Extracranial Carotid Artery Aneurysms

Incidence

True aneurysms account for a little more than half of all reported extracranial carotid artery aneurysms. These aneurysms affect men twice as often as women. The average age at recognition is 60 years. Although most true carotid aneurysms exhibit arteriosclerosis, arteriosclerosis is considered a secondary event rather than a primary etiologic factor.

The carotid artery bulb is the site of true aneurysms in more than 95% of cases ( Figures 1 and 2 ). Bilateral aneurysms are noted in 12% of cases, and no predilection exists for right- or left-sided involvement in patients with unilateral aneurysms. Because the normal carotid bulb is usually 40% greater in diameter than the more distal internal carotid artery, it requires very little expansion to reach the 50% dilation level. The latter is a generally accepted definition of an aneurysm. However, given the normal dilation of the carotid bulb, it becomes difficult to define the natural history of borderline-sized aneurysms. Because of concerns over one’s ability to differentiate a generous-sized carotid bulb from a small aneurysm, it has been proposed that an aneurysm only exists when the carotid bulb dilation at least is 200% greater than the extracranial internal carotid artery diameter or 150% of the common carotid artery diameter. Although true arteriosclerotic aneurysms have been encountered in the common carotid artery and the more distal internal carotid artery, trauma or some other vascular insult has likely preceded aneurysm development at these latter sites. Aneurysms affecting other arteries in patients with carotid artery aneurysms have been observed in nearly 25% of cases.

Manifestations

The natural history of true carotid artery aneurysms is poorly defined. Most aneurysms are likely to be asymptomatic, although the surgical literature does not support such a statement. Among patients described in surgical reports, approximately 60% have experienced transient ischemic attacks, including 33% with amaurosis and 21% with hemispheric symptoms. Frank strokes affected an additional 8% of patients.

Rupture of a true carotid aneurysm is rare, having been reported in fewer than a dozen patients. However, acute expansion of true carotid artery aneurysms does occur, and it can cause secondary cranial nerve dysfunction, such as hoarseness related to pressure on the recurrent laryngeal nerve. Severe hemicrania, often with Horner’s syndrome, can accompany acute expansion of an aneurysm, although such is more often caused by a carotid artery dissection. These aneurysms manifest as nontender cervical masses in a third of patients, and in some patients they may be mistaken for a deep peritonsillar abscess when they expand medially and encroach on the retropharyngeal space. More than 80% of patients with these aneurysms present with a pulsatile mass that may be difficult to distinguish from a tortuous artery or lymphadenopathy overlying a normal carotid bulb.

Duplex ultrasonography is adequate to define the size and extent of low-lying carotid artery aneurysms. However, computed tomography is necessary to define the relationship between high-lying aneurysms and surrounding structures above the angle of the mandible. Conventional cerebral arteriography or computed tomographic arteriography should be performed in all patients with suspected carotid aneurysms before proceeding to open operative or endovascular therapy. Arteriography is particularly useful to differentiate carotid artery aneurysms from carotid artery kinks and loops.