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Year : 2020  |  Volume : 7  |  Issue : 1  |  Page : 83-87

A rare case report of extensive extracranial internal carotid artery aneurysm and its endovascular management

1 Department of Vascular and Endovascular Surgery, Ruby Hall Clinic, Pune, Maharashtra, India
2 Ruby Hall Clinic, Pune, Maharashtra, India

Date of Submission11-Jun-2019
Date of Decision01-Jul-2019
Date of Acceptance31-Jul-2019
Date of Web Publication16-Mar-2020

Correspondence Address:
Dr. Bhushan D Shinde
Ruby Hall Clinic, Pune, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijves.ijves_36_19

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Aneurysms of the extracranial carotid arteries can occur as a result of atherosclerotic degeneration, traumatic injury, dissection, or local infection or as a complication after carotid endarterectomy. Extracranial carotid artery aneurysm (ECAA) is an uncommon but important clinical entity. Carotid aneurysms are extremely rare in comparison with atherosclerotic occlusive disease of the same location. These aneurysms are also rare in comparison with aneurysms involving the intracranial carotid arteries and their branches. The reported incidence of incidental intracranial aneurysms discovered in autopsy studies ranges from 0.8% to 18%. The incidence of ECAA is largely unknown, but it represents only 1%–1.5% of procedures performed for extracranial cerebrovascular disease at major referral centers.

Keywords: Arterial aneurysm, endovascular, extracranial carotid artery aneurysms

How to cite this article:
Kamerkar DR, Chavan R, Shinde BD, Tiwari K. A rare case report of extensive extracranial internal carotid artery aneurysm and its endovascular management. Indian J Vasc Endovasc Surg 2020;7:83-7

How to cite this URL:
Kamerkar DR, Chavan R, Shinde BD, Tiwari K. A rare case report of extensive extracranial internal carotid artery aneurysm and its endovascular management. Indian J Vasc Endovasc Surg [serial online] 2020 [cited 2020 Jul 14];7:83-7. Available from:

  Introduction Top

The normal carotid bifurcation is typically 40% greater in diameter than the more distal internal carotid artery (ICA).[1],[2],[3],[4] The accepted definition of most arterial aneurysms is “an artery having at least a 50% increase in diameter compared to the expected normal diameter of the artery.”[5] Given this definition, it does not require much dilatation of the carotid bulb to reach this threshold, a fact that has led to disagreement about what constitutes an extracranial carotid artery aneurysm (ECAA). de Jong et al. proposed that ECAA be defined as bulb dilatation greater than 200% of the diameter of the ICA or than 150% of the diameter of the common carotid artery (CCA).[6] This strict definition is used in many of the contemporary reports of ECAA and is helpful, given the normal physiologic dilatation of the carotid bulb.

True degenerative carotid aneurysms affect men twice as often as women,[7],[8] and there does not seem to be a predilection for the right or left side. Most patients are older than 60 years, but true degenerative carotid artery aneurysms have been reported in children.[9] There does not seem to be a specific racial distribution of true degenerative carotid aneurysms.

  Case Report Top

A 52-year-old female presented in the outpatient department with pulsatile painful neck swelling on the left side with pain during deglutition for 15 days.

There was no history of trauma or previous history of intervention. The patient did not have any comorbidity.

On examination, approximately 5 × 3 swelling was found on the left side of the neck anterior to the sternocleidomastoid muscle in the upper one-third with pulsation and tenderness. The upper extent of swelling cannot be negotiated. Intraoral examination showed bulge left-sided lateral pharyngeal wall which is suggestive of its internal extension. The patient was investigated with ultrasound which showed left ICA aneurysm partially thrombosed followed by CT angiography to see the extent and exact nature of swelling.

Computed tomography (CT) angiography is suggestive of extensive left ICA aneurysm which was partially thrombosed with extension from bifurcation up to the base of skull. It is 1.8 cm distal to the origin of ICA, extends about 7 cm in length, and it measures 2.7 cm in diameter [Figure 1]. There is no other aneurysm noticed and CT of the brain was normal.
Figure 1: Computed tomography angiography

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Routine blood investigation was found to be normal, although inflammatory markers erythrocyte sedimentation rate and C-reactive protein were significantly raised with ANA-positive status.

