{"title":"Gut dysfunction and intolerance to enteral nutrition in critically ill patients.","authors":"Frederick A Moore, Norman W Weisbrodt","doi":"10.1159/000072753","DOIUrl":null,"url":null,"abstract":"For patients who survive the first 48 h of intensive care, sepsis-related multiple organ failure (MOF) is the leading cause for prolonged intensive care unit (ICU) stays and deaths. Several lines of clinical evidence convincingly link gut injury and subsequent dysfunction to MOF [1]. First, patients who experience persistent gut hypoperfusion (documented by gastric tonometry) after resuscitation are at high risk for abdominal compartment syndrome (ACS), MOF, and death [2]. Second, epidemiologic studies have consistently shown that the normally sterile proximal gut becomes heavily colonized with a variety of organisms. These same organisms have been identified to be pathogens that cause late nosocomial infections. Thus, the gut has been called the ‘undrained abscess’ of MOF [3]. Third, gut-specific therapies (selective gut decontamination, early enteral nutrition (EN), and most recently immuneenhancing enteral diets) have been shown to reduce these nosocomial infections [4–7]. Of these gut-specific therapies, early EN is most widely employed. However, the most severely ill patients who should benefit most from early EN are frequently intolerant to it and are at increased risk for EN-related complications [8–11]. The purpose of this chapter will be to first provide a brief overview of why critically ill patients (using trauma patients as a model)","PeriodicalId":18989,"journal":{"name":"Nestle Nutrition workshop series. Clinical & performance programme","volume":"8 ","pages":"149-65; discussion 165-70"},"PeriodicalIF":0.0000,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000072753","citationCount":"12","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nestle Nutrition workshop series. Clinical & performance programme","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000072753","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 12
Abstract
For patients who survive the first 48 h of intensive care, sepsis-related multiple organ failure (MOF) is the leading cause for prolonged intensive care unit (ICU) stays and deaths. Several lines of clinical evidence convincingly link gut injury and subsequent dysfunction to MOF [1]. First, patients who experience persistent gut hypoperfusion (documented by gastric tonometry) after resuscitation are at high risk for abdominal compartment syndrome (ACS), MOF, and death [2]. Second, epidemiologic studies have consistently shown that the normally sterile proximal gut becomes heavily colonized with a variety of organisms. These same organisms have been identified to be pathogens that cause late nosocomial infections. Thus, the gut has been called the ‘undrained abscess’ of MOF [3]. Third, gut-specific therapies (selective gut decontamination, early enteral nutrition (EN), and most recently immuneenhancing enteral diets) have been shown to reduce these nosocomial infections [4–7]. Of these gut-specific therapies, early EN is most widely employed. However, the most severely ill patients who should benefit most from early EN are frequently intolerant to it and are at increased risk for EN-related complications [8–11]. The purpose of this chapter will be to first provide a brief overview of why critically ill patients (using trauma patients as a model)