Objective: Host response to infection and other forms of tissue injury have been termed systemic inflammatory response syndrome (SIRS). This inflammatory response can frequently be accompanied by oxidative injury in one or more organ systems in the body. The objective of this report was to clarify the possible role of oxidative stress in the development of multiple organ failure (MOF) in patients with SIRS.
Design: Prospective clinical study.
Setting: Intensive care unit in a university hospital.
Patients: A total of 214 consecutive patients (mean age, 57.1 +/- 17.4 yrs; range, 13 to 84 yrs; 148 men and 66 women). At the time of admission, 139 patients fulfilled the clinical criteria for SIRS.
Interventions: None.
Measurements and main results: We measured plasma concentrations of thiobarbituric acid reactant substances (TBARS), as an index of oxidative stress, every day from the point of admission to the intensive care unit until discharge or death. Furthermore, all variables of the SIRS score and the Sequential Organ Failure Assessment score were collected every day. At the time of admission, plasma TBARS concentrations in SIRS patients with MOF were significantly higher than those in SIRS patients without MOF (2.3 +/- 0.9 vs. 1.9 +/- 0.6 nmol/mL, p <.01), and there was a significant correlation between plasma TBARS concentration and Sequential Organ Failure Assessment score (r2 =.18, p <.001). Furthermore, the duration of SIRS persistence was significantly associated with the percentage increase in plasma TBARS concentration during SIRS persistence in those patients in whom the duration of SIRS was confirmed (r2 =.73, p <.001). The duration of SIRS was significantly higher in patients who developed MOF than in patients who did not develop MOF (6.9 vs. 3.2 days, p <.001). The percentage increase in plasma TBARS concentration during SIRS was also significantly higher in patients who developed MOF than in patients who did not develop MOF (57.1% vs. 15.8%, p <.001).
Conclusions: It can be concluded that processes of oxidative stress in connection with continued SIRS may promote the development of MOF.