Abstract
Posttraumatic coagulopathy involves disruption of both the coagulation and fibrinolytic
pathways secondary to tissue damage, hypotension, and inflammatory upregulation. This
phenomenon contributes to delayed complications after traumatic brain injury (TBI),
including intracranial hemorrhage progression and systemic disseminated intravascular
coagulopathy. Development of an early hyperfibrinolytic state may result in uncontrolled
bleeding and is associated with increased mortality in patients with TBI. Although
fibrinolytic assays are not routinely performed in the assessment of posttraumatic
coagulopathy, circulating biomarkers such as D-dimer and fibrin degradation products
have demonstrated potential utility in outcome prediction. Unfortunately, the relatively
delayed nature of these tests limits their clinical utility. In contrast, viscoelastic
tests are able to provide a rapid global assessment of coagulopathy, although their
ability to reliably identify disruptions in the fibrinolytic cascade remains unclear.
Limited evidence supports the use of hypertonic saline, cryoprecipitate, and plasma
to correct fibrinolytic disruption; however, some studies suggest more harm than benefit.
Recently, early use of tranexamic acid in patients with TBI and confirmed hyperfibrinolysis
has been proposed as a strategy to further improve clinical outcomes. Moving forward,
further delineation of TBI phenotypes and the clinical implications of fibrinolysis
based on phenotypic variation is needed. In this review, we summarize the clinical
aspects of fibrinolysis in TBI, including diagnosis, treatment, and clinical correlates,
with identification of targeted areas for future research efforts.
Keywords
traumatic brain injury - fibrinolysis - coagulopathy - intracranial hemorrhage - thromboelastography
