Blunt carotid and vertebral artery injuries

Injury, Int. J. Care Injured (2008) 39, 1232—1241

www.elsevier.com/locate/injury

Blunt carotid and vertebral artery injuries Zachary M. Arthurs a,*, Benjamin W. Starnes b a

Department of Surgery, Madigan Army Medical Center, Fitzsimmons Drive, Building 9040, Tacoma, WA 98431, United States b Chief, Division of Vascular Surgery, University of Washington, Seattle, WA, United States Accepted 15 February 2008

KEYWORDS Vascular; Carotid; Vertebral; Trauma; Stoke; Management; Endovascular

Summary The recognition and treatment of blunt cerebrovascular injuries has dramatically evolved over the past two decades. As imaging technology has improved both with respect to the image quality and acquisition times, its use has become a fundamental diagnostic tool in blunt trauma evaluation. The single greatest radiological advance in the past quarter century has been the refinement and increasing use of computed tomographic imaging for the diagnosis of surgical disease. Paralleling advances in noninvasive imaging, a heightened awareness of blunt cerebrovascular injuries has emerged, and the first screening protocols were developed at high volume trauma centres. Through aggressive screening, these injuries have increasingly been recognised before devastating neurological ischaemia and adverse neurocognitive outcomes. The mainstay of treatment for these injuries is antithrombotic therapy. However, all blunt cerebrovascular injuries require short and long-term follow-up. While the majority of injuries will resolve with medical management, a proportion will require further intervention in order to reduce the risk of subsequent stroke. # 2008 Elsevier Ltd. All rights reserved.

Introduction Blunt cerebrovascular injuries (BCVI) have been sporadically described since 1967 through a number of case series.55 Early case reports described patients with recognised symptoms of cerebral ischaemia, and nearly all were symptomatic at the time of the diagnosis. Presenting symptoms define the laterality of the cerebrovascular injury and isolate it to the respective extracranial arterial * Corresponding author. Tel.: +1 253 968 2200; fax: +1 253 968 0232. E-mail address: [email protected] (Z.M. Arthurs).

supply. Carotid injuries typically present with a contralateral sensory or motor deficit, and vertebral injuries present with ataxia, vertigo, emesis, and possible visual field deficits. A carotid-cavernous fistula may present with orbital pain, proptosis, hyperaemia, cerebral swelling, or seizure. The degree of symptoms is a variable depending on whether the vessel is occluded or whether the resultant injury acts as a nidus for subsequent embolic events. Patients typically have coexisting traumatic brain injuries that may mask signs and symptoms of BCVI. Three basic mechanisms of injury for BCVI are encountered: (1) extreme hyperextension and rota-

0020–1383/$ — see front matter # 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.injury.2008.02.042

Blunt carotid and vertebral artery injuries tion, (2) a direct blow to the vessel, and (3) vessel laceration by adjacent bone fractures.21 The most common mechanism causing blunt carotid injury results from hyperextension of the carotid vessels over the lateral articular processes of C1—3 at the base of the skull. There are also scattered case reports of chiropractic manipulation34 and rapid head turning with exercise causing BCVI.53 A direct blow to the artery typically occurs with a misplaced seatbelt across the neck during a motor vehicle crash or in the setting of hanging. This injury pattern typically occurs in the proximal internal carotid artery as opposed to the distal aspect. Injury to the carotid vessels can occur basilar skull fractures involving the petrous or sphenoid portions of the carotid canal. The most common accepted mechanism for vertebral artery injury is injury secondary to fractures of the transverse foramen through which the vessel courses (cervical vertebrae 2—6).19 In addition, the vertebral vessels are relatively fixed throughout the vertebral canal making it susceptible to hyperextension and stretch injuries. Depending on the nature of the injury, the traumatic event may cause intimal disruption, thrombosis, or rarely transection. Even though the patient may have a small intimal flap at the time of injury, the injury may progress to dissection, near-occlusion, or occlusion. All stages of injury are a nidus for platelet aggregation and a possible embolic source to the cerebral circulation. Since 1990, there have been two major advances that have altered the care of patients with BCVI: (1) the implementation of standardised screening protocols allowing diagnosis of BCVI prior to the development of neurological ischaemia, and (2) the recognition that antithrombotic therapy essentially eliminates the ischaemic events in asymptomatic patients. The vast majority of BCVI occur at the base of the skull, within the carotid canal, or within the vertebral canal. Traditional operative repair of these injuries is technically demanding, and if the lesion extends into the base of the skull, technically feasible but not without high surgical morbidity. Antithrombotic therapy has been recommended in the form of early heparinisation; however, many of these patients have coexisting traumatic brain injuries negating the use of heparin. Early anticoagulation has been shown to reduce the incidence of neurological events associated with BCVI, and it appears to impact BCVI related mortality as well. The ensuing review will address the following aspects of BCVI: screening, diagnostic imaging modalities, treatment, outcomes and follow-up.

