J ENDOVASC THER 2003;10:45–48 45 l CASE REPORT l Endovascular Management of Acute Carotid Artery Dissection With a Waxing and Waning Neurological Deficit Enrico Sbarigia, MD; Cesare Battocchio, MD; Maria A. Panico, MD; Davide Zaccagnini, MD; Filippo M. Salvatori, MD*; and Corrado Argentino, MD† Cattedra di Chirurgia Vascolare, *Dipartimento di Radiologia, and †Unità di Terapia Intensiva Neurologica, Università degli Studi di Roma ‘‘La Sapienza,’’ Rome, Italy l l Purpose: To evaluate the feasibility and efficacy of emergent carotid stenting for an acute internal carotid artery (ICA) dissection. Case Report: A 51-year-old man was admitted to our emergency department’s stroke unit 1 hour after the onset of left hemiparesis. Computed tomographic and transcranial Doppler scans showed no pathological findings, but the color Doppler study detected a double lumen in the right carotid bifurcation extending to the proximal ICA. Within the first 2 hours after admission, the patient’s neurological status began to fluctuate; the NIH Stroke Scale (NIHSS) and Rankin scores evaluated each hour after admission ranged from 0 to 12 and from 0 to 3, respectively. Emergency carotid angiography confirmed the dissection of the bulb and proximal right ICA, which prompted implantation of 2 Wallstents from the internal to common carotid artery. Forty-eight hours later, the patient was almost totally asymptomatic with an NIHSS score of 1 and a Rankin score of 0; he was discharged on postoperative day 3. At 3 months, the patient was free of neurological symptoms and the stented carotid artery was patent. Conclusions: In patients with fluctuating neurological signs and symptoms consistent with carotid artery dissection that are refractory to medical therapy, a stent can be placed to prevent permanent neurological deficits provided that the anatomical conditions are suitable. J Endovasc Ther 2003;10:45–48 Key words: internal carotid artery, dissection, neurological deficit, carotid artery stenting, microembolization, Wallstent endoprosthesis l Spontaneous dissection is a rare event in the extracranial carotid arteries, with a reported prevalence of ;2.5%.1 Surgery performed in the acute phase leads to failure in .60% of the cases.2 For this reason, the currently recommended treatment for acute carotid artery dissection is anticoagulant therapy with intravenous heparin. Medical treatment can achieve favorable results, reported as high as l 90% in some series.3–6 Despite these encouraging results, anticoagulant therapy does not avoid a residual deficit or late complications related to carotid dissection, such as stenosis, late occlusion, and pseudoaneurysm formation. Neither does it always protect the dissected wall from continuing embolization, causing unstable neurological symptoms.7 In these instances, various investigators have Address for correspondence and reprints: Enrico Sbarigia, MD, Università degli Studi di Roma ‘‘La Sapienza,’’ Viale del Policlinico, 00161 Rome, Italy. Fax: 39-06-4940532; E-mail: sbarigia@pbxfreenet.it Q 2003 by the INTERNATIONAL SOCIETY OF ENDOVASCULAR SPECIALISTS Available at www.jevt.org 46 EMERGENT CAROTID STENT FOR DISSECTION Sbarigia et al. J ENDOVASC THER 2003;10:45–48 Figure 1 l Ultrasound scan of the carotid arteries detected a double lumen on the posterior wall of the right carotid bulb. proposed the use of stents as an alternative to surgical therapy or for correcting surgical defects.8–15 In this report we describe the management of a patient with acute carotid artery dissection observed in the neurological intensive care unit (ICU) in a very early phase, which manifested as waxing and waning hemiplegia. CASE REPORT A 51-year-old hypertensive man was admitted to the neurological ICU of our University Hospital 1 hour after the onset of left hemiparesis. The National Institutes of Health Stroke Scale (NIHSS) score at admission was 9 and the Rankin score was 3. A computed tomographic (CT) scan of the brain performed within 1 hour after admission showed no cerebral infarct, but a color Doppler study of the carotid arteries detected a pathognomonic feature of arterial dissection, a double lumen (Fig. 1), along the posterior aspect of the right carotid bulb. A transcranial Doppler (TCD) scan documented the patency of all the intracranial arteries. After the cerebral CT scan excluded brain hemorrhage, heparin administration was begun with a 5000-unit intravenous bolus and continuous intravenous infusion of 1000 U/h. During and immediately after the diagnostic imaging procedures, the neurological deficit showed an unmistakable waxing and waning pattern; the NIHSS score varied from 0 to 12 (Rankin scale from 0 to 3) in the 2 hours immediately after admission. An emergency carotid angiogram (Fig. 2A) Figure 2 l (A) A dissection (arrow) extending proximally from the posterior wall of the carotid bulb is documented by arteriography. (B) Successful restoration of the carotid lumen with placement of 2 Wallstents. performed ;4 hours after admission demonstrated only irregularities extending for 1.5 cm along the posterior wall of the right carotid bulb, with persistent contrast medium, which confirmed the arterial dissection suggested by ultrasound. During angiography, the patient continued to show fluctuating hemiparesis. These findings, in addition to the ineffectiveness of the anticoagulant therapy, prompted us to insert 2 self-expanding carotid Wallstents (Boston Scientific Corp., Natick, MA, USA) between the internal and common carotid artery, without preliminary dilation; the heparin infusion was maintained