• M Keel, E Ecknauer, R Stocker, U Ungethüm, U Steckholzer, J Kenney, H Gallati, O Trentz, and W Ertel.
• Division of Trauma Surgery and Department of Surgery, University Hospital of Zurich, Switzerland.
• J Trauma. 1996 Jun 1;40(6):907-12; discussion 912-4.

BackgroundExcessive release of proinflammatory cytokines has been involved in pathogenesis of acute respiratory distress syndrome.DesignSince injured patients with chest trauma reveal a high risk for posttraumatic acute respiratory distress syndrome, local and systemic release of proinflammatory cytokines and their naturally occurring inhibitors were determined in the early posttraumatic period.Materials And MethodsProinflammatory and anti-inflammatory mediators were measured in plasma and bronchoalveolar lavage fluid (BALF) from 16 patients with multiple injuries including severe chest injury (Injury Severity Score of 34.4 +/- 2.3 points) and compared with healthy volunteers (n = 17).ResultsTumor necrosis factor-alpha was detectable neither in plasma nor in BALF. Interleukin-1beta and interleukin-8 were significantly increased in BALF from injured patients, while plasma levels were similar in both groups. Soluble tumor necrosis factor receptors p55 and p75 and interleukin-1ra were markedly elevated in plasma (p < or = 0.01) and BALF (p < or = 0.001) from injured patients compared with controls.ConclusionHighly increased concentrations of proinflammatory cytokines in BALF, but not in circulation, indicate a strong local inflammatory response early after multiple injuries combined with chest injury rather than severe systemic inflammation. In contrast, anti-inflammatory mechanisms seem to be activated locally and systemically.

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