1233

Screening for blunt cerebrovascular injury (BCVI) The overall incidence of BCVI has been universally reported as <1% of all trauma admissions for blunt trauma, but this relatively small population of patients has a stroke rate ranging from 25 to 58% and mortality rates of 31—59%.3,9,31 The variability in incidence of BCVI is 0.19—0.67% for unscreened populations as compared to 0.6—1.07% for screened populations.9 Common mechanisms of injury associated with BCVI include motor vehicle crash (41— 70%), direct cervical blow (10—20%), automobile versus pedestrian (12—18%), fall from height (5— 15%), and hanging (5%).3,9 Most common associated injuries include closed head injuries (50—65%), facial fractures (60%), and thoracic injuries (40— 51%).3,9 Nearly half of all patients will have cervical spine fractures at the time of diagnosis. Patients may present to the trauma centre with obvious signs of BCVI; however, significant proportions of patients are initially asymptomatic and subsequently develop symptoms after a latent period. The time from initial injury to the development of symptoms is variable, but several series have reported times from 1 h after injury to several weeks after injury.10,15,22,46 Prior to the initiation of screening protocols, Berne et al. found a median time to diagnosis of 12.5 h for survivors of BCVI and 19.5 h for nonsurvivors suggesting a sufficient window of opportunity for diagnosis and treatment.3 Neither admission GCS nor baseline neurological examination correlated with subsequent development of symptoms. Because a large number of these patients are asymptomatic on arrival to the trauma centre, initial markers are needed to identify patients at greatest risk of injury. In an attempt to identify patients in the asymptomatic latent period, screening protocols were first suggested in the early 1990s. While there is not consensus on the ideal screening protocol, several authors have found associations with signs, symptoms, and risk factors identified on admission. The first and most comprehensive screening protocol was initiated at the Denver Health Medical Center. These ‘‘Denver Criteria’’ are listed in Table 1.9,18 With this screening protocol, the authors reported an overall BCVI incidence of 0.86%. Exactly 4.8% of all trauma patients were screened based on defined risk criteria, and 18% of screened patients were found to have an injury. Fifty-two percent of these screened patients were asymptomatic. Neurological morbidity was 16%, and BCVI associated mortality was 15%.9 Using the Memphis criteria (Table 1), they found an incidence of 1.03%, 3.5% of all blunt trauma patients

1234

Z.M. Arthurs, B.W. Starnes

Table 1 Screening criteria for BCVI Denver criteria 9

Memphis criteria 41

Signs/symptoms Arterial hemorrhage or expanding hematoma

Cervical spine fracture Neurological exam not explained by brain imaging Horner’s syndrome LeForte II or III fracture pattern Basilar skull fracture with involvement of the carotid canal Neck soft tissue injury (seatbelt sign or hanging or hematoma)

Cervical bruit Focal neurological deficit Neurological exam inconsistent with head CT findings Stroke on follow-up head CT Risk factors LeForte II or III fracture pattern Cervical spine fracture Basilar skull fracture with involvement of the carotid canal Diffuse axonal injury with GCS < 6 Near hanging with anoxic brain injury

BCVI — blunt cerebrovascular injury, CT — computed tomography scan, GCS — Glascow coma scale.

were screened, and 29% of screened patients were found to have an injury.41 Both screening regimens, mandated four-vessel cerebral angiography if the patient met at least one of the screening criteria. Some authors have suggested a more restricted screening protocol in an effort to limit the number of negative examinations. Rozycki et al. prospectively screened only patients who had a cervical seatbelt sign.9 Their group screened 81 patients for BCVI, and found 4 injuries; however, 2 of the 4 patients died with resultant 50% mortality. Their reported 5% screening yield with a restricted screening protocol is much lower than more conservative series, but this reasoning is largely flawed with Type II error. DiPerna et al. also evaluated the importance of a ‘‘seat-belt sign’’ across the neck and found only 1 patient in a series of 131 patients to have a carotid injury.24 It is important to note that they did not use angiography on all patients and relied on duplex ultrasound for all of their examinations. Even so, relying on just physical signs of blunt injury to the neck fails to identify the majority of occult injuries. The utility of aggressive screening has been questioned altogether. Mayberry et al. reviewed a 10year experience and found 17 patients with BCVI.37 Their screening threshold included patients with focal neurological signs and neurological deficits not explained by head CT. Eleven patients developed a stroke and nine patients developed neurological symptoms within two hours of admission. Of the two delayed strokes, only one of the patients would have been identified with a more liberal screening protocol. The study questioned the impact of broad screening on BCVI outcomes. The major limitation of this analysis is that the total

number of occult injuries and their resultant outcomes in their population are unknown; therefore, the cost of a missed injury cannot be determined. All major trauma centres should have predetermined screening criteria for blunt cerebrovascular injury. Using the Denver criteria, an institution can expect a screening yield of 18%, and using the Memphis criteria, a screening yield of 29% can be obtained. Limiting screening criteria further is likely to miss occult injuries with an increased risk of morbidity.

