h1 class=”calibre8″>21 Role of Neurointerventional Techniques in Cervical Trauma

Neil Majmundar, Fawaz Al-Mufti, Michael Nosko, Anil Nanda, Sudipta Roychowdhury, and Gaurav Gupta

Keywords: carotid artery injury, vertebral artery injury, blunt cerebrovascular injury, endovascular, neurointerventional

21.1 Introduction

Traumatic injuries involving the carotid and vertebral arteries following cervical trauma can have devastating neurological outcomes. ¹ The incidence of carotid and vertebral artery injuries following cervical trauma has increased as comprehensive screening protocols with more specific and less invasive imaging methods have developed. The primary management of uncomplicated extracranial carotid/vertebral arterial injuries associated with trauma is mainly anticoagulation/antiplatelet therapy, the goal of which is to avoid potential ischemic complications. Neurointerventional techniques are generally reserved for more complicated and refractory injuries in cases where medical management fails or when systemic anticoagulation is contraindicated. These endovascular techniques, when indicated in the treatment of arterial injuries following cervical trauma, have become more common due to advances in imaging, improvements in the safety profiles of the devices used, and low complication rates.

21.2 Types of Vascular Injury After Cervical Trauma

21.2.1 Penetrating Injury

Penetrating trauma to the neck and cervical region, defined as violation of the platysma, is generally divided into three zones, with each zone mandating different management strategies. Zone 1 is defined as the region from the clavicle/sternum to the cricoid cartilage, zone 2 is the region from the cricoid cartilage to the angle of mandible, and zone 3 is the region from the angle of the mandible to the skull base. ² Carotid injury occurs in approximately 4.9 to 6% of penetrating neck trauma cases. ^3,4 Penetrating injury to either the carotid or vertebral arteries carries a mortality of 10%, while combined injuries carry a mortality of 50%. ⁵ These injuries can be highly lethal if left untreated, approaching a mortality rate of 100%. ⁶

Penetrating arterial injuries are most common secondary to gunshot or stab wounds and can result in extracranial carotid or vertebral artery pseudoaneurysms. ⁷ Although spontaneous resolution of these pseudoaneurysms has been described, ⁸ this pathology may result in stroke and if untreated, can enlarge and result in compression of local structures, regional pain, and arteriovenous (AV) fistulas. ^9,10,11,12

21.2.2 Nonpenetrating Injury

Blunt Cerebrovascular Trauma

Blunt trauma to the cervical spine can result in blunt cerebrovascular injury (BCVI) from high-energy nonpenetrating blunt force injury. ¹³ BCVI is seen in approximately 1 to 2% of blunt trauma patients, ^14,15,16 and in 2.4% of trauma patients who remain in the hospital over 24 hours. ¹⁵ The incidence of BCVI has significantly risen likely due to the development of improved screening protocols as well as advances in and availability of sophisticated noninvasive imaging. ^17,18 Comprehensive screening protocols resulting in earlier initiation of anticoagulation in patients diagnosed with BCVI have been shown to result in a significant reduction in stroke risk. ¹ The incidence of BCVI in the cervical internal carotid artery (ICA; 0.019–0.8%) is slightly higher than in the vertebral arteries (0.09–0.71%). ^{14,19,20,21,22}

BCVI carries significant neurosurgical morbidity and mortality rates of 56 and 30%, respectively. ¹⁴ The risk of ischemic stroke in patients with BCVI is 9 to 12%, and it typically occurs in patients who have not been started on anticoagulation or antiplatelet therapy. ^15,16

BCVI generally occurs secondary to a high energy transfer mechanism. Injuries which carry considerable risk of BCVI include Le Fort type 2 or 3 fractures, basilar skull fractures involving the carotid canal, traumatic brain injuries with diffuse axonal injury (with Glasgow Coma Scale < 6), cervical vertebral body or transverse foramen fractures/subluxations, cervical ligamentous injuries, near hanging injuries with anoxic brain injury, and clothesline/seat belt abrasions where the patient has local swelling, pain, and mental status change. ^20,23,24,25 Crissey and Bernstein identified four fundamental traumatic mechanisms which result in BCVI (▶ Table 21.1). Type 2 injuries, resulting from hyperextension and contralateral rotation of the head and neck, are the most common. ²⁶

