Dr. Bykowski is a Fellow in the Division of Neuroradiology, and Dr. Wong
is a Professor of Clinical Radiology, Interventional Neuroradiology,
Professor of Pain and Palliative Medicine, University of California–San
Diego Medical Center, San Diego, CA.
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
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 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.
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
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
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
Traumatic arteriovenous fistulae can occur
in the setting of arterial transection, with resulting communication
between the injured 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).
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 function. The balloon test occlusion is
typically maintained for 30 minutes or until the patient fails the
Extracranial arterial dissections and occlusions
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.
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 dissection27 (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.
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 event34 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 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
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
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).
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 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.
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.
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
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
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
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
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.
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.
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
serve these unique cases.
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