Abnormal Coagulation Tests Are Associated With Progression of Traumatic Intracranial Hemorrhage

Abstract

This study demonstrates an association between coagulopathy, diagnosed by routine laboratorial tests in the first 24 hours, with ICH progression; and ICH progression with mortality in patients with severe TBI. The causal relationship between coagulopathy and ICH progression will require further studies.

Endogenous plasminogen activators mediate progressive intracerebral hemorrhage after traumatic brain injury in mice

“…It is postulated that this exposure induces a procoagulant state that may help stem bleeding but may also cause a consumptive coagulopathy and secondary fibrinolysis that leads to delayed ICH. However, our data and those of others show that delayed bleeding often occurs in the absence of clinically relevant thrombocytopenia 49 or a clinically significant prolongation of clotting times, 3 suggesting that perturbations in other aspects of intracerebral hemostasis may predominate.…”

“…3,9,10 In support of this concept, high levels of D-dimers, prolongation of clotting times, thrombocytopenia, and increased plasmin/anti-plasmin complexes correlate with increased mortality. 7,11,12 However, measures that attenuate the consumptive coagulopathy fail to reduce mortality and/or disability.…”

“…1,2 Delayed intracerebral hemorrhage (ICH) is a strong predictor of morbidity and mortality. [3][4][5] Serial computed tomography scans reveal expansion of ICH in ;50% of patients post-TBI, [6][7][8] but intervention based on the current presumptive pathophysiology is often futile.…”

“…3,9,10 To pursue this hypothesis using independent experimental approaches, we examined the relationship between the intensity of posttraumatic endogenous fibrinolysis and activation of coagulation. We measured 2 global parameters of coagulation after TBI in WT, uPA mice developed elevated D-dimers and a significant fall in platelet count (P , .003) after CHI, comparable to findings in WT mice ( Figure 6C-D).…”

Hypocoagulability in Traumatic Brain Injury as Measured by Traditional Means and Thrombelastography

“…Abnormalities in admission PT, aPTT, INR, and fibrinogen degradation products have all been linked to increased morbidity and mortality in TBI patients [3,4,7,12,27,28,[32][33][34][35][36][37]. However, when we analyzed admission CCT values on 1924 of our highest-level trauma activations over 18 months, no statistically significant difference in the prevalence of coagulopathy based on these values was detected in TBI patients compared to non-TBI patients (Table 2).…”