Diagnostic modalities Selective digital subtraction angiography (DSA) was the initial diagnostic gold standard for screening patients with suspected BCVI. The Denver group designed an angiographic grading system for BCVI (Table 2).8 Most importantly, the grading scale held prognostic value for patients’ future risk of stroke. The stroke risk and mortality (%/%) for each grade are the following: Grade I (3%/11%), Grade II (11%/ 11%), Grade III (33%/11%), Grade IV (44%/22%), and Table 2

BCVI Grading Scale

8

Injury grade

Angiographic findings

I

Lumenal irregularity or a dissection/ intramural hematoma with <25% luminal narrowing Dissection or intramural hematoma of 25% of the lumen Pseudoaneurysm Vessel occlusion Vessel transection

II III IV V

Blunt carotid and vertebral artery injuries Grade V(100%/100%).8 The stroke risk reported pertains mainly to blunt carotid injuries; the grade of vertebral artery injuries does not correlate with increasing risk of stroke. The stroke risk of blunt vertebral arteries is 20% irrespective of grade.7 The Denver grading scale has become the standard for reporting BCVI. There are several limitations of DSA that make it a difficult diagnostic tool. First and foremost, it is an invasive procedure with technical limitations, and a complication profile that carries a small but real risk of stroke.9 Performing screening DSA on all patients at risk for BCVI may impose a large economic and workload burden on the interventional radiology suite; some institutions cannot support this type of demand. Early on, patients at high risk for BCVI were also at risk for blunt thoracic aorta injuries; therefore, patients would undergo both arch aortography as well as four-vessel cerebral angiography. Alternative diagnostic modalities have been evaluated. Duplex scanning has been compared against cerebral angiography at a cost savings of $1200/ patient examined.32 Fry et al. compared duplex scanning to angiography for a pilot study of 15 patients finding acceptable accuracy, and then proceeded to screen patients with duplex ultrasound. In the evaluation of carotid artery stenosis, duplex ultrasound is limited when evaluating lesions <60% stenosis; likewise, duplex will not often identify small intimal tears or non-occlusive dissections. It is often difficult to obtain adequate visualisation of the internal carotid artery at the base of the skull where the majority of these injuries occur, and duplex evaluation of the vertebral vessels is extremely limited. In addition, the study is techniciandependent which may make the test not readily available as part of the trauma evaluation. Magnetic resonance angiography (MRA) is an attractive noninvasive modality because of the resolution of images obtained in this anatomic region, the infinite number of projections of the vessel, and the ability to assess the intracranial architecture for signs of stroke.12,13 Limitations include availability and the time required for image acquisition. This modality is thus impractical in a trauma patient with multiple competing injuries. Adequately screening trauma patients for pacemakers or aneurysm clips prior to MRA scanning poses a challenge to this modality as well as the use of metallic orthopaedic traction devices in trauma patients. Helical computed tomographic angiography (CTA) offers several potential advantages over conventional DSA. It is a noninvasive study that can be obtained in less than 5 min, and as opposed to cerebral angiography, CTA obtains 3-dimensional images of the vessel wall. In addition, the work-up of blunt

1235 trauma patients will inevitably involve CT imaging of the head, chest, abdomen, or all the above; therefore, CTA of the carotid-vertebral circulation can easily be obtained during this examination sacrificing little in time (60 s/scan), contrast burden (approximately 100 cm3), or radiation exposure. Multi-detector CTA with 3-dimensional mulitplanar reformation has been found to have a sensitivity of 95% and specificity of 93% for detecting carotid artery stenosis >50% compared to digital subtraction cerebral angiography, but CTA does slightly underestimate the degree of stenosis.2 Several observational and retrospective studies have found CTA adequate for detecting BCVI,44,49 but only two prospective studies (performed by the Denver and Memphis groups) have compared CTA and MRA to conventional angiography for the evaluation of BCVI.11,41 Using DSA as the ‘‘gold standard,’’ CTA was found to have a sensitivity of 47— 68% and specificity of 67—99%. CTA missed 55% of Grade I, 14% of Grade II, and 13% of Grade III injuries.11,41 MRA had a sensitivity of 50—75% and specificity of 67—100%.11,41 Both study groups concluded that CTA and MRA while appealing should only be used for diagnosing BCVI when angiography was not available. It is important to note the CT scanners used in this study were single slice scanners. In addition, these results could represent the early experience with CTA to include initial limitations with timing contrast injection, image acquisition protocols, post-image processing delays (reformatting process), and inexperience with interpretation. All of these factors may have accounted for the poor accuracy of CTA in these two studies. In 2004, Berne et al. used CTA as a diagnostic modality in 486 patients and identified 25 BCVIs.4 Secondary to the constraints of using cerebral angiography in a busy trauma centre, the authors only obtained confirmatory DSA on patients with abnormal CTA. Negative CTAs, previously reported by Denver and Memphis to have a high rate of missed Grade I—III injuries, were only followed with clinical evaluation, and no patient developed documented neurological ischaemia. Their results were questioned because simultaneous DSA was not obtained to ensure that negative CTAs were true negatives. The authors suggested that improved CTA technology (4-slice scanners) may be approaching the accuracy of traditional DSA. During the same year, Bub et al. directly compared multidetector CTA (4- and 8slice scanners) to DSA and found a sensitivity of 83— 92% and specificity of 88—98% from three different radiologists.14 The interobserver reliability was also higher for CTA than DSA. For all three radiologists, the sensitivity and specificity for detecting verteb-

