(181) Thromboelastography With Platelet Mapping in Critically Ill Patients on Prostacyclin Analogues

Introduction: Prior literature has demonstrated in vitro platelet inhibition with the prostacyclin analogues (PGI2) epoprostenol (EPO) and treprostinil (TRE) used to treat pulmonary hypertension (PH), but their effects in critically ill patients remain unexplored. Thromboelastography with platelet mapping (TEG-PM) offers a novel approach to assess platelet activation pathways, including adenosine diphosphate (ADP) and arachidonic acid (AA), potentially providing insight into PGI2-induced platelet inhibition.

Methods: This is a retrospective review of adult patients with PH admitted to the intensive care unit (ICU) who had at least 1 TEG-PM collected while receiving a continuous intravenous (IV) or subcutaneous (SQ) PGI2. We sought to characterize reasons for use of TEG-PM, notable findings of platelet inhibition and incidence of bleeding.

Results: Nineteen TEG-PM tests were collected in 12 patients admitted to a medical (75%) or surgical (25%) ICU. Six patients (50%) were receiving IV TRE, 5 patients (42%) SQ TRE and 1 patient (8%) IV EPO. The median age was 54 years, 67% were female, 67% were on concomitant antithrombotics, and 25% were on venoarterial extracorporeal membrane oxygenation (VA-ECMO). Rationale for sending the initial TEG-PM included perceived high risk for bleeding (6/12), a bleeding event (5/12) or was unknown (1/12). A TEG-PM was repeated in 6 patients (range 2-3 tests). In 13/19 TEG-PM tests, the maximum amplitude (MA) ADP was < 50 mm [median 33 IQR (32, 41)], and in 12/19 tests, the MA AA was < 50 mm [median 33 (IQR 29, 37)]. Bleeding occurred in 8 patients, with 6/8 classified as major events, with 5/8 exhibiting significant platelet inhibition on TEG-PM, 5/8 with thrombocytopenia (platelets < 100× 109/L), and 6/8 with additional antithrombotic use that could have contributed. In response to major bleeding and TEG-PM results, 3 patients on VA-ECMO were titrated off PGI2 therapy and 1 patient had anticoagulation therapy interrupted. The remaining 8 patients had no changes to PGI2 or antithrombotic therapy based on TEG-PM results.

Conclusions: Consistent with previous in vitro data, critically ill PH patients on PGI2 therapy exhibited abnormal platelet function testing with TEG-PM. The clinical significance of these findings requires further investigation.