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European Journal of Radiology 64 (2007) 3–14

Imaging of blunt cerebrovascular injuries

Clint W. Sliker ∗, Stuart E. Mirvis 1

Department of Diagnostic Radiology, University of Maryland Medical Center, 22 South Greene Street, Baltimore, MD 21043, USA

Received 5 February 2007; accepted 14 February 2007

bstract

Blunt cerebrovascular injuries are uncommon but potentially devastating injuries that can lead to stroke and death. While uncommon, appreciation

f the seriousness of these injuries, a high index of suspicion in high risk patients, and aggressive screening of multitrauma patients leads to earlyiagnosis of asymptomatic lesions that may be amenable to treatment prior to the onset of ischemia. The radiologist can play a vital role in thearly diagnosis, follow-up, and, in some cases, treatment of these challenging injuries.

2007 Elsevier Ireland Ltd. All rights reserved.

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eywords: Blunt trauma; Carotid artery injury; Vertebral artery injury; Diagno

. Introduction

Historically, blunt cerebrovascular injuries (BCVI) were con-idered uncommon in the general blunt trauma population.lthough many of these lesions lead to stroke and death, diag-osis prior to onset of symptoms can be challenging. Withncreased appreciation of these injuries, increasing therapeu-ic options, and increasing access to ever advancing diagnosticmaging modalities, this group of injuries has received greaterttention in the trauma literature and from those caring forcutely traumatized patients.

The purpose of this article is to provide the radiologist withreview of blunt cerebrovascular injuries with special attention

o diagnosis and those clinical factors that impact diagnosis andhe radiologist’s role in patient management.

. Incidence

Blunt cerebrovascular injuries (BCVI) are generally consid-red uncommon injuries. Among all hospital admissions forlunt trauma, blunt carotid artery injuries (BCI) are encoun-

ered in 0.14–1.1% of patients [1–3] and blunt vertebral arterynjuries (BVI) are encountered in 0.4–0.53% [4,5]. Although theverall incidence of BCVI ranges from 1.1 to 1.4% [6,7] of all

∗ Corresponding author. Tel.: +1 410 328 7968; fax: +1 410 328 8925.E-mail addresses: csliker@umm.edu (C.W. Sliker),

mirvis@umm.edu (S.E. Mirvis).1 Tel.: +1 410 328 8845; fax: +1 410 328 8925.

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lunt trauma patients, it is more frequently diagnosed in moreeverely injured patients. For example, Mutze et al. [8] reportedn incidence as high as 2.7% in blunt patients with an injuryeverity score equal to or greater than 16.

. Outcomes

BCVIs result in high mortality and morbidity. For BCI, theverall mortality and morbidity rates are 17–38 and 32–67%1–3,5,7,9], respectively. Overall mortality and morbidity ratesor BVI are generally lower, although morbidity still ranges from4 to 24% [5,10] and mortality ranges from 8 to 18% [4,9].he high morbidity and mortality are, in part, attributable to

he severity of concurrent injuries frequently associated withCVI, although BCVI-specific mortality itself is high. In one

etrospective review of 22 patients with BCVI, McKevitt et al.11] reported a stroke rate of 60% and BCVI-specific mortalityf 25%. In a prospective study conducted by Cothren et al. [9],CI-specific mortality was 21%, while BVI-related mortalityas 18%. Moreover, reflecting a stroke’s globally deleterious

mpact on a patient, Cothren reported higher overall mortality inhose with BCVI-related stroke (32% for BCI and 18% for BVI)ompared to those without stroke (7% for both BCI and BVI).