1236 ral injuries was lower at 40—60% and 90—97%, respectively.14 These results refuted the early experience by both the Denver and Memphis groups when CT scanners and their interpretation were not near the quality available in 2005. In 2003, 16-slice CTscanners became readily available throughout the United States and with the improvement in image quality and experience of interrupting axial imaging, trauma surgeons began to meet resistance when trying to justify DSA for screening BCVI. While the only prospective experience in both Denver and Memphis showed CTA to be inferior to DSA, the radiology community considered the new generation CTA images equivalent to DSA. In 2005, Biffl et al. reported their experience using 16-slice CTA for the diagnosis of BCVIs, and contrary to the prior study in Denver disqualifying early generation CT scanners, DSA was not used as the ‘‘gold standard’’.6 Similar to Berne’s experience in 2004, Biffl was not able to perform a prospective comparative study. Over an 11-month period, 331 patients were screened, and 5.4% were diagnosed with BCVI. In this final study, negative CTA scans were followed with clinical observation, and no patients developed neurological symptoms consistent with delayed presentation of missed BCVI. All positive examinations were confirmed with DSA. Of the 18 injuries identified by CTA, 17 were correctly graded whereas one patient was upstaged to a Grade III on DSA (a small pseudoaneurysm was not identified on CTA, false-positive rate = 1.2%).6 Nine patients received antithrombotic therapy, and nine patients received no treatment. None of the patients experienced an ischaemic insult. Concern still persists regarding CTA’s accuracy as a screening modality. No prospective data are available comparing 16-slice CTA to DSA. With the current data available, it seems the false-negative rate, albeit unknown, has very little clinical impact. Until data is available verifying the accuracy of CTA, patients with a very high-suspicion of injury and found to have a negative CTA should be considered for DSA.

Treatment While operative intervention has been shown to reduce the mortality and stroke rate associated with these lesions,48 the majority of these lesions have limited embolic potential with early antithrombotic therapy.31 The results of recent series addressing treatment for BCVI are summarised in Table 3. Fabian et al. reported the first large series demonstrating improved neurological outcome associated with early use of antithrombotic therapy.31 Their analysis revealed the benefit of heparin therapy for

Z.M. Arthurs, B.W. Starnes decreasing the rate of neurological deterioration after symptoms developed and decreasing the rate of new neurological events. Heparin therapy was associated with a dramatic reduction in neurological morbidity and mortality as compared to previously reported rates as high as 58 and 31%, respectively. Additionally, in the 15 patients who presented with bilateral dissections, no patient on heparin therapy developed progression of symptoms. Biffl et al. confirmed that patients benefited from early anticoagulation documenting the greatest benefit to patients who were asymptomatic at the time of heparinisation.9 In the asymptomatic group, only one patient developed subsequent stroke. Analysing the symptomatic cohort, 93% of patients had improvement in their neurological deficits with anticoagulation as compared to only 67% without anticoagulation. After this landmark study, anticoagulation became the first line of treatment for BCVI. Complications associated with anticoagulation range from 25 to 54% in the trauma population.9 Most concerning are intracranial haemorrhage, but more common are gastrointestinal bleeds, retroperitoneal haemorrhage, blunt solid organ injury with hemorrhage, or re-bleeding from surgical wounds. Eachempati et al. noted few patients were able to receive heparin therapy at the time of BCVI diagnosis (14%), and they found a complication rate of 16% among those who received heparin therapy.27 Because of the complication profile of full anticoagulation therapy, several authors have focused on anti-platelet therapy as an alternative to traditional anticoagulation. In 2000, Biffl et al. examined isolated blunt vertebral artery injuries and noted the posterior circulation stroke rate to be 24%. Mortality was only 8% in that population. In addition, stroke evolution was independent of injury grade; however, heparin therapy reduced neurological events in the posterior circulation.7 Miller et al. also found that among heparin treated patients with BCVI only 6% of blunt carotid artery injuries and none of the blunt vertebral artery injuries developed a stroke.40 The apparent efficacy of heparin was similar to patients treated with aspirin (Table 3). One year later, Miller et al. reported a follow-up study in which aspirin therapy was increasingly used.41 Of 21 blunt carotid injuries in that study, 9 received aspirin with or without clopidogrel and 10 received heparin therapy. One patient in each group developed a stroke. Anti-platelet therapy was the dominant therapy for vertebral artery injuries. Of the 43 vertebral artery injuries, 32 received aspirin/clopidogrel, and only 8 patients received heparin therapy. None of the patients developed a stroke.

Blunt carotid and vertebral artery injuries

1237

Table 3 Literature review of treatment outcomes for bcvi utilizing heparin, anti-plateleta agents, and observation without antithrombotic therapy Author

Year

Inc. (%)

Fabian 31

1996

0.67

Biff 9

1998

Miller40

n

Sx (%)

Treatment

Neurological morbidity

All-cause mortality (%)

67

86

None Heparin

25% 75%

None Heparin

73% 29%

31

0.86

37

48

None Heparin

27% 73%

None Heparin

25% 25%

15

2001

0.5

96

34

None Anti-PLT Heparin

17% 21% 60%

None Anti-PLT Heparin

65% 10% 9%

13

Miller41

2002

1.03

63

None Anti-PLT Heparin

9% 63% 28%

None Anti-PLT Heparin

— 3% 5%

25

Wahl 54

2001

0.45

22

—

None Anti-PLT Heparin

36% 32% 32%

None Anti-PLT Heparin

—b — —

—

Edward 28

2007

0.35

111

18

None Anti-PLT Heparin Both

13% 38% 44% 5%

None Anti-PLT Heparin Both

0% 5% 8% 0%

6c

BCVI — blunt cerebrovascular injury, Inc. — incidence, n — number of patients, Sx — percentage of patients who were symptomatic at time of diagnosis. a Anti-platelet agents included aspirin, clopidogrel, and ticlopidine. b Stroke rate was not recorded. Authors documented no difference in neurological outcome among groups by a neurological assessment score. c BCVI-related mortality only; prior mortality rates are all-cause mortality.

