- Email: [email protected]
Vertebral Artery Occlusion and Recanalization After Cervical Facet Dislocation
Original Article
Vertebral Artery Occlusion and Recanalization After Cervical Facet Dislocation Zhengfeng Zhang, Honggang Wang, Zhiping Mu
OBJECTIVE: To investigate clinical features of vertebral artery (VA) occlusion and recanalization after cervical facet dislocation.
-
METHODS: During a 2-year period from January 2014 to December 2015, 29 consecutive patients with cervical facet dislocation were treated in investigator group. VA occlusion and recanalization were identified retrospectively by magnetic resonance imaging (MRI) at the time of injury and follow-up.
-
RESULTS: VA occlusion occurred in 6 of the 29 patients (20.7%). All patients were unilateral occlusion and had no vertebrobasilar symptoms. Surgical anterior spinal fusion was performed in 5 patients, and 1 was treated by posterior fusion. Follow-up MRIs revealed VA recanalization in 5 patients. One patient did not undergo MRI because he died of respiratory failure. The time course for VA recanalization was from 6 days after injury to 4 months after operation depending on the length of VA occlusion.
-
CONCLUSIONS: A fifth of patients with cervical facet dislocation will develop VA occlusion with rare symptomatic vertebrobasilar ischemia. VA recanalization occurs mainly within the first 4 months after injury, regardless of the length of VA occlusion.
-
INTRODUCTION
V
ertebral artery (VA) injuries have been reported to be present in 19%e39% of all blunt cervical spine traumas.1-3 The majority of VA injuries are clinically asymptomatic1,2,4; however, few of them have the potential for catastrophic
Key words Cervical facet dislocation - Magnetic resonance imaging - Occlusion - Recanalization - Vertebral artery -
Abbreviations and Acronyms ASIA: American Spinal Injury Association CT: Computed tomography MRI: Magnetic resonance imaging VA: Vertebral artery
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outcomes, such as posterior circulation stroke, cortical blindness, quadriplegia, and death.1,5 A one to three-quarters’ incidence of VA occlusion was reported in distractive flexion injury,4,6,7 which was closely related to pattern of facet dislocation. Therefore, it is hypothesized that facet dislocation patterns are a pathomechanism of VA occlusion with an independent incidence. VA injuries associated with facet dislocation, however, have not been reported in isolated case series; the cases of VA occlusion in facet dislocations have been described and derived only from few clinical series of blunt cervical spine trauma, including both fractures and dislocations.1-7 VA occlusion can be considered a common complication in approximately 20% of cervical spine fractures and dislocations.4 Using magnetic resonance imaging (MRI), we performed a retrospective study to investigate the clinical features of VA occlusion and recanalization after cervical facet dislocation.
MATERIALS AND METHODS During a 2-year period from January 2014 to December 2015, 29 patients with cervical facet dislocations were admitted or transferred to and treated surgically in the investigator’s group (Z.Z.). In these 29 patients (26 male and 3 female), the distribution of spine level was from C3/4 to C7/T1; the etiologic diagnosis included 5 unilateral and 24 bilateral facet dislocations; the neurologic status was comprised in 10 patients with American Spinal Injury Association (ASIA) Classification A, 5 with B, 4 with D, and 10 with E; the monthly follow-up ranged from 3 to 16 months (mean, 12 months). Before and after the surgery and at each 6 month follow-up, standard anteroposterior, lateral, and dual oblique films were taken to assess spinal injury, reduction, and internal fixation. All patients underwent computed tomography (CT) scans to define the precise spinal injury, spinal alignment, and fusion and 1.5-Tesla, T1-weighted and T2-weighted MRI to evaluate any cord compression and the extent of intramedullary MRI signals on
Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing, China To whom correspondence should be addressed: Zhengfeng Zhang, M.D., Ph.D. [E-mail: [email protected]] Citation: World Neurosurg. (2016) 95:190-196. http://dx.doi.org/10.1016/j.wneu.2016.08.002 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter ª 2016 Elsevier Inc. All rights reserved.
WORLD NEUROSURGERY, http://dx.doi.org/10.1016/j.wneu.2016.08.002
ORIGINAL ARTICLE
e/e/12
1 A/death/1 ? posterior fusion e/49.8 Average
VA, vertebral artery; ASIA, American Spinal Injury Association; M, male; F, female.
e/3.3
M/59 6
C5/6
B
Left
C2eC6/5
None
4 months postoperatively
B/D/9
3 months postoperatively
Anterior fusion None C2eC5/4
C3eC5/3 Right
Right B
U M/45
M/47 5
C5/6
sagittal and axial planes. Neurologic scores of all patients at admission and at each follow-up were determined following the International Standards for Neurological and Functional Classification of Spinal Cord Injury by the ASIA-International Medical Society of Paraplegia.8 All patients underwent early reduction and surgical stabilization with titanium instrumentation when clinical and radiographic evaluations had been completed. Anterior and/or posterior stabilization was selected properly in each case according to the type of spinal injuries. Retrospective MRI studies were performed to determine the VA occlusion for all patients at the time of injury and each followup. VA occlusion was diagnosed on MRIs with asymmetrical flow void and/or absence of flow void in either of both of the VAs.3,4 The diagnosis of VA occlusion also was achieved by consensus between 2 neuroradiologists to avoid clinical subjectivity. Neurologic status was reviewed carefully in all patients not only for specific findings of spinal cord injury but for vertebrobasilar ischemia (e.g., dizziness, vertigo, dysarthrias, dysphasia, visual field defect, blurry vision, drowsiness, and altered consciousness). For statistical analysis, comparisons were performed by with Student t tests and linear regression analyses. The results were reported by the use of P < 0.05 as the criterion for a significant difference. The odds ratio was reported with 95% confidence intervals. RESULTS
4
C5/6
None
Anterior fusion
D/E/15
3
2 D/E/15
6 days after injury
3 months postoperatively
Anterior fusion
A/A/16
VERTEBRAL ARTERY OCCLUSION AND RECANALIZATION
Anterior fusion None
None C3eC4/2
C3eC6/4 Right
Right B
B F/47 3
C5/6 M/52 2
C6/7
A/A/16 2 days postoperatively Anterior fusion None C3eC4/2 Right B C5/6 M/49 1
Side of VA Length of VA Occlusion Occlusion/Levels VA Symptoms Case No. Sex/Age, years Levels Unilateral/Bilateral
Table 1. Data for Patients With VA Occlusion and Recanalization
Treatment
Recanalization
ASIA Preoperative/Postoperative Follow-up, months Figure
ZHENGFENG ZHANG ET AL.
