Vertebral Artery Injury

Article Author:
Leslie Simon
Article Editor:
Michael Mohseni
Updated:
2/14/2019 7:48:15 AM
PubMed Link:
Vertebral Artery Injury

Introduction

Injuries to the vertebral artery may either be traumatic or spontaneous. Traumatic injuries are most frequently due to blunt injury to the head and neck but may be due to penetrating trauma. Spontaneous injuries are caused by intrinsic weakness of the vessel wall, often due to underlying vascular or connective tissue disorder, leading to dissection of the vessel. Spontaneous dissections are frequently associated with minor precipitating events. A grade of injury can range from irregularity of the vessel wall to complete transection with intracranial or extracranial hemorrhage. Patients commonly initially present with a headache and neck pain but may be asymptomatic. Vertebral artery injury is an important cause of stroke and transient ischemic attack, particularly in younger patients. The vertebral arteries perfuse the posterior fossa so the patient will present with stroke symptoms consistent with posterior circulation deficits. Symptoms may include difficulty speaking, swallowing or maintaining their balance. Loss of coordination or vision changes may also be present. The modified Denver screening criteria are used to identify patients at high risk for cerebrovascular injury. The initial diagnostic imaging study of choice is a CT angiogram. Treatment depends on location, symptoms, and degree of injury and may involve fibrinolysis, anticoagulation, antiplatelet therapy, endovascular therapy or open surgical repair.[1][2][3][4]

Etiology

Vertebral artery injuries can be due to blunt trauma, penetrating trauma or may be spontaneous. The majority of vertebral artery injuries are due to blunt trauma from motor vehicle crashes. Falls, strangulation, and pedestrian accidents are less common causes. Closed injuries to the vertebral arteries are usually due to hyperextension coupled with lateral flexion or rotation of the head.

Penetrating trauma to the neck, such as from a gunshot wound, is a rare but devastating cause of vertebral artery injury with high mortality. Injury to the vertebral artery may result from minimal trauma. Multiple case reports describe various sports, trampoline use, amusement park rides, coughing, sneezing, vomiting, childbirth, sexual intercourse, yoga, scuba diving and chiropractic neck manipulation among several other potential triggers. 

Spontaneous vertebral artery injuries occur when the structural integrity of the arterial wall is compromised. While this condition may be associated with vascular or connective tissue disorders such as fibromuscular dysplasia, Ehlers-Danlos syndrome and Marfan syndrome, the majority of patients diagnosed with a spontaneous cerebral artery dissection have no known history of the underlying predisposing disease. Most “spontaneous” cases are associated with a mildly traumatic event.[5][6][7]

Epidemiology

Spontaneous: Spontaneous cerebral artery dissections, both carotid and vertebral, account for about 20% of strokes in young adults. Vertebral artery dissections are less common than carotid dissections, occurring in about 1 in 100,000 individuals in population studies. The actual incidence may be higher since many may be asymptomatic. The mean age ranges from 44 to 46 years, and there is no clear racial or gender prevalence. Dissection may be more common in the winter but the reason for season variation is unclear.

Traumatic: Traumatic vertebral artery injury is a relatively rare condition, reported in less than 1% of trauma admissions. However, the incidence is increasing, most likely due to increased awareness and screening for this finding in high-risk patients.  Vertebral artery injury may be as high as 11% in patients with blunt traumas that meet specific clinical and physical examination criteria. The modified Denver screening criteria is used to identify patients at high risk for cerebral artery injuries. Patients with transverse foramen fractures or facet dislocations have an associated vertebral artery injury in 27.5% of cases.

Pathophysiology

The neurologic consequences of injury to the vertebral artery are due to cerebral ischemia from thromboembolism, hypoperfusion, hemorrhage, or a combination of the three. In most cases, vertebral artery injury is due to an intimal tear. The torn, exposed endothelium promotes platelet aggregation and thrombus formation. This may cause local occlusion of the vessel, but more commonly, the clot will embolize to the cerebral circulation resulting in a stroke. Intimal tears may also dissect and create a false lumen that may lead to arterial occlusion. Partial transection of the artery may result in pseudoaneurysm. A pseudoaneurysm can be a source of emboli or hemorrhage if it ruptures. Complete vertebral artery transections may result in hemorrhage, which may be intracranial or extracranial depending on the location.

