Introduction

Extracranial carotid artery aneurysms—mainly aneurysms of the cervical segment of the internal carotid artery (ICA)—are rare, accounting for only 0.4 to 4% of all peripheral artery aneurysms. Invasive treatment of extracranial carotid aneurysms comprises 0.6 to 3.8% of all extracranial carotid interventions. Furthermore, the morphology and causes of these aneurysms are diverse. Therefore, few reliable epidemiological data are available regarding immediate surgical outcomes or long-term follow-up. A retrospective review of aneurysm repair at one institution noted 67 cervical carotid aneurysms in 65 patients, representing a variety of causes, including atherosclerotic and traumatic factors and previous carotid procedures resulting in pseudoaneurysm. This observation was similar to the results of a review by Welleweerd and colleagues of pooled data on 1,239 patients from published reports of series with 10 or more patients available in the medical literature up to 2014.

The presenting symptoms of cervical carotid aneurysms vary but are due to mass effect in 33 to 58% and cerebral ischemia in 36 to 43% of cases ( 1 , 3, 4 in algorithm ). Some patients may have no symptoms at all ( 2, 5, 8 in algorithm ). A large number of other signs and symptoms have been noted in individual patients; these include cranial nerve dysfunction, pain (including headache), dysphagia, dizziness, tinnitus, hoarseness, pharyngeal mass, tracheal obstruction, and rupture (▶ Figs. 18.1 and 18.2 ).

Major controversies in decision making addressed in this chapter include:

1. 
   

   Whether or not treatment is indicated.

   
   
2. 
   

   Open versus endovascular treatment for cervical ICA aneurysms.

   
   
3. 
   

   Management of cervical ICA aneurysms causing mass effect.

   
   
4. 
   

   Management of cervical ICA pseudoaneurysms associated with arterial dissection.

Whether to Treat

Whether it is necessary to treat cervical carotid aneurysms is indeed an intriguing question. Because of their rarity, not enough data are available to accurately know the natural history and where the starting points for treatment should be. A review of the available data shows that there may be a difference, at least in 30-day outcomes, between surgically (open vascular and endovascular) treated cervical carotid aneurysms and conservatively managed cervical carotid aneurysms. However, as a result of the heterogeneous nature of the existing data and the diversity of open surgical, endovascular, and conservative treatments that have been reported, it is challenging to arrive at a single clinically reliable treatment method.

Anatomical Considerations

Anatomical considerations are similar to those for occlusive carotid disease. It is imperative to know the location of the common carotid artery bifurcation in relation to the cervical level, particularly with regard to the mandible. Determining its location is important because 65% of common carotid bifurcations occur between C3 and C4. Retrospective surgical and endovascular data show that complications are most commonly reflected in ischemic sequelae and cranial nerve dysfunction.

Exposure of the carotid artery requires identification of critical neurovascular structures. First, the jugular vein is encountered, and its medial and lateral borders are identified. Locating the common facial vein often helps to complete the venous dissection. Medial dissections along the jugular vein to identify the common, external, and internal portions of the carotid artery are critical steps in safe exposure. Identification and control of the superior thyroid artery are necessary to properly ensure vascular control. It is important to identify nerve structures that are likely to be distorted, depending on the location of the aneurysm. The hypoglossal nerve often travels medially to the jugular vein and courses laterally to medially over the cervical ICA. Careful dissection of the hypoglossal nerve at this juncture is crucial, given the likely distortion of the local anatomy. If the nerve is not adequately visualized and is retracted without identification, it may result in palsy. It is also essential to understand the relationship between the spinal accessory nerve and the sternocleidomastoid. The vagus nerve lies deep to the common carotid artery in the carotid sheath and could be injured when the vessels are clamped. With medial retraction in a high exposure of the cervical ICA, the marginal mandibular branch of the facial nerve is at risk. Injury to the pericarotid sympathetic chain has been described as resulting in transient Horner′s syndrome. Also, with high exposure of the ICA, identification of the posterior belly of the digastric muscle is useful, as its sacrifice can improve exposure without clinically significant morbidity.

Pathophysiology/Classification

The pathophysiological classifications of cervical carotid aneurysms in the literature are varied. These aneurysms can be classified morphologically as fusiform, saccular, or pseudoaneurysms (▶ Fig. 18.3 ). They can be further classified by their pathogenic origin as atherosclerotic, traumatic, mycotic, or other/miscellaneous. However, it is notable that many reports identify neither the morphological shape nor the pathophysiological source of cervical carotid aneurysms. In up to 16 to 20% of cases, the pathogenic origin is classified as other/miscellaneous (e.g., iatrogenic, Behçet′s disease, Ehlers–Danlos syndrome, or cryptogenic), or this information is missing.