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Carotid Artery Aneurysms: Serbian Multicentric Study
Carotid Artery Aneurysms: Serbian Multicentric Study äorCe Radak, MD, PhD,1 Lazar Davidovic , MD, PhD,2 Vladimir Vukobratov, MD, PhD,3 Nenad Ilijevski, MD, PhD,1 Dusan Kostic , MD, PhD,2 Zivan Maksimovic , MD, PhD,1 1 Goran Vuc urevic , MD, PhD, Slobodan Cvetkovic, MD, MrSc,2 and Svetolik Avramov, MD, PhD,3 Belgrade and Novi Sad, Serbia
This multicentric Serbian study presents the treatment of 91 extracranial carotid artery aneurysms in 76 patients (13 had bilateral lesions). There were 61 (80.3%) male and 15 (19.7%) female patients, with an average age of 61.4 years. The aneurysms were caused by atherosclerosis in 73 cases (80.2%), trauma in six (6.6%), previous carotid surgery in six (6.6%), tuberculosis in one (1.1%), and fibromuscular dysplasia in five (5.5%). The majority (61 cases or 67%) of the aneurysms involved the internal carotid artery, 29 (31.9%) the common carotid artery bifurcation, and one (1.1%) the external carotid artery. Forty-five (49.4%) aneurysms were fusiform, while 46 (50.6%) were saccular. Twenty-nine (31.9%) cases were totally asymptomatic at the time of diagnosis. The remainder presented with compression in 14 (15.4%) cases, stroke in 11 (12.1%) cases, transient ischemic attack in 33 (36.3%) cases, and rupture in four (4.4%) cases. In cases where the aneurysm involved the internal carotid artery, four surgical procedures were performed: aneurysmectomy with end-to-end anastomosis in 30 (33.0%) cases, aneurysmectomy with vein graft interposition in 20 (22.0%) cases, aneurysmectomy with anastomosis between external and internal carotid artery in eight (8.8%) cases, and aneurysmectomy followed by arterial ligature in three cases. One case of external carotid artery aneurysm also was treated by aneurysmectomy and ligature. Aneurysm replacement with Dacron graft was performed in 29 (31.9%) cases where common carotid artery bifurcation was involved. Two (2.2%) patients died after the operation due to a stroke. They had ruptured internal carotid artery aneurysm treated by aneurysmectomy and ligature. Including these, a total of five (5.5%) postoperative strokes occurred. In two (2.2%) cases, transient cranial nerve injuries were found. Excluding the five patients who were lost to follow-up, 69 other surviving patients were followed from 2 months to 12 years (mean 5 years and 3 months). In this period, there were no new neurological events and all reconstructed arteries were patent. Three patients died more than 5 years after the operation, due to myocardial infarction. Aneurysms of the extracranial carotid arteries are rare vascular lesions that produce a high incidence of unfavorable neurological sequelae. Because of their varied etiology, location, and extension, different vascular procedures have to be used during repair of extracranial carotid artery aneurysms. In all of these procedures, an aneurysmectomy with arterial reconstruction is necessary.
INTRODUCTION Extracranial carotid artery aneurysm (ECAA) is a very rare vascular lesion compared to occlusive disease.1-8 According to data from the largest series 1 Vascular Surgery Clinic, Dedinje Cardiovascular Institute, Belgrade, Serbia. 2 Vascular Surgery Clinic, Institute for Cardiovascular Diseases, Clinical Center of Serbia, Belgrade, Serbia. 3
Vascular and Transplant Surgery Clinic, Clinical Center, Novi Sad, Serbia.
published, their incidence ranges 0.27e0.6%.2-6 They are uncommon compared to aneurysms involving other peripheral arteries, particularly the abdominal aorta.1-8 Until 2000, about 2,600 ECAAs
Correspondence to: äorCe Radak, MD, PhD, Vascular Surgery Clinic, Dedinje Cardiovascular Institute, nh M. Tepic a 1, 11 000 Belgrade, Serbia, E-mail: [email protected] Ann Vasc Surg 2007; 21: 23-29 DOI: 10.1016/j.avsg.2006.10.004 Ó Annals of Vascular Surgery Inc. Published online: January 12, 2007
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24 Radak et al.
have been reported.1 Although rare, ECAAs have significant medical and surgical importance. Major neurological symptoms after embolization or thrombosis from the ECAA are relatively common.1-10 The stroke rate in such patients ranges 50-70%.8-11 In order to contribute to management guidelines, we present the clinical findings, surgical treatment, and results of 91 ECAAs.
