In Response

We thank Tanaka et al1 for their interest in our recent work describing fibrinolysis shutdown using rotational thromboelastometry in patients with traumatic injury.2 We agree that the viscoelastic coagulation tests have limitations when it comes to assessment in isolation a coagulation abnormality such as fibrinolysis and to advancement of the mechanistic understanding of fibrinolysis shutdown. Key determinants of clot degradation should be analyzed in future studies, for example, fibrinolysis pathway markers and platelet function, including clot retraction assessment. In particular, considering the clot retraction process as the tensile force of activated platelets over the fibrin clot that increases clot density and decreases its susceptibility to fibrinolytic activity,3 all the factors associated with fibrinolysis shutdown have the potential to attenuate the clot retraction. In our cohort, the fibrinolysis shutdown response encompassed a heterogeneous group of coagulation features that potentially reduce the clot retraction (higher transfusion volumes, a lower fibrinogen level, delayed dynamic clot parameters, and acidosis). Our findings are aligned with a recent post hoc analysis of the Pragmatic Randomized Optimal Platelet and Plasma Ratios trial that showed the fibrinolysis shutdown group had a lower fibrinogen level, a lower platelet count, and a worse platelet aggregation function when compared to physiologic fibrinolysis group. Also, 89% of patients in the fibrinolysis shutdown group had moderate to severe fibrinolytic activation as measured by plasmin–antiplasmin complexes.4 However, contrary to previous reports, we did not find an association with increased mortality in patients with fibrinolysis shutdown, and we speculated hemostatic activation (higher maximum clot formation was associated with fibrinolysis shutdown) potentially account for this finding. Overall, early fibrinolysis shutdown response suggests a hypocoagulable profile rather than a prothrombotic state of inhibition of the fibrinolytic activity and we hypothesize multiple underlying coagulation abnormalities convey into fibrinolysis shutdown. In contrast to hyperfibrinolysis, postinjury fibrinolysis shutdown response has only recently been described and is an evolving concept, and its clinical consequences remain to be fully elucidated. J. Carolina Gomez-Builes, MDAnesthesia DepartmentUniversity of TorontoToronto, Canada Sandro B. Rizoli, MD, PhD, FRCSC, FACSDepartment of SurgeryLi Ka Shing Knowledge InstituteSt Michael’s HospitalToronto, CanadaDepartment of SurgeryUniversity of TorontoToronto, Canada[email protected]

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