title: Hypocaloric support in the critically ill.
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.
authors.affiliation: Metabolic and Nutritional Support Service, Fundación Santa Fe de Bogotá, Calle 123 No. 8-20, Bogotá, D.C., Colombia.
authors.forename: J F
authors.initials: JF
authors.lastname: Patiño
authors.forename: S E
authors.initials: SE
authors.lastname: de Pimiento
authors.forename: A
authors.initials: A
authors.lastname: Vergara
authors.forename: P
authors.initials: P
authors.lastname: Savino
authors.forename: M
authors.initials: M
authors.lastname: Rodríguez
authors.forename: J
authors.initials: J
authors.lastname: Escallón
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D002245:Carbon Dioxide / Q000378:metabolism; D002302:Cardiac Output / Q000502:physiology; D003422:Critical Care; D016638:Critical Illness; D004040:Dietary Carbohydrates / Q000008:administration & dosage; D004044:Dietary Proteins / Q000008:administration & dosage; D002149:Energy Intake; D004734:Energy Metabolism; D005234:Fatty Liver / Q000209:etiology; D005260:Female; D005334:Fever / Q000503:physiopathology; D005947:Glucose / Q000008:administration & dosage; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology / Q000378:metabolism; D008066:Lipolysis; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption / Q000502:physiology; D010289:Parenteral Nutrition, Total; D011506:Proteins / Q000378:metabolism; D013312:Stress, Physiological / Q000378:metabolism / Q000503:physiopathology; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D001786:Blood Glucose; D004040:Dietary Carbohydrates; D004044:Dietary Proteins; D011506:Proteins; D002245:Carbon Dioxide; D005947:Glucose