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The incidence of blunt cerebrovascular injury (BCVI) varies depending on the criteria used and the sensitivity of the diagnostic test applied. Those using catheter angiography with fairly liberal criteria such as Biffl et al.1 described an alarming incidence of 1.07% for blunt carotid injuries and 0.53% for blunt vertebral artery injuries (BVI) amongst patients admitted with blunt trauma (those at risk) in the prospective arm of their 9-year study. Two other large series have, similarly, recorded rates above 1%. Bilateral lesions have been reported in up to 43%2. Up to 60% of asymptomatic patients with skull base fracture have shown BCI on angiography according to Kerwin et al3. Closed head injury, facial fracture, spinal (especially cervical spine) fracture and thoracic injury are also commonly associated. 53% of patients with cervical spine injuries identified on screening with CT angiography demonstrated BCVI, mainly of the vertebral arteries4.
A review of the literature5 done in 2002 showed a combined moderate and severe permanent neurologic deficit approximating 25% to 40% in survivors. Mortality varies from 15 – 40%5. Patients with an ipsilateral ischemic deficit on CT brain suffered a mortality of 47%, while mortality was 0% in those with a normal CT scan6. Death directly related to BCVI was documented in 8.3% (2/24) patients in a recent series of 2023 patients7. Recurrence rates for dissection and more importantly stroke have been reported between 1-4% over 2-5 years8,9. There is typically a latent period between the time of injury and the onset of symptoms. In the series at Denver Health Medical Centre, 44% of patients first had signs or symptoms 18 or more hours after the time of injury.
Further, 27% of asymptomatic patients had demonstrated BCVI and 20% of those with BCVI had none of the high-risk criteria1. Another study10 from Leipzig, Germany has shown delayed strokes after months to years of the traumatic event.
Until recently, these were occult injuries found mostly when patients had strokes. Yet since such patients usually had traumatic brain injuries (TBI) as well, it was seldom clear whether the TBI or blunt cerebrovascular injury was the cause. There is as yet no consensus in the literature on the value of screening. Patients who are diagnosed and treated while asymptomatic, have lower stroke rates and better neurologic outcomes according to Biffl et al.11 in 2006. Following are the Modified Denver Screening Criteria for BCVI12. If any of one or more of these criteria are present in a patient presenting with blunt injury, further investigation with a CT angiogram is recommended:
Adapted from Biffl et al.1
Using the above criteria for both symptomatic and asymptomatic patients Kerwin et al3 found a 44% positive angiography rate in 1941 patients. Back in 1996, the group from Memphis13, has reported a drop in BCI-associated mortality from 24% to 13% after instituting a broad screening protocol.
Current data does not support its role as a screening tool mainly because most injuries are close to the skull base and inaccessible as are the vertebral arteries. Indirect signs of turbulent flow disturbances obtained more caudal are unreliable when stenoses are <60%14. It does, however, have a role in follow up of lesions.
CT has the logistical advantage of patients already undergoing trauma imaging of other regions. Two studies in 1997 & 200014,15 have reported a sensitivity of 90-100% and specificity of 100% for CT in the diagnosis of BCVI. A recent prospective study11 on 331 patients screened (12% of 2,727 consecutive patients) demonstrated 5.4% positive results on 16-slice CTA. This accounted for 0.66% of all blunt-trauma admissions. Moreover, none of the patients with absent BCVI on CT developed neurological deficits11,7. There was a 1.2% false-positive rate on CTA. Subsequently, Eastman et al12, reported 146 patients who received both CTA and catheter angiography with 97.7% sensitivity, 100% specificity, 100% PPV and 99.3% negative predictive value.
Magnetic resonance imaging has the definite advantage of early recognition of reversible cerebral ischaemia, which is very important in BCVI. However, inaccessibility in the acute trauma situation due to incompatibility of devices and life supporting equipment remains a problem. No studies have as yet compared CTA and MRA directly. Comparing MRA with catheter angiography, Biffl et al16 reported a sensitivity of 75% and specificity of 67% in 16 patients. Corresponding positive predictive and negative predictive values were 43% and 89% respectively. Miller et al17 came out with even lower figures for 21 patients. False aneurysms are known to be missed due to turbulent flow. There clearly need to be further prospective studies in this direction. The role of MRI/MRA thus remains supportive rather than conclusive for this condition.
Digital Subtraction Angiography (DSA)
Still accepted as the gold standard in the diagnosis of BCVI. The complication rate of 2% still remains a concern18.
Luminal irregularity or dissection with < 25% stenosis
3% stroke rate
7% risk of progression
Dissections with > 25% luminal narrowing or a raised intimal flap
70% risk of progression
tend to persist
44% stroke rate
Transection of the carotid artery, with free extravasation of contrast or significant AV fistula
There are currently no published quality guidelines for the diagnosis and screening of traumatic vascular injury to the head and neck.
