endovascular management of extracranial carotid and ... · endovascular management of extracranial...

EndovascularManagement ofExtracranial Carotidand Vertebral Disease
Hjalti M.Thorisson, MDa,b, Michele H. Johnson, MDa,c,d,e,*
KEYWORDS� Carotid stenosis � Epistaxis � Carotid blowout� Carotid dissection � Endovascular management

The role of endovascular management in the treat- 29% of ischemic strokes are caused by extracra-
ment of extracranial carotid and vertebral vascularpathology is extensive and expanding. It is imper-ative for the neuroendovascular specialist to beproficient with diagnosis and treatment ofcommon extracranial pathologies. For this discus-sion, we divide extracranial vascular diseaseprocesses into atherosclerotic and nonathero-sclerotic vascular disease. The atheroscleroticdisease discussion includes a review of clinicaltrials for symptomatic and asymptomatic carotidstenosis and surgical, medical, and endovasculartreatments currently available. The nonathero-sclerotic injury category encompasses trauma,vascular injury attributable to cancer or cancertreatment, spontaneous dissection and sequelae,and idiopathic epistaxis. Although these under-lying pathologies differ, the diagnostic algorithmand therapeutic approaches are similar from theperspective of the neuroendovascular specialist.
ATHEROSCLEROTIC DISEASEExtracranial Carotid Stenosis

Ischemic stroke is a major cause of morbidity andmortality in the western world. An estimated 8% to

a Department of Diagnostic Radiology, Yale University SNew Haven, CT 06520, USAb Department of Radiology, University Hospital - Landspc Department of Surgery (Otolaryngology), Yale Unive208042, New Haven, CT 06520, USAd Department of Neurosurgery, Yale University SchooNew Haven, CT 06520, USAe Interventional Neuroradiology, Yale University SchooNew Haven, CT 06520, USA* Corresponding author. Department of Diagnostic RadiStreet, PO Box 208042, New Haven, CT 06520.E-mail address: [email protected] (M.H. Johns

Neurosurg Clin N Am 20 (2009) 487–506doi:10.1016/j.nec.2009.07.0111042-3680/09/$ – see front matter ª 2009 Published by E

nial atherosclerotic diseases (most frequentlycarotid bifurcation stenosis).1 Current treatmentmodalities for extracranial cervical carotid athero-sclerotic disease include medical management,carotid endarterectomy (CEA), and carotid angio-plasty and stenting (CAS).

Carotid endarterectomyFew surgical procedures have undergone the samerigorous scrutiny as CEA. Ever since its inception inthe 1950s, CEA for the treatment of carotid bifurca-tion stenosis has generated debate with respect toappropriate use. In the 1980s, CEA was the mostcommon vascular surgical procedure and ques-tions regarding appropriate use led to largerandomized trials both in North America and Eu-rope to evaluate its efficacy for treatment of symp-tomatic and asymptomatic lesions. Carotidstenosis is considered symptomatic if there isa history of ipsilateral stroke, ipsilateral transientischemic attack, or ipsilateral transient mono-ocular blindness within the preceding 6 months.

Symptomatic carotid stenosisThe North American Symptomatic Carotid End-arterectomy Trial (NASCET) randomized

chool of Medicine, 333 Cedar Street, PO Box 208042,

itali Haskolasjukrahus i Fossvogi, Reykjavik, Icelandrsity School of Medicine, 333 Cedar Street, PO Box

l of Medicine, 333 Cedar Street, PO Box 208042,

l of Medicine, 333 Cedar Street, PO Box 208042,

ology, Yale University School of Medicine, 333 Cedar

on).

lsevier Inc. neur

osur

gery

.thec

lini

cs.c

om

mailto:[email protected]

http://neurosurgery.theclinics.com

Thorisson & Johnson488

symptomatic patients from 50 centers to CEA withmedical management versus medical manage-ment alone. Initial results were reported in 1991and demonstrated a significant benefit to patientswith high-grade carotid stenosis (70% to 99%)who underwent CEA.2 The risk of an ipsilateralstroke over a 2-year period was 26% in themedical group but 9% in the CEA group, repre-senting an absolute risk reduction for the surgicalarm of the study of 17% decreased risk of any ipsi-lateral stroke over a 2-year period. These resultswere essentially corroborated in the EuropeanCarotid Surgery Trial (ECST) in 1998.3 Accountingfor differences in angiographic quantitation ofcarotid stenosis, the results of NASCET andECST were in agreement that CEA was of clearbenefit to symptomatic patients with carotidstenosis between 70% and 99% (when measuredusing the NASCET criteria).4 Further results of theNASCET study published in 1998 showed thatsymptomatic patients with moderate stenosis(50% to 69% by NASCET criteria) also benefitfrom CEA,5 although that benefit was less strikingand more apparent in men than women. Thesestudies established the legitimacy of CEA for treat-ment of symptomatic carotid stenosis greater than70%.

Asymptomatic carotid stenosisThe NASCET and ECST studies did not addressthe increasingly large, asymptomatic populationdiagnosed with carotid stenosis by imaging. TheAsymptomatic Carotid Atherosclerosis Studygroup (ACAS) trial, published in 1995, randomized1662 patients with greater than 60% carotidstenosis to CEA with medical management versusmedical management alone and found an esti-mated absolute risk reduction in the surgicallytreated group of 5.9% in the risk of ipsilateralstroke over a 5-year period as compared withmedical management alone. These results werefurther corroborated by the Asymptomatic CarotidSurgery Trial (ACST) published in 2004 that alsoshowed a 6% absolute risk reduction of ipsilateralstroke over a 5-year period in the surgically treatedgroup. Bear in mind that the patients randomizedin the ACAS trial were highly selected, withmultiple exclusion criteria (age older than 80,significant medical morbidities, and more), and inaddition, the surgeons performing the CEA hadto show a perioperative complication rate of lessthan 3% to be allowed to participate in thestudy.6,7 Previous trials had failed to show a benefitfor CEA in asymptomatic patients (Veterans Affairstrial8 and the Mayo Clinic trial9). The AmericanHeart Association guidelines for treatment recom-mend CEA for symptomatic extracranial carotid

stenosis (>70%) if the periprocedural rate of majorstroke or death was under 6% and treating asymp-tomatic extracranial carotid stenosis (>70%) if theperiprocedural rate of major stroke and death wasunder 3% and the life expectancy of the patientwas at least 5 years.10 Also of significance, bestmedical management has improved significantlysince these trials were performed, with a moredefined role for statin therapy, angiotensin-con-verting enzyme (ACE) inhibitors, and added anti-platelet therapy.