PATIENTS AND METHODS During a 12-year period (1992-2004), 861 patients with occlusive disease of the extracranial carotid arteries were surgically treated in our three institutions. During the same period, we treated 74 (0.94%) patients with 91 ECAAs (13 had bilateral lesions). Their mean age was 61.4 years (range 2187), and the male to female ratio was 61 (80.3%):15 (19.7%). The causes of the ECAA were divided among atherosclerosis in 73 cases (80.2%), trauma in six (6.6%), previous carotid endarterectomy with DacronÒ (DuPont, Wilmington, DE) patch in six (6.6%), tuberculosis in one (1.1%), and fibromuscular dysplasia in five (5.5%). Four false traumatic ECAAs developed after penetrating and two after blunt neck trauma. One of them developed in a patient who played water polo a few days before admission. During the course of the game, the head of our patient was twisted backward and to the right by the opponent player, after which he was hit by a ball in the left side of the neck. In our patient, a combination of two mechanisms took place. Accidental hyperextension of the neck exposed the common carotid artery to a subsequent sudden forceful compression against the transverse processus of the sixth cervical vertebra caused by the ball hit. One false traumatic aneurysm involved the external, two the common, and three the internal carotid artery (Fig. 1). In 61 (67.0%) cases, the aneurysms involved the internal carotid artery, 29 (31.9%) the common carotid artery bifurcation, and one (1.1%) the external carotid artery. Forty-five (49.4%) aneurysms were fusiform, while 46 (50.6%) were saccular. Twenty-nine (31.9%) cases were totally asymptomatic at the time ECAA was diagnosed. The remainder presented with compression in 14 (15.4%) cases, stroke in 11 (12.1%) cases, transient ischemic attack in 33 (36.3%) cases, and rupture in four (4.4%) cases. The diagnosis was established using duplex ultrasonography and angiography in all, while computed tomographic scan was performed in four cases (Table I).
Annals of Vascular Surgery
All our patients were treated surgically. Surgical treatment varied and was largely determined by several factors that included anatomic extent of the aneurysm, etiology, and the presence or absence of infection. The selection of various operative methods was influenced by the anatomic location of the aneurysm. Aneurysmectomy followed by replacement with Dacron graft was performed in 29 (31.9%) cases where common carotid artery bifurcation was involved. Out of them, in 23 cases a direct reimplantation of the external carotid artery into the Dacron graft was performed (Fig. 2A). In the other six cases, a new Dacron graft was used for the reconstruction of the external carotid artery by the ‘‘side arm technique’’ (Fig. 2B). In cases where the aneurysm involved the internal carotid artery, four surgical procedures were performed. Aneurysmectomy with end-to-end anastomosis was performed in 30 (33.0%) cases (Fig. 3). Aneurysmectomy with vein graft interposition was performed in 20 (22.0%) cases. Aneurysmectomy with anastomosis between the proximal external and distal internal carotid artery was performed in eight (8.8%) cases. Aneurysmectomy followed by arterial ligature was performed in three cases with ruptured, very highly localized internal carotid artery aneurysm where reconstruction was not possible. One of them had an infected internal carotid artery aneurysm. One case of false traumatic external carotid artery aneurysm also was treated by aneurysmectomy and ligature. Aneurysmectomy and arterial ligature was performed in a total of four (4.4%) cases. All reconstructive procedures were performed without insertion of an intraluminal shunt (Table II).
RESULTS Two (2.2%) patients died after the operation due to a stroke. They were patients with ruptured internal carotid artery aneurysm treated by aneurysmectomy and ligature. Including these, a total of five (5.5%) postoperative strokes occurred. One nonlethal stroke followed ligature of the internal carotid artery, while two followed aneurysmectomy of the carotid bifurcation and Dacron graft interposition. In two (2.2%) cases, transient cranial nerve (one facial and one hypoglossal) injuries were found. These patients made good progress postoperatively, and both hypoglossal and facial paresis regressed 4 months after surgery. Excluding the five patients who were lost to follow-up, 69 other surviving patients were followed from 2 months to 12 years
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Carotid artery aneurysms 25
Fig. 1. Common carotid artery saccular aneurysm caused by blunt neck injury a few years ago. A Asymptomatic pulsatile neck mass. B Angiography.
Table I. Clinical manifestations of extracranial carotid artery aneurysms Symptoms
n (%)
Asymptomatic neck mass Rupture Compression of cranial nerves Transient ischemic attacks Stroke Total
29 4 14 33 11 91
(31.9) (4.4) (15.4) (36.3) (12.1) (100.0)
(mean 5 years and 3 months). In this period, there were no new neurological events and all reconstructed arteries were patent. Three patients died more than 5 years after the operation due to myocardial infarction.
DISCUSSION Atherosclerosis causes over 75% of all ECAAs, as reported in published series.1-15 Seventy-three (80.2%) ECAAs in our series were atherosclerotic in origin. Other true ECAAs are caused by infection,12,13,16-25 inflammation,26,27 fibromuscular dysplasia,28,29 cystic necrosis of media,30,31 Behc¸et’s disease,32,33 protein C and S and antithrombin III deficiency, and idiopathic medial arteriopathy.34 We had one case of ruptured ECAA caused by tuberculous lymphadenitis of the neck. Very rare congenital ECAAs similar to intracranial carotid artery aneurysms have also been reported.4,12,35-39
Four groups of false ECAAs have been reported: traumatic, anastomotic, iatrogenic, and dissecting. False traumatic ECAAs are most frequently caused by blunt trauma of the neck.12,14,40-45 The precise mechanism by which blunt arterial injury produces ECAA is unclear. Extreme hyperextension,12,14,42,43 twisting of the neck,14,46 and compression against the internal carotid artery at the level of the first and second cervical vertebrae14,46 might be reasonable explanations for this. Another factor implicated in this condition is the association of mandibular fractures and ECAA.45 Anastomotic pseudoaneurysm is found as an early or late complication after carotid endarterectomy.1,3,6,12,13,15,47 We had six such cases after carotid endarterectomy and Dacron patch angioplasty. Data in the literature indicate that anastomotic pseudoaneurysm is found four times more frequently after endarterectomy with patching compared to endarterectomy alone.1,3,6,13,15,47 Although the overall incidence is low, significant morbidity is associated with such pseudoaneurysms, due to cerebral embolization. Iatrogenic carotid pseudoaneurysm occurs after various surgical procedures in the neck.48 Dissecting ECAAs, caused by spontaneous isolated carotid artery dissection, are rare.49-53 Major neurological events are the most common clinical manifestation of ECAA, occurring in more than 40% of patients.1-10,12-15,50,51,54-56 ECAAs produce either transient ischemic attacks (36.3% of our cases) or stroke (12.1% of our cases). According to Knight et al.,6 17% of ECAAs presented with compression of the cranial or cervical nerves. We had 15.4% such cases. Most frequently, ECAAs
