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  • Aspirin Does Not Promote Progression of Intracranial Hemorrhage

    Final Number:

    Jason B. Brill MD; Casey E. Dunne MPH; James D. Wallace MD; Paul R. Lewis DO; Jayraan Badiee MPH; Richard Y. Calvo PhD; Michael J. Sise MD; Vishal Bansal MD; Steven R. Shackford MD

    Study Design:
    Clinical Trial

    Subject Category:

    Meeting: Congress of Neurological Surgeons 2016 Annual Meeting - Late Breaking Science

    Introduction: No large studies examine the effect of aspirin monotherapy (aspirin as the sole antiplatelet agent) on progression of intracranial hemorrhage (pICH). Previous studies group antiplatelet medications together to analyze effects on pICH. Given recent work showing aspirin’s promise as a venous thromboprophylaxis agent in trauma, we examined pICH in patients with blunt traumatic brain injury (bTBI) taking pre-injury aspirin. We hypothesized that patient use of pre-injury aspirin monotherapy is not associated with an increased rate of pICH compared with patients not on any anticoagulant or antiplatelet agents (ACAP).

    Methods: We conducted a retrospective cohort study on all adult patients admitted to a level I trauma center 2010-2011 with ICH on any head computed tomography (HCT) after bTBI. Primary outcome was pICH on subsequent HCT per the radiologist’s dictation. Secondary outcomes included neurosurgical intervention, in-hospital mortality, and discharge to hospice. Patients on ACAP other than aspirin were excluded. Multiple logistic regression models evaluated the adjusted association of pre-injury aspirin and each outcome.

    Results: A total of 537 patients were identified with 1827 available HCTs, of whom 91 were excluded due to pre-injury ACAP use other than aspirin. Of the 446 eligible patients, 65 (14.6%) were on aspirin monotherapy. The incidence of pICH among patients taking aspirin was 24.6% vs. 28.9% without ACAP (p=0.48). Between aspirin and no ACAP groups, neurosurgical intervention was performed in 16.9% and 21.3%, respectively (p=0.42), and in-hospital mortality was 3.1% and 3.4%, respectively (p=1.00). Adjusted logistic regression models showed no statistically significant associations between aspirin and any outcome (table).

    Conclusions: In bTBI patients, pre-injury aspirin monotherapy is not associated with pICH. A prospective study would require 9166 patients to be powered adequately to show a 4% pICH rate difference. Our data suggest that aspirin is a low-risk therapy that may be safe to use in bTBI patients.

    Patient Care: As progression of intracranial hemorrhage after traumatic brain injury is clearly associated with worse outcomes, identification of risk factors for progression assists the clinician’s prognostic accuracy. The literature has established warfarin and clopidogrel as important risk factors, but extending that status to all antiplatelet medications is unfounded. Aspirin has a variety of prophylactic and therapeutic uses and is being investigated for venous thromboembolism prophylaxis in several trauma centers. Defining the risks associated with aspirin is essential, and this study clarifies the safety profile in blunt traumatic brain injured patients. The study also allows the practicing neurosurgeon to identify more appropriately the patients at higher risk for progression of intracranial hemorrhage, operative intervention, and mortality.

    Learning Objectives: By the conclusion of the session, participants should be able to: 1) Recognize that aspirin is not a risk factor for progression of intracranial hemorrhage after blunt traumatic brain injury, 2) Discuss the lack of association between aspirin and poor outcomes, such as operative intervention, mortality, and discharge to hospice, after blunt traumatic brain injury, and 3) Identify the impact of potential practice changes involving aspirin, other antiplatelet agents, and anticoagulants.

    References: see attached manuscript

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