. Mechanism of injury

Hyperextension and contralateral rotation of the head andeck, with the cervical internal carotid stretched against theransverse processes of the upper three cervical vertebrae, is

4 C.W. Sliker, S.E. Mirvis / European Journal of Radiology 64 (2007) 3–14

Fig. 1. A 82-year old woman with atlanto-occipital dissociation and bilateral vertebral artery injuries following motor vehicle collision. 3D volume rendered (a) andaxial images (b) obtained with whole-body multidetector computed tomography (WB-MDCT) protocol. Magnetic resonance angiogram (MRA) (c) and T1 weightedspin echo magnetic resonance image (MRI) (d). WB-MDCT demonstrates right vertebral artery segmental occlusion from C1 to foramen magnum (curved arrow),focal left vertebral artery central narrowing from intramural hematoma at level of foramen magnum, and bare occipital condyles (asterisks). MRA demonstratesabsent flow in distal right vertebral artery with focal narrowing of injured left vertebral artery (arrow). Left vertebral artery high T1 signal (arrowhead) indicatesintramural hematoma from dissection.

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Table 1Authors’ institutional guidelines for identifying trauma patients at high risk forblunt cerebrovascular injury

1. Cervical spine fracture withA. Foramen transversarium involvement, orB. 30% or more subluxation, orC. Significant rotation or distraction mechanism (e.g. unilateral interfacetal

dislocation, atlanto-occipital distraction, etc.)

2. Basilar skull fracture crossing carotid canal, foramen lacerum, or cavernoussinus

3. Severe facial fractures (LeFort II or III; naso-orbital ethmoid complex, facialsmash)

4. Carotid or vertebral artery perivascular hematoma by CT or MD-CTA5. Horner’s syndrome6. Glasgow Coma Score ≤ 6 at 24 h after initial assessment7. Neurologic examination incongruent with brain imaging8. Stroke or transient ischemic attack9. Hanging attempt with cervical hematomas or cervical spine fractures

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C.W. Sliker, S.E. Mirvis / Europea

onsidered the most common cause of BCI [12]. Also, exten-ion of basilar skull fractures through the carotid canal mayause petrous carotid injury [12]. Less common causes of BCInclude a direct blow to the neck (e.g. assault, near hanging,tc.) [12] and intraoral trauma from either a hard foreign objecte.g. falling against a toothbrush) [12] or posteriorly displacedandible fracture fragments [13].Since most of the vertebral arteries are fixated within the

ransverse foramina, they are vulnerable to injuries induced byisplaced bone fragments or stretching related to rotation andubluxation [14,15]. In cases of craniocervical junction distrac-ion or dislocation, the vertebral arteries may be crushed against1 [14] or stretched over the dura [16] (Fig. 1).

. Clinical presentation and associated injuries

The diagnosis of BCVI is typically suspected in patients pre-enting with overt signs of fixed neurologic deficits that arenexplained by cerebral computed tomography (CT). Otherigns, such as transient ischemic attacks, neck hematomas,orner’s syndrome, or cervical carotid bruit, also suggest BCVI,

lthough they can be difficult to identify in the acute multitraumaatient [17], especially those with concomitant traumatic brainnjury.

Several studies suggest prompt treatment reduces BCVI-elated stroke and mortality rates [4,5,7,18]. To this end, severaletrospective studies have described numerous clinical andmaging findings that may serve as triggers for screening of bluntrauma patients for BCVI [5,11,12,17,19–22]. Table 1 lists theuthors’ institutional guidelines for predicting BCVI. Despite

lack of consensus regarding the most significant independentredictors for BCVI, it has been shown that the greater the num-er of risk factors, the greater the likelihood of an associatedascular injury [12].

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ig. 2. A 40-year old with persistent low Glasgow Coma Score following motor vehiestricted diffusion related to diffuse axonal injury (curved arrows). (b) MRA demoarrowheads).

T, Computed tomography; MD-CTA, multidetector computed tomographicngiography. References: Lee et al. [16], Miller et al. [19], Kerwin et al. [20],othren et al. [21], Mirvis et al. [23] and Parbhoo et al. [24].

