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Abstract and Introduction

Abstract

A variety of head and neck vascular emergencies, such as nosebleeds or neoplastic hemorrhages, can occur spontaneously o

result from blunt or penetrating trauma. As most traumatic venous bleeding can be resolved with direct pressure, the main

focus is on arterial injury. The role of catheter angiography in the acute trauma setting has shifted over the past 15 years, with

the concomitant advances in computed tomography (CT) angiography for diagnosis, and development of microcatheters and

embolic agents for therapy.

Introduction

A variety of head and neck vascular emergencies, such as nosebleeds or neoplastic hemorrhages, can occur spontaneously o

result from blunt or penetrating trauma. As most traumatic venous bleeding can be resolved with direct pressure, the main

focus is on arterial injury. The role of catheter angiography in the acute trauma setting has shifted over the past 15 years, with

the concomitant advances in computed tomography (CT) angiography for diagnosis, and development of microcatheters andembolic agents for therapy.

Regional trauma associations have proposed algorithms for which patients should be evaluated by CT angiography and/or

catheter angiography for traumatic head and neck vascular injuries.[13] These include high-risk mechanisms such as: high-

energy collisions, neck hyperextension injury, intra-oral trauma, and near-hanging with anoxic brain injury. Additionally, CT or

catheter angiography should be considered in patients with LeFort/midface fractures, cervical spine or basilar skull fractures,

diffuse axonal injury with Glasgow Coma Scale (GCS) < 6, a new focal neurological deficit, neurological examination

incongruous with head CT findings, or imaging evidence of a new cerebral infarct in the setting of trauma.

Clinically occult head and neck vascular injury is rare; however, aggressive CT screening in asymptomatic patients has become

commonplace given the potentially devastating sequelae of a missed diagnosis,[46] combined with ease of access to CT

angiography. Ongoing discussion in the trauma community continues regarding patient selection criteria, given the concerns of

cost effectiveness of broad screening in asymptomatic patients as well as minimizing unnecessary radiation exposure.

There remain cases in which conventional angiogram remains the 'gold standard.' These include CT angiograms limited by

artifact from dental implants/amalgam, from metal or shrapnel, situations where appropriate bolus timing cannot be achieved,

and hemodynamically unstable patients with a high probability of requiring endovascular intervention. Diagnostic catheter

angiogram should always be considered in a patient with high suspicion for cervical vascular injury in the setting of a normal CT

angiogram, as this is a dynamic disease process and contrast opacification of a vessel on cross-sectional imaging may not

fully reflect flow dynamics and collateral pathways.

Large Arterial Lacerations, Pseudoaneurysms, and Arteriovenous Fistulae

Damage to the arterial wall can result in life-threatening hemorrhage, and patients with large arterial lacerations due to

penetrating trauma have significant mortality before reaching hospital care. Alternatively, hemorrhage may be contained by

development of a pseudoaneurysm or diverted through a traumatic arterial-venous fistula. In dealing with a patient with a

potential arterial laceration, it is crucial to maintain hemodynamic and ventilatory support throughout the search for and

treatment of the active bleeding site.

Exploration of anterior neck wounds is usually done surgically, given adequate exposure and direct visualization of the carotid

arteries.[7] In patients with active hemorrhage from a carotid or vertebral laceration, there is a high risk of stroke or even death

despite aggressive treatment, including surgical ligation or endovascular embolization of the vessel. Given the difficult surgical

approach to the carotid artery at the skull base and the vertebral arteries, [8,9] the interventional neuroradiologist can provide

great support to the trauma team with an endovascular approach to treatment at these sites. [10,11,12] Additionally, in patients

Angiographic Evaluation and Treatment for Head and Neck Vascular InjuryJulie Bykowski, MD; Wade Wong, DO, FACR, FAOCR

Posted: 04/26/2012; Appl Radio l. 2012;41(3):10-16. 2012 Anderson Publishing, Ltd.


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with extensive facial fractures or penetrating injuries, an endovascular approach to control bleeding is preferred (Figure 1).

Figure 1. (A) CT scan of a 22-year-old man with massive facial hemorrhage following a gunshot wound. (B) Early arterial

phase of left external carotid arteriogram shows active contrast extravasation (arrowhead). (C) Left external carotidarteriogram after embolization with gel foam slurry confirms cessation of extravasation.

