icu nutrition: treatment and problem solving topic 18

Copyright © by ESPEN LLL Programme 2011

ICU nutrition: Treatment and problem solving Topic 18

Module 18.2 Promoting homeostasis during nutrition support

Michael J. Hiesmayr

Learning Objectives:

• How to maintain homeostasis during nutrition care; • Clinical problem solving in case of problems; • Selected issues related to clinical nutrition in ICU;

Contents: 1. Introduction 2. Appropriateness of the amount of nutrients given

2.1. Excessive nutrient intake 2.2. Insufficient nutrient intake 2.3. Appropriate composition of diet

3. Brain 4. Cardiovascular system 5. Lung 6. Abdomen 7. Kidney function 8. Haematological system 9. Endocrine system / Metabolic equilibrium 10. Refeeding syndrome

10.1. Pathophysiology 10.2. Clinical symptoms

10.2.1. Fluid equilibrium 10.2.2. Glucose and lipid metabolism 10.2.3. Thiamine deficiency 10.2.4. Hypophosphataemia 10.2.5. Hypomagnesaemia 10.2.6. Hypokalaemia

10.3. Treatment and prevention of the refeeding syndrome 11. Summary 12. References Key messages: • Over- and undernutrition is frequent in clinical nutrition care • All organ systems can be affected individually by nutrition care • Acutely, electrolyte disorders are life-threatening complications of nutrition


• Patients with chronic nutritional abnormalities are at highest risk for complications associated with nutrition care • In the refeeding syndrome many complications may be combined • Use of protocols improves nutrition care 1. Introduction Nutrition care is considered to be a basic and mandatory (essential) element of modern intensive care treatment. Recommendations and guidelines exist from several professional organizations including ASPEN, Canadian Critical Care Group and ESPEN. Their focus is on indications for EN vs. PN, amounts of nutrients to be given, composition of all-in-one solutions and on specific nutrients such as glutamine. Not all guidelines give any practical advice on how to maintain homeostasis during nutrition care or on clinical problem solving in case of problems. Selected issues related to clinical nutrition will be addressed in depth in this LLL module. Nutrition care in the ICU presents several challenges because the usual control mechanisms such as hunger and thirst may be missing. On the one hand the control of intake is under external control and on the other hand nutrients may have complex interactions with various organ systems. These two factors indicate that an integrative view is essential. The refeeding syndrome may show various combinations of symptoms and problems of homeostasis that are due to an inadequate amount or composition of the diet given to patients at special risk.[1] The patient groups at highest risk for complications associated with nutrition care are obviously those at the extremes of body size, nutrient intake and current disease:

• BMI very low or very high • Higher age • Prolonged starvation • High level of organ support in the ICU • Severe physiological impairment

Tab. 1. Patient risk group.

2. Appropriateness of the amount of nutrients given The ESPEN guidelines state that: - 20-25 kcal.kg-1.h-1 should be given to patients in the acute and initial phase of critical illness and - 25-30 kcal.kg-1.h-1 in the anabolic recovery phase. ACCP guidelines recommend 25 kcal.kg-1.h-1. Little information about individualization of therapy is given, and thus only two options exist: measuring energy expenditure with indirect calorimetry or use of clinical observation, lab values and judgment to adjust nutrition care. The observation of trends is of crucial importance as is the combination of several signs and symptoms in any of these situations. Current guidelines do not offer problem solving algorithms for the diagnosis of under- or overnutrition. We consider that most of the recommendations apply for “mean” patients and that clinical judgment needs to be used for patients outside this category. A cartoon shows conceptually the adaptation of nutrient intake that may be considered for the young and the very old as well as those in the acute and stable phases of illness. The duration until stabilization certainly varies from patient to patient. Age is also an important factor for energy requirements. Energy requirements decrease at higher age.[2]