Many proposed predictors of BCVI can be readily identifieduring routine imaging of acutely injured patients [11,17,22].n a retrospective review of 75 patients with BCVI, Biffl et al.22] identified diffuse axonal injury (DAI) (Fig. 2), LeFort II orII fractures (Fig. 3), and petrous temporal bone fractures witharotid canal extension (Fig. 4) as independent risk factors forCI. Retrospective studies conducted by Berne et al. [25] andtter et al. [17] support the association of skull base fracturesith BCVIs. BVI and cervical spine injury have been strongly

ssociated in several studies [4,7,10,21,17,22,24,26]. In one

tudy [4], 38 patients with BVI were 11 times more likely thanot to have a cervical spine injury. In another study [21], 77%f patients with BVIs demonstrated cervical spine injuries, withost exhibiting either fracture involving a transverse foramen

cle collision. Diffusion weighted brain MRI (a) demonstrates corpus callosumnstrates distal cervical segment internal carotid artery (ICA) pseudoaneurysm

6 C.W. Sliker, S.E. Mirvis / European Journal of Radiology 64 (2007) 3–14

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ig. 3. A 44-year old male imaged with WB-MDCT following motor cycle crasnclude LeFort II and III patterns (arrowheads). Sagittal multiplanar reconstructCA just distal to carotid bulb (arrow).

Fig. 5), subluxation or dislocation, or injury level at C1 to3. Parbhoo et al. [24] report a high frequency of BVIs among

hose with unilateral facet dislocations, which is an associationupported by the authors’ experience.

Some significant clinical risk factors can be inferred byndings on routine imaging. For example, a very low (≤8)

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ig. 4. A 23-year old with skull base fractures following motor vehicle collision. Carotid canal (arrowheads). (b) Angiogram demonstrates petrous ICA (curved arrow)

volume rendered image (a) of face demonstrates extensive facial fractures thatPR) (b) demonstrates characteristic short-tapered post-traumatic occlusion of

lasgow Coma Score (GCS) [11,22] has been associated withCVI. Severe traumatic brain injury revealed by cerebral

maging may suggest a low GCS, and then allow the radiologisto propose evaluation for BCVI. Similarly, a high (≥3) thoracicbbreviated injury score (AIS) [11] has been linked to BCVIFig. 6). Since imaging plays the primary role in determining

omputed tomography (CT) (a) demonstrates displacement of fragments intoand cavernous ICA (arrow) pseudoaneurysms.

C.W. Sliker, S.E. Mirvis / European Journal of Radiology 64 (2007) 3–14 7

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ig. 5. A 22-year old male with vertebral artery injury induced brainstem strok6 left transverse process fractures involving foramen transversarium (black arrertebral artery (white arrow). Diffusion weighted (c) brain MRI performed 10

he thoracic AIS, if the radiologist diagnoses severe thoracicnjuries, he/she may then initiate the appropriate diagnosticvaluation for BCVI. Through awareness of the full spectrum ofisk factors for BCVI, the radiologist may be the first to considerts presence, thereby facilitating early diagnosis and treatment.

It is important to note that a large number of patients withCVI do not manifest any of the reported markers of injury.ccording to Biffl et al., approximately 20% of patients withCVI exhibit no recognized risk factors, and injuries are initially

linically occult [10] (Fig. 7). Supporting Biffl’s data, recentork by Stein et al. [42] found no major craniofacial or cervical

pine injury in 27% of 85 patients diagnosed with BCVI. As aeans to diagnose the large number patients with truly occult

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owing motor vehicle collision. Admission cervical spine CT (a) demonstrates) and angiogram demonstrates associated abrupt occlusion of the proximal left

later demonstrates rostral brain stem infarct (arrowhead).

cute injuries and limit resultant stroke, some [8] have suggestedhe routine use of computed tomographic angiography (CTA) toimultaneously examine the cervical spine and cervical arterialystem during assessment of acute multitrauma patients.

. Location and types of vascular injury

Blunt cerebrovascular injuries may occur anywhere along thearotid and vertebral artery distributions, and evaluation of both

irculations from their origins through their intracranial water-heds is vital. However, coinciding with the frequent associationith cervical spine injuries, most BVIs occur at the foraminal

i.e. V2) vertebral artery segments [26]. As predicted by the

8 C.W. Sliker, S.E. Mirvis / European Journal of Radiology 64 (2007) 3–14

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ig. 6. A 39-year old male scanned with WB-MDCT protocol following motoemonstrate a traumatic aortic injury with pseudoaneurysm (arrowheads), a righ

ominant mechanism of injury, BCIs typically affect the internalarotid artery just below the skull base [C.W. Sliker, unpublishedata], although a significant number occur at or above the skullase [12].

