis) of septiccomplications in severe acute necrotizing pancreatitis: a prospective,randomized, multicenter study comparing two regimens with imipenemcilastatin.Intensive Care Med 2003; 29: 1974-1980. PMID 14551680Xue P, Deng LH, Zhang ZD, Yang XN, Wan MH, Song B, et al. Effect of antibioticprophylaxis on acute necrotizing pancreatitis: results of a randomizedcontrolled trial. J Gastroenterol Hepatol 2009; 24:736-742. PMID19220676Jafri NS, Mahid SS, Idstein SR, Hornung CA, Galandiuk S. Antibiotic prophylaxisis not protective in severe acute pancreatitis: a systematic review andmeta-analysis. Am J Surg 2009; 197: 806-813. PMID 19217608

PATCH page 54Empiric approach in ICU to nutritional support. Effectiveness judged on clinicalgrounds, primarily. See PACT module on Basic clinical examination.Q. Estimated energy requirements on the basis of ideal body weight and actual preillnessbody weight amount to more than 1500 kcal/24h. The enteral feed suppliesapproximately 1000 kcal/d. Would you try to cover energy needs and if so, whichmeasures would you take to reach this goal?A. Mrs B's predicted total energy expenditure is about 1600-1800 kcal/d. Apparently,she does not tolerate full enteral nutrition at this stage. Residual stomach volumeshould not amount to more than 500 ml. Bowel distension should be absent and thepatient should produce stools. Prokinetics and enemas are questionable in thissetting. If tolerance does not improve the amount administered should be limited. Inthis case PN should be added to make up for the deficit in nutritional provision. It isnot always necessary to reach full requirements.Combination of EN and PNCalculation of total energy expenditureQ. Given the developing acute kidney injury, is it necessary to limit the proteincontent of the nutritional regimen? Explain your answer.A. Limitation of protein intake is rarely indicated. In this case the period of acuterenal failure will most likely be at least a few weeks. Normal protein quantities (1.2 gup to 1.5 g/kg/24h is generally recommended) should therefore be included, and ifnecessary the patient treated with haemodialysis or CVVH (Central Veno-VenousHaemoperfusion).Appropriate use of protein in the nutritional regimen in patients with acute orchronic renal failureQ. Would you limit the fat intake of Mrs B? Or would you aim for a high fat contentbecause of acute respiratory insufficiency? Why?A. High plasma triglyceride levels should caution against overloading the system withfat. It seems justified to give normal fat, monitor triglyceride levels in plasma andtaper fat content when triglycerides rise above 4-5 mmol/L. Abnormal liver enzymesindicating intrahepatic cholestasis often parallel the high triglyceride levels. Givinghigh quantities of fat to decrease CO 2 production is not supported by hard data.The management of hypertriglyceridaemia and steatosis in severe disease

PATCH page 55Q. What arguments do you give to start albumin administration or not?A. More and more authors share the view that albumin does not improve outcome inthis type of patient. There are certainly no data demonstrating a benefit. An exceptionmay be liver insufficiency with frequent ascites removal or very low levels ofalbuminaemia (e.g.

PATCH page 56Q. Do you again modify the nutritional regimen? If so, how?A. Although continuation of peri-operative enteral nutrition is advocated by some, inthe case of necrotising infected pancreatitis, temporary discontinuation of the enteralfeed is more usually favoured. Also limitation of PN to not more than 1000 kcal isoften advocated to prevent metabolic disturbances, specifically glucose intolerance. Ifan immune enhancing diet was instituted, it should be continued after operation.The potential deleterious role of hyperglycaemia in surgical ICU patients.A catheter jejunostomy was performed and enteral nutrition resumed one day afteroperation (12th day after admission). Parenteral nutrition was recommenced at 2000kcal/d (the infusion rate was reduced on the day of operation). On the 14th day thepatient develops overt sepsis and MOF of increasing severity. There is alsohypertriglyceridaemia (>7 mmol/L).Hypertriglyceridemia and potential untoward side-effectsQ. What measures do you now take? How do you treat hypertriglyceridaemia?A. The hypertriglyceridaemia has reached a point where, in general, a decrease of fatcontent in the nutritional regimen is indicated although it is not established at whichlevel this should be performed. At this moment there is no possibility to give Mrs B.full nutritional support. Fat administration through the TPN is reduced to twice aweek (but not removed because of risk of fatty acid deficiency) and enteral nutritionis given in very low quantities.Mrs B. is re-operated on the 15th day. Residual infected necrosis is removed,the omental sac is packed and the wound closed with a Vicryl® mesh. Due toenormous bowel distension primary closure is not possible. Enteral nutrition isdiscontinued before operation. Parenteral nutrition is administered at half strength(approximately 1000 kcal/d without fat).Q. When would you start enteral nutrition again via the jejunostomy catheter? Whenwould you try to resume full strength nutritional support? Is there a place for amodified formula both enterally or parenterally?A. Enteral nutrition should be resumed when bowel distension has abated and gastricaspirate volumes (GAV) are reduced. It is also more likely, that enteral nutrition willbe successful when the severity of disease has become less and bowel movementshave been recorded. Full requirements are possible only when fat clearance hasimproved to such a degree that fat can be included in the regimen on a daily basis.The administration of extra glucose is not an option because the ability to oxidiseglucose is limited to 4-5 g/kg/24h. Administering more will aggravate steatosis,which this patient has had all along.

