Operative V2 decompression for traumatic vertebrobasilar insufficiency: illustrative case

Abstract

BACKGROUND

Blunt vertebral artery injuries after cervical trauma due to the close anatomical relationship of the vertebral artery to the cervical spine may have fatal consequences because of posterior circulation ischemia and vertebrobasilar insufficiency. While the standard of care remains medical treatment by anticoagulation or antiplatelet therapy, surgical decompression of the vertebral artery is rarely indicated.

OBSERVATIONS

The authors present a case of selective decompression of a traumatically constricted vertebral artery within the transverse foramen of C2 presenting with vertebrobasilar insufficiency due to bilateral aplasia of the posterior communicating arteries and contralateral hypoplasia of the vertebral artery.

LESSONS

Because of their close relationship to the cervical spine, the vertebral arteries are at risk for blunt injury, which may present asymptomatically or with symptoms of posterior circulation ischemia or vertebrobasilar insufficiency either immediately or after a latency phase. The anatomical variability of (1) the vertebral arteries, (2) collateral brainstem perfusion, and (3) the individual injury pattern demands individualized treatment strategies. If endovascular treatment of hemodynamically relevant stenosis of the V2 segment of the vertebral artery poses too high a risk for vessel injury, decompression of the transverse foramen can be performed safely and without risk to the biomechanical stability of the cervical spine.

Blunt vertebral artery injuries (BVAIs) after head and cervical trauma due to the close anatomical relationship of the vertebral artery to the cervical spine and the biomechanical coupling of skull and cervical spine may have fatal consequences because of posterior circulation ischemia and vertebrobasilar insufficiency. Deceptively, BVAI may present either asymptomatically or with immediate or delayed symptom onset, leading to an ongoing controversy regarding optimal screening criteria to avoid missing initially asymptomatic BVAI. While the standard of care remains medical treatment by anticoagulation or antiplatelet therapy, surgical decompression of the vertebral artery is rarely indicated, as most hemodynamically relevant traumatic stenoses of the vertebral arteries are treated endovascularly.

We report a case of a hemodynamically relevant traumatic stenosis of the left vertebral artery in the transverse foramen of C2 after a C2 fracture presenting with vertebrobasilar insufficiency due to concomitant bilateral aplasia of the posterior communicating arteries and contralateral hypoplasia of the vertebral artery, rendering the stenotic vertebral artery the only major vessel perfusing the brainstem.

Illustrative Case

History and Examination

An 84-year-old female patient with chronic rotational vertigo and new neck pain after a fall on the back of the head was admitted to the neurosurgical department of an associated hospital. Computed tomography (CT) imaging of the head and neck showed a moderately dislocated C2 odontoid fracture similar to type III according to Anderson and D’Alonzo¹ with involvement of the transverse foramen (Fig. 1) and with traumatic stenosis of the V2 segment of the left vertebral artery as well as a fracture of the spinous process of C3. Stenosis of the left vertebral artery was confirmed by ultrasound and CT angiography (Denver grade 2). After extensive consultation with the patient, an attempt at conservative treatment with a cervical orthosis was made. However, after 2 days, the patient showed new symptoms of vertebrobasilar insufficiency with multiple syncope episodes and reduced consciousness after sitting up in bed. While repeat CT imaging of the cervical spine showed no change in the fractures, repeat ultrasound of the left vertebral artery showed progredient stenosis. Because of the increasing threat of brainstem perfusion with bilateral aplastic posterior communicating arteries and a hypoplastic right vertebral artery (Fig. 2), the patient was transferred to our institution for additional diagnostics and definitive treatment. Digital subtraction angiography showed high-grade stenosis of the V2 segment of the left vertebral artery in the transverse foramen of C2 (Fig. 2). While the fracture itself was treatable via a conservative approach, obstruction of the left vertebral artery led to clinical signs of increasing vascular insufficiency of the posterior circulation—being the only blood supply due to the individual anatomy of circle of Willis (Fig. 2). We discussed this case extensively in our neurovascular board. Given the obstruction by bone fragments, endovascular intervention was ruled out because of the risk of piercing the blood vessel. Without options for interventional therapy, the indication for selective surgical decompression of the left vertebral artery at the transverse foramen of C2 was given.

FIG. 1.

CT studies showing the extent of the C2 fracture. The fracture passes between the foramina transversa and crosses the odontoid root. Arrowheads indicate fracture fissure in multiple planes: coronal view (A), axial view (B), sagittal view (C).

