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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]‐α, 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‐α and IL‐6 concentrations were measured by using a radioimmunoassay, and IL‐1 concentrations were measured by using ELISA. Median serum concentrations on day 1 were: TNF‐α, 90 pg/mL; IL‐1, 7 pg/mL; and IL‐6, 5000 pg/mL. TNF‐α 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‐α serum concentrations were higher in bacteremic compared with nonbacteremic patients (151 vs. 73 pg/mL, p = .003). TNF‐α, 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‐α 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‐1 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‐α).