Citation

Gonzalez Rodriguez E, Cardenas JC, Cox CS, Kitagawa RS, Stensballe J, Holcomb JB, Johansson PI, Wade CE. Scand. J. Trauma Resusc. Emerg. Med. 2018; 26(1): e102.

Affiliation

Center for Translational Injury Research (CeTIR), Department of Surgery, McGovern Medical School, University of Texas Health Science Center, 6431 Fannin, MSB 5.204, Houston, TX, 77030, USA.

Copyright

(Copyright © 2018, Scandinavian Networking Group on Trauma and Emergency Management, Publisher Holtzbrinck Springer Nature Publishing Group - BMC)

DOI

10.1186/s13049-018-0565-3

PMID

30463625

Abstract

INTRODUCTION: Head injury and exsanguination are the leading causes of death in trauma patients. Hemorrhagic shock triggers systemic endothelial glycocalyx breakdown, potentially leading to traumatic endotheliopathy (EoT). Levels of syndecan-1, a main glycocalyx component, have been used to assess the integrity of the glycocalyx. In TBI patients, it remains unclear whether syndecan-1 shedding occurs and its correlation with outcomes. We aimed to determine the frequency of EoT+, defined as a syndecan-1 level of 40 ng/ml or higher, after TBI in isolated and polytraumatic injury. We also investigated how the presence of EoT+ affected outcomes in TBI patients.

METHODS: Severely injured trauma patients were enrolled. From blood samples collected upon patients' arrival to the hospital, we measured syndecan-1 (main biomarker of EoT+), soluble thrombomodulin (sTM, endothelial activation) adrenaline and noradrenaline (sympathoadrenal activation), and assessed TBI patients' coagulation capacity.

RESULTS: Of the enrolled patients (n = 331), those with TBI and polytrauma (n = 68) had the highest rate of EoT+ compared to isolated TBI (n = 58) and Non-TBI patients (n = 205) (Polytrauma-TBI 55.9% vs. Isolated-TBI 20.0% vs. non-TBI polytrauma 40.0%; p = 0.001). TBI patients with EoT+ exhibited marked increases in sTM, adrenaline and noradrenaline levels, and physiological and coagulation derangements. In isolated TBI patients, increasing syndecan-1 levels (β for every 10 ng/ml increase: 0.14; 95% CI: 0.02, 0.26) and hypocoagulability were negatively associated with survival.

CONCLUSIONS: This study provides evidence of syndecan-1 shedding after TBI supporting the notion that breakdown of the glycocalyx contributes to the physiological derangements after TBI.

Language: en

Keywords

Endothelium; Sympathoadrenal activation; Syndecan-1; Traumatic endotheliopathy