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Extracranial carotid artery aneurysm

Extracranial carotid artery aneurysm
Literature review current through: Jan 2024.
This topic last updated: Aug 16, 2023.

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 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 males were affected by pseudoaneurysm in this series, whereas for true aneurysm, the opposite was true. A later systematic review reported a distribution of 52 and 45 percent for true aneurysm and pseudo aneurysm, respectively [9].

Extracranial carotid aneurysms (true or false) have been classified according to affected anatomic segment, which is important for determining a treatment approach (figure 2) [10].

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. In a systematic review, Type I and III comprised more than two-thirds of extracranial carotid artery aneurysms (43 and 28 percent, respectively), followed by type V (15 percent), type IV (11 percent), and type II (3 percent) [9]. 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 [11-13]. 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 [8,13]. 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 [8,11,14,15].

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 [8,12]. 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. General risk factors for pseudoaneurysm formation include older age, female sex, calcified vessels, obesity, and anticoagulation [16]. Blunt or penetrating trauma can result in either type of aneurysm depending upon the mechanism and severity of the arterial wall injury [17]. One percent of aneurysms were of unknown etiology in one systematic review [9].

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 [18]. 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 [1,17,19]. 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 [7,10]. The male-to-female ratio is approximately 2:1 [19,20]. 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 [21-23]. Extracranial carotid artery aneurysms are increasingly being reported in association with human immunodeficiency virus [24].

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 [21]. (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 [25]. 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 [21,26]. (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 [27]. 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'.)

Most 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 [4,8,28,29]. 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 "Central venous catheters: Overview of complications and prevention in adults".)

Spontaneous carotid dissection — Among patients with spontaneous extracranial carotid artery dissection, up to 30 percent will develop pseudoaneurysms [30]. The time interval between the dissection and aneurysm formation is variable, as with cerebrovascular injury due to trauma. (See "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 [31], extracranial carotid artery pseudoaneurysm has also been reported [32,33]. 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 [34].

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 [1,35,36].

These include [8,37-52]:

Fibromuscular dysplasia

Connective tissue disease, including Marfan syndrome (table 1), Ehlers-Danlos syndrome, Loeys-Dietz syndrome, osteogenesis imperfecta, and pseudoxanthoma elasticum (see "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders" and "Clinical manifestations and diagnosis of Ehlers-Danlos syndromes")

Tuberous sclerosis (see "Tuberous sclerosis complex: Clinical features")

Arteritides, including Takayasu's arteritis, polyarteritis nodosa, and Behcet syndrome (see "Overview of and approach to the vasculitides in adults")

Cystic medial necrosis (see "Adventitial cystic disease")

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 [53]. 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 [54]. 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 [1,10,55-59]. 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) [1,17,54,60]. Although rare, a nonruptured aneurysm can compress the pharyngeal muscles resulting in dysphagia [8,61-63]. 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 [10,64]. (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 [12,54,65]. Infected aneurysms are more susceptible to rupture than noninfected aneurysms [12,22]. Pseudoaneurysms of the carotid artery secondary to radiation treatment have also been known to rupture [34].

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 [21].

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 [56-59]; there may be an associated systolic bruit [54].

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. A "yin-yang" pattern, described as persistent swirling blood flow on color Doppler imaging within the pseudoaneurysm sac, can help to differentiate a pseudoaneurysm from a hematoma [66]. Universally, however, a to-and-fro flow pattern should be seen in the neck of the pseudoaneurysm on spectral Doppler examination. The neck is the area connecting the carotid artery to the pseudoaneurysm masslike lesion [67].

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) [68]. 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 [69]. 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 [18]. In another review, 26 percent of patients with an extracranial carotid artery aneurysm had a coexistent abdominal aortic aneurysm [70]. Other arterial sites that have been reported include the thoracic aorta and the iliac, femoral, and subclavian arteries [10,18]. Coexistent intracranial carotid artery aneurysms can also occur [10].

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 [17] (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 [71]), 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 [17]. (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 [1,4,7,10,35,58,64,70,72-77]. 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 [78-81]. 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 [3,56,57,72,82-84]. 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 [61,78,79,85]. Later series report a lower, but still substantial, stroke rate for extracranial carotid artery aneurysms (true or pseudoaneurysm) [8,17,18,22,85]. (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 [29]. 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 [86]. In a later single-center retrospective review, 6 of 41 patients were managed conservatively; one patient had an ipsilateral stroke during the course of care [87].

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) [8,10,33,36,88-91].

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 [88]. 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 — 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.

Carotid artery ligation without bypass is associated with high rates of morbidity (up to 25 percent) and mortality (20 percent) [61,79] 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 [23,61].

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 [17].

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 [21,70].

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 "Overview of carotid artery stenting", section on 'Dual 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 [7,36,58,62,88-96]. 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 [88]. 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 [94,97,98]. 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 [3,4,13,18,64,70]. 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 [88]. 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 [10]. 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 [88].

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 [8,18].

In a systematic review that included 224 patients treated with endovascular repair, the reported stroke rate was 1.8 percent [88]. 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 percent for vein grafts [73]. 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 [88]. 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 [88].

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 aneurysm – 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.)

Etiology and risk factors – 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.)

Clinical features – 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.)

Diagnosis and further evaluation

The 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. (See 'Diagnosis' above.)

Brain imaging (CT or MR) should be routinely obtained to assess the intracerebral perfusion as well as identify any previous infarcts. 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.)

Natural history and management – 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.)

Approach to repair – 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.)

Mortality and complications – 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 17.0

References

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