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icle collision. 3D volume rendered image of the chest (a) and neck (b and c)dissection (black arrow), and a right vertebral artery dissection (white arrow).

Notably, a large number of those with BCVI manifest morehan one injured vessel (Figs. 1 and 6). Multiarterial injury, inarious combinations, has been reported in 18–38% of cases18,20,27,28]. Given the violent and complicated force vectors

C.W. Sliker, S.E. Mirvis / European Journal of Radiology 64 (2007) 3–14 9

Fig. 7. A 17-year old with female with femur fracture (not shown) and ICA injury following motor vehicle collision. Admission WB-MDCT (not shown) demonstratednarrowed distal left ICA cervical segment. Coronal maximum intensity projection (MIP) computed tomography angiogram (CTA) image (a) acquired day #2demonstrates left ICA pseudoaneurysm (white arrow) and normal adjacent lumen. Coronal MIP CTA image (b) acquired day #7 and angiogram acquired day #9(c) demonstrate larger pseudoaneurysm (black arrow) and near occlusion of adjacent ICA lumen (white arrowheads). Angiogram acquired after endovascular stentplacement (d) demonstrates normal ICA lumen (black arrowheads) and minimal pseudoaneurysm filling (curved arrow).

10 C.W. Sliker, S.E. Mirvis / European Jour

Table 2Biffl blunt cerebrovascular injury grading system

Injury grade Description

I Luminal irregularity (i.e. intimal injury) or dissection with<25% luminal narrowing

II Dissection or intraluminal hematoma with ≥25% luminalnarrowing, intraluminal thrombus, raised intimal flap, orhemodynamically insignificant AVF

III PseudoaneurysmIV OcclusionV

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Transection or hemodynamically significant AVF

VF, Arteriovenous fistula. Reference: Biffl et al. [27].

esponsible for many cases of multitrauma, this is not a surpris-ng injury characteristic. Given the propensity for multivesselnjuries, care should be taken to thoroughly assess all four vas-ular distributions during diagnostic imaging, especially duringngiography when one may be tempted to limit the evaluation toess than a complete four-vessel study in an attempt to avoid theotential consequences of progressive catheter manipulations.

The forms of injuries identified in the carotid and vertebralrteries are similar to those encountered in arteries elsewhere inhe body. Typical types of injury include intimal injury, spasm,issection with intramural hematoma, raised intimal flap, intra-ural hematoma, pseudoaneurysm, occlusion, transection with

ctive hemorrhage, and arteriovenous fistulae (AVF) [16,29,30].issections may vary in degree of luminal compromise frominimal to near occlusion. Combinations of injury can be seen

e.g. pseudoaneurysm with dissection, raised intimal flap withntraluminal thrombus, etc.) in the same artery. With occlu-ion or high grade luminal narrowing, inadequate collateralow and/or hypotension can lead to arterial insufficiency and

schemia, while intimal injury may promote platelet aggrega-ion and embolization [12]. Pseudoaneurysms may promotelatelet aggregation with distal embolization or compress theative vessel lumen [31] with resultant downstream underperfu-ion. Rarely, pseudoaneurysm rupture or transaction may leado ischemia or hemodynamic compromise [12].

In an effort to the predict risk of stroke, Biffl et al. [29] devisedblunt carotid artery injury grading scale based on the anatomic

eatures of injury. In a subsequent report [27], the scale (Table 2)as revised to include AVFs, and it was used to grade BVIs asell as BCIs. When BCVIs are reported with the Biffl scale,

he highest grade injury identified determines the score for thatarticular vessel. At the authors’ institution, all injuries in aarticular vessel are described, although only one may be used toetermine overall grade of injury. In addition to providing somerognostic information, the grading scale is a useful reportinghorthand that is easily understood by the traumatologist.

