HEPARIN-INDUCED THROMBOCYTOPENIA IN A PATIENT WITH ANTI-PHOSPHOLIPID SYNDROME AFTER AORTIC VALVE REPLACEMENT

Abstract

SESSION TITLE: Medical Student/Resident Critical Care SESSION TYPE: Med Student/Res Case Report PRESENTED ON: October 18-21, 2020 INTRODUCTION: Heparin-induced thrombocytopenia (HIT) is a feared complication of heparin exposure due to antibodies against platelet factor 4 (PF4) and heparin. The reported incidence of HIT ranges from 0.1 to 5% in patients exposed to heparin (1). Nearly all patients undergoing cardiac surgery are exposed to heparin and up to 50% of patients who undergo cardiopulmonary bypass develop antibodies to PF4. Though this does not necessarily correlate to a higher incidence, 1-2% of cardiac patients develop HIT. In these patients, alternative agents for anticoagulation are required, presenting unique challenges in monitoring. CASE PRESENTATION: A 44-year-old female with severe aortic insufficiency and moderate aortic stenosis was scheduled for aortic valve replacement (AVR). Her history was notable for anti-phospholipid syndrome (APLS) with an extensive history of thromboses including hepatic, renal, pulmonary and placental thrombosis, maintained on chronic warfarin. The patient had a remote history of HIT; however, pre-operatively she had a negative PF4 antibody and serotonin release assay (SRA), and bridging was done with enoxaparin. She underwent successful AVR with heparin use intra-operatively. Post-operatively, her platelet counts down-trended from 166,000/μL to 78,000/μL. Given her remote history of HIT, repeat antibody and SRA were sent and argatroban was used for post-op anticoagulation. As the patient’s baseline activated partial thromboplastin time (aPTT) was prolonged, argatroban was titrated using thrombin time (TT). Argatroban was started at 0.2 mcg/kg/min. TT was assessed every 6 hours after initiation with titration by 0.1mcg/kg/min until a therapeutic goal of 30-50 seconds was achieved. DISCUSSION: In healthy patients, aPTT is recommended for monitoring the effect of argatroban. However, in the case of APLS, antibodies interfere with coagulation tests that are phospholipid dependent, resulting in a prolonged baseline aPTT. Though there is no established range for the use of TT for monitoring argatroban, a recent study of agatroban in critically ill patients found TT to correlate with plasma drug concentrations (2). Low levels of argatroban were found to correlate with TT that are 30-50 seconds and intermediate plasma levels of argatroban correlate with TT that are approximately 50-100 seconds. Other options include fixed dose argatroban without monitoring of laboratory parameters or using non-phospholipid dependent measures such as thromboelastometry (3). CONCLUSIONS: As is demonstrated in this case, suspected HIT following cardiac surgery can be difficult to manage; this is further compounded in patients with APLS with baseline altered coagulation parameters. When a direct thrombin inhibitor is used, TT monitoring can be considered in patients that cannot be monitored using aPTT. Reference #1: Pishko AM, Cuker A. Heparin-Induced Thrombocytopenia in Cardiac Surgery Patients. Semin Thromb Hemost. 2017; 43(7):691–698. Reference #2: Beiderlinden M, Werner P, Bahlmann A, et al. Monitoring of argatroban and lepirudin anticoagulation in critically ill patients by conventional laboratory parameters and rotational thromboelastometry - a prospectively controlled randomized double-blind clinical trial. BMC Anesthesiol. 2018; 18(1):18. Reference #3: Pendleton, R., Wheeler, M. M., & Rodgers, G. M. Argatroban Dosing of Patients with Heparin-Induced Thrombocytopenia and an Elevated aPTT Due to Antiphospholipid Antibody Syndrome. Annals of Pharmacotherapy. 2006; 40(5): 972–976. DISCLOSURES: No relevant relationships by Ashley Budd, source=Web Response No relevant relationships by Prachi Patel, source=Web Response