Inflammatory cytokine response in patients with septic shock secondary to generalized peritonitis

Objectives: The aims of this study were the following: a) to assess the proinflammatory cytokine (tumor necrosis factor [TNF]-alpha, interleukin [IL]-1, and IL-6) response in patients with septic shock secondary to generalized peritonitis; and b) to evaluate the influence of bacteremic status, type of peritonitis (acute perforation or postoperative), and peritoneal microbial status (mono- or polymicrobial) on cytokine expression and mortality, Design: Prospective study. Setting: Surgical intensive care unit of a university hospital. Patients: Fifty-two consecutive patients with septic shock caused by generalized peritonitis. Interventions: Routine blood tests, blood cultures, and cytokine assays were performed during the first 3 days after onset of shock. Measurements and Main Results: Serum TNF-alpha and IL-6 concentrations were measured by using a radioimmunoassay, and IL-1 concentrations were measured by using ELISA. Median serum concentrations an day 1 were: TNF-alpha, 90 pg/mL; IL-l, 7 pg/mL; and IL-6, 5000 pg/mL, TNF-alpha. and IL-6 concentrations decreased significantly between the first and third days of septic shock (p = .0001), whereas IL-1 concentrations remained low. The decrease in IL-6 tended to be more pronounced in the survivors group (p = .057), Median TNF-alpha serum concentrations were higher in bacteremic compared with nonbacteremic patients (151 vs. 73 pg/mL, p = .003), TNF-alpha, IL-1, and IL-6 serum concentrations and mortality were not different between acute perforation vs, postoperative peritonitis and mono- versus polymicrobial peritonitis, Conclusions: The systemic release of TNF-alpha and IL-6 during septic shock caused by generalized peritonitis was maximal on day 1 and decreased rapidly during the next days. No systemic release of IL-l was observed, IL-6 serum concentrations remained higher in patients who subsequently died, Among the different features of peritonitis studied, only bacteremia influenced the systemic cytokine response (higher TNF-alpha).