. Diagnosis of BCVI

.1. Angiography

Four-vessel cervicocerebral angiography is considered theeference standard for diagnosing BCVI [10,20]. As an invasiveest, angiography carries an inherent risk of serious complica-

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ions, including stroke and hemorrhage. Yet, with experiencedperators, routine angiographic assessment of trauma patients,ho are generally young and without pre-existing vascular dis-

ase, is a safe procedure. For example, in one report by Cothren etl. [9], 727 blunt trauma patients were angiographically screenedor BCVI, and there was one instance (0.1%) of angiography-elated stroke and two cases (0.3%) of conservatively-manageduncture-site hematomas. In those in whom BCVI is stronglyuspected clinically, the risks would seem to be tolerable.till, in a screening population without hard clinical signs ofCVI, many may consider potential complications of angiog-

aphy unacceptable given the relative rarity of these injuries.oreover, angiography is also expensive and resource intensiveonsequently, other diagnostic modalities, including Dopplerltrasound, magnetic resonance angiography (MRA), and com-uted tomographic angiography (CTA), are being increasinglysed to diagnose BCVI.

.2. Multidetector computed tomographicngiography—scanning options

Computed tomography (CT) is an important tool commonlysed to evaluate multitrauma patients for head, spine, chest,bdomen, and pelvic injuries. With the advances in multidetectoromputed tomography (MDCT) technology, multidetector com-uted tomographic angiography (MD-CTA) is increasingly usedo evaluate the arterial systems throughout the body, and, recenteports describe it use to diagnose BCVI [6,7,17,32,33]. Withhe use of MDCT, routine diagnosis of BCVI does not need to beimited only to scans targeted to the craniocervical region. Cur-ent MDCT scanners, used in concert with contrast bolus timing,llow continuous scanning through all regions of interest in theypical multitrauma patient. Utilization of whole-body MDCTcanning techniques permits simultaneous detection of cranio-ervical vascular, skeletal, thoracic, and organ injuries whileorgoing the scanning time and excess radiation [34] inherent toraditional segmental scanning techniques.

In the authors’ trauma center, targeted neck MD-CTA andhole-body MDCT have been performed for over 3 years.urrently, both 16- and 40-detector row scanners are in use,

hough the 40-detector row scanner is preferred for most whole-ody and neck MD-CTA scans (Table 3). In most multitraumaatients, the whole-body scanning protocol is routinely used.he targeted neck MD-CTA protocol is utilized in those caseshere clinical interest is directed entirely to the cranicocervical

rterial system, in addition to cases where the patient is consid-red at risk for harboring a BCVI and the whole-body MDCTrovided suboptimal or equivocal evaluation of the neck vessels.ith both protocols, advanced post-processing techniques (e.g.

urved multiplanar reconstructions, volume rendering, etc.) aresed liberally on an as needed basis.

.3. Multidetector computed tomographic

ngiography—diagnostic accuracy

The relatively few studies that have investigated the accuracyf CTA when used to diagnose BCVI are limited by small cohorts

C.W. Sliker, S.E. Mirvis / European Journal of Radiology 64 (2007) 3–14 11

Table 3A 40-detector row MDCTa scanning protocols for evaluating craniocervical arterial system

Parameter Whole-body MDCT protocol Neck MD-CTA protocol

Patient positioning Arms extended superiorly over head Arms at his/her sidesDetector configuration and collimation 40 mm × 0.625 mm 40 mm × 0.625 mmPitch 0.926 0.67Rotation time 0.5 s 0.5 skV 120 120mA 250 400Area scanned Circle of Willis to lung bases (or ischial tuberosities) Vertex to aortic archContrast Iohexol (350 mg I/mL) Iohexol (300 mg I/mL)Contrast volume 100 mL contrast, 50 mL saline push 100 mL contrast, 50 mL saline pushContrast injection rate 6 mL/s for 60 mL, then 4 mL/s for 40 mL

(contrast followed by saline push)4 mL/s (contrast followed by saline push)