Carotid angioplasty and stentingInitial endovascular treatment of extracranialcarotid artery stenosis involved percutaneusballoon angioplasty with isolated case reportsand small series published in the early 1980s.11

The touted benefits of endovascular treatmentincluded minimally invasive approach allowingtreatment of patients with severe cardiac andpulmonary disease, decreased cranial nerveinjury, and suitablility for patients with anatomicallydifficult lesions for a surgical approach and inpatients with a prior history of neck radiation.Although CAS does avoid some of the complica-tions associated with CEA, such as cranial nerveinjury, there are specific procedural risks that areunique, such as groin or retroperitoneal hema-toma, vessel dissection related to catheterizationand contrast reaction, as well as the risk of stroke.There are anatomic configurations unfavorable forCAS such as severe tortuosity of the carotidvessels, or severe angulation between the aorticarch and origin of the brachiocephalic or carotidarteries (Fig. 1). It very quickly became apparentthat the major limitation of endovascular treatmentwas the risk of embolic stroke that initially seemedsignificantly higher for patients treated with percu-taneous transluminal angioplasty (PTA) with orwithout stenting versus those treated withsurgery.12

Randomized controlled trials of carotidendarterectomy versus carotid angioplastyand stentingWhen evaluating the literature comparing CEA andCAS, several issues must be considered:

1. Case series registries versus randomizedcontrolled trials (RCTs)

2. Symptomatic versus asymptomatic patients3. Low-risk surgical candidates versus high-risk

surgical candidates (and thus would havebeen excluded from the relevant surgical trials)

4. Periprocedural medical management5. Use of cerebral protection device during CAS6. Operator experience

Fig. 1. Unfavorable anatomy for CAS. (A) Symptomatic right internal carotid artery (ICA) stenosis accessed via highleft brachial approach owing to occlusive vascular disease in the femoral arteries. (B) Although diagnostic angi-ography was successful, the shuttle sheath could not be advanced into a position suitable for stent placement. (C)Symptomatic right ICA stenosis with tortuosity of the common carotid artery. (D) The tortuosity at the arch andthe angle of the right ICA origin prevented advancement of the protection device beyond the origin of theguiding catheter. The procedure was aborted and an awake endarterectomy performed. (E, F) Distal patch graftstenosis involves both internal and external carotid arteries, however there is a marked disparity in size betweenthe graft and the internal carotid artery precluding stent placement. (G) The external carotid artery is occluded inthis patient with oral bleeding and recurrent tonsilar cancer. The size disparity between the common and internalcarotid arteries and the acuteness of the angled precluded stent placement and the vessel was permanentlyoccluded with coils.

Extracranial Vascular Disease 489

The first RCT comparing CEA and CAS waspublished in 1998 and was a small trial that wasstopped prematurely because of a very high inci-dence (70%) of stroke in the CAS arm of the trial.12

The Carotid And Vertebral Transluminal Angio-plasty Study (CAVATAS) was published in 2001and showed no significant difference in 30-daymorbidity and mortality rates when comparingCEA and CAS.13 However, complication rates inboth groups were high by conventional standards,with a 30-day death or disabling stroke rate of10.0% and 9.9% for CAS and CEA respectively.Only about a quarter of endovascularly treated

patients received a stent and restenosis rateswere higher in the endovascular group.

The first RCT in high-risk patients was the Stent-ing and Angioplasty with Protection in Patients atHigh Risk for Endarterectomy (SAPPHIRE) trialpublished in 2004.14 Patients randomized for thetrial would likely have been excluded from thelarge surgical trials because of age and/or comor-bidity. Only experienced surgeons and interven-tionalists were allowed to participate in the trial.Most of the patients were asymptomatic (about70% in both arms); embolic protection devicesand stents were used in the endovascular arm of


the study. The results showed a significantly lower30-day mortality/major stroke/myocardial infarc-tion (MI) rate in the CAS group (4.8%) versus theCEA group (9.8%) and this benefit was still presentat 1 year after intervention. However, it is importantto realize that the vast majority of the differencebetween the two arms was because of a differencein the rate of MI (most MIs were non–Q-waveinfarctions detected on routine postoperativetests). If MI is excluded as an end point, therewas no statistically significant difference betweengroups.

The Stent Protected Angioplasty versus CarotidEndarterectomy (SPACE) trial was published in2006.15 A total of 1183 symptomatic patientswith over 70% stenosis were randomized to CASor CEA. Use of embolic protection devices wasleft to the discretion of the treating physician.Results showed a similar rate of complicationsbetween the groups. The 30-day mortality/majorstroke rate was 6.8% in the CAS arm and 6.3%in the CEA arm. The authors concluded that CEAwas still the gold standard because evidence ofthe equivalence or superiority of endovasculartreatment is lacking. The Endarterectomy VersusStenting in Patients with Symptomatic SevereCarotid Stenosis (EVA-3S) was also published in2006. After randomizing 527 patients to CAS orCEA, the trial was stopped because of concernsregarding the safety of CAS. Periprocedural30-day mortality and major stroke rates were9.6% in the CAS arm compared with 3.9% in theCEA arm. Since publication, the results of this trialhave been hotly debated, with concerns regardingdifferences in operator experience betweensurgeons and interventionalists. Also of note, thestroke rate before the mandatory use of embolicprotection devices was extraordinarily high (about25%) and rates improved significantly aftermandatory use of embolic protection deviceswas put in the study protocol.16

Ongoing studiesSeveral large prospective RCTs are currentlyenrolling patients. Perhaps the most eagerlyawaited study is the Carotid RevascularizationEndarterectomy versus Stenting (CREST) trial,which is funded by the National Institutes of Health(NIH). This trial plans to randomize 2500 patients toCEA or CAS and follow-up for 4 years. Optimalcurrent medical management is provided to botharms and intervention is performed in symptom-atic patients with 50% stenosis by angiography(70% by ultrasound) and in asymptomatic patientswith 60% stenosis by angiography (70% by ultra-sound). Some data from this trial has beenpublished indicating an increased risk for

octogenarians undergoing CAS.17 Other ongoingtrials comparing CEA and CAS are the Interna-tional Carotid Stenting Study (ICSS) evaluatinglow-risk symptomatic patients and the ACT 1 trial,which is evaluating low-risk asymptomaticpatients. The Transatlantic Asymptomatic CarotidIntervention Trial (TACIT) will enroll asymptomaticpatients to undergo CEA, CAS, or best medicalmanagement only. This trial is necessary becausethe best medical management represented in thelandmark surgical trials was not remotely similarto what has been established as best medicalmanagement today.18

Carotid angioplasty and stenting techniqueOur routine procedure for CAS is as follows. Theprocedure is performed with moderate sedationallowing for continuous neurologic monitoring.Before the procedure, antiplatelet therapy is initi-ated with aspirin and clopidogrel for at least 5days and is continued after the procedure. Prepro-cedural blood pressure control and initiation ofstatin therapy is also of paramount importance.All patients who have not undergone prior ipsilat-eral CEA have external pacemaker pads appliedbefore the start of the procedure as a precaution,if extreme bradycardia is encountered and wealso ensure that intravenous (IV) atropine is readilyavailable for rapid administration. Access isusually obtained with a common femoral arterypuncture and a thoracic angiogram frequently per-formed. Anticoagulation with heparin is initiatedand care taken to maintain an ACT above 250seconds for the remainder of the procedure.Selective angiography of the nontarget carotid isusually performed to assess potential collateralcirculation. Selective angiography of the targetvessel is performed in multiple projections toboth confirm the diagnosis of significant carotidartery stenosis and to ascertain the best workingprojection for the planned intervention (Fig. 2). An-teroposterior (AP) and lateral angiograms of thehead are also performed as a baseline examina-tion. Next, an exchange length wire is manipulatedinto a branch of the external carotid artery (ECA)and the diagnostic catheter exchanged over thewire for a 6-French 80- to 90-cm guiding sheath.An embolic protection device is then manipulatedacross the stenosis and the protection device de-ployed in the internal carotid artery (ICA) distal tothe segment to be treated. Predilatation is thenperformed if needed with a compliant angioplastyballoon. We tend to be more aggressive in predila-tation, as we feel this reduces the need for post-stent deployment dilatation by improving thestent approximation to the vessel wall. Next, anappropriately sized carotid stent is deployed

