The scope of this review is to provide practical guidelines for nutritional management of critically ill patients with sepsis with or without multiple organ failure (MOF). Basically, any nutritional intervention must be based on a better understanding of septic ‘autocannibalism’ [1
{"title":"Nutritional support in sepsis and multiple organ failure.","authors":"Gérard Nitenberg","doi":"10.1159/000072757","DOIUrl":"https://doi.org/10.1159/000072757","url":null,"abstract":"The scope of this review is to provide practical guidelines for nutritional management of critically ill patients with sepsis with or without multiple organ failure (MOF). Basically, any nutritional intervention must be based on a better understanding of septic ‘autocannibalism’ [1","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"8 ","pages":"223-40; discussion 240-4"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000072757","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22571608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Burn patients have the highest metabolic rate of all critically ill or injured patients. The metabolic response to a severe burn injury is characterized by a hyperdynamic cardiovascular response, increased energy expenditure, accelerated glycogen and protein breakdown, lipolysis, loss of lean body mass and body weight, delayed wound healing, and immune depression [1, 2]. This response is mediated by increases in circulating levels of the catabolic hormones, catecholamines, cortisol, and glucagon [3]. Catecholamines increase up to 10 times normal. Catabolism after major burn injury begins on the 5th day after injury and continues up to 9 months later [4]. Increasing age, weight, and delay in definitive surgical treatment predict increased catabolism in children. In adults, the response increases up to age 50 where it plateaus [5]. The body surface area burned increases catabolism until a 40% body burn is reached. The magnitude of metabolic expenditure is 1.5 to twice normal in burns of greater than 40% total body surface area (TBSA). Catabolism is further increased by 50% with environmental cooling or the development of sepsis. Hypermetabolism and muscle protein catabolism continue long after completion of wound closure [4]. Protein breakdown continues 6 and 9 months after severe burn. There is almost complete lack of bone growth for 2 years after injury resulting in long-term osteopenia which may adversely affect peak bone mass accumulation [6, 7]. Severely burned children with a burn size of 80% have a linear growth delay for years after injury [8].
{"title":"Modulation of the post-burn hypermetabolic state.","authors":"Jong O Lee, David N Herndon","doi":"10.1159/000072747","DOIUrl":"https://doi.org/10.1159/000072747","url":null,"abstract":"Burn patients have the highest metabolic rate of all critically ill or injured patients. The metabolic response to a severe burn injury is characterized by a hyperdynamic cardiovascular response, increased energy expenditure, accelerated glycogen and protein breakdown, lipolysis, loss of lean body mass and body weight, delayed wound healing, and immune depression [1, 2]. This response is mediated by increases in circulating levels of the catabolic hormones, catecholamines, cortisol, and glucagon [3]. Catecholamines increase up to 10 times normal. Catabolism after major burn injury begins on the 5th day after injury and continues up to 9 months later [4]. Increasing age, weight, and delay in definitive surgical treatment predict increased catabolism in children. In adults, the response increases up to age 50 where it plateaus [5]. The body surface area burned increases catabolism until a 40% body burn is reached. The magnitude of metabolic expenditure is 1.5 to twice normal in burns of greater than 40% total body surface area (TBSA). Catabolism is further increased by 50% with environmental cooling or the development of sepsis. Hypermetabolism and muscle protein catabolism continue long after completion of wound closure [4]. Protein breakdown continues 6 and 9 months after severe burn. There is almost complete lack of bone growth for 2 years after injury resulting in long-term osteopenia which may adversely affect peak bone mass accumulation [6, 7]. Severely burned children with a burn size of 80% have a linear growth delay for years after injury [8].","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"8 ","pages":"39-49; discussion 49-56"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000072747","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22570538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Key vitamins and trace elements in the critically ill.","authors":"Mette M Berger, René L Chioléro","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"8 ","pages":"99-111; discussion 111-7"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22570541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
That pancreatic rest and a reduction in exocrine secretion may allow a more expedient resolution of pancreatic inflammation is an important clinical precept in the management of patients with acute pancreatitis. Fortunately, the most common deleterious effect of early advancement to oral diet is an uncomplicated exacerbation of symptoms, which in one multi-center trial occurred in 21% of patients recovering from acute pancreatitis [1]. Of greater concern is a true exacerbation of pancreatitis, which occurs in less than one fifth of those patients who demonstrate an exacerbation of symptoms (or in 4.3% of patients overall) [1]. Relapse in response to early advancement to oral diet does impact patient outcome with regard to length of hospitalization. Length of hospitalization after advancement to oral diet was prolonged from 7 days in those patients who advanced successfully, to 18 days in those patients who suffered relapse [1]. Total length of hospitalization was nearly doubled from 18 to 33 days (p 0.002), when relapse occurred in response to early advancement to oral diet [1]. The development of late complications of major peripancreatic infection in response to early dietary advancement described in early retrospective studies [2] has not been demonstrated in more recent prospective studies. The understanding of what constitutes pancreatic rest has improved over the past decade. A reduction in the enzymatic protein portion of pancreatic exocrine secretion appears to be the most important factor in resolving the inflammatory response. While fluid volume and bicarbonate output from the pancreas are often simultaneously stimulated with increases in protein