FIG. 2.

Individual anatomical cerebrovascular aspects and pathology. A: CT angiogram demonstrated hypoplastic right vertebral artery. Arrowheads point to both vertebral arteries. B: Digital reconstruction of the circle of Willis based on CT angiography shows that both posterior communicating arteries are aplastic. This individual cerebrovascular anatomy perfusion of the posterior circulation— including the brainstem, cerebellum, posterior cerebral artery, and part of the thalamus—depends on only the left vertebral artery instead of all 4 arteries (both carotid arteries and both vertebral arteries). Thus, the patient’s cerebrovascular anatomy explains the loss of consciousness due to traumatic obstruction of the left vertebral artery. C: Digital subtraction angiography of the left vertebral artery. The arrowhead marks the stenosis due to obstruction by bone fragments and the traumatic disc herniation at the V2 segment of the vertebral artery at the transverse foramen of C2.

Operative Treatment

The patient was put in the prone position with a slightly elevated upper body and the head fixated in a head clamp. The left half of C0 to C3 was exposed via a dorsal median skin incision. Intraoperatively, an elongated left vertebral artery with a caudal curve of V3 beneath the stenosis of V2 in the transverse foramen of C2 was microsurgically exposed. The stenosis was confirmed by both a microDoppler ultrasound probe (16 MHz) and indocyanine green (ICG) videoangiography. Afterward, circumferentially constricting bone fragments and the intervertebral disc herniated laterally toward the transverse foramen were carefully removed from V2 with Kerrison punches and micro-scissors. Sufficient perfusion of the left vertebral artery after operative decompression was again confirmed by ICG videoangiography and microDoppler ultrasound before the patient was closed up. The extent of decompression is shown in Fig. 3.

FIG. 3.

Images reconstructed from CT angiography. Postoperative extent of decompression of the left transverse foramen of C2 (B, D, and F) in comparison to preoperative constriction of the left vertebral artery (A, C, and E). Arrowheads mark the site of stenosis.

Postoperative Course

CT angiography on postoperative day 1 showed complete removal of the vertebral artery stenosis. Postoperatively, all signs of vertebrobasilar insufficiency receded immediately, and the patient was mobilized with physiotherapy while still wearing a cervical orthosis due to her C2 fracture. While the patient was able to walk with a rollator, she remained insecure after her traumatic experience and still intermittently experienced attacks of chronic rotational vertigo, which differed significantly in character from the vertebrobasilar insufficiency experienced previously and subsided after a few weeks. The patient was able to climb 40 steps on a staircase when discharged. At the 3-month follow-up, the patient’s symptoms had resolved completely (Fig. 4), and magnetic resonance imaging and Doppler ultrasound showed a patent left vertebral artery without stenosis and an adequate healing process without increasing dislocation, pseudarthrosis, or spinal stenosis.

FIG. 4.

Patient at the 3-month follow-up. Clinical symptoms including vertigo, local pain, and syncope resolved completely. The patient shows how she can balance on the right leg only.

Discussion

Observations

The close anatomical relationship of the vertebral artery to the cervical spine predisposes it to blunt traumatic injury, which is commonly classified according to the Denver criteria, originally used to evaluate for angiographic diagnosis of blunt carotid arterial injuries and later transferred to blunt cerebrovascular injuries in general (Table 1).²

TABLE 1.

Classification of blunt arterial injuries

Grade	Description
I	Irregularity of the vessel wall or a dissection/intramural hematoma with <25% luminal stenosis
II	Intraluminal thrombus or raised intimal flap is visualized, or dissection/intramural hematoma with ≥25% luminal narrowing
III	Pseudo-aneurysms
IV	Vessel occlusion
V	Vessel transection

