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For patients who survive the first 48 hours 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 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. Third, gut-specific therapies (selective gut decontamination, early enteral nutrition, and most recently immune-enhancing enteral diets [IEDs]) have been shown to reduce these nosocomial infections.35 The purpose of this chapter will be to first provide a brief overview of why critically injured trauma patients develop gut dysfunction and how gut dysfunction contributes to adverse outcomes. The discussion will then focus on the pathogenesis and clinical monitoring of specific gut dysfunctions. Based on this information, potential therapeutic strategies to prevent and/or treat gut dysfunction to enhance patient outcome will be discussed.

Multiple Organ Failure

MOF occurs as a result of a dysfunctional inflammatory response and in two different patterns (i.e., early vs. late) (see ch68). After a traumatic insult, patients are resuscitated into a state of systemic hyperinflammation, now referred to as the systemic inflammatory response syndrome (SIRS). The intensity of SIRS is dependent upon (1) inherent host factors, (2) the degree of shock, and (3) the amount of tissue injured. Of the three, shock is the predominant factor.6 Mild-to-moderate SIRS is most likely beneficial, whereas severe SIRS can result in early MOF. As time proceeds, negative feedback systems downregulate certain aspects of acute SIRS to restore homeostasis and limit potential autodestructive inflammation (see ch67). This latter response has been dubbed the compensatory anti-inflammatory response syndrome (CARS) and results in delayed immunosuppression.7 Mild-to-moderate delayed immunosuppression is clinically insignificant, but severe immunosuppression is associated with late infections. These late infections can worsen early MOF or precipitate late MOF. Over the last decade, late CARS was characterized to include (a) apoptotic loss of intestinal lymphocytes and epithelial cells, (b) PMN and monocytic deactivation, (c) anergy characterized by suppressed T-cell proliferative responses, and (d) a shift from a TH1 to a TH2 phenotype.8,9

More recently, it has been hypothesized that SIRS and CARS are present concurrently following injury. With time though, SIRS ceases to exist and CARS is the predominant force. Debate exists over whether CARS is truly a compensatory response. In the laboratory, CARS does not occur unless preceded by SIRS.10 However, although the intensity of SIRS predicts early adverse outcomes, it does not predict late adverse outcome. CARS appears to occur in response to the injury (not to SIRS) (Fig. 58-1). This is ...

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