Figure 1. Graph BMI vs. caloric intake

2.1. Excessive nutrient intake Excessive nutrient intake is considered to be much less frequent than undernutrition but recent observational data from the NutritionDay ICU project 2007-2008 suggest that almost as many patients receive an amount of nutrients above the target zone of 20-30 kcal.kg-1.h-1 as below this. Prescription of parenteral nutrition may be associated with overfeeding in more than half of the patients.[3] Measured energy consumption may suggest an excessive intake if RQ is > 0.85 for patients who are not exercising during the measurement period. An elevated RQ suggests an increased CO2 production that may be related either to high energy intake or to high glucose load and ongoing lipogenesis.[4] The organ systems most affected by excessive intake are the lung, the heart and the endocrine system, but a few general symptoms such as fever or decreased level of consciousness may also relate to larger than tolerated intakes of single nutrients. The lung and ventilation: Elevated minute volume, e.g. above 150 ml.kg-1.min-1, persistently elevated arterial pCO2 despite normal minute ventilation, or difficulty in weaning from the ventilator in otherwise unstressed patients, should trigger thoughts about nutrient intake. In the case that an excessive nutrient intake appears to be an possibility, a trial of decreasing intake by 30% for a few days to allow weaning may be necessary.[5] The heart and circulation: Nutrient intake induces a typical response with an increase in oxygen consumption that is followed by an increase in cardiac output and a slight decrease in peripheral vascular resistance and thus no major change in blood pressure. In patients with decreased cardiovascular reserve, patients with congestive heart failure or patients who have lost heart muscle because of prolonged starvation, e.g. anorexia nervosa, this increase in demand for cardiac work may be associated with new or worsening heart failure.[1, 6, 7] Pulmonary oedema and new cardiac rhythm disturbances such as atrial fibrillation are possible. Cardiac inotropic support and careful volume adjustment may be the treatment of choice.


Endocrine system: Hyperglycaemia and hyperlipidaemia can be symptoms of excessive nutrient intake. In this case a decrease in nutrients needs to be considered. This decision is particularly difficult since acute disease states, injury and starvation for a few days are associated with increased insulin resistance.[8] This phenomenon is by far the most likely reason for hyperglycaemia. Tolerance to glucose also decreases with age.[9] General signs and symptoms: Fever may be a sign of an excessive load of amino acids given their thermogenic effect.[10] In some patients, especially those with a severe catabolic state, an increased load of amino acids that may appear indicated to prevent a further deterioration in nutritional status, may provoke a decreased level of consciousness due to a sharp rise in ammonium in blood. Hyperlipidaemia may occur in some patients and can be related either to a high glucose load or to poor lipid clearance. Lipid provision should probably only be reduced if triglyceride levels are very high and excessive glucose intake has been excluded. 2.2. Insufficient nutrient intake A cumulative deficit of nutrients compared with actual energy consumption has been found to be associated with an increase in complications [11, 12]. Especially infectious complications have been shown to be increased in patients with an energy deficit > 50% of needs compared with the recommendations for energy supply of the ACCP guidelines. Few centres routinely use indirect calorimetry to assess patients’ energy needs, thus most have to rely on formulas and clinical judgement.[13-15] Discrepancies between these and measured energy expenditure in different groups of critically ill patients have proved to be as high as between 1300 and 2200 calories.[15] The effect of an energy supply below needs is not easily detected since the clinical manifestations of semi-starvation need time to become obvious in an individual patient. Moreover the effect of semi-starvation is similar to the effect of severe catabolism induced by the acute disease process. Sleepiness, loss of physical strength, repeated skin defects, and pressure sores should raise the suspicion of a severe energy deficit. 2.3. Appropriate composition of diet Modifications in the composition of the diet are considered in three clinical situations: • Difficult to handle hyperglycaemia • Excessive hyperlipidaemia ( > 400 mg.dl-1) • High CO2 values and weaning problems In the case of hyperglycaemia which is difficult to control (usually considered when the need for insulin is > 100 IU. day-1) there are several possible causes. The first is excessive energy intake, the second, unbalanced nutrition with a relatively high glucose[16] content, or it may reflect a poorly controlled septic process. Elevated lipids (usually triglycerides > 400 mg.dl) happen from time to time in the ICU. There are several possibilities that need to be considered: • Excessive lipid intake (maximum clearance 3.5 g.kg-1.day-1) • Excessive glucose intake • Acquired poor lipid clearance • Acute renal failure • Chronic renal failure • Hypodynamic sepsis • Inborn poor lipid clearance or abnormal metabolism


