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B53-32 Heparin-induced Thrombocytopenia With Diffuse Thrombosis After Bilateral Lung Transplantation
Journal article   Peer reviewed

B53-32 Heparin-induced Thrombocytopenia With Diffuse Thrombosis After Bilateral Lung Transplantation

V Muldiiarov, M T Olson, S Biswas Roy and A Arjuna
American journal of respiratory and critical care medicine, Vol.212(Supplement_1)
05/01/2026

Abstract

Blood platelets Lung transplants Ostomy Thrombocytopenia Thrombosis
Introduction Heparin-induced thrombocytopenia (HIT) is a rare but life-threatening complication after solid organ transplantation. Its prothrombotic potential can result in widespread venous and arterial thromboses if not recognized early. Diagnosis requires high clinical suspicion, confirmatory testing, and prompt initiation of non-heparin anticoagulation. This case illustrates diffuse thrombosis secondary to HIT in the early postoperative period after lung transplantation and outlines a systematic management approach. Case Description A 55-year-old man with end-stage pulmonary hypertension underwent bilateral sequential lung transplantation without cardiopulmonary bypass or extracorporeal membrane oxygenation. He received unfractionated heparin 5,000 units subcutaneously every 8 hours for VTE prophylaxis. By postoperative day (POD) 3, platelets had fallen progressively. Despite a negative initial duplex, heparin was continued pending laboratory results. On POD 8, anti-platelet factor 4 antibodies returned positive, later confirmed by serotonin-release assay. Heparin was discontinued, and an argatroban infusion was initiated (2 µg/kg/min) with aPTT titrated to 1.5-3.0× baseline. Platelets were maintained above 50 × 109/L. On POD 11, CT pulmonary angiography revealed multiple emboli in the left pulmonary artery, and concurrent imaging demonstrated nonocclusive thrombus in the IVC, occluded right hepatic vein, and occlusive right iliofemoral thrombosis. Despite therapeutic argatroban, follow-up duplex showed progression to the popliteal segment. On POD 17, endovascular thrombectomy and IVC filter placement were performed without complications. After transient interruption for tracheostomy, argatroban was resumed, with subsequent imaging showing improvement. The patient was discharged on POD 39 in stable condition. Figure 1 depicts the platelet trend after lung transplantation. Discussion This case demonstrates the diagnostic and therapeutic challenges of HIT after lung transplantation. Clinicians must maintain vigilance for HIT when platelet counts decline during heparin therapy, particularly in the presence of thrombosis. Early transition to a direct thrombin inhibitor such as argatroban allows continued anticoagulation while accommodating procedures. Collaboration among transplant, hematology, and interventional teams is crucial to prevent catastrophic outcomes. This case reinforces the importance of rapid recognition, laboratory confirmation, and coordinated multidisciplinary management to safely navigate the competing risks of bleeding, thrombosis, and postoperative interventions in lung transplant recipients. This abstract is funded by: None

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