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AN ESICM MULTIDISCIPLINARY DISTANCE LEARNING PROGRAMME FOR INTENSIVE CARE TRAINING Nutrition Skills and techniques Update April 2010 Module Authors (Update 2010) RONAN THIBAULT Department of Gastroenterology and Nutritional Support, University Hospital (CHU) of Nantes, University of Nantes, Nantes, France CLAUDE PICHARD Clinical Nutrition, Geneva University Hospital, Geneva, Switzerland BRUNO RAYNARD Anaesthesia, Intensive Care and Infectious Diseases. Institut Gustave Roussy, Villejuif, France PIERRE SINGER General Intensive Care Department, Rabin Medical Center, Beilinson Hospital, Tikva, Israel Module Authors (first edition) Claude Pichard, Gerard Nitenberg, Philippe Jolliet, Peter Soeters Module Reviewers Gerard Nitenberg, Janice Zimmerman, Lia Fluit Section Editor Charles Hinds Nutrition Update April 2010 Editor-in-Chief Dermot PHELAN Intensive Care Dept Mater Hospital /University College Dublin, Ireland Deputy Editor-in-Chief Francesca Rubulotta, Imperial College, St Mary's Hospital, London, UK Medical Copy-editor Charles Hinds, Barts and The London School of Medicine and Dentistry Editorial Manager Kathleen Brown, Triwords Limited, Tayport, UK Business Manager Estelle Flament, ESICM, Brussels, Belgium Chair of Education and Training Committee Hans Flaatten, Bergen, Norway PACT Editorial Board Editor-in-Chief Dermot Phelan Deputy Editor-in-Chief Francesca Rubulotta Acute respiratory failure Anders Larsson Cardiovascular dynamics Jan Poelaert/Marco Maggiorini Neuro-intensive care and Emergency medicine Giuseppe Citerio HSRO / TAHI Carl Waldmann Environmental hazards Janice Zimmerman Systemic inflammation and Sepsis / Infection Johan Groeneveld Metabolism, endocrinology, nephrology, nutrition Charles Hinds Perioperative ICM and surgery Vacant (April 2010) ETC / Ethics Gavin Lavery Education and assessment Lia Fluit Consultant to the PACT Board Graham Ramsay Copyright© 2010. European Society of Intensive Care Medicine. All rights reserved. Contents Contents Introduction..................................................................................................................................................................... 1 1. Stress-related metabolic disturbances and rationale for feeding ..............................................................................2 Metabolic alterations in ICU patients.........................................................................................................................2 Rationale for feeding ...................................................................................................................................................4 2. Nutritional Assessment and Requirements................................................................................................................ 7 Nutritional assessment................................................................................................................................................ 7 Nutritional indices.......................................................................................................................................................8 Nitrogen (N) balance...................................................................................................................................................8 Measurement of body composition ............................................................................................................................9 Electrolytes ..................................................................................................................................................................9 Trace elements, vitamins, hormones, enzymes..........................................................................................................9 Practical assessment of nutritional status ..................................................................................................................9 Nutritional requirements ...........................................................................................................................................11 Energy and macronutrient requirements..................................................................................................................11 Micronutrient requirements ..................................................................................................................................... 13 3. Enteral and Parenteral Nutrition.............................................................................................................................. 15 Indications and contraindications............................................................................................................................ 15 Enteral nutrition: routes and formulas .................................................................................................................... 21 Nasogastric route .................................................................................................................................................. 21 Percutaneous route ...............................................................................................................................................22 Enteral nutrition formulas....................................................................................................................................23 Prescription of enteral nutrition...........................................................................................................................24 Early enteral nutrition ..........................................................................................................................................26 Pharmacomodulation............................................................................................................................................26 Parenteral nutrition: routes and formulas .............................................................................................................. 28 Route of access ..................................................................................................................................................... 28 Nutrients............................................................................................................................................................... 30 All-in-one PN solution .......................................................................................................................................... 31 Immunonutrients .................................................................................................................................................. 31 Combination of EN and PN.......................................................................................................................................33 4. Monitoring and Complications .................................................................................................................................34 Monitoring enteral nutrition.....................................................................................................................................34 Tube misplacement and bronchial aspiration .....................................................................................................34 Gastrointestinal dysfunction.................................................................................................................................34 Monitoring of parenteral nutrition...........................................................................................................................35 Catheter-related sepsis (CRS)...............................................................................................................................35 Non-septic complications due to the catheters....................................................................................................36 Metabolic complications of parenteral nutrition .................................................................................................36 Liver abnormalities ...............................................................................................................................................37 Pancreatic disorders..............................................................................................................................................37 Refeeding syndrome..............................................................................................................................................38 5. Nutritional Support for Specific Situations ..............................................................................................................39 Liver failure................................................................................................................................................................39 ARDS and acute respiratory failure..........................................................................................................................39 Renal dysfunction..................................................................................................................................................... 40 Sepsis ........................................................................................................................................................................ 40 Burns.......................................................................................................................................................................... 41 Neurotrauma ............................................................................................................................................................. 41 Catabolic states.......................................................................................................................................................... 41 Obesity .......................................................................................................................................................................42 Perioperative nutrition..............................................................................................................................................43 Conclusion .....................................................................................................................................................................44 Self-assessment..............................................................................................................................................................45 Patient Challenges……………………………………………………………………………………………………………………………………..49 Learning Objectives After studying this module on Nutrition, you should be able to: 1. Determine stress-related metabolic disturbances and rationale for feeding 2. Assess nutritional status and determine nutritional requirements for patients 3. Appropriately order enteral and parenteral nutrition 4. Review monitoring and complications 5. Assess nutritional support for specific situations Introduction INTRODUCTION Severe protein-calorie malnutrition (PCM) is a major problem in many intensive care unit (ICU) patients – in part due to increased catabolism and in 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 with discrepant data and difficult decision-making as to optimal timing and modalities of nutrient administration, estimation of patients' requirements, choice of parenteral or enteral nutrition solutions and feeding formulas, and method of monitoring. The purpose of this module is to provide practical guidelines on these issues. Nutritional care of the ICU patient presents challenges and choices The international guidelines regarding the use of enteral and parenteral nutrition 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 Society for Nutritional Medicine), Ebner C, Hartl W, Heymann C, Spies C; ESPEN (European Society for Parenteral and Enteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Intensive care Clin Nutr. 2006;25(2): 210-23. PMID 16697087 Singer 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 Parenteral Nutrition: intensive care Clin Nutr. 2009;28(4): 387-400. PMID 19505748 Heyland DK, Dhaliwal R, Drover JW, Gramlich L, Dodek P; Canadian Critical Care Clinical Practice Guidelines Committee. Canadian clinical practice guidelines for nutrition support in mechanically ventilated, critically ill adult patients JPEN J Parenter Enteral Nutr. 2003;27(5): 355-73. PMID 12971736 Martindale RG, McClave SA, Vanek VW, McCarthy M, Roberts P, Taylor B, Ochoa JB, Napolitano L, Cresci G; American College of Critical Care Medicine; A.S.P.E.N. Board of Directors. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition: Executive Summary Crit Care Med. 2009;37(5): 175761. Review. No abstract available. PMID 19373044 In this module five key tasks are presented. 1. Stress-Related Metabolic Disturbances And Rationale For Feeding 2. Nutritional Assessment and Requirements 3. Enteral And Parenteral Nutrition 4. Monitoring And Complications 5. Nutritional Support For Specific Situations Task 1. Stress-related metabolic disturbances and rationale for feeding p2 1. STRESS-RELATED METABOLIC DISTURBANCES AND RATIONALE FOR FEEDING The underlying nutritional status of the patient and the complexity of the metabolic response to injury/critical illness provide the basis for nutritional therapy. They are addressed under the headings ‘metabolic alterations in ICU patients’ and ‘rationale for feeding’. Metabolic alterations in ICU patients The metabolic response to injury/sepsis is theoretically characterised by an initial ‘ebb phase’ followed rapidly (< 24h) by a secondary ‘flow phase’. The metabolic disturbances are characterised by moderate to severe hypermetabolism, increased gluconeogenesis with insulin resistance, a large increase in endogenous lipolysis, and net loss of the lean body mass. Cytokines act synergistically with the stress hormones in mediating much of the metabolic disturbances seen after injury, trauma or sepsis. The major mediators involved in the Systemic Inflammatory Response are summarised in the list below, and the details reviewed in the following references. Plank LD, Hill GL. Sequential metabolic changes following induction of systemic inflammatory response in patients with severe sepsis or major blunt trauma World J Surg 2000; 24(6): 630-638. Review. PMID 10773114 Lin E, Calvano SE, Lowry SF. Inflammatory cytokines and cell response in surgery Surgery 2000; 127(2): 117-126. Review. PMID 10686974 Cytokines • Pro-inflammatory. Antiinflammatory • Tumour Necrosis Factor Lipid Mediators • Platelet Activating Factor • Prostaglandins • Thromboxanes (TxA2) • Leukotrienes (LTB4) Opioids and Neuromediators • Enkephalins • β-endorphin • Nitric Oxide Hormones • Thyroxine • Catecholamines • Glucocorticoids • Insulin • Glucagon • Growth Hormone • Insulin-like growth factor 1 • Growth Factors Fibronectin Complement (C3a, C5a, C1q) Enzymes • Proteases • Other lysosomal enzymes Peptides Oxygen Radicals The body's reaction to stress is associated with an elevation in body temperature, in cardiac output and in substrate turnover ICU care may profoundly influence the metabolic response Task 1. Stress-related metabolic disturbances and rationale for feeding p3 rate, all of which should lead to an increase in energy demand. The elevation in energy expenditure (EE), primarily controlled by the counter-regulatory hormones, is directly related to the extent and type of injury/sepsis. For example, minor or localised infections generally have