86 Examining the Use of Contact Pathway Activation to Characterize Burn Induced Coagulopathy Using Thromboelastography
Authors: Keyloun John W , Le Tuan D , Brummel-Ziedins Kathleen , Bravo Maria , Orfeo Thomas , McLawhorn Melissa M , Moffatt Lauren T , Pusateri Anthony , Shupp Jeffrey W 
Published: March 2020

Abstract

Introduction
Current studies on acute burn induced coagulopathy are discordant and often rely on laboratory tests examining fragments of the coagulation cascade. Viscoelastic measures such as thromboelastography (TEG) provide dynamic assessments and are used increasingly at the point-of-care. Clotting activators such as kaolin are used to decrease time to measurement. The aim of this work is to identify the impact of burns on coagulation over time using native (nTEG) or contact pathway activated kaolin TEG (kTEG)

Methods
A cohort of burn injured patients (n=156) presenting to a regional burn center from 2012 to 2017 were enrolled. Whole blood was assessed at set intervals from admission to 72 hours. Demographic data, injury characteristics, and laboratory measures were obtained from the medical chart. Blood samples underwent viscoelastic assay with both nTEG and kTEG. Patients were stratified into high (&gt;40%, n=33) and low (n=123) total body surface area (TBSA) burn categories. Statistical analyses of viscoelastic parameters (R, α, MA, and LY30) were performed using mixed-effect models. P-values &lt; 0.05 were considered significant.

Results
Of the 156 thermally injured patients, most were male (71%) with a mean age of 42.5 ±16.5 years, and a mean TBSA burn of 23.3 ±24.6%. Overall mortality was 13.3% (n=21). There were no significant differences in nTEG/kTEG R time or nTEG maximum amplitude (MA) between groups. nTEG showed lower α-angle values in patients in the high TBSA group until hour 24 and this difference was significant at Hour 0 (63.9 ±10.4° vs. 68.3 ±8.3°, p = 0.05). kTEG showed lower α-angles until hour 24 in the high TBSA group, at which point there was a transition to higher α-angle in the high TBSA group (67.7 ±5.9° vs. 71.6 ±4.6° vs., p = 0.03). MA trended lower in the high TBSA group on kTEG and this difference was significant on admission (53.6 ± 11.0 mm vs. 59.6 ±8.1 mm; P=0.02) and hour 2 (51.9 ±14.4 mm vs. 60.3 ±9.2 mm; P=0.006). Clot lysis at 30 minutes (LY30) was variable on admission but significantly lower in the high TBSA group on both kTEG (p=0.004) and nTEG (p=0.001) at Hour 72.

Conclusions
No difference in time to clot initiation (R) was observed between burn size cohorts. However, rate of clot development (α) and maximal clot strength (MA) were reduced during the first 24 hours in patients with larger burns. After 24 hours, increased MA and reduced fibrinolysis (LY30) in blood from patients with larger burns, suggested a transition from a relatively hypo-coagulable state to a potentially prothrombotic state by 72 hours.

Applicability of Research to Practice
kTEG may provide better resolution in the detection of burn induced coagulopathy. Further work to assess the applicability of TEG data to direct therapeutic interventions will depend on fully characterizing the extent to which TEG parameters correlate with the clinical coagulopathy.