多脏器功能衰竭的代谢与营养支持

Metabolism and nutritionalsupport during MOF

The problems of inflammation and infection leading to organ dysfunction and failure continue to be the major concerns after injury and operations and with the intensive care for many diseases and problems.When systemic inflammatory response syndrome (SIRS) goes to multiple organ dysfunction syndrome (MODS) and multiple organ failure (MOF),the mortality ecomes high,ranging from 30-80% depending on the number of failed organs.In MOF or MODS respiratory failure develops with the need for ventilaroty support,accompanied by circulatory instability with depression of cardiac output and a decrease in peripheral resistance,depression of the immune system,coagulation defects,gastrointestinal problems,a rising bilirubin denoting hepatic dysfunction and central nervous depression.The elevation in whole body protein turnover after sepsis and trauma usually is accompanied by an increase in metabolic rate Hepatic output of acute phase proteins rises,lean tissue is catabolized to provide energy substrates for wound and inflammatory tissue.Plasma proteins drop due to inhibition of hepathic synthesis,an increase in capillary permeability,and the dilutional effect of extracellular fluid expansion can be observed.Muscle protein synthesis seems to be decreased.These changes are driven by a combination of the counterregulatory hormones (catecholamines,glucagon,cortisol,growth hormone) and the direct and indirect actions fo the various inflammatory mediators (IL-1,IL-6,and TNF),prostaglandins and kallikreins.The changes in whole body protein turnover seen in MOF are similar to those described in overt sepsis and severe trauma:both synthesis and degradation are elevated,with a higher rate of degradation.This situation result in a loss of body mass, predominantly lean tissue.Although it is not oftern possible to identify the orgin of the “sepsis”,it must be reasonable to regard patients with MOF metabolically as “severely septic”.In recent years,the gastrointestinal tract was thought to be the ongoing inflammatory stimulus and the cause of MOF.In the presence of sepsis and shock and lack of nutrient intake,endotoxin and bacteria translocate from the lumen of the gut into the portal and systemic circulations and set up a systemic inflammatory reaction with release of inflammatory mediators.The evidence for the gastrointestinal tract as the “motor”for MOF,however,is derived largely from animal work,and the direct evidence duppotyinh gut permeability as a cause of MOF in man is less convincing,although early and aggressive enteral feeding afger major abdominal injury has been shown to diminish the incidence of major septic complications.On the other hand,there are problems associated with enteral feeding in MOF.This is due sometimes to local damage from peritoneal sepsis but often from deleterious effects of high levels of sympathetic activation on the gastrointestinal tract,combined with some fo the sedative and cardiovascular drugs used to facilitate artificial ventilation or to support the cardiovascular system that also adversely affect gastrointestinal motility.The use of parnteral nutrition in combination with the so-called minimal enteral nutritional support in critically ill patients is mandatory in order to preserve organ function and to avoid deleterious side effects.This strategy of combining the two ways of artificial nutrition is based on the idea to use the gut,if it works,and to complete the full range of essential nutrient supply by the parenteral route.As energy donors,lipid emulsions are an integral element of parenteral nutrition regiments for critically ill patients.Moreover lipids are not only structural building blocks of cells and tissues but at the same time suppliers of C atoms for a number of biosynthetic pathways as well as carriers of essential fatty acids and fat-soluble vitamins.In addition,faty acids are precursors of prostaglandins other eicosanoids and therefore have important metabolic functions.Over the years,for the supply of lipids in the filed of parenteral nutrition,different concepts have been developed.Lipid emulsions derived from soybean or safflower oil contain excessive quantities of PUFA and insufficient amounts of α-tocopherol.Their parenteral use can rapidly lead to an unbalanced pattern of eicosanoids and is associated with an increased production of peroxidative catabolites.In order to avoid negative effects from these metabolic procucts,it is recommended to use preparations with a reduced content of PUFA in combination with an enrichment in α-tocopherol.Indeed the physical mixture of MCT and LCT is a well-proven concept in the parenteral nutrition of critically ill patients.Having a demonstrably higher utilization rate,MCT-containing lipid emulsions do not impair liver function,produce less immune and no RES function compromise,and do not interfere with pulmonary hemodynmics or gas exchange.Newer preparations based on structured triglycenrides or lilve oil appear to achieve the same goal,I.e.reducing the n- PUFA intake.These new lipid emulsions are safe and wel tolerated.Further studies are necessary to investigate potential benefits compared to the physical mixture of MCT/LCT in a clinical environment.A promising substrato in the evolution of parenteral lipid emulsions can be seen in fish oils (n-3 fatty acids).Their fixed combination in a physical mixture of MCT/LCT displays a great number of fascinating aspects.With regard to current literature,n-3 fatty acids have a beneficial influence on the pathophysiological response to dndotoxins and exert important modulations on eicosanoid and cytokine biology.Furthermore their intravenous use may improve organ perfusion in different critical situations.