little effect on EE and increases above 5-15% are rarely observed. Elevations of 10-15% are frequently seen in patients presenting with severe infection or multiple trauma. The greatest increases in EE are documented in patients with uncontrolled sepsis, with or without the Acute Respiratory Distress Syndrome (ARDS), and in burn patients. On the other hand, prolonged starvation, severe PCM, physical immobilisation, sedation and/or muscle relaxation associated with critical illness decrease EE by 15-20% and counter the hypermetabolic effects of the underlying injury. Data on EE after severe injury are available in the following reference. Nitenberg G. Nutritional support in sepsis: still skeptical? Curr Opin Crit Care 2000; 6(4): 253-266. PMID 11329509 In the following table, examples are given of adequate energy supply in different clinical situations in the ICU, set against an arbitrary Resting Energy Expenditure of 20 kcal/kg/day. In the table, overweight is defined as a body mass index (BMI) between 25 and 29.9, and obesity as a BMI equal or higher than 30. Weight should be the actual weight of the patients, i.e. before admission to the unit, and mainly before fluid administration. If actual weight is unavailable, use the ideal body weight. Task 1. Stress-related metabolic disturbances and rationale for feeding p4 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 and Enteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Intensive care Clin Nutr 2006; 25(2): 210-223. PMID 16697087 Singer P, Berger MM, Van den Berghe G, Biolo G, Calder P, Forbes A, et al, ESPEN. ESPEN Guidelines on Parenteral Nutrition: intensive care Clin Nutr 2009; 28(4): 387-400. PMID 19505748 Thibault R, Pichard C. Nutrition and clinical outcome in intensive care patients Curr Opin Clin Nutr Metab Care. 2010; 13(2): 177-183. PMID 19996743 Martindale 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 in the adult critically ill patient: Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition: Executive Summary Crit Care Med 2009; 37(5): 1757-1761. Review. No abstract available. PMID 19373044 Q 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 increase EE by no more than 10–15%. Elevations of up to 50% are seen in patients presenting with severe infection or multiple trauma. The greatest increases in EE occur in patients with uncontrolled sepsis, with or without ARDS, and in burn patients. Prior malnutrition and sedation significantly reduce EE. Q Is the degree of hypermetabolism for all patients stable during the ICU stay? Explain your answer A. The course of an ICU patient is rarely uniform, and EE varies according to the secondary insults, infectious or not, complicating the ICU stay. On the other hand, it has 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 progressive active 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% for each 1 degree ° Celsius above 37 °. Conversely, profound sedation, with or without muscular paralysis, is able to totally counteract injury-induced hypermetabolism. Rationale for feeding Progress in intensive care has allowed prolonged survival of patients suffering from protracted catabolic disease such as sustained sepsis and multiple organ dysfunction. This situation has prompted heightened awareness of the importance of optimal nutritional support. The consequences of this support go beyond the supply of energy and proteins to Task 1. Stress-related metabolic disturbances and rationale for feeding p5 the body. Modulation of the host's immune response and the integrity of the gastrointestinal (GI) tract are also beneficially influenced. Feeding during During the initial ICU period, priority is given to management resuscitation is of the patient's cardiovascular and respiratory requirements inappropriate and and control of infection. Nutritional support, however, should may be detrimental be started before the onset of severe metabolic disorders and/or new events (second hits) which can precipitate irreversible Multiple Organ Failure (MOF). In the absence of cardio-respiratory instability, and especially when PCM has preceded ICU admission, nutritional intervention may be started 12-48 hours after admission to ICU if the patient is not expected to cover his/her energy needs by oral intake during the next 72 hours. For the rationale of early nutritional intervention in the ICU patient, see Heyland DK. Heyland DK. Nutritional support in the critically ill patients. A critical review of the evidence Crit Care Clin 1998; 14(3): 423-440. PMID 9700440 Marik PE, Zaloga GP. Early enteral nutrition in acutely ill patients: a systematic review. Crit Care Med 2001; 29(12): 2264-2270. Review. PMID 11801821 When the initial injury does not rapidly lead to death, the patient enters a period of relative stability characterised by hypermetabolism and major muscle catabolism. A state of post-injury wasting sets in, unless countered by nutritional and metabolic support. This state is worsened by bed rest that can lead to the loss of 20% of muscle mass without nutritional support. Nitrogen excretion can reach more than 20 g/day, which represents approximately 600 g of muscle. The duration of this phase varies between a few days and several weeks, according to the severity of the initial injury. Although a universal definition of PCM does not exist, it has Illness and PCM been repeatedly reported that 30-50% of hospitalised patients influence each other suffer from various levels of PCM due to the adverse effects of and can initiate a chronic and acute illnesses. Nutritional status, in turn, is a vicious cycle major determinant of the response to illness; in particular resistance to infection, maintenance of gut and lung function, wound healing. Nutritional support is aimed at limiting the degree of PCM and its consequences, particularly on the immune system and healing processes. It contributes to ‘buying the time’ necessary to restore adequate microcirculation and treat the underlying cause. The approach to metabolic and nutritional support in ICU patients depends on specific circumstances and should be flexible. A general outline of the metabolic alterations of injury and of a ‘phasic’ approach of nutritional support can be found in the following reference. Task 1. Stress-related metabolic disturbances and rationale for feeding p6 Biolo G, Grimble G, Preiser JC, Leverve X, Jolliet P, Planas M, et al; European Society of Intensive Care Medicine Working Group on Nutrition and Metabolism. Position paper of the ESICM Working Group on Nutrition and Metabolism. Metabolic basis of nutrition in intensive care unit patients: ten critical questions Intensive Care Med 2002; 28(11): 15121520. PMID 12415440 Biolo G, Ciocchi B, Stulle M, Bosutti A, Barazzoni R, Zanetti M, et al. Calorie restriction accelerates the catabolism of lean body mass during 2 wk of bed rest Am J Clin Nutr 2007; 86(2): 366-372. PMID 17684207 Nutritional intervention in critically ill patients is unlikely to produce ‘magical’ effects, in terms of morbidity or mortality. Recovery results from the combined effects of optimal therapeutic measures. Task 2. Nutritional Assessment and Requirements p7 2. NUTRITIONAL ASSESSMENT AND REQUIREMENTS The clinical assessment, supplemented by laboratory investigations, guides initial and ongoing nutritional therapy. These considerations are addressed under the headings ‘nutritional assessment’ and ‘nutritional requirements’. Nutritional assessment Nutritional assessment is performed with two goals in mind – to detect signs of PCM (or patients at risk of PCM) and to monitor and modify nutritional support according to need. PCM potentially limits recovery and, in addition, PCMrelated complications are believed to increase medical costs. Nutritional support should, therefore, be monitored with the goal of optimising risk-benefit and cost-efficacy ratios. An ideal clinical marker of nutritional status should be widely available, easily reproducible, highly specific to nutritional state and sensitive to its modifications. Unfortunately, no such marker is available. An ideal marker of nutritional status does not exist Physical signs Several 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 a nutritional point of view because of obesity, fluid movements due to stress, diuretic administration, oedema and ascites. Stable body weight can result from over hydration which masks a loss of body cell mass. Nevertheless, sequential body weight determination offers an integrated picture of all fluid intake and loss that computation of traditional ‘fluid balance’ cannot match. Examine the next ten ICU patients for features of PCM and relate such changes to eventual clinical outcome. Biological markers Serum protein Biological markers of PCM suffer from various shortcomings in levels have little ICU patients. Plasma albumin, transthyretin, transferrin, value in initial retinol-binding protein, fibronectin and insulin-like growth nutritional factor-1 have been used to assess nutritional status. However, assessment. the intravascular concentration of these factors mostly reflects Changes in levels, the net balance between hepatic synthesis, distribution and however, may be degradation. Stress and trauma-related hormones or infectionimportant related cytokines interact with amino acids and micronutrients to regulate the levels of the above-mentioned anabolic proteins together with acute phase proteins, such as C-reactive protein and alpha-1 glycoprotein acid. Low serum albumin is often correlated with a poor prognosis in hospitalised patients, but it is a weak short-term marker of the evolution of nutritional status Task 2. Nutritional Assessment and Requirements p8 because of its long half-life (20 days). Transferrin, transthyretin, and fibronectin, on the other hand, are sensitive to rapid changes of nutritional state and have shorter half-lives (7 days, 2 days and approximately 4 hours, respectively), but their serum levels are also markedly influenced by acute stress, transcapillary escape and the inflammatory response. Measurements of body composition by determination of skinfold thickness and arm muscle circumference, or by bioelectrical impedance analysis suffer from various shortcomings in ICU patients and are generally not relevant. Nutritional indices Since no single parameter adequately identifies PCM, nutritional indices integrating a number of parameters have been developed. These include the Instant Nutritional Assessment and the Prognostic Inflammatory and Nutritional Index. These examples are actually risk indices and should only be applied to patients in whom all items are applicable. Globally, the complexity and cost of these indices have rendered them obsolete except for research projects. For more information on nutritional indices, refer to the following references. Sungurtekin H, Sungurtekin U, Oner O, Okke D. Nutrition assessment in critically ill patients Nutr Clin Pract. 2008;23(6): 635-41. PMID 19033223 Downs JH, Haffejee A. Nutritional assessment in the critically ill Curr Opin Clin Nutr Metab Care. 1998;1(3): 275-9. Review. PMID 10565360 Nitrogen (N) balance In ICU patients, major non-urinary N losses may result from protein-losing bowel disease, extensive burns, renal replacement therapy, or high-output abdominal drains. Nitrogen balance becomes negative (–5-30 g/day), reflecting major protein catabolism. In practice, calculation of N balance is mainly aimed at 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 lost in skin and stool per day)]. Urinary N is usually directly measured by chemiluminescence or derived from routinely measured urinary urea using the following formula: Urinary N = [urinary urea (g/ 24h) / 2.14] + 2 to 4 g. The latter constant is an estimation of non-urea urinary losses of nitrogen (in the absence of nephrotic syndrome), and should not be confounded with losses from skin/stool. Urinary N should be measured in a 24-hour urine collection but in emergency a four hour collection may suffice. Exact determination of the duration and volume of the urine collection is crucial for accurate calculation of N balance. Mmol of urea may be converted to g using the following formula: Urea (g)=urea (mmol)/20.36 and 6.25 g of protein equals 1 g of N. Task 2. Nutritional Assessment and Requirements p9 Measure nitrogen balance in five of your patients and relate your findings to the nutritional support provided. Measurement of body composition Bioimpedance analysis (BIA) is a widely used method of body composition assessment, but its accuracy is limited in ICU patients due to rapid changes in electrolyte and fluid balance, themselves related to the severity of the disease. Therefore the measurement of body composition with this method is not recommended during the acute phase of critical illness. However, during the post-acute phase and the recovery phase, BIA can contribute to the assessment and the follow-up of nutritional status if the hydration status remains stable. Kyle UG, Bosaeus I, De Lorenzo AD, Deurenberg P, Elia M, Manuel Gómez J, et al. ESPEN Bioelectrical impedance analysis-part II: utilization in clinical practice. Clin Nutr 2004; 23: 1430-1453. PMID 15556267 Electrolytes PCM is associated with substantial gains of extra-cellular water and sodium gains, as well as changes in potassium, magnesium, calcium and phosphorus concentrations. These parameters should be initially assessed, and then corrected according to the severity of the observed changes. Special attention should be paid to the risk of early deficiencies in intracellular phosphorus, magnesium and potassium, even though plasma concentrations of these elements may remain normal. Trace elements, vitamins, hormones, enzymes Plasma concentrations of trace elements, vitamins, hormones and enzymes poorly reflect tissue concentrations. Determination of these parameters is only useful for metabolic research purposes or to confirm a clinical diagnosis (e.g. suspicion of Addison's disease, or B and C vitamin deficiencies in severe alcoholism). Practical assessment of nutritional status A practical approach to detecting PCM in critically ill patients is as follows: Patient history and clinical setting • Diseases associated with increased risk of malnutrition (e.g. chronic debilitating disease) • History of chronic low food intake, drug abuse, alcoholism, chronic psychiatric disorders Task 2. Nutritional Assessment and Requirements p10 • Diseases associated with hypermetabolism and prolonged catabolic activity (e.g. polytrauma, burns, persistent fever, sepsis, multiple organ failure) Clinical and anthropometric assessment • Signs of malnutrition on physical examination (e.g. cachexia, muscle atrophy, oedema) • Recent severe body weight loss (≥5% of usual body weight in one month or ≥ 10% in three months) • Body mass index (body weight in kg/(height in m2)) < 18.5 kg/m2 Biochemical 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: a practical approach. A position paper. Clin Nutr 1999; 18: 47-56). ESPEN Assess nutritional status in five of your patients at least two of whom should have PCM. Q Which factors of the clinical history will point to the risk, or the reality, of malnutrition? A. History of chronic low food intake Alcoholism Significant recent weight loss (≥ 5% of usual body weight in one month or ≥ 10% in three months) Chronic diarrhoeal or debilitating disease Drug abuse Q List two signs on physical examination indicating probable malnutrition. A. Muscular atrophy Loss of subcutaneous fat Oedema (in the absence of cardiovascular or renal disease) Mucosal lesions, including glossitis and skin rashes THINK 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 (see above). Task 