4.18 THROMBELASTOGRAPHY PERFOMRED WITHOUT AN ACTIVATOR ENHANCES DETECTION OF FIBRINOLYSIS

B. A. Quinn1,2, E. Gonzalez1, H. B. Moore1, M. P. Chapman1, A. Sauaia1, A. Banerjee1, C. C. Silliman1,3, E. E. Moore1,2  1University Of Colorado Denver,Department Of Surgery,Aurora, CO, USA 2Denver Health Medical Center,Department Of Surgery,Denver, CO, USA 3Bonfils Blood Center,Research Department,Denver, CO, USA

Introduction: The fibrinolytic response to trauma can be physiologic (preventing systemic clot propagation), pathologic (favoring bleeding), or shut-down (favoring un-regulated clotting). Thrombelastography (TEG) is used to quantify fibrinolysis and facilitate appropriate use of fibrinolysis inhibitors such as tranexamic acid in bleeding patients with hyperfibrinolysis. TEG in the trauma bay is typically performed with tissue factor as an activator (rapid-TEG). However, TEG can also be performed with kaolin as an activator or as a “native assay” with no activator. Which TEG modality is optimal for detecting fibrinolysis remains to be elucidated. We hypothesized that the use of kaolin or tissue factor as activators for TEG decreases the assay’s capability to detect tissue plasminogen activator (tPA)-induced fibrinolysis.

 

Methods: Citrated and non-citrated blood samples were collected from 10 healthy adults. Fibrinolysis was achieved by addition of tPA to whole blood samples prior to running the assay in five concentrations: 0, 50, 75, 150, and 300 (ng/mL). tPA-induced fibrinolysis was quantified by three different TEG methods—citrated native (CN) (no activator), citrated kaolin (CK), and non-citrated rapid (RT) (tissue factor). The TEG variable of fibrinolysis, LY30 (percent clot lysis at 30 minutes after reaching maximum clot strength), was compared at each tPA dose amongst CN, CK, and RT. The significance of differences between groups was tested by the Friedman’s test (p<0.05). Groups with significant differences were subjected to a post-hoc pairwise comparison with Bonferroni adjustment.

Results: At baseline (0 tPA), RT vs. CN detected a greater LY30 (2.8 vs. 1.7%, p=0.03). At 50 tPA the differences in LY30 among RT, CK, and CN were not statistically significant (p=0.050). At 75 tPA, CN vs. RT detected a greater LY30 (15.8 vs. 3.6%, p<0.001). At 150 tPA, CN vs. RT detected a greater LY30 (56.1 vs. 36.7%, p=0.005). At 300 tPA there were no significant differences.

Conclusion: Using a coagulation activator decreases the threshold for detecting tPA-induced fibrinolysis by TEG. When fibrinolysis was induced to levels of tPA previously reported in trauma patients (75 and 150 ng/mL), CN detected more fibrinolysis. Early detection of hyper-fibrinolysis in injured patients is imperative for triggering treatment with anti-fibrinolytics in order to control bleeding and decrease mortality. Our data demonstrates that TEG can be used with no activator (CN) for adequate quantification of fibrinolysis.