重症患者におけるｓｙｓｔｅｍｉｃ　ｉｎｆｌａｍｍａｔｏｒｙ　ｒｅｓｐｏｎｓｅ　ｓｙｎｄｒｏｍｅ（ＳＩＲＳ）の転帰および病態の検討

DOI 被引用文献9件 参考文献28件

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  • A study on the outcome and pathophysiology of systemic inflammatory response syndrome(SIRS) in critically ill patients.

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Objective: To investigate the outcome and pathophysiology of systemic inflammatory response syndrome (SIRS) in critically ill patients with the expectation that the concept and the criteria of SIRS are useful in elucidating the pathophysiology of the critically ill and provide us with an early warning of the development of organ failure. Patients and methods: We studied the incidence of SIRS, multiple organ failure complication rate and outcome of 922 critically ill patients treated at the ICU of Chiba University Hospital between 1986 and 1993, and investigated the relationship between the duration of SIRS and the date of the onset of MOF. In addition, we measured resting energy expenditure/basal energy expenditure (EE/BEE), cellular injury score (CIS), serum interleukin 6 (IL 6) and lipid peroxide (LPO) on the first postoperative day in patients who underwent gastrointestinal surgery and compared the results in SIRS patients and non-SIRS patients to investigate the pathophysiology of SIRS. Furthermore, to investigate the mechanism of deterioration of SIRS to organ failure we followed postoperative serial changes in serum IL-6 levels in non-SIRS, SIRS survivors and SIRS non-survivors. Results: SIRS developed in 63.7% of all ICU patients, and MOF developed in 14.3% of the SIRS patients and 1.2% of the non-SIRS patients, respectively. SIRS patient and non-SIRS patient mortality was 13.6% and 1.2%, respectively. Thus the MOF complication rate and mortality rate in the SIRS patients were significantly higher than in the non-SIRS patients. SIRS in non-MOF patients persisted for 4.0 days on average, and the average duration from the onset of SIRS to the onset of MOF was 8.2 days. There was no significant difference between CIS and serum LPO levels in SIRS patients and non-SIRS patients. However EE/BEE and serum IL-6 levels in SIRS patients were higher than in non-SIRS patients. Serial changes in serum IL-6 levels revealed that the levels in non-SIRS patients remained low, and that those in SIRS survivors were highest on the first postoperative day, but decreased the following day. The serial changes also showed that the IL-6 levels of SIRS non-survivors remained elevated and that non-survivors were unable to recover from SIRS. Conclusion: These findings indicate that SIRS is caused by overproduction of humoral mediators and also indicate that SIRS is not severe enough to cause cellular injury but is a condition which can easily deteriorate to organ failure. Furthermore, countermeasures against humoral mediators including cytokines seemed to be important in the prevention of organ failure in patients with persistent SIRS.

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