New Insight in Loss of Gut Barrier during Major Non-Abdominal Surgery

Abstract

BackgroundGut barrier loss has been implicated as a critical event in the occurrence of postoperative complications. We aimed to study the development of gut barrier loss in patients undergoing major non-abdominal surgery.Methodology/Principal FindingsTwenty consecutive children undergoing spinal fusion surgery were included. This kind of surgery is characterized by long operation time, significant blood loss, prolonged systemic hypotension, without directly leading to compromise of the intestines by intestinal manipulation or use of extracorporeal circulation. Blood was collected preoperatively, every two hours during surgery and 2, 4, 15 and 24 hours postoperatively. Gut mucosal barrier was assessed by plasma markers for enterocyte damage (I-FABP, I-BABP) and urinary presence of tight junction protein claudin-3. Intestinal mucosal perfusion was measured by gastric tonometry (PrCO2, Pr-aCO2-gap). Plasma concentration of I-FABP, I-BABP and urinary expression of claudin-3 increased rapidly and significantly after the onset of surgery in most children. Postoperatively, all markers decreased promptly towards baseline values together with normalisation of MAP. Plasma levels of I-FABP, I-BABP were significantly negatively correlated with MAP at ½ hour before blood sampling (−0.726 (p<0.001), −0.483 (P<0.001), respectively). Furthermore, circulating I-FABP correlated with gastric mucosal PrCO2, Pr-aCO2-gap measured at the same time points (0.553 (p = 0.040), 0.585 (p = 0.028), respectively).Conclusions/SignificanceThis study shows the development of gut barrier loss in children undergoing major non-abdominal surgery, which is related to preceding hypotension and mesenterial hypoperfusion. These data shed new light on the potential role of peroperative circulatory perturbation and intestinal barrier loss.

Selective bowel decontamination improves the survival of 90% hepatectomy in rats

“…Such results are consistent with previous studies [1,21,22]. Second, from the perspective of the intestinal bacterial flora, overgrowth has been shown to frequently occur during severe trauma or large operation [4,23] or liver diseases [24]. And apical exposure to LPS could increase epithelial permeability in the intestine [25], involving disruption of tight junction [26,27].…”

Protection against early intestinal compromise by lipid-rich enteral nutrition through cholecystokinin receptors*

“…In line with clinical studies showing rapid development of intestinal cell damage after severe trauma and nonabdominal surgery (13,14), in the current study, ileal cell damage was detected within 1 hr after shock. Enterocyte damage was defined as increased plasma levels of ILBP, an ileum-specific bile acid transporter confined to mature enterocytes (22,23,30).…”

“…Splanchnic hypoperfusion is considered to be crucial in the development of intestinal compromise (11,13,27). Therefore, in the current study, a model of hemorrhagic shock was selected in which perfusion of mesenteric organs is known to be severely restricted (27,28).…”

“…Furthermore, the associations that were established between the level of enterocyte damage in septic patients and poor clinical outcome indicate that events in the gut wall may be of extraintestinal significance (11,12). Recently, evidence was provided that intestinal epithelial damage is an early event in surgical and trauma patients that is related to the subsequently developing systemic inflammatory response and the occurrence of complications (13,14). These clinical observations support the importance of preserving early intestinal integrity under certain surgical conditions as a potential target for antiinflammatory therapies.…”

Nutritional Modulation of Immune Response via Vagus Nerve: Preclinical Studies and Future Perspectives

“…In critically ill and surgical patients, the early presence of enterocyte damage and a weakened intestinal barrier function have been demonstrated in association with poor clinical outcome (Derikx et al 2007(Derikx et al , 2008. Whereas such barrier loss may represent a generalized phenomenon that affects epithelial function in diverse organs, various lines of experimental and clinical evidence implicate early loss of the intestinal barrier in particular as a potential therapeutic target to prevent or treat dysregulated inflammation (MacFie et al 1999;Sambol et al 2000;Fink and Delude 2005).…”