PB0479 - A comparison of thrombin generation ex vivo circuit and in critically ill patients requiring Extracorporeal Membrane Oxygenation

Monday, July 11, 2022

6:30 PM – 7:30 PM

Location: Exhibition

Presentation Format: In-Person

Presenting Author(s)

Andrew J. Doyle, MBChB MRCP FRCPath

Consultant Haematologist
Guy's & St Thomas' NHS Foundation Trust
London, England, United Kingdom

Co-Author(s)

KP

Kiran Parmar

Biomedical Scientist
Guy's & St Thomas NHS Foundation Trust
London, England, United Kingdom
NG

Nigel Gooby

Perfusionist
Guy's & St Thomas NHS Foundation Trust
London, England, United Kingdom
Karen A. Breen, MD

Consultant Haematologist
Guy's & St Thomas' NHS Foundation Trust
London, England, United Kingdom
NB

Nicholas A. Barrett

Consultant Intensivist
Guy's & St Thomas NHS Foundation Trust
London, England, United Kingdom
AR

Andrew Retter

Consultant Intensivist
Guy's & St Thomas' NHS Foundation Trust
London, England, United Kingdom
Beverley J. Hunt, MD, FRCP, FRCPath

Professor of Thrombosis & Haemostasis, Consultant Haematologist
Guy's & St Thomas' NHS Foundation Trust
London, England, United Kingdom

Background: Thrombin generation (TG) is increased with the use of extracorporeal circuits such as cardiopulmonary bypass. TG is also increased in patients with critical illness. The combination of these factors in patients receiving ECMO may therefore be significantly elevated but at present is poorly described.

Aims: To assess changes in TG markers in an ex vivo circuit of ECMO and in patients receiving veno-venous ECMO for severe respiratory failure.

Methods: 6 ex vivo ECMO circuits with sodium citrate using healthy donor whole blood were run for 24-hours at a high-flow rate (4L/min). Blood samples were taken from 17 patients requiring ECMO prior to and 1-day after starting, and prior to decannulation and 1-day after. Samples were analysed by ELISA for Prothrombin Fragments (PF1+2, reference range 200-1200pmol/L), Thrombin-Antithrombin (TAT, 0.8-3.8µg/L) and D-Dimers ( < 400ng/ml FEU) according to manufacturer’s protocols. Ethical approval was gained for the study with nominated consultee consent for patient samples.

Results: In the ex vivo circuit, there was no significant increase prior to circuit initiation to 24-hours after in PF1+2 (median 97 to 101pmol/L, p=0.5), TAT (4.2 to 2.6 µg/L, p=0.3) and D-Dimers (462 to 506 ng/ml, p=0.3). No circuit thrombosis was seen in any circuit.

In critically ill patients, there was a significant increase prior to cannulation to 1-day after in PF1+2 (median 729 to 1305pmol/L, p=0.03) and non-significant increases in TAT (19.5 to 36.9µg/L, p=0.7) and D-Dimers (7398 to 9903ng/ml, p=0.3). There was a significant decrease from prior to decannulation to 1-day after in PF1+2 (median 1453 to 658pmol/L, p< 0.001), TAT (40.1 to 11.7µg/L, p< 0.001) and D-Dimer (15450 to 11200ng/ml, p=0.05).

Conclusion(s): ECMO circuits lead to reversible increases TG in critically patients but not shown in an ex vivo model. Given elevated preceding TG markers in patients, this suggests that patient-attributable factors may increase TG during ECMO.