Kidney Week

Abstract: PUB038

Plasmapheresis Before Heparinized Extracorporeal Mechanical Oxygenation in a Patient with Confirmed Heparin-Induced Thrombocytopenia

Session Information

• Publication Only

Category: Cardiovascular-Kidney-Metabolic Health

• 602 Cardiovascular-Kidney-Metabolic Health: Clinical

Authors

• Seol, Jaehoon, Independent Researcher, Seoul, Korea (the Republic of)

Jaehoon Seol, MD

• Prajapati, Vishal, Byramjee Jeejeebhoy Medical College, Ahmedabad, Gujarat, India

Vishal Prajapati, MBBS

• Milley, Lauren, University of South Florida, Tampa, Florida, United States

Lauren Milley, MD

• Reed, Hunter T., University of South Florida, Tampa, Florida, United States

Hunter T. Reed, MD

• Yi, Jia, University of South Florida, Tampa, Florida, United States

Jia Yi, MD

Introduction

Heparin-induced thrombocytopenia (HIT) is an immune-mediated complication of heparin exposure caused by antibodies to platelet factor 4–heparin complexes. Although typically avoided after diagnosis, heparin may be required in high-risk settings such as cardiac surgery. Therapeutic plasma exchange (TPE) has a Category III indication for HIT patients undergoing cardiopulmonary bypass or extracorporeal membrane oxygenation. Given the low incidence (0.1%–5%) data on heparin re-exposure after TPE are limited. We present a patient with advanced heart failure and HIT successfully re-exposed to heparin for left ventricular assist device (LVAD) implantation after TPE.

Case Description

A 60-year-old man with nonischemic cardiomyopathy, HFrEF (EF 10–15%), and atrial fibrillation who presented in cardiogenic shock. An intra-aortic balloon pump (IABP) was placed and heparin initiated. Heparin was stopped for thrombocytopenia concerning for HIT, then resumed after negative ELISA and platelet recovery. Recurrent thrombocytopenia prompted repeat testing which confirmed HIT by positive ELISA and serotonin release assay (SRA).
Streptococcal bacteremia delayed LVAD implantation, necessitating replacement of existing IABP with an Impella as a bridging device. Surgeon preference required intraoperative heparin for LVAD placement due to its quick intraoperative reversibility. The patient underwent three sessions of plasma exchange followed by intravenous immunoglobulin. First session was completed with IV albumin replacement followed by fresh frozen plasma for the second and third. Fibrinogen decreased during TPE but recovered. Repeat ELISA and SRA were negative. LVAD implantation proceeded without bleeding or thrombotic complications after heparin re-exposure. Platelets declined postoperatively but stabilized without recurrent HIT.

Discussion

Managing HIT in cardiac surgery requires balancing thrombotic and bleeding risks. In this case, TPE and IVIG reduced HIT antibodies, confirmed by ELISA and SRA, enabling safe heparin re-exposure for LVAD placement. Fibrinogen declined after initial TPE but recovered and remained within a safe range perioperatively without bleeding.