2. Nutritional Assessment and Requirements p11 Q What formula allows conversion of urea to nitrogen in order to calculate 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 requirements Optimal calorie and nitrogen requirements from nutritional support are difficult to define accurately. In addition, this approach is often complicated in critically ill patients by glucose and protein intolerance as well as the risk of fluid overload. Energy and macronutrient requirements A variety of techniques are available for evaluating energy needs but all have drawbacks in the critically ill patient. The reference method to evaluate energy needs consists of the measurement of energy expenditure by indirect calorimetry, which requires costly equipment and technical skills not widely available. The method is time-consuming, and is limited in patients under mechanical ventilation to those with an inspired oxygen concentration (FiO2) lower than 0.6-0.7. Some ventilators are currently sold with the ability to directly measure energy expenditure. However it is important to note that this method has never been validated 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 -4834 MV = minute ventilation in L/min, BT = body temperature in ⁰C 1kcal=4.184 kJ. The Harris-Benedict may be inaccurate in ICU patients for reasons discussed in detail in the following references. Walker RN, Heuberger RA. Predictive equations for energy needs for the critically ill. Respir Care 2009;54:509-21. PMID 19327188 Task 2. Nutritional Assessment and Requirements p12 McEvoy CT, Cran GW, Cooke SR, Young IS. Resting energy expenditure in nonventilated, non-sedated patients recovering from serious traumatic brain injury: Comparison of prediction equations with indirect calorimetry values. Clin Nutr 2009; 28: 526-32. PMID 19423202 Faisy C, Guerot E, Diehl JL, Labrousse J, Fagon JY. Assessment of resting energy expenditure in mechanically ventilated patients. Am J Clin Nutr 2003; 78: 241-9. PMID 12885704 Flancbaum L, Choban PS, Sambucco S, Verducci J, Burge JC. Comparison of indirect calorimetry, the Fick method, and prediction equations in estimating the energy requirements of critically ill patients. Am J Clin Nutr 1999; 69 : 461-466. PMID 10075331 In practice, a pragmatic estimate of total energy requirements is 25-35 (20-30 non-protein) kcal/kg/day in males and females, respectively. 10% should be added to energy needs for every degree of body temperature >37˚ C. Link to ESICM Flash Conference: Pierre Singer, ‘How do I evaluate energy requirements?’ ESICM congress, Vienna 2009 The main goal of nitrogen supply is to limit muscle catabolism, while maintaining an adequate nutrient supply to the liver. The body weight used for this computation should be the mean between ideal and measured weights in severely malnourished patients, and 20% higher than ideal weight in obese patients. It must be stressed that, in this context, equilibrium or positivity of nitrogen balance is not an end in itself and can even be detrimental if it leads to an accumulation of urea. It is generally accepted that protein intake should vary between 1.2 and 1.5 g/kg/day, and should certainly not exceed 2.0 g/kg/day except in patients with substantial losses (e.g. extensive burns, GI and/or urinary losses, etc.). For EN, standard polymeric diets, and for TPN, conventional crystalline amino acid solutions can be used. The requirements are modified 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 and lipid intakes between 0.5 to ≤ 2 g/kg/day. When oral or enteral intakes are possible, the lipid and carbohydrate requirements are the same as for healthy subjects, i.e. 30-35 % of total calorie intakes as lipids and 50-55% as carbohydrates. Identify all patients requiring nutritional support in your ICU for a week and determine appropriate initial prescription and the pathway to achieving caloric goal. Q Estimate the energy expenditure of a febrile (38.5 °C) 60-year-old man admitted to the ICU with a diagnosis of pneumonia; treatment includes mechanical ventilation. His body weight and height are 76 kg and 173 cm respectively. Task 2. Nutritional Assessment and Requirements p13 A. Resting energy expenditure (REE) can be calculated using the Harris-Benedict formula: REE = 66 + (13.75 x 76) + (5 x 173) - (6.76 x 60) = 1571 kcal/day (other formulae are available, and give approximately the same result). 10% increase in EE per ° Celsius above 37 °C = 1571 x 0.15 = 235 kcal Mechanical ventilation partially offsets the increase in EE due to fever, so that EE for this 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 are recommended for a 60-year-old woman (weight and height 56 kg and 162 cm respectively), with a chronic proteinuria of 25 g/day? A. Basal requirements = 1.5 x 56 = 84 g protein/day Replacement of renal losses is recommended (as is replacement of protein losses during haemodialysis or continuous venovenous haemofiltration (CVVH) Total protein requirements = 84 + 25 = 109 g/day Micronutrient requirements Minimal daily Trace elements and vitamins, also known as micronutrients, requirements of play an important role in various enzyme-catalysed key micronutrients should be reactions, many of which exhibit increased activity during the routinely administered by inflammatory response associated with critical illness. means of commercially Concomitantly, some critical conditions such as prolonged available, preparations. diarrhoea and extensive burns or treatments such as Supplementation is unnecessary when intake haemodialysis are accompanied by increased losses of trace occurs with ≥ 1000 kcal of elements, such as zinc and selenium. Requirements for vitamins B1 and B6 are considerably increased by sepsis and by commercial enteral formulas already enriched PN, particularly in malnourished patients, and Vitamin B1 with micronutrients. (about 100 mg/day) is essential to avoid lactic acidosis and other complications such as beri-beri, Korsakoff syndrome and Wernicke’s encephalopathy. Some vitamins, such as vitamins C, E and A are likely to prevent or counteract the cell damage caused by free radicals, which are generated during ischemia/reperfusion. When daily caloric intake of less than 1000kcals lasts for several days, or in severe conditions combining increased needs and large losses of trace elements, intravenous administration of vitamins B1, B6, C, E and A may be beneficial (see Task 2 sub-heading Practical assessment of nutritional status). Micronutrient requirements in critically patients are outlined in the following list. Vitamins Standard 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 I Task 2. Nutritional Assessment and Requirements p14 • • Zn (15-20 mg/day plus 10 mg/l of liquid stool) Se (120 mg/day) Electrolytes Based on clinical assessment of the patient’s volume, acid-base status and on daily plasma concentration (Na+, K+, Ca++) • P 2- (>16 mmol/day) • Mg 2- (>200 mg/day; 8.3 mmol) of specific nutritional needs Berger MM, Shenkin A. Update on clinical micronutrient supplementation studies in the critically ill. Curr Opin Clin Nutr Metab Care 2006;9:711-6. PMID 17053424 Berger MM, Chioléro RL. Antioxidant supplementation in sepsis and systemic inflammatory response syndrome. Crit Care Med. 2007;35(9 Suppl):S58490. PMID 17713413 By contrast, the administration of vitamin A and manganese should be avoided in those with severe liver insufficiency or unexplained liver enzyme abnormalities. Q Which vitamin is essential to avoid lactic acidosis due to PN in ICU patients? Please explain your answer. A. Vitamin B1 (about 100 mg/day) is essential to avoid lactic acidosis and other complications such as beri-beri, Korsakoff syndrome and Wernicke's encephalopathy. Particular attention should be paid when starting glucose administration to severely malnourished patients and patients with chronic alcoholism. Q All critically ill patients should receive vitamins and trace elements. Name two conditions when additional supplementary micronutrients should be considered in critically ill patients. A. High output intestinal fistulae Severe burns Severe inflammatory and septic diseases Multiple trauma ARDS Q Name two micronutrients with proven antioxidant properties. A. Vitamin A and β-carotene Vitamin E Vitamin C Selenium Task 3. Enteral and Parenteral Nutrition p15 3. ENTERAL AND PARENTERAL NUTRITION Nutritional therapy/support is effected via the enteral or parenteral approach. Indications and contraindications are initially outlined and then the practical considerations, including the prescriptions, relating to each of the enteral and the parenteral routes are detailed separately. Indications and contraindications Hinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. Saunders Ltd; 2008. ISBN: 978-0-7020259-6-9. p. 301 (Nutritional Support) Nutritional support is indicated for any critically ill patient in whom oral intake is not expected to cover the full energy needs in the first three days following ICU admission. The enteral route is recommended as the first-line nutritional support (ESPEN guidelines). In patients suffering from pre-existing PCM, parenteral nutrition should be initiated as soon as possible if EN is not feasible (ASPEN guidelines). The main indications and contraindications to nutritional support are summarised in the following list. Evidence-based indications • Well-nourished patients in whom oral intake is not expected to cover the full energy needs in the three days following ICU admission, including patients with prolonged fasting or insufficient oral intake. • Pre-existing malnutrition, whatever the aetiology, in a patient unable to cover their full energy needs by oral intake. Pragmatic indications • Severe stress in patients expected to be unable to eat for 5-7 days or more • Severe trauma and burns • After small bowel resection – especially if resection substantial or complicated • Resumption of gastrointestinal tract activity and preparation for oral feeding Although debate continues, the concept that EN should be the preferred route of feeding whenever possible has gained wide acceptance. Indeed, complete bypass of the gut leads to adverse structural and functional changes in the mucosal barrier, which can be reversed by EN. The advantages of enteral and parenteral nutrition are summarised below: Advantages of enteral nutrition: • Favours intestinal villous integrity and function, and reduces gut hyperpermeability • Maintains GI tract functions including Gut-associated Lymphoid Tissue (GALT) and Mucosa-associated Lymphoid Tissue (MALT) and production and secretion of IgA and hormones. 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 animals but not clearly relevant in humans) Avoids infectious complications associated with parenteral nutrition Reduces the risk of metabolic complications associated with parenteral nutrition: hyperglycaemia, insulin resistance, hypertriglyceridemia, fatty liver Less costly than parenteral nutrition Advantages 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 development of MOF and overwhelming sepsis in ICU patients? A. This question is highly controversial. There is often confusion between increased intestinal permeability for sugar probes – a common finding in the critically ill – and bacterial translocation, which has been shown to occur in a variety of clinical conditions. There is no correlation between bacteria in the mesenteric lymph nodes and MOF. To date no evidence exists for a cause and effect relationship between gut failure and generalised sepsis, MOF or death, especially in the absence of an identifiable source of infection. Hinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. Saunders Ltd; 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 the references below. Jeejeebhoy KN. Enteral and parenteral nutrition: evidence-based approach Proc Nutr Soc 2001; 60(3): 399-402. Review. PMID 11681815 Thibault R, Pichard C. Nutrition and clinical outcome in intensive care patients Curr Opin Clin Nutr Metab Care 2010; 13(2): 177-183. PMID 19996743 The contraindications to enteral and parenteral nutrition are detailed below: Contraindications to enteral nutrition Absolute • Adequate oral intakes (more than 80% of the energy target) • Non-functional gut: anastomotic disruption, lower GI obstruction, gut ischaemia/necrosis Absolute contraindications to • Generalised peritonitis nutritional support are rare, • Uncontrolled severe shock states except during the initial phase of resuscitation in severe illness Task 3. Enteral and Parenteral Nutrition p17 Relative • Expected period of fast ≤5 days, except in severely injured patients • Abdominal distension/severe protracted diarrhoea • Localised peritonitis, intra-abdominal abscess, active upper GI tract haemorrhage • 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, liver failure) • Terminal disease • Dementia, agitation, confusion Contraindications to parenteral nutrition Absolute • Adequate oral intake • Enteral nutrition feasible and covering more than 60% of the energy target within the three days following admission • Uncontrolled severe shock states Relative • 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, liver failure) • Incompatibility between intravenous drugs and parenteral nutrition solution in the absence of multiple port catheters • Dementia, agitation, confusion Adapted from: Kreymann KG, Berger MM, Deutz NE, Hiesmayr M, Jolliet P, Kazandjiev G, Nitenberg G, van den Berghe G, Wernerman J; DGEM (German Society for Nutritional Medicine), Ebner C, Hartl W, Heymann C, Spies C; ESPEN (European Society for Parenteral and Enteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Intensive care Clin Nutr. 2006;25(2): 210-23. PMID 16697087 Singer 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 Parenteral Nutrition: intensive care Clin Nutr. 2009;28(4): 387-400. PMID 19505748 Jolliet P, Pichard C, Biolo G, Chioléro R, Grimble G, Leverve X, et al.Enteral nutrition in intensive care patients: a practical approach. Clin Nutr. 1999; 18(1): 47-56.PMID 10459065 Nevertheless, problems linked to EN in ICU patients, such as functional ileus, gut failure, bacterial overgrowth, risk of nosocomial pneumonia, and technical problems with jejunal feeding, must be kept in mind. In patients with poor intestinal perfusion, due to prolonged or severe shock states, and unable to sustain digestion and nutrient absorption, EN should be PN should replace EN if patients develop major intolerance or other contraindication Task 3. Enteral and Parenteral Nutrition p18 administered with caution, and supplemented with or, if necessary, substituted by PN, to allow nutritional requirements to be met and to minimise excessive muscle wasting. Varga P, Griffiths R, Chiolero R, Nitenberg G, Leverve X, Pertkiewicz M, et al. Is parenteral nutrition guilty? Intensive Care Med 2003; 29(11): 18611864.PMID 14669752 Although animal studies indicate that the association between mucosal atrophy and an increase in gut permeability can induce translocation of bacteria from the gut lumen to the circulation, no proof exists that 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 the gastric residual volumes. Task 3. Enteral and Parenteral Nutrition p19 All around the world, cisapride has been taken off the market, due to concerns about side effects and drug interactions. There is no consensus about the amount of gastric residual volume that should 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 be checked, but once a day makes sense. Task 3. Enteral and Parenteral Nutrition p20 Poulard F, Dimet J, Martin-Lefevre L, Bontemps F, Fiancette M, Clementi E, Lebert C, Renard B, Reignier J. Impact of not measuring residual gastric volume