26 Radak et al.
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Fig. 2. A After aneurysmectomy, interposition of the Dacron graft between the common and internal carotid arteries with direct reimplantation of the external carotid artery into the Dacron graft was performed. B Reconstruction of the external carotid artery with Dacron graft (side arm technique).
Fig. 3. A Giant saccular aneurysm of the elongated internal carotid artery. B End-to-end anastomosis of the internal carotid artery was performed after aneurysmectomy.
compress the hypoglossal nerve.7,57 In 1994, Shimohata et al.57 described ECAA compression on both the hypoglossal and vagus nerves, which produced the so-called Tapia syndrome. Compression on glossopharyngeal and facial nerves, as well as on the stellate ganglion, has been reported.1,7,58,59 Dysphagia secondary to the bulking of the lesion or compression of the pharyngeal nerve has been described as a symptom of ECAA.1,59 ECAA rupture is a rare condition associated with high morbidity and mortality,7,58,60 due to extensive hemorrhage. We had four such cases. Some of the ruptured ECAAs presented with unusual hemorrhage to the pharynx, ear, and nose.61-69
In 1808, Sir Astley Cooper70 successfully performed a ligature of the internal carotid artery aneurysm. His patient lived without any neurological deficit for 13 years. According to reports that followed, this procedure carried very high mortality and morbidity rates.1-10,12,71,72 Ligature of the internal carotid artery was performed in three of our cases. In all of them, postoperative stroke occurred, and two patients died. Nowadays, a ligature of the internal carotid artery is indicated only in cases with aneurysm extending to the base of the skull and as an emergency procedure for massive, uncontrolled hemorrhage due to aneurysmal rupture.2,7,72 Since Cooper’s time numerous nonreconstructive
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Carotid artery aneurysms 27
Table II. Treatment of extracranial carotid artery aneurysms Type of treatment
n (%) a
Aneurysmectomy with Dacron graft Aneurysmectomy with end-to-end anastomosis b Aneurysmectomy with vein graft b Aneurysmectomy utilizing anastomosis between the external and the distal internal carotid artery b Aneurysmectomy with arterial ligature c Total
29 (31.9) 30 (33.0) 20 (22.0) 8 (8.8)
4 (4.4) 91 (100.00)
a The aneurysm involved bifurcation of the common carotid artery. b The aneurysm involved the internal carotid artery. c Three aneurysms involved the internal and one the external carotid artery.
our study, the early mortality rate (the first 30 postoperative days) was 2.2%. The most common complications after ECAA surgery are postoperative stroke and cranial nerve injuries. Five (5.5%) of our cases had a postoperative stroke. Knight et al.6 reported 6% of cases with postoperative reversible ischemic neurological deficit as well as 6% of cases with a postoperative stroke. Moreau et al.4 reported 5% of patients with postoperative stroke following surgery of ECAA, while Painter et al.2 found 8.2% such patients. Agrifoglio et al.78 described injuries of the superior laryngeal, facial, hypoglossal, glossopharyngeal, and vagal nerves after ECAA surgery. We had two (2.2%) cases with transient cranial nerve injuries.