Histopathology

Patients with spontaneous vertebral artery dissection have histopathologic findings of intramural hemorrhage with disruption of the intimal planes. Pathologic changes primarily involve the adventitial and medial layers of the vessel. This finding is not as common in patients with cerebrovascular injury resulting from acute trauma.

History and Physical

The history can be quite variable depending on whether the vertebral artery injury is spontaneous or due to acute trauma. Many cases thought to be spontaneous have antecedent minor trauma as an associated factor. Spontaneous dissections are more common in patients with connective tissue disorders, but most patients will not present with any known history of connective tissue disease.[8][9]

The most commonly reported symptoms are the head, and neck pain, vertigo, and dizziness but many patients with small dissections may be asymptomatic. In diagnosed cases, the presenting finding is often transient ischemic attack or acute stroke. The risk of stroke is greatest in the first two weeks after the dissection occurs. Young patients presenting with acute stroke should have cerebrovascular dissection considered especially if their symptoms are associated with a headache or neck pain. It is important to note that while neck pain is a common complaint, only 46% will initially report it. Additional clinical manifestations include scalp tenderness, tinnitus, bruits, or even cervical nerve root involvement. Vertebral artery dissection may also lead to lateral medullary infarction, posterior cervical vestibular symptoms, vision loss or spinal cord ischemia.

Patients presenting with acute trauma should first have a primary and secondary survey and should be stabilized following Advanced Trauma Life Support guidelines. Like with spontaneous dissections, some patients may initially have no neurologic findings. In one study by Biffl et al., a time lapse of 18 hours existed between the time of injury and onset of neurologic symptoms in 44% of cases. Patients with blunt cervical trauma who meet the modified Denver Screening criteria should be assessed for cerebrovascular injury.

Denver Screening Criteria:

  • Lateralizing neurologic deficit (not explained by head CT)
  • Infarct on head CT
  • Nonexpanding cervical hematoma
  • Massive epistaxis
  • Anisocoria /Horner’s syndrome
  • Glasgow coma score (GCS) less than 8 without significant CT finding
  • Cervical spine fracture
  • Basilar skull fracture
  • Le Forte II or III facial fractures
  • Seatbelt sign above the clavicle
  • Cervical bruit/thrill

Evaluation

CTA is the most reliable non-invasive neurovascular imaging modality and is the initial test of choice for patients with suspected cerebral artery injury. CTA should be performed in patients meeting the modified Denver Screening Criteria and in this population has a sensitivity of nearly 100%. Digital subtraction arteriography (DSA) has long been described as the gold standard but is more invasive, less readily available and requires more contrast than CTA. DSA itself also carries an increased risk of stroke (0.5%). DSA is still used when concurrent endovascular therapy is being considered or when other imaging modalities are inconclusive or unavailable. CTA has largely replaced DSA.

MRI is recommended to screen for vertebral artery injury in patients with blunt spinal cord or vertebral subluxation injuries. Magnetic resonance angiography (MRA) has shown inferior or equivalent specificity for detecting vertebral artery injury as compared to CTA and MR and is often unavailable or impractical in the emergency setting. MR angiography is not used independently to screen for blunt cerebrovascular injury. While duplex ultrasonography is the least invasive and perhaps the most widely available imaging modality, there is no data to support its use in assessing for vertebral artery injury. Ultrasound’s poor sensitivity for detecting vertebral artery injury is due to anatomic constraints that limit visibility in areas obscured by bone.

Young patients presenting with acute ischemic stroke should have spontaneous cerebral artery dissection considered as an inciting cause. CTA is commonly performed after non-contrast head CT to evaluate for this diagnosis.

