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1
Turk, Vito. Intracellular Protein Catabolism II. Springer London, Limited, 2012.
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2
Turk, Vito. Intracellular Protein Catabolism II. Springer, 2012.
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3
Blaser, Annika Reintam, and Adam M. Deane. Normal physiology of nutrition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0201.
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Energy is derived from three major categories of macronutrient—carbohydrate, lipid, and protein. While energy requirements to maintain stable weight can be estimated, it is uncertain if meeting these energy requirements improves outcomes in the critically ill. In health, excess energy is stored via non-oxidative metabolism and during periods of inadequate energy delivery catabolism of storage products occurs. Both storing and using the stores cost energy, each may require up to quarter of energy contained in stored nutrient. Excess carbohydrate stored as glycogen is easily available, albeit in a limited amount. Storage of lipid is the largest energy repository, but requires complex metabolism and is limited by low oxidative capacity. Protein catabolism normally contributes less than 5% of energy requirements, but during periods of inadequate energy delivery or increased catabolism there is a marked increase in endogenous protein breakdown.
4
Egreteau, Pierre-Yves, and Jean-Michel Boles. Assessing nutritional status in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0204.
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Decreased nutrient intake, increased body requirements, and/or altered nutrient utilization are frequently combined in critically-ill patients. The initial nutritional status and the extent of the disease-related catabolism are the main risk factors for nutrition- related complications. Many complications are related to protein energy malnutrition, which is frequent in the ICU setting. Assessing nutritional status pursues several different goals. Nutritional assessment is required for patients presenting with clinical evidence of malnutrition, with chronic diseases, with acute conditions accompanied by a high catabolic rate, and elderly patients. Recording the patient’s history, nutrient intake, and physical examination, and subjective global assessment allows classification of nutritional status. All the traditional markers of malnutrition, anthropometric measurements and plasma proteins, lose their specificity in the sick adult as each may be affected by a number of non-nutritional factors. Muscle function evaluated by hand-grip strength in cooperative patients and serum albumin provide an objective risk assessment. Several nutritional indices have been validated in specific groups of patients to identify patients at risk of nutritionally-mediated complications and, therefore, the need for nutritional support. A strong suspicion remains the best way of uncovering potentially harmful nutritional deficiencies.
5
Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0032.
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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
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Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_001.
Full textAbstract:
Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
7
Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_002.
Full textAbstract:
Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.
8
Rabier, Daniel. Hyperammonemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0078.
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Ammonia, an end-product of protein and amino acid catabolism toxic to the brain, must be removed quickly from the circulation. Its removal is achieved in two steps: glutamine synthesis and urea synthesis. Hyperammonemia results from either an excess of production or defective elimination. There are two main etiologies of hyperammonemia: inherited or acquired. Inherited causes are mainly related to defective elimination while acquired ones result either from excess production or deficient detoxification. Good laboratory diagnostic tools are necessary to make the right diagnosis.
9
Puthucheary, Zudin, Hugh Montgomery, Nicholas Hart, and Stephen Harridge. Skeletal Muscle Mass Regulation in Critical Illness. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0035.
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Muscle is a dynamic, plastic, and malleable tissue that is highly sensitive to mechanical and metabolic signals. Muscle mass is regulated by protein homeostasis, with protein being continually turned over, reflecting a balance between synthesis and breakdown. This chapter discusses the effect of critical illness on skeletal muscle mass, protein homeostasis, and the intracellular signalling driving anabolism and catabolism. The focus will be on the unique challenges to which the skeletal muscle are exposed, such as inflammation, sepsis, sedation, and inadequate nutrition, which, in combination with the disuse signals of immobilization and bed rest, engender dramatic changes in muscle structure and function. The mechanisms regulating muscle loss during critical illness are being unravelled, but many questions remain unanswered. Detailed understanding of these mechanisms will help drive strategies to minimize or prevent intensive care-acquired muscle weakness and the long-term consequences experienced by ICU survivors.
10
Wise, Matt, and Paul Frost. Nutritional support in the critically ill. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0334.
Full textAbstract:
Major injury evokes a constellation of reproducible hormonal, metabolic, and haemodynamic responses which are collectively termed ‘the adaptive stress response’. The purpose of the adaptive stress response is to facilitate tissue repair and restore normal homeostasis. If critical illness is prolonged, the adaptive stress response may become maladaptive, in essence exerting a parasitic effect leaching away structural proteins and impairing host immunity. Primarily therapy should be directed towards the underlying illness, as nutritional support per se will not reverse the stress response and its sequelae. Nonetheless, adequate nutritional support in the early stages of critical illness may attenuate protein catabolism and its adverse effects. This chapter covers nutritional assessment; detection of malnutrition; energy and protein requirements; monitoring the effectiveness of nutritional replacements; nutritional delivery; complications; and refeeding syndrome.
11
Rabier, Daniel. Amino Acids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0083.
