13 Traumatic and Iatrogenic Vertebral Artery Injury
Abstract
Vertebral artery injury (VAI) can result from direct cervical spine trauma, complications of spine surgery, or chiropractic manipulation. Patients can be asymptomatic or present with neck pain and/or cerebellar or brainstem neurological symptoms. If VAI is suspected, all patients should obtain magnetic resonance imaging (MRI) of the brain and computed tomography (CT) or MR angiography of the head and neck. Digital subtraction angiography is useful in identifying nonstenotic thrombus and defining the extent of collaterals. All asymptomatic patients should be treated medically with anticoagulation or antiplatelet treatment unless there is a contraindication. V4 segment VAI should be treated aggressively to minimize risk of subarachnoid hemorrhage. Endovascular or cerebrovascular options are indicated in patients who are symptomatic or who have failed medical therapy. Endovascular options include balloon test occlusion, vessel sacrifice, stent reconstruction (including flow-diverting stents) of dissection, pseudoaneurysms, and unstable thrombus. Open surgical repair is indicated in cases of intraoperative VAI if feasible. Patients should be followed up closely, 7 to 10 days after medical treatment initiation and 3 to 6 months after endovascular or surgical intervention, with a CT or MR angiography.
Introduction
Vertebral artery (VA) injury (VAI) is a potentially catastrophic complication that can be sustained from either iatrogenic events (e.g., manipulation by a chiropractor, cervical spine procedure) or trauma (e.g., traumatic brain or spine injury, blunt trauma). Outcomes can range from asymptomatic to more serious sequelae, including pseudoaneurysm, neurological deficit, late-onset hemorrhage, infarction, and death.
Approximately 0.5% of cervical trauma results in symptomatic VAI. Cervical injury with unstable fractures, particularly at the C2–C6 level, is associated with a higher risk of a VAI. Hypermobility in facet fractures, perched facets, jumped facets, and fractures involving the cortical boundary of the foramen transversarium are believed to compromise the VA within its osseous boundaries. In fact, the osseous canal may present less risk of injury to the VA from penetrating trauma than from blunt force trauma.
Procedures in the head and neck region can also injure the VA. Iatrogenic VAI has been reported during internal jugular vein catheterization, operative interventions on the cervical spine from an anterior or a posterior approach, and endovascular operations. Although the carotid artery in the midcervical spine is less well protected and is at greater risk of injury, the VA can take an aberrant course both before entry into the foramen transversarium (V1 segment) and after initial entry (V2 segment), with a subsequent extraosseous loop (V3 segment). Furthermore, during spine procedures, the V2 segment may be compromised. Iatrogenic VAI rate during cervical fusion procedures is reported to be 0 to 5.8%. Large, self-adjudicated series of anterior cervical decompression have documented VAIs in 0.18% of cases, whereas series of posterior cervical transarticular fixation (i.e., Magerl′s technique) have documented VAIs in 1.3%. Fusion procedures in the cervical spine requiring placement of instrumentation in the lateral mass may present a higher risk of VAI than decompressive techniques because of the proximity of the VA to the foramen transversarium.
Major controversies in decision making addressed in this chapter include:
The adequate and accurate diagnostic imaging tool.
Whether or not treatment is indicated.
The role of medical management.
Open versus endovascular treatment for VAI.
Whether to Treat
The management of patients with a VAI depends largely on the presence of symptoms in conjunction with radiographic abnormalities ( 1 –6, 8 in algorithm ). Most patients with noniatrogenic VAIs will have suffered blunt trauma and their presentation is usually silent rather than being associated with obvious signs of cervical trauma. A relatively high index of suspicion is therefore needed, depending on the traumatic mechanism in those patients who present without neurological symptoms. The primary management strategies for a VAI include observation, direct temporary vessel compression to achieve hemostasis, antithrombotic regimens, surgical repair, and endovascular therapy. The relatively high morbidity and mortality associated with an untreated VAI require that observation should be avoided unless there are strong contraindications to other strategies ( 3–11 in algorithm ). Aggressive screening to diagnose blunt VAIs results in early treatment, which leads to improved outcomes and a reduction in the rate of stroke. Asymptomatic patients with radiographic findings of a VAI should be considered for medical management with antithrombotic agents. Asymptomatic patients with a contraindication to anticoagulation or antiplatelet therapy should be considered for endovascular treatment that is based on the type of injury and its natural history. Patients with symptoms related to a VAI should be considered for immediate treatment ( 5, 8 in algorithm ). There is no level I evidence regarding the treatment of patients with blunt VAIs, but the preponderance of evidence in the form of retrospective reviews, case series, and meta-analyses points to intervention as an acceptable and safe form of treatment.
