title: New Insight in Loss of Gut Barrier during Major Non-Abdominal Surgery.
abstract: BACKGROUND
  Gut 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.
  
  
  RESULTS
  Twenty 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 (P(r)CO2, P(r-a)CO2-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 (1/2) hour before blood sampling (-0.726 (p<0.001), -0.483 (P<0.001), respectively). Furthermore, circulating I-FABP correlated with gastric mucosal P(r)CO2, P(r-a)CO2-gap measured at the same time points (0.553 (p = 0.040), 0.585 (p = 0.028), respectively).
  
  
  CONCLUSIONS
  This 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.
authors.affiliation: Department of Surgery, University Hospital Maastricht & Nutrition and Toxicology Research Institute (NUTRIM), Maastricht University, Maastricht, the Netherlands.
authors.forename: Joep P M
authors.initials: JP
authors.lastname: Derikx
authors.forename: Dick A
authors.initials: DA
authors.lastname: van Waardenburg
authors.forename: Geertje
authors.initials: G
authors.lastname: Thuijls
authors.forename: Henriëtte M
authors.initials: HM
authors.lastname: Willigers
authors.forename: Marianne
authors.initials: M
authors.lastname: Koenraads
authors.forename: Annemarie A
authors.initials: AA
authors.lastname: van Bijnen
authors.forename: Erik
authors.initials: E
authors.lastname: Heineman
authors.forename: Martijn
authors.initials: M
authors.lastname: Poeze
authors.forename: Ton
authors.initials: T
authors.lastname: Ambergen
authors.forename: André
authors.initials: A
authors.lastname: van Ooij
authors.forename: Lodewijk W
authors.initials: LW
authors.lastname: van Rhijn
authors.forename: Wim A
authors.initials: WA
authors.lastname: Buurman
mesh_terms: D000293:Adolescent; D001794:Blood Pressure; D002648:Child; D002675:Child, Preschool; D062465:Claudin-3; D013505:Digestive System Surgical Procedures; D050556:Fatty Acid-Binding Proteins / Q000097:blood; D005260:Female; D006801:Humans; D006913:Hydroxysteroid Dehydrogenases / Q000097:blood; D007410:Intestinal Diseases / Q000097:blood / Q000209:etiology* / Q000473:pathology / Q000652:urine; D007413:Intestinal Mucosa / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008365:Manometry; D008565:Membrane Proteins / Q000652:urine; D010539:Permeability; D011183:Postoperative Complications / Q000209:etiology* / Q000473:pathology; D012600:Scoliosis / Q000601:surgery*; D013123:Spinal Fusion / Q000009:adverse effects*; D045002:3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)
chemical_list: D062465:Claudin-3; D050556:Fatty Acid-Binding Proteins; D006913:Hydroxysteroid Dehydrogenases; D008565:Membrane Proteins; C568122:CLDN3 protein, human; C435496:AKR1C2 protein, human; D045002:3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)