Abstract
BACKGROUND: Antiphospholipid syndrome (APS) is a prothrombotic autoimmune disorder in which perioperative factors-particularly cardiopulmonary bypass-may amplify hypercoagulability. Evidence and consensus guidance for APS management around cardiovascular surgery remain limited. A 37-year-old man with a large, highly mobile thrombus in the ascending aorta underwent surgical thrombectomy under cardiopulmonary bypass. Preoperative testing showed only leukocytosis, slightly shortened activated partial thromboplastin time (APTT) and mild D-dimer elevation; all other findings were unremarkable. Ten days postoperatively, removal of a nontunneled right internal jugular central venous catheter (CVC) was unexpectedly impeded by catheter-related thrombosis (CRT) despite prophylactic anticoagulation. Noninvasive maneuvers failed to free the catheter, necessitating open surgical extraction. Subsequent evaluation revealed widespread venous thromboses and confirmed APS, likely underlying both the arterial event and the rapidly developing catheter-associated thrombosis. Aggressive multimodal therapy-including methylprednisolone, enteric-coated aspirin, warfarin, rituximab, unfractionated heparin, and fibrinogenase-achieved clinical stabilization and prevented further events. CONCLUSION: This case highlights the challenges in timely diagnosing APS and the management complexity of rapid, postoperative thrombus formation. Clinicians should maintain a high index of suspicion for early postoperative hypercoagulability-even when routine coagulation screens are unrevealing-escalate promptly when CVC removal meets resistance, and consider APS-tailored antithrombotic strategies. The possibility that fibrin sheaths and catheter-associated thrombosis can evolve quickly, even after short indwelling times, warrants vigilance and early multidisciplinary intervention. It also raises concern that, in this context, standard direct oral anticoagulants (DOACs) may be less effective.