In all cases where lipid intake is limited the minimal requirement for LCT of 10 g. week-1 should be considered. LCT are essential components for cell membranes. In patients with respiratory failure and elevated CO2 values there has been the idea to move from a balanced nutrition solution to more lipid focused nutrition because the RQ of lipids is 30% lower than the RQ for glucose. Research in this field demonstrates that a reduction in CO2 is achieved with limitation of the ratio of energy intake to consumption, but cannot be achieved by modification in the composition of the diet.[5, 16, 17] In severely obese patients a modification of the diet with low calories and 1.2 g of protein per kg actual body weight achieves similar nitrogen balance without provoking difficult hyperglycaemia.[18] 3. Brain The brain is affected by several nutrition related factors:[1, 7, 19, 20] • Glucose level • Hyperglycaemia • Hypoglycaemia • High ammonium • Electrolyte imbalance

Figure2. Neurological symptoms and nutrition abnormalities


4. Cardiovascular System Hypophosphataemia, hypokalaemia and the consequences of muscle loss during reduced nutrient intake favour the relatively frequent occurrence of severe cardiac complications in patie nts with malnutrition, severe catabolism and refeeding.

Figure 3. Cardiac symptoms and nutrition abnormalities

5. Lung The lungs can be affected by reduced cardiac function, diaphragmatic force, or by the levels of CO2 that need to be eliminated. Thus the main limiting factors are muscle loss during starvation or severe catabolism that impair both the heart and the respiratory muscles. The system is then stressed by the level of CO2 that needs to be eliminated. CO2 production is mainly affected by high energy intake or by a high glucose intake that is converted to fat with a RQ above 1.[5] As a third consequence of inadequate nutrient intake the risk of pneumonia is increased. 6. Abdomen The abdomen is not only affected directly by disease and the tolerance of enteral feeding but also by other nutrition related factors.


Figure 4. Abdominal symptoms and nutrition abnormalities

7. Kidney function Reduced kidney function has direct interactions with nutrition care. Poor excretion of waste products induces azotaemia. During acute illness it is usually not advisable to reduce protein intake or amino-acid infusion to a very low level. Thus renal replacement therapy is indicated to allow a sufficient protein intake. Other consequences such as hypokalaemia affect the capacity of the kidney to concentrate urine, or hinder the resolution of the metabolic alkalosis often seen after hypercapnic ventilatory failure or a shocked state. Hypomagnesaemia has been associated with renal failure.[21] Uncontrolled hyperglycaemia may be associated with osmotic diuresis and hypovolaemia. [22, 23] 8. Haematological system Leucocytes, erythrocytes and platelets are affected by deviations from electrolyte homeostasis. The main reason for impaired blood cell function is hypophosphataemia. Infection control, clot function and oxygen unloading may be affected. [24-26] 9. Endocrine system/Metabolic equilibrium The endocrine system is affected by starvation, malnutrition and acute illness. After a few days of reduced intake the capacity to metabolize glucose is reduced by almost 50%.[8] This effect is even more pronounced in phases of acute stress such as surgical interventions. Hyperglycaemia is a common feature in acute illness even in a high proportion of non-diabetic patients. [27-33] Hyperglycaemia is often associated with increased severity of illness and poorer prognosis especially in the group of patients without known diabetes before hospital admission.