CONCLUSION techniques have been employed in the management of ECAA. Because of the high incidence of neurological sequelae subsequent to such techniques, they have been largely abandoned in favor of reconstructive procedures, aimed at restoration of arterial flow.1-10,12-14 Surgical treatment of ECAA varied and was influenced by several factors that included size of the aneurysm, adequacy of cerebral blood flow, presence or absence of infection, and surgeon’s experience. Aneurysmectomy with arterial reconstruction is the treatment of choice. Direct end-to-end anastomosis (33.0% of our cases) can be performed if the aneurysm is saccular and the vessels elongated and tortuous.1-10,12,56,57 Whenever end-to-end anastomosis is difficult to perform, two alternative procedures are available: vein graft interposition1-25 (performed in 22.0% of our cases) and internal carotid artery reimplantation into the external or the common carotid artery2,9,57 (performed in 8.8% of our cases). Synthetic graft interposition is indicated when the bifurcation of the common carotid artery is involved1-10,13,15 (performed in 31.9% of our cases). Although ECAA repair is a much more demanding procedure than carotid endarterectomy, it is most frequently performed without intraluminal shunt. Endovascular procedures have also been described for treatment of ECAA.1,72-77 They are indicated for false traumatic aneurysms of the internal carotid artery localized high in the neck, at the base of the skull. Although surgical treatment of ECAA is more difficult compared to carotid endarterectomy, it is followed by a similar postoperative complication rate.9,26,74 After surgically treated ECAA, Painter et al.2 described an early mortality rate of 1.6%, Knight et al.6 3%, and McCollum et al.3 7%. In
Aneurysms of the extracranial carotid arteries are rare vascular lesions that produce a high incidence of unfavorable neurological events. Because of the various etiologies, locations, and extensions, different vascular procedures have to be used during repair of ECAA. In all of them, an aneurysmectomy with arterial reconstruction is necessary. REFERENCES 1. Goldstone J. Aneurysms of the external carotid artery. In: Rutherford RB, ed. Vascular Surgery, 5th ed. Philadelphia: W.B. Saunders, 2000, pp 1843-1853. 2. Painter TA, Hertzer N, Beven EG, O’Hara PJ. The significance of elongation and angulation of the carotid artery: a negative view. Surgery 1975;77:45-53. 3. McCollum CH, Wheeler WG, Noon GP, DeBakey ME. Aneurysms of the extracranial carotid artery: twenty-one years’ experience. Am J Surg 1979;137:196-200. 4. Moreau P, Albat B, Thevenet A. Surgical treatment of extracranial internal carotid aneurysm. Ann Vasc Surg 1994;8: 404-416. 5. Bower TC, Pairolero PC, Hallet JW, Jr. Brachiocephalic aneurysm: the case for early recognition and repair. Ann Vasc Surg 1991;5:125-132. 6. Knight GC, Hallman GL, Reuls GJ, et al. Surgical management of the extracranial carotid artery aneurysms. Tex Heart Inst J 1988;15:91-97. 7. Davidovic L, Kostic D, Maksimovic Z, et al. Carotid artery aneurysms. Vascular 2004;12:166-170. 8. Zwolak RM, Whitehouse WM, Knake JL. Atherosclerotic extracranial carotid artery aneurysms. J Vasc Surg 1984;1:415-422. 9. Mishaly D, Pasik S, Barzilai N, Mashiah A. Repair of internal carotid aneurysm under local anesthesia. J Cardiovasc Surg 1992;33:380-382. 10. Dehn TCB, Taylor GW. Extracranial carotid artery aneurysms. Ann R Coll Surg Engl 1984;66:247-250. 11. Winslow E. Extracranial aneurysm of the internal carotid artery. Arch Surg 1926;13:689. 12. Shipley AM, Winslow N, Walter WW. Aneurysms of the cervical portions of the internal carotid artery: an analytical
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36. Hazarika P, Sahota JS, Nayak DR, George S. Congenital internal carotid artery aneurysm. Int J Pediatr Otorhinolaryngol 1993;28:63-68. 37. Wagdi P, Aeschbacher B. Cerebrovascular symptoms in a patient with an aneurysm of the internal carotid artery, aneurysms of the interatrial septum, patent foramen ovale and redundant eustachian valve. Schweiz Med Wochenschr 1993;123:1448-1452. 38. Swany NK, Pope FM, Coakham HB. Giant aneurysm of internal carotid artery in a four year-old child: a case report. Neurology 1993;40:138-141. 39. Hammon JV, Silver D, Young WG. Congenital aneurysms of the extracranial carotid arteries. Ann Surg 1972;176:777-781. 40. Hebra A, Robinson JG, Elliott BM. Traumatic aneurysm associated with fibrointimal proliferation of the common carotid artery following blunt trauma. J Trauma 1993;34: 297-299. 41. Robinson NA, Floote CT. Traumatic aneurysms of the carotid arteries. Am Surg 1974;40:121-124. 42. Stonebridge PA, Carlson AL, Jenkins AM. Traumatic aneurysm of the extracranial internal carotid artery due to hyperextension of the neck. Eur J Vasc Surg 1990;4: 423-425. 43. Sharma S, Rajani M, Mishla N, et al. Extracranial carotid artery aneurysms following accidental injury: ten years experience. Clin Radiol 1991;43:162-165. 44. Sato M, Yamaguchi K, Tadaki T, et al. Traumatic carotid cavernous aneurysms after removal of cancer of the upper jaw. No Shinkei Geka 1995;23:515-519. 45. Tussanasunthornwong S, Ratanalert S. Direct approach to a traumatic intracavernous internal carotid artery aneurysm. J Med Assoc Thai 1995;78:157-163. 46. Sundt TM, Jr, Pearson BW, Piepgras DG. Surgical management of aneurysms of the distal extracranial internal carotid artery. J Neurosurg 1986;64:169-182. 47. Ehrenfeld WK, Hays RJ. False aneurysm after carotid endarterectomy. Arch Surg 1972;104:288-291. 48. Korovesis P, Michalopoulos B, Vassilakos P. Delayed recognition of a vascular complication, carotid artery aneurysms, 60 years after operation for muscular torticolis. Clin Orthop 1992;275:258-262. 49. Jentzer A. Dissecting aneurysm of the left internal carotid artery. Angiology 1954;5:232-234. 50. Miyamoto S, Kikuchi H, Karasawa J, Kuriyama Y. Surgical treatment for spontaneous carotid dissection with impending stroke. J Neurosurg 1984;61:382-386. 51. Bogousslovsky J, Despland PA, Regli F. Spontaneous carotid dissection with acute stroke. Arch Neurol 1987;44: 137-140. 52. Early TFM, Gregory RT, Wheeler JR, et al. Spontaneous carotid dissection: Duplex scanning in diagnosis and management. J Vasc Surg 1991;14:391-397. 53. Petro GR, Winter GA, Cacayorin ED, et al. Spontaneous dissection of the cervical internal carotid artery: correlation of arteriography, CT, and pathology. Am J Roentgenol 1987;148:393-398. 54. Spencer FC. Aneurysm of the common carotid artery treated by excision and primary anastomosis. Ann Surg 1957;154: 254-257. 55. Ito M, Nitta T, Sato K, Ishii S. Cervical carotid aneurysm presenting as transient ischemic attack and recurrent nerve palsy. Surg Neurol 1986;25:346-350. 56. Rhodes EL, Stanley JC, Hoffman GL, et al. Aneurysms of extracranial carotid arteries. Arch Surg 1976;11:339-343.
