Kidney Week

Abstract: PUB064

Not Just a Flush: Hemodialysis Catheter Heparin Exposure Causing Heparin-Induced Thrombocytopenia and Multisite Venous Thrombosis

Session Information

• Publication Only

Category: Dialysis

• 801 Dialysis: Hemodialysis and Frequent Dialysis

Authors

• Vazquez Morales, Emily, Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico

Emily Vazquez Morales, MD

• Pico-Ramirez, Alexandra C., Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico

Alexandra C. Pico-Ramirez, MD

• Ocasio Melendez, Ileana E., Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico

Ileana E. Ocasio Melendez, MD, FASN

• Rivera Rios, Jeaneishka Marie, Universidad de Puerto Rico Escuela de Medicina, San Juan, Puerto Rico

Jeaneishka Marie Rivera Rios, MD

Introduction

Heparin-induced thrombocytopenia (HIT) type II is an immune-mediated prothrombotic disorder caused by antibodies against platelet factor 4–heparin complexes. Although classically associated with systemic unfractionated heparin, even low-dose exposure from hemodialysis (HD) catheter locking flushes may trigger HIT. Because catheter flushes are often perceived as clinically insignificant, HD-related HIT may be underrecognized.

Case Description

A 57-year-old man with hypertension, coronary artery disease, heart failure with reduced ejection fraction, and chronic kidney disease developed oliguric acute kidney injury requiring intermittent HD after excessive NSAID use. A tunneled HD catheter was placed. During hospitalization, he received no systemic anticoagulation or heparin exposure other than intermittent heparin locking flushes for catheter maintenance.

Approximately 10 days after exposure, he developed progressive thrombocytopenia. Three days later, he reported right leg pain and right neck swelling. Examination revealed unilateral lower extremity edema, calf tenderness, and neck swelling.

Bedside ultrasound showed echogenic material in the right internal jugular vein. Doppler studies demonstrated extensive thrombosis involving the right lower extremity deep and superficial venous systems, with complete occlusion of the right internal jugular and subclavian veins. HIT was suspected, and PF4 antibody testing was positive.

All heparin was discontinued and argatroban initiated. Given extensive thrombotic burden, thrombectomy was performed with successful recanalization. He was transitioned to warfarin and discharged with strict avoidance of all heparin exposure, including catheter flushes.

Discussion

HIT is associated with high thrombotic morbidity and mortality. While most commonly linked to systemic heparin, even minimal exposure through HD catheter locking flushes may induce clinically significant HIT. This case demonstrates that catheter-lock heparin alone may be sufficient to trigger severe thrombosis. Dialysis patients are at increased risk due to repeated heparin exposure and frequent alternative causes of thrombocytopenia, which may delay recognition. Early diagnosis and prompt non-heparin anticoagulation are essential to prevent catastrophic complications.