Case Report

Endovascular Treatment of Traumatic Bilateral Internal Carotid Artery Dissection

*Paolo Pagnotta, MD, Carlo Briguori, MD, PhD, §Cesare Massa Saluzzo, MD, *Patrizia Presbitero, MD
*Paolo Pagnotta, MD, Carlo Briguori, MD, PhD, §Cesare Massa Saluzzo, MD, *Patrizia Presbitero, MD
Author Affiliations: From the *Laboratory of Interventional Cardiology, IRCCS Humanitas, Milan, and §Neuroradiology Unit, IRCCS Fondazione Policlinico San Matteo, Pavia, Italy. The authors report no conflicts of interest regarding the content herein. Manuscript submitted July 8, 2008 and final version accepted August 19, 2008. Address for correspondence: Patrizia Presbitero, MD, Laboratory of Interventional Cardiology, IRCCS Humanitas, Via Manzoni, 56, 20089 Rozzano, Milano, Italy. E-mail:


J INVASIVE CARDIOL 2009;21:E6-E7 Traumatic dissection of the internal carotid artery (ICA) is an uncommon but well-recognized entity.1 The accepted medical standard of therapy has consisted of systemic anticoagulation, which leads to a significant rate of subsequent resolution and healing.2,3 However, anticoagulation may be contraindicated in patients with multiple traumas, intracranial hematomas and penetrating injuries. Indeed, although most dissections of the carotid and vertebral arteries heal spontaneously, approximately 40% of traumatic dissections and the majority of pseudoaneurysms do not heal with anticoagulant therapy and constitute a long-term risk of embolization or flow-related complications.4,5 Surgical or endovascular treatment should be reserved for patients with contraindication to anticoagulation or who have persistent symptoms of ischemia and/or significant stenosis despite adequate anticoagulation.2,6 We describe a case of a 49-year-old male with a bilateral post-traumatic ICA. Case Report. A 49-year-old male was admitted to our hospital because of a cervical spine injury that occurred in a motor vehicle accident. His past history included systemic hypertension on pharmacological treatment. The patient presented with cervical “whiplash” syndrome due to the traumatic event with abrupt flexion-extension movement of the cervical spine. Symptoms included severe pain, loss of range of motion in the neck and occipital headache. The patient also suffered from a partial Horner’s syndrome (left eye miosis and ptosis) and sensorial deficit in the left hand. Three days later, the patient developed fluent (Werniche’s) aphasia. An X-ray showed fracture in the spinous processes of the cervical vertebral bodies C3 and C4. Angiographic magnetic resonance imaging (MRI) showed occlusive dissection in the C2 segments of both left and right ICA (Figure 1). Conventional digital subtraction angiography (DSA) confirmed the presence of an extensive occlusive dissection in the proximal and middle segment of both the right and left ICAs (Figure 2). Due to the bilateral ICA compromise, the case was discussed with the neurologist, vascular surgeon and interventional cardiologist, and the consensus was to treat the patient with stent implantation in both ICAs. The patient was loaded with 300 mg of clopidogrel prior to the procedure and was taking 100 mg/day of aspirin. The procedure was carried out via the femoral approach. Intravenous unfractionated heparin (total dose, 10,000 units; activated clotting time > 300 seconds) was administered. After cannulation of the right common femoral artery with a short (11 cm in length) 6 Fr sheath (Super Arrow-Flex®, Arrow International, Reading, Pennsylvania), a 5 Fr Judkins R4 diagnostic catheter was advanced into the right external carotid artery (ECA). The 0.035 inch super-stiff Amplatz long (260 cm) guidewire (Boston Scientific Corp., Natick, Massachusetts) was advanced through the lumen of the diagnostic catheter into the right ECA. Then the short sheath was replaced with a 6 Fr long (90 cm) sheath (Super Arrow-Flex®, Arrow International) and was advanced into the distal segment of the right common carotid artery. A distal embolic protection device Spider™ 6.0 mm (eV3, Inc., Plymouth, Minnesota) was advanced in the distal segment of the ICA. A self-expandable stent (Carotid Wallstent®; Boston Scientific; 8–10 mm in diameter x 50 mm in length) was advanced through the guidewire and positioned at the proximal segment of the ICA. Postdilatation was then performed using a 5.5 mm diameter x 20 mm long Ultrasoft balloon (Boston Scientific). The filter guidewire was retrieved and no macroscopic debris was observed. The final DSA of the right carotid system showed a good flow (Figure 3A). Therefore, the operator approached the left carotid artery system and the same procedure was performed. A self expandable stent (Carotid Wallstent®; Boston Scientific; 8–10 mm in diameter, 40 mm in length) was implanted in the proximal segment of the left ICA. The final DSA of the left carotid system showed a good flow (Figure 3B) and the patient’s intracranial flow was good. The femoral entry site was closed with an Angio-Seal™ STS Plus Platform device (St. Jude Medical, St. Paul, Minnesota). There were no neurological or other complications. Color-Doppler echography performed the day after the procedure confirmed optimal stent apposition. All neurological symptoms reverted and no neurological deficit was observed. The patient was discharged home on the third day after the procedure. No major adverse cerebrovascular events occurred at 8 months. A conventional DCA at 8 months confirmed good patency of both the right and the left ICAs (Figure 4). Discussion. Carotid artery dissection causes 10–25% of strokes in younger people and 2% of all ischemic strokes.3 Approximately 50% of patients with carotid dissection do not have identifiable predisposing factors.3 Traumatic dissection of the ICA is an uncommon but well-recognized entity.1 In the clinical set-up of neurotrauma it is easily missed because of multiple farsurized blood in the dissected medial defect.4 Surgical or endovascular treatment should be reserved for patients with contraindication to anticoagulation or who have persistent symptoms of ischemia and/or significant stenosis despite adequate anticoagulation.2,6 Surgical treatment (i.e., ligation of the carotid or vertebral artery, combined with an in situ or extracranial-to-intracranial bypass) is technically demanding and is associated with a substantial morbidity rate. Carotid artery stenting (CAS) entails a lower risk than surgical treatment and, in most instances, has supplanted surgery as the initial therapy of choice once medical therapy fails.2,7 CAS may provide immediate revascularization and avoids the need of anticoagulation.2,8 Cohen et al6 described 10 cases of post-traumatic ICA dissection treated by stenting. The dissection presented clinically with ischemic stroke in 4 patients, repetitive transient ischemic attacks in 2, local symptoms in 2 (Horner’s syndrome), and 2 patients were screened because of cervico-cranial penetrating injuries. The clinical manifestations of dissection appeared 4 hours to 19 days after the acute injury. Stenting was performed because of parenchymal hypoperfusion and impending stroke (5 patients), neurologic deterioration under anticoagulation (2 patients), and because of contraindication for anticoagulation (6 patients). The interval between the onset of focal ischemic signs and stenting ranged from 2–10 hours. There were no procedure-related complications. Six patients improved and 4 remained stable after 16 months of follow up. In the present case we observed a bilateral carotid flow-limiting dissection associated to neurological instability and clinical evidence of hemodynamic insufficiency. This severe anatomic damage would probably compromise any potential effective development of collateral circulation. Therefore, the combination of 1) a very high-risk vessel damage; and 2) the clinical evidence of hemodynamic instability suggests us to perform bilateral CAS. To the best of our knowledge, only Malek et al2 reported 2 cases of spontaneous bilateral ICA dissection. In both these cases, angiography showed unilateral occlusive dissection associated with critical stenosis in the contralateral carotid artery. Both cases were treated by CAS of the stenotic ICA. Significant drawbacks of stenting are: 1) the risk of distal embolization, which may be prevented by the used of protection devices; and 2) the lack of long-term data and large case series to establish the role of this approach as compared to medical therapy alone. Conclusion. CAS appears to be a feasible and safe strategy to treat bilateral and symptomatic ICA traumatic dissection.