In 2001 Greet van den Berghe from Leuven showed that, immediately after ICU admission, intensive control of glycaemia to levels of 80-110 mg.dl-1 (4.4-6.1 mmol.l-1) compared with treatment only for patients with glucose levels >180 mg.dl-1 (>10 mmol.l-1) significantly improved outcome and prevented morbidity.[34] This effect could be found also in medical ICU patients staying longer in the ICU and in children.[35] The Leuven approach combines early treatment of hyperglycaemia and simultaneous infusion of glucose, and the early start of enteral and parenteral nutrition therapy. These studies boosted the interest in hyperglycaemia and promoted research on treatment with continuous insulin to different targets and in specific populations. None of the multicentre trials could replicate the beneficial effects described by the Leuven group. Several trials were stopped prematurely because of a high proportion of hypoglycaemic events in the intensive treatment arm.[36] A very large multicentre trial (NICE-SUGAR) in 6104 patients showed a small unfavourable effect of intensive insulin control. A major debate on the reasons for these conflicting results is still ongoing.[35] Based on expert opinion and a recent meta-analysis, current recommendations can be summarized: • Hyperglycaemia should not be left uncontrolled in acute illness • The target should be to achieve values < 150 md.dl-1 (8.3 mmol.l-1) • Avoid large changes in glucose values • Avoid hypoglycaemic events to values < 60 mg.dl-1 (3.3 mmol.l-1) • Do not withhold appropriate nutrition care to avoid giving insulin • Use a protocol that includes the following elements • Target glucose range • Insulin dosage for deviations from the target • Step changes in insulin for rapid glucose changes • Avoid intravenous insulin boluses • Amount of glucose to be given in case of hypoglycaemia (usually 8-10 g as and enteral bolus) • Intervals of glucose measurement adapted to the most recent changes in glucose and insulin dosage • Definition of responsibilities • Who measures glucose • Who interprets glucose levels • Who is allowed to modify insulin dosage • Usually point of care glucose measurement is necessary unless glucose values can be obtained within 10 minutes of sampling 24 hours a day • Glucose measurement from blood gas machines is usually the most convenient, cost effective and reliable point of care approach The most important part is the analysis of the treatment process, to provide adequate training and to give the responsibility of measuring and modifying to one group of health-care providers that works near to the patient (usually nurses but may be physicians depending on local organization). An example protocol from the Cardio-thoracic ICU at the Medical University of Vienna is given below:


Figure 5. Example of a protocol for glycaemic control in the ICU Conversion to mmol/L requires mg/dL values to be multiplied by 0.06.

Treatment of stress induced hyperglycaemia outside the ICU has not been formally assessed until now.


10. Refeeding syndrome The refeeding syndrome is a potentially lethal and often forgotten condition associated with feeding of chronically malnourished individuals or individuals with little or no nutrient intake for 5-10 days (Table 1). The hallmark biochemical feature is hypophosphataemia but many other clinical signs are possible. The route of feeding does not have a specific effect on the refeeding syndrome. [1, 37] • Patients with anorexia nervosa • Patients with chronic alcoholism • Cancer patients • Postoperative patients • Elderly patients • Patients with uncontrolled diabetes mellitus • Patients with chronic malnutrition • Marasmus • Prolonged fasting or low energy diet • Morbid obesity with profound weight loss • High stress patients unfed for > 7 days • Inflammatory bowel disease • Chronic pancreatitis • Cystic fibrosis • Short bowel syndrome • Long term antacid use • Long term diuretic use Table 2. Patients at high risk of refeeding syndrome [37] Key pathophysiological features of the refeeding syndrome: • Fluid balance • Glucose homeostasis • Vitamin B1 deficiency. Hyperlactataemia/lactic acidosis • Hypophosphataemia • Hypomagnesaemia • Hypokalaemia The incidence of the refeeding syndrome may be as high as 25% for cancer patients, and as many as 34% of intensive care patients experience hypophosphataemia within 2 days of starting artificial nutrition. The clinical presentation may be variable, and some features are readily compatible with other disease processes and a poor general condition. Based on case reports the syndrome is potentially fatal, often unrecognized and poorly treated especially outside areas with close monitoring such as intensive care units. Refeeding should not be delayed until biochemical abnormalities have been corrected. According to the most recent NICE recommendations (Table 2), progressive increase in nutrient intake, correction of biochemical abnormalities and close monitoring allow early and safe refeeding.