WORLD NEUROSURGERY 95: 190-196, NOVEMBER 2016
VA occlusion was shown on MRI in 6 of the 29 patients (20.7%) (Table 1). There were 5 male and 1 female patients, with an average age of 49.8 years (range 45e59 years). All patients were followed up from 1 to 16 months (average, 12 months). Unilateral occlusion of the right VA occurred in 5 patients and of the left in 1. No patient had bilateral VA occlusions. Levels of cervical facet dislocations existed in C5/6 segment in 5 patients and C6/7 in 1. Of 6 patients with VA occlusion, 5 patients had bilateral facet dislocation and 1 patient had unilateral facet dislocation. VA occlusion was located in cephalic or dislocated vertebras (Figure 1). The length of VA occlusion was extended cephalad from 2 to 5 levels but had not reached C1. All 6 patients with VA occlusion had spinal cord injury (P < 0.05). There were 3 patients with ASIA A, 1 with B, and 2 with D. None of 6 patients with VA occlusion had radiographically detected brain trauma at injury. Regarding clinical manifestations related to vertebrobasilar ischemia, none of 6 patients with unilateral VA occlusion had symptoms, so no patient underwent systemic anticoagulation therapy. No neurologic impairment in terms of vertebrobasilar ischemia occurred during follow-up. Surgical anterior spinal fusion was performed in 5 patients. One patient was treated by posterior fusion because he had a chest injury and took a risk for tracheostomy after anterior surgical approach (case 6). Follow-up MRIs revealed VA recanalization in 5 patients. One patient had no chance of undergoing MRI because he was died of respiratory failure (case 6). The time course for VA recanalization was from 6 days after injury (case 2, Figure 2) to 4 months after operation (case 5, Figure 3). It was dependent on the length of VA occlusion, the shorter length of levels of VA occlusion, the
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ORIGINAL ARTICLE ZHENGFENG ZHANG ET AL.
VERTEBRAL ARTERY OCCLUSION AND RECANALIZATION
Figure 1. Imaging studies of the illustrative case with 5/6 bilateral facet dislocation with left vertebral artery (VA) occlusion from C2 to C6 (case 6). (AeB) Three-dimensional computed tomography (CT) reconstruction (A) and sagittal CT (B) showing C5/6 bilateral facet dislocation (arrows). (C) T2 sagittal magnetic resonance imaging (MRI) showing spine
shorter time of recanalization (Table 1) (P < 0.05). No adverse consequence associated with restoration of blood flow, such as distal embolization, occurred during follow-up.
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trauma and spinal cord injury. (DeI) T2 axial MRI showing intact VA at C1 (D), but left VA occlusion at C2 (E), C3 (F), C4 (G), C5 (H), and C6 (I) (arrows). (JeK) CT angiography showing left VA occlusion (arrows). (L) Postoperative anteroposterior radiograph and lateral radiograph showing the reduction and fixation of posterior pedicle screws.
DISCUSSION VA injury secondary to cervical spine trauma includes thrombosis, arteriovenous fistula, intimal dissection, pseudoaneurysm, and
WORLD NEUROSURGERY, http://dx.doi.org/10.1016/j.wneu.2016.08.002
ORIGINAL ARTICLE ZHENGFENG ZHANG ET AL.
Figure 2. Imaging studies of the illustrative case with 5/6 bilateral facet dislocation with right vertebral artery (VA) occlusion and recanalization for 6 days after injury (case 2). (AeB) Three-dimensional computed tomography (CT) reconstruction (A) and sagittal CT (B) showing C5/6 bilateral facet dislocation (arrows). (C) Postoperative lateral radiograph showing the reduction and fixation of anterior pedicle screw plate. (DeE) Postoperative axial CT images showing the placement of anterior pedicle screws at C5
occlusion.9 VA occlusion is considered the most common lesion.10,11 A pathomechanism of traumatic VA occlusion is: intimal disruption initially occurs, then secondary events such as thrombus formation may lead to clot occlusion of vessel lumen.11,12 The current study is the first report in which all the patients presented with VA occlusion after cervical facet dislocation with a long-term follow-up of VA recanalization in a single group. The incidence of VA occlusion after cervical facet dislocation was 20.7% in the current retrospective MRI study. In nonpenetrating cervical spine trauma, including fractures and/or
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VERTEBRAL ARTERY OCCLUSION AND RECANALIZATION
and C6. (F) T2 sagittal magnetic resonance imaging (MRI) showing spine trauma and spinal cord injury. (GeJ) T2 axial MRI showing right VA occlusion at C3 (G) and C4 (H) but VA intact at C5 (I) and C6 (J) (arrows). (K) T2 sagittal MRI 6 days after injury. (LeO) T2 axial MRI showing right VA recanalization at C3 (L) and C4 (M), and blood flow of C5 (N) and C6 (O) (arrows). (P) T2 sagittal MRI 2 weeks after injury. (QeT) axial MRI showing blood flow of right VA at C3 (Q), C4 (R), C5 (S), and C6 (T) (arrows).