The aim of early treatment is to prevent development of a neurological deficit or prevent the progression of an existing one. There are two possible mechanisms for this: either haemodynamically important occlusion, or the formation of small thrombi, which subsequently embolize to the cerebral circulation. Embolic events are likely to be the more significant of the two. Treatment options include:
Anticoagulation – There have been no randomised trials to advocate treatment with anticoagulation and all recommendations are based on level III evidence. Some studies have shown that the cerebrovascular complications that accompany these injuries are often preventable with simple anticoagulation. Two studies of small groups of patients have shown benefits of anticoagulation, although the risks of hemorrhagic complications remains a concern. Treatment with Aspirin and/or other antiplatelet regimens is equally contentious. So far, no prospective studies have been conducted comparing antiplatelet regimen with Heparin. A larger series reported only 1 of 18 patients with Grade II lesions (dissections with > 25% luminal narrowing or a raised intimal flap) developing a stroke in spite of angiographic progression in 70%.
Stenting +/- thrombolysis – Endovascular stenting has evolved into an attractive alternative to surgery with lower risks than surgery in patients where anticoagulation is contraindicated.
Surgery – reports in the literature have not been very encouraging. A recent series on 50 spontaneous and traumatic carotid dissections (treated 9 months after injury) reported a 90% success but 20% early postoperative failure and 58% cranial nerve damage.
Following are the recommendations of the American Heart Association/American Stroke Association Council on Stroke published in 2006 for the treatment of BCVI:
For patients with ischemic stroke or TIA and extracranial arterial dissection, use of warfarin for 3 to 6 months or use of antiplatelet agents is reasonable (Class Iia, Level of Evidence B). Beyond 3 to 6 months, long-term antiplatelet therapy is reasonable for most stroke or TIA patients. Anticoagulant therapy beyond 3 to 6 months may be considered among patients with recurrent ischemic events (Class Iib, Level of Evidence C).
For patients who have definite recurrent ischemic events despite adequate antithrombotic therapy, endovascular therapy (stenting) may be considered (Class IIb, Level of Evidence C). Patients who fail or are not candidates for endovascular therapy may be considered for surgical treatment (Class IIb, Level of Evidence C).
Biffl WL, Moore EE, Offner PJ et al. Blunt carotid arterial injuries: implications of a new grading scale. J. Trauma 1999; 47: 845–53.
Davis JW, Holbrook TL, Hoyt DB et al. Blunt carotid artery dissection: incidence, associated injuries, screening, and treatment. J. Trauma1990; 30: 1514–17.
Kerwin AJ, Bynoe RP, Murray J et al. Liberalized screening for blunt carotid and vertebral artery injuries is justified. J. Trauma 2001; 51: 308–14.
Screening test for clinically significant blunt cerebrovascular injuries. J Trauma 2006;60:745-752
Nunnink L. Blunt carotid artery injury. Emergency Medicine (2002) 14, 412–421
Cogbill TH, Moore EE, Meissner M et al. The spectrum of injury to the carotid artery: a multicenter perspective. J. Trauma 1994; 37: 473–9.
Berne JD, Reuland KS, Villarreal DH, et al. Sixteen-Slice Multi-Detector Computed Tomographic Angiography Improves the Accuracy of Screening for Blunt Cerebrovascular Injury. J Trauma 2006; 60: 1204–1210
Bassetti C, Carruzzo A, Sturzenegger M, Tuncdogan E. Recurrence of cervical artery dissection: a prospective study of 81 patients. Stroke 1996;27:1804-1807
Touze E, Gauvrit JY, Moulin T, et al. for the Multicenter Survey on Natural History of Cervical Artery Dissection. Risk of stroke and recurrent dissection after a cervical artery dissection: a multicenter study. Neurology. 2003;61:1347-1351.
Scheid R, Zimmer C, Schroeter ML, et al. The clinical spectrum of blunt cerebrovascular injury. The Neurologist 2006; 12: 255–262.
Biffl WL, Egglin T, et al. Sixteen-slice computed tomographic angiography is a reliable noninvasive screening test for clinically significant blunt cerebrovascular injuries. J Trauma 2006;60:745-752
Eastman AL, Chason DP. Perez CL, et al. Computed Tomographic Angiography for the Diagnosis of Blunt Cervical Vascular Injury: Is It Ready for Primetime? J Trauma 2006; 60: 925-929
Fabian TC, Patton JH, Croce MA et al. Blunt carotid injury: importance of early diagnosis and anticoagulant therapy. Ann. Surg.1996; 223: 513–25.
Biffl WL. Diagnosis of blunt cerebrovascular injuries. Curr Opin Crit Care 2003; 9:530–534.
LeBlang SD, Nunez DB Jr, Rivas LA, et al. Helical computed tomography angiography in penetrating neck trauma. Emerg Radiol 1997, 4:200–206.
Biffl WL, Ray CE Jr., Moore EE, et al. Noninvasive diagnosis of blunt cerebrovascular injuries: A preliminary report. J Trauma 2002;53:850–856.
Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries: Analysis of diagnostic modalities and outcomes. Ann Surg. 2002;236:386–395.
Willinsky RA, Taylor SM, terBrugge K, et al. Neurologic complications of cerebral angiography: prospective analysis of 2,899 procedures and review of the literature. Radiology. 2003; 227: 522–528.
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