Extracranial Carotid Artery Aneurysm

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Extracranial carotid artery aneurysm

Author: Melissa L Kirkwood, MD
Section Editors: John F Eidt, MD, Joseph L Mills, Sr, MD
Deputy Editor: Kathryn A Collins, MD, PhD, FACS
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2020. | This topic last updated: Sep 03, 2019.
INTRODUCTION
Extracranial carotid artery aneurysms are uncommon and occur in a broad range of patients due to many etiologies. True
aneurysms involving all layers of the carotid arterial wall and false aneurysms both occur. Overall, extracranial carotid
artery aneurysm accounts for less than 1 percent of all arterial aneurysms and approximately 4 percent of peripheral
artery aneurysms [1-3]. Repair of extracranial carotid artery aneurysm represents 0.2 to 5 percent of carotid procedures
depending upon the reporting institution [4].
A diagnosis may be made incidentally in asymptomatic patients or suspected based upon clinical manifestations that may
include neurologic symptoms, a pulsatile mass in the neck, mass effects, or bleeding due to rupture. Any segment of the
carotid artery (common, external, internal) can be affected, although the internal carotid artery is most commonly involved.
The treatment approach depends on the symptoms, etiology, and location of the carotid aneurysm. Observation is safe for
some small, asymptomatic aneurysms, but repair is indicated for enlarging asymptomatic aneurysms to prevent stroke
and aneurysm rupture, and for all symptomatic aneurysms. In most series, open surgical repair is more often selected for
true aneurysms, infected aneurysms, and larger aneurysms causing mass effects. Endovascular repair is more often
initially chosen for patients with pseudoaneurysms due to traumatic mechanisms or as a result of carotid dissection.
The classification, clinical features, and management of extracranial carotid artery aneurysm are reviewed here.
Intracranial carotid artery aneurysms are discussed in detail separately. (See "Unruptured intracranial aneurysms" and
"Treatment of cerebral aneurysms".)
ANATOMY AND CLASSIFICATION
The extracranial carotid arteries include the common carotid artery, which originates in the chest, the external carotid
artery, and the internal carotid artery to the base of the skull. The anatomy of the carotid arteries is illustrated in the
figures (figure 1A-C).
Aneurysms are categorized as either true or false aneurysms. True aneurysms are a segmental, full-thickness dilation of a
blood vessel having at least a 50 percent increase in diameter compared with the expected normal diameter [5,6]. False
aneurysm (pseudoaneurysm) is due to a localized disruption of the arterial wall, which can occur as a result of carotid
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trauma or prior carotid dissection, and represents a contained hematoma that has maintained a persistent connection with
the arterial lumen.
The proportion of true aneurysm to pseudoaneurysm varies widely in case series, likely related to the specific
demographics at individual institutions. As examples, one review of 42 cases from 1984 to 2004 at Baylor reported that 48
percent of extracranial carotid artery aneurysms were pseudoaneurysms and 52 percent were true aneurysms [7].
However, a separate review over a 15 year study period (1998 to 2012) from the Mayo Clinic that included 141 carotid
aneurysms reported that 82 percent were pseudoaneurysms and 18 percent were true aneurysms [8]. More men were
affected by pseudoaneurysm in this series, whereas for true aneurysm, the opposite was true.
Extracranial carotid aneurysms (true or false) have been classified according to affected anatomic segment, which is
important for determining a treatment approach (figure 2) [9].
● Type I – Isolated aneurysms of the internal carotid artery