dislocations, the reported incidence of VA injury varies from different diagnostic methods. In the past, VA injury was thought to be infrequent because it was rarely symptomatic, but its incidence was reported to be 46%e75% when evaluated by angiography in a small sample case series study.6,11 It was found to occur at a lower rate, between 17.2% and 25.5%, in studies that use MRI and magnetic resonance angiography,4,7,10,12-14 which is comparable with that found in our results in cervical facet dislocation. Although the limitation of this retrospective study includes small sample cases, VA occlusion can be considered a common complication in approximately 20% of cervical facet dislocation.
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VERTEBRAL ARTERY OCCLUSION AND RECANALIZATION
Figure 3. Magnetic resonance imaging (MRI) studies of the illustrative case with 5/6 bilateral facet dislocation with right vertebral artery (VA) occlusion and recanalization for 4 months after injury (case 5). (A) T2 sagittal MRI showing spine trauma and spinal cord injury. (BeD) T2 axial MRI showing right VA occlusion at C4 (B) and C5 (C), but VA intact at C6 (D) (arrows).
Diagnosis of VA occlusion should be made on the basis of cervical 4-vessel angiography, digital subtraction angiography, CT angiography, magnetic resonance angiography, and MRI.4,8,11,13,15-17 Angiography is the most definitive method for detecting VA injury, which was considered as the gold standard for diagnoses; however, it is an invasive technique with risk of complications and is risky in critically ill patients with unstable spines. CT angiography with more than 16-slice scanners has been shown to have sensitivity and specificity close to that of conventional angiography.1,18 Axial T2 MRI scans are very useful because they show an absence of flow when there is an occlusion and a high signal when there is an intraluminal clot. They also are more sensitive for identifying some of the sequelae of VA dissection, such as back lifting, cerebellar, and parieto-occipital infarction.14 Thus, the axial T2 sequence can be used to analyze both the fracture and the possibility of VA injury. Magnetic resonance angiography is less sensitive for detecting VA injury than angiography but may be performed during the magnetic resonance study, for it is not necessary to change the position of the patient. Angiography is reserved for cases in which MRI
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(E) T2 sagittal MRI at 1 week after operation. (FeJ) T2 axial MRI showing partial recanalization of right VA at C2 (F), C3 (G), C4 (H), and C5 (I), and blood flow of C6 (J) (arrows). (K) T2 sagittal MRI 4 months after operation. (LeP) T2 axial MRI showing recanalization of right VA at C2 (L), C3 (M), C4 (N), and C5 (O), and blood flow of C6 (P) (arrows).
is not diagnostic.14 Because it is always coincident with the positive results when magnetic resonance angiography was performed in patients with absent flow (signal void) in MRI, VA occlusion in the current retrospective study was diagnosed only based on a noninvasive MRI method. The clinical features of VA occlusion in cervical facet dislocation are somewhat similar to those reported in previous cervical spine trauma studies. For example, the most frequent site of the VA occlusion was C5eC6; VA occlusion was unilateral in major cases; VA occlusion was located in the injured or cephalic segment; most patients had no occlusion of the intracranial segment; and most patients with VA occlusion had traumatic spinal cord injury.11,12,14 Furthermore, the present series demonstrated that the length of VA occlusion was extended cephalad from 2 to 5 levels. There was no significant correlation between VA occlusion and severity of spinal cord injury in this study (P < 0.05) (Table 1). Cerebellar infarction has been reported in some conditions of VA occlusion.1,5 Unilateral VA occlusion rarely results in a neurologic deficit because of collateral supply through the contralateral VA and the posterior inferior cerebellar arteries,19
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ORIGINAL ARTICLE ZHENGFENG ZHANG ET AL.
VERTEBRAL ARTERY OCCLUSION AND RECANALIZATION
Although approximately 15% of patients have hypoplasia of one VA, which emphasizes the fact that there may not always be sufficient collateral arterial supply in a patient with unilateral occlusion.6,20 A low frequency of bilateral VA occlusion with cervical spine trauma has been shown in published reports; however, the consequence of its vertebrobasilar ischemia can have a mortality rate from 75% to 86%,21 although a few cases of asymptomatic posttraumatic bilateral artery occlusion also have been reported.6,12-14,20,22 The artery lesion was unilateral in all cases in the present series. The length of VA occlusion was extended cephalad from 2 to 5 levels but did not reach to C1. Therefore, no patients had neurologic symptoms due to VA occlusion in the present series. The treatment of symptomatic VA occlusion has been reported for cases of distal embolism, including anticoagulation, catheter embolization ligation, surgical ligation, and surgical resection and grafting23-27; however, the protocol or strict criteria for treatment are still lacking. Asymptomatic VA occlusion need not be embolized or ligated because there is adequate collateral flow through the opposite artery, or it will be recanalized for restoration of blood flow. Recanalization of VA occlusion has been reported in a few case series, with an incidence ranging from 17% to 85%.12,28,29 In the present series, VA recanalization was observed in 5 of 6 patients (83%) within a 4-month follow-up, even with 1 case lost follow-up. Therefore, the restoration rate of blood flow may be underestimated because follow-ups with magnetic resonance angiography were not long enough (e.g., 1 month) in some patients in
REFERENCES 1. Biffl WL, Moore EE, Elliott JP, Ray C, Offner PJ, Franciose RJ, et al. The devastating potential of blunt vertebral arterial injuries. Ann Surg. 2000;231: 672-681. 2. Miller PR, Fabian TC, Croce MA, Cagiannos C, Williams JS, Vang M, et al. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg. 2002;236:386-393 [discussion: 93-95]. 3. Even J, McCullough K, Braly B, Hohl J, Song Y, Lee J, et al. Clinical indications for arterial imaging in cervical trauma. Spine. 2012;37:286-291. 4. Taneichi H, Suda K, Kajino T, Kaneda K. Traumatically induced vertebral artery occlusion associated with cervical spine injuries: prospective study using magnetic resonance angiography. Spine. 2005;30:1955-1962. 5. Yoshihara H, VanderHeiden TF, Harasaki Y, Beauchamp KM, Stahel PF. Fatal outcome after brain stem infarction related to bilateral artery occlusion-case report of a detrimental complication of cervical spine trauma. Patient Saf Surg. 2011; 5:18. 6. Louw JA, Mafoyane NA, Small B, Neser CP. Occlusion of the vertebral artery in cervical spine dislocation. J Bone Joint Surg. 1990;72-B:679-681.