Pseudoaneurysms result from arterial bleeding into the wall of an injured vessel. This can manifest as a focally expanded

dissection with containment by the adventitia, or containment of leakage outside of the vessel wall by a layer of clot. While

some extremity pseudoaneurysms have been reported to resolve spontaneously, [13] asymptomatic pseudoaneurysms of the

carotid arteries are generally treated to preclude thromboembolic stroke and reduce the risk of re-bleeding. Endovascular

embolization with coils or balloon occlusion is often favored over direct surgical exploration; [14,15] however, it should be done

with care as re-bleeding is common given the fragility of structures containing the site of injury (Figure 2). In some situations, a

stent may be sufficient to divert flow, allowing the pseudoaneurysm to thrombose without coil deployment.[1618] Some

controversy persists regarding the risks and benefits of stent placement, with long-term stent occlusion rates reported in up to

45% of patients in early series.[19] Discussion continues about the ideal timing of treatment, perceived benefits of different sten

features, and optimal concomitant antiplatelet therapy in these patients.[20]


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Figure 3. (A) 38-year-old woman complained of "swooshing" sound after whiplash injury. Right external carotid

arteriogram confirms arteriovenous fistula, supplied by small branches of the right occipital artery. (B) A microcatheter was

advanced into the right occipital artery and successful embolization of feeder branches was performed with 200-micron

polyvinyl alcohol (PVA) particles.

Figure 4. (A) CT scan in 18-year-old-man with facial trauma revealed an enlarged left superior ophthalmic vein. (B) Left

internal carotid arteriogram confirmed the presence of a carotid cavernous fistula. (C) Arteriogram repeated after

detachable balloon placement in the single hole shunt of the fistula shows occlusion of the fistula.

In situations where vessel sacrifice is considered, occlusion by balloons or coils should only be done after a thorough test

balloon occlusion to ensure there will not be undesired, irreversible neurological sequelae. Unilateral vertebral artery occlusion

is considered more forgiving as long as the contralateral, uninjured vertebral artery has adequate caliber and the embolization

material can be deployed proximal to the posterior inferior cerebellar artery (PICA), preserving collateral supply on the side of

injury.[24,25] A typical balloon test occlusion is performed by anticoagulating the patient with heparin and then advancing an

occlusive balloon across or distal to the site of injury, to cause cessation of blood flow. Neurological testing for the carotid

artery would include evaluation of pronator drift, motor, sensory, and memory function. Vertebral artery neurological testing

during balloon occlusion is less reliable, however, and emphasis should be placed on coordination, motor, and sensory


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function. The balloon test occlusion is typically maintained for 30 minutes or until the patient fails the procedure.

Extracranial Arterial Dissections and Occlusions

Arterial dissections in the head and neck usually are associated with deceleration and shear injuries. These include injuries to

the proximal cervical vertebral artery, and the distal internal carotid and vertebral arteries below the skull base. Vertebral artery

dissections can also occur at the sites of transverse foramen fractures, and these areas should be carefully evaluated in the

setting of cervical spine trauma.[26] Occlusions can result from sluggish flow in the dissected vessel, compounded by

underlying atherosclerotic disease.

In the acute setting, CT angiography is commonly used to evaluate for vessel irregularity and filling defects. MR imaging,

particularly T1 fat-saturated sequences, is sensitive for the detection of methemoglobin in a false lumen of a dissection [27]

(Figure 5). However, within the first 3 days after the traumatic event, the blood products often have only intermediate signal

changes. Diagnostic catheter angiography may be needed in patients with artifact from bullet fragments or dental amalgam or

difficult evaluation at the skull base.

Figure 5. (A) MR imaging reveals T1-hyperintense methemoglobin (black arrowhead) surrounding a narrowed left internal

carotid artery, confirming dissection. (B) Corresponding angiogram confirms focal vessel narrowing at the point of

dissection (lower arrowhead). Thrombus is also noted distally within the left internal carotid artery (upper arrowhead), as

an intraluminal filling defect.