Anatomical Considerations/Pathophysiology
VAIs are more common in persons younger than 30 years. Nonvalidated mechanisms that have been identified as supporting an association between younger age and VAIs include increased exposure to trauma because of the relative flexibility of musculoskeletal structures at the thoracic inlet in younger patients. Cadaveric studies have demonstrated a 90% decrease in flow rate during normal range of motion, and transbrachial arteriography has confirmed this pattern in healthy persons. Younger patients may have an increased risk of injury at the transition points between the V1 and V2 segments, as well as between the V2 and V3 segments, where a relatively mobile VA transitions into a relatively fixed VA. For example, a left VA dissection was identified during a stroke workup of a 19-year-old patient who presented initially with transient weakness in his right arm that started during physical activity and progressed to contralateral weakness (▶ Fig. 13.1a ). After a 3-month regimen of anticoagulation, provocative testing (i.e., right head turn) continued to demonstrate obliteration of the left VA at the C2 level and preserved flow in the right VA (▶ Fig. 13.1b,c ). This case illustrates the concept of increased risk in active, flexible patients at the segmental transition points of the VA.
Numerous patients with VAIs may present during standard trauma evaluation or in an asymptomatic fashion. However, vessel injury may result in the formation of a pseudoaneurysm, with resulting local mass effect, thromboembolic complications, and hemodynamic instability ( 2, 8 in algorithm ). The characteristics of large pseudoaneurysms may include soft-tissue protrusion, which can also cause dysfunction of adjacent cervical structures from mass effect. Such patients may present with dysphagia, hoarseness, or airway compromise. Compression of the neurovascular bundle may provoke lower cranial nerve deficits. Subintimal injury and associated intramural thrombus will cause stenosis of the vessel lumen, which can manifest as vertebrobasilar insufficiency and posterior circulation hypoperfusion symptoms. Propagating thrombi also lead to ischemia in the vascular distribution of the vessel via focal occlusion or via thromboembolism. Distinct from these ischemic complications, intracranial extension of a VAI can also result in subarachnoid hemorrhage.
Surgical Anatomy of the Cervical Spine Related to the V2 Segment
The anatomy of the V2 segment of the VA requires special attention because a VAI that occurs during anterior cervical spine surgery can be a devastating complication. VAIs are more common in patients with degenerative spinal disease or anomalies in which the anatomical landmarks are disturbed. Approximately 5 to 7% of patients have an anomalous VA entry, and approximately 2 to 5% have medial displacement of the foramen transversarium. Degeneration can also distort the position of the VA because the disk space collapses as the intertransverse process space narrows; this condition produces redundant vessel length that can create tortuosity or aberrant loops and direct compression from osteophytes. Rare medial VA looping into the disk space can also occur, endangering the success of a diskectomy. Although the transverse foramen has relatively abundant space for the VA, the artery usually occupies the medial section. Branches of the VA should also be kept in mind. The V1 and V3 vertebral segments do not have radicular or radiculomedullary branches. However, the V2 segment has several small branches with diameters ranging from 0.5 to 1.1 mm; these branches feed muscles, vertebrae, nerve roots, spinal dura, the spinal cord, and lower cranial nerves. Muscular branches occur under the bellies of longus capitis and longus colli muscles in 58% of segments, and these are at risk for injury during dissection around the V2 segment. Posterior branches arise in 39% of segments between C4 and C6, and they follow the corresponding nerve root in an ascending fashion, giving rise to ligamentous and radicular VA branches. The latter contribute to the vascular supply of the spinal cord. At the C3 level, the V2 segment consistently gives rise to a medial branch for the retro-odontoid arterial arch and to a lateral branch that crosses the extraforaminal portion of the cervical nerve root and unites with the ascending cervical artery. An awareness of small side branches will help the surgeon to avoid avulsion during spinal procedures and during the handling, retraction, and dissection of the VA for repair.