previous studies.28,29 It is reported that the restoration of blood flow is greater in compression injuries than in distraction injuries4; however, different results of distractive flexion injury-related cervical facet dislocation were observed in the present series. The mechanism of occlusion is unlikely to be subjected to relatively minor stretching in compressive or distractive injuries. The current study is the first report in which the time course for VA recanalization was from several days after injury to 4 months after operation. The short length of levels of VA occlusion can be restored within a short period. There are several limitations to this study. First, it was retrospective. Second, although eligible cases are hard to amass, the small sample size (only 6 patients) is certainly a major limitation. Third, VA occlusion and recanalization in the current study were diagnosed in noninvasive MRI; however, MRI was not found to be more sensitive than angiography, CT angiography, or magnetic resonance angiography because of the retrospective study. Finally, this study reflected the experience at a single specialized spinal injuries center with a bias epidemiologic feather. In summary, the incidence of VA occlusion after cervical facet dislocation was 20.7%, which is comparable with nonpenetrating cervical spine injuries. VA occlusion rarely was symptomatic because of sufficient collateral blood supply. VA recanalization was observed in more than 80% patients and occurred mainly within the first 4 months after injury. The time course of VA recanalization was dependent on the length of VA occlusion.
7. Giacobetti FB, Vaccaro AR, Bos-Giacobetti MA, Deeley DM, Albert TJ, Farmer JC, et al. Vertebral artery occlusion associated with cervical spine trauma. A prospective analysis. Spine. 1997;22: 188-192. 8. DiTunno JF, Young W, Creasey G. International standards for neurological and functional classification of spinal cord injury: revised 1992. Paraplegia. 1994;32:70-80. 9. Hayes P, Gerlock AJ, Cobb CA. Cervical spine trauma. A cause of vertebral artery injury. J Trauma. 1980;20:904-905. 10. Friedman D, Flanders A, Thomas C, Millar W. Vertebral artery injury after acute cervical spine trauma: rate of occurrence as detected by MR angiography and assessment of clinical consequences. AJR Am J Roentgenol. 1995;164:443-447 [discussion: 448-449]. 11. Willis BK, Greiner F, Orrison WW, Benzel EC. The incidence of vertebral artery injury after midcervical spine fracture or subluxation. Neurosurgery. 1994;34:435-441 [discussion: 441-442]. 12. Vaccaro AR, Klein GR, Flanders AE, Albert TJ, Balderston RA, Cotler JM. Long-term evaluation of vertebral artery injuries following cervical spine trauma using magnetic resonance angiography. Spine. 1998;23:789-794 [discussion: 795].
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13. Parbhoo AH, Govender S, Corr P. Vertebral artery injury in cervical spine trauma. Injury. 2001;32: 565-568. 14. Veras LM, Pedraza-Gutiérrez S, Castellanos J, Capellades J, Casamitjana J, Rovira-Cañellas A. Vertebral artery occlusion after acute cervical spine trauma. Spine. 2000;25:1171-1177. 15. Gambee MJ. Vertebral artery thrombosis after spinal injury: case report. Paraplegia. 1986;24: 350-357. 16. Golueke P, Sclafani S, Phillips T, Goldstein A, Scalea T, Duncan A. Vertebral artery injury—diagnosis and management. J Trauma. 1987;27:856-865. 17. Raskind R, North CM. Vertebral artery injuries following chiropractic cervical spine manipulation. Case reports. Angiology. 1990;41:445-452. 18. Bromberg WJ, Collier BC, Diebel LN, Dwyer KM, Holevar MR, Jacobs DG, et al. Blunt cerebrovascular injury practice management guidelines: the eastern association for the surgery of trauma. J Trauma. 2010;68:471-477. 19. Hartkamp MJ, van Der Grond J, van Everdingen KJ, Hillen B, Mali WP. Circle of Willis collateral flow investigated by magnetic resonance angiography. Stroke. 1999;30:2671-2678. 20. Weller SJ, Rossitch E, Malek AM. Detection of vertebral artery injury after cervical spine trauma
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using magnetic resonance angiography. J Trauma. 1999;46:660-666. 21. Becker KJ, Monsein LH, Ulatowski J, Mirski M, Williams M, Hanley DF. Intraarterial thrombolysis in vertebrobasilar occlusion. AJNR Am J Neuroradiol. 1996;17:255-262. 22. Rodriguez M, Tyberghien A, Matge G. Asymptomatic vertebral artery injury after acute cervical spine trauma. Acta Neurochir (Wien). 2001;143:939-945. 23. Cothren CC, Moore EE, Biffl WL, Ciesla DJ, Ray CE Jr, Johnson JL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg. 2004;139:540-545 [discussion: 545-546]. 24. Hoshino Y, Kurokawa T, Nakamura K, Seichi A, Mamada T, Saita K, et al. A report on the safety of
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unilateral vertebral artery ligation during cervical spine surgery. Spine. 1996;21:1454-1457. 25. Schwarz N, Buchinger W, Gaudernak T, Russe F, Zechner W. Injuries to the cervical spine causing vertebral artery trauma: case reports. J Trauma. 1991;31:127-133. 26. Alexander JJ, Glagov S, Zarins CK. Repair of a vertebral artery dissection. J Neurosurg. 1986;64: 662-666. 27. Shintani A, Zervas NT. Consequence of ligation of the vertebral artery. J Neurosurg. 1972;36:447-450.
