Blunt Cerebrovascular Injury

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CHAPTER 352 Blunt Cerebrovascular Injury

Gregory G. Heuer, Robert W. Hurst, Peter D. LeRoux

Blunt injury to the carotid or vertebral vessels (blunt cerebrovascular injury) is uncommon and is diagnosed in about 1 of 1000 (0.1%) patients hospitalized for trauma in the United States.¹ This incidence increases to 1% when all blunt trauma patients are screened.² In patients presenting to a trauma center for major trauma, the incidence of blunt carotid injury is 0.08% to 0.67%.³^–⁵ Most of these injuries, however, are diagnosed only after symptoms (e.g., cerebral ischemia) develop. Consequently, the mortality and morbidity associated with blunt cerebrovascular injury are often high.³ Several injury patterns can occur that cause both immediate and long-term symptoms; these include intimal flap or dissection, pseudoaneurysm formation, thrombosis, fistula formation, complete transection, and progressive narrowing of the lumen, contributing to vessel occlusion, thrombosis, or continued thromboembolism.⁶ Both blunt and penetrating injuries to the vertebral artery can occur and include similar injuries to those seen in the carotid artery.⁷^–⁹ The incidence of vertebral artery injury after blunt trauma is 0.20% to 0.77%.¹⁰

It is important to recognize which patients should be screened for asymptomatic injury and how they should be evaluated, what treatment is required for asymptomatic and symptomatic disease, and what follow-up is needed. This chapter reviews the pathology, clinical presentation, imaging, diagnosis, and treatment of blunt carotid and vertebral artery injuries. The chapter focuses on carotid artery injuries, but unique aspects of vertebral artery injuries are also reviewed. Penetrating injury (stab or gunshot wound) will not be discussed. There is a paucity of specific recommendations for blunt cerebrovascular injury in children.

Pathology

Location and Risk Factors

Injury to the extradural portions of the internal carotid artery (ICA) and vertebral artery are more common than intradural injury. Injury to the extradural ICA is more common than extradural vertebral artery injury. Most extradural ICA injuries involve the cervical portion of the ICA, with petrous or cavernous involvement being less common. Among intradural injuries, injury to the vertebral artery is more common than injury to the ICA or its intracranial branches.

Most injuries that involve the ICA occur at the base of the skull.¹¹ Extradural arteries (i.e., the cervical ICA or the vertebral artery) are at greater risk for dissection than the intradural portions because they are more mobile, are not protected by the skull, and may be damaged by surrounding bony structures. In particular, injury may occur where a mobile vessel segment traverses a fixed location, such as the skull base foramina. In addition, injury such as dissection may be seen extending from above the relatively fixed common carotid artery bifurcation along the ICA to the foramen lacerum and carotid canal. The vertebral artery is mobile in its proximal (V1) and distal (V3) extradural segments. The foraminal or V2 portion of the vertebral artery is less commonly injured because it is less mobile and is protected by the bony walls of the transverse foramina. Intradural vertebral artery injuries (V4) may occur from extension from the V3 segment.

The risk for injury may be increased among patients with certain connective tissue disorders, such as fibromuscular dysplasia (FMD), Marfan’s syndrome, or Ehlers-Danlos syndrome (type IV), among others. Redundancy and loops of the cervical ICA also may increase the risk for injury, including spontaneous dissection.¹²

Mechanisms of Injury

There are a number of causes of injury to the carotid artery, but generally it results after overt head and neck trauma. In particular, blunt vascular injuries occur with cervical hyperextension and rotation, hyperflexion, or a direct blow.² However, dissection also may occur with apparently trivial traumatic events, such as nose blowing or head turning.¹³ One of the most common mechanisms of blunt vascular injury is a motor vehicle collision (MVC). During an MVC, the injury results from rapid deceleration, with the neck hyperextended or flexed and rotated. The carotid arteries are immobile at the skull base, and the traumatic motion stretches the carotid artery over the upper cervical vertebrae and tears the vessel intima. Other mechanisms of blunt carotid injury include strangulation, basilar skull fractures, and facial fractures. Extradural vertebral artery dissections or injuries are associated with cervical spine fractures, particularly those with a rotational component.

The carotid or vertebral artery occasionally may suffer iatrogenic injury during neurosurgical or angiographic procedures that involve vessel exposure, passage of hardware near or through the artery, or direct manipulation of the vessel.¹⁴ Specific procedures during which ICA injury may occur include proximal vascular control during aneurysm surgery, exposure for anterior cervical spine procedures, placement of posterior high cervical hardware (e.g., C1 lateral mass screw), or transsphenoidal surgery.¹⁴^–¹⁸ The vertebral arteries also are at risk for iatrogenic injury during neurosurgical procedures; during procedures on the cervical spine, posterior or anterior iatrogenic injury occurs in 0.3% to 0.5% of cases.¹⁹^–²⁴ The vessels also may be damaged during endovascular procedures when catheters are passed through the common or internal carotid artery or balloons are deployed in the vessel. Iatrogenic arterial dissection occurs in 0.07% to 0.3% of patients undergoing diagnostic cerebral angiograms.^25,²⁶