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57. Shimohata T, Nakano R, Sato S, Tsuji S. A patient with aneurysm of extracranial internal carotid artery presenting lower cranial palsy neuropathy similar to Tapia’s syndrome. Rinsho Shinkeigaku 1994;34:707-711. 58. Rittenhouse EA, Radke HM, Summer DS. Carotid artery aneurysm: review of the literature and report of case with rupture into the oropharynx. Arch Surg 1972;105:786-789. 59. Row JG, Hosni AA. A common carotid artery aneurysm causing severe dysphagia. J Laryngol Otol 1994;108:67-68. 60. Harrison DE. Two cases of bleeding from the ear from carotid aneurysm. Guy’s Hosp Rep 1954;103:207-212. 61. Teitelbaum GP, Halbach VV, Larsen DW, et al. Treatment of massive posterior epistaxis by detachable coil embolization of a cavernous internal carotid artery aneurysm. Neuroradiology 1995;37:334-336. 62. Shike T, Hishino H, Takagi M, et al. Bacterial intracavernous carotid aneurysm presented as massive epistaxis. Rinsho Shinkeigaku 1995;35:531-536. 63. Constanatino PD, Russell E, Reisch D, et al. Ruptured petrous carotid aneurysm presenting with otorrhagia and epistaxis. Am J Otol 1991;12:378-383. 64. Romaniuk CS, Bartlett RJ, Kavanaghi G, Salam MA. An unusual cause of epistaxis: non-traumatic intracavernous carotid aneurysm. Br J Radiol 1993;66:942-945. 65. Saim L, Rejale E, Hamaz M, et al. Massive epistaxis from traumatic aneurysm of the internal carotid artery. Aust Surg 1993;63:906-910. 66. Pritz MB. Ruptured nontraumatic fusiform aneurysm of the cavernous carotid artery presenting with multiple episodes of epistaxis. Surg Neurol 1994;42:293-296. 67. Destian S, Tung H, Gray R, et al. Giant infectious intracavernous carotid artery aneurysm presenting as intractable epistaxis. Surg Neurol 1994;41:472-476.
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68. Ildan F, Uzuneyupopglu Z, Boyar B, et al. Traumatic giant aneurysm of the intracavernous internal carotid artery causing fatal epistaxis. J Trauma 1994;36:565-567. 69. Young N. Bleeding from the ear as a sign of leaking aneurysm of the extracranial portion of the internal carotid artery. J Laryngol Otol 1991;56:35-64. 70. Cooper A. Account of the first successful operation, performed on the carotid artery, for aneurysm, in the year 1808; with the post-mortem examination in 1821. Guy’s Hosp Rep 1836;1:53-58. 71. Nicholson ML, Horrocks M. Leaking carotid artery aneurysms. Eur J Vasc Surg 1988;2:197-198. 72. Kawauchi M, Symon L. Magnetic resonance demonstration of the effect of carotid artery ligation for a giant internal carotid artery aneurysm. Br J Neurosurg 1991;5:387-391. 73. Graves VB, Strother CM, Rappe AH. Treatment of experimental canine carotid aneurysm with platinum coils. Am J Neuroradiol 1993;14:987-993. 74. Coldwell DM, Novak Z, Ryu RK, et al. Treatment of posttraumatic internal carotid arterial pseudoaneurysms with endovascular stents. J Trauma 2002;48:470-472. 75. Duke BJ, Ryu RK, Coldwell DM, Brega KE. Treatment of blunt injury to the carotid artery by using endovascular stents: an early experience. J Neurosurg 1997;87: 825-829. 76. Weber W, Nahser HC, Henkes H, et al. Pseudoaneurysm of the extracranial internal carotid artery: treatment by stent and coil implantation. Nervenarzt 1999;70:870-877. 77. Simionato F, Righi C, Scotti G. Post-traumatic dissecting aneurysm of extracranial internal carotid artery: endovascular treatment with stenting. Neuroradiology 1999;41:543-547. 78. Agrifoglio M, Rona P, Spiriot R. Extracranial carotid artery aneurysms. J Cardiovasc Surg 1989;30:942-944.