{"title":"Nutritional support in acute pancreatitis.","authors":"Stephen A McClave","doi":"10.1159/000072756","DOIUrl":"https://doi.org/10.1159/000072756","url":null,"abstract":"That pancreatic rest and a reduction in exocrine secretion may allow a more expedient resolution of pancreatic inflammation is an important clinical precept in the management of patients with acute pancreatitis. Fortunately, the most common deleterious effect of early advancement to oral diet is an uncomplicated exacerbation of symptoms, which in one multi-center trial occurred in 21% of patients recovering from acute pancreatitis [1]. Of greater concern is a true exacerbation of pancreatitis, which occurs in less than one fifth of those patients who demonstrate an exacerbation of symptoms (or in 4.3% of patients overall) [1]. Relapse in response to early advancement to oral diet does impact patient outcome with regard to length of hospitalization. Length of hospitalization after advancement to oral diet was prolonged from 7 days in those patients who advanced successfully, to 18 days in those patients who suffered relapse [1]. Total length of hospitalization was nearly doubled from 18 to 33 days (p 0.002), when relapse occurred in response to early advancement to oral diet [1]. The development of late complications of major peripancreatic infection in response to early dietary advancement described in early retrospective studies [2] has not been demonstrated in more recent prospective studies. The understanding of what constitutes pancreatic rest has improved over the past decade. A reduction in the enzymatic protein portion of pancreatic exocrine secretion appears to be the most important factor in resolving the inflammatory response. While fluid volume and bicarbonate output from the pancreas are often simultaneously stimulated with increases in protein","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"8 ","pages":"207-15; discussion 215-21"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000072756","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22570547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lipid metabolism is altered in the critically ill patient as a result of changes in the status of hormones and other mediators [for reviews see, 1–3]. Enhanced mobilization of adipose tissue triacylglycerol stores is characteristic of the metabolic response to severe stress. This process is promoted by catecholamines and inflammatory cytokines, such as tumor necrosis factor (TNF)and interleukin (IL)-1, and is exaggerated by the decreased insulin sensitivity of adipose tissue. The release of fatty acids from adipose tissue is frequently in excess of energy requirements. Those fatty acids not oxidized may be re-esterified into triacylglycerols in the liver and packaged into very low-density lipoproteins (VLDLs). Hepatic triacylglycerol production is increased in critical illness and this can lead to lipid deposition (steatosis) in the liver. Nevertheless, hepatic triacylglycerol output (as VLDLs) is also increased in critical illness. In some conditions (e.g. trauma or after surgery) triacylglycerol clearance is not impaired (or may even be increased) and so plasma triacylglycerol concentrations remain normal (or may even be decreased). However, in some conditions (e.g. sepsis), the activity of adipose tissue lipoprotein lipase is suppressed by inflammatory cytokines (e.g. TNF and IL-1) and insulin resistance, and so triacylglycerols are not efficiently cleared from the circulation. Thus, hypertriacylglycerolemia occurs in such patients. VLDLs can bind endotoxin and target it for degradation in liver parenchymal cells. Thus, the increase in VLDL concentration may be, in part, a protective mechanism. The plasma cholesterol concentration is decreased in stress conditions, with the concentrations of both low(LDLs) and highdensity lipoproteins (HDLs) being decreased. This decrease occurs despite increased hepatic cholesterol production. The decreased HDL concentration
{"title":"Lipids and the critically ill patient.","authors":"Philip C Calder","doi":"10.1159/000072749","DOIUrl":"https://doi.org/10.1159/000072749","url":null,"abstract":"Lipid metabolism is altered in the critically ill patient as a result of changes in the status of hormones and other mediators [for reviews see, 1–3]. Enhanced mobilization of adipose tissue triacylglycerol stores is characteristic of the metabolic response to severe stress. This process is promoted by catecholamines and inflammatory cytokines, such as tumor necrosis factor (TNF)and interleukin (IL)-1, and is exaggerated by the decreased insulin sensitivity of adipose tissue. The release of fatty acids from adipose tissue is frequently in excess of energy requirements. Those fatty acids not oxidized may be re-esterified into triacylglycerols in the liver and packaged into very low-density lipoproteins (VLDLs). Hepatic triacylglycerol production is increased in critical illness and this can lead to lipid deposition (steatosis) in the liver. Nevertheless, hepatic triacylglycerol output (as VLDLs) is also increased in critical illness. In some conditions (e.g. trauma or after surgery) triacylglycerol clearance is not impaired (or