• One or more • BMI < 16 • Unintentional weight loss > 15 % in 3-6 months • Little or no nutritional intake for > 10 days • Low potassium, phosphate, magnesium before feeding

• Two or more • BMI <18.5


• Unintentional weight loss > 10 % in 3-6 months • Little or no nutritional intake for > 5 days • History of alcohol misuse or chronic drug use (insulin, antacids, diuretics)

Table 3. NICE recommendations to identify high risk patients based on cases and expert opinion[1]

10.1. Pathophysiology The pathophysiology is determined by the occurrence of starvation followed by refeeding. During starvation the basal needs for glucose must be supplied by gluconeogenesis from protein when glycogen stores have been depleted. The metabolic and hormonal changes aim to minimize this protein break-down. The main source of energy is lipid, and increased levels of ketone bodies stimulate the brain to utilize ketone bodies instead of glucose. The metabolic rate progressively decreases by 20-25%. During this phase cells tend to shrink and lose large amounts of intracellular electrolytes. The serum levels may however remain normal despite severe depletion. With refeeding, insulin levels increase and glucagon levels decrease. Protein, glycogen and fat synthesis is stimulated and cell volumes increase again. This anabolic phase necessitates a supply of nutrients, but also of large amounts of phosphate and magnesium as well as cofactors such as thiamine. The role of depletion of micronutrients has not yet been well investigated. Insulin stimulates glucose uptake into cells with the help of the Na-K ATPase symporter. Magnesium and phosphate are also taken up by the cells. Water follows by osmosis, cell volume tends to increase. This is by itself a strong anabolic signal. As a consequence the serum levels of these electrolytes may decrease dramatically within a short period of time and the metabolic rate may increase above the physiological tolerance of the cardio-respiratory system.

10.2. Clinical symptoms:

10.2.1. Fluid equilibrium Refeeding with carbohydrate can induce reduced sodium and water excretion, with extracellular volume expansion and weight gain. Volume expansion and poor fluid tolerance due to the reduced cardiac mass of malnutrition may result in cardiac failure.[23, 38] Refeeding predominantly with protein and lipid may however result in fluid loss. 10.2.2. Glucose and lipid metabolism The capacity to metabolize glucose decreases within a few days of even partial starvation. During refeeding with glucose gluconeogenesis will be suppressed or at least reduced in critically ill patients, but the tolerance for glucose is limited. Hyperglycaemia with osmotic dieresis and metabolic acidosis is possible and should be detected early with proper monitoring. Thus relative overnutrition and insufficient treatment of the insulin resistance of starvation may promote lipogenesis. Maximal lipid tolerance is 3.8 g.kg-1.day-1 and can be much lower during critical illness.[39]


10.2.3. Thiamine deficiency Thiamine is a cofactor of several enzymes such as the transketolases. The vitamin deficiency of malnutrition may be exacerbated with refeeding and an increased intracellular need for vitamins. Thiamine deficiency is associated with Wernicke’s encephalopathy (confusion, ocular disturbance, ataxia, coma) and Korsakov’s syndrome (short-term memory impairment and confabulation). Thiamine deficiency is also associated with hyperlactataemia (lactic acidosis) without other shock symptoms.[40] 10.2.4. Hypophosphataemia Hypophosphataemia is the most frequent sign of the refeeding syndrome. Phosphate is the major intracellular anion involved - in the form of ATP - in energy storage, and in intracellular buffering, as an essential initial step in glycolysis, and as a structural part of cell membranes. Many enzymes are activated by phosphate binding.[24, 25] Phosphate has multiple functions: • General cell function • Metabolic pathways • Intracellular buffer • Control of enzyme function • Excitation-stimulus coupling and nervous system conduction • Chemotaxis & phagocytosis of leucocytes • Platelets: clot retraction • Erythrocyte oxygen affinity • Muscle function • Neurological function • Avoidance of thrombocytopenia Phosphate is the major intra-cellular anion and is shifted rapidly between the intracellular and extracellular compartments. The driving forces for these shifts are the metabolic rate, the ingestion of carbohydrates and lipids, and finally the acid-base balance. The majority of phosphate (85%) is stored in the organic matrix of bone as hydroxyl-apatite crystals, 14% is in cells and 1% in the blood. The intracellular concentration is typically 100 mmol.l-1. A small proportion is in the inorganic form while the majority is bound to intermediary carbohydrates, proteins and lipids. In the blood, phosphate is present in organic and inorganic forms at an overall concentration of 3.5-4 mmol.L-1. Typically only the inorganic form is measured by standard laboratory methods and the normal concentration of phosphate is therefore 0.9-1.3 mmol.L-1. Phosphate is present in sufficient amounts in a mixed diet; phosphate balance is determined primarily by the kidneys. Hypophosphataemia is categorized into • Mild 0.6-0.85 mmol/L • Moderate 0.3-0.6 mmol/L • Severe < 0.3 mmol/L In moderate and severe hypophosphataemia immediate intravenous replacement therapy is indicated. Current guidelines recommend the administration of 9 or 18 mmol respectively within a 12 hour period.[1] The next dose should be given after a repeat estimation of serum phosphate. In the intensive care setting supplementation with 45 mmol over a 3 hour period normalized phosphate in 98% of patients with moderate or severe hypophosphataemia.[41] The amount proposed should always be seen in addition to continuous background phosphate provision with typically 0.5 mmol.kg-1.d-1. Either inorganic phosphate or organic phosphate has been used. K PO4