during the endovascular procedure. The completion angiogram (Fig. 2B) documented disappearance of the posterior irregularity in the carotid artery. At the end of the endovascular procedure, about 6 hours after admission, the patient suffered complete hemiparesis (NIHSS: 12, Rankin: 3). Standard post-stenting therapy consisting of ticlopidine (500 mg/d) and aspirin (320 mg/d) was begun immediately after the stent was positioned. Over the next few hours, the neurological deficit progressively regressed; heparin infusion was discontinued 24 hours after the procedure. At 48 hours, the hemiparesis had completely cleared (NIHSS 1, Rankin 0) and only upper limb paresthesia remained. Postpro- J ENDOVASC THER 2003;10:45–48 EMERGENT CAROTID STENT FOR DISSECTION Sbarigia et al. cedural CT scans at 12 and 24 hours were negative for cerebral infarct, and color Doppler and TCD investigations at 24 and 72 hours showed a well-positioned stent and patent right carotid and intracranial arteries. The patient was discharged on postoperative day 3 with no residual neurological deficit. Postprocedural followup studies at 12 months confirmed the absence of neurological symptoms and patency of the stented carotid artery. symptoms consistent with carotid artery dissection can avoid permanent neurological deficits in selected patients. Stenting can bring about immediate symptomatic improvement rather than acute deterioration followed by gradual recovery. DISCUSSION The distinctive features in this case were the patient’s fluctuating neurological deficit and the early detection of a carotid bulb dissection in its initial stages. Prompt diagnosis provided an opportunity to treat the dissection with carotid stenting, which was considered appropriate because the lesion was small and there was no irreversible brain damage on CT scan. The time needed for intravenous anticoagulation to take effect could have put the patient at risk for a permanent neurological deficit. Although we could not determine the microembolic origin for the waxing and waning neurological deficit, the imaging studies excluded all other causes but the carotid lesion. Despite anticoagulant therapy, the patient’s neurological signs and symptoms continued to fluctuate and repeatedly worsened. The last deficit developed during the stenting procedure and reached maximum expression before stent positioning but did not continue thereafter, thus the acute clinical deterioration was not owing to a massive distal embolus but to a small embolic source in the intimal flap, similar to other reported cases.7,8 After the procedure, the patient’s clinical condition markedly improved, and no neurological deficits of any kind developed. None of the postoperative CT scans showed evidence of new infarctions. We used a self-expanding carotid stent to avoid predilation and minimize the risk of further embolization. Complete resolution of clinical symptoms within 48 hours, as evaluated by the neurologists, confirmed the hypothesis of microembolization from the minimal wall defect visualized on ultrasound and angiography. In conclusion, emergent carotid stenting in the face of fluctuating neurological signs and 47 REFERENCES 1. Schievink WI, Mokri B, Whisnant JP. Internal carotid artery dissection in a community. Rochester, Minnesota, 1987–1992. Stroke. 1993;24: 1678–1680. 2. Hart RG. Easton JD. Dissections of cervical and cerebral arteries. Neurol Clin. 1983;1:155–182. 3. Sturzenegger M. Spontaneous internal carotid artery dissection: early diagnosis and management in 44 patients. J Neurol. 1995;242:231–238. 4. Rothrock JF, Lim V, Press G, et al. Serial magnetic resonance and carotid duplex examinations in the management of carotid dissections. Neurology. 1989;39:686–692. 5. Woll MM, Goff JM, Gillespie DL, et al. Bilateral spontaneous dissection of the internal carotid arteries. Vasc Surg. 2001;35:221–224. 6. Muller BT, Luther B, Hort W, et al. Surgical treatment of 50 carotid dissections: indications and results. J Vasc Surg. 2000;31:980–988. 7. Molina CA, Alvarez-Sabin J, Schonewille W, et al. Cerebral microembolism in acute spontaneous internal carotid artery dissection. Neurology. 2000;55:1738–1740. 8. Malek AM, Higashida RT, Phatouros CC, et al. Endovascular management of extracranial carotid artery dissection achieved using stent angioplasty. AJNR Am J Neuroradiol. 2000;21: 1280–1292. 9. Yamashita K, Okamoto S, Kim C, et al. Emergent treatment of iatrogenic dissection of the internal carotid artery with the Palmaz-Schatz stent—a case report. Neurol Med Chir (Tokyo). 1997;37:336–339. 10. Hong MK, Satler LF, Gallino R, et al. Intravascular stenting as a definitive treatment of spontaneous carotid artery dissection. Am J Cardiol. 1997;79:538. 11. Liu AY, Paulsen RD, Marcellus ML, et al. Longterm outcomes after carotid stent placement for treatment of carotid artery dissection. Neurosurgery. 1999;45:1368–1374. 12. Anzuini A, Briguori C, Roubin GS, et al. Emergency stenting to treat neurological complications occurring after carotid endarterectomy. J Am Coll Cardiol. 2001;37:2074–2079. 13. Bejjani GK, Monsein LH, Laird JR, et al. Treat- 48 EMERGENT CAROTID STENT FOR DISSECTION Sbarigia et al. J ENDOVASC THER 2003;10:45–48 ment of symptomatic cervical carotid dissections with endovascular stents. Neurosurgery. 1999;44:755–761. 14. DeOcampo J, Brillman J, Levy DI. Stenting: a new approach to carotid dissection. J Neuro- imaging. 1997;7:187–190. 15. Albuquerque FC, Han PP, Spetzler RF, et al. Carotid dissection: technical factors affecting endovascular therapy. Can J Neurol Sci. 2002;29: 54–60.