This multicentric Serbian study presents the treatment of 91 extracranial carotid artery aneurysms in 76 patients (13 had bilateral lesions). There were 61 (80.3%) male and 15 (19.7%) female patients, with an average age of 61.4 years. The aneurysms were caused by atherosclerosis in 73 cases (80.2%), trauma in six (6.6%), previous carotid surgery in six (6.6%), tuberculosis in one (1.1%), and fibromuscular dysplasia in five (5.5%). The majority (61 cases or 67%) of the aneurysms involved the internal carotid artery, 29 (31.9%) the common carotid artery bifurcation, and one (1.1%) the external carotid artery. Forty-five (49.4%) aneurysms were fusiform, while 46 (50.6%) were saccular. Twenty-nine (31.9%) cases were totally asymptomatic at the time of diagnosis. The remainder presented with compression in 14 (15.4%) cases, stroke in 11 (12.1%) cases, transient ischemic attack in 33 (36.3%) cases, and rupture in four (4.4%) cases. In cases where the aneurysm involved the internal carotid artery, four surgical procedures were performed: aneurysmectomy with end-to-end anastomosis in 30 (33.0%) cases, aneurysmectomy with vein graft interposition in 20 (22.0%) cases, aneurysmectomy with anastomosis between external and internal carotid artery in eight (8.8%) cases, and aneurysmectomy followed by arterial ligature in three cases. One case of external carotid artery aneurysm also was treated by aneurysmectomy and ligature. Aneurysm replacement with Dacron graft was performed in 29 (31.9%) cases where common carotid artery bifurcation was involved. Two (2.2%) patients died after the operation due to a stroke. They had ruptured internal carotid artery aneurysm treated by aneurysmectomy and ligature. Including these, a total of five (5.5%) postoperative strokes occurred. In two (2.2%) cases, transient cranial nerve injuries were found. Excluding the five patients who were lost to follow-up, 69 other surviving patients were followed from 2 months to 12 years (mean 5 years and 3 months). In this period, there were no new neurological events and all reconstructed arteries were patent. Three patients died more than 5 years after the operation, due to myocardial infarction. Aneurysms of the extracranial carotid arteries are rare vascular lesions that produce a high incidence of unfavorable neurological sequelae. Because of their varied etiology, location, and extension, different vascular procedures have to be used during repair of extracranial carotid artery aneurysms. In all of these procedures, an aneurysmectomy with arterial reconstruction is necessary.
INTRODUCTION Extracranial carotid artery aneurysm (ECAA) is a very rare vascular lesion compared to occlusive disease.1-8 According to data from the largest series 1 Vascular Surgery Clinic, Dedinje Cardiovascular Institute, Belgrade, Serbia. 2 Vascular Surgery Clinic, Institute for Cardiovascular Diseases, Clinical Center of Serbia, Belgrade, Serbia. 3
Vascular and Transplant Surgery Clinic, Clinical Center, Novi Sad, Serbia.
published, their incidence ranges 0.27e0.6%.2-6 They are uncommon compared to aneurysms involving other peripheral arteries, particularly the abdominal aorta.1-8 Until 2000, about 2,600 ECAAs
Correspondence to: äorCe Radak, MD, PhD, Vascular Surgery Clinic, Dedinje Cardiovascular Institute, nh M. Tepic a 1, 11 000 Belgrade, Serbia, E-mail: [email protected] Ann Vasc Surg 2007; 21: 23-29 DOI: 10.1016/j.avsg.2006.10.004 Ó Annals of Vascular Surgery Inc. Published online: January 12, 2007
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24 Radak et al.
have been reported.1 Although rare, ECAAs have significant medical and surgical importance. Major neurological symptoms after embolization or thrombosis from the ECAA are relatively common.1-10 The stroke rate in such patients ranges 50-70%.8-11 In order to contribute to management guidelines, we present the clinical findings, surgical treatment, and results of 91 ECAAs.
PATIENTS AND METHODS During a 12-year period (1992-2004), 861 patients with occlusive disease of the extracranial carotid arteries were surgically treated in our three institutions. During the same period, we treated 74 (0.94%) patients with 91 ECAAs (13 had bilateral lesions). Their mean age was 61.4 years (range 2187), and the male to female ratio was 61 (80.3%):15 (19.7%). The causes of the ECAA were divided among atherosclerosis in 73 cases (80.2%), trauma in six (6.6%), previous carotid endarterectomy with DacronÒ (DuPont, Wilmington, DE) patch in six (6.6%), tuberculosis in one (1.1%), and fibromuscular dysplasia in five (5.5%). Four false traumatic ECAAs developed after penetrating and two after blunt neck trauma. One of them developed in a patient who played water polo a few days before admission. During the course of the game, the head of our patient was twisted backward and to the right by the opponent player, after which he was hit by a ball in the left side of the neck. In our patient, a combination of two mechanisms took place. Accidental hyperextension of the neck exposed the common carotid artery to a subsequent sudden forceful compression against the transverse processus of the sixth cervical vertebra caused by the ball hit. One false traumatic aneurysm involved the external, two the common, and three the internal carotid artery (Fig. 1). In 61 (67.0%) cases, the aneurysms involved the internal carotid artery, 29 (31.9%) the common carotid artery bifurcation, and one (1.1%) the external carotid artery. Forty-five (49.4%) aneurysms were fusiform, while 46 (50.6%) were saccular. Twenty-nine (31.9%) cases were totally asymptomatic at the time ECAA was diagnosed. The remainder presented with compression in 14 (15.4%) cases, stroke in 11 (12.1%) cases, transient ischemic attack in 33 (36.3%) cases, and rupture in four (4.4%) cases. The diagnosis was established using duplex ultrasonography and angiography in all, while computed tomographic scan was performed in four cases (Table I).
