Blunt cerebrovascular injuries in acute trauma care: a screening protocol.

Löhrer L, Vieth V, Nassenstein I, Hartensuer R, Niederstadt T, Raschke MJ, Vordemvenne T

Abstract

INTRODUCTION Blunt cerebrovascular injuries (BCVI) of the extra- or intracerebral vessels are frequently observed lesions which may lead to thrombembolic events with focal neurological deficits, stroke or death particularly in patients <60 years. However, a comprehensive standardised clinical algorithm for screening and management of these secondary injuries is still lacking. MATERIALS AND METHODS We developed a standardised screening protocol applicable for mild as well as severely injured patients. In this prospective cohort study, we evaluated the feasibility of this diagnostic algorithm in a level 1 trauma centre setting. Trauma patients who met the inclusion criteria underwent a computed tomographic angiography (CTA) as part of standard diagnostic procedure at admission. All suspicions or positive findings were reevaluated by a conventional four-vessel catheter angiography within the first 72 h after trauma. Within this period, anticoagulation with low-dose heparin was started. BCVI confirmation indicated a shift to systemic heparinisation with overlapping phenprocoumon therapy for at least 6 months. All patients were reevaluated after 6 months by another four-vessel angiography. Depending on the diagnostic findings, oral anticoagulation may be discontinued or continued for another 6 months. RESULTS A total of 44 patients (8 male, 6 female, age range 19-95 years) were included in the study. 20 BCVIs were detected in 16 patients (36.3%). The most common injuries identified were Biffl Type II (40%) and Type IV lesions (30%). 86.4% of the patients received a CTA upon admission, 93.2% of which were conducted within 12 h posttrauma. None of the patients had a secondary thrombembolic neurological event during the hospital stay or within 3 months postdischarge. CONCLUSION Our results indicate that implementation of the screening protocol can prevent strokes in patients without primary thrombembolic neurological deficits.