Scan trigger threshold 90 HUb Time to peak cervical ICA enhancement + 2 sc

Axial images (thickness × interval) 2 mm × 2 mm 1 mm × 0.5 mmSagittal and coronal MPR images (thickness × interval) 2 mm × 2 mm 2 mm × 2 mmSagittal and coronal MIP images (thickness × interval) n/a 5 mm × 2 mmThin section axial images to independent workstation

(thickness × interval)2 mm × 1 mm 1 mm × 0.5 mm

n/a, MIP images through neck not part of routine whole-body MDCT protocol. MDCT, Multidetector computed tomography; MD-CTA, multidetector computedtomographic angiography; MPR, multiplanar reconstruction; MIP, maximum intensity projection.

a Philips Brilliance-40 scanner (Philips Medical Systems, Cleveland, OH, USA).b Bolus Pro triggering system (Philips Medical Systems) with region of interest at the distal ascending aorta.

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f injured patient and varied study designs. Compared to the ref-rence standard, angiography, reports of single-slice spiral CTAielded disappointing results; sensitivities for BCI and BVI were7–68% [10,19] and 53% [10], respectively. Recently, studiesnvestigating the accuracy of MD-CTA have emerged. In 2006,iffl et al. [32] and Berne et al. [6] reported their experience

creening 331 and 435 patients, respectively, for BCVI with 16-lice MD-CTA. In both studies, injuries (combined total of 42atients) were confirmed with angiography while those patientsith normal (i.e. no BCVI) MD-CTA results were followed clin-

cally for signs of neurovascular complications. Neither groupeported delayed neurological complications of BCVI in thoseith normal MD-CTA examinations, though neither followedormal MD-CTA examinations with angiography. Therefore,n both reports, true accuracy of 16-slice MD-CTA for detect-ng BCVI was not determined. In a prospective study that alsoppeared in 2006, Eastman et al. [33] evaluated 146 at-riskatients with both 16-slice MD-CTA and angiography, and theyetermined 16-slice MD-CTA to have a sensitivity of 97.7%nd specificity of 100% when used to diagnose BCVI. Despitehese impressive results, the BCVI cohort consisted of only 43atients [33], which is a small number when studying an uncom-on entity; this is a limitation shared by the other two studies.oreover, Eastman et al. [33] report only 46 injuries in the

3 patients diagnosed with BCVI, which is far from the pre-iously reported multivessel injury rate of 18–32% in patientsith BCVI [18,20,28], Although the results of this study areromising, the small cohort of injured patients and the atyp-

cally small number of patients with multiple injured vesselsuggest the data may not reflect the true accuracy of 16-slice

D-CTA when used to evaluate to the blunt trauma populationt large for BCVI. Controversies not withstanding, the authors

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eel that MD-CTA (16-slice or greater) plays a valuable role invaluating patients with suspected BCVI, but, until proven by aarge (preferably multicenter and prospective) trial, the authorso not think that MD-CTA should be considered diagnosticallyquivalent to angiography.

.4. Magnetic resonance angiography

Few studies have assessed the diagnostic accuracy of mag-etic resonance angiography (MRA) relative to angiographyhen used to detect BCVI. In one study by Biffl et al. [10],6 patients at risk for BCVI were examined with both MRA andngiography. Angiography confirmed BCVI in three patients,nd the collective sensitivity and specificity of MRA for BCVIere 75 and 67%, respectively. In a slightly larger study con-ucted by Miller et al. [19] 21 at-risk patients were examinedith both MRA and angiography. Among the four patients withCI, the sensitivity of MRA was 50% and its specificity was00%. Vertebral artery injuries were found in 17 patients, andhe sensitivity and specificity of MRA were 47 and 97%, respec-ively.

Though its sensitivity is limited, the use MRA to diagnoseCVI has several potential advantages relative to other diag-ostic options. Among them, the examination does not utilizeonizing radiation or require intravenous contrast. However, in

ost centers, magnetic resonance (MR) imaging is not as rapidlyccessible as CT. In addition to the time and personnel requiredo transport the patient to the MR suite, which is remote from

atient care areas in many centers, the MR environment itself isot conducive to the management of the acutely injured patient.onsequently, even if future well-designed studies demonstrate

hat contemporary MRA techniques have diagnostic accuracies

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omparable or exceeding those of CTA, the authors feel that thehysical limitations of MRA should limited it use in favor ofD-CTA (16 detector row or greater) or angiography, with the

se of MRA relegated to instances when the other two diagnos-ic options are unavailable, their results are equivocal, or whenhe use of iodinated contrast material and/or ionizing radiations contraindicated.

