Surgical outcome of degenerative versus postreconstructive extracranial carotid artery aneurysms
Article Outline
Objectives
Extracranial carotid artery aneurysms (ECAAs) are rare vascular lesions, and large series with short-term and long-term outcomes are seldom reported. This study compared the clinical presentation and conventional treatment outcomes of different ECAA types according to their etiology.
Methods
We retrospectively reviewed the data of 55 consecutive patients (47 men, 8 women) with 61 ECAAs who were treated from January 1986 to December 2007 by conventional surgical techniques. The patients were a mean age of 65 ± 11 years (range, 30-92 years). Thirty-two ECAAs (52.5%) occurred postoperatively after previous carotid endarterectomy, of which 26 patients had 29 degenerative aneurysms (47.5%). Clinical presentation included cerebral stroke in three patients (4.9%) and transient ischemic attack in 26 (42.7%). Mean follow-up was 42.7 ± 22.0 months. Statistical analysis was performed within and between degenerative and post-reconstructive ECAA subgroups of patients.
Results
Open aneurysm resection included 27 extended polytetrafluoroethylene interposition grafts, 12 venous grafts, and 22 closures using synthetic patch. Cumulative 1-year primary patency rates were 86.9% for the degenerative ECAAs and 96% for the postoperative ECAAs, with respective secondary patency rate at 5 years of 80% and 93.3%. The 5-year patency rate was 88.9% for synthetic grafts compared with 66.7% for vein grafts and 86.4% for synthetic patches. These differences were not statistically significant (P > .05). Complications for the degenerative ECAAs included two reconstruction thromboses <30 days, two cerebral strokes, and one myocardial infarction. The patients with postoperative ECAAs experienced one early thrombosis and two strokes postoperatively. Two patients (3.6%) from the degenerative ECAA subgroup died of cardiac decompensation (n = 1) and cerebral ischemic event (n = 1).
Conclusions
Despite the different trends, no significant differences were found between degenerative ECAA and postoperative ECAA patients in clinical presentation, localization, and surgery outcomes. The good middle-term and long-term patency rates of synthetic graft reconstruction justify its use in the treatment of ECAAs, and it is less time consuming and technically demanding compared with vein interposition graft.
Extracranial carotid artery aneurysms (ECAAs) are quite rare lesions that count for <1% of all peripheral aneurysms and <1.5% of all carotid procedures.1 Atherosclerosis is the most common reported etiologic factor for the formation of a true and usually fusiform-shaped ECAA. In contemporary series, nearly 50% of the reported cases were false aneurysms of the ECA that occurred after carotid endarterectomy (CEA) and patching.1 Rare causes of ECAA include arterial dysplasia, dissection, blunt or penetrating trauma, connective tissue disorders, and a previous mycotic infection.1, 2, 3
The goal of the present study was the retrospective analysis of prospectively collected data of 61 ECAAs that were treated by conventional surgical techniques during a 22-year period. A further aim of our investigation was the detection of possible differences in clinical features, treatment options, and outcomes between degenerative (dECAAs) and postoperative anastomotic aneurysms (pECAAs).
Patients and methods
Between January 1986 and December 2007, 9567 carotid procedures were performed in our department for treatment of carotid occlusive disease. Data from these procedures were collected prospectively and were analyzed retrospectively for this study. The following procedures were performed: 5549 eversion CEAs (58%), 2918 CEAs (30.5%) with synthetic patch closure, of which 2099 were with expanded polytetrafluoroethylene (ePTFE) and 604 with Dacron; 602 CEAs (6.3%) with venous patch closure; and 325 CEAs (3.4%) with primary closure. Finally, 172 patients (1.8%) underwent carotid artery stenting as the primary treatment.
During the study period, 55 patients (47 men and 8 women; male/female ratio, 5.8:1) with 61 ECAAs were diagnosed and treated surgically. An anastomotic pseudoaneurysm developed in 29 patients (52.5%) after previous carotid surgery (pECAA) that was performed in our institution. Twenty-six patients had 29 dECAA (47.5%). The mean age of the patients was 65 ± 11 years (range, 30-92 years). Three patients had bilateral dECAAs, and another three had bilateral pECAAs. Table I summarizes the demographics and cardiovascular risk factors of the two subgroups.