may even be increased) and so plasma triacylglycerol concentrations remain normal (or may even be decreased). However, in some conditions (e.g. sepsis), the activity of adipose tissue lipoprotein lipase is suppressed by inflammatory cytokines (e.g. TNF and IL-1) and insulin resistance, and so triacylglycerols are not efficiently cleared from the circulation. Thus, hypertriacylglycerolemia occurs in such patients. VLDLs can bind endotoxin and target it for degradation in liver parenchymal cells. Thus, the increase in VLDL concentration may be, in part, a protective mechanism. The plasma cholesterol concentration is decreased in stress conditions, with the concentrations of both low(LDLs) and highdensity lipoproteins (HDLs) being decreased. This decrease occurs despite increased hepatic cholesterol production. The decreased HDL concentration","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"8 ","pages":"75-91; discussion 91-8"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000072749","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22570540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Obesity is a common medical condition affecting more than 1 in 10 adults in Western European countries [1]. Its prevalence varies considerably in different countries. In Europe, it amounts to about 10–15% of the middleaged population. It is highest in Eastern European countries, in North America, high in Africa and Eastern Asian countries, where it is strongly associated with poverty, but lower in Japan and China. There has been a progressive rise in the overall prevalence of obesity during the last decade, both in adults and children. The medical and economical consequences are enormous. The medical spectrum of obesity is wide, ranging from simple overweight without associated medical risk, to morbid obesity with severe associated comorbidities [1]. Various diagnostic criteria have been used; the most useful and simplest relies on the body mass index (BMI) scale. According to the International Obesity Task Force of the Word Health Organization, the severity of obesity is classified into 3 main categories: (1) overweight: BMI 25–30; (2) obesity: BMI 30–40, and (3) morbid obesity: BMI over 40 kg/m2. In addition to the absolute amount of body fat, as reflected by the BMI, body fat distribution is important: centralization of body fat to the abdominal visceral stores is associated with the development of systemic and metabolic complications [2]. Body fat distribution can easily be assessed in clinical practice using simple anthropometric measurements, such as waist circumference: a circumference over 102 cm in European men and 88 cm in women is an independent risk factor for a cluster of medical and metabolic
{"title":"Nutritional support of obese critically ill patients.","authors":"René L Chioléro, Luc Tappy, Mette M Berger","doi":"10.1159/000072755","DOIUrl":"https://doi.org/10.1159/000072755","url":null,"abstract":"Obesity is a common medical condition affecting more than 1 in 10 adults in Western European countries [1]. Its prevalence varies considerably in different countries. In Europe, it amounts to about 10–15% of the middleaged population. It is highest in Eastern European countries, in North America, high in Africa and Eastern Asian countries, where it is strongly associated with poverty, but lower in Japan and China. There has been a progressive rise in the overall prevalence of obesity during the last decade, both in adults and children. The medical and economical consequences are enormous. The medical spectrum of obesity is wide, ranging from simple overweight without associated medical risk, to morbid obesity with severe associated comorbidities [1]. Various diagnostic criteria have been used; the most useful and simplest relies on the body mass index (BMI) scale. According to the International Obesity Task Force of the Word Health Organization, the severity of obesity is classified into 3 main categories: (1) overweight: BMI 25–30; (2) obesity: BMI 30–40, and (3) morbid obesity: BMI over 40 kg/m2. In addition to the absolute amount of body fat, as reflected by the BMI, body fat distribution is important: centralization of body fat to the abdominal visceral stores is associated with the development of systemic and metabolic complications [2]. Body fat distribution can easily be assessed in clinical practice using simple anthropometric measurements, such as waist circumference: a circumference over 102 cm in European men and 88 cm in women is an independent risk factor for a cluster of medical and metabolic","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"8 ","pages":"187-200; discussion 200-5"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000072755","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22570546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Enteral versus parenteral nutrition: alterations in mechanisms of function in mucosal host defenses.","authors":"Nicholas A Meyer, Kenneth A Kudsk","doi":"10.1159/000072752","DOIUrl":"https://doi.org/10.1159/000072752","url":null,"abstract":"","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"8 ","pages":"133-42; discussion 142-8"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000072752","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22570543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Body protein homeostasis primarily depends on protein intake, even if other dietary factors, such as the energy content of the diet also play a role. However, protein intake can affect protein homeostasis in a variety of ways. First and obviously, the quantity of dietary proteins plays a major role. During short-term adaptation, an increased protein intake results in a temporarily higher nitrogen balance. However, over the long term, nitrogen balance stabilized itself, unless an excess energy intake is associated with the increased protein