Pathologic Findings

Arterial walls are composed of three layers: an internal or endothelial layer (tunica intima), a middle or muscular layer (tunica media), and an external or connective tissue layer (tunica adventitia). Dissection is a common manifestation of blunt injury and usually results from a tear or disruption of the intima. This tear starts a cascade of events that includes subintimal exposure causing platelet adherence and a site for thrombus formation and embolization. The subsequent course depends on the surrounding environment (i.e., where the initial injury occurs in the vessel course), extent of injury, and hemodynamic features of the injury site. Extradural injuries therefore are less likely to cause hemorrhage unless the injury is in the skull base cavities. Ischemic symptoms (embolic or hypoperfusion) therefore are more common after extradural injuries, whereas aneurysm enlargement and hemorrhage (subarachnoid hemorrhage) are more frequent with intradural lesions.

Blood that penetrates and extends into the vessel wall causes an intramural hematoma. This may narrow or occlude the lumen, particularly if located between the intimal and medial layers and thus causing hypoperfusion. Intramural hematomas also compromise the structural integrity of the vessel wall, so a traumatic aneurysm occurs particularly when the hematoma extends between the medial and adventitial layers. When the walls of the dilated aneurysmal segment are composed of the incomplete remaining elements of the vessel, a dissecting aneurysm forms. Complete disruption of the arterial wall leads to blood extravasation into the surrounding structures. In extradural regions, the hemorrhage is into soft tissue, and a pseudoaneurysm forms. The walls of this aneurysm are not composed of vessel wall layers. Dissecting aneurysms may continue to communicate with flowing blood, and therefore delayed growth may occur. Alternatively, because of slow flow in the aneurysm, intraluminal thrombosis occurs, leading to embolization.

Clinical Presentation

Clinical features of extradural blunt cerebrovascular injury and, in particular, of dissection include headache, neck pain, transient ischemic attack (TIA), ischemic stroke, pulsatile tinnitus, and cranial nerve palsy. Intradural injuries most often present with either ischemic stroke or subarachnoid hemorrhage (SAH). The patient may present with acute symptoms or in a subacute fashion, or symptoms may develop in a delayed fashion (hours to weeks). In addition, many patients with blunt cerebrovascular injuries are completely asymptomatic.^5,²⁷ Some studies (retrospective), however, suggest a reduced risk for stroke when patients are treated before ischemia develops (6%), whereas 50% of untreated patients develop a stroke.²⁸ Other studies have failed to demonstrate this effect, and no randomized trial has been performed.²⁸ Consequently, there is debate about which trauma patients should be screened for blunt cerebrovascular injury.

There are limited data to make firm recommendations on screening, but it is reasonable to screen asymptomatic patients with significant blunt head trauma and the following risk factors for carotid injury: Glasgow Coma Scale (GCS) score of 8 or greater, petrous bone fracture, diffuse axonal injury, and LeFort II or III facial fractures.^29,³⁰ Overall, among these patients, traumatic cerebrovascular injuries may be identified in up to 44% of screened patients using angiography,³⁰ but this incidence may be as high as 90% when all carotid risk factors are present. Risk factors for vertebral artery injuries include cervical spine fractures, particularly those associated with severe flexion or extension; upper cervical spine injuries; and fractures through the foramen transversarium.^29,³⁰ The frequency of vertebral artery injury when these risk factors are present is between 11% and 24%.^31,³² In addition, any patient with a neurologic abnormality that is not explained by the injury or with epistaxis from a suspected arterial source following injury should be screened. Patients who are victims of near hanging, those with seat belt abrasions of the neck, and those with soft tissue swelling of the anterior neck are also candidates for screening.

Symptoms and Signs

The clinical manifestations of blunt cerebrovascular injury vary according to the pathology and where the lesion is located. The clinical manifestations may be associated with local effects (e.g., a neck hematoma) or result from distal ischemia.

Extradural Carotid Injury

Nonspecific headache is a common presentation of blunt carotid injury in the awake trauma patient. Similarly, patients may present with neck pain, ear ache, or facial pain. Ophthalmologic manifestations, including an ipsilateral Horner’s syndrome, are frequent.³³ Emboli from the carotid injury may cause optic neuropathy or central retinal artery infarction. Other cranial nerve findings are less frequent. Cerebral ischemia may occur in up to half of patients³⁴ from hemodynamic or embolic factors, and the presentation can range from hemispheric transient ischemic events, to a cerebrovascular accident (CVA), to coma or brain death. Epistaxis may occur in some cavernous carotid injuries.