Fig. 2. 57-year-old male with symptomatic left internal carotid artery (ICA) stenosis. (A) Left anterior oblique archarteriogram demonstrates right ICA occlusion and a 98% stenosis of the left ICA approximately 1 cm above thelevel of the common carotid bifurcation. (B) Selective left common carotid artery arteriogram demonstrates 98%eccentric stenosis (arrow). (C) Poststent arteriogram reveals marked improvement in lumen caliber with mildresidual stenosis (arrow).


and postdeployment angiography performed. Ifpossible, we avoid poststent deployment balloonangioplasty because it has been our anecdotalexperience that a significant number of intraproce-dural embolic complications occur during ordirectly after poststenting balloon angioplasty.This observation may be attributable to a gratingeffect of the stent on the atheromatous plaqueand subsequent emboli during poststentingballoon angioplasty. As a rough guideline, we willaccept a 30% or less residual stenosis after stentdeployment. Next, the embolic protection deviceis retrieved and AP and lateral angiograms of thehead performed along with a brief on-table neuro-logic examination. If no complications are encoun-tered, the guiding sheath is exchanged over a wirefor a closure device to achieve hemostasis. Thepatient is then monitored in an ICU setting untilthe next morning with frequent neurologic exami-nations and close monitoring of blood pressure.

Long-term efficacy of carotid stenting in termsof stroke prevention appears to be equivalentto carotid endarterectomy but periproceduralmorbidity may be increased for patients under-going carotid stenting. CAS is reserved forselected symptomatic patients with such comor-bidities as post CEA re-stenosis, a history ofneck irradiation, contralateral laryngeal nervepalsy, anatomically surgically difficult lesions, orpoor surgical candidates because of major comor-bidities (Fig. 3). Low-risk patients should undergoCAS only in the setting of a RCT. Although

currently the standard of care for patients withextracranial carotid stenosis is carotid endarterec-tomy, it is likely that CAS will have an increasingrole to play in the treatment of carotid stenosis inthe future. We eagerly await the results of largeRCTs comparing the treatment modalities, and totechnological improvements to protection devicesand stents to further define the role of CAS in thetreatment of carotid artery stenosis.

EXTRACRANIALVERTEBRAL ARTERY STENOSIS

About 25% of all strokes involve the posteriorcirculation.19 The association between posteriorcirculation strokes and vertebral artery stenosisis less well defined than the relationship betweenanterior circulation stroke and carotid stenosis.The vertebral artery origin is the most commonlocation for vertebral artery stenosis and tends tobe associated with adjacent atherosclerosis inthe subclavian artery (similar to renal arterystenosis and aortic disease). One registry20 found20% of patients with symptoms of vertibrobasilarischemia to have a proximal vertebral arterystenosis (defined as at least 50% stenosis) andabout half of these patients also had contralaterallesions. The risk of stroke after posterior circula-tion transient ischemic attack has been reportedbetween 25% and 29% during 5- to 6-yearfollow-up.21 Despite medical therapy with warfarinor aspirin, these patients have a high recurrenceand death rate, reported as 16% to 18%.22

Fig. 3. Accelerated atherosclerosis post radiation (multiple vessels). (A) Arch arteriogram demonstrates markedirregularity of both common carotid arteries as well as the origins of the vertebral arteries bilaterally in a patientwith laryngeal carcinoma 5 years post radiation therapy. (B) Selective right vertebral artery arteriogram demon-strates diffuse irregularity in the proximal vertebral segment. (B) Selective left common carotid artery arterio-graphy demonstrates marked irregularity and a focal 1-cm stenosis with ulceration. (D, E) AP and lateral viewsfrom a right common carotid artery (RCCA) arteriogram in a 63-year-old with history of mantle therapy forlymphoma demonstrates occlusion of the internal carotid artery and a marked stenosis of the common carotidartery with ulceration (arrow). The external carotid artery provides collateral flow to the brain via ethmoidalcollaterals. (F) Following stent placement into the RCCA there was significant improvement in intracranial flow.


A number of case series have been publisheddescribing the primary deployment of balloonexpandable stents to treat lesions greater than50% with high technical success rates. Theseseries also report a low incidence of majorprocedure-related complications (0% to 3.4%)and low incidence of recurrence (1.7% to 3.0%)

on short- and intermediate-term follow-up (3 to37 months). Periprocedural posterior circulationtransient ischemic attacks (TIAs) were reportedat rates of 0% to 4.8%.23 Recently, use of anembolic protection device has been advocatedduring vertebral artery stenting to minimize risk ofintraprocedural stroke.24 The only randomized


controlled evaluation of vertebral artery PTA andstenting compared with medical managementwas a small subgroup of patients within theCAVATAS trial where 16 patients were random-ized. Results were nonrevealing owing to the smallsample size.13 A large RCT comparing extracranialvertebral artery stenting with best medicalmanagement has yet to be performed. Vertebralartery angioplasty and stenting can be consideredas an emerging therapy for patients with symp-tomatic vertebral artery stenoses that have failedbest medical management.

NONATHEROSCLEROTIC ARTERIAL INJURY

Patients with nonatherosclerotic vascular injuriesusually present with symptoms, often hemorrhageand/or stroke. This etiologically diverse categoryencompasses multiple pathologies includingtrauma (blunt, penetrating, and iatrogenic),vascular injury attributable to cancer or cancertreatment, spontaneous dissection and sequelae,and idiopathic epistaxis. Although these under-lying pathologies differ, the diagnostic algorithmand therapeutic approaches are similar allowingus to consider them together.

Management of these patients varies with theacuity of presentation, for example a patient withoral or nasal bleeding, or severe blunt or pene-trating trauma, would receive general supportivemeasures such as airway and hemodynamic resus-citation, before imaging including diagnostic angio-gram. CT scan and in many cases CT angiographycan be helpful for triage and evaluation of the site ofbleeding or vascular compromise. Once the lesionhas been diagnosed and defined, diagnostic angi-ography can be targeted and decisions can bemade about appropriate therapeutic options suchas distal embolization of the involved vessel, occlu-sion (sacrifice) of the vessel, or reconstructiveendovascular management such as placement ofa (covered) stent to treat the lesion. Arteriographymust include selective arteriography, assessmentof potential collaterals, especially the Circle ofWillis, in addition to identification of perilous extra-cranial-to-intracranial communications that couldlead to nontarget embolization if not appreciated.