Wahl et al. reported 22 patients with BCVI, and 8 of the 22 had contraindications to anticoagulation (head injuries, blunt aortic injury, and recent surgical wounds).54 Seven patients were anticoagulated with heparin and four patients experienced major bleeding complications requiring transfusion. Seven patients were treated with aspirin alone, and there were no identifiable differences in neurological outcomes (measured by neurological assessment score) compared to anticoagulation.54 The primary treatment for acute non-occlusive dissections of the carotid artery should be anticoagulation therapy. However when anticoagulation is not feasible, the patient develops a pseudoaneurysm, or the patient develops a chronic dissection, endoluminal treatment with either a bare or covered stent is an alternative to open repair.1,16 Balloon expandable and self-expanding stents have been used in this location, and in all cases, apposition of the dissection to the wall was achieved with no neurological events reported.1,35 Bejjani et al. treated four acute symptomatic carotid dissections with endovascular bare stents, and all patients had improvement in their neurological examination.1 The failure of pseudoaneurysms to resolve has been reported by other authors,42 and Fabian et al. noted that 29% of acute non-occlusive dissections

treated with anticoagulation developed pseudoaneurysms on follow-up arteriography.31 Of the 6 initial pseudoaneurysms in that series, none resolved and one patient developed complete occlusion. Once a pseudoaneurysm or chronic non-occlusive dissection has developed, it is unlikely to resolve spontaneously with continued anticoagulation therapy. These lesions have a very low risk of rupture, but they tend to be the source of embolic events or thrombosis.26,47 The natural history of traumatic pseudoaneurysms without antithrombotic therapy is for them to have a high association of subsequent neurological sequelae. El-Sabrout reported 43% of patients presented with ischaemic symptoms prior to operative repair,29 and Moreau et al. reported 74% of patients presented with ischaemic symptoms prompting surgical repair.43 Because of the potential for embolic stroke, it is foreseeable that modern antithrombotic therapy or exclusion of the pseudoaneurysm could reduce the risk of stroke. In fact, Fabian et al. initial report of anticoagulation had a remarkable impact on ischaemic events secondary to pseudoaneurysms, but none of the aneurysms decreased in size and there was a tendency for lesions to enlarge.31 Therefore, exclusion of the pseudoanuerysms has been reserved for lesions that

1238 fail to resolve, enlarge, or result in ischaemic complications. Schievink et al. addressed blunt carotid pseudeoaneurysms with operative repair in 22 patients.51 In order to exclude the lesions, 5 patients required carotid ligation, 13 underwent resection with reconstruction, and 4 required cervical to intracranial carotid bypass. In their series, two patients experienced ischaemic stroke, and the most common complications were cranial nerve neuropraxia secondary to high surgical exposure. Because of the location in the distal third of the internal carotid artery, endovascular approaches offer a less invasive alternative to open repair. Self-expanding covered stents can be safely delivered to these locations with limited morbidity.17,25,30,39 Initial reports from Parodi et al. relied on balloon expandable bare Palmaz stents (Cordis, Johnson and Johnson, Miami Lakes, FL) to cover the orifice of the pseudoaneurysm.45 Covering the orifice will typically promote thrombosis of the pseudoaneurysm, but if the sac fails to thrombose, an option has been to coil embolise the sac through the interstices of the bare stent.33 In these series, the mean follow-up was 3.5 years without neurological sequelae, but thrombosis and embolic potential as well as the potential for re-stenosis, remain a concern after endovascular placement of devices in the carotid artery.38 While thromboembolic complications are most common after stent placement, patients should be committed to lifelong follow-up for unforeseen complications such as stent fracture.23 Post-stent therapy is variable, but extrapolating data from carotid artery stenting for atherosclerotic disease, a regimen of dual anti-platelet therapy (aspirin and clopidogrel) appears adequate to prevent stent thrombosis and embolic ischaemic events.5 In their series, patients were treated with anticoagulation for 8 weeks if tolerated or dualanti-platelet therapy without any events; however, there are reports of early stent thrombosis if antiplatelet therapy is discontinued.25 Cothren et al. reported their 3-6 month follow-up analysis of post-traumatic carotid pseudoaneurysms excluded with carotid stents.20 Patients who had a persistent pseudoaneurysm 7—10 days after injury were considered candidates for stent therapy. Twenty-three patients were treated with carotid wallstents, and a sobering 3(13%) of the patients experienced ischaemic complications (2-periprocedural and 1-attributed to patient noncompliance).20 Of the 23 patients not treated with stents (anticoagulation and/ or anti-platelet agents), only one patient developed a stroke who was not on medication secondary to bleeding risk. None of the medically treated patients returned for follow-up DSA; how-