● Type II – Aneurysms of the complete internal carotid artery with involvement of the bifurcation
● Type III – Aneurysms of the carotid bifurcation
● Type IV – Combined aneurysm of the internal and common carotid artery
● Type V – Isolated aneurysm of the common carotid artery
All segments of the carotid artery are susceptible to aneurysm formation; however, aneurysms affecting the very proximal
carotid artery within the chest are rare.
For true aneurysm (typically atherosclerotic), the most frequent site reported in the literature reviews is the bifurcation of
the carotid artery or proximal internal carotid artery [10-12]. Aneurysms at this site are typically fusiform. The middle and
distal portions of the internal carotid artery are the next most common sites, and the appearance is typically saccular
[8,12]. In the Mayo Clinic review, 114 (81 percent) involved the internal carotid, 11 (8 percent) the common carotid, 15 (10
percent) the bifurcation, and 1 (1 percent) the external carotid [8]. Bilateral aneurysms can also occur [8,10].
Infected pseudoaneurysms typically occur at the site of a prior patch repair in the proximal internal carotid artery, while
traumatic pseudoaneurysms are more likely to affect the distal internal carotid artery. (See "Blunt cerebrovascular injury:
Mechanisms, screening, and diagnostic evaluation".)
ETIOLOGY AND RISK FACTORS
The factors leading to true aneurysm or pseudoaneurysm differ. True aneurysms are predominantly related to
atherosclerosis, particularly in older individuals. However, other etiologies such as fibromuscular dysplasia, connective
tissue disorders, inflammatory diseases, congenital defects, and irradiation can all predispose to full-thickness
aneurysmal degeneration [8,11]. Primary infection of the carotid artery wall can lead to true aneurysm, whereas, for those
who have had prior carotid surgery or other intervention, secondary infection usually results in pseudoaneurysm. Blunt or
penetrating trauma can result in either type of aneurysm depending upon the mechanism and severity of the arterial wall
injury [13].
The most common etiology of extracranial carotid artery aneurysm is atherosclerosis (34 to 42 percent), followed by
trauma (35 to 51 percent) and pseudoaneurysm at prior endarterectomy sites (26 to 57 percent) [8].
● In a review of 42 patients with extracranial carotid artery aneurysms, 50 percent were due to atherosclerosis, 30
percent were pseudoaneurysms, and 12 percent were related to trauma [7].
● In another report that included 48 patients, 71 percent were atherosclerotic, 25 percent pseudoaneurysm, and 4
percent related to infection [14]. These are in contrast to an older series that found that 57 percent of extracranial
carotid artery aneurysms were the result of degeneration or infection of a previous carotid endarterectomy patch, and
43 percent were secondary to atherosclerosis and trauma [1].
Factors that increase the risk of extracranial carotid aneurysm are discussed briefly below, and in detail in the linked topic
reviews, where available.
Atherosclerosis — Atherosclerosis is the most common etiology for true extracranial carotid artery aneurysm [1,13,15].
The patient often has severe hypertension and other comorbidities, such as coronary artery disease and chronic
obstructive pulmonary disease. The mean ages in two studies were 56 and 62 years [7,9]. The male-to-female ratio is
approximately 2:1 [15,16]. Histologic features include disruption of the internal elastic lamina and thinning of the arterial
media.
Infection — Extracranial carotid artery aneurysm can be due to primary infection of the carotid arterial tissues, or
infection secondary to prior carotid surgery or other instrumentation [17-19]. Extracranial carotid artery aneurysms are
increasingly being reported in association with human immunodeficiency virus [20].
Primary infection — Infected primary extracranial carotid artery aneurysm is rare, with only approximately 100 cases
reported in the literature. These are the result of infection affecting the carotid artery wall, leading to acute inflammatory
changes, weakening of the arterial wall, and subsequent dilation [17]. (See "Overview of infected (mycotic) arterial
aneurysm", section on 'Etiology'.)
● Septic emboli that lodge at the carotid bifurcation most commonly arise from infected cardiac valves. (See
"Complications and outcome of infective endocarditis".)
● Contiguous infection, typically from meningitis or cervical lymphadenitis, can spread to involve the periarterial
lymphatics and the vasa vasorum. This mechanism is the most common cause of carotid artery aneurysm in children
[21]. Since the widespread use of antibiotics, the incidence of infected aneurysms due to peritonsillar and middle ear
infections has declined. The most common pathogens associated with infected extracranial carotid artery aneurysm
are Staphylococcus aureus, Salmonella, streptococci, Escherichia coli, and Klebsiella [17,22]. (See "Overview of
infected (mycotic) arterial aneurysm", section on 'Microbiology'.)
Postprocedural — The incidence of carotid pseudoaneurysm after carotid endarterectomy remains low, occurring in
less than 1 percent of all carotid endarterectomies performed [23]. These aneurysms can be related to suture line
disruption or a result of deep wound infection. S. aureus was the most commonly cultured organism. (See "Complications
of carotid endarterectomy", section on 'Infection'.)
The majority of cases occur after endarterectomy with a synthetic patch, but aneurysms have also been reported after
vein patch repair and following primary carotid closure. In a review of 141 extracranial carotid artery aneurysms,
pseudoaneurysms at the site of prior endarterectomy accounted for 28 (24 percent) of all pseudoaneurysms and
presented at a mean of 82 months from the time of surgery [8]. All of the affected arteries were originally patched
(Dacron: 79 percent, saphenous vein: 7 percent, bovine pericardium: 4 percent, unknown patch: 10 percent). In another
small series, all post-carotid-endarterectomy aneurysms occurred in patched arteries presenting between 2 and 20 years
after the original surgery [4].
Cerebrovascular injury — Blunt or penetrating cerebrovascular injury can lead to extracranial carotid artery aneurysm,
which can present acutely or in a delayed manner years after the inciting event; a time interval between 1 and 20 years
has been reported [4,8,24,25]. Blunt carotid injury mechanisms, including cervical hyperextension, cervical hyperflexion,
and intraoral injury, are illustrated in the figure (figure 3). Penetrating injury can result from a gunshot or stab wound, or
from incidental carotid artery puncture or cannulation during central line placement. (See "Blunt cerebrovascular injury:
Mechanisms, screening, and diagnostic evaluation" and "Complications of central venous catheters and their prevention".)
Spontaneous carotid dissection — Among patients with spontaneous extracranial carotid artery dissection, up to 30
percent will develop pseudoaneurysms [26]. The time interval between the dissection and aneurysm formation is variable,
as with cerebrovascular injury due to trauma. (See "Spontaneous cerebral and cervical artery dissection: Clinical features
and diagnosis".)
Radiation — Although carotid artery stenosis may be more frequently reported as a complication of radiation therapy
[27], extracranial carotid artery pseudoaneurysm has also been reported [28,29]. The etiology of pseudoaneurysm due to
radiation is multifactorial but is related to arterial wall injury. Pseudoaneurysm is more common after a second course of
radiation therapy. In one review, 70 percent of patients had been treated with a second course of radiotherapy [30].
Others — True aneurysms can result from a variety of other pathologies that are known to weaken the integrity of the
arterial wall, although extracranial carotid artery aneurysm as a manifestation of connective tissue disease is rare
[1,31,32].
These include [8,33-47]:
● Fibromuscular dysplasia
● Connective tissue disease, including Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome,
osteogenesis imperfecta, and pseudoxanthoma elasticum (see "Genetics, clinical features, and diagnosis of Marfan
syndrome and related disorders")
● Tuberous sclerosis (see "Tuberous sclerosis complex: Genetics, clinical features, and diagnosis")
● Arteritides, including Takayasu's arteritis, polyarteritis nodosa, and Behcet syndrome (see "Overview of and approach
to the vasculitides in adults")
● Cystic medial necrosis
CLINICAL FEATURES
Symptoms from extracranial carotid artery aneurysm can be due to local mass effect or embolism. Rupture is very rare
unless there is associated infection. Thrombotic occlusion is likewise pretty rare. Because of the wide range of etiologies,
extracranial carotid artery aneurysm can present in patients of any age. In the past, the onset of symptoms most often led