- has often been used when concomitant hypokalaemia exists. Organic preparations such as glucose-1-phosphate or fructose-1-6-diphosphate have the advantage of minimizing the risk of precipitation when


calcium is also present in the solution. In all cases where phosphate is added to parenteral nutrition solutions organic preparations should be preferred. Unfortunately organic preparations have not received approval in all countries. Nutrition therapy should not be delayed until hypophosphataemia has been corrected. Both interventions: nutrition and correction of electrolytes should be done in parallel.[42] 10.2.5. Hypomagnesaemia Hypomagnesaemia is also frequent with refeeding and several acute severe disease states. Magnesium is a predominantly intracellular divalent cation. Magnesium levels < 0.5 mmol.L-1 are considered to be severely deficient and are often accompanied by clinical symptoms. Magnesium is an important cofactor in many enzyme systems such as those involved in ATP production, maintains the structural integrity of DNA, RNA and ribosomes, and affects the membrane potential of cells. The most prominent clinical features are cardiac arrhythmias including torsade de pointes, abdominal discomfort and anorexia, and neurological manifestations such as tremor, paraesthesia, tetany, seizures, weakness, etc.[43, 44] Supplementation is best achieved with a continuous infusion until normalization. The maintenance dose is 4-8 mmol.d-1. Oral magnesium supplementation can be associated with diarrhoea. 10.2.6. Hypokalaemia Hypokalaemia is frequently present in acute disease states especially those associated with an increased catecholamine release, but also during aggressive refeeding. Potassium is the most abundant monovalent intracellular cation. Its main function is to maintain the electrochemical membrane potential. A potassium < 3 mmol.L-1 is considered to be severely low. The most serious consequences are cardiac arrhythmias, but many other systems are also affected. Gastrointestinal features include ileus and constipation, the kidney has impaired concentration capacity, compensation of metabolic alkalosis is delayed, neuro-muscular function is impaired, but also endocrine function is disturbed with impaired glucose tolerance. 10.3. Treatment and prevention of the refeeding syndrome Stepwise approach: • Identify patients at risk • Check electrolytes • Start refeeding with 50% (or less) of energy intake recommendations • 8-10 kCal.kg-1.d-1 (actual body weight) • Increase gradually to reach recommendations within 3-5 days • Rehydrate carefully and monitor cardio-circulatory function • Replace electrolytes in sufficient amounts • Potassium 2-4 mmol.kg-1 • Phosphate 0.3-0.6 mmol.kg-1 • Magnesium 0.05-0.1 mmol.kg-1 • Calcium 0.05-0.1 mmol.kg-1 • Monitor electrolytes, metabolic tolerance and the clinical situation closely during the first 5-10 days of refeeding.


