VPB0129 - Thromboelastography Six: redefining heparin resistance in post COVID syndrome

Sunday, July 10, 2022

6:30 PM – 7:30 PM

Location: Exhibition

Presentation Format: Virtual

Presenting Author(s)

JP

Joshua Payne

Surgical Critical Care Fellow
Henry Ford Hospital
Royal Oak, Michigan, United States

Co-Author(s)

VC

Victor Coba

Cardiac Surgery ICU Director
Henry Ford Hospital
Detroit, Michigan, United States
AM

Anna Marrocco

Cardiac Surgery Nurse Practitioner
Henry Ford Hospital
Detroit, Michigan, United States
TL

To Long

Cardiac Surgery Pharmacist
Henry Ford Hospital
Detroit, Michigan, United States
NG

Nitish Gupta

Cardiac Anesthesiology Fellow
Henry Ford
Detroit, Michigan, United States
AH

Ariella Hodari-Gupta

Surgical ICU Director
Henry Ford Hospital
Detroit, Michigan, United States
IL

Ileana Lopez-Plaza

Division Head - Pathology and Blood Bank
Henry Ford Hospital
Detroit, Michigan, United States

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/hr (65,000 IU/day), see figure one. With the prolonged R time, heparin was descalated to 16 IU/kg/hr 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.