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.
Highlights
Patients undergoing major surgery or sustaining severe trauma are at risk of developing morbidity and mortality from postoperative or posttraumatic systemic inflammatory response syndrome (SIRS), sepsis and multiple organ failure (MOF)
Thirteen patients showed an increase in plasma I-Fatty Acid Binding Proteins (FABP) levels of at least twofold during surgery; while 7 patients had relatively unchanged circulating Intestinal-Fatty Acid Binding Protein (I-FABP) values
The data showing an early increase of circulating FABP and urinary claudin-3, followed by rapid return towards baseline values, indicate that the patients suffered transient injury to the mature enterocytes and their tight junctions
Summary
Patients undergoing major surgery or sustaining severe trauma are at risk of developing morbidity and mortality from postoperative or posttraumatic systemic inflammatory response syndrome (SIRS), sepsis and multiple organ failure (MOF). The development of such potentially lethal complications in relatively healthy surgical or trauma patients is poorly understood [1,2]. Experimental animal models, resembling the clinical situation of major surgery and trauma, show that haemorrhagic shock leads to disruption of the gut barrier, measured by elevated circulating levels of Fatty Acid Binding Proteins (FABP), originating from damaged intestinal epithelial cells and derangement of tightjunctions [7,8]. We aimed to study the development of gut barrier loss in patients undergoing major non-abdominal surgery
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