11. Summary In acute illness nutrition care needs specific attention. Patients often develop a stress-induced hyperglycaemia that is associated with more severe disease, and careful treatment with appropriate protocols improves outcome. The target for optimal glucose control is still unclear. All organ systems can be affected by nutrition care. Frequent complications are associated with over- and undernutrition. Knowledge of possible complications and regular monitoring of patient is mandatory, especially during the first 10 days of nutrition care. Checking for electrolyte disorders, metabolic abnormalities and clinical signs of heart and lung failure need to be routine in critically ill patients. Manifestations of the refeeding syndrome are frequent in patients with chronic and acute starvation, severe malnutrition, cancer and acute severe illness. Hypophosphataemia is the most frequent manifestation of the refeeding syndrome. 12. References: 1. Mehanna, H.M., J. Moledina, and J. Travis, Refeeding syndrome: what it is, and how to prevent and treat it. Bmj, 2008. 336(7659): p. 1495-8. 2. Poehlman, E.T., Energy expenditure and requirements in aging humans. J Nutr, 1992. 122(11): p. 2057-65. 3. Nardo, P., et al., Clinical relevance of parenteral nutrition prescription and administration in 200 hospitalized patients: a quality control study. Clin Nutr, 2008. 27(6): p. 858-64. 4. Acheson, K.J., et al., Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. Am J Clin Nutr, 1988. 48(2): p. 240-7. 5. Pingleton, S.K., Enteral nutrition in patients with respiratory disease. Eur Respir J, 1996. 9(2): p. 364-70. 6. Cumming, A.D., J.R. Farquhar, and I.A. Bouchier, Refeeding hypophosphataemia in anorexia nervosa and alcoholism. Br Med J (Clin Res Ed), 1987. 295(6596): p. 490-1. 7. Kohn, M.R., N.H. Golden, and I.R. Shenker, Cardiac arrest and delirium: presentations of the refeeding syndrome in severely malnourished adolescents with anorexia nervosa. J Adolesc Health, 1998. 22(3): p. 239-43. 8. Svanfeldt, M., et al., Effects of 3 days of "postoperative" low caloric feeding with or without bed rest on insulin sensitivity in healthy subjects. Clin Nutr, 2003. 22(1): p. 31-8. 9. Watters, J.M., et al., Aging exaggerates the blood glucose response to total parenteral nutrition. Can J Surg, 1996. 39(6): p. 481-5. 10. Henneberg, S., J. Sjolin, and H. St Jernstrom, Over-feeding as a cause of fever in intensive care patients. Clin Nutr, 1991. 10(5): p. 266-71. 11. Dvir, D., J. Cohen, and P. Singer, Computerized energy balance and complications in critically ill patients: an observational study. Clin Nutr, 2006. 25(1): p. 37-44. 12. Villet, S., et al., Negative impact of hypocaloric feeding and energy balance on clinical outcome in ICU patients. Clin Nutr, 2005. 24(4): p. 502-9. 13. Pirat, A., et al., Comparison of measured versus predicted energy requirements in critically ill cancer patients. Respir Care, 2009. 54(4): p. 487-94. 14. Walker, R.N. and R.A. Heuberger, Predictive equations for energy needs for the critically ill. Respir Care, 2009. 54(4): p. 509-21. 15. Weekes, C.E., Controversies in the determination of energy requirements. Proceedings of the Nutrition Society, 2007. 66: p. 367-377. 16. Talpers, S.S., et al., Nutritionally associated increased carbon dioxide production. Excess total calories vs high proportion of carbohydrate calories. Chest, 1992. 102(2): p. 551-5. 17. Pingleton, S.K. and G.S. Harmon, Nutritional management in acute respiratory failure. Jama, 1987. 257(22): p. 3094-9. 18. Choban, P.S., et al., Hypoenergetic nutrition support in hospitalized obese patients: a simplified method for clinical application. Am J Clin Nutr, 1997. 66(3): p. 546-50.