The signs and symptoms of BCVI may not always be obvious in trauma patients who generally present with a complex picture. These patients often arrive intubated (precluding an accurate neurological assessment) and generally have multisystem injuries. Signs and symptoms of BCVI include hemorrhage from the nose, mouth, or neck, a cervical bruit in patients aged less than 50 years, a rapidly expanding cervical hematoma, a region of stroke on computed tomography (CT) or magnetic resonance imaging (MRI), Horner syndrome, hemiparesis, vertebrobasilar insufficiency, and a neurological deficit which is inconsistent with imaging findings. ²⁵ As mentioned earlier in the chapter, early and comprehensive screening protocols have led to an increase in the frequency with which BCVI is diagnosed and, in turn, earlier treatment and better prognoses for patients with this injury. Screening protocols developed at the University of Colorado and the University of Tennessee in Memphis have assisted in identifying risk factors, presenting signs and symptoms, and treatment paradigms. ^20,23,24

Stretch injuries to the cervical vessels may result in intimal injuries leading to vessel wall dissection. These injuries can occur secondary to cervical chiropractic manipulation and generally follow hyperextension and rotation of the neck. ^6,27

Occlusive injuries to the carotid or vertebral arties can occur secondary to fractures resulting in subluxation or dislocation. The vertebral artery may be occluded secondary to external force from fractures of the transverse foramen or in cases where the facets are jumped or perched. These injuries are not typically dealt directly via neurointerventional procedures, but they may require proximal occlusion if the patient has active extravasation of blood, or if open reduction will result in further injury to the vessel.

21.3 Pathophysiology of Vascular Injury

21.3.1 Mechanism

Blunt vascular injuries result from high energy transfer after trauma. ²⁸ The injury can result in the development of an intimal flap, which in turn can lead to a dissection of the vessel. The denuded subintimal layer provides a nidus for platelets to aggregate, initiating a series of events resulting in the formation of a thrombus. The thrombus can cause occlusion of the vessel, stenosis of the vessel, or embolization distally resulting in an infarction. ²⁸

Dissections of the extracranial carotid and vertebral arteries are more common than intracranial dissections as the cervical segments are longer and dissections occur more frequently where a relatively mobile segment of the artery is stretched against an immobile/relatively fixed segment at the base of the skull. ²⁹ Arterial dissection involves the creation of a false lumen due to the extravasation of blood secondary to an intimal tear. As the media and adventitia of the intracranial segments of the vessels weaken, dissection can lead to intradural subarachnoid hemorrhage (SAH) and/or extradural hematomas. Subintimal dissections are more common with intracranial dissections, whereas extracranial vessels usually dissect at the media or between the media and adventitia.

21.3.2 Pseudoaneurysms

Also referred to as “traumatic aneurysms,” these result from a disruption of the internal elastic lamina and eventually all layers of the arterial wall. ²⁸ This results in the formation of another channel within the arterial wall which causes the adventitia to expand. Pseudoaneurysms, lacking the normal layers of the vessel wall, are formed when the intramural thrombus weakens the vessel wall and allows for the hematoma to extravasate into the surrounding tissue. A hematoma forms within the false lumen, thus compressing the true lumen of the vessel resulting in stenosis.

These traumatic aneurysms account for approximately 10% of all patients presenting with BCVI. ³⁰ Pseudoaneurysms can form in the acute setting or later as the initial injury to the vessel wall progresses. Approximately 8% of carotid injuries, which initially only consist of a luminal irregularity, may later progress to form a pseudoaneurysm. ³¹ Extracranial carotid artery pseudoaneurysms reportedly form in 10.3 to 23% of BCVI patients, primarily affecting the upper and middle parts of the vessel. ^15,30,32 Pseudoaneurysms of the vertebral artery are not as common and are found in 3.7 to 6.5% of BCVI patients. ^15,30

Pseudoaneurysms may have two different basic structures: saccular and fusiform. Saccular pseudoaneurysms are less common, but have a greater potential to enlarge (33.3%). These form secondary to any mechanism causing a tear or other disruption in the normal vascular wall anatomy. ²⁸ They also have a higher risk of leading to ischemic complications. ²⁸ Fusiform aneurysms form secondary to an arterial stretch injury. They are relatively more benign and approximately half of all can be treated and resolve with antiplatelet therapy. ^28,30