.5. Sonography

Although operator dependent, ultrasound is a portable, inex-ensive tool in common use by traumatologists, and Duplexoppler techniques are established means for diagnosing andonitoring non-traumatic cerebrovascular disease. Therefore,

ltrasound is an attractive option for diagnosing BCVI. How-ver, since the intracranial internal carotid arteries and most ofhe vertebral arteries are encompassed by bony canals, the abil-ty of ultrasound to detect potentially significant injuries (e.g.ntimal flaps, pseudoaneurysms) without associated flow distur-ances can be limited. The few studies that have discussed theensitivity of Doppler ultrasound for detecting BCVI report dis-ppointing results. In one early study [35], Doppler ultrasoundiagnosed 14 patients with BCI within the neck for a sensitivityf 86%, although it missed two injuries near the skull base. Inmore recent study, Mutze et al. [8] detected BCVI in 0.9%

f 1471 patients screened with Doppler ultrasound with sen-itivity of only 38.5%. The eight patients in whom Dopplerltrasound missed injury came to clinical attention as resultf cerebrovascular ischemia, supporting the notion that injuriesissed by sonography are potentially significant. Given its lim-

tations, Doppler ultrasound should only be utilized when these of other imaging techniques is impossible.

. Injury evolution

Both blunt carotid and vertebral arteries tend to be dynamicesions. That is, over the course of days or weeks, the sever-ty of both treated and untreated lesion may either progress oregress. In their review of 114 carotid artery and 65 vertebralrtery injuries followed with angiography 7–10 days after sus-aining injury, Biffl et al. [27] noted that grade I and II injuriesrequently healed by initial follow-up, and therapy could thene discontinued in 57% of grade I and 8% of grade II lesions.onversely, 8% of grade I lesions and 43% of grade II lesionsrogressed, leading to more aggressive therapeutic interven-ions. Ninety-three percent of grade III injuries and 82% of gradeV injuries were unchanged, although in the authors’ experience,hese lesions, especially carotid injuries, change with greaterrequency. Notably, Biffl et al. noted no significant differencen injury progression or regression among patient populationseceiving systemic anticoagulation, antiplatelet therapy, or noedical therapy [27].At the authors’ trauma center, blunt cerebrovascular injuries

re followed with the imaging modality that most satisfacto-ily characterized it during the initial work-up; this is usuallyn MDCT angiogram. The first follow-up imaging is typicallyerformed between 24 and 72 h after initial diagnosis. Dur-

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nal of Radiology 64 (2007) 3–14

ng this brief interval, BCVI frequently change enough to alteranagement, which is particularly important given the relative

requency of coexisting injuries (e.g. unstable cervical spinenjury requiring surgery, major visceral injury, etc.) that mayomplicate treatment with anti-thrombotic agents. A secondollow-up examination is usually obtained within 1 week to 1onth (Fig. 7a and b). Beyond this point, the timing of repeat

maging is generally based on injury morphology and responseo management. Uncommonly, rapid morphologic changes ren-er differentiation between injury progression and vascularemodeling associated with healing difficult, and, in these cases,ore frequent follow-up imaging can be especially useful.

. Treatment

Though treatment of some BCVI may be impossible orruitless due to early extensive stroke or other contraindica-ions (e.g. intracranial hemorrhage, spinal cord injury) [36],

ultiple authors have suggested that treatment with either med-cal therapy or endovascular techniques can either prevent orimit BCVI-related neurologic deficits [2–5,18,19,37,38]. Tohis date, the optimum treatment regimen has yet to be deter-

ined, but the current trend is towards medical therapy asption of choice. Many consider anticoagulation first line ther-py [2–5,9,18,19,29], with antiplatelet therapy reserved forhose with contraindications to anticoagulation. In one studyonducted by Miller et al. [5], timely treatment with either anti-oagulation or antiplatelet therapy lowered stroke incidence to% in patients diagnosed with BCI and to 0% in those with BVIcompared to 50% for both untreated BCI and BVI). Antiplateletas been proposed by others [37] to exhibit efficacy comparableo anticoagulation while reducing the risk of hemorrhagic com-lications. At this time, the superiority of one approach over thether is unproven.

