Blunt cerebrovascular injuries (BCVIs), injuries to the extracranial carotid and vertebral arteries, historically have been considered rare, yet are recognized as potentially devastating events. Given the limited experience with BCVI, even in busy trauma centers, there is no large body of literature to guide the treatment of these injuries. As a result, BCVIs continue to be challenging in terms of risk assessment, screening, diagnosis, and treatment.

Regional Anatomy

The left common carotid artery (CCA) originates from the aortic arch and is therefore intrathoracic, whereas the right CCA originates from the innominate artery and has no intrathoracic portion. The left and right cervical CCAs divide into the internal (ICA) and external (ECA) carotid arteries at the level of the C3-4 disc space, which corresponds to the superior border of the thyroid cartilage. The ECA does not supply circulation directly to the brain but, in the presence of carotid or vertebral artery (VA) occlusive disease, the ECA branches provide significant collateral blood flow to the intracranial contents. The ICA begins at the bifurcation of the CCA, terminates at its intracranial bifurcation into the anterior cerebral artery (ACA) and middle cerebral artery (MCA), and provides blood supply to the cerebral hemispheres. The ICA can be separated into four segments: cervical, petrous, cavernous, and cerebral (supraclinoid). The cervical portion of the ICA has no named branches. The petrous segment of the ICA traverses the carotid canal in the petrous portion of the temporal bone. The cavernous portion of the ICA is the first part of the course of the ICA within the cranial vault. It is suspended between the layers of the dura mater that form the cavernous sinus. The supraclinoid, or cerebral, segment is the fourth portion of the ICA and begins where the artery passes through the dura.

The left and right VA arise from the upper and posterior portion of the first segment of their respective subclavian arteries. The VA, like the ICA, is composed of four segments. The first segment begins at its subclavian origin and courses superiorly and posteriorly to the point where it enters the transverse foramen of C6. The second segment ascends through the transverse foramina of the upper 6 cervical vertebrae. The third portion of the VA curves posteriorly behind the lateral mass of the atlas, and the fourth segment pierces the dura. There is considerable asymmetry in the vertebral system, to the point of unilateral VA agenesis.

The circle of Willis is a vascular ring that effectively forms an arterial manifold balancing anterior (ICA) and posterior (VA) inflow with the outflow to the ACA, MCA, and posterior cerebral artery. A symmetric circle of Willis is present as described in only 20% of individuals. The frequency of variations in the collateral circulatory routes can help explain unusual clinical presentations of arterial injuries. In addition, it underscores the need to image the intracranial circulation in cases of cervical vessel injury.

Injury Mechanism

There appear to be four fundamental mechanisms of blunt carotid arterial injury. The most common type results from hyperextension and contralateral rotation of the head and neck. This may be explained by anatomic relationships unique to the upper cervical region. The lateral articular processes and pedicles of the upper 3 cervical vertebrae project more anteriorly than do those of the lower 4 cervical vertebrae. As a result, the overlying distal cervical ICA is prone to stretch injury during cervical hyperextension. A direct blow to the neck may crush the artery or it may be compressed between the mandible and vertebral prominence in acute cervical hyperflexion injuries. Intraoral trauma may injure the ICA, most typically in children who have fallen with a hard object (eg, pencil) in their mouth. Finally, basilar skull fractures that involve the sphenoid or petrous bones may result in laceration of the artery.

The third segment of the VA, which extends from the level C2 to the dura, is most commonly injured by blunt trauma because of the increased degree of stretching and compression that occurs at the atlantoaxial and atlanto-occipital joints during head rotation. In addition, the relationship between the VA and the cervical vertebral bodies puts the VA at risk when the vertebral body, particularly the foramen transversarium, is fractured. Although high-speed motor vehicle crashes and falls account for most ICA and VA injuries, virtually any mechanism involving acute hyperextension, flexion, or rotation of the neck (even after “trivial trauma”) may result in BCVI.

Pathophysiology

Tearing of the intima exposes the thrombogenic subendothelial collagen surface, which promotes platelet aggregation and the potential for embolization, partial thrombosis with low flow, or complete thrombosis. In addition, the intimal tear offers a portal of egress for a dissecting column of blood that may narrow the lumen with subsequent partial or complete vessel occlusion. The end result is cerebral ischemia. Less commonly, partial or complete transection of the artery occurs, resulting in pseudoaneurysm formation or free rupture.

Signs and symptoms

There are several premonitory signs and symptoms that are associated with the vessel injury itself, which may suggest the presence of BCVI before the onset of cerebral ischemia. These include neck, ear, face, periorbital, posterior neck, and occipital pain and Horner’s syndrome. Cerebral ischemic neurologic events may be classified as transient ischemic attack (lasting less than 24 hours), reversible ischemic neurologic deficit (lasting less than 1 week), or ischemic infarction (signs and symptoms do not clear completely). A decrease in the patient’s level of consciousness, although a common finding in traumatic brain injury, is decidedly unusual in acute stroke.

