Treatment of Blunt Cerebrovascular Injury - A Systematic Review and Meta-Analysis, Multicenter Retrospective Review, and Protocol for a Feasibility Randomized Controlled Trial
Abstract
Blunt cerebrovascular injury (BCVI) is an often-overlooked clinical problem that can result in stroke and cause devastating, potentially permanent, neurologic disabilities in young and otherwise healthy trauma patients. Early diagnosis and treatment of BCVI can reduce the risk of stroke and prevent disability, however, treatment also carries a risk of bleeding complications. More research is needed to understand the optimal management strategy to reduce the risk of stroke while minimizing bleeding complications.
The aim of this thesis is to review and critically appraise the literature to better understand the efficacy of various treatment strategies in preventing stroke following BCVI, evaluate current practice patterns and patient outcomes at Canadian Level I Trauma Centers, and create a feasibility randomized controlled trial protocol to assess practicability of a future randomized control trial determining the optimal dose of antiplatelet therapy in the treatment of BCVI.
Systematic review and meta-analysis of existing literature revealed a slightly lower risk of stroke with the use of antiplatelets compared to anticoagulants (4.5% vs. 5.2%; OR 0.57; 95% CI 0.33 – 0.96, p = 0.04), although there was no difference in stroke rate when evaluating the use of specific agents, acetylsalicylic acid (ASA) vs. heparin (OR 0.43; 95% CI 0.15 – 1.20, p = 0.11). Bleeding complications were significantly higher with the use of anticoagulants and led to more severe bleeding requiring invasive intervention, suggesting better tolerance of antiplatelets in the trauma population. Retrospective review of trauma registries at two Canadian Level I Trauma Centers revealed that patients were more likely to develop stroke after BCVI if they were injured as a result of a motor vehicle collision (MVC), had a lower initial Glasgow Coma Scale (GCS) and higher Injury Severity Scale (ISS), did not meet Denver screening criteria, or had carotid artery injuries. Patients who suffered a stroke were more likely to require intensive care. Treatment interruptions or delays were not associated with increased risk of stroke, and the dose of therapy (81 mg ASA vs. 325 mg ASA) was not independently associated with an increase in stroke rate after adjustment for initial GCS, injury location, and grade of injury (OR 2.244; 95% CI 0.660-7.628).
Current research suggests that early detection and treatment of BCVI can significantly reduce the risk of stroke. ASA has shown similar efficacy as heparin for stroke risk reduction but was associated with less bleeding complications. Currently, the optimal dose of ASA is still unknown. Data from retrospective reviews suggests that there is no difference in stroke rates when using low-dose (81 mg) vs. high-dose (325 mg) ASA but no experimental studies exist to evaluate this question. A randomized controlled trial is required to further assess different doses of ASA to determine the optimal dose that reduces the risk of stroke while minimizing bleeding complications.