Z.M. Arthurs, B.W. Starnes ever, 18 of the 23 carotid stent patients returned at 3—6 months. An alarming 8 (45%) returned with occluded carotid stents (55% patency).20 All of these patients received periprocedural heparin and were discharged on coumadin. As opposed to the experience by Cothren et al., Edwards et al. placed 22 carotid stents for BCVI. Eighteen patients had pseudoaneurysms, and four patients were treated for extensive dissections. They experienced no periprocedural complications. Twelve patients were treated with post-procedural anti-platelet therapy, and 8 received anticoagulation. With a mean angiographic follow-up of 7 months, none were occluded (100% patency).28 Follow-up for this patient cohort is imperative, and further studies with long-term follow-up are needed to determine the risks and efficacy of carotid stents for BCVI. Compliance with medications and followup surveillance should be considered when planning appropriate therapy for trauma patients. In summary, it is clear that treatment reduces the neurological morbidity and mortality associated with BCVI. Whether to treat the patient with heparin, aspirin, adenosine diphosphate (ADP) receptor inhibitors, or combination therapy remains less clear. Unfortunately, patients who sustain blunt carotid injuries typically have associated closed head injuries, solid organ injuries, or pelvic fractures that prevent the use of early anticoagulation. Small intimal based flaps with minimal or no dissection are best managed with anti-platelet therapy or observation with transcranial doppler examination.52 Similarly, asymptomatic acute non-occlusive dissections may be treated with heparin therapy or anti-platelet therapy with monitoring for ischaemic symptoms. Symptomatic patients should undergo heparinisation if the bleeding risk is acceptable and undergo selective cerebral arteriography. Prospective outcome based trials are needed to evaluate the appropriate management of pseudoaneurysms. Initial antithrombotic therapy is appropriate. Persistent, enlarging, or symptomatic pseudoaneurysms should be excluded from circulation secondary to their embolic risk and failure to resolve with antithrombotic therapy alone. Pseudoaneurysms in the proximal internal carotid can be approached through an open repair, whereas pseudoaneurysms in the distal internal carotid can be approached with an endovascular stent.

Outcomes and follow-up The trauma population is notoriously non-compliant, and obtaining long-term follow-up imaging of BCVI has been challenging for trauma centres. Both the Denver and Memphis group obtain 7—10 days follow-up angiography after diagnosis of the injury

Blunt carotid and vertebral artery injuries and treatment with antithrombotic therapy. This experience has shown that 50—62% of Grade I injuries will heal completely, and thus, antithrombotic therapy can be discontinued.10 Four to thirteen percent will develop pseudoaneurysms, and the remaining 29—46% remain unchanged. Only 10% of Grade II injuries will heal, 29—47% will develop pseudoaneurysms, and 3% will thrombose. Grade III injuries are unlikely to resolve (5%) and unlikely to thrombose (5%); however, 91—100% of pseudoaneurysms persist.10 Grade IV injuries have a low rate of recanalisation (14—25%).10 Again, this data only represents 7—10 day follow-up. Reporting a mean angiographic follow-up of 4 months, Edwards et al. found 72% of Grade I injuries completely healed.28 Grade II injuries are fairly evenly distributed: 33% improved, 33% were stable, and 33% progressed to pseudoaneurysms.28 Grade III injuries tended to either remain unchanged (50%) or enlarge (40%), which prompted the authors to intervene with carotid stenting. Grade IV injuries universally did not improve and probably do not warrant follow-up DSA.28 There is no consensus on definitive follow-up. Repeat DSA and possible intervention (either open surgery or endoluminal therapy) is warranted for patients who become symptomatic on anticoagulation. Grade I-II injuries should have repeat imaging at 7—10 days prior to discharge since a proportion of patients will be able to discontinue antithrombotic therapy. Grade III injuries should be treated for a period of 4-8 weeks, and should then undergo repeat DSA with possible intervention versus continued close observation. Grade IV injuries universally do not resolve and should not undergo repeat DSA. Since BCVI has been increasingly recognised, diagnosed, and treated, the neurological morbidity and BCVI-related mortality has markedly decreased. Delayed recognition of occult blunt carotid injuries carries an increased mortality,50 and compared to penetrating carotid injuries which are easily diagnosed at the time of injury, patients have an overall decrease in functional outcome measures.36 This small patient population requires tremendous resources in the post-injury period, and many will have permanent disability. Only 37% are able to independently transfer themselves, necessitating discharge to a rehabilitation or nursing facility for the majority of patients.36 Twenty-four percent of patients are unable to feed themselves, and 20% are unable to form expressive speech.36 The functional loss of this young population cannot be overstated, and the potential yield of preventing one ischaemic event can dramatically improve the trauma patient’s rehabilitation potential.

1239

Conclusions Over the past two decades, BCVI has been increasingly recognised. Screening protocols have identified patients with injury patterns at greatest risk. Imaging technology continues to improve, and currently, 16-slice CTA is rivalling the accuracy of conventional DSA. Increased awareness and screening protocols have identified a population of patients that are asymptomatic. Recognition and early antithrombotic therapy has reduced the neurological morbidity of this injury, and if the patient is asymptomatic at the time of treatment, future embolic events can nearly be eliminated. Although a rare injury at trauma centres, the morbidity associated with this injury cannot be overstated; trauma specialists should continue to screen patients at risk for BCVI.

Conflict of interest None.

