For patients who survive the first 48 hours of intensive care, multiple organ failure (MOF) is the leading cause of death among patients in the intensive care unit (ICU) (see Chapter 61). 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), which can lead to early MOF, and even death.2,3 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 after the ischemia–reperfusion insult weakens the gut barriers.4,5,6,7,8,9,10,11,12 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.13,14,15,16,17,18,19 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 overall morbidity and mortality. 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.
HOW GUT DYSFUNCTION CONTRIBUTES TO ADVERSE PATIENT OUTCOME
Multiple organ failure results from a dysfunctional, hyperinflammatory response producing two distinct patterns (ie, early vs late) (see Chapter 55). Soon after a traumatic insult, patients are found to be in a state of systemic hyperinflammation, now referred to as the systemic inflammatory response syndrome (SIRS).20,21,22 The intensity of SIRS is dependent upon (1) innate host factors, (2) the degree of shock, and (3) the amount of tissue injured. Of the three, shock is the predominant factor that produces a maladaptive, over exuberant SIRS response.23,24 Mild-to-moderate SIRS is most likely beneficial, whereas severe SIRS can result in early organ failure and death. As time proceeds, negative feedback systems down regulate certain aspects of acute SIRS to restore homeostasis and limit potential auto-destructive inflammation (see Chapter 61).
Reiterated in a recently published Glue Grant Study by Tompkins et al, they took blood samples of 167 patients at varying time intervals to better understand the genomic make-up after severe trauma or burn using microarray analysis. They referred to what they found as “genomic storm” in that “circulating white cells of the 167 patients studied when compared with those of the 35 normal volunteers, more than 80% of the WBC genes changed significantly.25 Tompkins et al further described the genomic patterns of complicated patients (thus that got MOF ...