29. Quint DJ, Spickler EM. Magnetic resonance demonstration of vertebral artery dissection. Report of two cases. J Neurosurg. 1990;72: 964-967. Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Received 3 July 2016; accepted 1 August 2016 Citation: World Neurosurg. (2016) 95:190-196. http://dx.doi.org/10.1016/j.wneu.2016.08.002 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com
28. Deen HG Jr, McGirr SJ. Vertebral artery injury associated with cervical spine fracture. Spine. 1992; 17:230-234.
1878-8750/$ - see front matter ª 2016 Elsevier Inc. All rights reserved.
WORLD NEUROSURGERY, http://dx.doi.org/10.1016/j.wneu.2016.08.002
Vertebral Artery Occlusion and Recanalization After Cervical Facet Dislocation Zhengfeng Zhang, Honggang Wang, Zhiping Mu
OBJECTIVE: To investigate clinical features of vertebral artery (VA) occlusion and recanalization after cervical facet dislocation.
-
METHODS: During a 2-year period from January 2014 to December 2015, 29 consecutive patients with cervical facet dislocation were treated in investigator group. VA occlusion and recanalization were identified retrospectively by magnetic resonance imaging (MRI) at the time of injury and follow-up.
-
RESULTS: VA occlusion occurred in 6 of the 29 patients (20.7%). All patients were unilateral occlusion and had no vertebrobasilar symptoms. Surgical anterior spinal fusion was performed in 5 patients, and 1 was treated by posterior fusion. Follow-up MRIs revealed VA recanalization in 5 patients. One patient did not undergo MRI because he died of respiratory failure. The time course for VA recanalization was from 6 days after injury to 4 months after operation depending on the length of VA occlusion.
-
CONCLUSIONS: A fifth of patients with cervical facet dislocation will develop VA occlusion with rare symptomatic vertebrobasilar ischemia. VA recanalization occurs mainly within the first 4 months after injury, regardless of the length of VA occlusion.
-
INTRODUCTION
V
ertebral artery (VA) injuries have been reported to be present in 19%e39% of all blunt cervical spine traumas.1-3 The majority of VA injuries are clinically asymptomatic1,2,4; however, few of them have the potential for catastrophic
Key words Cervical facet dislocation - Magnetic resonance imaging - Occlusion - Recanalization - Vertebral artery -
Abbreviations and Acronyms ASIA: American Spinal Injury Association CT: Computed tomography MRI: Magnetic resonance imaging VA: Vertebral artery
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outcomes, such as posterior circulation stroke, cortical blindness, quadriplegia, and death.1,5 A one to three-quarters’ incidence of VA occlusion was reported in distractive flexion injury,4,6,7 which was closely related to pattern of facet dislocation. Therefore, it is hypothesized that facet dislocation patterns are a pathomechanism of VA occlusion with an independent incidence. VA injuries associated with facet dislocation, however, have not been reported in isolated case series; the cases of VA occlusion in facet dislocations have been described and derived only from few clinical series of blunt cervical spine trauma, including both fractures and dislocations.1-7 VA occlusion can be considered a common complication in approximately 20% of cervical spine fractures and dislocations.4 Using magnetic resonance imaging (MRI), we performed a retrospective study to investigate the clinical features of VA occlusion and recanalization after cervical facet dislocation.
MATERIALS AND METHODS During a 2-year period from January 2014 to December 2015, 29 patients with cervical facet dislocations were admitted or transferred to and treated surgically in the investigator’s group (Z.Z.). In these 29 patients (26 male and 3 female), the distribution of spine level was from C3/4 to C7/T1; the etiologic diagnosis included 5 unilateral and 24 bilateral facet dislocations; the neurologic status was comprised in 10 patients with American Spinal Injury Association (ASIA) Classification A, 5 with B, 4 with D, and 10 with E; the monthly follow-up ranged from 3 to 16 months (mean, 12 months). Before and after the surgery and at each 6 month follow-up, standard anteroposterior, lateral, and dual oblique films were taken to assess spinal injury, reduction, and internal fixation. All patients underwent computed tomography (CT) scans to define the precise spinal injury, spinal alignment, and fusion and 1.5-Tesla, T1-weighted and T2-weighted MRI to evaluate any cord compression and the extent of intramedullary MRI signals on
Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing, China To whom correspondence should be addressed: Zhengfeng Zhang, M.D., Ph.D. [E-mail: [email protected]] Citation: World Neurosurg. (2016) 95:190-196. http://dx.doi.org/10.1016/j.wneu.2016.08.002 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter ª 2016 Elsevier Inc. All rights reserved.
