IS TRANSLOCATION OF BACTERIA AND ENDOTOXIN FROM THE GASTROINTESTINAL-TRACT A SOURCE OF SEPSIS IN CRITICALLY ILL PATIENTS

In recent years many investigators have focused on the role of the gut as a reservoir for pathogens which can enter the host if conditions a re favourable and cause systemic inflammatory response (SIRS), sepsis and multiple organ failure (MOF). Patients who have been resuscitated after severe trauma,circulatory shock, sepsis or other critical condit ions appear to be particularly vulnerable. The term translocation is u sed to describe the passage of viable bacteria from the lumen of the g astrointestinal tract to mesenteric lymph nodes, liver, spleen, pancre as, peritoneum and blood. However, absorption of bacterial toxins from the gut lumen is probably just as important as alive bacteria and the refore, some authors have recently included endotoxin in the definitio n of translocation. Experimental studies have demonstrated that bacter ia translocate in haemorrhagic shock, acute pancreatitis, burns, mesen teric ischaemia, intestinal obstruction, cardiogenic shock, endotoxic shock and sepsis. Lack of enteral food intake, lack of non-fermentable dietary fibres, protein malnutrition, broad spectrum antibiotics, cyt otoxic drugs and transient endotoxaemia are all factors that increase translocation. Due to difficult access, a rather limited number of cli nical studies has been performed on translocation. However, the availa ble data still shows without reasonable doubt that translocation of ba cteria does also occur in humans. There are indications that transloca tion of bacteria and endotoxin occurs in small amounts even in healthy individuals, but are rapidly inactivated by the reticuloendothelial s ystem and therefore of limited clinical relevance. However, in critica lly ill patients this otherwise insignificant phenomenon can become li fe threatening due to injured gut-mucosal barrier and immune suppressi on from acute illness or trauma. Thus, the current experimental and cl inical literature strongly suggests that there is a connection between unhealthy gastrointestinal tract and the subsequent development of SI RS, sepsis and MOF. It also suggests that therapy aimed at preserving the gastrointestinal structure and function (immune-nutrition) in crit ically ill or injured patients does improve outcome. On the other hand , whether this apparent relationship between the gut and sepsis is due to translocation of bacteria and endotoxin or due to mediator release (for example tumor necrosis factor alpha, interleukin-1 and interleuk in-6) from hypoperfused gastrointestinal tract (including the liver) r emains to be determined.