Hypocaloric Support in the Critically Ill
. The critically ill patient exhibits a well defined endocrine and metabolic adaptive response to stressor agents, characterized by incremented resting energy expenditure (hypermetabolism, which is believed to signify increased energy requirements), accelerated whole‐body proteolysis (hypercatabolis...
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Published in | World journal of surgery Vol. 23; no. 6; pp. 553 - 559 |
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Main Authors | , , , , , |
Format | Journal Article Conference Proceeding |
Language | English |
Published |
Berlin/Heidelberg
Springer‐Verlag
01.06.1999
Springer Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Abstract | .
The critically ill patient exhibits a well defined endocrine and metabolic adaptive response to stressor agents, characterized by incremented resting energy expenditure (hypermetabolism, which is believed to signify increased energy requirements), accelerated whole‐body proteolysis (hypercatabolism), and lipolysis. These phenomena occur in the acute stage, which is also characterized by hyperglycemia, typically accompanied by a hyperdynamic cardiovascular reaction manifested by high cardiac output, increased oxygen consumption, high body temperature, and decrease peripheral vascular resistance. High provisions of glucose‐derived calories tend to accentuate these reactions and increase the degree of hyperglycemia. We have adopted a hypocaloric‐hyperproteic regimen which is provided only during the first days of the flow phase of the adaptive response to injury, sepsis, or critical illness. Our regimen includes a daily supply of 100 to 200 g of glucose and 1.5 to 2.0 g of protein (synthetic amino acids) per kilogram of ideal body weight. We have analyzed the data on 107 critically ill patients, 70 men and 37 women, who were admitted to the surgical intensive care unit and who received nutritional support by the TPN hypocaloric modality for a minimum of 3 days. We found that the high caloric loads contained in TPN regimens results in additional metabolic stress, with consequent hyperdynamic cardiorespiratory repercussion, high CO2 production, and frequently hepatic steatosis. In contrast, our hypocaloric‐hyperproteic approach has resulted in a more physiologic clinical course and considerable reduction in cost. The infusion of high glucose loads, such as those used in hypercaloric TPN, does not seem to suppress the excessive endogenous production of glucose but instead markedly exacerbates the hyperglycemia of the postinjury and acute stress condition. We believe that the hypocaloric‐hyperproteic regimen we utilize during the first few days of the stress situation is more in accordance with the inflammatory and hormonal mediator climate of the initial stages of the flow phase and thus appears to be beneficial vis‐à‐vis the hypercaloric loads that many use as routine metabolic support in critically ill patients. |
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AbstractList | .
The critically ill patient exhibits a well defined endocrine and metabolic adaptive response to stressor agents, characterized by incremented resting energy expenditure (hypermetabolism, which is believed to signify increased energy requirements), accelerated whole‐body proteolysis (hypercatabolism), and lipolysis. These phenomena occur in the acute stage, which is also characterized by hyperglycemia, typically accompanied by a hyperdynamic cardiovascular reaction manifested by high cardiac output, increased oxygen consumption, high body temperature, and decrease peripheral vascular resistance. High provisions of glucose‐derived calories tend to accentuate these reactions and increase the degree of hyperglycemia. We have adopted a hypocaloric‐hyperproteic regimen which is provided only during the first days of the flow phase of the adaptive response to injury, sepsis, or critical illness. Our regimen includes a daily supply of 100 to 200 g of glucose and 1.5 to 2.0 g of protein (synthetic amino acids) per kilogram of ideal body weight. We have analyzed the data on 107 critically ill patients, 70 men and 37 women, who were admitted to the surgical intensive care unit and who received nutritional support by the TPN hypocaloric modality for a minimum of 3 days. We found that the high caloric loads contained in TPN regimens results in additional metabolic stress, with consequent hyperdynamic cardiorespiratory repercussion, high CO2 production, and frequently hepatic steatosis. In contrast, our hypocaloric‐hyperproteic approach has resulted in a more physiologic clinical course and considerable reduction in cost. The infusion of high glucose loads, such as those used in hypercaloric TPN, does not seem to suppress the excessive endogenous production of glucose but instead markedly exacerbates the hyperglycemia of the postinjury and acute stress condition. We believe that the hypocaloric‐hyperproteic regimen we utilize during the first few days of the stress situation is more in accordance with the inflammatory and hormonal mediator climate of the initial stages of the flow phase and thus appears to be beneficial vis‐à‐vis the hypercaloric loads that many use as routine metabolic support in critically ill patients. The critically ill patient exhibits a well defined endocrine and metabolic adaptive response to stressor agents, characterized by incremented resting energy expenditure (hypermetabolism, which is believed to signify increased energy requirements), accelerated whole-body proteolysis (hypercatabolism), and lipolysis. These phenomena occur in the acute stage, which is also characterized by hyperglycemia, typically accompanied by a hyperdynamic cardiovascular reaction manifested by high cardiac output, increased oxygen consumption, high body temperature, and decrease peripheral vascular resistance. High provisions of glucose-derived calories tend to accentuate these reactions and increase the degree of hyperglycemia. We have adopted a hypocaloric-hyperproteic regimen which is provided only during the first days of the flow phase of the adaptive response to injury, sepsis, or critical illness. Our regimen includes a daily supply of 100 to 200 g of glucose and 1.5 to 2.0 g of protein (synthetic amino acids) per kilogram of ideal body weight. We have analyzed the data on 107 critically ill patients, 70 men and 37 women, who were admitted to the surgical intensive care unit and who received nutritional support by the TPN hypocaloric modality for a minimum of 3 days. We found that the high caloric loads contained in TPN regimens results in additional metabolic stress, with consequent hyperdynamic cardiorespiratory