VASCULAR TRAUMAOF THE FACE AND NECK

Trauma to the extracranial carotid or vertebralarteries may be either blunt or penetrating. Pene-trating trauma is by far the more common, withgunshot wounds accounting for most penetratingtraumatic injuries in the United States (Fig. 4).25

Although less common, blunt injury to the majorarteries of the head and neck can be devastating

with major neurologic morbidity and mortality ratesestimated around 60% and 30% respectively.26 Ofall comers to a level 1 trauma center with blunttrauma, 0.24% (37 of 15,331 patients) sustainedblunt carotid injury in a study published in 1999.This same study maintained that screening forblunt carotid injury identified a number of asymp-tomatic patients with serious injuries. Twenty-fiveof 2902 (0.86%) patients screened were diag-nosed with blunt carotid injury and 13 of those(52%) were asymptomatic.27

Prompt diagnosis and treatment are critical topatient outcome. CT angiography has becomethe imaging modality of choice in the emergencyroom setting. To our knowledge, no comprehen-sive comparison studies between CTA and angi-ography exist for screening of trauma patients.CT/CTA findings of vascular injury can vary widely(Fig. 5). Frank extravasation of contrast is rarelyencountered, but when present, is easily identifiedas nonvascular contrast. Complete traumaticocclusion of extracranial vessels often involvesthe cervical ICA 1 to 3 cm above the carotid bifur-cation or the vertebral artery at the level of cervicalfracture. Intramural hematoma and dissection canresult from blunt or penetrating trauma with vari-able compromise of the involved vessel lumen.Contained rupture of the injured major vessel(pseudoaneurysm) is most often initially irregularin shape but has a tendency to take on a moresmooth fusiform or saccular shape over time,depending on the vessel of origin.

Treatment of traumatic injury to the cervicalvasculature varies based on the mechanism, typeand location of injury, neurologic status, and thepresence of associated injuries. Extensive concur-rent injuries may preclude the use of antiplateletregimen needed to place and sustain covered stentgraft placement for major vessel injury. With pene-trating traumatic vascular injury, diagnostic angio-gram followed by endovascular treatmenttargeted specifically to the injury including distalvessel embolization with particulates, or liquidembolic agents. With blunt traumatic injury leadingto pseudoaneurysm or traumatic dissection seenon CTA, without hemorrhage or stroke, treatmentdecisions are less clear cut. Many advocate closeobservation in these patients, and if no contraindi-cations exist, treatment is with an anticoagula-tion/antiplatelet regimen, as complications fromthese injuries are usually embolic. However, if serialimaging demonstrates interval worsening ofimaging findings, or the patient becomes symp-tomatic from the lesion, intervention may be neces-sary. Vertebral artery dissection and/or occlusionmay be initially treated with vertebral artery sacri-fice to prevent recanalization and subsequent

Fig. 4. (A) Axial CT following gunshot wound to the right nose demonstrates bullet fragments traversing thecourse of the vertebral artery at C-1. (B) Lateral subtracted arteriogram demonstrates the path and occlusionof the vertebral artery proximal to the metallic fragments. (C) The vertebral artery was occluded with platinumcoils below the level of the bullet fragments with contrast stasis demonstrated in the distal arterial remnant.


distal embolization and stroke, particularly inpatients requiring cervical manipulation or othersurgery (Fig. 6). A recent review of the literaturefound favorable results for placement of coveredstents in the setting of ICA pseudoaneurysm(Fig. 7).28 If major vessel occlusion is seen on theCTA, endovascular options are limited. Althoughthere have been some good outcomes withopening occluded carotids in the setting of athero-sclerotic disease, there are few data on recanaliz-ing traumatically occluded vessels. Emergentsurgical bypass and/or thrombectomy are seldomused in this setting.

CAROTID BLOWOUT SYNDROME

Carotid blowout syndrome (CBS) is defined as therupture of the extracranial carotid arteries or one ofits major branches, with oral, nasal, or peritrachealbleeding and has been coined in the setting ofhead and neck neoplasm, most often squamouscell carcinoma. Carotid blowout is the most fearedsequela of head and neck cancer. Prior radiationtherapy or brachytherapy are believed to playa key role in the pathogenesis of carotid blowout,possibly because of the obliterating effects onthe vasa vasorum caused by radiation and theassociated weakening of the arterial wall. Prior

Fig. 5. CTA findings of vascular injury. (A) Oblique reformat CTA image demonstrates a pseudoaneurysm origi-nating from the distal common carotid artery at the level of the bulb with an expanding left cervical mass. (B)Lateral left common carotid arteriogram demonstrates the opacification of the pseudoaneurysm limit withdraping of the superior thyroid artery around partially thrombosed portion of the mass. (C) Axial CTA followingendarterectomy in a patient with expanding left cervical hematoma, demonstrates pseudoaneurysm at the levelof the anastomosis, best illustrated in continuity on the oblique reformatted image (D). (E) Axial CTA demon-strates typical appearance of a distal cervical ICA dissection with pseudo aneurysmal dilatation.


Fig. 6. (A) A 29-year-old male status post motor vehicle accident with bilateral perched facets and apparent verte-bral artery (VRT) occlusion. Note the proximal and distal segments of the vertebral artery (arrows). (B) Arterio-gram 5 days later demonstrates recanalization of the vertebral artery and focal irregularity at the level of theperched facets (arrows). (C) MRI diffusion weighted imaging demonstrates restrictive diffusion (arrow) consistentwith infarct in the distal vertebral territory.


radiation treatment has been associated witha sevenfold increase of CBS in patients withhead and neck cancer.29 Although not confinedwithin the classic definition of carotid blowoutsyndrome, it is important to keep in mind thatsignificant hemorrhage can also occur fromerosion of tumor into the internal jugular vein andfrom the tumor itself. In the past few years therehas been significant improvement in both diag-nosis and treatment of CBS.

The reported incidence of CBS in patients witha history of neck dissection is reported to rangefrom 3% to 4%.30 In the past, carotid blowout hasresulted in very significant mortality and morbidity.Recent improvement in care has markedly reducedboth mortality and morbidity.31 Carotid blowout isnow approached as a syndrome, with manifesta-tions that can range from acute life-threateninghemorrhage to asymptomatic encasement ofa carotid artery. CBS can be categorized into oneof three categories: threatened, impending, andacute carotid blowout. Threatened carotid blowoutisdefinedasphysical examination or imaging resultsthat suggest inevitable hemorrhage from one of thecarotid arteries or its branches if no action is taken.Impending carotid blowout (also called sentinelhemorrhage) is defined as transient hemorrhagethat resolves spontaneously or with packing/pres-sure. Acute carotid blowout represents hemorrhagethat cannot be controlled by packing or pressure.32

Once carotid blowout syndrome is clinically sus-pected, the conventional gold standard for diag-nosis has been digital subtraction angiography(DSA). However, we believe that noncontrast CTand/or CT angiography have an important role indiagnosis in clinically stable patients. It is usefulto understand the extent of tumor, prior surgery,or region treated with brachytherapy seeds beforeangiography (Fig. 8). Unfortunately, there is a lackof literature on the sensitivity and specificity ofangiography, and to our knowledge, there is nodirect comparison between DSA and CTA for eval-uation of carotid blowout syndrome.