in mechanically ventilated patients receiving early enteral feeding: a prospective before-after study. JPEN J Parenter Enteral Nutr 2010; 34(2): 125-130. PMID 19861528 Moreira TV, McQuiggan M. Methods for the assessment of gastric emptying in critically ill, enterally fed adults Nutr Clin Pract 2009; 24(2): 261-273. Review. PMID 19321900 Optimal combination of enteral and parenteral nutrition Q What is the only (temporary) contraindication to nutritional support? A. Severe shock prior to haemodynamic and respiratory stabilisation. Q Specify at least three reasons why patients should be fed enterally rather than parenterally? Explain your answer. A. Maintenance of gut integrity Prevention of bacterial (or endotoxin) translocation (not proven) Maintenance of adequate splanchnic blood flow Maintenance of adequate immune functions of the gut Avoidance of catheter-related sepsis Cost-savings Q Specify one situation in which PN is preferable to EN. Explain your answer. A. Bowel obstruction Mesenteric infarction and/or complete gut failure Very short bowel (<70 cm) Peritonitis (relative contraindication) Task 3. Enteral and Parenteral Nutrition p21 Enteral nutrition: routes and formulas Enteral nutrition may be administered through a nasogastric or nasojejunal tube, or through percutaneous routes such as gastrostomy or jejunostomy. Hinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. Saunders Ltd; 2008. ISBN: 978-0-7020259-6-9. p.302 (Administration followed by Choice of Feed p.303) Schmidt H, Martindale R. The gastrointestinal tract in critical illness: nutritional implications. Curr Opin Clin Nutr Metab Care 2003; 6(5): 587-591.PMID 12913678 Nasogastric route Gastric feeding provides the most normal route for enteral nutrition, but poor tolerance of gastric feeding in the critically ill patient is common. Tolerance is essentially limited by the severity of disease. In these circumstances, it may be difficult to maintain an infusion rate higher than 1000 ml/24 hours and a global energy load higher than 1500 kcal/day. Use of prokinetics decreases (but does not eliminate) the incidence of aspiration in the presence of a competent pyloric sphincter. Gastrostomy or post-pyloric positioning of the feeding tube does not decrease the risk of aspiration. The nasogastric route is used for the majority of enteral nutrition in ICU patients, for short (<2 weeks) and intermediate terms (<4 weeks). When aspiration of gastric contents is not necessary (e.g. prior to endotracheal intubation), small diameter (6-12 Fr.) silicone or polyurethane tubes are preferred to larger tubes because they are more comfortable and associated with less naso-pharyngeal trauma. Their length varies according to preferred site (stomach 90 cm, duodenum 110 cm, jejunum at least 120 cm). The majority of tubes for EN are radiopaque and can therefore be seen on chest radiography. Spontaneous transpyloric passage of enteral tubes in critically ill patients is commonly unsuccessful even when gut prokinetics are intravenously administered (metoclopramide, erythromycin, cisapride). Nasoenteral tubes with inner stylets are therefore recommended for postpyloric EN placement, which can be routinely placed via ‘blind bedside’ technique, with a success rate ranging from 70% to more than 90%. In some instances, the procedure has to be performed either under fluoroscopic guidance (at the bedside using portable equipment) or with endoscopic assistance. Recently, ‘self-propelling’ nasoenteral tubes) have been developed and are currently being evaluated. The position of the nasoenteral tube could be controlled by transnasal re-endoscopy as recently shown in the following reference. Task 3. Enteral and Parenteral Nutrition p22 Wiegand N, Bauerfeind P, Delco F, Fried M, Wildi SM. Endoscopic position control of nasoenteral feeding tubes by transnasal re-endoscopy: a prospective study in intensive care patients Am J Gastroenterol. 2009; 104(5): 1271-1276. PMID 19319127 Although frequently advised, the clinical benefits of duodenal placement of the nasogastric tube have never been clearly demonstrated. Hsu CW, Sun SF, Lin SL, Kang SP, Chu KA, Lin CH, Huang HH. Duodenal versus gastric feeding in medical intensive care unit patients: a prospective, randomized, clinical study Crit Care Med 2009; 37(6): 1866-1872. PMID 19384225 An abdominal radiograph is strongly recommended after placement of a nasogastric tube. In US, it is only required for the smaller bore feeding tubes. X-ray should 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 lower oesophagus, and silent intrabronchial or tracheal placement have all been recorded. To reduce the risk of bronchoaspiration, tolerance to gastric feeding should be monitored e.g. by measuring gastric residual volume at least once per day (see figure p.19), especially in unintubated, comatose or sedated patients. Percutaneous route Percutaneous endoscopic gastrostomy (PEG) tube placement has become common for ICU patients requiring prolonged EN support (≥4-6 weeks) especially when there is intolerance or complications of NG tubes. Tubes in the range of 9 to 24 F are available. This procedure should be considered in patients who have normal gastric emptying and no sign of gastrointestinal intolerance and can be performed at the bedside in the ICU. The methods and clinical utility for measuring of gastric emptying are discussed in the following reference. Moreira TV, McQuiggan M. Methods for the assessment of gastric emptying in critically ill, enterally fed adults Nutr Clin Pract. 2009; 24(2): 261-273. Review. PMID 19321900 If postpyloric feeding is necessary in such patients, percutaneous endoscopy (PEJ) or radiology-guided jejunostomy may be performed. Task 3. Enteral and Parenteral Nutrition p23 PEJ utilises the same approach as for PEG but after tube insertion into the stomach the tube is guided into the duodenum under endoscopic control. Surgical placement of a gastrostomy or jejunostomy is usually performed as the last phase of gastrointestinal surgery (gastrectomy, pancreatectomy), the goal being to administer perioperative nutritional support. Selection of gastrostomy, needle-catheter jejunostomy or transgastric jejunostomy depends on the primary diagnosis, the status of the patient, and hospital facilities and skills. The insertion of a percutaneous gastrostomy or a jejunostomy must be avoided in those with uncontrolled hyperthermia or infections. A delay of 7 days without any fever is warranted to limit the risk of abdominal abcess. The procedure of percutaneous gastrostomy or jejunostomy is covered by an antibiotic prophylaxis. Relative contraindications for gastrostomy or jejunostomy are: ascites, portal hypertension, local abdominal infectious problems, gastroparesis, poor gastric emptying, gastric cancer, gastric ulcer, previous laparotomy and coagulation disorders. All the issues relating to the technical aspects of EN are extensively discussed in the following reference. Gopalan S, Khanna S. Enteral nutrition delivery technique Curr Opin Clin Nutr Metab Care 2003; 6(3): 313-317. Review. PMID 12690265 Q Name two conditions contraindicating percutaneous gastric positioning of enteral feeding tube. A. Ascites Gastric cancer/ulcer Severe coagulation disorders Poor gastric emptying or gastroparesis Q List three criteria prompting the performance of a gastrostomy in an ICU patient. A. Enteral nutrition planned for longer than 4–6 weeks Mechanical obstruction or severe mucosal oesophageal lesions Patient intolerance of nasogastric tube. Enteral nutrition formulas Standardised, commercially produced formulas are recommended, in the form of iso-osmotic (approximately 300 Fibre-enriched polymeric solutions are theoretically more physiological. Elemental formulas are not indicated in adult patients Task 3. Enteral and Parenteral Nutrition p24 mosm/l) polymeric solutions containing 1-1.5 kcal/ml, 45-60% of which should be in the form of carbohydrates, 20-35% as lipids, and 15-20% as proteins. Solutions are gluten and lactosefree. Polymeric EN solutions contain homogenised substrates similar to those found in normal nutrition. The type of feeding preparations available for enteral nutrition are listed below. These preparations generally contain between 500-1000 kcal/500 ml and 23-45 g protein/500 ml. There are no available data to recommend the use of semielemental solution in ICU patients, even in those with severe malabsorption or gut dysfunction. However, in a situation of proven or suspected intestinal malabsorption, a semi-elemental EN solution may be introduced in patients with severe and persistent diarrhoea associated with the administration of a polymeric solution. Nitrogen free amino-acids Carbohydrate glucose or oligosaccharide s Semielemental Peptides (hydrolised proteins) oligosaccharide s Polymeric Whole protein polysaccharides Elemental * Lipid mediumchain triglycerid es mediumchain triglycerid es long-chain triglycerid es Fibre none none availa ble *not available in all European countries More details on the composition of enteral diets can be found in the following reference. Kreymann KG, Berger MM, Deutz NE, Hiesmayr M, Jolliet P, Kazandjiev G, Nitenberg G, van den Berghe G, Wernerman J; DGEM (German Society for Nutritional Medicine), Ebner C, Hartl W, Heymann C, Spies C; ESPEN (European Society for Parenteral and Enteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Intensive care Clin Nutr. 2006;25(2): 210-23. PMID 16697087 Modified formulas containing increased proportions of lipids Semi-elemental solutions and less carbohydrate (to reduce CO2 production in acute may facilitate digestion respiratory failure), or reduced protein content or increased and absorption in a branched-chain amino-acids (for patients with acute renal or minority of patients with hepatic failure) have been developed. No convincing data, severe gut dysfunction however, support their use. Prescription of enteral nutrition Various techniques for administration of EN are available. We recommend the use of 500 mL bottles/cans: this option facilitates storage, manipulation and organisation at the bedside. Furthermore, the use of 1-2 L containers leads to a waste of feeding solution if only part of the solution can be administered due to changes in the rate of administration or relative intolerance. There is also an increased risk of bacterial contamination if large containers are left connected to Task 3. Enteral and Parenteral Nutrition p25 the patient for prolonged periods (>24h), unless a closed system is used, at an increased cost. Finally, the tubing connecting the container to the patient's feeding tube should be specific to EN (not interchangeable with an IV connection) and changed once a day, to minimise the risk of bacterial contamination. Tolerance to EN can be improved by progressive increase of the feed volume prescription (e.g. 25-50 ml/h during the first 24h, then 25 ml/h or 500 ml daily step by step increase), by providing sufficient intraluminal sodium (above 80 mmol/L of diet) and by prokinetic drug administration such as metoclopramide or erythromycin. For more information about the respective advantages of these prokinetics, see the following reference. Röhm KD, Boldt J, Piper SN. Motility disorders in the ICU: recent therapeutic options and clinical practice Curr Opin Clin Nutr Metab Care. 2009;12(2): 161-7. Review. PMID 19202387 There 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 tolerance to EN. Thus, a quality assurance programme can be implemented and has been shown to improve the risk-benefit ratio of EN in the critically ill. Design an EN regimen for five of your newly admitted patients and compare your suggested formulation with that prescribed. Overly enthusiastic EN prescription may result in aspiration, aggravated gut ischemia, dangerous intestinal distension and diarrhoea, especially when the infusion rate is greater than 100 ml/h. Q Why should polymeric enteral feeds be preferred to semielemental feeds? A. Polymeric products mimic standard food, stimulate the gut mucosa and GI tract functions, can be enriched with fibre, are less expensive and tend to be better tolerated than 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 a reduction in gut mucosa stimulation). Gut allergy to macromolecules such as protein (because semi-elemental diet contains hydrolysed peptides). Q What is an abnormal gastric residual volume during EN? Task 3. Enteral and Parenteral Nutrition p26 A. Volumes exceeding 500 mL. However this figure remains controversial in the literature. Q What are the recommended dosages of metoclopramide and erythromycin as prokinetic drugs? A. 6 mg erythromycin/kg/day (IV route) 10 mg metoclopramide TID (IV route) Early enteral nutrition Early EN may decrease mortality, infectious morbidity and reduce both length of stay and overall costs – all highly favourable effects. Thanks to these beneficial effects, EN has been proven superior to PN particularly in patients with major trauma and in GI surgery – mainly in relation to the increased infection rate in severe and septic ICU patients. The institution of EN is frequently and erroneously delayed by radiologic or endoscopic examinations, GI intolerance (prolonged gastric emptying, regurgitation of enteral feeds, diarrhoea). Under these circumstances EN and PN appear to give similar results. Indeed, the timing of the initiation of the nutritional support seems to be more critical than the root of administration. Early PN is associated with reduced infection rates and mortality in comparison with delayed EN. Even small amounts (250-500 ml/day) of EN started early can be beneficial Thibault R, Pichard C. Nutrition and clinical outcome in intensive care patients Curr Opin Clin Nutr Metab Care 2010; 13(2): 177-183. PMID 19996743 Biffl WL, Moore EE, Haenel JB. Nutrition support of the trauma patient. Nutrition 2002; 18(11-12): 960-965. PMID 12431718 Bisgaard T, Kehlet H. Early oral feeding after elective abdominal surgery--what are the issues? Nutrition 2002; 18(11-12): 944-948. Review. PMID 12431715 Q. List three clinical conditions in which enteral nutrition carries a high risk of complications. A. Vomiting (risk of bronchoaspiration). Sphenoidal fracture (risk of nasogastric tube malposition). Clearly patients with these fractures should not undergo blind placement of nasoenteric tubes to avoid malposition, but many of these patients can be fed enterally as long as their GI tract can be accessed safely. Severe ileus (risk of intestinal distension and/or intestinal rupture). Pharmacomodulation Hinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. Saunders Ltd; 2008. ISBN: 978-0-7020259-6-9. p.303-305 Immunonutrition Task 3. Enteral and Parenteral Nutrition p27 On the assumption that modification of EN might reverse the immunosuppression and modulate the inflammatory status related to PCM and/or injury, the innovative concept of pharmaconutrition has been introduced. Enrichment of conventional nutritive mixtures with arginine, glutamine, omega-3 fatty acids, nucleotides, antioxidants, etc., has been proposed over the last two decades. Six currently available products are listed below. Pharmaconutrition is the use of nutrients for their abilities to modulate inflammatory and/or immune response, healing or endocrine function, independently from their nutritional properties. High-risk patients after major elective abdominal surgery, patients with multiple trauma, burns >30% of body surface area and possibly some medical ICU patients on mechanical ventilation may benefit from pharmaconutrition, if patients are without severe sepsis and if pharmaconutrition is initiated immediately after ICU admission. Current evidence does not support routine immunonutrition in all ICU patients Several randomised trials suggest that supplementation of EN solutions with omega 3 fatty acids improved clinical outcome (reduced mortality, reduced length of ICU and hospital stay, reduced duration of mechanical ventilation) f of critically ill patients with ARDS. A grade A recommendation has been given by ESPEN for the use of EN or PN supplemented with omega 3 polyunsaturated fatty acids in this group of patients. Link to ESICM Flash Conference: Pierre Singer, ‘Are omega 3 fatty acids safe for critically ill patients?’ ESICM congress, Vienna 2009 Task 3. Enteral and Parenteral Nutrition p28 There is not enough data to recommend the systematic use of antioxidant micronutrient in the setting of ICU, except in severe burns – see specific paragraph 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 and Enteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Intensive care Clin Nutr 2006; 25(2): 210-223. PMID 16697087 Singer 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 Parenteral Nutrition: intensive care Clin Nutr 2009; 28(4): 387-400. PMID 19505748 Heyland DK, Novak F, Drover JW, Jain M, Su X, Suchner U. Should immunonutrition become routine in critically ill patients? A systematic review of the evidence. JAMA 2001; 286(8): 944-953. Review. PMID 11509059 Montejo 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 and consensus statement Clin Nutr. 2003;22(3): 221-33. Review. PMID 12765660 Singer P, Shapiro H.Enteral omega-3 in acute respiratory distress syndrome. Curr Opin Clin Nutr Metab Care 2009; 12(2): 123-128. Review. PMID 19202383 [No authors listed]. Consensus recommendations from the US summit on immune-enhancing enteral therapy. JPEN J Parenter Enteral Nutr 2001; 25(2 Suppl): S61-63. PMID 11288926 Parenteral nutrition: routes and formulas Two large meta-analyses involving 19 randomised or quasi-randomised trials suggest that PN is associated with slightly increased morbidity and is mainly beneficial in those surgical patients who are malnourished prior to ICU admission, but does not contribute to reduced morbidity or mortality in ‘true’ critically ill patients. On this basis, PN should only by used when EN is contraindicated (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/necrosis Generalised peritonitis Severe shock states Patient unable to eat adequate amounts of food Route of access Hinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. Saunders Ltd; 2008. ISBN: 978-0-7020259-6-9. p .306 Administration Task 3. Enteral and Parenteral Nutrition p29 The vast majority of PN solutions are hyperosmotic and necessitate central venous administration. Central catheter insertion and maintenance require strict adherence to aseptic and antiseptic protocols in order to reduce the risk of catheterrelated infection, which has become in the recent years a less important problem of PN in critically ill patients. Subclavian vein access is recommended. Subcutaneous tunnelling of internal jugular and femoral catheters reduces infection Pronovost P, Needham D, Berenholtz S, Sinopoli D, Chu H, Cosgrove S, et al. An intervention to decrease catheter-related bloodstream infections in the ICU. N Engl J Med 2006; 355: 2725-2732. PMID 17192537 In particular, the tubing connecting the PN bag to the patient's catheter should be changed once per day to avoid bacterial contamination. O'Grady NP, Alexander M, Dellinger EP, Gerberding JL, Heard SO, Maki DG, et al; Healthcare Infection Control Practices Advisory Committee. Guidelines for the prevention of intravascular catheter-related infections. Am J Infect Control 2002; 30(8): 476-489. PMID 12461511 PN may also be given by peripherally inserted venous catheters, midline finebore catheters (for PN expected to exceed six days) and by standard short cannulae. For peripheral PN, a Teflon or polyurethane catheter should be selected, placed in an upper extremity site preferably, and changed every 3 or 4 days to minimise the risk of phlebitis and infection. With peripherally inserted catheters, full provision of nutritional needs is only possible if 2.5 to 3.5 litres of iso- to slightly hyperosmotic (≤900 mosm/l) solutions can be tolerated. Use of a single lumen polyurethane or silicone catheter is preferable, unless one port of a multi-lumen catheter is exclusively assigned to PN administration. The risk of drug incompatibility is thereby reduced. Routine replacement of central catheters in a new site or by guide wire exchange increases the risk of mechanical complications. Contrary to previous studies, the guide-wire catheter replacement did not increase the risk of infection. Randolph AG, Cook DJ, Gonzales CA, Brun-Buisson C. Tunneling short-term central venous catheters to prevent catheter-related infection: a metaanalysis of randomized, controlled trials. Crit Care Med 1998; 26: 14521457. PMID 9710109 Task 3. Enteral and Parenteral Nutrition p30 Nutrients Nitrogen is provided by a balanced mixture of amino acids (AA). There are no convincing 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 pharmacological agents (see below). Because of the relatively poor tolerance of carbohydrates together with the well known risks of excessive glucose administration (hyperglycaemia, hypertriglyceridemia, infections, liver steatosis), the recommended daily quantity of glucose is ≤ 6g/kg/day (cf p.6) and should not be administered at rates exceeding 5 mg/kg/min in critically ill patients. Excessive (>23 mg/kg/min or 60% of total energy input) lipid supply can also cause hepatic steatosis. Lipid emulsions contain energy in a small volume (9 kcal/g) reduce the osmolarity of nutritional mixtures and provide essential fatty acids necessary for cell membrane structure and stability, and for synthesis and action of the prostaglandin system. An initial supply of 0.5 to 1 g/kg/day of long chain triglycerides (LCT) seems to be best; this can be increased up to a maximum of 2 g/kg/day as long as plasma lipid clearance is regularly monitored (triglyceridemia, serum lactescence), and the infusion is given continuously over a 24h period. There is still no consensus, however, regarding the ideal quantity of lipid for critically ill patients. Whether supplementation with more than the minimum LCT requirement is of benefit during severe stress also remains debatable. As the severity of injury/sepsis increases, lipid oxidation and clearance from the blood decrease rapidly, which suggests poor utilisation. The relative advantages and risks of glucose and lipid-based PN regimens have been examined by Tappy L et al in the reference below. Some ICU patients receive high doses of propofol which contains long chain triglycerides. The lipid emulsion administration has to be adapted to take account 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 nutrition on glucose metabolism, de novo lipogenesis, and respiratory gas exchanges in critically ill patients. Crit Care Med 1998; 26 (5): 860-867. PMID 9590315 In addition, stimulation of alveolar macrophages could partially explain the abnormal pulmonary vascular tone and transient episodes of arterial desaturation seen during intermittent infusion of lipid emulsions. Such deleterious effects, however, are unlikely as long as the infusion rate is not excessive; it is therefore preferable to administer a continuous 24h infusion. Task 3. Enteral and Parenteral Nutrition p31 Controversy remains about the possible immunosuppressive effect of standard lipid emulsions in the acutely ill patient. It seems reasonable within the context of severe trauma/sepsis to limit the lipid supply to about 40-50% of the non-protein calorie input, or even less (≤ 30%) in patients who are severely septic. All-in-one PN solution All-in-one (ternary) PN bags, containing protein, carbohydrate,Uninterrupted administration of PN lipid, or binary bags containing carbohydrate and protein, reduces the risk of supplemented with trace elements, vitamins and electrolytes, metabolic complications are generally recommended for their convenience and good metabolic tolerance. Binary bags are less expensive and allow modification of lipid administration. THINK In which kind of patients might use of binary PN bags be important? Patient with liver steatosis Elevated blood liver enzymes or triglycerides Patients receiving high doses of propofol Pichard C, Schwarz G, Frei A, Kyle U, Jolliet P, Morel P, et al. Economic investigation of the use of three-compartment total parenteral nutrition bag: prospective randomized unblinded controlled study. Clin Nutr 2000; 19: 245-251. PMID 10952795 Convenient and simplified administration protocols are possible, and adjustment of infusion rate, when indicated, is easier. Immunonutrients Parenterally administered immunonutrients include glutamine, omega-3 fatty acids, trace elements and vitamins. In inflammatory conditions such as injury and sepsis, glutamine becomes a conditionally essential aminoacid and the preferred fuel for rapidly dividing cells such as lymphocytes, macrophages and enterocytes (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. Glutamine Several randomised controlled trials indicate that the supplementation of PN solutions with glutamine improves the clinical outcome (reduced mortality, reduced length of ICU and hospital stay, reduced duration of mechanical ventilation) of abdominal surgery and critically ill trauma patients. A grade A recommendation is given by ESPEN for the use of PN supplementation with glutamine in these groups of patients. Task 3. Enteral and Parenteral Nutrition p32 Immunonutrients in trauma, sepsis and inflammation Lymphocyte Macrophage Enterocyte PUFA: polyunsaturated fatty acids OKG: ornithine alpha-ketoglutarate SCFA: short chain fatty acids Omega-3 PUFAs, derived from fish oils, give rise to 10 to 100fold less platelet activation and thrombogenesis compared with omega-6 PUFA (derived from vegetable oils), the usual component of standard lipid emulsions. Therefore, omega-3 PUFAs are less liable to induce an inflammatory response to the activation of target cells by cytokines. The following four references describe in more detail the impact of immunonutrients on the clinical course of ICU patients. Sacks GS, Genton L, Kudsk KA. Controversy of immunonutrition for surgical critical-illness patients Curr Opin Crit Care 2003; 9(4): 300-305. Review. PMID 12883285 McCowen KC, Bistrian BR. Immunonutrition: problematic or problem solving? Am J Clin Nutr. 2003; 77(4): 764-770. Review. PMID 12663270 Marik PE, Zaloga GP. Immunonutrition in critically ill patients: a systematic review and analysis of the literature. Intensive Care Med 2008; 34(11): 1980-1990. Review. PMID 18626628 Dupertuis YM, Meguid MM, Pichard C. Advancing from immunonutrition to a pharmaconutrition: a gigantic challenge Curr Opin Clin Nutr Metab Care 2009; 12(4): 398-403. Review. PMID 19474715 Link to ESICM Flash Conference: Pierre Singer, ‘Immunonutrition in trauma patients’ ESICM congress, Vienna 2009 Task 3. Enteral and Parenteral Nutrition p33 Design a PN regimen for five of your newly admitted ICU patients and compare your suggested formulation with that prescribed. Combination of EN and PN It is clear that PN does not support mucosal structure and/or function of the gastrointestinal tract. In fact, except in cases of frank intestinal occlusion, partial EN is almost always feasible, even following major abdominal surgery. The only frequent annoying complication of EN in the ICU patient is the onset of severe diarrhoea. However, EN is not a dogma, and the keyword should be flexibility: the two methods are complementary. The decision to use one and/or the other will depend on the expertise, experience and training of the dieticians, medical and nursing staff, as well as the individual patient’s tolerance of EN. The type of nutritional support provided must be continuously adapted to the clinical situation (see p. 19). EN is preferable. PN is more expensive, bypasses the alimentary tract and the entero-pancreatic axis, thus potentially facilitating intestinal hyperpermeability and bacterial translocation. The indications for combined EN and PN are expected to increase in the future. Several studies have shown that the protein-energy deficit frequently observed with the use of EN alone is associated with increased morbidity and mortality. Thus, avoiding nutritional deficiencies is a key objective of nutritional therapy in intensive care. As EN is often difficult to fully optimise in the first three days following ICU admission, supplementing EN with PN could allow a better coverage to help achieve the energy target and limit the protein-energy deficit. This concept is particularly important given the expected changes in the characteristics 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 the number of ICU patients with loss of lean body mass and pre-existing nutritional deficiencies or undernutrition. The early optimisation of nutritional support will be necessary to improve their clinical outcome and enhance their chances of rapid recovery. Q Name at least one clinical situation in which the combination of EN 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 needs and EN to promote gut adaptation) Task 4 Monitoring and Complications p34 4. MONITORING AND COMPLICATIONS Assessment and monitoring of nutritional support is mandatory in critically ill patients; nutritional and metabolic disorders are frequent and are important determinants of patient outcome. This process should be integrated with other aspects of ICU patient care, as discussed in the two following reviews. Monitoring of nutrition is an integral part of overall ICU patient monitoring Hinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. Saunders Ltd; 2008. ISBN: 978-0-7020259-6-9. p. 305 Complications and p.308310 Complications and monitoring patients receiving TPN Downs JH, Haffejee A. Nutritional assessment in the critically ill Curr Opin Clin Nutr Metab Care 1998;1(3): 275-279. Review. PMID 10565360 Jolliet P, Pichard C, Biolo G, Chiolero R, Grimble G, Leverve X, et al. Enteral nutrition in intensive care patients: a practical approach. Working Group on Nutrition and Metabolism, ESICM. Intensive Care Med 1998; 24 (8): 848-859. PMID 9757932 Monitoring enteral nutrition A number of practical clinical considerations are inherent to the safe and smooth provision of enteral nutrition. They are addressed under the headings ‘tube misplacement and bronchial aspiration’ and ‘gastrointestinal dysfunction’. Tube misplacement and bronchial aspiration X-rays are generally recommended after the placement of a nasogastric tube and are repeated at least every week, especially with fine bore tubes in comatose patients. Malpositioning of (particularly) fine bore tubes is frequent Serious complications can occur when nutrients are infused outside the gastrointestinal tract, particularly into the airways. Bronchial aspiration may occur in patients with swallowing disturbances even if they are intubated; the risk is partially reduced by raising the head 30 to 45° above the supine position during EN administration. Gastrointestinal dysfunction If gastric feeding is used, monitoring of residual volume can decrease the risk of pulmonary aspiration. If the volume is greater than 500 ml, the infusion rate should be decreased by half for four hours and prokinetic agents used. If the residual volume is less than 200 ml, the collected fluid should be reinstilled and feeding resumed at the previous rate (see figure p.19). Abdominal cramps, nausea, vomiting and diarrhoea may occur when an enteral solution is infused at a high rate (greater than 80-100 ml/h). Cramps and nausea 