intake. The amino acid composition is the second classical and important factor. The amount of indispensable amino acids ingested should meet the amino acid requirements. These amino acids will be utilized for protein synthesis, but also as precursors of metabolically active compounds or for regulatory purposes. Digestibility is the other factor affecting the ‘quality’ of dietary proteins. It is classically lower for vegetal than for animal proteins, although recent data show that many plant proteins are highly digestible [1]. The overall quality of a protein can be assessed by global approaches such as the measurement of postprandial nitrogen utilization, using 15N-labeled proteins. More recently a third factor modulating protein retention has been identified. The bioavailability of dietary amino acids over time can be modified by two different means: the pattern of feeding, and the rate of digestion. The influence of the pattern of feeding has been studied for years, for example in the setting of parenteral nutrition. However, it was demonstrated only recently that modifying the repartition of the daily protein intake over a day modulates protein retention [2]. With respect to the influence of the rate of digestion, we recently proposed the concept of ‘slow and fast’ dietary proteins [3] and
{"title":"Optimization of dietary protein intake during aging.","authors":"B. Beaufrère","doi":"10.1159/000067506","DOIUrl":"https://doi.org/10.1159/000067506","url":null,"abstract":"Body protein homeostasis primarily depends on protein intake, even if other dietary factors, such as the energy content of the diet also play a role. However, protein intake can affect protein homeostasis in a variety of ways. First and obviously, the quantity of dietary proteins plays a major role. During short-term adaptation, an increased protein intake results in a temporarily higher nitrogen balance. However, over the long term, nitrogen balance stabilized itself, unless an excess energy intake is associated with the increased protein intake. The amino acid composition is the second classical and important factor. The amount of indispensable amino acids ingested should meet the amino acid requirements. These amino acids will be utilized for protein synthesis, but also as precursors of metabolically active compounds or for regulatory purposes. Digestibility is the other factor affecting the ‘quality’ of dietary proteins. It is classically lower for vegetal than for animal proteins, although recent data show that many plant proteins are highly digestible [1]. The overall quality of a protein can be assessed by global approaches such as the measurement of postprandial nitrogen utilization, using 15N-labeled proteins. More recently a third factor modulating protein retention has been identified. The bioavailability of dietary amino acids over time can be modified by two different means: the pattern of feeding, and the rate of digestion. The influence of the pattern of feeding has been studied for years, for example in the setting of parenteral nutrition. However, it was demonstrated only recently that modifying the repartition of the daily protein intake over a day modulates protein retention [2]. With respect to the influence of the rate of digestion, we recently proposed the concept of ‘slow and fast’ dietary proteins [3] and","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"33 1","pages":"103-15; discussion 115-8"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85202334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In the practice of nutritional intervention as it relates to the sick patient, the future is today! Predicting future developments in nutritional intervention depends on technical innovations, yet to be realized, which will facilitate the implementation of advances in nutritional support. These innovations include delivery devices, ranging from catheters to packaging and enhanced nutrient substrate composition, based on greater understanding of their function in health and disease. But, by merely expanding the use of contemporary nutritional support to the field of obstetrics, heart disease, human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS) and bone marrow transplantation (BMT), we can immediately amplify our application of nutritional intervention, bringing the future to it. This would benefit patient populations in whom nutritional support is not routinely considered, despite medical evidence to the contrary.
{"title":"Nutritional intervention: what of the future?","authors":"Michael M Meguid","doi":"10.1159/000067504","DOIUrl":"https://doi.org/10.1159/000067504","url":null,"abstract":"In the practice of nutritional intervention as it relates to the sick patient, the future is today! Predicting future developments in nutritional intervention depends on technical innovations, yet to be realized, which will facilitate the implementation of advances in nutritional support. These innovations include delivery devices, ranging from catheters to packaging and enhanced nutrient substrate composition, based on greater understanding of their function in health and disease. But, by merely expanding the use of contemporary nutritional support to the field of obstetrics, heart disease, human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS) and bone marrow transplantation (BMT), we can immediately amplify our application of nutritional intervention, bringing the future to it. This would benefit patient populations in whom nutritional support is not routinely considered, despite medical evidence to the contrary.","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"7 ","pages":"277-96; discussion 296-300"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000067504","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22155640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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