Management and Angiographic Approachto Carotid Blowout Syndrome

Initial management of these complex patientsrevolves around the airway. Controlling the airwayis paramount and intubation to prevent aspirationis necessary. Oral, nasal, or wound packing isadjunctive to fluid resuscitation measures andtransfusion. Manipulation of the neck woundshould be minimized. Once the patient has beenstabilized, direct diagnostic and therapeutic strat-egies can be used.

It is critically important to discuss treatmentoptions and expectations with the patient and/orfamily representatives with regard to decisionmaking regarding stroke/death risk versus

Fig. 7. (A) MRA multiple intensity projection (MIP) image in a patient with chronic neck pain demonstrates pseu-doaneurysm of the internal carotid artery near the skull base. Following angiographic confirmation (B), overlap-ping stents were placed using a protection device to exclude the pseudoaneurysm from the circulation (C).


bleeding/death risk in the treatment of CBS. Patientand family wishes and preferences, including resus-citation status, should be taken into account ifbleeding cannot be stopped without significantstroke risk. There are some patients who prefer notto accept the risk of carotid occlusion in spite ofthe grave prognostic implications of untreated CBS.

Diagnostic angiography varies slightly based onthe nature and location of the hemorrhage. Bilat-eral imaging of the common carotids, the internalcarotids, the external carotids, and the vertebralarteries will establish the bleeding site as well asthe integrity of the Circle of Willis. This is importantin patients who may require carotid artery sacri-fice. Selective external carotid branch arteriog-raphy is often required to identify a bleeding site

not demonstrable on more global injections.31,33

Internal maxillary, facial, lingual, ascendingpharyngeal, and superior thyroid arteries are thevessels most commonly affected. In patients withperitracheal bleeding, the thyrocervical trunksmust also be examined bilaterally.

MAJOR VESSEL LESIONS

During the initial angiographic assessment, cath-eter placement should be proximal to the sus-pected carotid injury. The location of surgicalclips and brachytherapy seeds are local indicatorsof the potential site of vascular compromise. Forfrank rupture, sacrifice of the carotid artery aboveand below the point of rupture will prevent the

Fig. 8. (A–D) A 72-year-old status post salvage laryngectomy for squamous cell carcinoma of larynx with intrac-table oral bleeding. Axial (A) and coronal (B) CTA demonstrates air (white arrows) dissecting within the carotidspace directly adjacent to the left internal carotid artery (ICA) (black arrow) and a local soft tissue mass. Note theabsence of the internal jugular vein (IJV) on the left. (C) AP LCCA arteriogram demonstrates marked irregularityof the distal CCA, stenosis at the origin of the ICA with marked irregularity to the level of the skull base. A stump(white arrow) is seen at the origin of the external carotid artery. (D) AP RCCA angiogram demonstrates robustcollaterals filling the left intracranial vasculature from the right ICA and the right vertebral arteries. Note thecoil mass on the left. (E–G) A 60-year-old male with nasopharyngeal carcinoma and oral bleeding. (E) Narrowingof the internal carotid artery with a small angular contrast collection consistent with pseudoaneurysm withina soft tissue tumor mass (white arrows). The IJV is occluded. (F) Angiography confirms the PSA and the adjacentICA stenosis. (G) The ICA and the PSA were permanently occluded using detachable platinum coils. Control arte-riography demonstrates prompt filling of distal ethmoidal branches of the IMA to collateralize with theophthalmic artery (OPH) that is filling retrogradely to reconstitute the supraclinoid ICA.

498

Fig. 9. A62-year-old patient 2 weeks post endoscopic resection of presumed recurrent nasopharyngeal carcinoma.(A) AP view of a left internal carotid artery (ICA) arteriogram demonstrates narrowing and irregularity of thepetrous internal carotid artery (arrows) adjacent to the site of recent surgery. (B) Following successful left ICABOT, the ICA was occluded permanently using a combination of platinum detachable coils and the AmplatzerPlug (AP).


creation of a pattern of unreachable collateral flow.Often both the internal and external carotidbranches must be occluded (see Fig. 8). Carotidsacrifice was formerly performed with detachablesilicone or latex balloons; however, these are notcurrently available in the United States. Currentlywe perform carotid sacrifice with detachable coils,with variable adjunctive use of the Amplatzervascular plug (AGA Medical Corporation, Ply-mouth, MN) for occlusion of the proximal aspectof the vessel (Fig. 9).

In CBS patients with a lesion of the common orinternal carotid, such as pseudoaneurysm, ulcera-tion, or long-segment irregularity, sacrifice of theinvolved carotid may be the only life-saving option.Ideally, when time permits, a temporary balloonocclusion test (BOT) is performed to ascertaintolerance of carotid artery occlusion before theprocedure. The three components of a temporaryballoon occlusion test include diagnostic arteriog-raphy for collateral assessment, clinical testingduring temporary occlusion, and TC-hexamethyl-propyleneamine oxime–single-photon emissioncomputed tomography (HMPAO-SPECT) or xenonCT evaluation of cerebral blood flow duringtemporary occlusion. Balloon occlusion testing isfurther described elsewhere in this issue.

Covered stent (stent graft) placement has beenused for salvage of major vessels in carotidblowout. This technology is limited in the settingof open wounds, active infection, and unfavorableanatomy. The use of covered stents may be anoption in some patients; however, one must beprepared to convert a stent procedure into carotidocclusion if hemostasis cannot be maintained

(Fig. 10).34,35 When carotid sacrifice cannot besafely performed because of lack of collateralflow or a lack of tolerance of temporary balloonocclusion testing, and stent placement is not anoption, surgical extracranial-to-intracranial bypasstechniques may be considered, in association withcarotid sacrifice, to augment cerebral blood flow.36

When CBS manifests as uncontrollable hemor-rhage, carotid sacrifice must then be performedwithout clinical preocclusion testing (as a life-saving procedure). In this situation, HMPAO-SPECT is sometimes performed followingocclusion to assist in postocclusion ICU hyperten-sive and hypervolemic management. Theocclusion balloon is withdrawn and the carotidsacrificed using retrievable and/or detachablecoils. Alternatively, the occlusion balloon cathetercan be left in place with the balloon inflated anda microcatheter advanced through the lumen ofthe occlusion balloon and embolization of thedistal ICA performed during balloon occlusion ofthe proximal ICA. This allows immediate controlof bleeding and the ability to raise blood pressureto enhance cerebral perfusion during the perma-nent occlusion. Clinical management in the ICUincludes neurologic monitoring and hemodynamicmeasures to maintain cerebral perfusion pressure.CT scan of the head can be adjunctive followingpatient stabilization.

