Blunt traumatic vertebral artery injury: a clinical review

Abstract

Blunt traumatic vertebral injury (TVAI) is frequently associated with head and neck injury and is being detected with increasing frequency due to improved imaging of the trauma patient. In a few cases, it can lead to potentially fatal posterior circulation ischaemia There is debate in the literature regarding whether TVAI should be actively screened for and, if so, how. Management of TVAI may be conservative, medical (antiplatelet agents or anticoagulation), endovascular or open surgery. We review the literature concerning the mechanisms and presentation of TVAI following blunt injury and the current screening recommendations. Management strategies proposed are based on the radiological grade and clinical severity of TVAI, where high-grade symptomatic injuries and high-grade injuries in patients where anticoagulation is contraindicated are treated endovascularly and asymptomatic or low-grade injuries are managed with anticoagulation where it is not contraindicated. Follow-up is via CT angiography to assess for resolution of the injury.

Fig. 1

The vertebral arteries are composed of four segments. V1, the extraosseous segment, starts at the origin of the vertebral artery and runs to the transverse foramen of the C6. V2 is the foraminal segment where the artery passes through the transverse foramina from C6 to C1. V3, the extraspinal segment begins at the foramen transversarium of C2. The vertebral artery then passes along the superior aspect of the posterior ring of C1, then twists antero-superior towards the foramen magnum where it pierces the dura. Then begins V4, the intradural segment which courses to the pontomedullary junction, where the basilar artery is formed

Fig. 2

Images from a 64-year-old man who presented with acute vertigo and vomiting 2 weeks after a flexion–extension injury of his neck with continued neck pain. At the time of the injury, X-rays and a CT scan (a sagittal reformat) showed an unstable type 2 odontoid fracture, which was managed with a hard collar. An MRI (b axial FLAIR sequence) following admission with clinical features of a cerebellar ischaemic event 2 weeks later showed high signal in the left PICA territory compatible with acute infarction. A CT angiogram (c coronal maximum intensity projection) showed occlusion of the left vertebral artery arising from a dissection at the level of the C1/2 junction. He was managed with immediate anticoagulation using heparin, which was temporarily stopped after 3 days to allow surgery to stabilise the fracture via C1–C3 sublaminar wiring (d AP and lateral post-operative X-rays). He made a good recovery with rehabilitation and his anticoagulation was converted to warfarin, target INR 2–3, and then stopped after 6 months with no further adverse events

Fig. 3

Algorithm for assessment, screening and management of TVAI^a