作者: Sunjay Kanwar , Alistair C. J. W. Windsor , Fenella Welsh , G. Robin Barclay , Pierre J. Guillou
DOI: 10.1097/00000658-200001000-00013
关键词:
摘要: The pathophysiology of sepsis and multiple organ failure remains the subject intense investigation. Several hypotheses exist to explain a common end-organ injury that results from diverse etiologies. In recent years, considerable attention has focused on gastrointestinal tract its barrier function, there is an emerging consensus gut function may fuel systemic component inflammatory response syndrome (SIRS), sepsis, failure. 1 The origin hypothesis suggests as result major stress insult permits bacterial endotoxin translocation, which triggers splanchnic cytokines perpetuate exacerbate immunoinflammatory in This concept supported by data animal studies experimental models, including surgical trauma, 2 malnutrition, 3,4 jaundice, 5 pancreatitis, 6–8 hemorrhagic shock, 9,10 thermal injury. 11–13 These have demonstrated presence translocation measured recovery viable enteric organisms regional lymph nodes, liver, other organs, increased intestinal permeability macromolecules, endotoxemia. The situation humans less clear, 14 particularly with respect where poor concordance studies. Increased index dysfunction has, however, been observed after burns, 15 16 sepsis. 17 Moreover, endotoxemia be evident patient 18 or burns 19 20 Although this indirectly corroborate evidence proving occurs under similar defined insults humans, significance relevant clinical scenarios poorly understood. Two specific based role current paradigm SIRS were tested study—first, compromised preoperative predisposes SIRS, resections, second, pattern change postoperative period correlates septic course.