NON^MAJOR VESSEL SOURCESOF HEMORRHAGE

Significant oral, nasal, or peritracheal bleedingmay result from tumoral neovascularity or erosion

Fig.10. (A) Carotid blowout with massive oral bleeding into the pharynx demonstrates marked irregularity withextravasation. Note extensive radiation seeds. (B) Following failed BOT, two overlapping covered stents wereplaced in the common carotid artery with the achievement of hemostasis. (C) Twenty-four hours later, therewas recurrent oral bleeding, and despite placement of two additional overlapping stents, contrast extravasationwas again demonstrated. The carotid artery was sacrificed permanently. The patient survived without neurologicdeficit for 18 months. (From Johnson MH. Carotid blowout syndromes. Endovascular Today 15–18 Jan/Feb 2003;with permission.)


through the wall of a small external carotid branchvessel, rather than major vessel erosion. Selectiveexternal carotid branch arteriography is oftenrequired to demonstrate the bleeding site. Micro-catheterization both permits identification of thebleeding site and allows for more selective place-ment of embolic material. Selection of embolicmaterial depends on the site and the nature ofthe hemorrhage source. In our experience, in thetrauma setting, embolization is most often per-formed with particulate such as polyvinyl alcoholfoam (PVA) or gelfoam, with or without adjunctiveplacement of coils. In the setting of head andneck cancer, radiation, and infection, liquidembolic agents are more durable in these fragile,diffusely diseased vessels (Fig. 11).

TUMORAL HEMORRHAGE

Hemorrhage derived from neovascularity of thetumor or local granulation tissue can be treatedwith medium-sized, 250-micron to 350-micronparticles of PVA suspended in dilute contrastmedia. We introduce the particles into the tumorunder roadmap guidance using a microcatheterand 1-cc syringes until the neovascularity is suffi-ciently reduced. Proximal gelfoam pledgets maybe adjunctive. This is a temporizing measure thatmay allow for healing of friable tumor. One should

avoid using small 50-micron to 150-micron parti-cles if additional surgery is not planned, to avoidfrank tumor necrosis and subsequent secondaryinfection.

VASCULAR LACERATIONOR PSEUDOANEURYSM

Vascular laceration or pseudoaneurysm (PSA) maybe treated directly with microcatheter embolizationto address the specific bleeding site in the setting oftrauma or head and neck cancer/tumor/radiation(CBS). Embolic materials vary with the setting. Gel-foam with or without complex helical coils may beused for a discrete vessel laceration in the settingof trauma. This will control bleeding in an otherwiseintrinsically normal lacerated vessel; we use Trufilln-BCA Liquid Embolic System (Cordis Corpora-tion, a Johnson & Johnson company, Miami, FL),where possible, for pseudoaneurysm or focalextravasation (Fig. 12). Proximal vessel coil embo-lization should be avoided, because it does notdirectly address the site of pathology. In mostcases, when attempts at proximal occlusion havefailed to control hemorrhage, small microcatheterscan navigate beyond proximally placed clips orcoils for more distal embolization. When choosingan embolic agent, pay attention to the site of thelesion, the nature of adjacent collaterals, the distal

Fig. 11. (A) Lateral common carotid artery angiogram in a patient with a base of tongue cancer demonstratesmarked irregularity of the facial artery (black arrow) and marked narrowing and irregularity with pseudoa-neurysm of the lingual artery. (B) Selective lingual arteriogram demonstrates marked narrowing and irregularityand a pseudoaneurysm of the lingual artery at the tongue base. (C) The lingual artery and pseudoaneurysm wereembolized with NBCA (see the radio-opaque glue cast in the lingual artery after embolization).


parenchymal territory, and the role of embolization(ie, presurgical or palliative).

EXTRACRANIAL CAROTID AND VERTEBRALARTERY SPONTANEOUS DISSECTION

Arterial dissection is an intimal tear in the wall of anartery allowing intrusion of blood products withinthe layers of the arterial wall. As this hematomain the false lumen between the intima and mediaexpands, it may compress the true lumen, result-ing in stenosis, occlusion, and/or pseudoaneur-ysm formation with weakening of the media andadventitia. Spontaneous or nontraumatic dissec-tion of the extracranial carotid and vertebraldissection were once thought to be rare, but mayaccount for as many as 20% of strokes in patientsyounger than 45 years.37

The pathogenesis of spontaneous dissection isincompletely understood. A history of minor necktrauma is often present although not universal.Patients with underlying connective tissue disor-ders such as fibromuscular dysplasia, Ehlers-Dan-los syndrome, Marfan’s syndrome, and alfa 1antitrypsin deficiency syndrome may be more

vulnerable to cervical vascular dissection. Therehas been speculation that recent infection mayplay a role in the pathogenesis of dissection, inpart supported by some seasonal variance.38 Ithas also been speculated that migraine history,hypertension, and smoking may contribute toincreased risk of dissection.

Carotid and vertebral dissection are classifiedinto extradural (extracranial) and intradural(intracranial) dissections. Extradural/extracranialdissection is far more common although intraduralextension of dissection is usually more significantand carries a poorer prognosis and a risk ofsubarachnoid hemorrhage. Spontaneous dissec-tion is more common in the carotid arteries (80%)than in the vertebral arteries.39 The arterialsegments affected differ between dissection andatherosclerosis. Dissection often involves the distalpart of the ICA near the point of fixation at the entryinto the carotid canal at the skull base, whereasatherosclerosis most often affects the carotidbulb and the origin of the ICA. Vertebral dissectionfrequently occurs near points of fixation such as theentry or exit from the foramen transversarium andwhere the vertebral artery pierces the dura at the

Fig.12. (A) Recurrent epistaxis following left internal carotid artery occlusion demonstrates a PSA of the secondportion of the IMA. (B) Acrylic glue is identified within the PSA. (C) Oral bleeding 7 days post resection and graftplacement for treatment of floor of mouth cancer demonstrates a PSA of the graft at the anastomosis (whitearrows). (D) Acrylic glue cast demonstrated within the PSA. The graft remained viable.


foramen magnum. Atherosclerosis tends to involvethe origin of the vertebral artery.

Classic clinical features of spontaneous dissec-tion are often not present, but include neck pain,Horner’s syndrome, headache, cranial nervepalsies, and neurologic deficits secondary todistal embolization or ischemia from flow compro-mise. Embolic phenomena are most commonbecause of platelet aggregation at the site ofinjury and distal embolization. A study from 2004demonstrated territorial infarcts (presumedembolic in origin) in all patients with dissectioncontrasted with watershed infarcts (secondary tohemodynamic phenomena) in only 5% of thesepatients.40

Extracranial dissection is readily diagnosed withnoninvasive methods such as Doppler ultrasound,MRI/MR angiography (MRA), and most recentlywith CT angiography (CTA). Identification of thefalse lumen filled with thrombus on the T1 fat satu-ration image is diagnostic. Irregularity of the lumenor sharp edges rather than curves on the axial CTAimages are equally diagnostic when the studiesare technically of good quality (Fig. 13). Catheterangiography is usually performed only for prob-lematic cases or when intervention is considered.

Treatment is essentially medical and rarely dothese patients require endovascular or operativemanagement. Once diagnosed, thromboembolismis the most feared possible sequalae. Management

Fig. 13. (A) Axial CTA demonstrates a spontaneous dissection of the internal carotid artery with surroundingthrombus (*). Spontaneous dissection is similarly well demonstrated on fat-saturation T1-weighted images (B).


revolves around minimizing the risk of embolicphenomenon using antiplatelet agents as themainstay of treatment. In cases with severeluminal compromise, short-term heparin and/orwarfarin administration is sometimes used.