to a diagnosis of extracranial carotid artery aneurysm, but asymptomatic aneurysms are increasingly discovered on cross-
sectional imaging performed for unrelated reasons. Carotid aneurysms can also present as asymptomatic cervical or
parapharyngeal masses, which may or may not be pulsatile [48]. In one series, approximately one half of extracranial
carotid artery aneurysms were asymptomatic and discovered incidentally [8].
Symptoms — Symptoms related to extracranial carotid artery aneurysm can be related to embolization of thrombus lining
the aneurysm sac, local compression of surrounding structures from mass effects, or aneurysm rupture. In a review of
141 carotid aneurysms, approximately one half manifested with symptoms (44 percent true aneurysm, 52 percent
pseudoaneurysm): painless mass in 28, transient ischemic attacks in 10, vision symptoms in 10, rupture in 9, strokes in 8,
painful mass in 4, dysphagia in 1, tongue weakness in 1, and bruit in 1 [8]. The average diameter of true aneurysms
causing symptoms was 23 mm, compared with 13 mm for asymptomatic aneurysms.
● Neurologic symptoms – The most common symptomatic presentation is either a transient ischemic attack or a stroke.
Although most neurologic symptoms are related to embolization, some neurologic symptoms may be related to
decreases in cerebral blood flow as a large aneurysm compresses the internal carotid artery when the head is turned.
In several series, neurologic symptoms were the initial presenting symptom in 37 to 100 percent of cases [1,9,49-52].
Transient ischemic attack occurs approximately twice as often as stroke and, as an initial warning sign, may allow a
sufficient interval of time for recognition and repair of the aneurysm prior to developing disabling stroke.
● Compressive symptoms – Extracranial carotid artery aneurysm can also cause compression of surrounding
structures or nerve compression, each of which can cause pain (neck, retro-orbital, headache) [1,13,48]. Although
rare, a nonruptured aneurysm can compress the pharyngeal muscles resulting in dysphagia [8,53-55].
Glossopharyngeal nerve compression can cause auricular pain as well as pharyngeal dysfunction and dysphagia. If
the sympathetic chain is involved, Horner's syndrome (ptosis, miosis, anhidrosis) can result. Vagal compression can
also result in hoarseness, and hypoglossal compression can cause tongue deviation and decreased function [9,56].
(See "The detailed neurologic examination in adults".)
● Rupture – Rupture with extramural hemorrhage can lead to airway compression, which can be fatal. Bleeding may
manifest as pharyngeal hemorrhage, epistaxis, or bleeding from the ear [11,48,57]. Infected aneurysms are more
susceptible to rupture than noninfected aneurysms [11,18]. Pseudoaneurysms of the carotid artery secondary to
radiation treatment have also been known to rupture [30].
● Neck infection/cellulitis – Infected extracranial carotid artery aneurysms often present as an expanding, pulsatile
cervical mass associated with local pain, tenderness, fever, dysphonia, or dysphagia. Overlying erythema is not a
common finding [17].
Physical findings — In up to 90 percent of patients with extracranial carotid artery aneurysm, a pulsatile neck mass is
palpable below the angle of the mandible [49-52]; there may be an associated systolic bruit [48].
A detailed neurologic examination should be documented and will identify the presence of any associated cranial nerve
abnormalities.
DIAGNOSIS
Although the diagnosis of extracranial carotid artery aneurysm may be suspected based upon history and physical
examination, the diagnosis relies upon the demonstration of the aneurysm on imaging studies. Further evaluation is
aimed at determining the etiology of the aneurysm (eg, post-endarterectomy, post-trauma), which can be challenging in
some patients. Ultrasound is the initial imaging study to evaluate most neck masses, but advanced imaging is usually
needed to further define the aneurysm (diameter, presence of thrombus, intracranial circulation, collateral circulation) and
suggest an etiology, which may affect treatment decisions. Computed tomographic (CT) angiography and magnetic
resonance (MR) angiography have replaced conventional catheter-based arteriography for diagnostic purposes at most
vascular centers. (See "Evaluation of a neck mass in adults".)
Carotid imaging — Ultrasound is the initial imaging study for any pulsatile neck mass. Sonographically, carotid
pseudoaneurysms may be largely thrombosed with only a small amount of blood flow or may show large areas of swirling
blood flow with little thrombus. Universally, however, a to-and-fro flow pattern should be seen in the neck of the
pseudoaneurysm on spectral Doppler exam. The neck is the area connecting the carotid artery to the pseudoaneurysm
masslike lesion [58].
CT or MR angiography are useful confirmatory tests because they can assess the extent of aneurysmal dilation, thrombus
formation, and the relationship of the aneurysm with surrounding structures (image 1). Multidetector three-dimensional CT
angiography and MR imaging can be reconstructed to create three-dimensional images that provide additional information
and a higher level of detail compared with angiography.
Arteriography is no longer necessary for making a diagnosis; however, it still has a role in the management of extracranial
carotid artery aneurysm when a balloon occlusion test is necessary to assess collateral circulation, which is helpful to
obtain preoperatively if ligation of the carotid artery is being considered [8]. During a balloon occlusion test, in which a
balloon catheter is advanced into the carotid artery and inflated, the patient is monitored for several minutes for neurologic
changes [59]. If the patient remains stable and has no neurologic symptoms, then carotid ligation/occlusion is an option, if
revascularization is not possible. (See 'Indications for and approach to repair' below.)
Further evaluation — Brain imaging (CT or MR angiography) should be routinely obtained to assess the intracerebral
perfusion as well as identify any previous infarcts. Patients with true carotid artery aneurysms should also be evaluated
for other aneurysms. (See "Screening for intracranial aneurysm".)
Prior to carotid aneurysm surgery, otolaryngologic examination, which may include laryngoscopy, should be performed in
patients who have vocal disturbance (tone change, hoarseness).
Screening for other aneurysm — True extracranial carotid artery aneurysms are frequently associated with
aneurysms in other vascular beds. In a review of 48 patients with extracranial carotid artery aneurysm, 24 percent of
those with true aneurysms had an associated aneurysm in another vascular territory, most commonly the abdominal aorta
[14]. In another review, 26 percent of patients with an extracranial carotid artery aneurysm had a coexistent abdominal
aortic aneurysm [60]. Other arterial sites that have been reported include the thoracic aorta and the iliac, femoral, and
subclavian arteries [9,14]. Coexistent intracranial carotid artery aneurysms can also occur [9].
Screening for heritable conditions — For patients with extracranial carotid aneurysm in whom a predisposing
heritable condition is suspected, further investigation is warranted and should include family history, pathology
consultation, and imaging of other affected arterial beds. Genetic testing and counseling should be considered. (See
'Others' above and "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders".)
DIFFERENTIAL DIAGNOSIS
A palpable neck mass can be due to any one of a number of pathologies, including enlarged lymph nodes, cystic
hygroma, neoplastic lesions of the neck, peritonsillar abscess, and branchial cleft cysts. (See "Differential diagnosis of a
neck mass".)
Many neck masses can be differentiated from carotid artery aneurysm based upon their location away from the normal
course of the carotid artery, and by being nonpulsatile in nature. However, a thrombosed carotid artery aneurysm will also
be nonpulsatile. It is important to distinguish carotid artery aneurysm from peritonsillar abscess. Attempted incision and
drainage of a peritonsillar abscess that is really a carotid artery pseudoaneurysm can be fatal. (See 'Physical findings'
above.)
A pulsatile neck mass may be vascular in origin, but a nonvascular mass that is closely related to the carotid or other
artery in the neck can also seem to be pulsatile. Vascular etiologies causing a mass in the neck include carotid kinks and
coils, and carotid tumors. Carotid kinks and coils are an anatomic variant. These redundant, tortuous carotid arteries can
produce a large, pulsatile mass in the neck that is indistinguishable from extracranial carotid artery aneurysm on physical
examination. Although it has been suggested that tortuosity can be distinguished on physical examination by evaluating