WORLD NEUROSURGERY, http://dx.doi.org/10.1016/j.wneu.2016.08.002
ORIGINAL ARTICLE
e/e/12
1 A/death/1 ? posterior fusion e/49.8 Average
VA, vertebral artery; ASIA, American Spinal Injury Association; M, male; F, female.
e/3.3
M/59 6
C5/6
B
Left
C2eC6/5
None
4 months postoperatively
B/D/9
3 months postoperatively
Anterior fusion None C2eC5/4
C3eC5/3 Right
Right B
U M/45
M/47 5
C5/6
sagittal and axial planes. Neurologic scores of all patients at admission and at each follow-up were determined following the International Standards for Neurological and Functional Classification of Spinal Cord Injury by the ASIA-International Medical Society of Paraplegia.8 All patients underwent early reduction and surgical stabilization with titanium instrumentation when clinical and radiographic evaluations had been completed. Anterior and/or posterior stabilization was selected properly in each case according to the type of spinal injuries. Retrospective MRI studies were performed to determine the VA occlusion for all patients at the time of injury and each followup. VA occlusion was diagnosed on MRIs with asymmetrical flow void and/or absence of flow void in either of both of the VAs.3,4 The diagnosis of VA occlusion also was achieved by consensus between 2 neuroradiologists to avoid clinical subjectivity. Neurologic status was reviewed carefully in all patients not only for specific findings of spinal cord injury but for vertebrobasilar ischemia (e.g., dizziness, vertigo, dysarthrias, dysphasia, visual field defect, blurry vision, drowsiness, and altered consciousness). For statistical analysis, comparisons were performed by with Student t tests and linear regression analyses. The results were reported by the use of P < 0.05 as the criterion for a significant difference. The odds ratio was reported with 95% confidence intervals. RESULTS
4
C5/6
None
Anterior fusion
D/E/15
3
2 D/E/15
6 days after injury
3 months postoperatively
Anterior fusion
A/A/16
VERTEBRAL ARTERY OCCLUSION AND RECANALIZATION
Anterior fusion None
None C3eC4/2
C3eC6/4 Right
Right B
B F/47 3
C5/6 M/52 2
C6/7
A/A/16 2 days postoperatively Anterior fusion None C3eC4/2 Right B C5/6 M/49 1
Side of VA Length of VA Occlusion Occlusion/Levels VA Symptoms Case No. Sex/Age, years Levels Unilateral/Bilateral
Table 1. Data for Patients With VA Occlusion and Recanalization
Treatment
Recanalization
ASIA Preoperative/Postoperative Follow-up, months Figure
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VA occlusion was shown on MRI in 6 of the 29 patients (20.7%) (Table 1). There were 5 male and 1 female patients, with an average age of 49.8 years (range 45e59 years). All patients were followed up from 1 to 16 months (average, 12 months). Unilateral occlusion of the right VA occurred in 5 patients and of the left in 1. No patient had bilateral VA occlusions. Levels of cervical facet dislocations existed in C5/6 segment in 5 patients and C6/7 in 1. Of 6 patients with VA occlusion, 5 patients had bilateral facet dislocation and 1 patient had unilateral facet dislocation. VA occlusion was located in cephalic or dislocated vertebras (Figure 1). The length of VA occlusion was extended cephalad from 2 to 5 levels but had not reached C1. All 6 patients with VA occlusion had spinal cord injury (P < 0.05). There were 3 patients with ASIA A, 1 with B, and 2 with D. None of 6 patients with VA occlusion had radiographically detected brain trauma at injury. Regarding clinical manifestations related to vertebrobasilar ischemia, none of 6 patients with unilateral VA occlusion had symptoms, so no patient underwent systemic anticoagulation therapy. No neurologic impairment in terms of vertebrobasilar ischemia occurred during follow-up. Surgical anterior spinal fusion was performed in 5 patients. One patient was treated by posterior fusion because he had a chest injury and took a risk for tracheostomy after anterior surgical approach (case 6). Follow-up MRIs revealed VA recanalization in 5 patients. One patient had no chance of undergoing MRI because he was died of respiratory failure (case 6). The time course for VA recanalization was from 6 days after injury (case 2, Figure 2) to 4 months after operation (case 5, Figure 3). It was dependent on the length of VA occlusion, the shorter length of levels of VA occlusion, the
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Figure 1. Imaging studies of the illustrative case with 5/6 bilateral facet dislocation with left vertebral artery (VA) occlusion from C2 to C6 (case 6). (AeB) Three-dimensional computed tomography (CT) reconstruction (A) and sagittal CT (B) showing C5/6 bilateral facet dislocation (arrows). (C) T2 sagittal magnetic resonance imaging (MRI) showing spine
shorter time of recanalization (Table 1) (P < 0.05). No adverse consequence associated with restoration of blood flow, such as distal embolization, occurred during follow-up.
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trauma and spinal cord injury. (DeI) T2 axial MRI showing intact VA at C1 (D), but left VA occlusion at C2 (E), C3 (F), C4 (G), C5 (H), and C6 (I) (arrows). (JeK) CT angiography showing left VA occlusion (arrows). (L) Postoperative anteroposterior radiograph and lateral radiograph showing the reduction and fixation of posterior pedicle screws.
