Traumatic Intracranial Hemorrhage Correlates with Preinjury Brain Atrophy, but Not with Antithrombotic Agent Use: A Retrospective Study

Abstract

BackgroundThe impact of antithrombotic agents (warfarin, clopidogrel, ASA) on traumatic brain injury outcomes is highly controversial. Although cerebral atrophy is speculated as a risk for acute intracranial hemorrhage, there is no objective literature evidence.Materials and MethodsThis is a retrospective, consecutive investigation of patients with signs of external head trauma and age ≥60 years. Outcomes were correlated with antithrombotic-agent status, coagulation test results, admission neurologic function, and CT-based cerebral atrophy dimensions.ResultsOf 198 consecutive patients, 36% were antithrombotic-negative and 64% antithrombotic-positive. ASA patients had higher arachidonic acid inhibition (p = 0.04) and warfarin patients had higher INR (p<0.001), compared to antithrombotic-negative patients. Antithrombotic-positive intracranial hemorrhage rate (38.9%) was similar to the antithrombotic-negative rate (31.9%; p = 0.3285). Coagulopathy was not present on the ten standard coagulation, thromboelastography, and platelet mapping tests with intracranial hemorrhage and results were similar to those without hemorrhage (p≥0.1354). Hemorrhagic-neurologic complication (intracranial hemorrhage progression, need for craniotomy, neurologic deterioration, or death) rates were similar for antithrombotic-negative (6.9%) and antithrombotic-positive (8.7%; p = 0.6574) patients. The hemorrhagic-neurologic complication rate was increased when admission major neurologic dysfunction was present (63.2% versus 2.2%; RR = 28.3; p<0.001). Age correlated inversely with brain parenchymal width (p<0.001) and positively with lateral ventricular width (p = 0.047) and cortical atrophy (p<0.001). Intracranial hemorrhage correlated with cortical atrophy (p<0.001) and ventricular width (p<0.001).ConclusionsIntracranial hemorrhage is not associated with antithrombotic agent use. Intracranial hemorrhage patients have no demonstrable coagulopathy. The association of preinjury brain atrophy with acute intracranial hemorrhage is a novel finding. Contrary to antithrombotic agent status, admission neurologic abnormality is a predictor of adverse post-admission outcomes. Study findings indicate that effective hemostasis is maintained with antithrombotic therapy.

Formation of Microparticles in the Injured Brain of Patients with Severe Isolated Traumatic Brain Injury

“…This latter effect has been considered to be mediated by nuclear factor kappa B (NF-κB) [264]. Although there is a potential risk of bleeding complications in a TBI situation when using ASA [265], the results of two studies showed no hazardous effects of ASA intake prior to injury [266,267].…”

DRINet for Medical Image Segmentation

“…In the future, we plan extend the proposed approach to segment lesions as well as CSF using a single DRINet. This is useful in clinical settings for prognostication after stroke [44] or estimating cerebral haemorrhage risk [45], [46].…”

Major trauma in the older patient: Evolving trauma care beyond management of bumps and bruises

“…By virtue of their common cortical atrophy and high use of antiplatelet/anticoagulant medications, older persons are at higher risk of intracranial injury despite normal GCS . While the incidence of traumatic intracranial bleeds is extensively researched for warfarin, new oral anticoagulation (NOAC) therapies include direct thrombin (dabigatran) or Factor Xa (rivaroxaban and apixaban) inhibitors .…”