the pulsation [13] (the pulsation of a kinked carotid artery is said to run parallel to the long axis of the vessel as opposed
to radiating laterally, as occurs in an aneurysm [61]), we do not rely on examination, but rather on carotid imaging to make
the distinction.
A carotid body tumor can also present as a painless, pulsatile mass given its close proximity to typically the carotid
bifurcation. These masses are vertically fixed but laterally mobile, which contrasts with carotid aneurysms, which are fixed
in location [13]. (See "Paragangliomas: Epidemiology, clinical presentation, diagnosis, and histology", section on 'Head
and neck paragangliomas'.)
NATURAL HISTORY AND MANAGEMENT
As with aneurysms at other sites, the natural history of extracranial carotid artery aneurysm may be one of continued
expansion, which can eventually lead to symptoms. There are few large reviews to guide management of extracranial
carotid artery aneurysm, and most decisions regarding care are derived from single-institution series
[1,4,7,9,31,51,56,60,62-67]. Although specific management depends upon the factors discussed below, we generally
repair all symptomatic extracranial carotid artery aneurysms (open or endovascular), as well as asymptomatic aneurysms
that are large (>2 cm), those with intraluminal thrombus (regardless of symptoms), and small asymptomatic aneurysms
that demonstrate expansion on serial imaging (algorithm 1).
The mortality rate for untreated extracranial carotid artery aneurysm was historically quite high [68-71]. In the absence of
advanced three-dimensional imaging that identifies small aneurysms, often incidentally, these older studies likely reflected
predominantly aneurysms that were symptomatic and large enough to be identified on physical examination
[3,49,50,62,72-74]. Nevertheless, the reported mortality rate was at least twice as high as the mortality rate for the most
morbid surgical procedure, which is carotid artery ligation [53,68,69,75]. Later series report a lower, but still substantial,
stroke rate for extracranial carotid artery aneurysms (true or pseudoaneurysm) [8,13,14,18,75]. (See 'Indications for and
approach to repair' below.)
Observation — The risk of embolism due to extracranial carotid artery aneurysm is not well defined but is potentially
related to aneurysm diameter and presence of thrombus or associated calcification. Observation of small, asymptomatic
aneurysms and pseudoaneurysms (eg, blunt trauma, dissection) is acceptable, but we have a low threshold to proceed
with repair in any patient with signs of aneurysm expansion, or the development of thrombus within the aneurysm on
serial imaging (algorithm 1). Symptomatic patients who are not candidates for any repair due to comorbidities may also be
observed, but with the availability of endovascular techniques most symptomatic patients can be treated. (See
'Endovascular repair' below.)
In one case series, 10/25 true aneurysms (40 percent) and 65/116 pseudoaneurysms (56 percent) were managed
nonoperatively [8]. Nonoperative management was more frequent in asymptomatic patients than in symptomatic patients
(71 versus 31 percent). The average diameters of true and pseudoaneurysms treated nonoperatively were 12.0 and 10.2
mm, respectively, compared with those that were managed operatively at 21.2 and 20.9 mm. No aneurysm managed
nonoperatively required intervention during a mean follow-up of 77 months. In a separate review of traumatic extracranial
cerebrovascular injuries, the majority of patients were managed nonoperatively with antiplatelet therapy and serial
imaging [25]. Saccular aneurysms were more likely to enlarge than fusiform aneurysms (33 versus 12 percent). In a
review of 43 traumatic pseudoaneurysms occurring in 39 patients, among internal carotid pseudoaneurysms treated with
aspirin and observation alone, 9 (28 percent) increased in size, 17 (53 percent) decreased or stabilized, and 6 (19
percent) resolved [76].
Indications for and approach to repair — Treatment is clearly appropriate for symptomatic aneurysms (eg, mass effect,
embolism) regardless of aneurysm diameter (algorithm 1). We also treat asymptomatic extracranial carotid artery
aneurysms that are large or expanding; however, what defines large or expanding is not firmly established. Some
vascular specialists repair asymptomatic carotid artery aneurysms larger than 1.5 times the diameter of the adjacent
normal artery (which essentially defines aneurysm), but based upon available observational data, we generally use a
cutoff of around 2 cm. The presence of thrombus in a carotid aneurysm may increase the risk for neurologic events; thus,
we feel that the identification of thrombus, regardless of symptoms, is also an indication for repair.
● Options for open surgical repair include carotid artery ligation with or without bypass, and carotid aneurysm excision
with reconstruction. (See 'Open surgical repair' below.)
● Options for endovascular repair include bare metal stent placement with or without trans-stent coil embolization of the
aneurysm sac, exclusion of the aneurysm using a stent-graft, or endovascular occlusion of the carotid artery. (See
'Endovascular repair' below.)
The choice of treatment is often determined by patient factors (eg, comorbidities, symptoms, individual anatomy),
physician-related factors (eg, experience, training), and facility-related factors (eg, advanced imaging, devices)
[8,9,29,32,77-80].
● Factors favoring an open approach:
• True aneurysm (atherosclerotic, related to connective tissue disorders).
• Infected primary aneurysm.
• Pseudoaneurysm due to carotid patch disruption. Some clinicians believe that disruptions that occur shortly after
an endarterectomy, that do not appear to be due to infection, may be amenable to an endovascular approach to
reduce potential complications related to the intense inflammatory changes in the immediate postoperative
period surrounding the carotid artery.
● Factors favoring an endovascular approach:
• Pseudoaneurysm related to trauma (often affect the distal carotid).
• Aneurysm of the distal internal carotid.
• Hostile neck anatomy (prior irradiation, prior neck surgery).
Open surgical intervention remains the primary treatment choice for carotid artery aneurysms. Ruptured extracranial
carotid artery aneurysm or rapidly expanding pseudoaneurysm mandates rapid control of the patient's airway and
emergent open surgery to control hemorrhage. Ligation may be necessary to control bleeding in patients with ruptured
carotid aneurysm or acute traumatic carotid pseudoaneurysm. Although not a preferred technique for elective extracranial
carotid aneurysm repair, ligation may also be needed for some mycotic aneurysms or other circumstances for which distal
control for bypass cannot be obtained for anatomic reasons. Some clinicians believe that disruptions that occur shortly
after an endarterectomy, that do not appear to be due to infection, may be amenable to an endovascular approach to
reduce potential complications related to the intense inflammatory changes in the immediate postoperative period
surrounding the carotid artery.
As with other vascular pathologies, an endovascular approach is becoming increasingly popular. In a retrospective review
at a single institution, patients treated during the first 10 years of the study period underwent open surgical repair
exclusively [7]. By comparison, during the second 10 years, only 30 percent were treated with open surgery, while the
remainder underwent endovascular repair. Another single-institution review noted a similar trend for more endovascular
intervention in more recent years [8]. Potential advantages of the endovascular approach are avoidance of cranial nerve
injury, access to lesions that may be difficult to access or control with an open approach, and avoidance of general
anesthesia. A concern about endovascular treatment compared with open surgery is the lack of long-term data. Thus,
endovascular intervention is reserved for elective situations that involve a high inaccessible lesion, a hostile neck where
the risk of cranial nerve injury is high, or in a poor surgical candidate with multiple comorbidities who cannot tolerate
general anesthesia.
There are no randomized trials comparing open surgery and endovascular repair for the treatment of extracranial carotid
artery aneurysm. Given the rarity of carotid aneurysm, and the generally low morbidity and mortality rates associated with
intervention, it is unlikely that recruitment of a sufficient number of patients could be achieved to meaningfully compare
these approaches. It should be noted, though, that the results of trials comparing open and endovascular therapy for
carotid atherosclerotic occlusive disease are not sufficiently generalizable to carotid aneurysm to justify choosing one
approach over the other, given that the etiology, pathology, location of disease, and patient populations are sufficiently