Treatment of carotid and vertebral arterial dissections remains somewhat controversial. [2] The most conservative approach

includes medical management, with ongoing debate as to whether anticoagulation with heparin and/or antiplatelet therapy is

more effective.[19,26,28,30] There remains concern about the use of these agents in the setting of acute multitrauma,[30] althoug

successful treatment with antiplatelet agents has also been described in the setting of pre-existing intracranial hemorrhage. [31]

Medical management has resulted in 50% to 70% successful arterial recanalization rates. [32,33] However, these patients

remain at risk for thromboembolic events in the days to weeks following the traumatic event [34] or delayed formation of

dissecting aneurysms. Much of the healing of dissections occurs 36 months after the inciting event.[35,36]

Stents have been used to treat patients who have contraindications to anticoagulation or antiplatelet therapy, [37] although

adjunctive antiplatelet therapy is often used to ensure long-term stent patency.[20] Endovascular treatment with stents has also

been described in patients who fail medical management either with ongoing or new neurological symptoms, or enlargement of

a dissecting aneurysm on follow-up evaluation. [38]


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If an ischemic stroke has occurred, coordination with the stroke neurology team is essential. Brain imaging, including diffusion-

and perfusion-weighted imaging, should be a consideration, understanding that there may be time constraints if

revascularization is indicated. If imaging suggests an embolic mechanism for the stroke, techniques similar to stroke

thrombolysis or thromboembolectomy may be used. If a large vessel occlusion is present, angioplasty or stenting may not be

wise as this may cause a reperfusion hemorrhage in the brain.

Branch Vessel Arterial Lacerations

Trauma to the face, neck, and scalp can result in damage to branches of the external carotid arteries that cannot be controlled

by direct pressure alone. Understanding the trauma mechanism and having cross-sectional imaging of the head and neck arehelpful in the acute setting to tailor the angiogram most expeditiously to areas of interest. One should always consider the rich

collateral supply to the face and neck, and the thyrocervical trunk, vertebral artery, and internal carotid artery branches should

also be scrutinized (Figure 6).

Figure 6. (A) Right common carotid arteriogram in patient with hematochezia reveals active extravasation from a branch

of right superior thyroid artery (arrowhead). (B) Selective arteriogram after embolization with 200-micron PVA particles

confirms cessation of flow distal to the micrcatheter and absence of further extravastion from the right superior thyroid

artery.

The goal is to decrease the pressure head within the injured vessel with resulting cessation of bleeding. Generally, it is

important to place the tip of the catheter as close to the bleeding site as practical to avoid occlusion of normal branches.

Additionally, prior to any particle embolization, one should be well aware of potential dangerous anastamotic collaterals.[39]


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These include: distal external carotid artery ethmoidal perforators to the ophthalmic artery, superficial temporal artery to the

middle cerebral artery, middle meningeal artery to the ophthalmic artery, and occipital artery to the vertebral artery (Figure 7).

Additional embolization hazards, such as scalp necrosis, should be kept in mind when targeting sites in the superficial

temporal and occipital arteries.

Figure 7. (A) Retrograde flow can be seen from the external carotid into the distal internal carotid via ethmoidal

perforators and the ophthalmic arteries (arrowhead). (B) Collateral flow is identified from the occipital artery branch of the

external carotid artery, to the vertebral artery (arrowheads). This can present hazards during embolization.

In areas where potential neurological deficit or collateral flow would be detrimental, provocative testing with 2 ml 1% lidocaine

(20 mg) with concomitant neurological testing can be helpful. For example, provocative testing can reveal neurological deficits o

cranial nerves V, VII, and X associated with the ascending pharyngeal artery before embolization, allowing for appropriate

change in the therapy plan.

Temporary occlusive agents, such as gel foam and particles, are the preferred embolization material in most situations, as

coils, glue, and balloons may preclude access in the setting of re-bleeding. Gel foam can be made into a slurry with contrast,

allowing safe, targeted delivery through a 3 or 4 French catheter. Particles, such as 200700 micron polyvinyl alcohol, are

usually mixed with Iohexol 240 contrast to create an evenly distributed isobaric solution. Polyvinyl alcohol particles are injected

via a microcatheter fast enough to be visualized but not so fast as to create reflux into normal vessels. As the embolization

progresses, the injection rate typically slows until stagnation and flow are angiographically evident. The use of smaller particles

increases the risk of nontarget embolization by particle migration via small collateral vessels.

