title: The inflammatory response in transgastric surgery: gastric content leak leads to localized inflammatory response and higher adhesive disease.
abstract: BACKGROUND
  Risk of gastric spillage during transgastric surgery is a potential complication of NOTES procedures. The aim of this study was to determine risk outcomes from gastric spillage in a rat survival model by measuring local and systemic inflammatory markers, adhesive disease, and morbidity.
  
  
  METHODS
  We performed a minilaparotomy with needle aspiration of 2 ml of gastric contents mixed with 2 ml of sterile saline (study group, SG) or 4 ml of sterile saline (control group, CG) injected into the peritoneal cavity of 60 male rats. Inflammatory markers (TNFalpha, IL-6, and IL-10) were analyzed at 1, 3, 6, and 24 h postoperatively by obtaining plasma levels and peritoneal washings. At necropsy, the peritoneal cavity was examined grossly for adhesions.
  
  
  RESULTS
  Adhesions were seen more frequently in the SG versus the CG (100% vs. 33.3%, p < 0.014). There was a significant difference in the peritoneal TNFalpha levels in the SG compared with the CG, which peaked 1 h after surgery (p < 0.02). Both peritoneal IL-6 and IL-10 levels were higher in the SG versus the CG, which peaked 3 h after surgery (p < 0.005 and p < 0.001, respectively). All peritoneal inflammatory markers returned to undetectable levels at 24 h for both groups. Plasma cytokines were undetectable at all time intervals.
  
  
  CONCLUSIONS
  The inflammatory response was found to be a localized and not systemic event, with plasma cytokine levels remaining normal while peritoneal washings revealed a brisk, short-lived localized inflammatory response. There was a significantly higher rate of adhesive disease in the SG compared with the CG; this, however did not translate into a difference in apparent clinical outcome. We conclude that gastric leakage in this NOTES rodent model induces a localized inflammatory response, followed by mild to moderate adhesive disease. This may be important in human NOTES.
authors.affiliation: Center for the Future of Surgery, Department of Surgery, University of California, San Diego Medical Center, San Diego, CA, USA. sramamoorthy@ucsd.edu
authors.forename: Sonia L
authors.initials: SL
authors.lastname: Ramamoorthy
authors.forename: Jeffrey K
authors.initials: JK
authors.lastname: Lee
authors.forename: Linda
authors.initials: L
authors.lastname: Luo
authors.forename: Yoav
authors.initials: Y
authors.lastname: Mintz
authors.forename: John
authors.initials: J
authors.lastname: Cullen
authors.forename: David W
authors.initials: DW
authors.lastname: Easter
authors.forename: Michelle K
authors.initials: MK
authors.lastname: Savu
authors.forename: Alana
authors.initials: A
authors.lastname: Chock
authors.forename: John
authors.initials: J
authors.lastname: Carethers
authors.forename: Santiago
authors.initials: S
authors.lastname: Horgan
authors.forename: Mark A
authors.initials: MA
authors.lastname: Talamini
mesh_terms: D000818:Animals; D016009:Chi-Square Distribution; D004797:Enzyme-Linked Immunosorbent Assay; D005766:Gastrointestinal Contents / Q000737:chemistry*; D018836:Inflammation Mediators / Q000032:analysis*; D016753:Interleukin-10 / Q000032:analysis*; D015850:Interleukin-6 / Q000032:analysis*; D007813:Laparotomy; D023421:Models, Animal; D011183:Postoperative Complications / Q000209:etiology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D013270:Stomach / Q000601:surgery*; D000267:Tissue Adhesions / Q000209:etiology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*
chemical_list: D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10
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