Table I. Patient demographics and cardiovascular risk factors
| Variable | pECAA | dECAA | Pa |
|---|---|---|---|
| Demographics | |||
 Age, mean ± SD, y | 65.1± 11.2 | 61.1± 4.2 | .654 |
| Male/female ratio | 5.4:1 | 4.1:2 | .343 |
| Risk factors, No. (%) | |||
| Hypertension | 25(61.0) | 16(39.0) | .432 |
| Dyslipidemia | 10(41.7) | 14(58.3) | .234 |
| Smoking | 12(60.0) | 8(40.0) | .321 |
| Diabetes mellitus | 5(62.5) | 3(37.5) | .345 |
| Coronary artery disease | 12(36.4) | 21(63.6) | .332 |
| PAOD | 17(63.0) | 10(37.0) | .232 |
| Aneurysm in another locationb | 3(33.3) | 7(63.7) | .234 |
aNo significant differences (P > .05) between the two subgroups in terms of demographic features (P < .05 is significant.) |
bPopliteal, aortic, or iliac artery. |
The pECAAs occurred in 43.4% after venous patching (14 patients in 602 procedures), 34.4% after eversion CEA (11 of 5549), and 22.2% after operative treatment of severe carotid stenosis by synthetic patching (7 of 2918). The mean period during which anastomotic pseudoaneurysms developed was 49.5 ± 4.0 months after the previous carotid surgery using vein patching and 34.5 ± 3.1 months after eversion CEA. The mean time period for the development of pECAAs after previous carotid restoration of blood flow by synthetic patching was 39 ± 2.9 months.
The definition of ECAA was based on the maximum vessel diameter using measurements from duplex ultrasound (DUS) imaging and computed tomography (CT) scanning. Patients with vessel dilatation ≥150% of the common carotid artery diameter or ≥200% of the internal carotid artery diameter were diagnosed as having an ECAA.4, 5 In asymptomatic patients or in small ECAAs with a diameter <20 mm, the presence of intraluminal thrombus in the aneurysm sack ensured the diagnosis of ECAA and the need for surgical treatment to avoid cerebral thromboembolism. Mean diameters were 23.9 ±7.2 mm for dECAAs and 22.1 ± 3.7 mm for pECAAs.
Clinical presentation of the ECAAs included cerebral stroke in three patients (5.4%), transient ischemic attack (TIA) in 26 (47.3%), a palpable pulsatile mass of the neck in 18 patients (32.7%), difficulty swallowing in four (6.0%), and aneurysm rupture in two (2.7%). Finally, 21 patients (32.4%) were asymptomatic. Aneurysm morphology was saccular in 27 ECAAs (44.3%) and fusiform shaped in 34 (57.3%). The clinical presentation and diagnosis data of the two ECAA subgroups are compiled in Table II.
Table II. Clinical presentation and diagnostic data of the 61 extracranial carotid artery aneurysms
| Variable | dECCA (n = 29) | pECCA (n = 32) | P |
|---|---|---|---|
| Symptoms, No. (%) | |||
| Asymptomatic | 9(31.1) | 12(37.6) | .232 |
| Transient ischemic attack | 10(34.5) | 16(50) | .122 |
| Stroke | 1(3.4) | 2(6.2) | .223 |
| Pulsatile masse | 9(31.1) | 9(28.1) | .123 |
| Swallowing difficulties | 3(10.3) | 1(3.1) | .234 |
| Rupture | 1(3.4) | 1(3.1) | .234 |
| Other not specific symptoms | 7(24.1) | 9(28.1) | .345 |
| Localization, No. (%) | |||
| Right side | 14(48.3) | 9(28.1) | .321 |
| Left sidea | 15(51.7) | 23(71.9) | .023 |
| Bilateral | 3(10.3) | 3(9.3) | .342 |
| Common carotid | 4(13.8) | 5(15.6) | .223 |
| Internal carotid | 14(48.3) | 12(37.5) | .145 |
| Entire bifurcation (3 vessels) | 11(37.9) | 15(46.9) | .123 |
| Morphology | |||
| Sacculara, No. (%) | 9(31.1) | 18(56.2) | 031 |
| Diameter, mean (SD), mm | 24.9±1.9(7.1) | 22.9±1.7(4.0) | .334 |
| Fusiform, No. (%) | 20(68.9) | 14(43.8) | .113 |
| Diameter, mean (SD), mm | 23.4 ± 1.2(7.3) | 21.1 ± 1.7(3.2) | .234 |
| CVI stage, No. (%) | |||
| Stage I | 18(62.1) | 14(43.8) | .233 |
| Stage II | 8(27.6) | 14(43.8) | .342 |
| Stage III | 2(6.9) | 2(6.2) | .234 |
| Stage IV | 1(3.4) | 2(6.2) | .243 |
aDifferences between two groups were significant in left vs right side localization (P = .023) and saccular vs fusiform morphology (P = .031). |