distinct (particularly carotid pseudoaneurysm). Nevertheless, similar to other studies comparing open and endovascular
approaches, in retrospective reviews and institutional case series, an endovascular approach for extracranial carotid
artery aneurysm appears to be associated with lower rates of perioperative morbidity and mortality but may be at the
expense of device-related complications.
● In a single-institution review, the authors noted their practice was to use an endovascular approach only in the
treatment of pseudoaneurysms due to their belief that the causes of the pseudoaneurysms were self-limited, whereas
the pathology of true aneurysms (including those related to connective tissue disease) was ongoing with further
aneurysmal degeneration a possibility if treated by endovascular means [8].
● In a single-center cohort study, the rates of cranial nerve injury, 30 day mortality, and major stroke were significantly
reduced in the cohort that underwent predominantly endovascular repair [7].
● A systematic review that evaluated the outcomes of 224 patients from 113 separate reports who underwent
endovascular stenting concluded that the endovascular approach had comparable, if not better, clinical outcomes
compared with historical rates for stroke, cranial nerve injury, and mortality following open repair [77]. In this series,
following endovascular repair, the stroke rate was 1.8 percent, cranial nerve injury occurred in 0.5 percent, and in-
hospital mortality was 4.1 percent; none of the postoperative deaths were considered procedure related.
OPEN SURGICAL REPAIR
The conduct of anesthesia, surgical exposure, neuromonitoring, and carotid shunting are similar to that of carotid
endarterectomy, which is reviewed in detail elsewhere. Some form of neurologic monitoring during surgery is required, as
with all carotid surgeries. Shunting is one tool, as is electroencephalography (EEG) monitoring; the choice is surgeon
dependent. No data exist related to shunting and stroke risk for carotid artery aneurysms, only stroke risk for repair in
carotid artery aneurysms. (See "Carotid endarterectomy", section on 'Surgical anatomy and physiology' and "Carotid
endarterectomy", section on 'Anesthesia' and "Carotid endarterectomy", section on 'Carotid shunting'.)
Open surgical options include carotid artery ligation with or without bypass, and aneurysm excision with reconstruction.
Carotid artery ligation with or without bypass — Carotid artery ligation without bypass is associated with high rates of
morbidity (up to 25 percent) and mortality (20 percent) [53,69] and is reserved for cases where distal control for bypass
cannot be obtained due to anatomic reasons or for difficult-to-control hemorrhage as with carotid aneurysm rupture.
Carotid ligation alone without reconstruction also may be necessary for some mycotic aneurysms following excision of the
aneurysm and debridement to healthy tissues [19,53].
Some type of bypass or reconstruction of the carotid is preferred to ligation alone. Following ligation above and below the
aneurysm, bypass to the distal internal carotid can be performed using a vein graft or prosthetic graft with inflow typically
from the proximal carotid artery, but inflow from other vessels (eg, ipsilateral subclavian artery) can also be used.
Aneurysm excision and reconstruction — Following excision of any degenerated aneurysmal tissue, carotid artery
reconstruction can be performed primarily, or by using an interposition graft or patch angioplasty depending upon whether
a portion of the vessel wall remains intact [13].
Aneurysm excision with interposition graft is the most common approach. Vein conduit is preferred, particularly in the
setting of infection. To perform a bypass, normal proximal and distal arterial segments must be able to be exposed. To
obtain appropriate distal exposure, the mandible may need to be subluxed, as some extracranial carotid artery aneurysms
involve the mid and distal internal carotid artery (ICA). Other possible conduits if vein is not available are
polytetrafluoroethylene (PTFE), Dacron, or autologous arterial segments including the external carotid artery, internal iliac
artery, and superficial femoral artery [17,60].
If the carotid artery is redundant, resection of the aneurysm and primary end-to-end anastomosis may be possible after
appropriate mobilization. Another technique partially excises the carotid artery followed by patch angioplasty, which may
be a good option if resection is difficult because of large aneurysm diameter, distal extent of the aneurysm, or close
proximity to cranial nerves [1].
ENDOVASCULAR REPAIR
Carotid artery stenting can be performed with general anesthesia or with moderate sedation. The procedure is carried out
in a similar fashion as carotid artery stenting for managing carotid stenosis due to atherosclerosis. Endovascular
treatment of carotid artery aneurysm with a stent-graft differs from conventional carotid artery angioplasty and stenting
with respect to the need for a larger sheath due to the larger device profile. When possible, we feel that a distal embolic
protection device should be used; however, the presence of mural thrombus lining the aneurysm requires extra care when
delivering the cerebral protection device to avoid inadvertent embolization. We recommend perioperative antiplatelet
therapy prior to and following carotid artery stenting or stent grafting for extracranial carotid artery aneurysm. (See
"Anesthesia for carotid endarterectomy and carotid stenting" and "Carotid artery stenting and its complications", section
on 'Antiplatelet therapy'.)
Options for endovascular repair include bare metal stent placement with or without trans-stent coil embolization of the
aneurysm sac (image 2), exclusion of the aneurysm using a stent-graft, or endovascular occlusion of the carotid artery
[7,32,51,54,77-83]. In a systematic review of 224 patients, indications for endovascular stenting rather than open surgery
included a high distal extent of the aneurysm and hostile neck anatomy due to previous neck surgery or radiation [77].
Covered stents were used in 68 percent of patients, and bare metal stents were used in the remaining cases. A distal
protection device was employed only 2.3 percent of the time. Stent-graft patency at a mean follow-up of 15 months was
93.2 percent. Compared with patients with pseudoaneurysms, patients with true aneurysms had higher rates of overall
late complications, including stent-graft migration and late stroke. Covered stents and bare metal stents had similar
procedural success rates, but compared with bare stents, covered stents had an increased rate of aneurysm sac
thrombosis and significantly decreased rates of reintervention and overall late complications.
The sac can also be embolized with coils or other agents using microcatheters to inject the coils between the interstices of
the stents [81,84,85]. The proximal and distal landing sites are critical. For aneurysms that span the bifurcation, two
overlapping stent-grafts with different diameters may be needed rather than a single stent-graft to account for the
difference in diameter between the internal and common carotid artery.
Follow-up imaging — Following the procedure, carotid artery stent/stent-graft patency should be monitored at regular
intervals with ultrasound or computed tomography (CT) angiography at 30 days, three months, six months, and then
annually.
MORBIDITY AND MORTALITY
Perioperative mortality is similar for open compared with endovascular repair of extracranial carotid artery aneurysm.
Complications of treatment include cranial nerve injury, stroke (perioperative and late), and graft/stent-specific
complications. For open repair, mortality ranges from 1.5 to 7 percent [3,4,12,14,56,60]. Patients without infection as an
etiology for the aneurysm typically fare better. In one study, during a mean follow-up of 4.6 years, 16 of 42 patients died,
with 11 due to cardiac causes [7]. In a review that included 224 patients treated with endovascular repair of their carotid
artery aneurysms, in-hospital mortality was 4.1 percent [77]. However, none of the postoperative deaths were considered
procedure related. After a mean follow-up period of 15 months, the non-procedure-related death rate was 2.4 percent.
Cranial nerve injury — Injury to cranial nerves IX, X, and XII are a possible consequence of open repair. Cranial nerve
injury is the most common complication of open extracranial carotid artery aneurysm repair, occurring in 5 to 44 percent of
patients [4]. Risk factors for cranial nerve injury include distal internal carotid anatomy aneurysm, redo operations,
infection, and prior irradiation. The incidence is higher for open extracranial carotid aneurysm repair compared with other
elective carotid surgeries related to distorted anatomy and displacement of the cranial nerves in the neck. In addition, the
nerves can firmly adhere to the aneurysm due to inflammation changes. Transient nerve dysfunction is more common