See also Desouza et al.⁴

BVAIs can have fatal consequences due to posterior circulation ischemia in up to 25% of cases and show an overall mortality of 4%–8%.^3,4 Particularly the V2 segment of the vertebral artery appears to be at risk of injury due to its relative immobilization within the foramina transversa. Characteristic patterns of cervical spine fractures associated with BVAI are fractures of the foramen transversum, subluxation, and fractures of C1–3. Overall, these injury types comprise approximately 70% of all cervical spine fractures.^5–7 Multisegmental fractures of the foramina transversa show a particular predilection for BVAI.⁸ Within the upper cervical spine, fractures of C2 are a high-risk constellation with an incidence of BVAI of approximately 17% in odontoid fractures and 27% in traumatic spondylolistheses of C2.⁹ However, depending on the individual degree of collateralization of the posterior circulation, BVAI may stay asymptomatic or show delayed development of symptoms after hours to days, which impedes screening for BVAI solely based on clinical grounds.⁴ Therefore, screening of trauma patients for BVAI with CT angiography has been widely established, with ongoing controversy regarding the exact indications for radiological screening for BVAI. The early diagnosis of BVAI could be increased to almost 100% through the use of expanded Denver screening criteria, which take into account major concomitant injuries in addition to spine fractures and which have since been evaluated for CT angiography.^10–12 Nevertheless, 4-vessel cerebrovascular angiography remains the gold standard of BVAI diagnosis due to relevant rates of false-positive and false-negative results after CT angiography, depending on the technique used.¹³ Either anticoagulation or antiplatelet therapy is considered the standard of care for BVAI, while endovascular stenting or vertebral artery occlusion remain in case anticoagulation is contraindicated.^4,6,14 Surgical treatment of BVAI is technically challenging with high morbidity and mortality, which is why it is usually reserved for traumatic transections with severe hemorrhage or as an individual case-by-case decision.⁴ Iatrogenic surgical injury of the vertebral artery is a feared complication in surgery of the upper cervical spine, with an incidence of up to 1.35% in posterior fixation of C1–2.¹⁵

Here, we present a rare case of selective surgical decompression of a BVAI by external compression of the left vertebral artery by fracture fragments in the foramen transversum, which presented with clinical signs of vertebrobasilar insufficiency due to lack of collateralization (bilateral aplastic posterior communicating artery and hypoplastic right vertebral artery). Endovascular treatment was ruled out by our neuro-interventionalist. Based on the cross-sectional imaging, a cause of the severe stenosis seemed to be spotty compression by a fracture fragment in the foramen transversum. An intraluminal lesion like an intimal flap or intramural hematoma could be ruled out. In the case of endovascular therapy—stent implantation—the luminal narrowing could not be treated properly because of massive external compression. On the contrary, it could provoke an iatrogenic vessel dissection. This left surgery as the remaining option for treating the patient’s life-threatening vertebrobasilar insufficiency.

This surgery was deliberately carried out in a minimally invasive way by sole decompression of the left transverse foramen without stabilizing the C2 fracture. This is in accordance with Zaidi et al.,¹⁶ who already emphasized the adequacy of selective decompression without fusion via resection of a part of the posterior C1 arch for bow hunter syndrome without a traumatic etiology. We chose not to stabilize this patient despite a dislocated cervical fracture for multiple reasons. First, the patient’s age was considered a significant risk factor for a bigger surgery such as a combined ventro-dorsal approach for posterior decompression of the transverse foramen and anterior instrumentation of the odontoid process or a purely dorsal instrumentation of the upper cervical spine. Second, any instrumented surgery of C1 and C2 bears a relevant risk of injury to the patient’s last remaining vessel perfusing the brainstem. The compressed left vertebral artery displayed an aberrant ecstatic course with a larger risk for injury. Last, we considered limited decompression of an already fractured and dislocated transverse foramen not to be a significant contribution to destabilization of the upper cervical spine. The craniocervical junction possesses a wide array of ligamentous support structures, and a C2 fracture with abundant surface area of cancellous bone at the interface of fracture fragments usually shows a good healing tendency.

Lessons

In summary, this case illustrates one option for the rare surgical treatment of a BVAI in high-risk patients. The anatomical variability of (1) the vertebral arteries, (2) collateral brainstem perfusion, and (3) the individual injury pattern demands individualized treatment strategies. If endovascular treatment of hemodynamically relevant stenosis of the V2 segment of the vertebral artery poses too high a risk for vessel injury, decompression of the transverse foramen can be performed safely and without particular risk to the biomechanical stability of the cervical spine.

Disclosures

The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Author Contributions

Conception and design: ML Moskopp, Sannwald, D Moskopp. Acquisition of data: all authors. Analysis and interpretation of data: all authors. Drafting of the article: ML Moskopp, Sannwald. Critically revising the article: all authors. Reviewed submitted version of the manuscript: all authors. Approved the final version of the manuscript on behalf of all authors: ML Moskopp. Administrative/technical/material support: all authors. Study supervision: D Moskopp. Operating surgeon: D Moskopp.