Epistaxis

Nosebleeds are common and can be spontaneous, traumatic, or secondary to underlying telangiectasia, arteriovenousmalformations or neoplasms, such as juvenile nasal angiofibromas. The first step is to identify the site of bleeding.

Most commonly, the bleeding site is anterior, supplied from Kiesselbach plexus (sphenopalatine, descending palatine, superior

labial branches from ECA and anterior and posterior ethmoidal arteries from the ophthalmic artery). [40,41] Anterior nasal

bleeding can often be stopped with direct pressure, packing, or cautery, given the ease of access. If the bleeding site is

posteriorly located, endovascular embolization is preferred over arterial ligation, as it allows repeated access in the event of re-

bleeding via collateral branches.[42, 43] This is usually best accomplished via the internal maxillary arteries (Figure 8), with

microcatheter placement distal to the origins of the middle meningeal and accessory meningeal arteries.


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Figure 8. (A) 62-year-old woman presented with nasal congestion. Coronal CT scan reveals a right nasal cavity mass.

Extensive uncontrolled hemorrhage occurred after biopsy. (B) Right external carotid arteriogram reveals active contrast

pooling after the arterial stage, indicating active bleeding. This was successfully treated with microcatheter selection of the

distal internal maxillary artery (arrowhead) and embolization with 300-micron PVA particles.

In all cases of nasal and facial embolization, it is essential to evaluate collateral supply via the ophthalmic and facial arteries to

avoid undesirable non-target embolization.[44] Collateral supply can occur via the artery of the foramen rotundum, the vidian andascending pharyngeal arteries, as well as communications between the facial, sphenopalatine and ophthalmic arteries.

Preferred treatment is with temporary occlusive agents, such as 200500 micron polyvinyl alcohol particles. It is important to

closely monitor the injection rate, to avoid reflux into other branch vessels. If subselective arterial positioning cannot be

achieved or the vascular anatomy is altered by prior surgical intervention, gelfoam injection into the larger, feeding artery may

sufficiently diminish the pressure and stop the bleeding. We typically avoid using coils to treat epistaxis, as these permanent

devices preclude future access, if re-bleeding occurs. Having to access the bleed via collateral sources such as the ophthalmic

artery makes the embolization procedure much more hazardous.

Neoplastic Bleeds

Vascular head and neck neoplasms, such as thyroid cancer and paraganglioma, may bleed spontaneously and be difficult to

control externally. Often, the only finding is hypervascular oozing. In such cases, partial embolization of the tumor may

sufficiently shut down the vascular bed.

More commonly, head and neck cancers can erode into a blood vessel wall and cause spontaneous hemorrhage. The search

for neoplastic bleeding source can be challenging (Figure 9), and surgical exploration can be difficult in patients with prior neck

dissection or radiation therapy. In the setting of neoplastic bleeding, one may see hypervascular tumor blush or there may be

actual active extravasation.[45] In some cases, such as carotid blow-out, bleeding can be profuse and life-threatening. In this

setting, emergent endovascular therapy with stents, balloon occlusion and liquid glue have been reported, [46,47,48] with the

understanding that these are often palliative measures.


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Figure 9. (A) 81-year-old with metastatic thyroid cancer eroding into the right mainstem bronchus, with intermittent

hematochezia. In this case, left subclavian angiography demonstrated that the expected thyrocervical artery (white

arrowhead) was not the actual source. (B) Vascular contribution to the tumor mass originated from the right superior

thyroid artery, demonstrated on subselective catheterization. (C) After treatment with 200-micron PVA particles, right

superior thyroid arteriogram shows successful embolization.

Conclusion

Catheter angiography continues to serve a role in the diagnosis of head and neck vascular trauma, particularly in cases with


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high suspicion for vascular injury or where CT angiography is limited due to artifact from dental amalgam or gunshot debris. The

neurointerventionalist continues to play an increasing role in the acute setting to identify and stop bleeding, with an increasing

number of temporary and permanent agents within their armamentarium. Before embolization, it is crucial to assess collateral

vascular supply, both to avoid nontarget embolization and undesired permanent sequelae when vessel sacrifice is required.

Endovascular procedures can also be a useful adjunct in patients who have failed conservative management. The population of

head and neck vascular trauma and bleeding is heterogeneous and techniques continue to advance to serve these unique

cases.