than permanent nerve injury [4]. In one study that included 57 patients who underwent open repair, transient and
permanent cranial nerve injury rates were 20.3 and 6.3 percent, respectively [9]. The incidence of cranial nerve injury is
significantly lower for endovascular repair compared with open surgical repair. In one systematic review of endovascular
stenting, the incidence of cranial nerve injury was only 0.5 percent [77].
Stroke — Following open surgical repair, the reported perioperative stroke rate ranged from 0 to 23 percent in a review
that included series reported in 2000 through 2010 [4]. In this review, the late stroke rate was 0 to 6.2 percent. Two later
series have reported perioperative and late stroke rates of 0 and 10 percent and 3 and 15 percent, respectively [8,14].
In a systematic review that included 224 patients treated with endovascular repair, the reported stroke rate was 1.8
percent [77]. Compared with patients with pseudoaneurysms, patients with true aneurysms had higher rates of overall late
complications, including late stroke. Patients treated with covered stents had a significant decrease in overall late
complications.
Graft/stent specific complications — Like carotid endarterectomy, graft or patch thrombosis is a significant early
complication that mandates an intervention, whereas late thrombosis is often asymptomatic and can be managed
nonoperatively. One study reported a five-year primary patency for synthetic grafts at 89 percent compared with 66
https://www.uptodate.com/contents/extracranial-carotid-artery-aneurysm/print?csi=c55ddc3a-91fb-472f-ad06-dab7ed9510c8&source=contentS… 10/25
percent for vein grafts [63]. They attributed the high postoperative stroke rate (three out of five patients) with vein grafts to
kinking of the graft.
Although endovascular repair confers some benefits over open repair, unique device-related complications such as
endoleak and stent graft occlusion can occur. In addition, the placement of a stent graft does not necessarily relieve the
mass effect and compressive symptoms caused by a larger aneurysm.
In a systematic review that included 224 patients, the leading in-hospital complication with endovascular repair was
endoleak, occurring in 8.1 percent of cases [77]. After a mean follow-up period of 15 months, the rate of late complication
was 11.7 percent, with the most frequent complication being stent-graft occlusion at 6.3 percent. Late reintervention rates
and surgical conversion were 4.7 and 2.4 percent, respectively. Additionally, stent migration and fracture with stenosis,
persistent endoleak, late stroke, and carotid artery rupture were all reported. Compared with patients with
pseudoaneurysms, patients with true aneurysms had higher rates of overall late complications, including stent-graft
migration and late stroke. A subgroup analysis of covered versus bare metal stents had similar procedural success rates.
However, patients treated with covered stents had a significant decrease in reinterventions and in overall late
complications [77].
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided
separately. (See "Society guideline links: Aortic and other peripheral aneurysms".)
SUMMARY AND RECOMMENDATIONS
● Extracranial carotid artery aneurysms are uncommon and occur in a broad range of patients due to many etiologies.
Extracranial carotid aneurysms (true or false) have been classified according to affected anatomic segment, which is
important for determining a treatment approach. The internal carotid artery is the most commonly involved segment.
(See 'Anatomy and classification' above.)
● The factors leading to true aneurysm or pseudoaneurysm differ. The most common etiology of true extracranial
carotid artery aneurysm is atherosclerosis. Pseudoaneurysm is often a consequence of carotid trauma or dissection,
or related to a prior carotid endarterectomy site. Factors that predispose to carotid artery aneurysm include those that
increase the risk for atherosclerosis, primary or secondary carotid artery infection, cerebrovascular injury (trauma or
dissection), and carotid artery irradiation. A variety of other pathologies that are known to weaken the integrity of the
arterial wall are also associated with carotid artery aneurysm. (See 'Etiology and risk factors' above.)
● A diagnosis of extracranial carotid artery aneurysm may be suspected based upon symptoms related to embolization
of thrombus lining the aneurysm sac, local compression of surrounding structures from mass effects, or, rarely,
aneurysm rupture. The most common symptomatic presentation is transient ischemic attack, or stroke. In many
patients with extracranial carotid artery aneurysm, a pulsatile neck mass can be palpated below the angle of the
mandible. (See 'Clinical features' above.)
● A diagnosis of extracranial carotid artery aneurysm relies upon the demonstration of the aneurysm on imaging
studies. Ultrasound is the initial imaging study to evaluate most neck masses, but advanced imaging (computed
tomography [CT] angiography, magnetic resonance [MR] angiography) is usually needed to further define the
aneurysm and confirm a suspected etiology. Brain imaging (CT or MR) should be routinely obtained to assess the
intracerebral perfusion as well as identify any previous infarcts. (See 'Carotid imaging' above and 'Further evaluation'
above.)
● Other evaluation includes screening for other aneurysms in those with true extracranial carotid artery aneurysms, and
for patients in whom a predisposing heritable condition is suspected, further investigation should include family
history, pathology consultation, and imaging of other affected arterial beds, and possibly genetic testing and
counseling. (See 'Further evaluation' above.)
● The natural history of asymptomatic extracranial carotid artery aneurysm is uncertain but may be one of continued
expansion, which eventually can lead to symptoms. Patients with symptomatic extracranial carotid artery aneurysms
should undergo repair. We also repair asymptomatic aneurysms that are large (>2 cm), those with intraluminal
thrombus (regardless of symptoms), and small, asymptomatic aneurysms that demonstrate expansion on serial
imaging. (See 'Natural history and management' above.)
● The approach to repair is individualized based upon aneurysm etiology and location (proximal and distal extent of the
aneurysm), patient comorbidities, and available surgical and endovascular expertise and resources. (See 'Indications
for and approach to repair' above.)
• Options for open surgical repair include carotid artery ligation with or without bypass, and aneurysm excision and
carotid reconstruction. Features favoring an open approach include true aneurysm, infected primary aneurysm,
and pseudoaneurysm due to carotid patch disruption. (See 'Open surgical repair' above.)
• Options for endovascular repair include bare metal stent placement with or without trans-stent coil embolization
of the aneurysm sac, exclusion of the aneurysm using a stent-graft, or endovascular occlusion of the carotid
artery. Features favoring an endovascular approach include pseudoaneurysm related to trauma, aneurysm of the
distal internal carotid artery, and hostile neck anatomy. (See 'Endovascular repair' above.)
● Perioperative mortality is similar for open and endovascular repair of extracranial carotid artery aneurysm.
Complications include cranial nerve injury with open repair, stroke (perioperative and late), and graft-/stent-specific
complications. (See 'Morbidity and mortality' above.)
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Topic 14939 Version 11.0
GRAPHICS
Anatomy of the cerebral arterial circulation
Frontal view of the carotid arteries, vertebral arteries, and intracranial vessels and their
communication with each other via the circle of Willis.
Reproduced with permission from: Uflacker R. Atlas Of Vascular Anatomy: An Angiographic Approach,
Second Edition. Philadelphia: Lippincott Williams & Wilkins, 2006. Copyright © 2006 Lippincott Williams &
Wilkins.
Graphic 51410 Version 6.0
External carotid artery anatomy
External carotid artery and its branches in the lateral view.
Reproduced with permission from: Uflacker R. Atlas Of Vascular Anatomy: An Angiographic Approach, Second
Edition. Philadelphia: Lippincott Williams & Wilkins, 2007. Copyright © 2007 Lippincott Williams & Wilkins.
Lateral view of the internal carotid artery
Lateral view of a schematic drawing of the carotid arteries, vertebral arteries, and intracranial vessels
and their relationships in the neck and brain.
Reproduced with permission from: Uflacker R. Atlas Of Vascular Anatomy: An Angiographic Approach, Second
Edition. Philadelphia: Lippincott Williams & Wilkins, 2007. Copyright © 2007 Lippincott Williams & Wilkins.
Classification extracranial carotid artery aneurysm
Morphological classification of the extracranial carotid artery aneurysm:

Type I: Aneurysm of the internal carotid artery above the carotid bulb
Type II: Aneurysm of the internal carotid artery
Type III: Aneurysm of the carotid bifurcation
Type IV: Aneurysm of the internal carotid artery and the common carotid artery
Type V: Aneurysm of the common carotid artery
Modified from: Attigah N, Külkens S, Zausig N, et al. Surgical therapy of extracranial carotid artery
aneurysms: long-term results over a 24-year period. Eur J Vasc Endovasc Surg 2009; 37:127.
Mechanism of blunt cerebrovascular injury
(A) Cervical hyperextension stretches the internal carotid artery across the lateral articular
processes of the first through third cervical vertebrae, causing intimal tearing.
(B) Cervical hyperflexion may directly compress the internal carotid artery between the
mandible and the upper cervical vertebrae, causing intimal disruption or mural hematoma.
(C) Falling with a hard object in the mouth (eg, toothbrush) can lead to injury of the internal
carotid artery at the angle of the jaw.
Carotid pseudoaneurysm on neck CT
This coronal view of a neck CT scan shows a large pseudoaneurysm (arrow) of the right carotid artery.
CT: computed tomography.
Management of extracranial carotid artery aneurysm
TIA: transient ischemic attack.

* Imaging every six months after diagnosis, then if stable, annual surveillance.
¶ Open repair preferred for: Most true aneurysms, infected aneurysm, ruptured
aneurysm. Endovascular repair may be preferred for: Pseudoaneurysm, distal internal
carotid artery, prior neck surgery.
Pseudoaneurysm of the internal carotid artery with subsequent stent placement
An internal carotid angiogram (A) shows a focal dissection (arrow) in the cervical portion of the carotid artery. An angiogram performed two years
later (B) shows a pseudoaneurysm at the previous site of dissection (arrow). Image C shows stent placement (arrowheads) across the mouth of
the pseudoaneurysm. Six months later (D), an angiogram shows resolution of the pseudoaneurysm (arrowhead).
Courtesy of Thanh Nguyen, MD.
Contributor Disclosures
Melissa L Kirkwood, MD Nothing to disclose John F Eidt, MD Nothing to disclose Joseph L Mills, Sr, MD Grant/Research/Clinical
Trial Support: Voyager Trial [Peripheral artery disease (Rivoxaraban)]. Consultant/Advisory Boards: Innomed [Peripheral artery disease
(Femoral artery stent)]. Equity Ownership/Stock Options: NangioTx [Peripheral artery disease (Self-assembling nanotubules)]. Other
Financial Interest: Elsevier; Rutherford [Vascular surgery (Rutherford and Comprehensive Vascular and Endovascular Surgery
textbooks)]. Kathryn A Collins, MD, PhD, FACS Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through
a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced
content is required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

