(P-TA-12) Therapeutic Plasma Exchange for Management of Heparin-Induced Thrombocytopenia and Thrombosis: Results of a Single Center Based Study

Background/Case Studies: Heparin-induced thrombocytopenia and Thrombosis (HIT/HITT) is a life-threatening thrombotic disorder caused by the formation of anti-heparin/platelet factor four (anti-HPF4) antibody immune complexes. The common management involves heparin cessation and initiation of a direct thrombin inhibitor (DTI). To minimize HIT-related complications, therapies like therapeutic plasma exchange (TPE) are used to remove intravascular anti-HPF4 antibody complexes. We sought to define TPE in HIT/HITT practice pattern using single center-based study.

Study

Design/Methods: A retrospective chart review between January 2019 and December 2020 retrieved perioperative clinical and laboratory data for 15 adults with history of HIT/HITT and a current positive anti-HPF4 antibody titer, managed with TPE and heparin anticoagulation.

Results/Findings: 11 males and 4 females with a median age of 59 years (range: 20-73) were retrieved. All patients had thrombocytopenia onset between 5 to 10 days of heparin exposure. Immediate heparin cessation and bivalirudin initiation was performed in all 15 patients. The pre-procedure median anti-HPF4 antibody titer on IgG- specific enzyme-link immunosorbent assay (ELISA) was 2.0 OD (range: 0.5-3) with positive platelet serotonin release assay (SRA) in only 47%. Majority (86%) patients underwent 1-3 TPE sessions. The most common TPE indications were cardiovascular procedures (100%) and HIT-associated thrombosis (47%). 47% had pre-procedure and 53% had post-procedure TPE. The plasma volume processed was 1.0 -1.5 and the replacement fluid used was fresh frozen plasma (FFP) in 87% cases and FFP plus albumin in 13% cases. Post-TPE; 53% had negative anti-HPF4 titers, 6% had equivocal results, and 40% remain positive with reduced titers. Only 13% remain SRA positive post-TPE. None reduced titers developed clinical HIT/HITT. Heparin-dependent antibodies do not invariably reappear with subsequent heparin use in 47%.

Conclusions: TPE removes sufficient anti-HPF4 IgG titers to achieve negative SRA and negative/decreased EIA ELISA results. This potentially decreases the thrombotic risks associated with high anti-HPF4 antibody titers and also permits necessary heparin re-exposure for cardiovascular procedures. However, large prospective studies are needed to more clearly define the role of TPE in HIT/HITT.

Importance of research: Heparin-induced thrombocytopenia (HIT) is a life-threatening thrombotic disorder commonly caused by the formation of anti-heparin/platelet factor four (PF4) antibody immune complexes. HIT complications include high rates of death, limb amputation, thrombosis and bleeding. To minimize HIT-related complications, therapeutic plasma exchange (TPE) is used to remove large intravascular anti-heparin/PF4 antibody complexes and preventing complications.