Carotid Artery Aneurysms

Introduction

Extracranial carotid artery aneurysms (ECAA) are rare in comparison with atherosclerotic occlusive disease in the same location. ECAA can occur as a result of atherosclerosis, trauma, dissection, local infection, or after carotid endarterectomy (CEA). These aneurysms occur less frequently than 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 true incidence is unknown, but repair represents only 0.6% to 3.8% of procedures performed for extracranial cerebrovascular disease, and is probably <2% of all carotid diseases.

An ECAA is defined as a fusiform or saccular aneurysm which occurs between the common carotid artery (CCA) origin at the aortic arch and the internal carotid artery (ICA) at the skull base. The external carotid artery may also be involved. The definition of arterial aneurysm is “an artery having at least a 50% increase in diameter compared to the expected normal diameter of the artery.” This definition is easily applied to fusiform aneurysms of the ICA and the CCA. However, the normal carotid bifurcation is typically 40% greater in diameter than the more distal ICA. Therefore, it does not require much dilation to reach this threshold. de Jong et al. proposed that ECAA be defined as bulb dilation >200% of the ICA diameter or >150% of the common carotid artery diameter. This definition has been internationally accepted and applied in the surgical literature. However, strict diameter criteria have not been applied to saccular ECAA, which have been defined more loosely as a distended sac of any size affecting only part of the ICA or CCA circumference (ECCA Registry). This chapter describes contemporary management of ECAAs, including open surgery and endovascular options.

Historical Review

Sir Astley Cooper is credited with the first unsuccessful and successful operations for ECAA in London in 1806 and 1808, respectively. Ligation of the common carotid artery was the sole treatment. Winslow reported an exhaustive review of 124 reported cases through 1925, including 82 patients treated by carotid ligation with a mortality rate of 28%. The first resection of a carotid aneurysm with primary anastomosis was described by Shea et al. in 1955. The first successful resection and repair was in 1952. When inadequate length of vessels precludes primary anastomosis, an interposition graft must be used. Beall et al. performed the first prosthetic graft replacement in 1959. By the 1970s, direct arterial reconstruction or autogenous vein grafting (or both) had supplanted carotid ligation. Endovascular techniques were first applied for ECAAs in the 1990s and continue to have an increasing role.

Epidemiology

Population Affected

The population affected and age at diagnosis are directly related to the cause of the aneurysm. The relative frequency of various causes of ECAA has changed over the years. Syphilis, tuberculosis, middle ear, and tonsillar infections were the most common causes of carotid artery aneurysms before the advent of antibiotics. The majority of these early cases were pseudoaneurysms related to trauma or “erosions” from middle ear infections and tonsillitis, rather than true atherosclerotic aneurysms. Therefore, most patients were between 20 and 40 years of age, and the surgical morbidity and mortality were excessive. Increasing the use of antibiotics for head and neck infections significantly reduced the incidence of mycotic arterial infections from local extension of a septic process. Mycotic ECAAs should not be entirely dismissed as a problem of the past, since modern series suggest that mycotic ECAAs may still be encountered in immunocompromised patients.

Atherosclerotic degeneration, dissection, trauma, and previous carotid surgery have supplanted infection as the most frequent causes of ECAA ( Table 97.1 ). ^, True degenerative atherosclerotic carotid aneurysms affect men twice as often as women, ^, and affect right and left sides equally. Most patients are older than 60 years, but degenerative carotid artery aneurysms have also been reported in children. There does not seem to be a specific racial distribution. Earlier reports suggested that the incidence of ECAAs in patients with other aneurysmal disease ranged from 14% to 25%. ^, Most modern series have not reported similar findings.

TABLE 97.1

Aneurysm Characteristics

From Welleweerd et al. Management of ECAA. Eur J Vasc Surg . 2015;50:141–147, Table 1.