References 1. Bejjani GK, Monsein LH, Laird JR, et al. Treatment of symptomatic cervical carotid dissections with endovascular stents. Neurosurgery 1999;44(4):755—60 [discussion 760—1]. 2. Berg M, Zhang Z, Ikonen A, et al. Multi-detector row CT angiography in the assessment of carotid artery disease in symptomatic patients: comparison with rotational angiography and digital subtraction angiography. AJNR Am J Neuroradiol 2005;26(5):1022—34. 3. Berne JD, Norwood SH, McAuley CE, et al. The high morbidity of blunt cerebrovascular injury in an unscreened population: more evidence of the need for mandatory screening protocols. J Am Coll Surg 2001;192(3):314—21. 4. Berne JD, Norwood SH, McAuley CE, Villareal DH. Helical computed tomographic angiography: an excellent screening test for blunt cerebrovascular injury. J Trauma 2004;57(1):11—7 [discussion 17—9]. 5. Bhatt DL, Kapadia SR, Bajzer CT, et al. Dual antiplatelet therapy with clopidogrel and aspirin after carotid artery stenting. J Invasive Cardiol 2001;13(12):767—71. 6. Biffl WL, Egglin T, Benedetto B, et al. Sixteen-slice computed tomographic angiography is a reliable noninvasive screening test for clinically significant blunt cerebrovascular injuries. J Trauma 2006;60(4):745—51 [discussion 751—2]. 7. Biffl WL, Moore EE, Elliott JP, et al. The devastating potential of blunt vertebral arterial injuries. Ann Surg 2000;231(5): 672—81. 8. Biffl WL, Moore EE, Offner PJ, et al. Blunt carotid arterial injuries: implications of a new grading scale. J Trauma 1999;47(5):845—53. 9. Biffl WL, Moore EE, Ryu RK, et al. The unrecognized epidemic of blunt carotid arterial injuries: early diagnosis improves neurologic outcome. Ann Surg 1998;228(4):462—70. 10. Biffl WL, Ray Jr CE, Moore EE, et al. Treatment-related outcomes from blunt cerebrovascular injuries: importance

1240

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25. 26.

27.

28.

29.

30.

of routine follow-up arteriography. Ann Surg 2002;235(5): 699—706 [discussion 706—7]. Biffl WL, Ray Jr CE, Moore EE, et al. Noninvasive diagnosis of blunt cerebrovascular injuries: a preliminary report. J Trauma 2002;53(5):850—6. Bok AP, Peter JC. Carotid and vertebral artery occlusion after blunt cervical injury: the role of MR angiography in early diagnosis. J Trauma 1996;40(6):968—72. Bousson V, Levy C, Brunereau L, et al. Dissections of the internal carotid artery: three-dimensional time-of-flight MR angiography and MR imaging features. AJR Am J Roentgenol 1999;173(1):139—43. Bub LD, Hollingworth W, Jarvik JG, Hallam DK. Screening for blunt cerebrovascular injury: evaluating the accuracy of multidetector computed tomographic angiography. J Trauma 2005;59(3):691—7. Cogbill TH, Moore EE, Meissner M, et al. The spectrum of blunt injury to the carotid artery: a multicenter perspective. J Trauma 1994;37(3):473—9. Cohen JE, Ben-Hur T, Rajz G, et al. Endovascular stentassisted angioplasty in the management of traumatic internal carotid artery dissections. Stroke 2005;36(4):e45—7. Coldwell DM, Novak Z, Ryu RK, et al. Treatment of posttraumatic internal carotid arterial pseudoaneurysms with endovascular stents. J Trauma 2000;48(3):470—2. Cothren CC, Moore EE, Biffl WL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg 2004;139(5):540—5 [discussion 545—6]. Cothren CC, Moore EE, Biffl WL, et al. Cervical spine fracture patterns predictive of blunt vertebral artery injury. J Trauma 2003;55(5):811—3. Cothren CC, Moore EE, Ray Jr CE, et al. Carotid artery stents for blunt cerebrovascular injury: risks exceed benefits. Arch Surg 2005;140(5):480—5 [discussion 485—6]. Crissey MM, Bernstein EF. Delayed presentation of carotid intimal tear following blunt craniocervical trauma. Surgery 1974;75(4):543—9. Davis JW, Holbrook TL, Hoyt DB, et al. Blunt carotid artery dissection: incidence, associated injuries, screening, and treatment. J Trauma 1990;30(12):1514—7. de Vries JP, Meijer RW, van den Berg JC, et al. Stent fracture after endoluminal repair of a carotid artery pseudoaneurysm. J Endovasc Ther 2005;12(5):612—5. DiPerna CA, Rowe VL, Terramani TT, et al. Clinical importance of the ‘‘seat belt sign’’ in blunt trauma to the neck. Am Surg 2002;68(5):441—5. Duane TM, Parker F, Stokes GK, et al. Endovascular carotid stenting after trauma. J Trauma 2002;52(1):149—53. Duke BJ, Ryu RK, Coldwell DM, Brega KE. Treatment of blunt injury to the carotid artery by using endovascular stents: an early experience. J Neurosurg 1997;87(6):825—9. Eachempati SR, Vaslef SN, Sebastian MW, Reed Jr RL. Blunt vascular injuries of the head and neck: is heparinization necessary? J Trauma 1998;45(6):997—1004. Edwards NM, Fabian TC, Claridge JA, et al. Antithrombotic therapy and endovascular stents are effective treatment for blunt carotid injuries: results from longterm followup. J Am Coll Surg 2007;204(5):1007—13 [discussion 1014—5]. El-Sabrout R, Cooley DA. Extracranial carotid artery aneurysms: Texas Heart Institute experience. J Vasc Surg 2000;31(4):702—12. Ellis PK, Kennedy PT, Barros D’Sa AA. Successful exclusion of a high internal carotid pseudoaneurysm using the Wallgraft endoprosthesis. Cardiovasc Intervent Radiol 2002;25(1): 68—9.