21.3.3 Stroke

In cases of arterial injury, mechanisms completely disrupting blood flow, such as total occlusion of the vessel or transection, have the highest risk of resulting in ischemic stroke. ^15,32,33 Although complete occlusions and transections of the cervical vessels are relatively rare, the most common cause of ischemic strokes in patients with cervical trauma is thromboembolism resulting from injury to the arterial wall. ^16,34 In these cases patients can develop ischemic stroke from thrombosis/stenosis causing a significant reduction in blood flow, embolization from a thrombus formed after intimal injury, or SAH which is more common in posterior circulation injuries. Pseudoaneurysms carry a significant risk of ischemic stroke (15.4%) due to the potential for distal emboli. ³⁰ The individual risks of stroke with carotid and vertebral artery injuries will be discussed in the upcoming sections (▶ Table 21.2).

21.4 Injury to the Carotid Artery

A basilar skull fracture is the strongest predictor of blunt injury to the carotid artery. ^20,24 Motor vehicle collisions are by far the most common etiology of blunt carotid injuries, accounting for more than half of the cases. ^23,35,36 Other less common etiologies include strangulation and spinal chiropractic manipulation therapy, although vertebral artery dissection is more common following manipulation. ³⁷ Patients with fibromuscular dysplasia are also predisposed to multiple extracranial dissections.

The cervical ICA is most prone to injury over the second and third cervical vertebrae, especially in cases of hyperextension, lateral flexion, and rotation. ²⁸ In cases of significant hyperextension, the ICA can be compressed by the angle of the mandible, and in cases of rotation, by the styloid process. ^36,38 The distal cervical ICA can also be injured in cervical trauma resulting in stretching over the lateral masses of the cervical vertebrae. ³⁹

The risk of stroke with ICA dissection varies with the grade of injury. The grading scale is summarized in ▶ Table 21.3. Grade 1 injuries carry a 3% risk of stroke, and most injuries (70%) will resolve with or without anticoagulation. Approximately 4 to 12% will persist, and progress to a higher grade of injury. ^27,28 The use of anticoagulation lowers the risk of progression. ^27,40 Approximately 70% of grade 2 injuries, which carry an 11% risk of stroke, progress to a higher grade of injury despite anticoagulation with heparin. Most grade 3 and 4 injuries will persist despite medical treatment. Over time, patients may develop neurological deficits as the initial injury develops. Neurological sequelae develop within 1 to 24 hours of injury in 57 to 75% of cases, explaining the higher rate of BCVI seen in trauma patients hospitalized for greater than 24 hours. ²⁷ Management of these injuries is discussed later in this chapter.

21.5 Injury to the Vertebral Artery

BCVIs involving the vertebral arteries affect 0.5 to 2% of patients who present with blunt trauma to treatment centers with aggressive screening protocols. ^{25,41,42,43,44} Most blunt vertebral artery injuries are caused by motor vehicle collisions. Chiropractic spinal manipulation therapy, sudden neck turning, and direct trauma to the back of the neck can also result in BCVI of the vertebral artery. ^27,45,46

Vertebral artery injuries generally occur in the V2 and V3 segments of the vertebral artery, as these are the fixed segments. ⁴⁷ These segments correspond to the artery’s location within the transverse foramina, and as it exits the transverse foramina of C1 and travels around the occipitocervical junction.

The risk of stroke following blunt injury to the vertebral artery is listed in ▶ Table 21.4. Unlike the increasing risk of stroke seen with grade of injury, the risk of stroke in vertebral artery injuries is highest (40%) with grade 2 injuries. ⁴⁰ Grade 1 injuries carry a relatively high risk of 19%, when compared with grade 1 carotid injuries that carry a 3% risk of stroke. Vertebral artery injuries usually do not have a warning sign, such as a transient ischemic attack, prior to a stroke. ²⁷ The average time from injury to stroke is 4 days, ranging from 8 hours to 12 days. ²⁷