Annals of Vascular Surgery
All our patients were treated surgically. Surgical treatment varied and was largely determined by several factors that included anatomic extent of the aneurysm, etiology, and the presence or absence of infection. The selection of various operative methods was influenced by the anatomic location of the aneurysm. Aneurysmectomy followed by replacement with Dacron graft was performed in 29 (31.9%) cases where common carotid artery bifurcation was involved. Out of them, in 23 cases a direct reimplantation of the external carotid artery into the Dacron graft was performed (Fig. 2A). In the other six cases, a new Dacron graft was used for the reconstruction of the external carotid artery by the ‘‘side arm technique’’ (Fig. 2B). In cases where the aneurysm involved the internal carotid artery, four surgical procedures were performed. Aneurysmectomy with end-to-end anastomosis was performed in 30 (33.0%) cases (Fig. 3). Aneurysmectomy with vein graft interposition was performed in 20 (22.0%) cases. Aneurysmectomy with anastomosis between the proximal external and distal internal carotid artery was performed in eight (8.8%) cases. Aneurysmectomy followed by arterial ligature was performed in three cases with ruptured, very highly localized internal carotid artery aneurysm where reconstruction was not possible. One of them had an infected internal carotid artery aneurysm. One case of false traumatic external carotid artery aneurysm also was treated by aneurysmectomy and ligature. Aneurysmectomy and arterial ligature was performed in a total of four (4.4%) cases. All reconstructive procedures were performed without insertion of an intraluminal shunt (Table II).
RESULTS Two (2.2%) patients died after the operation due to a stroke. They were patients with ruptured internal carotid artery aneurysm treated by aneurysmectomy and ligature. Including these, a total of five (5.5%) postoperative strokes occurred. One nonlethal stroke followed ligature of the internal carotid artery, while two followed aneurysmectomy of the carotid bifurcation and Dacron graft interposition. In two (2.2%) cases, transient cranial nerve (one facial and one hypoglossal) injuries were found. These patients made good progress postoperatively, and both hypoglossal and facial paresis regressed 4 months after surgery. Excluding the five patients who were lost to follow-up, 69 other surviving patients were followed from 2 months to 12 years
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Carotid artery aneurysms 25
Fig. 1. Common carotid artery saccular aneurysm caused by blunt neck injury a few years ago. A Asymptomatic pulsatile neck mass. B Angiography.
Table I. Clinical manifestations of extracranial carotid artery aneurysms Symptoms
n (%)
Asymptomatic neck mass Rupture Compression of cranial nerves Transient ischemic attacks Stroke Total
29 4 14 33 11 91
(31.9) (4.4) (15.4) (36.3) (12.1) (100.0)
(mean 5 years and 3 months). In this period, there were no new neurological events and all reconstructed arteries were patent. Three patients died more than 5 years after the operation due to myocardial infarction.
DISCUSSION Atherosclerosis causes over 75% of all ECAAs, as reported in published series.1-15 Seventy-three (80.2%) ECAAs in our series were atherosclerotic in origin. Other true ECAAs are caused by infection,12,13,16-25 inflammation,26,27 fibromuscular dysplasia,28,29 cystic necrosis of media,30,31 Behc¸et’s disease,32,33 protein C and S and antithrombin III deficiency, and idiopathic medial arteriopathy.34 We had one case of ruptured ECAA caused by tuberculous lymphadenitis of the neck. Very rare congenital ECAAs similar to intracranial carotid artery aneurysms have also been reported.4,12,35-39
Four groups of false ECAAs have been reported: traumatic, anastomotic, iatrogenic, and dissecting. False traumatic ECAAs are most frequently caused by blunt trauma of the neck.12,14,40-45 The precise mechanism by which blunt arterial injury produces ECAA is unclear. Extreme hyperextension,12,14,42,43 twisting of the neck,14,46 and compression against the internal carotid artery at the level of the first and second cervical vertebrae14,46 might be reasonable explanations for this. Another factor implicated in this condition is the association of mandibular fractures and ECAA.45 Anastomotic pseudoaneurysm is found as an early or late complication after carotid endarterectomy.1,3,6,12,13,15,47 We had six such cases after carotid endarterectomy and Dacron patch angioplasty. Data in the literature indicate that anastomotic pseudoaneurysm is found four times more frequently after endarterectomy with patching compared to endarterectomy alone.1,3,6,13,15,47 Although the overall incidence is low, significant morbidity is associated with such pseudoaneurysms, due to cerebral embolization. Iatrogenic carotid pseudoaneurysm occurs after various surgical procedures in the neck.48 Dissecting ECAAs, caused by spontaneous isolated carotid artery dissection, are rare.49-53 Major neurological events are the most common clinical manifestation of ECAA, occurring in more than 40% of patients.1-10,12-15,50,51,54-56 ECAAs produce either transient ischemic attacks (36.3% of our cases) or stroke (12.1% of our cases). According to Knight et al.,6 17% of ECAAs presented with compression of the cranial or cervical nerves. We had 15.4% such cases. Most frequently, ECAAs