The prognosis depends largely on the severity ofneurologic deficit incurred before diagnosis, but isgenerally good with vessel wall healing with extra-cranial dissection. Recurrence rates are very low inthe absence of underlying connective tissuedisease.

IDIOPATHIC EPISTAXIS

A majority of the adult population will experienceepistaxis during their lifetime although only a smallminority will experience bleeding requiring medicalattention.41 There is a small group of patients whodo not respond to conservative therapies such aslocal packing. Epistaxsis is deemed idiopathic ifthere is no known underlying etiology such astrauma or tumor. These patients are treated withvarious forms of therapy including posterior andanterior packing, vasoconstrictors, endoscopiccautery, surgical ligation and/or endovascularembolization. Patients with posterior epistaxisare said to be particularly difficult to manageconservatively and often require a more aggres-sive treatment regimen including endovascularembolization.42 Endovascular embolization of idio-pathic epistaxis was first described in 1974 by So-koloff and colleagues.43 Since that time, numerousseries have been published detailing results andtechnique. A recent review of the literature showedan average technical success rate of 88% andaverage postprocedural complication rate to be12%.44 The most common agent used in theseseries was PVA, with particle size varying from50 to 750 micrometers although many differentdistal particulates were used such as embo-spheres and gelfoam. Endovascular embolization

has a high success rate and low morbidity rate.Primary success rates range from 79% to 96%with recurrence after embolization ranging from0% to 24%. Major complications secondary toepistaxis embolization were rare, 3%, consistingof stroke (most common), monocular blindness,skin sloughing, ICA dissection and postproceduralMI.44 Minor complications such as self-limitingfacial pain and numbness have also beendescribed. Randomized comparison of emboliza-tion to other forms of treatment, such as surgery,have not been performed.

An important caveat is worth mentioning.Epistaxis in the setting of hereditary hemorrhagictelangiectasia (HHT or Osler-Weber-Rendudisease) is, in our experience, refractory to effec-tive treatment with embolization. It has been ourexperience and confirmed in the literature thatpatients with HHT do not have a durable resultafter embolization and fare much better with oper-ative septal dermoplasty as the initial therapeuticstrategy to control severe epistaxis.45

When performing endovascular embolization forepistaxis, a complete diagnostic angiogram isabsolutely essential. This includes detailed evalua-tion of the external and internal carotid arteries.The primary vascular supply to the nasal mucosaincludes the internal maxillary and distal facialarteries (Fig. 14). The distal most branches of theophthalmic artery may also contribute and maybecome more prominent following embolizationof the internal maxillary and facial nasal supply.Rarely, epistaxis may be caused by internalcarotid pathology, particularly in the setting ofprior radiation treatment or trauma (see Fig. 9).Evaluation of the ICA is also critical to minimizethe risk of nontarget embolization and to delineateanastamoses between the ECA and ICA circula-tions. It has been our experience that a definitebleeding site is very infrequently seen duringangiography for idiopathic epistaxis. Traditionally,

Fig. 14. (A) The blood supply to the nasal mucosa and septum is derived from the IMA and facial artery (FAC),which provide a balanced circulation (white arrows). (B) Microcatheter injection into the distal internal maxillarynasal branches demonstrates a normal nasal arterial arcade. (C) Distal facial microcatheter arteriogram demon-strates extensive arterial vascular supply to the nasal mucosa and septum.


embolization for idiopathic epistaxis has involvedangiography of the distal nasal branches of theinternal maxillary and facial arteries followed byparticulate (PVA) embolization of three of the fourbranches (usually both distal internal maxillaryartery [IMA] and the dominant facial artery) toreduce the opportunity for collateral flow to friablenasal vessels before they have time to heal. A keycomponent to decision making is laterality. If theside of bleeding has been determined before angi-ography, some authors feel that single-vesselembolization, usually the IMA is sufficient forcontrol. The ipsilateral facial nasal branches maythen be embolized if there is significant vascularcontribution to the nasal mucosa.46

SUMMARY

It is imperative for the neuroendovascularspecialist to be proficient with diagnosis and treat-ment of common extracranial pathologies. Foratherosclerotic vascular disease, technologiescontinue to improve and potentially expand therole of endovascular techniques for treatmentwhile study trials are ongoing and results areanxiously awaited to determine the ultimate roleof CAS in disease management. For traumaticvascular injury, embolization for vessel closureand vessel preservation using stents and stentgrafts are a routine part of patient management.Although carotid blowout remains a challenge for


rapid triage and treatment, our expanding toolsand aggressive ICU management help manypatients to survive potentially catastrophic hemor-rhage. The neuroendovascular techniques areuniquely suited to treat a wide variety of extracra-nial vascular diseases.

REFERENCES

1. Meyers PM, Schumacher HC, Higashida RT, et al.

Use of stents to treat extracranial cerebrovascular

disease. Annu Rev Med 2006;57:437–54.

2. North American Symptomatic Carotid Endarterec-

tomy Trial Collaborators. Beneficial effect of carotid

endarterectomy in symptomatic patients with high-

grade carotid stenosis. N Engl J Med 1991;325:

445–53.

3. Randomised trial of endarterectomy for recently

symptomatic carotid stenosis: final results of the

MRC European Carotid Surgery Trial (ECST). Lancet

1998;351:1379–87.

4. Eliasziw M, Smith RF, Singh N, et al. Further

comments on the measurement of carotid stenosis

from angiograms. North American Symptomatic

Carotid Endarterectomy Trial (NASCET) Group.

Stroke 1994;25(12):2445–9.

5. Barnett HJ, Taylor DW, Eliasziw M, et al. Benefit of

carotid endarterectomy in patients with symptomatic

moderate or severe stenosis. North American Symp-

tomatic Carotid Endarterectomy Trial Collaborators.

N Engl J Med 1998;339:1415–25.

6. Endarterectomy for asymptomatic carotid artery

stenosis. Executive Committee for the Asymptomatic

Carotid Atherosclerosis Study. JAMA 1995;273:

1421–8.

7. Asymptomatic Carotid Surgery Trial (ACST) Collab-

orative Group. Prevention of disabling and fatal

strokes by successful carotid endarterectomy in

patients without recent neurological symptoms:

randomized controlled trial. Lancet 2004;

363(9420):1491–502.

8. Mayberg MR, Wilson SE, Yatsu F, et al. Carotid

endarterectomy and prevention of cerebral ischemia

in symptomatic carotid stenosis. Veterans Affairs

Cooperative Studies Program 309 Trialist Group.

JAMA 1991;266:3289–94.

9. Results of a randomized controlled trial of carotid

endarterectomy for asymptomatic carotid stenosis.

Mayo Asymptomatic Carotid Endarterectomy Study

Group. Mayo Clin Proc 1992;67:513–8.

10. Moore WS, Barnett HJ, Beebe HG, et al. Guidelines

for carotid endarterectomy. A multidisciplinary

consensus statement from the Ad Hoc Committee,

American Heart Association. Stroke 1995;26:

188–201.