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 p35 diarrhoea. In those with gastrointestinal symptoms, daily examination for abdominal distension is performed to detect a possible mesenteric ischaemia as early as possible. In patients receiving antibiotics, pseudomembranous enterocolitis due to the toxin of Clostridium difficile should be considered as a cause of diarrhoea. Stool cultures (with stool Clostridium toxin assays) are indicated when diarrhoea persists for more than three days after exclusion of other common causes. A Spanish study (see below) has reviewed the incidence of the complications of EN in critically ill patients. Montejo JC. Enteral nutrition-related gastrointestinal complications in critically ill patients: a multicenter study. The Nutritional and Metabolic Working Group of the Spanish Society of Intensive Care Medicine and Coronary Units. Crit Care Med 1999; 27 : 1447-1453. PMID 10470748 Monitoring of parenteral nutrition The adverse effects of parenteral nutrition are a major limitation to its clinical use. These are addressed as catheter related (including septic) and as metabolic/organ-specific complications. Catheter-related sepsis (CRS) Body temperature and insertion sites of intravenous catheters must be carefully monitored. A low-grade fever, in the absence of an obvious source of infection, or a dirty, inflamed or purulent insertion site may be a sign of catheter infection. Rigorous infection control measures are mandatory in all patients receiving PN If CRS is suspected to be the cause of severe sepsis or septic shock, the catheter must be removed immediately, PN temporarily interrupted, central and peripheral blood and catheter cultures obtained. In the case of mild infection, to avoid unjustified central venous catheter removal and the risks associated with the placement of a new catheter in a new site, the physician has two options – either guide wire exchange for quantitative culture of the catheter tip, or taking cultures ‘in situ’. The pros and cons of these options are discussed in the following references. In the absence of local or systemic signs of sepsis, routine line changes do not decrease the incidence of infection Blot F, Nitenberg G, Chachaty E, Raynard B, Germann N, Antoun S, Laplanche A, Brun-Buisson C, Tancrède C. Diagnosis of catheter-related bacteraemia: a prospective comparison of the time to positivity of hub-blood versus peripheral-blood cultures Lancet 1999; 354(9184): 1071-1077. PMID 10509498 Brun-Buisson C. Suspected central venous catheter-associated infection: can the catheter be safely retained? Intensive Care Med 2004; 30(6): 1005-1007. No abstract available. PMID 14991086 Task 4 Monitoring and Complications p36 Non-septic complications due to the catheters Complications associated with catheter insertion, such as air embolism, injury to thoracic structures (lung, pleura, arteries) and cardiac arrhythmias, are not uncommon. General safety guidelines, not specific to PN, should be strictly applied. Catheter thrombosis can occur any time after insertion and is often associated with catheter infection. Heparinisation of PN bags or solutions has been advocated. Metabolic complications of parenteral nutrition Hyperglycaemia is frequently observed in the critically ill, especially in patients with infection, liver or pancreatic dysfunction, diabetes mellitus, and those receiving diabetogenic drugs such as corticosteroids and cephalosporins. Therefore blood glucose values should be checked at least daily. The monitoring of urine glucose could be used to guide insulin therapy in an ICU patient, since it can detect ketonuria. The association between hyperglycaemia and adverse outcome in postoperative (mainly post cardiac surgery) patients has been documented. Blood glucose control lower than 10 mmol/L (1.8 mg/dL) with insulin can dramatically improve morbidity and/or mortality of surgical/medical ICU patients. Indeed, the NICE-SUGAR multicentre randomised study has recently indicated that the maintenance of a blood glucose lower than 10 mmol/L is associated with a reduced mortality rate as compared with “tight” glycaemic control (4.5-6 mmol/L (0.8-1.1 mg/dL). Thus, the glycaemic control is necessary in medical critically ill patients treated with PN, but not as “tight” as previously indicated by van den Berghe et al. However, it remains to be seen whether tight glycaemic control should be used in specific subsets of ICU patients, such as surgical patients. Hypoglycaemia is much less common, and may be caused by the sudden cessation of a hypertonic glucose infusion (e.g. due to kinking of the perfusion tubing), 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 result when carbohydrates are given in excess of needs, and can result in hepatic steatosis. NICE-SUGAR Study Investigators, Finfer S, Chittock DR, Su SY, Blair D, Foster D, Dhingra V, et al. Intensive versus conventional glucose control in critically ill patients. N Engl J Med 2009; 360(13): 1283-1297. PMID 19318384 van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R. Intensive insulin therapy in the critically ill patients. N Engl J Med 2001; 345(19): 13591367.PMID 11794168 Task 4 Monitoring and Complications p37 Liver abnormalities Levels of aspartate aminotransferase, alanine aminotransferase and bilirubin should be checked regularly e.g. every second day. The differential diagnosis of ICU-jaundice is often difficult due to the numerous possible aetiologies such as sepsis, hypoxaemia, ischaemia, mechanical ventilation, drugs, and nutrition that can damage hepatocytes. Sludge in the biliary tract and stasis in the biliary ducts causing chronic acalculous cholecystitis may be associated with prolonged PN and may be prevented by small volume EN (100–200 ml/day). Gangrenous cholecystitis is a rare but often severe, life-threatening complication of total parenteral nutrition in mechanically ventilated patients that has been described in patients with liver dysfunction. More than 60% of ICU patients receiving PN for more than two weeks have abnormal liver function tests. These mulitfactorial abnormalities are usually benign but may herald 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. PMID 10589378 Ziegler TR. Parenteral nutrition in the critically ill patient. N Engl J Med 2009; 361(11): 1088-1097. Review. No abstract available. PMID 19741230 Pancreatic disorders Pancreatitis in the ICU most often results from drug toxicity. In view of the rather 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 the results appear to be better than in the case of PN (see the following reference for details). 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 be interrupted 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 Nutr 2009; 28(4): 428-435. PMID 19464771 Marik PE. What is the best way to feed patients with pancreatitis? Curr Opin Crit Care 2009; 15(2): 131-138. Review. PMID 19300086 Task 4 Monitoring and Complications p38 Q List at least five laboratory parameters reflecting metabolic disturbances correctable by nutritional support. A. Hypoglycaemia and/or high acetonaemia Hypokalaemia Hypocalcaemia Hypomagnesaemia Hypophosphoraemia Hypovitaminosis Q What should be checked or corrected when hypertriglyceridaemia exceeds 6 mmol/L (540 mg/dL)? A. Look for sepsis, hyperglycaemia, acute pancreatitis are common; familial hypertriglyceraemia (e.g. type IV) is rare Correct excessive total energy and/or lipid administration Q In hyperglycaemia ≥12 mmol/L (218 mg/dL), what nutrition regimen 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 for infection should be initiated. Refeeding syndrome Patients with severe PCM (body weight loss ≥20%) have major metabolic disturbances. Prevention of lactic acidosis, beri-beri and/or Wernicke’s encephalopathy is achieved by high vitamin B1 levels when (or even before) hypertonic glucose is started. Reversal of acidaemia following the establishment of mechanical ventilation may result in hypophosphataemia due to a shift of phosphate from the extracellular to the intracellular compartment. In addition, when nutritional support is started in a malnourished patient, the intracellular demands for phosphate and potassium are increased due to enhanced glycolysis and stimulation of the Na/K-pump. In practice, the rate of phosphate and potassium infusion should increase from 15-30 to 30-60 mmol PO4 /day and from 80-120 to 120-200 mmol KCl /day. Phosphate, potassium, calcium and magnesium should be closely monitored, and replaced as necessary. Further details on the management of the refeeding syndrome can be found in the following reference. Q What are the two major risks related to rapid initiation of feeding of a severely malnourished patient? A. Severe hypokalaemia and hypophosphataemia Cardiac arrhythmia Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. BMJ 2008; 336(7659): 1495-1498. PMID 1858368 Task 5. Nutritional Support for Specific Situations p39 5. NUTRITIONAL SUPPORT FOR SPECIFIC SITUATIONS Liver failure Energy and protein intakes should not be modified, except in the case of severe encephalopathy clearly due to liver failure. In this case, protein intake can be transiently decreased to 0.6 g/kg/day to avoid the worsening of porto-caval encephalopathy. Intravenous manganese and molybdenum administration should be limited to three standard doses per week, instead of one daily if the patient is receiving PN. Finally, the use of a modified nutrient profile, such as increased branched-chain amino acids for patients with acute hepatic failure, has never been shown to prevent or control encephalopathy. No data support the concept of low calorie or low lipid PN in ICU patients with liver failure. ARDS and acute respiratory failure In the presence of significant respiratory muscle weakness, and/or when weaning from the ventilator is proving difficult, the added ventilatory demand may exacerbate respiratory muscle fatigue and jeopardise extubation. Generally, the excess in total caloric load and the rate of administration, rather than the proportion of glucose and lipids, are responsible for these undesirable effects. Accordingly, the use of modified-feeds containing increased proportions of lipids and less carbohydrate to reduce carbon dioxide production is not recommended. Recent data suggest that the enrichment of feeding with omega-3 fatty acids can improve respiratory function in ARDS patients, and even reduce the length of stay in the ICU. . Singer P, Theilla M, Fisher H, Gibstein L, Grozovski E, Cohen J. Benefit of an enteral diet enriched with eicosapentaenoic acid and gamma-linolenic acid in ventilated patients with acute lung injury. Crit Care Med 2006; 34(4): 10331038. PMID 16484911 Singer 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 Parenteral Nutrition: intensive care Clin Nutr 2009; 28(4): 387-400. PMID 19505748 For patients on EN, interruption of flow rate 3-6 hours before nasotracheal extubation after prolonged mechanical ventilation is frequently advocated to reduce the risk of aspiration. This procedure could potentially worsen respiratory muscle dysfunction at a time when energy needs are increased to support spontaneous breathing. We advocate continuation of EN until fifteen minutes before extubation when the nasogastric tube should be switched to gentle suction to empty the stomach. Task 5. Nutritional Support for Specific Situations p40 Q To facilitate weaning of ARDS patients from MV, is it better to reduce total energy input, glucose loading and/or lipid supply? A. Weaning from mechanical ventilation increases respiratory muscle work. The nutritional support strategy needs to be carefully considered. Excessive glucose loading may increase carbon dioxide production and respiratory work. Excessive lipid load may result in impaired gas exchange. It is recommended that a balanced nutritional intake be maintained at a level representing 80 to 100% of the patient's energy needs. Renal dysfunction The value of Nutritional therapy in patients with acute renal failure (ARF) branched-chain should not be tailored to the impairment of renal function but to amino acids for the severity of MOF. Renal failure occurring in ICU patients usually patients with acute renal failure has requires treatment with continuous or intermittent renal never been proven replacement therapy, which allows administration of nutrition as dictated by the individual patient’s needs. Hence, the usual protein intake restrictions for non-dialysed end-stage renal disease patients are unnecessary. The optimal composition of protein intake is not known, but a mixture of balanced standard solution of amino acids for PN and a standard polymeric diet for EN seems sensible. Finally, the losses of glucose and amino acids in the dialysate (lipids are not dialysable) should be taken into account. The metabolic features of both haemodialysis and continuous haemofiltration are detailed in the following reference. Chan LN. Nutritional support in acute renal failure Curr Opin Clin Nutr Metab Care 2004; 7(2): 207-212. Review. PMID 15075713 Q In a patient on continuous haemodialysis, is it necessary to reduce the quantity of electrolytes and protein given by enteral or parenteral routes? Explain your answer and consider whether intermittent haemodialysis (IHD) is different. A. Continuous haemodialysis allows for full provision of nutritional needs, while intermittent haemodialysis may necessitate reduced administration of fluid, electrolytes and protein. Sepsis There is no specific nutritional or metabolic support for critically ill septic patients. All our efforts must be concentrated on the immediate treatment of the underlying cause and careful symptomatic, goal-directed management of the patient. Early metabolic (nutritional) support is required, however, once haemodynamic stability has been achieved. Task 5. Nutritional Support for Specific Situations p41 Some simple guidelines can facilitate optimal nutritional management of these patients: restriction of energy supply (both carbohydrates and lipids) or even hypocaloric support (<1000 kcal/day) for two to three days, cautious increase in nitrogen supply above 0.20 g/kg/day, and prevention of cellular deficiencies in electrolytes (phosphorus, magnesium), trace elements (zinc, selenium) and vitamins (E, K). In severe sepsis, it is difficult to demonstrate any real benefit from the use of (very) early enteral nutrition, to determine the appropriate amount and nature of the nitrogen supply, or to assess the risk/benefit ratio of lipids. Nutritional pharmacology, aimed at immunomodulation and/or anti-inflammatory effects, together with prevention of gut failure in stress, are the major ambitions of the modern metabolic approach in septic patients. However, early enteral immunonutrition could be deleterious in severe sepsis patients, where the role of immune nutrients, such as arginine and n-3 fatty acids, deserve further investigations. Further details, including economic and ethical issues, are available in the following review article. Nitenberg G. Nutritional support in sepsis: still skeptical? Curr Opin Crit Care. 2000; 6(4): 253-266. PMID 11329509 Burns For further information see the PACT module on Burns. In burn patients, the supplementation of anti-oxidant micronutrients (selenium, zinc, vitamins A et E) is recommended to improve morbidity and mortality. Neurotrauma For further information see Task 4 (Treatment of Severe Head Injury) of the PACT module on Traumatic brain injury, subheadings ‘General Intensive Care’ and ‘Nutrition’. Catabolic states Hinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. Saunders Ltd; 2008. ISBN: 978-0-7020259-6-9. p. p.310 Modifying the Catabolic Response Limitation