As aneurysm was symptomatic, decision was taken for active intervention.

As aneurysm was extended up to the base of skull, open surgical intervention would have resulted in extensive morbidity to the patient, so endovascular approach to the aneurysm was preferred.

Digital subtraction angiography with balloon occlusion test

The procedure was done under local anesthesia and done with bilateral femoral punctures. Large fusiform aneurysm was seen involving the cervical portion of left ICA with probably some intimal injury and dissection in it [Figure 2]. It shows a significant dilatation with ectasia. Thrombus with filling defect was seen with slow distal antegrade flow opacifying intracranial ICA and left middle cerebral artery branches. The rest of the neck and intracranial arteries are normal.
Figure 2: Digital subtraction angiography image

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Balloon occlusion test was performed with 6 mm × 20 mm submarine balloon (Medtronic Rapido – usually used for carotids and renals inflated in left CCA). Stasis suggestive of total occlusion of lumen. The patient was monitored for 15 min for vision, memory, cognitive functions, and right-sided weakness. The patient passed the balloon occlusion test. Simultaneous angiogram obtained from the right ICA and vertebral showed good cross-flow across the anterior communicating artery (ACOM) and posterior communicating artery (PCOM).

As there was good collateral circulation, decision was taken to occlude the aneurysmal ICA with CCA to external carotid artery (ECA) covered stent with distal coiling.

Endovascular treatment for left internal carotid artery aneurysm

  • Procedure was done under general anesthesia (GA)
  • Bilateral femoral arterial access was taken [Figure 3]
  • 6F sheath on the left side and 9F sheath on the right side were inserted
  • There was unchanged left ICA (cervical portion) aneurysm
  • Amplatz (exchange length) wire parked in the left superficial temporal artery
  • Two selectively detachable long Axium coils were deployed through Echelon microcatheter
  • Embolization protection device is not used because plan is to jail ICA with covered stent from CCA to ECA
  • Fluency plus vascular stent graft (8 mm × 40 mm) was then deployed from the left ECA to the CCA across origin of left ICA
  • Complete obliteration left ICA is noted
  • Good crossflow was seen across ACOM and left PCOM arteries on the right ICA and vertebral angiograms
  • No retrograde opacification of cervical ICA aneurysm noted
  • Patient extubated without any neurological deficit.
Figure 3: Endovascular coiling and covered stent

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The patient was discharged on postprocedure day 4 with no neurological deficit.

The patient was followed on day 10 and found to be symptom free.

The patient was advised to continue follow-up with a rheumatologist for etiology (? inflammatory) of aneurysm.

  Discussion Top

Anatomy and classification

The extracranial carotid arteries include the CCA, which originates in the chest, the ECA, and the ICA to the base of the skull.

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% increase in diameter compared with the expected normal diameter.[7],[10] 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.

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

  • Type I – Isolated aneurysms of the ICA
  • Type II – Aneurysms of the complete ICA with involvement of the bifurcation
  • Type III – Aneurysms of the carotid bifurcation
  • Type IV – Combined aneurysm of the internal and CCA
  • Type V – Isolated aneurysm of the CCA.

Etiology and risk factors

Factors that increase the risk of extracranial carotid aneurysm are discussed briefly below, and in detail in the linked topic reviews, where available.


Atherosclerosis is the most common etiology for true ECAA.[7],[10] The patient often has severe hypertension and other comorbidities, such as coronary artery disease and chronic obstructive pulmonary disease.


ECAA can be due to primary infection of the carotid arterial tissues or infection secondary to prior carotid surgery or other instrumentation.[11],[12]

Cerebrovascular injury

Blunt or penetrating cerebrovascular injury can lead to ECAA, 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.[13],[14]

Spontaneous carotid dissection

Among patients with spontaneous extracranial carotid artery dissection, up to 30% will develop pseudoaneurysms.[15] The time interval between the dissection and aneurysm formation is variable.


Although carotid artery stenosis may be more frequently reported as a complication of radiation therapy,[16] extracranial carotid artery pseudoaneurysm has also been reported.[17],[18]

Clinical features

Symptoms from ECAA can be due to local mass effect or embolism. Rupture is very rare unless there is an associated infection. Thrombotic occlusion is likewise pretty rare. 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.[19] In one series, approximately one-half of ECAAs were asymptomatic and discovered incidentally.


