35fcthrombotic Occlusion of the Common Carotid Artery 1233912120856263 2

7/30/2019 35fcthrombotic Occlusion of the Common Carotid Artery 1233912120856263 2

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Thrombotic Occlusion of the Common

Carotid Artery in Acute Ischemic Stroke

Vijay K Sharma

Consultant Neurologist

National University HospitalSingapore

[email protected]


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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.

1. Cull DL et al.Ann Vasc Surg1999;13:73-76.

2. Zardi EM et al. Eur J Neurol2006;13:423-424.

3. Tsai CF et al.J Neuroimaging2005;15:50-56.


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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.


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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.


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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 internalcarotid (ICA) and external carotid (ECA) arteries were seen inall 3 patients.

CCA occlusions were also seen on CT angiography of neck(n=3)

Conventional digital subtraction angiography, performed inone case confirmed the presence of CCA thromus in onecase.


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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


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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.


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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).



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.


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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.




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Some salient features

All 3 patients had a history of atrial fibrillation andhypertension

Blood pressure was lowered with nicardipine andmaintained in the systolic range of 160 180 mm

Hg range during the IV-TPA infusion andimmediately thereafter.

All the patients were kept in the head-down (flat)position.1

1. Wojner-Alexander AW et al. Neurology2005;64:1354-1357.


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Some salient features

At 2 hours after IV-TPA bolus, TCD showed complete proximalMCA recanalization in 2 cases despite persistent occlusions ofthe proximal CCA/ICA.

None of our patients achieved CCA or ICA recanalization.

None of our cases showed intracerebral hemorrhage onsubsequent 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 pointsat discharge from the hospital (case 3).


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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 innature.1,2,3

We excluded dissections in the carotid arteries oraortic arch by ultrasound and other imagingmodalities (CTA or DSA).

1. Cull DL et al.Ann Vasc Surg1999;13:73-76.

2. Zardi EM et al. Eur J Neurol2006;13:423-424.3. Tsai CF et al.J Neuroimaging2005;15:50-56.


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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.

1. Gerlock AJ et al. Applications of noninvasive vascular

techniques. Philadelphia: WB Saunders;1988:88-111.


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DiscussionImportance of intracranial collaterals in CCA occlusions

When acute CCA occlusions extend into the cervical ICA,intracranial collateral flow through communicating arteriesbecomes of utmost significance.

Similar to an isolated ICA occlusion, the competence andefficiency of the circle of Willis collaterals determine theextent and severity of ischemic damage.1,2

T-occlusion of the terminal ICA carries a relatively poorprognosis with failed recanalization by systemicthrombolysis.3

Two out of three of our patients had collateral flows throughthe anterior communicating artery, and milder strokeseverity compared to the patient with CCA occlusion andtandem T-type ICA occlusion.

1. Linfante I et al. Stroke 2002 ;33:2066-2071.

2. El-Mitwalli A et al. Stroke 2002;33:99-102.3. Georgiadis D et al. Neurology2004;63:22-


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Discussion- therapeutic options

Acute thrombus in a large artery like CCArepresents a high clot-burden.

Endovascular therapy1, clot removal by

Mechanical embolectomy 2, and combinedintravenous-intra-arterial thrombolysis3,

alone or in combination, may help in

achieving recanalization in acute largeartery occlusions in acute stroke.

1. Snugg RM et al.AJNR2005;26:2591-2594.

2. Smith WS et al. Stroke 2005;36:1432-1440.

3. The IMS study investigators. Stroke 2004;35:904-

912.


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Conclusions

We have described the sonographic and imaging featuresof CCA occlusions with tandem lesions treated withintravenous 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 thromboticocclusions and accompanying tandem lesions may benefitfrom systemic thrombolysis.1,2,3

Acute CCA occlusions should not be considered to belargely associated with poor outcome and a contra-indication for IV-TPA.

1. Linfante I et al. Stroke 2002 ;33:2066-2071.

2. El-Mitwalli A et al. Stroke 2002;33:99-102.

3. Christou I et al. J Neuroimaging2002;12:119-

123.


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Contributors

Tsivgoulis Georgios, MD

Lao, Annabelle Y, MD

Flaster, Murray, MD, PhD Frey, James L MD

Malkoff, Marc D, MD

Alexandrov Andrei V, MD

35fcthrombotic Occlusion of the Common Carotid Artery 1233912120856263 2

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