title: Does reoperation for abdominal sepsis enhance the inflammatory host response?
abstract: OBJECTIVE
  To determine the effect of reoperation for severe abdominal sepsis on the course of proinflammatory mediators and hemodynamic factors.
  
  
  METHODS
  Inception cohort.
  
  
  METHODS
  A university hospital and a secondary care hospital.
  
  
  METHODS
  Fifteen patients suffering from severe peritonitis due to intestinal perforation or infected necrotizing pancreatitis were studied following 19 subsequent operations. Plasma samples were obtained immediately before and after reoperation, as well as at 1, 3, 6, 12, and 24 hours after operation to determine endotoxin, tumor necrosis factor alpha, and interleukin-6 levels. Clinical factors and therapeutic support were recorded at the corresponding times.
  
  
  METHODS
  Postoperative hemodynamic instability as defined by changes of the mean arterial pressure, pulmonary capillary wedge pressure, and vasopressor support. Courses of proinflammatory mediators were correlated to the hemodynamic findings.
  
  
  RESULTS
  Mean arterial pressure decreased from 94 mm Hg postoperatively to 80 mm Hg at 3 hours (P = .006) and 81 mm Hg at 6 hours postoperatively (P = .005). Pulmonary capillary wedge pressure dropped from 14 mm Hg postoperatively to 12 mm Hg at 1 hour (P = .05). Vasopressor support significantly increased from 1 to 6 hours postoperatively (P = .02). Neither endotoxin nor tumor necrosis factor alpha levels showed significant changes in the postoperative course. Interleukin-6 levels continously increased from 586 pg/mL preoperatively to 910 pg/mL at 1 hour (P = .02) and 931 pg/mL at 3 hours postoperatively (P = .04). Overall interleukin-6 levels (R = -0.38, P = .003) and especially early postoperative interleukin-6 levels inversely correlated with postoperative mean arterial pressure.
  
  
  CONCLUSIONS
  Reoperation for abdominal sepsis frequently causes substantial hypotension, and is, thus, potentially harmful to the patient. Reoperative trauma may induce an early postoperative increase in interleukin-6 levels. Because this increase occurs before the development of hypotension, a relationship between the kinetics of this cytokine and the observed hemodynamic instability may be present.
authors.affiliation: Department of Surgery, University of Vienna, Austria.
authors.forename: T
authors.initials: T
authors.lastname: Sautner
authors.forename: P
authors.initials: P
authors.lastname: Götzinger
authors.forename: E M
authors.initials: EM
authors.lastname: Redl-Wenzl
authors.forename: K
authors.initials: K
authors.lastname: Dittrich
authors.forename: M
authors.initials: M
authors.lastname: Felfernig
authors.forename: P
authors.initials: P
authors.lastname: Sporn
authors.forename: E
authors.initials: E
authors.lastname: Roth
authors.forename: R
authors.initials: R
authors.lastname: Függer
mesh_terms: D000328:Adult; D000368:Aged; D016207:Cytokines / Q000097:blood; D004731:Endotoxins / Q000097:blood; D005260:Female; D006439:Hemodynamics; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D010538:Peritonitis / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology / Q000601:surgery*; D012086:Reoperation; D018805:Sepsis / Q000276:immunology / Q000503:physiopathology / Q000601:surgery*; D012720:Severity of Illness Index
chemical_list: D016207:Cytokines; D004731:Endotoxins; D018836:Inflammation Mediators