repercussion, high CO2 production, and frequently hepatic steatosis. In contrast, our hypocaloric-hyperproteic approach has resulted in a more physiologic clinical course and considerable reduction in cost. The infusion of high glucose loads, such as those used in hypercaloric TPN, does not seem to suppress the excessive endogenous production of glucose but instead markedly exacerbates the hyperglycemia of the postinjury and acute stress condition. We believe that the hypocaloric-hyperproteic regimen we utilize during the first few days of the stress situation is more in accordance with the inflammatory and hormonal mediator climate of the initial stages of the flow phase and thus appears to be beneficial vis-à-vis the hypercaloric loads that many use as routine metabolic support in critically ill patients. The critically ill patient exhibits a well defined endocrine and metabolic adaptive response to stressor agents, characterized by incremented resting energy expenditure (hypermetabolism, which is believed to signify increased energy requirements), accelerated whole-body proteolysis (hypercatabolism), and lipolysis. These phenomena occur in the acute stage, which is also characterized by hyperglycemia, typically accompanied by a hyperdynamic cardiovascular reaction manifested by high cardiac output, increased oxygen consumption, high body temperature, and decrease peripheral vascular resistance. High provisions of glucose-derived calories tend to accentuate these reactions and increase the degree of hyperglycemia. We have adopted a hypocaloric-hyperproteic regimen which is provided only during the first days of the flow phase of the adaptive response to injury, sepsis, or critical illness. Our regimen includes a daily supply of 100 to 200 g of glucose and 1.5 to 2.0 g of protein (synthetic amino acids) per kilogram of ideal body weight. We have analyzed the data on 107 critically ill patients, 70 men and 37 women, who were admitted to the surgical intensive care unit and who received nutritional support by the TPN hypocaloric modality for a minimum of 3 days. We found that the high caloric loads contained in TPN regimens results in additional metabolic stress, with consequent hyperdynamic cardiorespiratory repercussion, high CO^sub 2^ production, and frequently hepatic steatosis. In contrast, our hypocaloric-hyperproteic approach has resulted in a more physiologic clinical course and considerable reduction in cost. The infusion of high glucose loads, such as those used in hypercaloric TPN, does not seem to suppress the excessive endogenous production of glucose but instead markedly exacerbates the hyperglycemia of the postinjury and acute stress condition. We believe that the hypocaloric-hyperproteic regimen we utilize during the first few days of the stress situation is more in accordance with the inflammatory and hormonal mediator climate of the initial stages of the flow phase and thus appears to be beneficial vis-à-vis the hypercaloric loads that many use as routine metabolic support in critically ill patients. [PUBLICATION ABSTRACT] The critically ill patient exhibits a well defined endocrine and metabolic adaptive response to stressor agents, characterized by incremented resting energy expenditure (hypermetabolism, which is believed to signify increased energy requirements), accelerated whole‐body proteolysis (hypercatabolism), and lipolysis. These phenomena occur in the acute stage, which is also characterized by hyperglycemia, typically accompanied by a hyperdynamic cardiovascular reaction manifested by high cardiac output, increased oxygen consumption, high body temperature, and decrease peripheral vascular resistance. High provisions of glucose‐derived calories tend to accentuate these reactions and increase the degree of hyperglycemia. We have adopted a hypocaloric‐hyperproteic regimen which is provided only during the first days of the flow phase of the adaptive response to injury, sepsis, or critical illness. Our regimen includes a daily supply of 100 to 200 g of glucose and 1.5 to 2.0 g of protein (synthetic amino acids) per kilogram of ideal body weight. We have analyzed the data on 107 critically ill patients, 70 men and 37 women, who were admitted to the surgical intensive care unit and who received nutritional support by the TPN hypocaloric modality for a minimum of 3 days. We found that the high caloric loads contained in TPN regimens results in additional metabolic stress, with consequent hyperdynamic cardiorespiratory repercussion, high CO 2 production, and frequently hepatic steatosis. In contrast, our hypocaloric‐hyperproteic approach has resulted in a more physiologic clinical course and considerable reduction in cost. The infusion of high glucose loads, such as those used in hypercaloric TPN, does not seem to suppress the excessive endogenous production of glucose but instead markedly exacerbates the hyperglycemia of the postinjury and acute stress condition. We believe that the hypocaloric‐hyperproteic regimen we utilize during the first few days of the stress situation is more in accordance with the inflammatory and hormonal mediator climate of the initial stages of the flow phase and thus appears to be beneficial vis‐à‐vis the hypercaloric loads that many use as routine metabolic support in critically ill patients. |
Author | Savino, Patricia Rodríguez, Mario Vergara, Arturo Patiño, José Félix Escallón, Jaime de Pimiento, Sonia Echeverri |
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Keywords | Human Critical state Increase Supplemented diet Metabolism Lipolysis Protein Parenteral administration Feeding Energetic cost Proteolysis Total Low calorie diet |
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SubjectTerms | Adolescent Adult Aged Biological and medical sciences Blood Glucose - analysis Carbon Dioxide - metabolism Cardiac Output - physiology Critical Care Critical Illness Dietary Carbohydrates - administration & dosage Dietary Proteins - administration & dosage Energy Intake Energy Metabolism Fatty Liver - etiology Female Fever - physiopathology Flow Phase Glucose Glucose - administration & dosage Hepatic Steatosis Humans Hyperglycemia Hyperglycemia - etiology Hyperglycemia - metabolism Ideal Body Weight Lipolysis Male Medical sciences Metabolic diseases Middle Aged Nutrition Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...) Oxygen Consumption - physiology Parenteral Nutrition, Total Proteins - metabolism Stress, Physiological - metabolism Stress, Physiological - physiopathology Surgical Intensive Care Unit Tropical medicine Vascular Resistance - physiology |
Title | Hypocaloric Support in the Critically Ill |
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