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.

Tight glycemic control in critical care – The leading role of insulin sensitivity and patient variability: A review and model-based analysis

“…Absolute and relative insulin deficiency is a further cause. Finally, high glucose content nutritional regimes exacerbate hyperglycemia and thus mortality [18][19][20][21][22][23], whereas reducing glucose intake from all sources has reduced glycemic levels [19,22,[24][25][26] and can alleviate the impact of the hyperglycemic counter-regulatory response that drives the problem [1, 4,27,28]. Equally, insulin, with TGC, can ameliorate these inflammatory responses and improve insulin sensitivity and glycemic response [17,[29][30][31].…”

Serial plasma glucose changes in dogs suffering from severe dog bite wounds

“…The net effect of these hormones, coupled with a defective suppression of gluconeogenesis and resistance to the peripheral action of insulin, is hyperglycaemia. This is all part of the hypermetabolic response to trauma 12,30,34 , which may last for 7-10 days 12 . This phenomenon has been described in human medicine in response to acute injury and has been termed 'diabetes of injury' 42 .…”

“…Patients with severe injury therefore undergo an accelerated form of starvation 7,11,37 . During the hypermetabolic state, a number of alterations in carbohydrate metabolism are induced, these include 1,23,34,42 : • Enhanced peripheral uptake and utilisation of glucose by the wound and other organs such as the liver and spleen, which are involved in the immune response; • Increased glucose production stimulated by the release of epinephrine, cortisol, glucagon and growth hormone; • Hyperlactataemia due to hypoperfusion; • Decreased glucose production due to the release of gram-negative bacterial endotoxin, interleukin-6, insulin-like factors and decreased hepatic export or increased utilisation; • Depressed glycogenesis due to the persistent high rate of glycogen breakdown under the influence of epinephrine and glucagon, decreased glycogen synthetase activity or the presence of tumour necrosis factor (TNF); • A rise in extra-cellular glucose concentrations due to defective suppression of gluconeogenesis, glucose intolerance and resistance to the peripheral action of insulin, also termed 'diabetes of injury'. Tissue trauma with or without infection can initiate the systemic inflammatory response syndrome (SIRS), in which multiple inflammatory, immunological, coagulation and fibrinolytic cascades are activated and interact 18,20 .…”

Hypocaloric peripheral parenteral nutrition with lipid emulsion in postoperative gastrointestinal cancer patients

“…Surgical trauma induces a catabolic response with hypermetabolism and insulin-resistant hyperglycemia [3] . Traditionally, postoperative parenteral nutrition with full calories and high glucose loads results in deteriorating hyperglycemia, hyperosmolar state, increased carbon dioxide generation [4] , and net fat synthesis-deposition when the capacity of oxidation is overwhelmed.…”

“…HPPN is a method using lower glucose loads mixed with soluble alternatives via the peripheral venous route to avoid the complications of hypermetabolism, hyperglycemia and the use of central venous catheters in stressed patients [1,2] . Currently, HPPN (15-20 kcal/kg per day) has been a trend for managing postoperative patients in a situation of moderate malnutrition and short-term fast [3] . Our current study was designed as a prospective, randomized clinical trial to explore the effects of shortterm HPPN using lipid emulsion for patients with GI cancers following surgery.…”