Estimation of d lactat level as amarker of bacterial translocation in gut failure in critically ill pediatric patients

Abstract

Today, multiple organ failure (MOF) is still a common cause of death in ICU despite the efforts to prevent this ultimate evolution of critical illness. Among the different mechanisms involved in the complex pathophysiology of MOF, injury to the gut may play a key role. The gut mucosa constitutes a barrier protecting the internal milieu from the intraluminal content. Since any insult to the barrier results in increased permeability to large molecules, it has been hypothesized that bacteria or bacterial products such as endotoxin, could be "translocated" into the blood stream, subsequently promoting systemic inflammatory responses and development of MOF. Lactic acid, like many organic molecules, consists of two mirror-image isomers. L-lactate is produced by the human body and is the isomer tested for in common “lactate” assays. D-lactate, the mirror image of L-lactate, is produced in minute concentrations in human Measurement of plasma D-lactate has been suggested to be a marker of splanchnic hypoperfusion. D-lactate is produced by bacterial fermentation in the colonic lumen and subsequently absorbed into the blood. Bacterial overgrowth and increased gut permeability are both features of gastrointestinal dysfunction during septic shock. During hypoperfusion in the gut, both L-lactate and D-lactate are produced in increased amounts. Because humans lack the enzyme D-lactate dehydrogenase, liver metabolism of D-lactate is slower than that of L-lactate. D-Lactate may therefore reflect the intestinal perfusion than L-lactate. The aim of work of the current study was to test effect of lactoferrin supplementation for improving gut barrier function, prognosis