of catabolism during the initial phase of the stress response and promotion of anabolism as soon as the catabolic phase is over are among the major nutritional therapeutic goals in ICU patients with severe and prolonged illness. Potential countermeasures to stress-related catabolism, including anabolic compounds, are and covered in the Concise Textbook and in the next reference. At present no anabolic agent can be recommended for routine use Task 5. Nutritional Support for Specific Situations p42 However, insulin administration in ICU patients is limited to the control of glycaemia, while recombinant human growth hormone (rhGH), recombinant human insulin-like growth factor-1 (rhIGF-1), and anabolic steroids have been investigated but their use cannot be recommended. Anabolic factors can promote lean body mass Reid CL, Campbell IT, Little RA. Muscle wasting and energy balance in critical illness Clin Nutr 2004; 23(2): 273-280. PMID 15030968 Obesity Excessive fat stores do not preclude the need for an external source of energy and other substrates. Indeed, ICU stay is not a favourable period for weight loss management, except if weight loss is the critical issue for improving lung/cardiac functions. Energy needs of obese patients can be estimated (see paragraph on energy and protein requirements), from ideal body weight increased by 20% to adjust for extra lean body mass related to obesity. The energy requirements could be estimated as 15 kcal/kg actual BW/day or 20 kcal/kg ideal BW/day. Daily protein needs vary between 1.2 and 1.5 g/kg adjusted body weight, specific losses not included. More details about this poorly recognised problem can be found in the following reference. Task 5. Nutritional Support for Specific Situations p43 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 and Enteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Intensive care Clin Nutr 2006; 25(2): 210-223. PMID 16697087 Thibault R, Pichard C. Nutrition and clinical outcome in intensive care patients Curr Opin Clin Nutr Metab Care 2010; 13(2): 177-183. PMID 19996743 Martindale 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 in the adult critically ill patient: Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition: Executive Summary Crit Care Med 2009; 37(5): 1757-1761. Review. No abstract available. PMID 19373044 Perioperative nutrition Malnourished patients undergoing surgery, mainly for gastrointestinal tumours, are at a higher risk of morbidity and mortality. A number of studies have shown that nutritional support has beneficial metabolic effects, reduces morbidity (including that due to infection) and decreases mortality. See guidelines and review below. Braga M, Ljungqvist O, Soeters P, Fearon K, Weimann A, Bozzetti F; ESPEN. ESPEN Guidelines on Parenteral Nutrition: surgery. Clin Nutr 2009; 28(4): 378386.PMID 19464088 Fearon KC, Luff R.The nutritional management of surgical patients: enhanced recovery after surgery. Proc Nutr Soc 2003; 62(4): 807-811. PMID 15018479 The small bowel recovers its ability to absorb nutrients almost immediately following surgery, even in the absence of peristalsis. In abdominal surgery, placement of a nasoenteric tube or the creation of a feeding jejunostomy is clearly appropriate to ensure nutrient delivery and to avoid the inconvenience and cost of PN. The French and North-American consensus conferences held in 1995 and 1997 concluded that 7 to 10-day preoperative PN nutrition was of value only in malnourished gastrointestinal cancer patients, and that these patients should continue with nutritional support postoperatively for at least five days. Postoperative complications may be reduced by 10%. Preoperative PN is not recommended in other cases, as it could increase the risk of complications. Task 5. Nutritional Support for Specific Situations p44 Recent (European Society of Parenteral and Enteral Nutrition) ESPEN guidelines on PN in Surgery concur. Braga M, Ljungqvist O, Soeters P, Fearon K, Weimann A, Bozzetti F; ESPEN. ESPEN Guidelines on Parenteral Nutrition: surgery. Clin Nutr 2009; 28(4): 378-386. PMID 19464088 It is suggested that postoperative nutritional support should be given to patients who cannot resume around 60% of their calculated nutritional intake within five days following the operation. Enteral nutrition is the preferred route in this indication. Perioperative EN or PN can be made more effective by the use of pharmaconutrients. The following two references review the evidence. Martindale RG, Maerz LL. Management of perioperative nutrition support Curr Opin Crit Care 2006; 12(4): 290-294. Review. PMID 16810037 Calder PC. Immunonutrition in surgical and critically ill patients Br J Nutr. 2007; 98 Suppl 1: S133-S139. Review. PMID 17922951 CONCLUSION It is relatively easy to maintain adequate nutritional status, but a more difficult and prolonged task to cure PCM. ‘PCM is a sign of poverty in the Third World but of ignorance in hospitals of industrialised countries’ (Sir A. Wretlind 1981). Enteral nutrition is always the first choice. Parenteral nutrition should be restricted to those situations in which there are contraindications to enteral nutrition. The value of immunonutrition remains uncertain. Self-assessment p45 SELF-ASSESSMENT EDIC-style Type K 1. Type K. Resting energy expenditure (REE) is defined as the energy expenditure (EE) of the body in the resting state. Which of the following statements of REE is true: A. REE is always less than or equal to EE B. REE is not affected by body temperature C. REE, measured in terms of body mass, is equal in males and females D. REE is often in the range of 20-30 kcal/kg body weight in ICU patients 2. Type K. What is the ideal marker of protein-calorie malnutrition? A. Body mass index B. Serum albumin C. Nitrogen balance D. Bio-impedance analysis 3. Type K. A 54-year-old female patient with chronic pancreatitis because of alcohol abuse during several years is admitted to the ICU with a severe pneumonia. She is 173 cm high and weights 43 kg. Regarding the energy requirements in this patient: A. The goal of total energy delivery is around 2200 kcal/24h B. 50-55% of her energy intake should be carbohydrates. C. Lipid intake should not exceed 2 g/kg/day D. Glucose requirement is usually 6-10 g /kg/day 4. Type K. Contraindications to start enteral nutrition include: A. Uncontrolled acute circulatory failure B. Gastric atonia (Gastroparesis) C. Peritonitis D. Absent bowel sounds Self-assessment p46 5. Type K. A 57-year-old male, body weight 72 kg, with COPD is treated with non-invasive ventilation (NIV) applied with a mask. He is given full enteral nutrition (1750 ml, approximately 75 ml/hour) on day 3 after admission. He is awake and cooperative. On the morning of day 4, the ICU nurse reports a gastric residual volume of 650 ml. Which of the following options related to the nutritional management this day is appropriate? A. Reduce infusion rate to 50% 4-6 hours then progressively increase over the next 1-2 days B. Permanently reduce the amount to 1250 ml/day because the present amount is too much in COPD C. Stop all EN and give him parenteral nutrition for 1-2 days, then progressively increase over the next 1-2 days D. Consider giving i.v. erythromycin 6. Type K. After a successful placement of a fine-bore nasogastric (NG) tube the 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 position C. Installation of air through the NG and listen for characteristic sounds (bubble) in the epigastric region D. Gastroscopy to confirm correct position of the NG tube 7. Type K. Metabolic complications of parenteral nutrition (PN) include: A. Hyperglycaemia B. Hypertriglyceridaemia C. Hypoglycaemia D. Hypophosphataemia Self-assessment p47 EDIC-style Type A 8. Type A. The ‘low-phase’ of the metabolic response to injury and severe infections is characterised by the following disturbances EXCEPT: A. Increased energy expenditure B. Decreased gluconeogenesis C. Increased endogenous lipolysis D. Loss of lean body mass E. Increased insulin resistance 9. Type A. The advantages of enteral nutrition include all the following EXCEPT: A. Maintains normal IgA secretion in the gut mucosa B. Reduces the risk of hyperglycaemia C. Reduces intestinal motility D. Less costly than parenteral nutrition (PN) E. Decrease infectious complications compared to PN 10. Type A. Regarding enteral nutrition formulas, the following statements are true with the EXCEPTION of: A. A standard EN solution contains 1 kcal/ml B. Additional vitamins and trace elements should be added when the volume of EN <1500 ml C. A standard EN contains 1g protein/ml D. A standard EN contains fat mainly as LCT (long-chain triglycerides) E. The protein content of a so called ‘elemental’ diet contains only individual aminoacids or oligopeptides 11. Type A. Suggested dosing of parenteral nutrition (PN) in critical ill adults includes the following EXCEPT: A. Recommended dose of amino-acid/protein nitrogen is equivalent of 0.3 to 0.5 g N/kg/24 hour B. More than 6 g glucose/kg/24 hour should not be given C. Recommended dose of lipids is 1-2 g/kg/24 hour D. Short-chain fatty acids (SCFA) are never a part of PN E. It is not necessary to give all non-essential amino acids during PN Self-assessment p48 Self-assessment Answers 1. A. B. C. D. T F F T A. B. C. D. F F F F A. B. C. D. F T T F A. B. C. D. T F T F A. B. C. D. T F F T A. B. C. D. T F T F A. B. C. D. T T T T 2. 3. 4. 5. 6. 7. 8. Answer B is correct 9. Answer C is correct 10. Answer C is correct 11. Answer A is correct PATCH page 49 Nutrition PATIENT CHALLENGES Mrs B., a 54-year-old, previously healthy, woman presented with acute abdominal pain. She had a 10 year history of abdominal discomfort and nausea after fatty meals and ingestion of coffee. Stools and urine were said to be normal. She did not consume excessive amounts of alcohol, which was confirmed by her family. She has been obese since the birth of her children and at present has a stable weight of 82 kg and is 1.62 m tall. She suffered from moderate hypertension but otherwise her history was unremarkable. The pain was located in the mid upper abdomen and radiated 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 palpation of the upper abdomen. There was no referred discomfort and bowel sounds were audible. Core temperature was 38.3° C. Abnormal findings on investigation: ultrasound upper abdomen; stone shadows in the gallbladder and suspicion of hepatic steatosis. Intrahepatic bile ducts slightly dilated, no stone shadows visible in bile ducts. Pancreas difficult to evaluate due to gas in stomach and colon. Plank LD, Hill GL. Sequential metabolic changes following induction of systemic inflammatory response in patients with severe sepsis or major blunt trauma World J Surg 2000; 24(6): 630-638. Review. PMID 10773114 Venneman NG, van Brummelen SE, van Berge-Henegouwen GP, van Erpecum KJ. Microlithiasis: an important cause of "idiopathic" acute pancreatitis? Ann Hepatol 2003; 2(1): 30-35. Review. PMID 15094703 Napoléon B, Lefort C, Gincoul R. State of the art lecture: lithiasis and pancreatitis. Endoscopy 2006; 38 Suppl 1: S35-40. Review. No abstract available. PMID 16802221 Laboratory tests: Hb 8.2 g/dL Leukocytes 21.4 /fL ESR 18 mm/h Albumin 32 g/L CRP 60 mg/L Urinary Amylase 1800 IU γGT 124 IU Alk Phosph 217 IU ASAT 55 IU ALAT 40 IU PATCH page 50 Amylase 748 IU Creat 75 µmol/L Blood Urea 8.3 mmol/L Bilirubin - total 41 µmol/L - direct 80% Gluc 8.9 mmol/L Mrs 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. Nasogastric suction 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 a necrotising pancreatitis is present. In patients with interstitial pancreatitis, no benefit of artificial nutrition has been demonstrated. Indications for artificial nutrition in acute disease of short duration, and in acute pancreatitis Gianotti L, Meier R, Lobo DN, Bassi C, Dejong CH, Ockenga J, Irtun O, MacFie J; ESPEN. ESPEN Guidelines on Parenteral Nutrition: pancreas Clin Nutr 2009; 28(4): 428-435. PMID 19464771 Meier R, Ockenga J, Pertkiewicz M, Pap A, Milinic N, Macfie J; DGEM (German Society for Nutritional Medicine), Löser C, Keim V; ESPEN (European Society for Parenteral and Enteral Nutrition). ESPEN Guidelines on Enteral Nutrition: Pancreas Clin Nutr. 2006; 25(2): 275-284. PMID 16678943 Marik PE. What is the best way to feed patients with pancreatitis? Curr Opin Crit Care 2009; 15(2): 131-138. Review. PMID 19300086 Indications for artificial nutrition in patients with normal body composition PACT module on Pancreatitis Q. Presuming your answer was no, would you have instituted artificial nutrition if she weighed 54 kg? A. Only if the 54 kg is the result of recent substantial weight loss (e.g. about 5-6 kg in the past 3 months) might one consider early artificial nutrition. Since 54 kg is close to ideal body weight for 1.62 m there is no indication for artificial nutrition. PATCH page 51 After 2 days Mrs B's clinical state deteriorates. Urine output diminishes to 25 ml/h prompting additional fluid support. She is slightly confused and has a slight tachycardia (110 b/min). Arterial blood pressure is maintained. Additional investigation. Plain abdominal and chest X-ray: still gas in transverse colon, little gas in small intestine, some pleural effusion in the left hemi-thorax. Laboratory tests: Hb 6.2 g/dL Leukocytes 21/fL Thrombocytes 580 /fL Alb 21 g/L CRP 180 mg/L Liver enzymes no changes Gluc 12.9 mmol/L Creat 121 µmol/L Amylase 1200 IU Urinary Amylase 23000 IU Triglycerides 2.1 mmol/L Bilirubin 18 µmol/l Necrotising pancreatitis is suspected and a prolonged clinical course is expected. With appropriate fluid support, her haemodynamic parameters remain stable. Symptomatology of severe acute disease. See PACT module on Oliguria and anuria. Werner J, Hartwig W, Uhl W, Müller C, Büchler MW. Useful markers for predicting severity and monitoring progression of acute pancreatitis Pancreatology 2003; 3(2): 115-127. Review. PMID 12748420 Lempinen M, Stenman UH, Puolakkainen P, Hietaranta A, Haapiainen R, Kemppainen E. Sequential changes in pancreatic markers in acute pancreatitis Scand J Gastroenterol 2003; 38(6): 666-675. PMID 12825877 Aoun E, Chen J, Reighard D, Gleeson FC, Whitcomb DC, Papachristou GI. Diagnostic Accuracy of Interleukin-6 and Interleukin-8 in Predicting Severe Acute Pancreatitis: A Meta-Analysis Pancreatology 2010; 9(6): 777785. PMID 20110745 Q. 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 of necrotising pancreatitis in this context. Also the low haemoglobin, albumin, the high leukocytes, thrombocytes, glucose and creatinine are indicators of severe inflammation and disease. Therefore a long clinical course is rightfully expected. Artificial nutrition should be instituted on the basis of these considerations. Mrs B's obesity does not alter this indication. Prediction of severity of illness and consequently indications for artificial nutrition PATCH page 52 Q. Why is there a substantial drop in haemoglobin? A. The drop in haemoglobin is mainly the result of haemodilution. The drop is still moderate, which makes it unlikely to be due to haemorrhagic necrotising pancreatitis. Nutritional requirements in obesity Q. 