References

1. Biffl WL, Cothren CC, Moore EE, et al. Western Trauma Association critical decisions in trauma: screening for and

treatment of blunt cerebrovascular injuries. JTrauma. 2009;67:11501153.

2. Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries: Analysis of diagnostic

modalities and outcomes.Ann Surg. 2002;236:386393.

3. Bromberg WJ, Collier BC, Diebel LN, et al. Blunt cerebrovascular injury practice management guidelines: The Eastern

Association for the Surgery of Trauma. J Trauma. 2010;68:471477.

4. Cogbill TH, Moore EE, Meissner M, et al. The spectrum of blunt injury to the carotid artery: A mult icenter perspective. J

Trauma. 1994;37: 473479.

5. Biffl WL, Moore EE, Ryu RK, et al. The unrecognized epidemic of blunt carotid arterial injuries: Early diagnosis improves

neurologic outcome.Ann Surg. 1998;228:462470.

6. Berne JD, Norwood SH, McAuley CE, et al. The high morbidity of blunt cerebrovascular injury in an unscreened

population: More evidence of the need for mandatory screening protocols. J Am Coll Surg. 2001;192:314321.

7. Feliciano DV. Management of penetrating injuries to the carotid artery. World J. Surg. 2001; 25:10281035.

8. Sclafani SJ, Panetta T, Goldstein AS, et al. The management of arterial injuries caused by penetration of Zone III of the

neck. J Trauma. 1985;25:871881.

9. Sclafani AP, Sclafani SJ. Angiography and transcatheter arterial embolization of vascular injuries of the face and neck.

Laryngoscope. 1996;106:168173.

10. Reuben BC, Whitten MG, Sarfati M, Kraiss LW. Increasing use of endovascular therapy in acute arterial injuries:

Analysis of the National Trauma Data Bank. J Vasc Surg. 2007;46:12221226.

11. Rao PM, Ivatury RR, Sharma P, et al. Cervical vascular injuries: A trauma center experience. Surgery. 1993;114:527

531.

12. Herrera DA, Vargas SA, Dublin AB. Endovascular treatment of penetrating traumatic injuries of the extracranial carotid

artery. J Vasc Interv Radiol. 2011;22:2833.13. Toursarkissian B, Allen BT, Petrinec D, et al. Spontaneous closure of selected iatrogenic pseudoaneurysms and

arteriovenous fistulae. J Vasc Surg. 1997;25:803809.

14. Cox MW, Whittaker DR, Martinez C, et al. Traumatic pseudoaneurysms of the head and neck: Early endovascular

intervention. J Vasc Surg. 2007;46:12271233.

15. Herrera DA, Vargas SA, Dublin AB. Endovascular treatment of traumatic injuries of the vertebral artery.AJNR Am J

Neuroradiol. 2008;29:15851589.

16. Berne JD, Reuland KR, Villarreal DH, et al. Internal carotid artery stenting for blunt carotid artery injuries with an

associated pseudoaneurysm. J Trauma. 2008;64:398405.

17. Yi AC, Palmer E, Luh GY, et al. Endovascular treatment of carotid and vertebral pseudoaneurysms with covered stents.

AJNR Am J Neuroradiol. 2008;29:983987.

18. Coldwell DM, Novak Z, Ryu RK, et al. Treatment of posttraumatic internal carotid arterial pseudoaneurysms with

endovascular stents. J Trauma. 2000;48:470472.

19. Cothren CC, Moore EE, Biffl WL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce

stroke rate.Arch Surg. 2004;139:540545.

20. DuBose J, Recinos G, Teixeira PG, et al. Endovascular stenting for the treatment of traumatic internal carotid injuries:

Expanding experience. J Trauma. 2008;65:15611566.

21. Gemmete JJ, Ansari SA, Gandhi DM. Endovascular techniques for treatment of carotid-cavernous fistula. J Neuro-

Ophthalmol. 2009;29:6271.

22. Higashida RT, Halbach VV, Tsai FY, et al. Interventional neurovascular treatment of traumatic carotid and vertebral arter

lesions: Results in 234 cases.AJR Am J Roentgenol. 1989;153:577582.

23. Kirsch M, Henkes H, Liebig T, et al. Endovascular management of dural carotid-cavernous sinus fistulas in 141 patients

Neuroradiology. 2006;48:486490.


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