Treatment / Management

Symptomatic patients who present with acute ischemic stroke due to spontaneous vertebral artery dissection without associated injuries or contraindications should be considered for systemic thrombolytic therapy if they present within 3 hours of onset of symptoms. Patients who present up to 4.5 hours from symptom onset and those who are otherwise not candidates for systemic thrombolytic therapy should be considered for catheter-directed thrombolysis. Patients who are not appropriate for thrombolytic therapy are managed with anticoagulation, antiplatelet therapy, endovascular or open operative repair depending on the grade of injury.[3][10][11]

Asymptomatic patients are managed with anticoagulation versus antiplatelet therapy based on bleeding risk, the location of lesion and grade of injury. Endovascular therapy and operative repair are reserved for patients with higher-grade lesions and those with contraindications to anticoagulation or antiplatelet therapy that are at high risk for progression.

There are no proven methods to reduce the risk of a neurologic event or recurrent dissection in patients with know dissections, but patients are advised to limit contact sports, neck manipulation or any other activity that involves the abrupt movement of the neck. Hypertension should be well-controlled and estrogen-containing medications avoided.

Staging

Denver Radiologic Grading Scale for Blunt Cerebrovascular Injury:

Grade I: Irregularity of the vessel wall or dissection/intramural hematoma with less than 25% stenosis

  • Management: Anticoagulation or antiplatelet therapy, endovascular repair for symptomatic patients who are not candidates for anticoagulation or antiplatelet therapy

Grade II: Intramural thrombus or raised intimal flap or dissection/intramural hematoma with greater than 25% stenosis

  • Management: endovascular therapy if symptomatic, anticoagulation, antiplatelet therapy, deferred endovascular repair in high-risk asymptomatic patients

Grade III: Pseudoaneurysm

  • Management: endovascular therapy if symptomatic, anticoagulation, antiplatelet therapy, deferred endovascular repair in high-risk asymptomatic patients

Grade IV: Vessel Occlusion

  • Management: endovascular therapy if symptomatic, anticoagulation, antiplatelet therapy, deferred endovascular repair in high-risk asymptomatic patients

Grade V: Vessel transection

  • Management: Vascular sacrifice, either open or endovascular if symptomatic followed by anticoagulation or antiplatelet therapy. Asymptomatic patients may be managed with observation, operative or endovascular treatment for ongoing hemorrhage.

Prognosis

Traumatic vertebral artery injuries can have devastating complications. Sanelli et al. reported a stroke rate of 24% and a death rate of 8% in patients with traumatic vertebral artery injury. Mortality in patients with associated cervical spine injury is even higher and approaches 40%. Highest mortality occurs in those with bilateral injury or injury due to penetrating, high-velocity trauma such as blast injury or gunshot wound.

The prognosis in patients with spontaneous vertebral artery dissections depends on location as well as the degree of associated ischemic stroke or subarachnoid hemorrhage. In patients with extracranial dissections, an excellent outcome is reported in up to 85% with 5% to 25% have poor neurologic outcome or death. Poor outcome is associated with older age, arterial occlusion and higher stroke scores at diagnosis.

Enhancing Healthcare Team Outcomes

Injury to the vertebral artery is managed by a multidisciplinary team that consists of a vascular surgeon, radiologist, neurologist and an internist. Once the diagnosis is made, the treatment depends on whether the patient is symptomatic or asymptomatic

Symptomatic patients who present with acute ischemic stroke due to spontaneous vertebral artery dissection without associated injuries or contraindications should be considered for systemic thrombolytic therapy if they present within 3 hours of onset of symptoms. Patients who present up to 4.5 hours from symptom onset and those who are otherwise not candidates for systemic thrombolytic therapy should be considered for catheter-directed thrombolysis. Patients who are not appropriate for thrombolytic therapy are managed with anticoagulation, antiplatelet therapy, endovascular or open operative repair depending on the grade of injury.

Asymptomatic patients are managed with anticoagulation versus antiplatelet therapy based on bleeding risk, the location of lesion and grade of injury. Endovascular therapy and operative repair are reserved for patients with higher-grade lesions and those with contraindications to anticoagulation or antiplatelet therapy that are at high risk for progression.

The prognosis for patients with vertebral injury varies from a stroke rate o 24% to a death rate of 8%. Mortality rates are even higher in the presence of other brain injury. Poor outcome is associated with older age, arterial occlusion and higher stroke scores at diagnosis. [12][13](Level V)


References

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