The role of the gastrointestinal tract in the development of burn sepsis.
Conceptualization of the gastrointestinal tract as the "motor" that drives sepsis and multiple-system organ failure has only recently been appreciated. Most of the investigation into the pathophysiology of gut-derived sepsis involves using animal models; however, some of the findings are already being corroborated in human studies. The gastrointestinal tract is a dynamic organ whose function as a front-line defense against infection needs to be appreciated. The development of lethal sepsis is a function of the microbial load and virulence, the status of the gastrointestinal barrier, and the magnitude of the host defense response. In assuming care of a critically ill patient, we must be judicious in the use of antibiotics in order to prevent intestinal overgrowth of potential pathogens. Providing proper nutrition by an enteral route (when possible) not only satisfies caloric needs but regulates the microflora and maintains the integrity of the mucosal barrier. Burn patients should receive enteral nutrition early, the first day if possible. This not only will protect the intestinal mucosa but also will blunt the hypermetabolic response following thermal injury. Lastly, the patient should not receive an excessive amount of narcotic or sedative, for these drugs have an inhibitory effect on gastrointestinal motility, encouraging bacterial overgrowth. In the near future, new therapeutic modalities may soon become available to protect and treat the compromised gastrointestinal barrier. These modalities may include, but certainly are not limited to, the use of glutamine and xanthine oxidase inhibitors to prevent stress-related injury to the gastrointestinal mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)
Epstein
M D
MD
Division of Plastic and Reconstructive Surgery, Milton S. Hershey Medical Center, Pennsylvania State University.
Banducci
D R
DR
Manders
E K
EK
D000818:Animals; D016470:Bacteremia / Q000382:microbiology; D001424:Bacterial Infections / Q000209:etiology*; D018407:Bacterial Physiological Phenomena; D002056:Burns / Q000382:microbiology*; D004064:Digestive System / Q000382:microbiology; D004068:Digestive System Physiological Phenomena; D006801:Humans