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 increased both intravascularly but also extravascularly because of the vascular expansion caused by fluid support. In addition the transcapillary escape rate of albumin has increased. Furthermore the synthesis rate of albumin is generally not decreased but breakdown most probably is increased. Kinetics of albumin. See the PACT module on High risk surgical patient Q. If you start artificial nutrition now, how and what? A. Although it is important to initiate enteral nutrition it is unlikely that this will meet the patient's full requirements at this stage. Therefore PN is appropriate until oral or enteral nutrition can be resolved. Does enteral nutrition worsen the severity of pancreatitis by stimulation of the pancreas? Outcome of acute pancreatitis: nasogastric versus nasojejunal feeding? O'Keefe SJ.Physiological response of the human pancreas to enteral and parenteral feeding.Curr Opin Clin Nutr Metab Care 2006; 9(5): 622-628. PMID 16912561 Kaushik N, Pietraszewski M, Holst JJ, O'Keefe SJ.Enteral feeding without pancreatic stimulation. Pancreas. 2005; 31(4): 353-359. PMID 16258370 Eatock FC, Chong P, Menezes N, Murray L, McKay CJ, Carter CR, et al. A randomized study of early nasogastric versus nasojejunal feeding in severe acute pancreatitis. Am J Gastroenterol 2005; 100(2): 432-439. PMID 15667504 Kumar A, Singh N, Prakash S, Saraya A, Joshi YK. Early enteral nutrition in severe acute pancreatitis: a prospective randomized controlled trial comparing nasojejunal and nasogastric routes J Clin Gastroenterol 2006; 40(5): 431-434. PMID 16721226 PATCH page 53 Enteral nutrition Parenteral nutrition Although the efficacy of antibiotic prophylaxis for the prevention of infections is not established and remains controversial in acute pancreatitis (see ESICM-SCCM consensus statement and references below), IV imipenem® is commenced together with enteral nutrition via a nasojejunal tube. 500 ml of a nutrition formula of polymeric composition is administered as a continuous 24h pump driven enteral infusion. Three days later (5d after admission to the ICU) Mrs B. still requires large volume loads and is in positive fluid balance. She is confused, is suffering from acute respiratory insufficiency, necessitating oxygen administration. Mechanical ventilation is considered. The volume of enteral nutrition has been increased to 1000 mL/d. On examination Mrs B. is hyperventilating, her abdomen is distended with occasional high-pitched bowel sounds, and her upper abdomen is tender on palpation. She has not passed a motion, and 800 ml of clear slightly brownish fluid have been aspirated via her stomach tube. Additional investigation. Laboratory tests: Hb 5.4 mmol/L Creat 213 µmol/L Blood Urea 21.0 mmol/L Alb 14 g/L Gluc repeatedly above 10 mmol/L Persistent leukocytosis Triglycerides 3.2 mmol/L CRP 250 mg/L Nathens AB, Curtis JR, Beale RJ, Cook DJ, Moreno RP, Romand JA, Skerrett SJ, Stapleton RD, Ware LB, Waldmann CS. Management of the critically ill patient with severe acute pancreatitis. Crit Care Med 2004; 32(12): 25242536. Review. PMID 15599161 Maraví-Poma E, Gener J, Alvarez-Lerma F, Olaechea P, Blanco A, DominguezMuñoz JE; Spanish Group for the Study of Septic Complications in Severe Acute Pancreatitis. Early antibiotic treatment (prophylaxis) of septic complications in severe acute necrotizing pancreatitis: a prospective, randomized, multicenter study comparing two regimens with imipenemcilastatin. Intensive Care Med 2003; 29: 1974-1980. PMID 14551680 Xue P, Deng LH, Zhang ZD, Yang XN, Wan MH, Song B, et al. Effect of antibiotic prophylaxis on acute necrotizing pancreatitis: results of a randomized controlled trial. J Gastroenterol Hepatol 2009; 24:736-742. PMID 19220676 Jafri NS, Mahid SS, Idstein SR, Hornung CA, Galandiuk S. Antibiotic prophylaxis is not protective in severe acute pancreatitis: a systematic review and meta-analysis. Am J Surg 2009; 197: 806-813. PMID 19217608 PATCH page 54 Empiric approach in ICU to nutritional support. Effectiveness judged on clinical grounds, primarily. See PACT module on Basic clinical examination. Q. Estimated energy requirements on the basis of ideal body weight and actual preillness body weight amount to more than 1500 kcal/24h. The enteral feed supplies approximately 1000 kcal/d. Would you try to cover energy needs and if so, which measures 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 volume should not amount to more than 500 ml. Bowel distension should be absent and the patient should produce stools. Prokinetics and enemas are questionable in this setting. If tolerance does not improve the amount administered should be limited. In this case PN should be added to make up for the deficit in nutritional provision. It is not always necessary to reach full requirements. Combination of EN and PN Calculation of total energy expenditure Q. Given the developing acute kidney injury, is it necessary to limit the protein content of the nutritional regimen? Explain your answer. A. Limitation of protein intake is rarely indicated. In this case the period of acute renal failure will most likely be at least a few weeks. Normal protein quantities (1.2 g up to 1.5 g/kg/24h is generally recommended) should therefore be included, and if necessary the patient treated with haemodialysis or CVVH (Central Veno-Venous Haemoperfusion). Appropriate use of protein in the nutritional regimen in patients with acute or chronic renal failure Q. Would you limit the fat intake of Mrs B? Or would you aim for a high fat content because of acute respiratory insufficiency? Why? A. High plasma triglyceride levels should caution against overloading the system with fat. It seems justified to give normal fat, monitor triglyceride levels in plasma and taper fat content when triglycerides rise above 4-5 mmol/L. Abnormal liver enzymes indicating intrahepatic cholestasis often parallel the high triglyceride levels. Giving high quantities of fat to decrease CO2 production is not supported by hard data. The management of hypertriglyceridaemia and steatosis in severe disease PATCH page 55 Q. 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 in this type of patient. There are certainly no data demonstrating a benefit. An exception may be liver insufficiency with frequent ascites removal or very low levels of albuminaemia (e.g. <12 g/l), in the absence of haemodilution. Albumin by infusion is of unproven value Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R; SAFE Study Investigators. A comparison of albumin and saline for fluid resuscitation in the intensive care unit N Engl J Med 2004; 350(22): 2247-2256. PMID 15163774 Mrs B's nutritional regimen is modified: enteral nutrition is limited to 500 mL/d containing approximately 500 kcal. In addition parenteral nutrition is added to meet her calculated energy requirements. Insulin is administered by continuous infusion for glycaemic control. Prokinetics and enemas are given to stimulate bowel movements and the production of stools. She passes malodorous diarrhoea. Imipenem® is continued. On the 8th day, a spiral CT scan reveals patchy necrosis in the body of the pancreas and peri-pancreatic necrosis. The situation remains relatively stable although renal function is compromised. Attempts to increase enteral nutrition are unsuccessful and bowel distension becomes worse. On the 10th day Mrs B's clinical condition deteriorates. She becomes haemodynamically unstable, requires more volume support and develops hypoxia despite extra oxygen and renal failure. She is intubated, and mechanically ventilated. CT guided aspiration of the necrotic area reveals Gram negative micro-organisms. At subsequent operation infected necrosis is debrided. Q. Should a catheter jejunostomy be performed? A. Some surgeons advocate the insertion of a catheter jejunostomy during operation. Others favour the view that in a type of patient any extra hole made in the intestine may increase the risk of complications as in Mrs B's case. For some, intestinal feeding is feasible via a double-lumen nasoenteral tube inserted and located intraoperatively by the surgeon. The pros and cons for performing a catheter jejunostomy during the operation PATCH page 56 Q. Do you again modify the nutritional regimen? If so, how? A. Although continuation of peri-operative enteral nutrition is advocated by some, in the case of necrotising infected pancreatitis, temporary discontinuation of the enteral feed is more usually favoured. Also limitation of PN to not more than 1000 kcal is often advocated to prevent metabolic disturbances, specifically glucose intolerance. If an 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 after operation (12th day after admission). Parenteral nutrition was recommenced at 2000 kcal/d (the infusion rate was reduced on the day of operation). On the 14th day the patient develops overt sepsis and MOF of increasing severity. There is also hypertriglyceridaemia (>7 mmol/L). Hypertriglyceridemia and potential untoward side-effects Q. What measures do you now take? How do you treat hypertriglyceridaemia? A. The hypertriglyceridaemia has reached a point where, in general, a decrease of fat content in the nutritional regimen is indicated although it is not established at which level 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 a week (but not removed because of risk of fatty acid deficiency) and enteral nutrition is 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 to enormous bowel distension primary closure is not possible. Enteral nutrition is discontinued 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? When would you try to resume full strength nutritional support? Is there a place for a modified formula both enterally or parenterally? A. Enteral nutrition should be resumed when bowel distension has abated and gastric aspirate volumes (GAV) are reduced. It is also more likely, that enteral nutrition will be successful when the severity of disease has become less and bowel movements have been recorded. Full requirements are possible only when fat clearance has improved 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 oxidise glucose is limited to 4-5 g/kg/24h. Administering more will aggravate steatosis, which this patient has had all along. PATCH page 57 The utilisation of fat and carbohydrates in critical illness Two more drainage procedures are necessary but on the 21st day the last gauze pack is removed from the lesser sac, the wound granulates and inflammatory parameters become stable and subsequently improve. During one of the drainage procedures the jejunostomy catheter is dislodged, reinserted and oversewn. Mrs B. is artificially ventilated, is on CVVH (Central Veno-Venous Haemoperfusion) and she can be brought into negative fluid balance. She needs less oxygen and less inotropic support. Attempts to increase her caloric intake by adding fat have until now failed because of increasing plasma triglyceride levels. Five hundred mL of enteral feed is administered via the jejunostomy catheter, which on the 25th day is increased to 1000 kcal/d, implying that energy requirements are approximately met (EN and PN together). On the 28th day after admission the oversewn entry site of the jejunostomy catheter opens and in a few days a high output fistula (over 1500 ml per day) develops which drains into the left side of the open granulating wound. Surgical treatment of infected, pancreatic necrosis and the integrated approach to effective enteral and parenteral nutrition. See PACT Module on Pancreatitis Raraty MG, Connor S, Criddle DN, Sutton R, Neoptolemos JP. Acute pancreatitis and organ failure: pathophysiology, natural history, and management strategies Curr Gastroenterol Rep 2004; 6(2): 99-103. Review. PMID 15191686 Singh VK, Wu BU, Bollen TL, Repas K, Maurer R, Mortele KJ, Banks PA. Early systemic inflammatory response syndrome is associated with severe acute pancreatitis Clin Gastroenterol Hepatol. 2009;7(11): 1247-1251. PMID 19686869 Mole DJ, McClymont KL, Lau S, Mills R, Stamp-Vincent C, Garden OJ, Parks RW. Discrepancy between the extent of pancreatic necrosis and multiple organ failure score in severe acute pancreatitis World J Surg. 2009; 33(11): 2427-2432. PMID 19641951 Although almost all organ functions improve Mrs B. becomes jaundiced with rapid rises in Alk Phosph, γGT and direct Bilirubin. Transaminases are only slightly elevated. Triglyceride levels have stabilised at 3 mmol/L, and inflammatory parameters indicate only modest inflammation. Albumin is rising to above 20 g/L without albumin infusion. PATCH page 58 Q. Which nutritional regimen do you prescribe? What is the cause of the intrahepatic cholestasis? A. Reactivation of distal small bowel function has been shown to decrease the severity of intrahepatic cholestasis. This may involve reinfusion of chyme, collected from the proximal part of the fistula, into the distal small bowel with or without a liquid enteral formula. Somatostatin or somatostatin analogs may diminish fistula output, but only in certain circumstances and when the bowel and adjacent tissues are healthy. The causes of intrahepatic cholestasis are multifactorial. The PN as well as the actual short bowel and the defunctionalised distal small bowel, as a result of the fistula, are implicated in the intrahepatic cholestasis. The pathogenesis is not yet well defined but may include endotoxin-induced cytokine cascades. The multifactorial origin of intrahepatic cholestasis in severely ill patients receiving parenteral nutrition Calicis B, Parc Y, Caplin S, Frileux P, Dehni N, Ollivier JM, Parc R. Treatment of postoperative peritonitis of small-bowel origin with continuous enteral nutrition and succus entericus reinfusion Arch Surg 2002; 137(3): 296300. PMID 11888452 Frileux P, Attal E, Sarkis R, Parc R. Anastomic dehiscence and severe peritonitis Infection 1999; 27(1): 67-70. Review. PMID 10206794 Effects of somatostatin or analogs on pancreatitis and fistula output and healing. See PACT Module on Pancreatitis Initially 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 together with an enteral formula. It soon becomes possible to administer 1000 mL of enteral feed per day together with a large part of the proximal pancreatic and biliary secretions. PN is diminished to 1000 kcal/d. Finally Mrs B. improved physically, mentally and biochemically. Albumin and haemoglobin rose to normal levels, intrahepatic cholestasis, including jaundice, disappeared almost completely. Thirty-five days after admission to ICU she was transferred to the normal ward. After 56 days of hospital stay Mrs B. had further surgery. Her jejunal fistula was closed as was the abdominal wound and cholecystectomy was done. The skin was left open. Mrs B. resumed oral intake a few days after the operation and was discharged 70 days after her admission to ICU. Balancing enteral and parenteral nutrition Route of feeding Combination of enteral and parenteral nutrition PATCH page 59 On reflection, the intensive care course of this patient was prolonged and involved the collaborative and dedicated efforts of many doctors, nurses and other healthcare professionals. Fortunately, the outcome was positive and the patient returned to her family. Q. Apart from the technical skills demonstrated by the carers in this case what other components of care would you consider would have been important? A. Clearly, communication between members of the ICU team and with surgical and dietetic colleagues would have been critically important. The fact that many of the decisions taken were based on clinical experience as well as laboratory findings underscores the importance of 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 Communication Q. Once the patient left ICU what would have been the important points in her subsequent management? A. Again detailed communication with ward staff before and during the patient's transfer to the ward would b essential to ensure a smooth transition. After the patient's return home, skilled and experienced support would continue to be important since patients recovering from prolonged illness, particularly when complicated by PCM, are both physically and psychologically vulnerable.