Of special interest to radiologists, endovascular repair withtent placement has been used to treat BCIs when lesions areefractory to medical therapy [31,38] (Fig. 7c and d), medicalherapy is contraindicated [38], or either angiography or perfu-ion imaging demonstrates evidence of cerebral hypoperfusion38]. In a study reported by Cohen et al. [38], 10 patients withost-traumatic cervical internal carotid artery (ICA) dissectionsere treated with endovascular stent placement. There wereo procedure-related complications or stent occlusions, andt a mean clinical follow-up time of 16 months four patientsemonstrated no deterioration in neurologic status while sixatients improved. In contrast, Cothren et al. [39] reported a1% complication rate (three strokes and one subclavian arteryissection) and an occlusion rate of 45% among 23 patientsith post-traumatic cervical ICA pseudoaneurysms treated with

tents. In a cohort of 18 patients who received only medical ther-py, none suffered stroke or progressive deficit after initiation ofreatment, and one suffered carotid artery occlusion despite anti-oagulation. Interestingly, this report contradicts an earlier one

rom the same institution, in which Coldwell et al. [31] describedncomplicated endovascular treatment of cervical ICA pseu-oaneurysms in 14 patients in whom a mean clinical follow-upf 16 months revealed no evidence of stroke or delayed stent

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C.W. Sliker, S.E. Mirvis / Europea

omplication. It must be noted that in Cohen’s study, all patientseceived antiplatelet therapy with aspirin and clopidogrel [38],hile those suffering stent occlusion in Cothren’s study only

eceived anticoagulation [39], thereby suggesting that thentiplatelet therapy either alone or in combination with thetents contributed to the more promising results reported byohen. Clearly, the role and methods of endovascular repair ofCI remain areas in need of continued investigation.

Endovascular therapy of vertebral artery injuries is also aiagnostic option. Although emergent coil embolization of ver-ebral artery transections is an appropriate approach [40], the

erits of a comparable approach to less severe injuries remainncompletely explored. Since Biffl et al. [27] suggest the highestate of BVI-related stroke (38%) occurs with grade II injuries,nd up to 75% of traumatic vertebral artery occlusions canecanalize [24], coil embolization of occluded vessels has beenroposed [41] to prevent reconstitution and the risk of dis-al thromboembolization. While this approach may pose nodditional harm to the patient, its long term merits measuredgainst those of medical therapy and the immediate risks of anndovascular procedure are unproven. Although dissections andseudoaneurysms can be addressed with endovascular occlu-ion, this should be done with caution with documentationf adequate collateral flow through the contralateral vertebralrtery and circle of Willis established.

0. Conclusion

Blunt cerebrovascular injuries are infrequently encountered,nd a high index of suspicion coupled with understanding ofnjury mechanism and recognition of associated injuries facil-tates early diagnosis and treatment of asymptomatic lesions.ased on available resources, each institution must determine

n what setting and with what means will the evaluation forCVI be initiated. Although its accuracy remains unproven,

iberal screening with 16-slice (or higher) MD-CTA facili-ates early diagnosis and treatment. In cases where MD-CTAesults are suspicious, equivocal or normal in high-risk patients,r clearly positive in those whom endovascular therapy is anption, prompt follow-up with four-vessel cerebral angiographys recommended. Regardless of the diagnostic and therapeuticpproaches utilized to address blunt cerebrovascular injuries,he authors advocate that institutions caring for blunt traumaatients adopt a coordinated and systematic approach in orderfficiently utilize resources while optimizing the outcomes ofhose diagnosed with these uncommon but potentially devastat-ng injuries.

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