Z.M. Arthurs, B.W. Starnes 31. Fabian TC, Patton Jr JH, Croce MA, et al. Blunt carotid injury. Importance of early diagnosis and anticoagulant therapy. Ann Surg 1996;223(5):513—22 [discussion 22—5]. 32. Fry WR, Dort JA, Smith RS, et al. Duplex scanning replaces arteriography and operative exploration in the diagnosis of potential cervical vascular injury. Am J Surg 1994;168(6): 693—5 [discussion 695—6]. 33. Horowitz MB, Miller III G, Meyer Y, et al. Use of intravascular stents in the treatment of internal carotid and extracranial vertebral artery pseudoaneurysms. AJNR Am J Neuroradiol 1996;17(4):693—6. 34. Lee KP, Carlini WG, McCormick GF, Albers GW. Neurologic complications following chiropractic manipulation: a survey of California neurologists. Neurology 1995;45(6):1213—5. 35. Liu AY, Paulsen RD, Marcellus ML, et al. Long-term outcomes after carotid stent placement treatment of carotid artery dissection. Neurosurgery 1999;45(6):1368—73 [discussion 1373—4]. 36. Martin MJ, Mullenix PS, Steele SR, et al. Functional outcome after blunt and penetrating carotid artery injuries: analysis of the National Trauma Data Bank. J Trauma 2005;59(4):860—4. 37. Mayberry JC, Brown CV, Mullins RJ, Velmahos GC. Blunt carotid artery injury: the futility of aggressive screening and diagnosis. Arch Surg 2004;139(6):609—12 [discussion 612—3]. 38. McCready RA, Divelbiss JL, Bryant MA, et al. Endoluminal repair of carotid artery pseudoaneurysms: a word of caution. J Vasc Surg 2004;40(5):1020—3. 39. McNeil JD, Chiou AC, Gunlock MG, et al. Successful endovascular therapy of a penetrating zone III internal carotid injury. J Vasc Surg 2002;36(1):187—90. 40. Miller PR, Fabian TC, Bee TK, et al. Blunt cerebrovascular injuries: diagnosis and treatment. J Trauma 2001;51(2):279— 85 [discussion 285—6]. 41. Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic modalities and outcomes. Ann Surg 2002;236(3):386—93 [discussion 393—5]. 42. Mokri B. Traumatic and spontaneous extracranial internal carotid artery dissections. J Neurol 1990;237(6):356—61. 43. Moreau P, Albat B, Thevenet A. Surgical treatment of extracranial internal carotid artery aneurysm. Ann Vasc Surg 1994;8(5):409—16. 44. Ofer A, Nitecki SS, Braun J, et al. CT angiography of the carotid arteries in trauma to the neck. Eur J Vasc Endovasc Surg 2001;21(5):401—7. 45. Parodi JC, Schonholz C, Ferreira LM, Bergan J. Endovascular stent-graft treatment of traumatic arterial lesions. Ann Vasc Surg 1999;13(2):121—9. 46. Perry MO, Snyder WH, Thal ER. Carotid artery injuries caused by blunt trauma. Ann Surg 1980;192(1):74—7. 47. Pretre R, Kursteiner K, Reverdin A, Faidutti B. Blunt carotid artery injury: devastating consequences of undetected pseudoaneurysm. J Trauma 1995;39(5):1012—4. 48. Ramadan F, Rutledge R, Oller D, et al. Carotid artery trauma: a review of contemporary trauma center experiences. J Vasc Surg 1995;21(1):46—55 [discussion 55—6]. 49. Rogers FB, Baker EF, Osler TM, et al. Computed tomographic angiography as a screening modality for blunt cervical arterial injuries: preliminary results. J Trauma 1999;46(3):380—5. 50. Rozycki GS, Tremblay L, Feliciano DV, et al. A prospective study for the detection of vascular injury in adult and pediatric patients with cervicothoracic seat belt signs. J Trauma 2002;52(4):618—23 [discussion 623—4]. 51. Schievink WI, Piepgras DG, McCaffrey TV, Mokri B. Surgical treatment of extracranial internal carotid artery dissecting aneurysms. Neurosurgery 1994;35(5):809—15 [discussion 815—6].

Blunt carotid and vertebral artery injuries 52. Srinivasan J, Newell DW, Sturzenegger M, et al. Transcranial Doppler in the evaluation of internal carotid artery dissection. Stroke 1996;27(7):1226—30. 53. Traflet RF, Babaria AR, Bell RD, et al. Vertebral artery dissection after rapid head turning. AJNR Am J Neuroradiol 1989;10(3):650—1.

1241 54. Wahl WL, Brandt MM, Thompson BG, et al. Antiplatelet therapy: an alternative to heparin for blunt carotid injury. J Trauma 2002;52(5):896—901. 55. Yamada S, Kindt GW, Youmans JR. Carotid artery occlusion due to nonpenetrating injury. J Trauma 1967;7(3): 333—42.