Variables	N	(%)
Reports included	39
Patients	1239
Aneurysms	1322
Etiology
Atherosclerosis	509	38
Traumatic	144	11
Mycotic	65	5
Other	329	25
Not reported	275	21
Symptoms ^a
Cerebral ischemia	476	36
Mass	442	33
Asymptomatic	172	13
Compression	119	9
Local pain	39	3
Other	185	14
Location
ICA	608	46
Bifurcation	261	20
CCA	108	8
ECA	9	1
Not reported	336	25

Note . Other etiology includes granulomatous diseases, connective tissue disorders, iatrogenic aneurysms, post-carotid endarterectomy cystic medial necrosis, and arteritis.

CCA , common carotid artery; ECA , external carotid artery; ICA , internal carotid artery.

a Some patients experienced multiple symptoms from one aneurysm.

Blunt trauma, dissection, and penetrating injury to the neck can result in a carotid pseudoaneurysm. Such lesions are typically encountered in a younger population. Pseudoaneurysms after CEA performed for occlusive disease usually affect individuals in their sixth or seventh decades of life. ECAAs also occur in patients who have undergone extensive surgery and radiation therapy for head and neck cancer. There have been several reports of ECAAs in patients with connective tissue disorders, including Ehlers–Danlos syndrome, neurofibromatosis, Behçet disease and Marfan syndrome. In such patients, it is unwise to use autologous vein for arterial reconstruction due to unacceptable risk of late aneurysmal degeneration.

Incidence

Because these aneurysms are rare, it is difficult to quantify the true incidence or to determine if the frequency is increasing. A search of the world’s literature from 1687 to 1977 found only 853 ECAAs. ^, A more recent systematic review of single-center series with at least 10 patients from 1900 to 2014 reported 1239 patients with 1322 ECAAs. Advances in vascular and soft tissue imaging may have contributed to greater recognition, at least partially accounting for the larger number of ECAAs reported over a shorter time period.

Other authors have quantified ECAA repairs as a percentage of their total operative carotid workload. Pooled data from the largest single-center series (1960–1995) that included CEA volume during that same period demonstrated a total of 17,854 carotid procedures, 276 of which were performed for ECAA, for a relative incidence of 1.54%. El-Sabrout and Cooley from the Texas Heart Institute reported 67 ECAAs treated between 1960 and 1995. During the same period, their institution performed 7394 peripheral aneurysm repairs and 4991 carotid operations. Their 1.31% relative incidence is consistent with other published series. ^, The low incidence at large referral centers suggests that the true incidence of ECAAs is probably less than 1% of all carotid disorders.

Pathogenesis

Etiology

Degenerative/Atherosclerotic

The most common cause of ECAAs is atherosclerosis and subsequent degeneration accounting for up to 40% of ECAAs. Degenerative aneurysms are true aneurysms which demonstrate disruption of the internal elastic lamina and thinning of the media on histology. They tend to be fusiform rather than saccular and are most commonly located at the bifurcation and proximal ICA, where atherosclerosis is common ( Fig. 97.1 ). Atherosclerotic aneurysms that do not involve the carotid bifurcation are frequently saccular and occur in patients with severe hypertension. Most bilateral, nontraumatic ECAAs are also saccular.

Figure 97.1, Arch ( A ) and right carotid ( B , C ) arteriograms showing a large extracranial carotid artery aneurysm involving the proximal internal carotid artery.

Post-Traumatic Causes

The incidence of carotid artery injury in civilian trauma series ranges from 12% to 17% of penetrating neck injuries (see Ch. 180 , Vascular Trauma of the Head and Neck). The internal jugular vein is the most frequently injured vascular structure and the common carotid artery is the most frequent site of arterial injury from penetrating neck trauma. Penetrating injuries involving the extracranial carotid arteries can have two important vascular sequelae: arteriovenous fistula and pseudoaneurysm formation. Carotid pseudoaneurysm has also been reported due to iatrogenic injury from attempted placement of a catheter in the internal jugular vein.

