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|LETTER TO EDITOR
|Year : 2014 | Volume
| Issue : 3 | Page : 310-313
Vertebral artery thrombosis in a case of traumatic atlanto-axial dislocation with delayed presentation: Emphasis on preoperative evaluation and operative steps to prevent a catastrophe
Pravin Salunke1, Sushanta K Sahoo1, Mandeep S Ghuman2
1 Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Radiodiagnosis, Postgraduate Institute of Medical Education and Research, Chandigarh, India
|Date of Submission||10-May-2014|
|Date of Decision||25-May-2014|
|Date of Acceptance||02-Jun-2014|
|Date of Web Publication||18-Jul-2014|
Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Salunke P, Sahoo SK, Ghuman MS. Vertebral artery thrombosis in a case of traumatic atlanto-axial dislocation with delayed presentation: Emphasis on preoperative evaluation and operative steps to prevent a catastrophe. Neurol India 2014;62:310-3
|How to cite this URL:|
Salunke P, Sahoo SK, Ghuman MS. Vertebral artery thrombosis in a case of traumatic atlanto-axial dislocation with delayed presentation: Emphasis on preoperative evaluation and operative steps to prevent a catastrophe. Neurol India [serial online] 2014 [cited 2021 Jan 16];62:310-3. Available from: https://www.neurologyindia.com/text.asp?2014/62/3/310/136993
Vertebral artery (VA) thrombosis and dissection has been documented in cervical spine injuries. , These vascular injuries are often asymptomatic and their pick up rates have increased with the advent of magnetic resonance imaging (MRI) and MR-angiogram.  VA thrombosis following traumatic atlanto-axial dislocation (TAAD) has rarely been reported. Few case reports have described early reduction and management of injured VA. The intraoperative steps to prevent a catastrophe while handling an injured VA have not been described. , Furthermore, such dislocation and fracture odontoid may present in a delayed manner, taking away attention from these vascular injuries.
A 32-year-old male presented with neck pain and progressive spastic quadriparesis of 4 months duration following a road traffic accident that occurred 6 months ago. He was partially dependant for activities of daily living. X-ray craniovertebral junction showed apparently malunited C2 type fracture. Computed tomography (CT) showed fractured dens with C1 arch dislocated anteriorly over the C2 body [[Figure 1]-upper row]. The fracture line extended onto the C2 facet and body. Apart from partially locked C1-2 facets the jagged margins of the fractured fragments appeared to the cause of irreducibility. Part of the fractured line appeared to be united. Dynamic X-rays showed angular movements with jagged margin of the edge of fractured fragments acting as a pivot. Magnetic resonance imaging (MRI) showed cervcio-medullary junction compression. CT-angiography revealed thrombosed V3 segment of right VA, extending from C2 to C1 transverse foramina. Beyond C1 transverse foramina, the right VA opacified again possibly due to back flow from the opposite VA [[Figure 1]-middle and lower row]. The gradual increase in the caliber of right VA beyond C1 transverse foramen suggested thrombosis and not congenital aplasia [[Figure 1] lower row]. Left VA showed good opacification and appeared to be the dominant one. Progression of the lesion could not be assessed as the patient had not been evaluated prior to this admission. In view of progression of symptoms and delayed presentation, operative treatment was chosen over the usual conservative management for C2 body fracture. Though there was no reduction on traction, a direct posterior approach was chosen as there was some angular mobility seen on dynamic X rays suggesting non-union rather than malunion. Bilateral C2 root ganglia were cut. The C1 facets were seen anterior to ventral edge of C2 facets. Both vertebral arteries were traced laterally from the exit of transverse foramina and the loop was lax despite significant anterior subluxation. A posterior edge of C1 facet and anterior edge of C2 facet was drilled to unlock the facets after which reduction could be achieved with distraction. Care was taken not to over distract to avoid indirect injury to the VA. Post operatively he improved rapidly and is doing well at 6 month follow up. Follow-up CT of craniovertbral junction (CVJ) showed bony fusion. And repeat angiogram showed similar findings with no recanalization of VA.
