78.13 Evaluating Endothelial Dysfunction in Burn Patients with Syndecan-1 as Marker of Glycocalyx Shedding

R. L. Ball1,3, M. C. Bravo2, K. Brummel-Ziedins2, T. Orfeo2, L. Moffatt3, J. W. Shupp1,3  1Washington Hospital Center,Washington, DC, USA 2University Of Vermont College Of Medicine / Fletcher Allen Health Care,Burlington, VT, USA 3Firefighters’ Burn And Surgical Research Laboratory,Washington, DC, USA

Introduction:  Endotheliopathy is a complex process that can be initiated by insults such as tissue damage and leads to poor outcomes for critically ill patients. The role of endothelial dysfunction in burn pathophysiology is largely unknown. Syndecan-1 is a component of the endothelial glycocalyx released into the bloodstream upon endothelial disruption and serves as a potential biomarker for endotheliopathy. This study aims to investigate the relationship between total body surface area (TBSA) affected and syndecan-1 levels at multiple time points during a burn patient’s hospitalization.

Methods:  Blood samples were serially collected from 30 burn patients with varying degrees of TBSA.  Baseline samples were collected within 4 hours of the injury using IRB approved protocols.  Additional blood samples were collected approximately 4, 8, and 12 hours after the baseline.  Syndecan-1 levels were quantified by ELISA.  For analysis, patients were grouped by extent of TBSA: <10% (n=12), 10-30% (n=10), and >30% (n=8).   ANOVA and t-tests were performed.

Results: At baseline, mean syndecan-1 levels were higher in groups with more severe burn injury: <10% TBSA = 19.4 ng/mL, 10-30% TBSA = 36.0, >30% TBSA = 51.5.  However, the differences were not statistically significant (p = 0.198).  Intragroup variability of baseline syndecan-1 levels was captured by large standard deviations (11.7, 53.0, and 42.8 respectively).  Similarly at hours 4 and 8, mean syndecan-1 levels increased with increasing TBSA, but the differences were not significant with a large intragroup variability.  At hour 12, significant differences in mean syndecan-1 levels were observed with increasing TBSA: <10% TBSA = 26.6 ±14.9 ng/mL, 10-30% TBSA = 56.2±43.7, >30% TBSA = 76.3±42.9, (p = 0.012).  

Conclusion: Thermal injury itself is impressively heterogeneous, which is evidenced by the large intragroup variation in syndecan-1 levels observed in this study. Although a consistent pattern from the earliest time points of increasing syndecan-1 levels with increasing TBSA was observed, it was not until hour 12 when syndecan-1 levels were related to injury size in burn patients with statistical significance. Additional markers of endothelial dysfunction need to be evaluated along with a thorough review of outcomes of these patients to establish the clinical relevance of these findings.