11. Bockenheimer SA, Mathias K. Percutaneous translu-

minal angioplasty in arteriosclerotic internal carotid

artery stenosis. AJNR Am J Neuroradiol 1983;4:

791–2.

12. Naylor AR, Bolia A, Abbott RJ, et al. Randomized

study of carotid angioplasty and stenting versus

carotid endarterectomy: a stopped trial. J Vasc

Surg 1998;28:326–34.

13. Endovascular versus surgical treatment in patients

with carotid stenosis in the Carotid and Vertebral

Artery Transluminal Angioplasty Study (CAVATAS):

a randomised trial. Lancet 2001;357:1729–37.

14. Yadav JS, Wholey MH, Kuntz RE, et al. Protected

carotid-artery stenting versus endarterectomy in

high-risk patients. N Engl J Med 2004;351:

1493–501.

15. Ringleb PA, Allenberg J, Bruckmann H, et al. 30 day

results from the SPACE trial of stent-protected angio-

plasty versus carotid endarterectomy in symptom-

atic patients: a randomised non-inferiority trial.

Lancet 2006;368:1239–47.

16. Mas JL, Chatellier G, Beyssen B, et al. Endarterec-

tomy versus stenting in patients with symptomatic

severe carotid stenosis. N Engl J Med 2006;355:

1660–71.

17. Hobson RW, Howard VJ, Roubin GS, et al. Carotid

artery stenting is associated with increased compli-

cations in octogenarians: 30-day stroke and death

rates in the CREST lead-in phase. J Vasc Surg

2004;40:1106–11.

18. Gaines PA, Randall MS. Carotid artery stenting for

patients with asymptomatic carotid disease (and

news on TACIT). Eur J Vasc Endovasc Surg 2005;

30:461–3.

19. Bogousslavasky J, van Melle G, Regli F. The Lau-

sanne Stroke Registry: analysis of 1,000 consecu-

tive patients with first stroke. Stroke 1988;19:

1083–92.

20. Wityk RJ, Chang HM, Rosengart A, et al. Proximal

extracranial vertebral artery disease in the New

England Medical Center Posterior Circulation

Registry. Arch Neurol 1998;55:470–8.

21. Hornig CR, Lammers C, Butter T, et al. Long term

prognosis of intratentorial transient ischemic attacks

and minor strokes. Stroke 1992;23:199–240.

22. Mohr JP, Thompson JL, Lazar RM, et al. A compar-

ison of warfarin and aspirin for the prevention of

recurrent ischemic stroke. N Engl J Med 2001;345:

1444–51.

23. Zavala-Alarcon E, Emmans L, Little R, et al. Percuta-

neous intervention for posterior fossa ischemia. A

single center experience and review of the literature.

Int J Cardiol 2008;127:70–7.

24. Henry M, Polydorou A, Henry I, et al. Angioplasty

and stenting of extracranial vertebral artery stenosis.

Int Angiol 2005;24:311–24.

25. Davis JM, Zimmerman RA. Injury of the carotid

and vertebral arteries. Neuroradiology 1983;25:

55–69.


26. Cogbill TH, Moore EE, Meissner M, et al. The spec-

trum of blunt injury to the carotid artery: a multicenter

perspective. J Trauma 1994;37:473–9.

27. Biffl WL, Moore EE, Ryu RK, et al. The unrecognized

epidemic of blunt carotid artery injuries. Ann Surg

1999;228(4):462–9.

28. Maras D, Lioupis C, Magoufis G, et al. Covered

stent-graft treatment of traumatic internal carotid

artery pseudoaneurysms: a review. Cardiovasc

Intervent Radiol 2006;29:958–68.

29. Maran AGD, Amin M, Wilson J. A radical neck

dissection: a 19 year experience. J Laryngol Otol

1989;10:760–4.

30. Koch WM. Complications of surgery of the neck. In:

Eisele D, editor. Complications in head and neck

surgery. St Louis (MO): Mosby; 1993. p. 393–413.

31. Morrissey DD, Andersen PE, Nesbit GM, et al. Endo-

vascular management of hemorrhage in patients

with head and neck cancer. Arch Otolaryngol

Head Neck Surg 1997;123(1):15–9.

32. Chaloupka JC, Roth TC, Putman CM, et al. Recur-

rent carotid blowout syndrome: diagnostic and ther-

apeutic challenges in newly recognized subgroup of

patients. AJNR Am J Neuroradiol 1999;5:1069–77.

33. Chaloupka JC, Putman CM, Citardi MJ, et al. Endo-

vascular therapy for the carotid blowout syndrome in

head and neck surgical patients: diagnostic and

managerial considerations. Am J Neuroradiol 1996;

17:843–52.

34. Lee S, Huddle D, Awad IA. Indications and manage-

ment strategies in therapeutic carotid occlusion.

Neurosurg Q 2000;10:211–23.

35. Roth TC, Chaloupka JC, Putman CM, et al. Percuta-

neous direct-puncture acrylic embolization of

a pseudoaneurysm after failed carotid stenting for

the treatment of acute carotid blowout. Am J Neuro-

radiol 1998;19(5):912–6.

36. Toyoda T, Sawatari K, Yamada T, et al. Endovascular

therapeutic occlusion following bilateral carotid

artery bypass for radiation-induced carotid artery

blowout: a case report. Radiat Med 2000;18(5):

315–7.

37. Bogousslavsky J, Pierre P. Ischaemic stroke in

patients under age 45. Neurol Clin 1992;10:113–24.

38. Grau AJ, Brandt T, Buggle F, et al. Association of

cervical artery dissection with recent infection.

Arch Neurol 1999;56:851–6.

39. Schievink WI, Mokri B, Whisnant JP. Internal carotid

artery dissection in a community: Rochester, Minne-

sota, 1987–1992. Stroke 1993;24:1678–80.

40. Benninger DH, Georgiadia D, Kremer C. Mechanism

of ischaemic infarction in spontaneous carotid

dissection. Stroke 2004;35:482–5.

41. Shaw CB, Wax MK, Wetmore SJ. Epistaxis:

a comparison of treatment. Otolaryngol Head Neck

Surg 1993;109:60–5.

42. Sinuloto TM, Leinonen ASS, Karttunen AI, et al. Embo-

lization for the treatment of posterior epistaxis. Arch

Otolaryngol Head Neck Surg 1993;119:837–41.

43. Sokoloff J, Wickborn I, McDonald D, et al. Thera-

peutic percutaneous embolization in intractable

epistaxis. Radiology 1974;111(2):285–7.

44. Christensen NP, Smith DS, Barnwell SL, et al. Arterial

embolization in the management of posterior

epistaxis. Otolaryngol Head Neck Surg 2005;133:

748–53.

45. Layton KF, Kallmes DF, Gray LA, et al. Endovascular

treatment of epistaxis in patients with hereditary

hemorrhagic telangiectasia. AJNR Am J Neuroradiol

2007;28:885–8.

46. Johnson MH, Chiang VL, Ross DA. Interventional

neuroradiology adjuncts and alternatives in patients

with head and neck vascular lesions. Neurosurg Clin

N Am 2005;16:547–60.

endovascular management of extracranial carotid and ... · endovascular management of extracranial...

Documents