All patients were treated with conventional techniques under general endotracheal anesthesia. Intraoperative cerebral monitoring included transcranial Doppler imaging, somatosensory evoked potentials (SSEP), and measurement of regional brain tissue oxygen saturation (rSo2) by near-infrared spectroscopy. The simultaneous reduction of rSo2 was <55% in all patients. In 39 ECAA (63.9%) that were fusiform shaped or saccular with large neck, the preferable treatment option was aneurysm resection and the continuation of cerebral flow by interposition graft (PTFE in 27 and venous graft from saphenous vein in 12). In saccular ECAAs with narrow necks, the resection was done using synthetic patch (PTFE in 16; Dacron in 6). In addition, in 23 ECAAs (37.7%; 8 degenerative and 15 post-reconstructive) ligation of the external carotid artery was necessary before restoration of cerebral flow. Nine patients (16.4%) underwent operations with intraluminal shunting, without any perioperative neurologic deficit.
To be more precise with the preoperative clinical manifestation of the aneurysms, we classified the cerebrovascular insufficiency in following stages:
Microbiologic culture analysis did not reveal a specific microorganism in any of the exampled specimens nor in the two aneurysms that ruptured. However, the macroscopic appearance and histologic analysis showed significant data. Specimens from atherosclerotic aneurysms had typical evidence of atherosclerosis, with intimal and medial degeneration/disruption. Specimens from post-reconstructive aneurysms had evidence related to the primary carotid procedure and the ECAAs morphology. No evidence of fibromuscular dysplasia was detected.
Mean follow-up was 42.7 ± 22.0 months and included DUS scans at 1, 3, 6, and 12 months, and yearly thereafter, as well as an independent postoperative neurologic examination before the patient was discharged and in any cerebral event that was diagnosed during the entire follow-up period.
Statistical analysis was performed within groups and between atherosclerotic and post-reconstructive ECAA patients, using SPSS software (SPSS Inc, Chicago, Ill). Continuous data were compared using the t test and categoric variables with the Fisher exact test, as appropriate. The 1- and 5-year primary and secondary patency rates for patients of the two groups with immediate (30-day) successful outcomes were estimated using Kaplan-Meier life-table analysis. The same analysis was used to compare the early- and long-term primary patency rates between the three different types of ECAA reconstruction techniques (PTFE graft vs venous graft vs synthetic patch)
Results
Morbidity
Three patients presented with permanent cerebral stroke, two from the dECAA subgroup due to early thrombosis of the reconstruction (1 vein graft; 1 synthetic patch) and one patient due to intraoperative cerebral thromboembolism. One patient sustained a myocardial infarction on postoperative day 5, and another patient died because of fatal cardiac decompensation.
For the pECAA subgroup, cerebral stroke was noted in two of 29 patients due to early reconstruction thrombosis in one patient (vein graft) and because of clamping intolerance in the other, having no evidence of a thromboembolism event based on the angiography postoperatively and significant changes in the intraoperative neuromonitoring. In addition, one patient experienced an episode of prolonged reversible ischemic neurologic deficit with contralateral arm paresis.
In 61operations, cranial nerve injuries resulting in paresis of recurrent laryngeal nerve occurred in six patients (transient in 3), and three patients had a transient paresis of the hypoglossal nerve. Cranial nerve deficits, such as hoarseness, dysphagia, and Horner syndrome, were present in six patients. Respiratory complications included pneumonia in one patient in both groups.