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ANATOMY AND CLASSIFICATION

● Type I – Isolated aneurysms of the internal carotid artery

ETIOLOGY AND RISK FACTORS

These include [8,33-47]:

● Cystic medial necrosis

NATURAL HISTORY AND MANAGEMENT

● Factors favoring an open approach:

• True aneurysm (atherosclerotic, related to connective tissue disorders).

• Infected primary aneurysm.

● Factors favoring an endovascular approach:

• Pseudoaneurysm related to trauma (often affect the distal carotid).

• Aneurysm of the distal internal carotid.

• Hostile neck anatomy (prior irradiation, prior neck surgery).

OPEN SURGICAL REPAIR

MORBIDITY AND MORTALITY

SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

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Anatomy of the cerebral arterial circulation

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External carotid artery anatomy

External carotid artery and its branches in the lateral view.

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Lateral view of the internal carotid artery

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Classification extracranial carotid artery aneurysm

Morphological classification of the extracranial carotid artery aneurysm:

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Mechanism of blunt cerebrovascular injury

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Carotid pseudoaneurysm on neck CT

CT: computed tomography.

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Management of extracranial carotid artery aneurysm

TIA: transient ischemic attack.

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Pseudoaneurysm of the internal carotid artery with subsequent stent placement

Courtesy of Thanh Nguyen, MD.

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