1. Watridge CB, Muhlbauer MS, Lowery RD. Traumatic carotid artery dissection: Diagnosis and treatment. J Neurosurg 1989;71:854–857.
2. Malek AM, Higashida RT, Phatouros CC, et al. Endovascular management of extracranial carotid artery dissection achieved using stent angioplasty. Am J Neuroradiol 2000;21:1280–1292.
3. Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med 2001;344:898–906.
4. Pozzati E, Giuliani G, Acciarri N, Nuzzo G. Long-term follow-up of occlusive cervical carotid dissection. Stroke 1990;21:528–531.
5. Fabian TC, Patton JH Jr, Croce MA, et al. Blunt carotid injury. Importance of early diagnosis and anticoagulant therapy. Annals Surg 1996;223:513–522.
6. Cohen JE, Ben-Hur T, Rajz G, et al. Endovascular stent-assisted angioplasty in the management of traumatic internal carotid artery dissections. Stroke 2005;36:e45–e47.
7. Liu AY, Paulsen RD, Marcellus ML, et al. Long-term outcomes after carotid stent placement treatment of carotid artery dissection. Neurosurgery 1999;45:1368–1373.
8. Bejjani GK, Monsein LH, Laird JR, et al. Treatment of symptomatic cervical carotid dissections with endovascular stents. Neurosurgery 1999;44:755–760.