DISCUSSION VA injury secondary to cervical spine trauma includes thrombosis, arteriovenous fistula, intimal dissection, pseudoaneurysm, and
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Figure 2. Imaging studies of the illustrative case with 5/6 bilateral facet dislocation with right vertebral artery (VA) occlusion and recanalization for 6 days after injury (case 2). (AeB) Three-dimensional computed tomography (CT) reconstruction (A) and sagittal CT (B) showing C5/6 bilateral facet dislocation (arrows). (C) Postoperative lateral radiograph showing the reduction and fixation of anterior pedicle screw plate. (DeE) Postoperative axial CT images showing the placement of anterior pedicle screws at C5
occlusion.9 VA occlusion is considered the most common lesion.10,11 A pathomechanism of traumatic VA occlusion is: intimal disruption initially occurs, then secondary events such as thrombus formation may lead to clot occlusion of vessel lumen.11,12 The current study is the first report in which all the patients presented with VA occlusion after cervical facet dislocation with a long-term follow-up of VA recanalization in a single group. The incidence of VA occlusion after cervical facet dislocation was 20.7% in the current retrospective MRI study. In nonpenetrating cervical spine trauma, including fractures and/or
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and C6. (F) T2 sagittal magnetic resonance imaging (MRI) showing spine trauma and spinal cord injury. (GeJ) T2 axial MRI showing right VA occlusion at C3 (G) and C4 (H) but VA intact at C5 (I) and C6 (J) (arrows). (K) T2 sagittal MRI 6 days after injury. (LeO) T2 axial MRI showing right VA recanalization at C3 (L) and C4 (M), and blood flow of C5 (N) and C6 (O) (arrows). (P) T2 sagittal MRI 2 weeks after injury. (QeT) axial MRI showing blood flow of right VA at C3 (Q), C4 (R), C5 (S), and C6 (T) (arrows).
dislocations, the reported incidence of VA injury varies from different diagnostic methods. In the past, VA injury was thought to be infrequent because it was rarely symptomatic, but its incidence was reported to be 46%e75% when evaluated by angiography in a small sample case series study.6,11 It was found to occur at a lower rate, between 17.2% and 25.5%, in studies that use MRI and magnetic resonance angiography,4,7,10,12-14 which is comparable with that found in our results in cervical facet dislocation. Although the limitation of this retrospective study includes small sample cases, VA occlusion can be considered a common complication in approximately 20% of cervical facet dislocation.
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Figure 3. Magnetic resonance imaging (MRI) studies of the illustrative case with 5/6 bilateral facet dislocation with right vertebral artery (VA) occlusion and recanalization for 4 months after injury (case 5). (A) T2 sagittal MRI showing spine trauma and spinal cord injury. (BeD) T2 axial MRI showing right VA occlusion at C4 (B) and C5 (C), but VA intact at C6 (D) (arrows).
Diagnosis of VA occlusion should be made on the basis of cervical 4-vessel angiography, digital subtraction angiography, CT angiography, magnetic resonance angiography, and MRI.4,8,11,13,15-17 Angiography is the most definitive method for detecting VA injury, which was considered as the gold standard for diagnoses; however, it is an invasive technique with risk of complications and is risky in critically ill patients with unstable spines. CT angiography with more than 16-slice scanners has been shown to have sensitivity and specificity close to that of conventional angiography.1,18 Axial T2 MRI scans are very useful because they show an absence of flow when there is an occlusion and a high signal when there is an intraluminal clot. They also are more sensitive for identifying some of the sequelae of VA dissection, such as back lifting, cerebellar, and parieto-occipital infarction.14 Thus, the axial T2 sequence can be used to analyze both the fracture and the possibility of VA injury. Magnetic resonance angiography is less sensitive for detecting VA injury than angiography but may be performed during the magnetic resonance study, for it is not necessary to change the position of the patient. Angiography is reserved for cases in which MRI
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(E) T2 sagittal MRI at 1 week after operation. (FeJ) T2 axial MRI showing partial recanalization of right VA at C2 (F), C3 (G), C4 (H), and C5 (I), and blood flow of C6 (J) (arrows). (K) T2 sagittal MRI 4 months after operation. (LeP) T2 axial MRI showing recanalization of right VA at C2 (L), C3 (M), C4 (N), and C5 (O), and blood flow of C6 (P) (arrows).