|Figure 1: Top row: Preoperative imaging showing odontoid with AAD and Postoperative CT showing reduction. Middle row (right to left): 2D coronal CTA showing left dominant VA and right VA (white arrows) not fi lling beyond C2 transverse foramina. 3D reconstructed CTA left and right oblique views showing well opacifi ed Left V3 segment (black arrow) and non-fi lling right VA beyond C2 transverse foramina. Just distal to the C1 transverse foramina the VA is seen again, initially narrow & then fi lling well (3 black arrows). Bottom row: Axial CTA showing non-visualization of Right VA at C2 level, but is|
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Traumatic AAD may cause injury to the V3 segment of VA directly due to associated fracture of the edges of transverse foramen or indirectly by excessive distraction during the dislocation or simple compression due to severe dislocation. ,, It may lead to VA dissection or thrombosis. These are usually asymptomatic not only due to flow from opposite VA but also from the circle of Willi's.  In cases where the dislocation progresses with time, the artery is likely to be stretched beyond its physiological limit. A rotational component may stretch one VA more than the other. Additional movements may cause intimal tears in an already stretched artery. The intimal tears would lead to thrombosis. The thrombus may extend with time or shower emboli giving rise to posterior circulation strokes. Such strokes have been described in cases of congenital AAD.  Thus the cause of delayed onset myelopathy in patients with traumatic AAD can be direct cord compression or vascular compromise due to involvement of VA. VA thrombosis was unlikely to be the cause of myelopathy in our patient as there was rapid clinical improvement following surgery. Besides, the thrombosed VA was non-dominant. However, manipulation of thrombosed VA during surgery may shower emboli and lead to catastrophe.
A preoperative CT-angiogram helps in identifying these vascular injuries. Though asymptomatic after injury, distraction while trying to reduce it may lead to catastrophe. So a preoperative evaluation of these vessels is imperative. The atlantoaxial joint provides about 45 degrees of rotation. VA has to be redundant between C2 and C1 transverse foramina to allow this movement. The minimum length of this segment to allow this movement has to be √[a 2 +(d/2*sin11°) 2 ], where a is the distance between the C1 and C2 transverse foramen in neutral position and d is the distance between both C1 transverse foramina. So the length of the VA measured on angiogram more than the calculated minimal length of VA in rotation, allows the amount of distraction in a dislocated position.
The intraoperative management of injured VA in traumatic AAD has not been clearly delineated though operative steps to safeguard anomalous VA in congenital AAD have been described.  Few steps would be the common to safeguard the stretched artery in a traumatic AAD. During surgery, the VA needs to be identified from the exit of the C2 transverse foramen. The artery is usually lateral to the facets unless anomalous. The lateral dislocation or rotational dislocation makes one VA away from the C2 facet and the opposite VA closer to it. It is better to start dissecting from the side where the VA is away from the C2 facet. The distraction of the facets while trying to reduce the dislocation needs to be calculated as described above (preferably not more than 10 mm). A non-dominant VA is unlikely to shower emboli during manipulation due to back flow, though extension of thrombus is possible. Furthermore a non-dominant VA can be sacrificed if need be, in case of dissection. But manipulation needs to be extremely gentle while handling an injured dominant VA. Anticoagulation is preferable while handling such vessels during surgery. In case of dissection of the dominant artery, immediate post operative stenting or thrombolysis in case of thromboembolic phenomenon is the only option.
Apart from highlighting the importance of preoperative evaluation of the VA in traumatic AAD this report emphasizes on intraoperative steps to prevent catastrophe in presence of injured vessel. Operative intervention needs to be tailored depending on the dominance and its relation to the involved facets.
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|6.||Salunke P, Futane S, Sahoo SK, Ghuman M, Khandelwal NK. Operative nuances to safeguard anomalous vertebral artery without compromising the surgery for congenital atlantoaxial dislocation: Untying a tough knot between vessel and bone. J Neurosurg Spine 2014;20:5-10. |
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