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Thrombotic Occlusion of the Common Carotid Artery in Acute Ischemic Stroke

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Slide 1 :

Thrombotic Occlusion of the Common Carotid Artery in Acute Ischemic Stroke Vijay K Sharma Consultant Neurologist National University Hospital Singapore drvijay@singnet.com.sg

Slide 2 :

Introduction Common carotid artery (CCA) occlusion is a rare finding in patients evaluated for cerebrovascular diseases.1 CCA occlusions are seen in less than 2% of cases.1 A wide range of presentations can be seen from completely asymptomatic to a devastating stroke.2,3 Riles TS et al. Ann Surg 1984;199:363-366. Levine SR et al. Neurology 1989;39:2084-2093. Cull DL et al. Ann Vasc Surg 1999;13:73-76.

Slide 3 :

Introduction The commonest cause of CCA occlusion is attributed to atherosclerosis. Less frequent causes include1,2,3 Takayasu arteritis post-radiation arteriopathy cardiac embolism Syphilis trauma homocystinuria etc. Cull DL et al. Ann Vasc Surg 1999;13:73-76. Zardi EM et al. Eur J Neurol 2006;13:423-424. Tsai CF et al.J Neuroimaging 2005;15:50-56.

Slide 4 :

Introduction Acute internal carotid artery (ICA) occlusions have been widely described in acute ischemic stroke. Acute CCA thrombosis has rarely, if ever, been reported in detail in patients with acute cerebral ischemia.

Slide 5 :

CCA thrombi in acute ischemic stroke From September 2005 through May 2006, 47 ischemic stroke patients received IV-TPA therapy. Rapid sequence transcranial Doppler (TCD) and cervical duplex ultrasound were performed in all cases before TPA bolus. Most of these patients underwent CT angiography of head and neck immediately following the brain CT scan. CCA patency was assessed in all patients during the cervical duplex examination. 3 out of the 47 patients (6%) were found to have CCA occlusions before TPA bolus.

Slide 6 :

CCA thrombi in acute ischemic stroke Times elapsed between symptom onset and TPA bolus were Case 1- 145 minutes Case 2- 115 minutes Case 3- 160 minutes Mobile and acute CCA thrombi extending into the internal carotid (ICA) and external carotid (ECA) arteries were seen in all 3 patients. CCA occlusions were also seen on CT angiography of neck (n=3) Conventional digital subtraction angiography, performed in one case confirmed the presence of CCA thromus in one case.

Slide 7 :

Clinical, imaging, sonographic characteristics with recanalization patterns, neurological recovery and disposition data of the three cases with acute CCA occlusions Sharma VK et al. Eur J Neurol 2007;14:237-240

Slide 8 :

Case 1- Sonographic and imaging findings Acute mobile thrombi on transverse (a) and longitudinal (b) views on B-mode cervical duplex sonography. Computerized tomographic (c) of neck showing non-opacification (arrows) of right CCA. Final cerebral infarctions seen on diffusion weighted MRI (d) Note the thrombus in ICA also (b). Schematic representation of CCA occlusion & intracranial flow patterns..Note anterior cross-filling of ipsilateral MCA via ACOM and flow reversal in ipsilateral ACA. 1- Aortic arch; 2-Innominate artery; 3- CCA; 4- ECA; 5-ICA; 6-Subclavian artery; 7-Veretbral artery; 8- intracranial ICA; 9-A1 segments of ACA; 10-M1 segments of MCA; 11-A2 segments of ACA; 12-Anterior communicating artery; 13-Ophthalmic artery; 14-Basilar artery.

Slide 9 :

Case 2- Sonographic and imaging findings Acute mobile thrombi on transverse (a) and longitudinal (b) views on B-mode cervical duplex sonography. s CT angiogram of neck (c) showing non-opacification of left CCA. Final cerebral infarctions seen on brain CT scan (d). 1- Aortic arch; 2-Innominate artery; 3- CCA; 4- ECA; 5-ICA; 6-Subclavian artery; 7-Veretbral artery; 8- intracranial ICA; 9-A1 segments of ACA; 10-M1 segments of MCA; 11-A2 segments of ACA; 12-Anterior communicating artery; 13-Ophthalmic artery; 14-Basilar artery. Schematic representation of CCA occlusion and intracranial flow patterns. It shows thrombotic occlusion of left CCA, ICA, ECA,intracranial ICA, ipsilateral MCA and ACA. No intracranial collateral flow is seen.

Slide 10 :

Case 3- Sonographic and imaging findings Acute mobile thrombi on transverse (a) and longitudinal (b) views on B-mode cervical duplex sonography. Digital subtraction angiograms (c) of neck showing non-opacification of right CCA. Final cerebral infarctions seen on diffusion weighted MRI (d) Schematic representation of CCA occlusion and intracranial flow patterns. Thrombotic occlusion of right CCA, ECA, ECA and intracranial ICA with anterior cross-filling of ipsilateral MCA via ACOM and flow reversal in ipsilateral ACA. 1- Aortic arch; 2-Innominate artery; 3- CCA; 4- ECA; 5-ICA; 6-Subclavian artery; 7-Veretbral artery; 8- intracranial ICA; 9-A1 segments of ACA; 10-M1 segments of MCA; 11-A2 segments of ACA; 12-Anterior communicating artery; 13-Ophthalmic artery; 14-Basilar artery.