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Amino acids present in the different biological fluids belong to two groups: the protein group, with the 21 classical amino acids constituting the backbone of the protein, and the nonprotein group, appearing in different metabolic pathways as intermediate metabolites. It is important to know and to be able to recognize the latter, as they are the markers of many inherited metabolic diseases. Three kinds of pathways must be considered: the catabolic pathways, the synthesis pathways, and the transport pathways. A disorder on a catabolic pathway induces an increase of all metabolites upstream and so an increase of the starting amino acid in all fluids. Any disorder on the synthetic pathway of a particular amino acid will induce a decrease of this amino acid in all fluids. When a transporter is located on a plasma membrane, its deficiency will result in normal or low concentration in plasma concomitant to a high excretion in urine.
12
Keshav, Satish, and Alexandra Kent. Unintentional weight loss. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0080.
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Body weight is determined by the combination of metabolic rate, calorie intake, and activity levels. Natural weight loss is usually due to declining muscle mass, with the redistribution of muscle mass in the extremities, leading to greater truncal fat stores. Unintentional weight loss refers to weight loss that is not voluntary, and can reflect serious underlying pathology. It can be caused by inadequate nutritional intake, increased metabolism, malabsorption, or a combination of these factors. Weight loss of 5% of body weight over 6–12 months should be investigated. Cachexia is a complex syndrome in which loss of body mass (fat and protein) cannot be reversed nutritionally, that is, is due to underlying disease processes inducing catabolism, rather than to inadequate nutritional intake.
13
Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B7 (biotin) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0011.
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Biotin is a water-soluble B vitamin (vitamin B7) which acts as a coenzyme to carboxylases and has roles in gluconeogenesis, fatty acid synthesis, and amino acid catabolism. Reduced activity of biotin-dependent enzymes (acetyl-CoA carboxylase I and II, and propionyl-CoA carboxylase) alters lipid metabolism and may impair synthesis of polyunsaturated fatty acids and prostaglandins; in addition, biotin has effects on gene expression by binding covalently to histones. Deficiency can be caused by prolonged consumption of egg whites, which contain the biotin-binding protein avidin. Smoking accelerates the degradation of biotin, which can result in marginal biotin deficiency. The effects of deficiency include disruption of immune function and lipid metabolism, with some evidence of teratogenicity in animals. Dietary deficiency is unlikely, although high consumption of egg whites should be avoided in pregnancy.
14
Baracos, Vickie E., Sharon M. Watanabe, and Kenneth C. H. Fearon. Aetiology, classification, assessment, and treatment of the anorexia-cachexia syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0205.
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Anorexia-cachexia is a heterogeneous and multifactorial syndrome most likely driven by systemic inflammation and neuroendocrine activation. Key diagnostic features include reduced appetite, weight loss, and muscle wasting. Key clinical problems include management of anorexia without resort to artificial nutritional support, and muscle wasting that cannot be completely arrested/reversed even with such intervention. Assessment should cover domains such as body stores of energy and protein, food intake, performance status, and factors resulting in excess catabolism. Intervention should be early rather than late, informed by the assessment process and focused on a multimodal approach (nutrition, exercise, and pharmacological agents). This chapter aims to discuss these issues and provide (a) the reader with some background principles to classification, (b) a simple approach to patient assessment and a robust algorithm for basic multimodal treatment, and (c) an overview of the evidence base for different pharmacological interventions.
15
Kumar, Navneet, Heather Henderson, Beverly D. Cameron, and Peter A. McCullough. Malnutrition, obesity, and undernutrition in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0106_update_001.
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Both overnutrition resulting in obesity and undernutrition leading to protein energy wasting contribute to chronic kidney disease-related morbidity and adverse outcomes. Early in the course of chronic kidney disease, goals should be set for a healthy body weight and lifelong efforts should be encouraged to attain and keep this goal. For patients with progressive chronic kidney disease, the development of weight loss and protein energy wasting is an ominous sign and is a clinical signal for a myriad of adverse catabolic processes that have been associated with poor outcomes including hospitalization and death, particularly for those with end-stage renal disease. Renal nutrition consultation at all stages of chronic kidney disease with frequent visits and education and counselling is needed to intercede early in both ends of the nutrition continuum in patients with chronic kidney disease.
16
Fervenza, Fernando C. Evaluation of Kidney Function, Glomerular Disease, and Tubulointerstitial Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0472.
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Several measures are used to evaluate kidney function: serum creatinine, urinalysis, renal clearance, and renal imaging. Creatinine is an end product of muscle catabolism and is commonly used as a filtration marker. Dysmorphic erythrocytes in the urinary sediment indicate bleeding in the upper urinary tract. A urine pH less than 5.5 excludes type 1 renal tubular acidosis. A pH greater than 7 suggests infection. Acidic urine is indicative of a high-protein diet, acidosis, and potassium depletion. Alkaline urine is associated with a vegetarian diet, alkalosis and urease-producing bacteria. Clearance of p-aminohippurate is a measure of renal blood flow. Kidney function is evaluated to determine disease states such as glomeruluar disease or tubulointerstitial disease. Clinical manifestations of glomerular injury can vary from the finding of isolated hematuria or proteinuria, or both. In addition, some patients who present with advanced renal insufficiency, hypertension, and shrunken, smooth kidneys are presumed to have chronic glomerulonephritis. Acute and chronic interstitial disease preferentially involves renal tubules.