26 Radak et al.
Annals of Vascular Surgery
Fig. 2. A After aneurysmectomy, interposition of the Dacron graft between the common and internal carotid arteries with direct reimplantation of the external carotid artery into the Dacron graft was performed. B Reconstruction of the external carotid artery with Dacron graft (side arm technique).
Fig. 3. A Giant saccular aneurysm of the elongated internal carotid artery. B End-to-end anastomosis of the internal carotid artery was performed after aneurysmectomy.
compress the hypoglossal nerve.7,57 In 1994, Shimohata et al.57 described ECAA compression on both the hypoglossal and vagus nerves, which produced the so-called Tapia syndrome. Compression on glossopharyngeal and facial nerves, as well as on the stellate ganglion, has been reported.1,7,58,59 Dysphagia secondary to the bulking of the lesion or compression of the pharyngeal nerve has been described as a symptom of ECAA.1,59 ECAA rupture is a rare condition associated with high morbidity and mortality,7,58,60 due to extensive hemorrhage. We had four such cases. Some of the ruptured ECAAs presented with unusual hemorrhage to the pharynx, ear, and nose.61-69
In 1808, Sir Astley Cooper70 successfully performed a ligature of the internal carotid artery aneurysm. His patient lived without any neurological deficit for 13 years. According to reports that followed, this procedure carried very high mortality and morbidity rates.1-10,12,71,72 Ligature of the internal carotid artery was performed in three of our cases. In all of them, postoperative stroke occurred, and two patients died. Nowadays, a ligature of the internal carotid artery is indicated only in cases with aneurysm extending to the base of the skull and as an emergency procedure for massive, uncontrolled hemorrhage due to aneurysmal rupture.2,7,72 Since Cooper’s time numerous nonreconstructive
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Carotid artery aneurysms 27
Table II. Treatment of extracranial carotid artery aneurysms Type of treatment
n (%) a
Aneurysmectomy with Dacron graft Aneurysmectomy with end-to-end anastomosis b Aneurysmectomy with vein graft b Aneurysmectomy utilizing anastomosis between the external and the distal internal carotid artery b Aneurysmectomy with arterial ligature c Total
29 (31.9) 30 (33.0) 20 (22.0) 8 (8.8)
4 (4.4) 91 (100.00)
a The aneurysm involved bifurcation of the common carotid artery. b The aneurysm involved the internal carotid artery. c Three aneurysms involved the internal and one the external carotid artery.
our study, the early mortality rate (the first 30 postoperative days) was 2.2%. The most common complications after ECAA surgery are postoperative stroke and cranial nerve injuries. Five (5.5%) of our cases had a postoperative stroke. Knight et al.6 reported 6% of cases with postoperative reversible ischemic neurological deficit as well as 6% of cases with a postoperative stroke. Moreau et al.4 reported 5% of patients with postoperative stroke following surgery of ECAA, while Painter et al.2 found 8.2% such patients. Agrifoglio et al.78 described injuries of the superior laryngeal, facial, hypoglossal, glossopharyngeal, and vagal nerves after ECAA surgery. We had two (2.2%) cases with transient cranial nerve injuries.
CONCLUSION techniques have been employed in the management of ECAA. Because of the high incidence of neurological sequelae subsequent to such techniques, they have been largely abandoned in favor of reconstructive procedures, aimed at restoration of arterial flow.1-10,12-14 Surgical treatment of ECAA varied and was influenced by several factors that included size of the aneurysm, adequacy of cerebral blood flow, presence or absence of infection, and surgeon’s experience. Aneurysmectomy with arterial reconstruction is the treatment of choice. Direct end-to-end anastomosis (33.0% of our cases) can be performed if the aneurysm is saccular and the vessels elongated and tortuous.1-10,12,56,57 Whenever end-to-end anastomosis is difficult to perform, two alternative procedures are available: vein graft interposition1-25 (performed in 22.0% of our cases) and internal carotid artery reimplantation into the external or the common carotid artery2,9,57 (performed in 8.8% of our cases). Synthetic graft interposition is indicated when the bifurcation of the common carotid artery is involved1-10,13,15 (performed in 31.9% of our cases). Although ECAA repair is a much more demanding procedure than carotid endarterectomy, it is most frequently performed without intraluminal shunt. Endovascular procedures have also been described for treatment of ECAA.1,72-77 They are indicated for false traumatic aneurysms of the internal carotid artery localized high in the neck, at the base of the skull. Although surgical treatment of ECAA is more difficult compared to carotid endarterectomy, it is followed by a similar postoperative complication rate.9,26,74 After surgically treated ECAA, Painter et al.2 described an early mortality rate of 1.6%, Knight et al.6 3%, and McCollum et al.3 7%. In
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