Skip to main content
Fig. 1 | Critical Care

Fig. 1

From: The digestive tract as the origin of systemic inflammation

Fig. 1

Pathogenic events in the course of gastro-intestinal failure. Potential toxic components in the small intestine are contained in the lumen under homeostatic conditions, whilst enterocytes allow the uptake of nutrients such as short-chain fatty acids (SCFA) across the epithelial barrier. In the critically ill patient suffering from major trauma or burns or undergoing surgery, protective mechanisms that maintain the gut barrier fail due to circulatory and neuroendocrine dysregulation. This results in gastro-intestinal (G-I) failure, which coincides with clinical signs such as oral intolerance, gastrointestinal hemorrhage, or ileus. G-I failure is a progressive clinical syndrome in which an early stage of predominantly gastrointestinal symptoms may be followed by extraintestinal derangements, such as acute respiratory distress syndrome (ARDS), liver failure, cholecystitis, pancreatitis, or kidney failure. G-I failure is associated with epithelial denudation, villus shortening, and inflammatory cell infiltration in the small intestine at the tissue level. Finally, various clinical biomarkers may aid in the diagnosis of G-I failure, including plasma or urinary levels of intestinal-type fatty acid-binding protein (I-FABP), liver-type fatty acid-binding protein (L-FABP), ileal bile acid-binding protein (I-BABP) or citrulline. CRP C-reactive protein

Back to article page