CAR-T Cell Therapy-Associated Coagulopathy: From Immunothrombotic Storm Mechanisms to Precision Management Strategies

Chimeric antigen receptor T-cell (CAR-T) therapy has transformed the management of relapsed or refractory hematologic malignancies, yet its benefit is constrained by immune-mediated vascular toxicities. CAR-T-associated coagulopathy (CARAC) is an under-recognized, potentially fatal syndrome driven by endothelial activation, cytokine amplification and disordered fibrinolysis. In this review, we synthesize current evidence on CARAC pathobiology, emphasizing its dynamic transition from early procoagulant endothelial conversion to secondary hyperfibrinolysis and consumptive coagulopathy. We delineate disease-specific phenotypes, including hemorrhage-prone B-cell acute lymphoblastic leukemia, thrombotic large B-cell lymphoma and assay-confounded multiple myeloma, and highlight key diagnostic pitfalls such as tocilizumab-associated fibrinogen decline. To support standardization, we propose a phase-adapted conceptual framework integrating laboratory kinetics, clinical events and functional coagulation assessment. Finally, we outline precision management strategies spanning risk-adapted anticoagulation, hemostatic rescue and targeted treatment of delayed inflammatory and endothelial complications.