Angiographic Evaluation and Treatment for Head and Neck Vascular Injury

8/14/2019 Angiographic Evaluation and Treatment for Head and Neck Vascular Injury

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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

or 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

or 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.

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.[1–3] 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,

[4–6]

combined with ease of access toCT 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

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

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

Appl Radio l. 20 12;41(3):10-16 .

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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 carotid arteriogram 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.[16–18] 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

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





Figure 2.

(A) T1-weighted post-contrast MR image of a 52-year-old man reveals enhancing squamous cell carcinoma of the left sphenoid

sinus and cavernous sinus. Massive arterial hemorrhage occurred after endoscopic biopsy. (B) Left internal carotid arteriogram

reveals development of a cavernous sinus pseudoaneurysm. (C) After test balloon occlusion, coils were deployed into the

pseudoaneurysm. Not surprisingly, several coils ruptured beyond the encasing thrombus. (D) The left internal carotid was

therefore sacrificed with coil occlusion. Post-treatment arteriogram confirms complete occlusion of the left internal carotid with

filling only of the left external carotid. The patient had intact collateral supply from the right internal carotid via the anterior

communicating artery.

Traumatic arteriovenous fistulae can occur in the setting of arterial transection, with resulting communication between theinjured artery and adjacent vein. Most commonly, these occur in the facial arterial or at the cavernous carotid artery, due to the

prevalence of facial and skull base injury, respectively.

Different methods of embolization have been described, depending on the flow rate, site, and available technology.[21–23]

Small fistulous communications may be embolized with polyvinyl alcohol particles (Figure 3). In larger fistulae, deployment of

micro coils, detachable balloons or liquid embolic agents through the fistula may be necessary to obtain cessation of shunting

(Figure 4).





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 embolizationmaterial 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





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

Extracranial Arterial Dissections and Occlusions

Arterial diss ections 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 fillingdefect.

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]

although 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 3–6 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 hasalso 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]

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 are

helpful 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]

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

of 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 200–700 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, arteriovenous

malformations 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.





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

and ascending pharyngeal arteries, as well as communications between the facial, sphenopalatine and ophthalmic arteries.

Preferred treatment is with temporary occlusive agents, such as 200–500 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.









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

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 servethese unique cases.

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Angiographic Evaluation and Treatment for Head and Neck Vascular Injury

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