PATCH page 57The utilisation of fat and carbohydrates in critical illnessTwo more drainage procedures are necessary but on the 21st day the lastgauze pack is removed from the lesser sac, the wound granulates and inflammatoryparameters become stable and subsequently improve. During one of the drainageprocedures the jejunostomy catheter is dislodged, reinserted and oversewn. Mrs B. isartificially ventilated, is on CVVH (Central Veno-Venous Haemoperfusion) and shecan be brought into negative fluid balance. She needs less oxygen and less inotropicsupport. Attempts to increase her caloric intake by adding fat have until now failedbecause of increasing plasma triglyceride levels. Five hundred mL of enteral feed isadministered via the jejunostomy catheter, which on the 25th day is increased to1000 kcal/d, implying that energy requirements are approximately met (EN and PNtogether).On the 28th day after admission the oversewn entry site of the jejunostomy catheteropens and in a few days a high output fistula (over 1500 ml per day) develops whichdrains into the left side of the open granulating wound.Surgical treatment of infected, pancreatic necrosis and the integrated approach toeffective enteral and parenteral nutrition. See PACT Module on PancreatitisRaraty MG, Connor S, Criddle DN, Sutton R, Neoptolemos JP. Acute pancreatitisand organ failure: pathophysiology, natural history, and managementstrategies Curr Gastroenterol Rep 2004; 6(2): 99-103. Review. PMID15191686Singh VK, Wu BU, Bollen TL, Repas K, Maurer R, Mortele KJ, Banks PA. Earlysystemic inflammatory response syndrome is associated with severe acutepancreatitis Clin Gastroenterol Hepatol. 2009;7(11): 1247-1251. PMID19686869Mole DJ, McClymont KL, Lau S, Mills R, Stamp-Vincent C, Garden OJ, ParksRW. Discrepancy between the extent of pancreatic necrosis and multipleorgan failure score in severe acute pancreatitis World J Surg. 2009;33(11): 2427-2432. PMID 19641951Although almost all organ functions improve Mrs B. becomes jaundiced with rapidrises in Alk Phosph, γGT and direct Bilirubin. Transaminases are only slightlyelevated. Triglyceride levels have stabilised at 3 mmol/L, and inflammatoryparameters indicate only modest inflammation. Albumin is rising to above 20 g/Lwithout albumin infusion.

PATCH page 58Q. Which nutritional regimen do you prescribe? What is the cause of the intrahepaticcholestasis?A. Reactivation of distal small bowel function has been shown to decrease the severityof intrahepatic cholestasis. This may involve reinfusion of chyme, collected from theproximal part of the fistula, into the distal small bowel with or without a liquidenteral formula. Somatostatin or somatostatin analogs may diminish fistula output,but only in certain circumstances and when the bowel and adjacent tissues arehealthy.The causes of intrahepatic cholestasis are multifactorial. The PN as well as the actualshort bowel and the defunctionalised distal small bowel, as a result of the fistula, areimplicated in the intrahepatic cholestasis. The pathogenesis is not yet well definedbut may include endotoxin-induced cytokine cascades.The multifactorial origin of intrahepatic cholestasis in severely ill patients receivingparenteral nutritionCalicis B, Parc Y, Caplin S, Frileux P, Dehni N, Ollivier JM, Parc R. Treatment ofpostoperative peritonitis of small-bowel origin with continuous enteralnutrition and succus entericus reinfusion Arch Surg 2002; 137(3): 296-300. PMID 11888452Frileux P, Attal E, Sarkis R, Parc R. Anastomic dehiscence and severe peritonitisInfection 1999; 27(1): 67-70. Review. PMID 10206794Effects of somatostatin or analogs on pancreatitis and fistula output and healing.See PACT Module on PancreatitisInitially full PN is administered with normal amino acid and fat content.The proximal jejunal output is re-infused into the distal part of the jejunum togetherwith an enteral formula. It soon becomes possible to administer 1000 mL of enteralfeed per day together with a large part of the proximal pancreatic and biliarysecretions. PN is diminished to 1000 kcal/d.Finally Mrs B. improved physically, mentally and biochemically. Albumin andhaemoglobin rose to normal levels, intrahepatic cholestasis, including jaundice,disappeared almost completely. Thirty-five days after admission to ICU she wastransferred to the normal ward. After 56 days of hospital stay Mrs B. had furthersurgery. Her jejunal fistula was closed as was the abdominal wound andcholecystectomy was done. The skin was left open. Mrs B. resumed oral intake a fewdays after the operation and was discharged 70 days after her admission to ICU.Balancing enteral and parenteral nutritionRoute of feedingCombination of enteral and parenteral nutrition

PATCH page 59On reflection, the intensive care course of this patient was prolonged andinvolved the collaborative and dedicated efforts of many doctors, nurses and otherhealthcare professionals. Fortunately, the outcome was positive and the patientreturned to her family.Q. Apart from the technical skills demonstrated by the carers in this case what othercomponents of care would you consider would have been important?A. Clearly, communication between members of the ICU team and with surgical and dieteticcolleagues would have been critically important. The fact that many of the decisions takenwere based on clinical experience as well as laboratory findings underscores the importanceof regular sharing of information and ensuring that all carers are involved in the process.Frequent and sensitive communication with relatives would be equally important.Link to Pact module on CommunicationQ. Once the patient left ICU what would have been the important points in hersubsequent management?A. Again detailed communication with ward staff before and during the patient'stransfer to the ward would b essential to ensure a smooth transition. After thepatient's return home, skilled and experienced support would continue to beimportant since patients recovering from prolonged illness, particularly whencomplicated by PCM, are both physically and psychologically vulnerable.