Symptoms related to ECAA can be related to embolization of thrombus lining the aneurysm sac, local compression of surrounding structures from mass effects, or aneurysm rupture.

  • Neurologic symptoms – The most common symptomatic presentation is either a transient ischemic attack or a stroke
  • Compressive symptoms – 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, and anhidrosis) can result. Vagal compression can also result in hoarseness, and hypoglossal compression can cause tongue deviation and decreased function.

Physical findings

In up to 90% of patients with ECAA, a pulsatile neck mass is palpable below the angle of the mandible;[20],[21],[22] there may be an associated systolic bruit.[23]

A detailed neurologic examination should be documented and will identify the presence of any associated cranial nerve abnormalities.


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.

Computed tomography or magnetic resonance angiography

Computed tomography (CT) and magnetic resonance angiography (MRA) are useful confirmatory tests because they can assess the extent of aneurysmal dilation, thrombus formation, and the relationship of the aneurysm with surrounding structures.


Arteriography is no longer necessary for making a diagnosis; however, it still has a role in the management of ECAA 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. 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.[24] If the patient remains stable and has no neurologic symptoms, then carotid ligation/occlusion is an option, if revascularization is not possible.

Further evaluation

Brain imaging (CT or MRA) 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.

Screening for other aneurysms

True ECAAs are frequently associated with aneurysms in other vascular beds. In a review of 48 patients with ECAA, 24% of those with true aneurysms had an associated aneurysm in another vascular territory, most commonly the abdominal aorta. In another review, 26% of patients with an ECAA had a coexistent abdominal aortic aneurysm.[25] Other arterial sites that have been reported include the thoracic aorta and the iliac, femoral, and subclavian arteries. Coexistent intracranial carotid artery aneurysms can also occur.

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.

Natural history and management

As with aneurysms at other sites, the natural history of ECAA may be one of the continued expansions, which can eventually lead to symptoms, although specific management depends on the factors discussed below.


The risk of embolism due to ECAA is not well defined but is potentially related to aneurysm diameter and the presence of thrombus or associated calcification. Observation of small, asymptomatic aneurysms and pseudoaneurysms (e.g., blunt trauma and 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. 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.

Indications for repair

Treatment is appropriate for symptomatic aneurysms (e.g., mass effect and embolism) regardless of aneurysm diameter.

Asymptomatic ECAAs 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).

The presence of thrombus in a carotid aneurysm may increase the risk for neurologic events.

  • Options for open surgical repair include carotid artery ligation with or without bypass and carotid aneurysm excision with reconstruction
  • 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
  • Factors favoring an open approach:

    • True aneurysm (atherosclerotic, related to connective tissue disorders)
    • Infected primary aneurysm
    • Pseudoaneurysm due to carotid patch disruption.

  • 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 and prior neck surgery).

Open surgical repair

Open surgical options include carotid artery ligation with or without bypass and aneurysm excision with reconstruction.

Some form of neurologic monitoring during surgery is required, as with all carotid surgeries. Shunting is one tool and is electroencephalography monitoring; the choice is surgeon dependent. No data exist related to shunting and stroke risk for carotid artery aneurysms and only stroke risk for repair in carotid artery aneurysms.

Endovascular repair

Carotid artery stenting can be performed with GA 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. Perioperative antiplatelet therapy prior to and following carotid artery stenting or stent grafting for ECAA is recommended.

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. 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.[26] Covered stents were used in 68% of patients, and bare-metal stents were used in the remaining cases. A distal protection device was employed only 2.3% of the time. Stent-graft patency at a mean follow-up of 15 months was 93.2%. 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.[27] 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 ICA and CCA.

Follow-up imaging

Following the procedure, carotid artery stent/stent-graft patency should be monitored at regular intervals with ultrasound or CT angiography at 30 days, 3 months, 6 months, and then annually.

Morbidity and mortality

Perioperative mortality is similar for open compared with endovascular repair of ECAA.

  Conclusion Top

In extensive extracranial ICA aneurysm involving up to the base of skull, endovascular approach is treatment of choice.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

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  [Figure 1], [Figure 2], [Figure 3]


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