Mortality
Two patients from the dECAA group died, one each of cardiac decompensation and because of stroke after early thrombosis and revision surgery. The overall mortality for the 55 patients with 61 ECAA open reconstructions was 3.6%.
Patency
The 1-year primary patency rates were 86.9% for dECAA patients and 92.8% for pECAA patients, and the respective secondary patency rates were 95.6% and 100%. The 5-year primary patency rates were 80% for the dECAA group and 93.3% for the pECAA group, and the respective secondary patency rates were 93.3% and 100%. Fig 1 shows the 5-year primary patency rates according to whether the ECAAs were postoperative or degenerative.
Fig 1.
Cumulative primary patency rates at 5-years for degenerative (dECAA, broken line) and postoperative (pECAA, solid line) extracranial carotid aneurysms.
The patency rates of the different types of reconstruction (vein graft, synthetic graft, and synthetic patch) during a 5-year period are shown in Fig 2. The early (<30-day) patency rates were 96.3% for synthetic grafts, 83.3% for vein grafts, and 95.5% for and synthetic patching. A sustained good patency rate of 88.9% for the synthetic grafts was recorded over a period of 1 and 5 years. On the other hand, the patency rate for synthetic patching was slightly inferior, at 90.9% and 86.4%, and for the vein grafts, 66.7%. These differences were not statistically significant (P > .05).
Fig 2.
Cumulative primary patency rates of the three techniques of reconstructions—synthetic patch (solid line), polytetrafluoroethylene (PTFE) graft (small broken line), and venous graft (large broken line)—during a 5-year period.
Fusiform-shaped aneurysms were more frequent in venous patch and eversion CEA cases, and saccular ECAAs were usually located in the medial or lateral suture line of a synthetic patch or of an eversion CEA closure. Fusiform-shaped aneurysms had histologic evidence of intimal fibrosis and sclerosis, disruption of elastic and muscular fibers, and wall dissection. Examination of saccular ECAAs revealed chronic inflammatory response due to foreign body reaction with foam cells and histiocytosis. Finally, in venous patch cases, the main evidence was sclerosis and degeneration of the venous wall.
Statistical analysis did not reveal any significant difference between dECAA and pECAA patients for the etiology and size, the clinical presentation, and cerebrovascular insufficiency stage status, or in the immediate, 1-year, and 5-year outcomes. The difference between two groups was significant only in morphology. The incidence of saccular ECAAs (56.2%) was higher in the pECAA group and fusiform shaped (68.9%) in the dECAA group. In addition, a within-group analysis showed a difference between post-reconstructive patients in localization in favor of the left side (Table II, P = .023) and in the type of primary operation (venous patch vs other types, P = .05, Table II).
Discussion
ECAAs are rare vascular lesions that account for approximately 1% of all carotid operations performed at major vascular centers.1 Primary ECAA are classified as either fusiform or saccular. Fusiform lesions are usually degenerative, have a bilateral predilection, and occur at the carotid bifurcation. The saccular type is usually unilateral and mostly located in the middle segment of the internal carotid artery.
Atherosclerosis remains the main cause of all ECAAs. Numerous reports have published different causes for the development of true ECAAs, such as infection, inflammation, fibromuscular dysplasia, cystic necrosis of media, Behçet-Adamantiades disease, protein C and S and antithrombin III deficiency, and idiopathic medial arteriopathy.2, 3, 4 Radak et al5 reported that tuberculous lymphadenitis of the neck was underlying cause for ruptured ECAA.
Four groups of false aneurysms have been reported: traumatic, anastomotic developing after previous carotid surgery, iatrogenic, and dissecting.5 False traumatic ECAAs are caused by blunt trauma of the neck.6 Possible explanations for this may be extreme hypertension, twisting of the neck, and mandibular fractures.7 Anastomotic pseudoaneurysms are thought to be more common after CEA with patching than after CEA alone.5 Iatrogenic carotid pseudoaneurysms occur after various surgical procedures in the neck. Dissecting ECAAs are rare and are caused by spontaneous carotid dissection.5
The present study reports one of the largest series in the literature of surgery of ECAA, with equal number of patients with dECAAs (47.5%) and pECAAs (52.5%). We have reviewed in Table III1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16 the largest series during the last 15 years that present complete data of the number of the treated aneurysms, the length of follow-up, and the immediate adverse events and death rat.