19. Sedlacek, M., A.C. Schoolwerth, and B.D. Remillard, Electrolyte disturbances in the intensive care unit. Semin Dial, 2006. 19(6): p. 496-501. 20. Silvis, S.E. and P.D. Paragas, Jr., Paresthesias, weakness, seizures, and hypophosphatemia in patients receiving hyperalimentation. Gastroenterology, 1972. 62(4): p. 513-20. 21. Whang, R., M.P. Ryan, and J.K. Aikawa, Magnesium deficiency: a cause of reversible renal failure. Lancet, 1973. 1(7795): p. 135-6. 22. Bloom, W.L., Carbohydrates and water balance. Am J Clin Nutr, 1967. 20(2): p. 157-62. 23. Bloom, W.L. and W. Mitchell, Jr., Salt excretion of fasting patients. Arch Intern Med, 1960. 106: p. 321-6. 24. Amanzadeh, J. and R.F. Reilly, Jr., Hypophosphatemia: an evidence-based approach to its clinical consequences and management. Nat Clin Pract Nephrol, 2006. 2(3): p. 136-48. 25. Bugg, N.C. and J.A. Jones, Hypophosphataemia. Pathophysiology, effects and management on the intensive care unit. Anaesthesia, 1998. 53(9): p. 895-902. 26. Camp, M.A. and M. Allon, Severe hypophosphatemia in hospitalized patients. Miner Electrolyte Metab, 1990. 16(6): p. 365-8. 27. Capes, S.E., et al., Stress hyperglycaemia and increased risk of death after myocardial infarction in patients with and without diabetes: a systematic overview. Lancet, 2000. 355(9206): p. 773-8. 28. Foo, K., et al., A single serum glucose measurement predicts adverse outcomes across the whole range of acute coronary syndromes. Heart, 2003. 89(5): p. 512-6. 29. Gandhi, G.Y., et al., Intraoperative hyperglycemia and perioperative outcomes in cardiac surgery patients. Mayo Clin Proc, 2005. 80(7): p. 862-6. 30. Marfella, R., et al., Effects of stress hyperglycemia on acute myocardial infarction: role of inflammatory immune process in functional cardiac outcome. Diabetes Care, 2003. 26(11): p. 3129-35. 31. Norhammar, A., et al., Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus: a prospective study. Lancet, 2002. 359(9324): p. 2140-4. 32. Ouattara, A., et al., Poor Intraoperative Blood Glucose Control Is Associated with a Worsened Hospital Outcome after Cardiac Surgery in Diabetic Patients. Anesthesiology, 2005. 103(4): p. 687-694. 33. Umpierrez, G.E., et al., Hyperglycemia: an independent marker of in-hospital mortality in patients with undiagnosed diabetes. J Clin Endocrinol Metab, 2002. 87(3): p. 978-82. 34. Van den Berghe, G., et al., Intensive insulin therapy in the critically ill patients. N Engl J Med, 2001. 345(19): p. 1359-67. 35. Van den Berghe, G., et al., Intensive insulin therapy in critically ill patients: NICE-SUGAR or Leuven blood glucose target? J Clin Endocrinol Metab, 2009. 36. Brunkhorst, F.M., et al., Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med, 2008. 358(2): p. 125-39. 37. Crook, M.A., V. Hally, and J.V. Panteli, The importance of the refeeding syndrome. Nutrition, 2001. 17(7-8): p. 632-7. 38. Veverbrants, E. and R.A. Arky, Effects of fasting and refeeding. I. Studies on sodium, potassium and water excretion on a constant electrolyte and fluid intake. J Clin Endocrinol Metab, 1969. 29(1): p. 55-62. 39. Druml, W., et al., Fat elimination in acute renal failure: long-chain vs medium-chain triglycerides. Am J Clin Nutr, 1992. 55(2): p. 468-72. 40. Madl, C., et al., Lactic acidosis in thiamine deficiency. Clin Nutr, 1993. 12(2): p. 108-11. 41. Charron, T., et al., Intravenous phosphate in the intensive care unit: more aggressive repletion regimens for moderate and severe hypophosphatemia. Intensive Care Med, 2003. 29(8): p. 1273-8. 42. NICE, National Institute for Health and Clinical Excellence: Nutrition support in adults., in Clinical guideline CG322006.


43. Weisinger, J.R. and E. Bellorin-Font, Magnesium and phosphorus. Lancet, 1998. 352(9125): p. 391-6. 44. Whang, R., Magnesium deficiency: pathogenesis, prevalence, and clinical implications. Am J Med, 1987. 82(3A): p. 24-9.

icu nutrition: treatment and problem solving topic 18

Documents