is not diagnostic.14 Because it is always coincident with the positive results when magnetic resonance angiography was performed in patients with absent flow (signal void) in MRI, VA occlusion in the current retrospective study was diagnosed only based on a noninvasive MRI method. The clinical features of VA occlusion in cervical facet dislocation are somewhat similar to those reported in previous cervical spine trauma studies. For example, the most frequent site of the VA occlusion was C5eC6; VA occlusion was unilateral in major cases; VA occlusion was located in the injured or cephalic segment; most patients had no occlusion of the intracranial segment; and most patients with VA occlusion had traumatic spinal cord injury.11,12,14 Furthermore, the present series demonstrated that the length of VA occlusion was extended cephalad from 2 to 5 levels. There was no significant correlation between VA occlusion and severity of spinal cord injury in this study (P < 0.05) (Table 1). Cerebellar infarction has been reported in some conditions of VA occlusion.1,5 Unilateral VA occlusion rarely results in a neurologic deficit because of collateral supply through the contralateral VA and the posterior inferior cerebellar arteries,19
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Although approximately 15% of patients have hypoplasia of one VA, which emphasizes the fact that there may not always be sufficient collateral arterial supply in a patient with unilateral occlusion.6,20 A low frequency of bilateral VA occlusion with cervical spine trauma has been shown in published reports; however, the consequence of its vertebrobasilar ischemia can have a mortality rate from 75% to 86%,21 although a few cases of asymptomatic posttraumatic bilateral artery occlusion also have been reported.6,12-14,20,22 The artery lesion was unilateral in all cases in the present series. The length of VA occlusion was extended cephalad from 2 to 5 levels but did not reach to C1. Therefore, no patients had neurologic symptoms due to VA occlusion in the present series. The treatment of symptomatic VA occlusion has been reported for cases of distal embolism, including anticoagulation, catheter embolization ligation, surgical ligation, and surgical resection and grafting23-27; however, the protocol or strict criteria for treatment are still lacking. Asymptomatic VA occlusion need not be embolized or ligated because there is adequate collateral flow through the opposite artery, or it will be recanalized for restoration of blood flow. Recanalization of VA occlusion has been reported in a few case series, with an incidence ranging from 17% to 85%.12,28,29 In the present series, VA recanalization was observed in 5 of 6 patients (83%) within a 4-month follow-up, even with 1 case lost follow-up. Therefore, the restoration rate of blood flow may be underestimated because follow-ups with magnetic resonance angiography were not long enough (e.g., 1 month) in some patients in
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previous studies.28,29 It is reported that the restoration of blood flow is greater in compression injuries than in distraction injuries4; however, different results of distractive flexion injury-related cervical facet dislocation were observed in the present series. The mechanism of occlusion is unlikely to be subjected to relatively minor stretching in compressive or distractive injuries. The current study is the first report in which the time course for VA recanalization was from several days after injury to 4 months after operation. The short length of levels of VA occlusion can be restored within a short period. There are several limitations to this study. First, it was retrospective. Second, although eligible cases are hard to amass, the small sample size (only 6 patients) is certainly a major limitation. Third, VA occlusion and recanalization in the current study were diagnosed in noninvasive MRI; however, MRI was not found to be more sensitive than angiography, CT angiography, or magnetic resonance angiography because of the retrospective study. Finally, this study reflected the experience at a single specialized spinal injuries center with a bias epidemiologic feather. In summary, the incidence of VA occlusion after cervical facet dislocation was 20.7%, which is comparable with nonpenetrating cervical spine injuries. VA occlusion rarely was symptomatic because of sufficient collateral blood supply. VA recanalization was observed in more than 80% patients and occurred mainly within the first 4 months after injury. The time course of VA recanalization was dependent on the length of VA occlusion.
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13. Parbhoo AH, Govender S, Corr P. Vertebral artery injury in cervical spine trauma. Injury. 2001;32: 565-568. 14. Veras LM, Pedraza-Gutiérrez S, Castellanos J, Capellades J, Casamitjana J, Rovira-Cañellas A. Vertebral artery occlusion after acute cervical spine trauma. Spine. 2000;25:1171-1177. 15. Gambee MJ. Vertebral artery thrombosis after spinal injury: case report. Paraplegia. 1986;24: 350-357. 16. Golueke P, Sclafani S, Phillips T, Goldstein A, Scalea T, Duncan A. Vertebral artery injury—diagnosis and management. J Trauma. 1987;27:856-865. 17. Raskind R, North CM. Vertebral artery injuries following chiropractic cervical spine manipulation. Case reports. Angiology. 1990;41:445-452. 18. Bromberg WJ, Collier BC, Diebel LN, Dwyer KM, Holevar MR, Jacobs DG, et al. Blunt cerebrovascular injury practice management guidelines: the eastern association for the surgery of trauma. J Trauma. 2010;68:471-477. 19. Hartkamp MJ, van Der Grond J, van Everdingen KJ, Hillen B, Mali WP. Circle of Willis collateral flow investigated by magnetic resonance angiography. Stroke. 1999;30:2671-2678. 20. Weller SJ, Rossitch E, Malek AM. Detection of vertebral artery injury after cervical spine trauma
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using magnetic resonance angiography. J Trauma. 1999;46:660-666. 21. Becker KJ, Monsein LH, Ulatowski J, Mirski M, Williams M, Hanley DF. Intraarterial thrombolysis in vertebrobasilar occlusion. AJNR Am J Neuroradiol. 1996;17:255-262. 22. Rodriguez M, Tyberghien A, Matge G. Asymptomatic vertebral artery injury after acute cervical spine trauma. Acta Neurochir (Wien). 2001;143:939-945. 23. Cothren CC, Moore EE, Biffl WL, Ciesla DJ, Ray CE Jr, Johnson JL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg. 2004;139:540-545 [discussion: 545-546]. 24. Hoshino Y, Kurokawa T, Nakamura K, Seichi A, Mamada T, Saita K, et al. A report on the safety of
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unilateral vertebral artery ligation during cervical spine surgery. Spine. 1996;21:1454-1457. 25. Schwarz N, Buchinger W, Gaudernak T, Russe F, Zechner W. Injuries to the cervical spine causing vertebral artery trauma: case reports. J Trauma. 1991;31:127-133. 26. Alexander JJ, Glagov S, Zarins CK. Repair of a vertebral artery dissection. J Neurosurg. 1986;64: 662-666. 27. Shintani A, Zervas NT. Consequence of ligation of the vertebral artery. J Neurosurg. 1972;36:447-450.
29. Quint DJ, Spickler EM. Magnetic resonance demonstration of vertebral artery dissection. Report of two cases. J Neurosurg. 1990;72: 964-967. Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Received 3 July 2016; accepted 1 August 2016 Citation: World Neurosurg. (2016) 95:190-196. http://dx.doi.org/10.1016/j.wneu.2016.08.002 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com
28. Deen HG Jr, McGirr SJ. Vertebral artery injury associated with cervical spine fracture. Spine. 1992; 17:230-234.
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