Blunt cerebrovascular injury (BCVI) occurs in 0.18% to 2.7% of blunt trauma patients, and typically involves the distal ICA just below the skull base. Traumatic dissections can degenerate into pseudoaneurysms, which can enlarge, embolize thrombus, or rupture. Some authors advocate treatment of grade 3 pseudoaneurysms that persist beyond a week. Many of these patients have associated head injuries precluding antiplatelet therapy and anticoagulation initially. Enlarging or symptomatic pseudoaneurysms from blunt trauma are typically diagnosed some time after the original injury, at which point patients can safely be treated with preprocedural clopidogrel and intraprocedural heparin.

Post-Endarterectomy Aneurysms

CEA-related pseudoaneurysms are frequently reported aneurysms of the extracranial carotid arteries. El-Sabrout and Cooley demonstrated that 57% of their 67 cases were a result of previous CEA. Zhou et al., in a later series from the Baylor College of Medicine, found post-CEA pseudoaneurysm to be the principal etiology in 36% of 42 cases. The development of post-CEA pseudoaneurysm can be caused by suture line failure or patch degeneration with or without infection. El-Sabrout and Cooley reported seven patients in whom the silk sutures, used before the advent of monofilament sutures, degenerated. Infectious complications have been reported in a third of post-CEA pseudoaneurysms. Patients typically have local signs and symptoms of infection, including pain and erythema at the operative site or draining neck sinuses. Infection of synthetic patches may also be identified at the time of removal, with Staphylococcus species being the most commonly cultured causative organism. Aneurysmal degeneration of saphenous vein patches has also been reported.

Arterial Dysplasia

Arterial dysplasia, usually a fibromuscular variant, is a frequent reported cause of ECAAs in some smaller series. ^, ^, The arteries of patients with fibromuscular dysplasia typically display a beaded appearance caused by alternating stenotic webs and dilations. These lesions may lead to ICA dissection and pseudoaneurysm formation.

Pathology

The rarity of primary carotid artery aneurysm in comparison with carotid occlusive disease makes it difficult to accept atherosclerosis as the sole cause. Histologic study of carotid artery aneurysms, however, reveals many of the findings seen in atherosclerotic specimens: fragmentation of the elastic lamina, lipid-laden foam cells, extracellular accumulation of cholesterol, deposition of hemosiderin, degeneration of the media, and neoangiogenesis. Thinning of the media and fragmentation of the internal elastic lamina are also seen, as in aging arteries. Just as many authorities propose for abdominal aortic aneurysms, atherosclerosis is clearly a coexisting finding for many ECAAs but may not be the only cause. ^,

Clinical Findings

Physical Findings/Symptoms

The symptoms of ECAAs vary according to their location, size, and etiology. The most common finding is a painless pulsatile neck mass, which was the initial symptom in 93% of patients in the series reported by Zhou et al. Tenderness and overlying erythema, especially if associated with fever, should raise suspicion for an infected aneurysm.

An ICA aneurysm is occasionally recognized as a pulsating mass in the tonsillar fossa or pharynx with little or no manifestation of its presence externally in the neck. The classic analytic study by Shipley et al. emphasized that aneurysms of the ICA are directed inward into the throat, whereas those of the common carotid artery are directed outward into the neck. The absence of cervical swelling in the former is attributed to the dense, deep cervical fascia and muscles attached to the styloid process anteriorly and the cervical vertebrae posteriorly, which crowd the gradually dilating aneurysm inward toward the tonsillar fossa, where the thin superior pharyngeal constrictor muscle and mucous membrane offer only minimal resistance to inward protrusion.

Aneurysms that arise at or proximal to the carotid bifurcation are readily palpable and usually pose no diagnostic difficulty. Those arising from the ICA near the base of the skull can cause diagnostic problems. A chronic unilateral swelling of the posterior pharynx should raise the level of suspicion, especially when other physical signs are lacking, bizarre, or atypical. Otolaryngologists are often the first to see these lesions. A high index of suspicion usually leads to computed tomography angiography (CTA), magnetic resonance angiography (MRA), or catheter-based angiography, any of which is nearly always diagnostic when an aneurysm is present.

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