Clinicopathogenetic aspects of systemic inflammatory response development in polytrauma

Introduction

The aim of the study was identification of common regularities and pathogenetic significance of changes in the ratio between primary and secondary inflammatory mediators in development of systemic inflammatory response syndrome (SIRS) in polytrauma.

Methods

Three hundred and eighty-seven patients with polytrauma hospitalized to the ICU were examined. There was infection confirmed by microbiology in 175 (pneumonia, bronchitis, osteomyellitis, acute urethritis, and so forth); 212 patients had no infection (acute respiratory distress syndrome, disseminated intravascular coagulation, fat embolism, and so forth). In 87% two or more signs of SIRS were noted according to the criteria of the Consensus Conference ACCP/SCCM (2003). C-reactive protein (CRP) in venous blood serum was measured on 1, 3, 5, 7, 10, 15 and 17 days after admission using the biochemical analyzer HITACI-912 with reagents Tina-Quant CRP (Roche Diagnostic GMBH), lipopolysaccharide-binding protein (LPSBP) and cytokines TNFα, IL-2R, IL-6, IL-8, IL-10 using the immunochemiluminescent analyzer IMMULITE with the reagents DPC (USA). Constant variables were compared using Student's t test and the Mann-Whitney U test. The differences were significant at P < 0.05.

Results

On admission, increased serum LPSBP and TNFα were noted in all patients with infection compared with the patients without it (1.8 and 3 times respectively, P < 0.01). Moreover, the infectious patients had the apparent increase of IL-2R, IL-6, IL-8 and CRP: 5, 13, 18 and 5 times, respectively (P < 0.05). At that, generalized manifestation of inflammatory reaction in the infectious patients was characterized by at mean fivefold increase in IL-8 on day 3 of the follow-up. It was not accompanied by adequate anti-inflammatory response that was indicated by an absence of IL-10 dynamics. A direct correlation was found between an increase in inflammatory mediator concentration (IL-6, IL-8, IL-10) and respiratory rate (r = 0.73; 0.46; 0.59), CRP and heart rate (r = 0.48, P < 0.05), and an inverse correlation between inflammatory mediators (TNFα, IL-2R, LPSPB) and arterial pressure level (r = -0.42; -0.63; -0.48) and respiratory function values (vital lung capacity and forced expiratory volume, r = -0.42).

Conclusions

Hyperproduction of proinflammatory cytokines is closely connected with ventilation disturbances and clinical variants of the post-traumatic period course in patients with polytrauma.