Table III. Review of the largest series regarding a surgical approach to repair of aneurysmal disease of the extracranial carotid artery
| First author | Year | Aneurysms, No. | Patients, No. | Length of follow-up | Immediate adverse eventsarate, No. (%) | Immediate death rate, No. (%) |
|---|---|---|---|---|---|---|
| Moreau8 | 1994 | 38 | 35 | 6-30y | 10(29) | 1(2.9) |
| Schievink9 | 1994 | 22 | 22 | 6.2y | 2(9) | 0 |
| Liapis10 | 1994 | 12 | 12 | 5.5 y | 1(8) | 0 |
| Faggioli11 | 1996 | 24 | 20 | 8y | 1(4.5) | 0 |
| Pulli12 | 1997 | 21 | 21 | 2y | 1(4.7) | 0 |
| Zhang13 | 1999 | 66 | 63 | NA | 4(6) | 1(1.6) |
| Rosset3 | 2000 | 25 | 25 | 5.5y | 14(56) | 0 |
| El-Sabrout2 | 2000 | 65 | NA | 5.9y | 10(15.4) | 4(6.1) |
| Alberti14 | 2002 | 19 | 17 | 1980-2000 | 7(63.4) | 0 |
| Davidovic15 | 2004 | 17 | 16 | 5.3y | 3(17.6) | 1(5.9) |
| Bakoyannis16 | 2006 | 10 | 9 | 6mon-10y | 0 | 0 |
| Radak5 | 2007 | 91 | 76 | 5.3y | 5(5.5) | 2(2.2) |
| This study | 2008 | 64 | 58 | 5y | 5(7.8) | 2(3.4) |
aEarly postoperative myocardial infarction and stroke. |
The subgroup analysis of the pECAAs and dECAAs showed an apparent predominance of the pECAAs in the clinical manifestation with a neurologic event (43.8% vs 27.6%, P > .05). Almost 72% of pECAAs vs 51.7% of dECAAs occurred at the left side. One possible explanation may be the greater length of the left internal carotid artery and its predisposition to kinking and torsion with subintimal tearing requiring extensive and technically more demanding arteriotomy.7 Further investigation in this issue is necessary. One other difference between the two subgroups was the morphology of the aneurysms: 64.6% of the dECCAs were fusiform compared with the pECAAs, which had 50% fusiform and 46.8% saccular.
The most common first manifestation of the ECAA is a TIA, which occurred in approximately 60% of the patients. In our series, the aneurysms had a varied clinical presentation. The pulsatile neck mass caused difficulty in swallowing in 14 patients (25.4%). Neurologic manifestations were noted in 29 of 55 patients (52.7%) in the form of TIA (n = 26) or hemispheric brain ischemia (n = 3) and were the leading symptom.
Surgical treatment aims to eliminate the aneurysm and restore arterial continuity. In small, elongated ECAAs, resection and direct end-to-end anastomosis is feasible. Other possible techniques with satisfactory results are replacement or interposition by a vein graft or the use of synthetics grafts. Bakoyannis et al16 recommend an extended cervical incision to approach large and high-lying aneurysms above the Blaisdell line (an imaginary line connecting the mastoid to the angle of the mandible) and even construction of a distal anastomosis into the carotid foramen. For longer distances, other approaches, such as cervical-petrous, posterior-lateral, and anterior-lateral are more suitable.
Synthetic (ePTFE or Dacron) graft or patch was used to treat 63.9% of the patients in our series. Saphenous vein interposition was used in 12 of 61. In contrast with the recommendation of many authors that synthetic graft remain the second choice if appropriate saphenous vein is unavailable, we recorded a primary patency rate of 88.9% during a 5-year period. The sustained good patency rate of the PTFE reconstructions should ensure the use of synthetic material as the first choice for the reconstruction owing to less time duration and challenge compared with the vein interposition graft.
