Acute lung injury in TBI patients with SIRS: role of vascular endothelial damage

Introduction

The pathological organ dysfunction that occurs in patients with SIRS or sepsis is believed to be related to vascular endothelial damage. We investigated the role of vascular endothelial damage in the occurrence of acute lung injury in severe TBI patients with SIRS.

Methods

The subjects were 20 severe TBI patients with SIRS. The P/F ratio was calculated from arterial blood gas analysis data obtained for seven consecutive days from the time of admission. Peripheral blood samples were collected four times to measure the serum levels of IL-6 and IL-8, and the levels of ICAM-1 and granulocyte elastase (GE) as markers of vascular endothelial damage.

Results

The P/F ratio decreased with time and was below 300 from day 4 onwards. However, the survivors maintained a P/F ratio of 300 or more. In the patients with a fatal outcome, the ratio continued to decline and the subjects developed acute lung injury on day 3. From day 5 onward, they showed a significant decrease of the ratio, with values of 200 or less and symptoms of adult respiratory distress syndrome. The levels of IL-6, IL-8, ICAM-1, and GE increased after admission, but then decreased again in the survivors. In the patients who died, these levels continued to rise and there was a significant increase of IL-6, IL-8, and ICAM-1 after 1 week. The correlation between the blood level of IL-6 and the level of IL-8, ICAM-1, or GE was strong, while that between the IL-8 level and the ICAM-1 or GE levels was also strong and that between the ICAM-1 and GE level was weaker. In contrast, the correlations between the P/F ratio and the blood levels of IL-6, IL-8, ICAM-1, or GE were moderate and negative. Therefore, inverse correlations were noted between the P/F ratio and all these parameters.

Conclusions

By determining the changes of humoral mediators, we demonstrated that vascular endothelial damage was involved in the occurrence of the pathological state of acute lung injury, which occurs in severe TBI patients with SIRS.