Physical Findings

On physical examination, patients may present with a neck hematoma, bruits, pulsatile neck mass, or a palpable thrill (Table 352-1).^36,³⁷ One third of trauma patients with blunt carotid injury may have other associated cerebral vascular injuries.¹¹ Also, many patients will have associated traumatic injuries, in particular to the head or chest.^38,³⁹ There are conflicting reports on whether the type of injury or the presence of associated injuries increases the likelihood of a patient having a blunt carotid injury.^11,³⁹

TABLE 352-1 Manifestations of Internal Carotid Dissections

MANIFESTATION	FREQUENCY (%)
Headache	58-92
Cerebral ischemia	63-90
Horner’s syndrome	9-75
Neck pain	18-46
Scalp tenderness	8-27
Bruit	12-39
Carotid tenderness	8-19
Cranial nerve palsy	5-12
Syncope	11
Amaurosis fugax	4-6
Dysgeusia	3

Modified from Zetterling M, Carlstrom C, Konrad P. Review article: internal carotid artery dissection. Acta Neurol Scand. 2000;101:1-7; and Singh RR, Barry MC, Ireland A, Bouchier Hayes D. Current diagnosis and management of blunt internal carotid artery injury. Eur J Vasc Endovasc Surg. 2004;27:577-584.

Imaging and Diagnosis

Head computed tomography (CT) scans are almost universally obtained in patients admitted with a head injury (Figs. 352-1A, 352-2A, and 352-3A). Blunt cerebrovascular injury should be considered when there is a neurologic deficit that cannot be explained by the head CT scan, particularly when it is normal, or by the initial injury. In some series of blunt cerebrovascular injuries, this is how 18% to 34% of patients present.^4,¹¹

FIGURE 352-1 Imaging of a patient with an internal carotid injury resulting from a skull fracture. A, Serial axial computed tomography images demonstrating a fracture that involves the skull base around the right internal carotid artery. B, Digital subtraction angiography (DSA) demonstrating a right internal carotid artery dissection. C, Postcoiling DSA image. D, Postcoiling DSA angiogram demonstrating reconstitution of the right distal intracranial vasculature from the left internal carotid artery.

FIGURE 352-2 Radiographic imaging of a patient with bilateral carotid artery injury. A, Axial unenhanced computed tomography (bone windows) demonstrates a peripherally calcified aneurysm adjacent to the left internal carotid artery (ICA). Left common carotid artery angiogram lateral (B), anteroposterior (C), and three-dimensional oblique (D) views show irregular dissection beginning about 1 to 2 cm distal to the origin of the ICA, expanding into the aneurysm and resuming normal caliber at the skull base. Right common carotid artery angiogram lateral (E), anteroposterior (F), and three-dimensional oblique (G) views illustrate an additional dissection that involves the right ICA.

FIGURE 352-3 A, Computed tomography scan demonstrating a hypodensity in the left frontoparietal region consistent with a stroke. Magnetic resonance angiography (B) and digital subtraction angiography (C) demonstrate a left internal carotid artery dissection.

Because blunt cerebrovascular injury can be progressive, it is important to identify these lesions early and to have effective follow-up. There should be a high index of suspicion in the patients who have a mechanism of injury that places the ICA or vertebral artery at risk.³ Blunt cerebrovascular injury may be diagnosed noninvasively using ultrasonography, computed tomography angiography (CTA), magnetic resonance imaging (MRI), and magnetic resonance angiography (MRA). Duplex ultrasound alone is not an adequate test to diagnose traumatic cerebrovascular injury because of limited sensitivity, although Duplex ultrasonography may be used for screening.^3,^5,²⁷ Transcranial Doppler may be used to listen for distal emboli. Recent advances in noninvasive imaging have made MRI or MRA, followed by CT or CTA, the initial screening study of choice in most patients with suspected dissection. The “gold standard” imaging modality to detect injury of the cerebral cervicocranial vessels is digital subtraction angiography (DSA). The use of these CT- and particularly MRI-based modalities may be limited in trauma patients. Therefore, DSA retains a major role in both diagnosis and treatment (Figs. 352-1B; 352-2B, C, E, and F; and 352-3C). The various imaging modalities, however, have yet to be systematically compared.

Noninvasive Imaging

Contrast-enhanced CT imaging of the neck or CT angiography may be used to detect symptomatic or occult lesions.^40,⁴¹ In particular, multislice (eight or more slices), multidetector CTA may be a reasonable screening modality to use instead of DSA because their detection rates are similar. However, CTA using four of fewer slices is an inadequate imaging study. On CT, patients will have a focal area of low density within the vessel, and the dissection may be further visualized and defined with CTA (Fig. 352-2D and G).

MRA, because it is noninvasive and requires no contrast administration, is used as an alternative to DSA to image carotid injury (Fig. 352-3B). When compared with DSA, MRA has 95% sensitivity and 99% specificity in some studies.⁴² On T1-weighted fat-saturated MRI, intramural hematoma will appear as a crescent of intensity encircling the carotid, with narrowing of the adjacent lumen compared with the contralateral carotid. The extent of injury can further be defined with MRA (see Fig. 352-3B

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