Workup
Clinical Evaluation
Many patients will present in an asymptomatic fashion without significant trauma despite an in-depth review of their history. Patients who have collagen vascular disease are at increased risk of arterial injury with minimal trauma, but most patients with an atraumatic presentation are not found to have connective tissue disorders. Recent respiratory infection is often proposed as an alternative mechanism for an isolated VAI.
Risk factors for VAIs include a history of chronic migraine, hypertension, and hyperhomocysteinemia, which may predispose the arterial substrate to injury. However, unlike the pathophysiological mechanisms for connective tissue disorders, logical pathophysiological mechanisms for these associations have not been demonstrated. These associations are also weaker than those of connective tissue disorders, and thus these conditions may not justify indefinite anti-platelet anticoagulation treatment.
Imaging
After a comprehensive patient history and physical examination have been conducted, noninvasive imaging can confirm the diagnosis of a VAI and can define the anatomical irregularity. The most common techniques are computed tomography (CT) and CT angiography (CTA), magnetic resonance (MR), ultrasound, and digital subtraction angiography (DSA). CTA and MR are noninvasive, readily available, and sensitive means of assessing both the injury and the intracranial sequelae. CTA is often the earliest available modality and can demonstrate the anatomical VAI as well as any sequelae, which can include subarachnoid hemorrhage, cerebral infarction, hematoma, and pseudoaneurysm. Congenitally hypoplastic or atretic VAs can be mistaken for stenotic VAs from dissection. In patients who have undergone acute trauma, CTA of the cervical vessels is often an efficient and safe means of screening for a VAI, particularly in the presence of a high-risk mechanism or imaging findings suggesting significant force in proximity to the vessel.
MR is a particularly useful imaging modality that is capable of identifying and helping to assess the vessel lumen, the vessel wall, thrombi, soft tissue, and ischemia and infarction. T1- and T2-weighted sequences are particularly useful in identifying hematoma. The addition of a fat suppression sequence is also useful, given cervical adipose tissue. Time-of-flight MR angiography (MRA) is useful in assessing the caliber of the VA, although it may be limited in VAs with tortuous or turbulent flow. Gadolinium-enhanced MRA can increase the sensitivity of lumen detection. In addition to diagnosis of a VAI, MR also provides the greatest spatial resolution and sensitivity for detecting intracranial ischemia, which is the primary complication of an extracranial VAI. Diffusion sequences, susceptibility-weighted imaging, and phase-shifted sequences can provide prognostic information for recovery from symptoms and can also provide greater sensitivity than CT for intracranial hemorrhage, a significant complication of an intracranial VAI and a feared complication of antiplatelet or anticoagulation treatment regimens.
DSA can facilitate the formulation of the management plan, but it is likely to be less sensitive than MR in diagnosing a VAI. However, patients with implants causing significant MR artifact or precluding the safe application of MR can often be evaluated with DSA. In particular, one must be aware of the risk of missing a nonstenotic thrombus with DSA. DSA can also better define the extent of the collateral vascular supply, which must be known in order to plan deconstructive treatment modalities. The demonstration of adequate collateral supply is critical before VA sacrifice. DSA and high-resolution cross-sectional imaging can demonstrate small branches with VA-dependent supply, such as the posterior inferior cerebellar artery and the anterior spinal artery. The involvement of these vessels may complicate the management of VAIs, and both reconstructive and deconstructive treatments should account for perfusion to these end arteries.
Cross-sectional imaging is useful in evaluating the configuration of the injury. Ultrasound and MR are more likely to demonstrate an intramural thrombus, whereas CT and DSA are particularly prone to missing this pathology because CT may be limited by poor soft-tissue resolution and DSA lacks extraluminal evaluation. Cross-sectional imaging can also effectively determine intracranial extension, which supports intervention for reduction of hemorrhagic risk. All modalities may demonstrate a dissection flap in the presence of a false lumen, but the dynamic nature of ultrasound and DSA may increase the sensitivity of these modalities. A dissection flap in the direction of flow may be particularly prone to cause occlusion and/or thromboembolic phenomena. In contrast, an anterograde flap supports intervention for reduction of ischemic risk.
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