Thromboelastography Six: Redefining heparin resistance in post COVID syndrome
Recommended Citation
Payne J, Coba V, Marrocco A, Long T, Gupta N, Hodari‐Gupta A, Lopez‐Plaza I. Thromboelastography Six: Redefining heparin resistance in post COVID syndrome. Research and Practice in Thrombosis and Haemostasis 2022; 6(Supplement 1).
Document Type
Conference Proceeding
Publication Date
10-1-2022
Publication Title
Research and Practice in Thrombosis and Haemostasis
Keywords
antithrombin, endogenous compound, heparin, heparin lyase, adult, bleeding, blood clotting, blood transfusion, clinical article, conference abstract, controlled study, coronavirus disease 2019, drug resistance, drug therapy, heparinization, human, long COVID, male, platelet count, thromboelastography
Abstract
Background: In the literature there has been minimal discussion of heparin resistance with regards to the post-COVID syndrome. Since the COVID pandemic began, patients with COVID were suffering complications from VTE that suggested the presence of a hypercoagulable state. Generally this hypercoagulable state is described through the use of thromboelastogram six (TEG6) with a short R time, wide alpha angle and a very large amplitude. Aims: In this case we were using the TEG6 as a guide for heparin therapy by following the CK-R time compared to the CKH-R time (with heparinase). We observed no bleeding or clotting events. While the patient was on ECMO, there were no changes in the delta-P and the circuit was not replced during his clinical course. Additionally, he required no blood transfusions during this time. Methods: An observational analysis of TEG6 in COVID-19 ECMO patient while using an anti-Xa heparin based protocol for therapeutic heparin therapy. Results: On the initial TEG6, there was a significantly prolonged R time that was partially corrected with heparinase -with heparin dosing of 24 IU/kg/h (65,000 IU/day), see figure one. With the prolonged R time, heparin was descalated to 16 IU/kg/h and the coagulation profile was resent, see figure two. Additionally, the TEG6 MA remained elevated -consistent with the hypercoagulable post-COVID syndrome. This occurred in the setting of a normal anti-thrombin three level and platelet counts. Conclusion(s): Through the use of TEG6, we were able to better characterize his coagulation profile and we were able to deescalate his dosing of heparin using the CK and CKH-R time comparison. We propose using TEG6 to redefine heparin resistance in the post-COVID syndrome of hypercoagulopathy, as older modalities may not be accurately reflecting this modern pathology. (Figure Presented).
Volume
6
Issue
Supplement 1