C-spine injuries, most frequently transverse foramina fractures, facet fracture-dislocations, and vertebral subluxations, are the strongest risk factors for vertebral artery injury. ^20,23,24,48 The incidence of vertebral artery injury jumps to 6% in cases of cervical spine fractures or ligamentous injuries, although this number varies and has been reported to be as high as 70%. ^40,41,48 The overall mortality associated with single vertebral artery BCVI is 16%; bilateral vertebral artery injury is always almost fatal. ⁴¹ In certain extreme cases, a vertebrovenous fistula has been reported to form between the vertebral artery and its surrounding venous plexus. ^49,50,51

21.6 Imaging

CT of the head and cervical spine are generally the initial imaging modalities ordered in trauma patients presenting after mechanisms concerning for head and neck injuries. CT angiography (CTA) of the head and neck follows noncontrast imaging as the primary screening modality for vascular injury. SAH secondary to intracranial extension of an extracranial dissection must be ruled out in the presence of traumatic SAH on CT scan following trauma. In all cases of suspected vascular injuries, CTA of the head and neck must be performed.

21.6.1 Computed Tomography

CT scans of the head and neck are useful in identifying strokes, fractures, and grossly obvious hematomas. Rarely, arterial injuries can be seen on noncontrast scans as crescent shaped thickenings in the arterial wall secondary to hematoma formation. ⁵² Vertebral artery dissections (20%) may also present with posterior fossa SAH. ⁵³

21.6.2 Computed Tomographic Angiography

CTA of the head and neck is the preferred screening tool for vascular injuries in trauma patients, as it is relatively quick, sensitive, specific, and provides a prompt diagnosis. ^44,54 In addition to the vasculature, CTA provides relevant bone and soft-tissue anatomy. In many cases, digital subtraction angiography (DSA) may not need to be performed in addition to CTA imaging.

21.6.3 Magnetic Resonance Imaging

MRI of the head and neck is not as accurate as CTA or DSA. The optimal MRI study is axial T1-weighted imaging (T1WI) with fat suppression. This sequence is helpful in differentiating an intimal flap from a fusiform aneurysm. On T2-weighted imaging (T2WI), a hematoma in the wall can be seen as a bright signal in the vessel wall, referred to as the “crescent sign.” The most effective use of MRI is to investigate for regions of infarction, not readily visualized on CTA as MRI is more effective in visualizing potential regions affected by embolic phenomenon. The ideal MRI for a dissection includes a magnetic resonance angiography (MRA) of the neck and/or brain with and without contrast with axial black blood sequences. ⁵⁵

In the setting of trauma, MRI is not utilized frequently due to the amount of time required for the study. In patients who do not have any obvious signs or symptoms of vascular injury and are undergoing an MRI of the cervical spine to investigate for ligamentous injury, MRA (comparable to CTA) can be performed in combination with the MRI of the cervical spine.

21.6.4 Digital Subtraction Angiography

DSA is the gold standard for diagnosing carotid and vertebral artery injury following trauma. DSA provides both a superior anatomical visualization of the artery itself in an individual frame and an exceptional visualization of real-time flow of blood within the artery allowing the physician to visualize both obvious injury to the vessel wall and more subtle flow-altering injuries. It offers the ability to treat the lesion during the same exam and afford visualization of the contralateral and anterior/posterior circulation collaterals, which is extremely important in deciding upon a particular treatment modality.

In cases of dissection, the intimal flap is usually seen at the most proximal portion of the dissection. The false lumen exists within the intimal flap and will have slower flow of contrast, which will remain within the false lumen well into the venous phase of the study. Dissections may also change configuration on repeat angiograms. ⁵³ In cases of occlusion, the injured artery will taper to the point of occlusion, resulting in stagnation of blood flow at that point. Kinking of the vessels can be seen with mass effect from a coexisting fracture or subluxation. Suspicious traumatic vascular lesions (pseudoaneurysms) must be followed with a repeat CTA or DSA in 7 to 10 days and at the 6-week interval.

21.7 Management of Vascular Injuries in Cervical Trauma

Several treatment modalities are available for patients presenting with vascular injuries following cervical trauma. Treatment options include conservative management/observation, anticoagulation, antiplatelet therapy, neuroendovascular intervention, and surgery. In cases of penetrating injury to the carotid/vertebral artery, there is a limited role for medical management. ▶ Fig. 21.1 and ▶ Fig. 21.2 provide a basic algorithm for treatment of uncomplicated injuries involving the carotid and vertebral arteries.

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