Whereas a long vein graft in the extremities accommodates to this additional length by assuming a gentle curve in the thigh, a short vein graft as in the case of carotid procedures instead tends to kink within the tight confines of the neck. It tends to elongate as well as dilate once flow has been restored. Therefore, a carotid interposition vein graft must be trimmed precisely to its estimated postperfusion length before the final anastomosis is completed. This may explain the apparent inferior patency rate of the vein interposition grafts in our series, especially as Fig 2 suggests the occlusions of these grafts during the early postoperative period. Another reason may be the smaller number of patients who were treated by this type of reconstruction.
Whether to use an intraluminal shunt during the aneurysm repair remains controversial. Difficulties in its placement into the artery and its use can lead to distal embolization and cerebral events. We performed continuous neurophysiologic monitoring by measuring the short latency SSEP, rSo2 by near-infrared spectroscopy, and transcranial DUS during the operation. The simultaneous reduction of rSo2 <55% and great changes in SSEP amplitude, or history of ipsilateral stroke or contralateral occlusive lesions were absolute indications to use an intraluminal shunt.
The literature provides for the moment scant information concerning endovascular techniques in the treatment of ECAAs. Bergeron et al17 reported that covered stents and endografts offer a new therapeutic option for ECAAs, excluding nerve injury from procedural complications.4 They treated five ECAAs endovascularly, and no in-hospital complications or adverse events were observed during a follow-up period of 3.6 ± 1.3 years. The stents were patent without evidence of in-stent stenosis. Severe complications have also been reported, however, such as recoil or deforming of the prosthesis.18 It is important to mention that first-generation stent grafts were used, which tended to have device-related complications.
Conclusion
ECAAs produce a high incidence of severe neurologic deficits. This condition justifies an aggressive surgical approach to restore the arterial continuity. The primary rate of cumulative major adverse cardiovascular events, including stroke, myocardial infarction, and death, of the entire series was 9.3%. Nevertheless, the operative treatment of these lesions is technically demanding and strongly related to a high risk of cranial nerve injuries and neurologic events. Reliable alternatives are needed to simplify the challenging surgical approach, such as the use of synthetic grafts as first line reconstruction type.
Author contributions
References
- . Aneurysms of the extracranial carotid artery (Twenty-one years' experience). Am J Surg. 1979;137:196–200
- . Extracranial carotid artery aneurysms: Texas Heart Institute experience. J Vasc Surg. 2000;31:702–712
- . Surgical treatment of extracranial internal carotid artery aneurysms. J Vasc Surg. 2000;31:713–723
- . Extracranial carotid artery aneurysms. Eur J Vasc Surg. 1989;3:557–562
- . Carotid artery aneurysms: Serbian Multicentric Study. Ann Vasc Surg. 2007;21:23–29
- . Selective management of extracranial cervical carotid aneurysms. Am J Surg. 1991;146:85–91
- . Surgical aspects of fusiform and saccular extracranial carotid artery aneurysms. Cardiovasc Surg. 1997;5:190–195
- . Surgical treatment of extracranial internal carotid aneurysm. Ann Vasc Surg. 1994;8:409–416
- . Surgical treatment of extracranial internal carotid artery dissecting aneurysms. Neurosurgery. 1994;35:809–815
- . Surgical treatment of extracranial carotid artery aneurysms. Int Angiol. 1994;13:290–295
- . Extracranial internal carotid artery aneurysms: results of a surgical series with long-term follow-up. J Vasc Surg. 1996;23:587–594
- . Extracranial carotid artery aneurysms. J Cardiovasc Surg (Torino). 1997;38:339–346
- . Management of extracranial internal carotid artery aneurysms: 17 years' experience. Eur J Vasc Endovasc Surg. 1999;18:162–165
- . Surgical treatment of extracranial carotid aneurysms. Chir Ital. 2002;54:31–36
- Carotid artery aneurysms. Vascular. 2004;12:166–170
- Surgical management of extracranial internal carotid aneurysms by cervical approach. ANZ J Surg. 2006;76:612–617
- . Long-term results of endovascular exclusion of extracranial internal carotid aneurysms and dissecting aneurysm. J Interven Cardiol. 2004;17:245–252
- Carotid artery aneurysm: evolution of management over two decades. J Vasc Surg. 2006;43:493–497
Competition of interest: none.
PII: S0741-5214(08)01334-7
doi:10.1016/j.jvs.2008.08.006
© 2009 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
