Blunt cerebrovascular injury (BCVI)

Brommeland, T., Helseth, E., Aarhus, M. et al. Best practice guidelines for blunt cerebrovascular injury (BCVI). Scand J Trauma Resusc Emerg Med 26, 90 (2018). https://doi.org/10.1186/s13049-018-0559-1

Background

BCVI is a non-penetrating injury to the carotid and/or vertebral artery that can cause stroke in trauma patients. Rare, but perhaps 1-2% in trauma populations and up to 9% in those with severe head injury.

Due to stretching or impingement of vascular walls due to forceful movement of the head and neck; causing subintimal exposure and secondary thrombus formation, wall hematoma, and possibly lumen occlusion. Can lead to pseudoaneurysm.

Clearly associated with severe facial injuries and fractures of the skull base and C-spine.

Can lead to a stroke (local occlusion, embolic shower). In the carotid artery, stroke rates increase with increasing injury grade. By contrast, stroke incidence and neurologic outcomes are independent of blunt vertebral injury grade.

BCVI is an independent predictor for poor outcome with higher morbidity and mortality rates in trauma patients with this injury, reported as high as 25–50% for those suffering a stroke.

Diagnosis of BCVI

  1. Use the expanded Denver screening criteria (includes the Memphis screening tool) for trauma patients (adults and children) with signs or symptoms of BCVI, or a high-energy trauma mechanism with 1+ risk factors below:
    1. 300
    2. will help identify asymptomatic BCVI and perhaps reduce the rate of stroke
  2. CTA of the precerebral carotids and vertebral arteries should be done (to the base of the skull including COW) in patients meeting 1+ Denver screening critieria.
    1. CTA may detect almost all clinically significant BCVIs as very few strokes have been observed in trauma patients with a negative CTA
    2. few studies using MR angiography for BCVI have been performed
  3. Biffl injury grading scale should be used to classify the BCVI on imaging:

Treatment of BCVI

  1. Start antithrombotic treatment as soon as considered safe (even with severe TBI or solid organ/MSK injury).
    1. Recent studies on BCVI and concomitant intracranial, intraspinal or solid organ injuries have shown no difference in hemorrhagic worsening between treated or untreated patients
    2. Eastman et al. demonstrated a reduced stroke rate from 15.3 to 3.8% when time to diagnosis and thus start of treatment was lowered
  2. Treatment consists of antiplatelet or anticoagulation.
    1. Suggested regimen per Brommeland CPG: LMWH (full-dose) within 24-48h of the diagnosis followed by transition to oral ASA 75-81 mg daily "when appropriate". For kids, the ASA dose is 3-5 mg/kg.
    2. Suggested regimen per UTD: IV UFH initially; then transition to either antiplatelet vs long-term oral anticoagulant.
    3. No randomized study has been performed comparing antiplatelet to anticoagulation in BCVI patients.
    4. There is no evidence that double platelet inihibitors or a combination of drugs is more effective than a single-drug regimen
  3. Treatment continues for at least 3 months.
    1. There is a paucity of data and most studies with long-term follow-up are on patients with spontaneous dissections.
    2. Whether a remaining vessel narrowing after 3–6 months in an asymptomatic trauma patient represent an indication for continued medical treatment or endovascular intervention is undetermined.
  4. Follow CTA in 7d and 3 months is recommended as the initial CTA can show false-positive findings.
    1. If negative, stop treatment
    2. If positive, consider continuing treatment (clinical decision)

For pseudoaneurysms progressing in size or severe luminal stenosis producing thrombotic/ischemic events, consult a neurointerventionalist with endovascular expertise.