A systematic neurologic examination will help to localize the distribution of cerebral ischemia. Occlusion of the ICA generally results in contralateral sensorimotor deficits in the arm, face, and leg (in decreasing order of severity). Global aphasia indicates involvement of the dominant hemisphere, and contralateral neglect is typical of nondominant hemisphere involvement. Carotid-cavernous sinus fistulae usually occur in the cavernous or cerebral segments of the ICA, typically the result of a basilar skull fracture that lacerates the artery. Common features include conjunctival hyperemia, chemosis, exophthalmos, ophthalmoplegia, and orbital pain. There is often a cephalic bruit and a palpable thrill over the orbit.

The MCA is the larger of the 2 terminal branches of the ICA and is the most common site of embolization. Infarction in the MCA distribution results in contralateral hemiparesis and hemisensory loss and ipsilateral deviation of the eyes and head. Broca’s (expressive) aphasia may be present if the dominant hemisphere is involved, whereas involvement of Wernicke’s speech area results in receptive aphasia. Hemineglect is encountered with nondominant hemisphere lesion. The MCA distribution is large, and infarctions of the entire distribution can lead to significant swelling and increased intracranial pressure. The ACA is the smaller of the 2 terminal branches of the ICA. Compared with MCA infarctions, the smaller territory creates less of a risk for the development of late intracranial pressure problems.

Cervical VA occlusions are less likely than carotid arterial occlusions to result in neurologic deficits. Vertebrobasilar ischemia may result in a combination of contralateral sensorimotor abnormalities and ipsilateral cranial nerve or cerebellar abnormalities. Embolic strokes in the vertebrobasilar distribution often result in the lateral medullary (Wallenberg’s) syndrome, which may include ipsilateral facial analgesia, contralateral body analgesia. Horner’s syndrome, and ataxia. Posterior fossa swelling can result in obstruction of the fourth ventricle and hydrocephalus or brainstem compression and herniation. Unilateral occlusion of the posterior cerebral artery may result in contralateral homonymous hemianopsia, and bilateral posterior cerebral artery infarction leads to cortical blindness (Anton’s syndrome). In general, brainstem lesions can be identified best by their crossed patterns of deficits with cranial nerve palsies ipsilateral and hemiparesis contralateral to the infarction.

Rationale for screening

A latent period before the appearance of clinical manifestations of the injury is characteristic of BCVI. Presumably, this reflects the time it takes for platelets to aggregate at sites of intimal disruption and to embolize, limit flow, or occlude the vessel. In large series, 23% to 50% of patients experience the manifestation of symptoms more than 24 hours after injury. In our experience, 42% of patients experienced the manifestation more than 18 hours after injury. Moreover, delayed recognition of BCVI is common because associated head injuries preclude a meaningful neurologic examination and other critical associated injuries demand immediate intervention.

Previous multicenter reviews suggested the incidence of BCVI to be one per 1000 blunt trauma admissions. Over the past 2 decades, however, there has been a steady increase in the reported numbers of BCVI. We documented blunt carotid arterial lesions in 3.5% of a subgroup of patients undergoing thoracic aortography after blunt trauma. One half of the blunt carotid arterial lesions were unsuspected on clinical grounds. This prompted a more aggressive screening approach. Patients who sustain blunt trauma with severe hyperextension or hyperflexion, strangulation, or direct blow mechanisms and those patients with cervical vertebral or basilar skull carotid canal fractures are screened with cerebral arteriography for BCVIs. We have identified BCVIs in 27% of asymptomatic patients selected on the basis of our screening criteria. The incidence of BCVI at our center in the past 8 years has been 1.1% among patients admitted after blunt trauma.

Diagnosis

The gold standard test is cerebral arteriography. Unfortunately, the noninvasive alternatives duplex ultrasonography, transcutaneous Doppler ultrasonography, computed tomographic angiography, and magnetic resonance angiography have yet to be established as accurate as arteriography although CTA appears promising. We have developed a grading scale based on the literature and our collective experience. Grade I injuries are defined by the arteriographic appearance of irregularity of the vessel wall or a dissection without stenosis of the lumen. Grade II injuries include dissections or intramural hematomas with associated luminal narrowing, or a visible raised intimal flap. Pseudoaneurysms have been designated grade III BCVIs; occlusions have been designated grade IV, and arterial transsections have been designated grade V.

Management

Surgical therapy is appropriate for accessible lesions. Unfortunately, most injuries are too distal for operative repair. The current standard treatment is anticoagulation and most authorities recommend systemic heparin. However, there is justification for evaluation of alternative agents (eg, antiplatelet agents) in this setting. Endovascular stenting of the carotid arteries for atherosclerotic disease has enjoyed tremendous popularity recently, but its overall efficacy for BCVI remains to be defined.