Slide 11 :

Some salient features All 3 patients had a history of atrial fibrillation and hypertension Blood pressure was lowered with nicardipine and maintained in the systolic range of 160 – 180 mm Hg range during the IV-TPA infusion and immediately thereafter. All the patients were kept in the ‘head-down’ (flat) position.1 1. Wojner-Alexander AW et al. Neurology 2005;64:1354-1357.

Slide 12 :

Some salient features At 2 hours after IV-TPA bolus, TCD showed complete proximal MCA recanalization in 2 cases despite persistent occlusions of the proximal CCA/ICA. None of our patients achieved CCA or ICA recanalization. None of our cases showed intracerebral hemorrhage on subsequent imaging studies. No immediate neurological improvement was noted during IV-TPA infusion. NIHSS scores dropped from 10 points at TPA bolus to 5 points at discharge from the hospital (case 1). NIHSS scores dropped from 12 points at TPA bolus to 3 points at discharge from the hospital (case 3).

Slide 13 :

Discussion Our patients had CCA occlusions with mobile intraluminal thrombi. In presence of AF, these thrombi are presumed to have originated from the heart. No evidence for a significant underlying atheromatous lesions were noted ultrasonography. This is in contrast to the existing literature on chronic CCA occlusions that are mostly atherosclerotic in nature.1,2,3 We excluded dissections in the carotid arteries or aortic arch by ultrasound and other imaging modalities (CTA or DSA). Cull DL et al. Ann Vasc Surg 1999;13:73-76. Zardi EM et al. Eur J Neurol 2006;13:423-424. Tsai CF et al.J Neuroimaging 2005;15:50-56.

Slide 14 :

Discussion- types of CCA occlusions Types of CCA occlusion- Type I- isolated CCA occlusion, ICA is patent and perfused by a retrograde flow originating at the circle of Willis or in the ECA.1 Type II- CCA occlusion accompanied by occlusions of ipsilateral ECA and ICA Type-I CCA occlusions are more frequent. All our patients had type-II CCA occlusions. Gerlock AJ et al. Applications of noninvasive vascular techniques. Philadelphia: WB Saunders;1988:88-111.

Slide 15 :

Discussion Importance of intracranial collaterals in CCA occlusions When acute CCA occlusions extend into the cervical ICA, intracranial collateral flow through communicating arteries becomes of utmost significance. Similar to an isolated ICA occlusion, the competence and efficiency of the circle of Willis collaterals determine the extent and severity of ischemic damage.1,2 T-occlusion of the terminal ICA carries a relatively poor prognosis with failed recanalization by systemic thrombolysis.3 Two out of three of our patients had collateral flows through the anterior communicating artery, and milder stroke severity compared to the patient with CCA occlusion and tandem “T”-type ICA occlusion. Linfante I et al. Stroke 2002 ;33:2066-2071. El-Mitwalli A et al. Stroke 2002;33:99-102. Georgiadis D et al. Neurology 2004;63:22-26.

Slide 16 :

Discussion Role of cerebrovascular ultrasound Bedside ultrasound examination in acute cerebral ischemia provides useful real-time information about thrombus presence and its location, collateral blood supply and monitor recanalization and re-occlusion.

Slide 17 :

Discussion- therapeutic options Acute thrombus in a large artery like CCA represents a ‘high clot-burden’. Endovascular therapy1, clot removal by Mechanical embolectomy 2, and combined intravenous-intra-arterial thrombolysis3, alone or in combination, may help in achieving recanalization in acute large artery occlusions in acute stroke. Snugg RM et al. AJNR 2005;26:2591-2594. Smith WS et al. Stroke 2005;36:1432-1440. The IMS study investigators. Stroke 2004;35:904-912.

Slide 18 :

Conclusions We have described the sonographic and imaging features of CCA occlusions with tandem lesions treated with intravenous TPA. Acute occlusions of the carotid arteries in acute ischemic strokes are associated with poor outcomes. However, given the potential for an intracranial recanalization, patients with acute CCA thrombotic occlusions and accompanying tandem lesions may benefit from systemic thrombolysis.1,2,3 Acute CCA occlusions should not be considered to be largely associated with poor outcome and a contra-indication for IV-TPA. Linfante I et al. Stroke 2002 ;33:2066-2071. El-Mitwalli A et al. Stroke 2002;33:99-102. Christou I et al. J Neuroimaging 2002;12:119-123.

Slide 19 :

Contributors Tsivgoulis Georgios, MD Lao, Annabelle Y, MD Flaster, Murray, MD, PhD Frey, James L MD Malkoff, Marc D, MD Alexandrov Andrei V, MD

	drvijay 1 Years ago. Category: Neurology

Tags:	Neurology

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PowerPoint Presentation on Thrombotic Occlusion of the Common Carotid Artery in Acute Ischemic Stro more PowerPoint Presentation on Thrombotic Occlusion of the Common Carotid Artery in Acute Ischemic Stroke or PowerPoint Presentation on Ultrasonographic and imaging characteristics of 3 patients with acute ischemic stroke and acute thrombi in CCA have been described. All three patients were treated with intravenous-TPA. Their intracranial flow patterns and outcomes are described. less

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