Common Carotid Artery Occlusion and Retrograde Flow

8/9/2019 Common Carotid Artery Occlusion and Retrograde Flow

1/8

Journal of Diagnostic Medical Sonography

29(6) 269 –274

© The Author(s) 2013Reprints and permissions:

sagepub.com/journalsPermissions.nav

DOI: 10.1177/8756479313510402 jdms.sagepub.com

Case Study

The carotid arteries, as all other arteries in the body, are

susceptible to atherosclerotic plaque development. Not

uncommonly, there may be atheromatous plaque at the

origin of the internal carotid artery (ICA) causing a total

occlusion. Rarely, the common carotid artery (CCA) may

become occluded, often associated with ipsilateral ICA

occlusion1; however, in the case presented below, the

ipsilateral ICA and external carotid artery (ECA)

remained patent.The extracranial cerebrovascular duplex and Doppler

ultrasound protocol requires imaging the CCA, ICA,

ECA, vertebral artery (VA), and subclavian artery (SCA).

If significant pathology is demonstrated, the examination

may be expanded to include the ophthalmic arteries

(OAs). The criteria used to diagnose an occlusion typi-

cally include increased echogenicity throughout the

course of the vessel, lack of radial pulsation of the vessel,

absence of any color flow filling of the vessel, and no

detectable spectral Doppler signal throughout the

vessel.2–5

Case Report

A woman in her late 80s referred from the Stroke

Prevention Clinic presented with transient right arm

weakness that had persisted for approximately 6 hours.

The patient had a history of atrial fibrillation and was

being treated with warfarin. Laboratory analysis demon-

strated a subtherapeutic international normalized ratio

(INR) of 1.4. Therapeutic levels for this laboratory test

that monitors the relative degree of anticoagulation

should be between 2.0 and 3.0.6 At that time, her warfarin

dose was readjusted to regulate her INR into the thera-

peutic range, and she was referred for a carotid duplex

sonogram. Her past history included a mild stroke in

2004 with residual left facial asymmetry.

The carotid sonogram was performed by a registered

vascular technologist using a Philips IU 22 ultrasound

machine (Philips Healthcare, Andover, MA), with the

results interpreted by a neurologist from the Neuro

Sonography Unit. A linear probe with a 9-MHz center fre-quency was used. Two-dimensional (B-mode) examina-

tion of the left side showed multifocal plaques at the carotid

bifurcation and in the proximal ICA. Spectral Doppler

analysis demonstrated normal flow dynamics of the left

ICA (Figure 1) with normal flow hemodynamics seen in

the left CCA and ECA as well. B-mode examination of the

right side demonstrated echogenic material within the

lumen of the mid and distal CCA with multifocal plaques

at the CCA bifurcation and proximal ICA (Figure 2a,b).

Spectral Doppler analysis of the proximal right CCA dem-

onstrated a high-pulsatility to-and-fro flow with low veloc-

ity, typical of a flow waveform proximal to an occlusion

(Figure 3). No flow was detected by color, power, or spec-tral Doppler in the mid and distal segments of the CCA

(Figure 4), even with the spectral Doppler sample volume

box size increased. Color Doppler flow assessment of the

10402 JDMXXX10.1177/8756479313510402Journal of DiagnosticMedica l Sonography Whiteand Chakraborty2013

1The Ottawa Hospital, Ottawa, ON, Canada

Corresponding Author:

Megan A. White, BMRSc, RDMS, RVT, CRGS, CRVS, Medical Imaging,

The Ottawa Hospital, 1053 Carling Avenue, Ottawa, ON K1Y4E9,

Canada.

Email: [email protected]

Common Carotid Artery Occlusion With Retrograde Flow in the InternalCarotid Artery: A Case Report

Megan A. White, BMRSc, RDMS, RVT, CRGS, CRVS1,

and Santanu Chakraborty, MRCP, FRCR1

Abstract

In most cases of common carotid artery (CCA) occlusion, the internal carotid artery (ICA) is also occluded. This casepresents a patient with a patent ICA distal to a thrombotic CCA occlusion, likely secondary to cardiac embolization

related to chronic atrial fibrillation, with retrograde filling of the extracranial ICA via intracranial collateral flows.

Keywords

CCA occlusion, retrograde ICA, antegrade ECA, Doppler


2/8

270 Journal of Diagnostic Medical Sonography 29(6)

ICA demonstrated retrograde blood flow. Spectral Doppler

analysis confirmed retrograde ICA flow with a peak sys-

tolic velocity of only 14 cm/s. Color flow assessment of the

ECA showed antegrade flow, which was confirmed by

spectral Doppler; the identification of the ECA was con-

firmed by the presence of an arterial branch and visualiza-tion of a temporal tap response (Figure 6). Antegrade flow

signals were noted in the vertebral arteries bilaterally.

Throughout the spectral Doppler evaluation, note was

made of an irregular heart rhythm (Figures 3 and 5).

Based on the results of the carotid sonogram, the

patient was sent for a computed tomography (CT) scan of

the head without intravenous (IV) contrast and CT angi-

ography (CTA) of the neck and head with IV contrast.

The CT and CTA were performed using a General Electric

Figure 2. (a) B-mode image of the right carotid arterybifurcation region demonstrating evidence of a diffuseatherosclerotic plaque with heterogeneous echogenicity. (b)Transverse B-mode image of the distal right common carotidartery showing a more homogeneous, somewhat hypoechoicmaterial characteristic of thrombus within the lumen of thevessel.

Figure 3. Color and spectral Doppler evaluation of theproximal right common carotid artery showing low velocitieswith a pulsatile, to-and-fro flow waveform characteristic of amore distal occlusion.

Figure 4. Color and spectral Doppler evaluation of the distalright common carotid artery showing a complete absenceof flow. Note the increased sample volume size to maximizesensitivity to any low flow signals.

Figure 1. Color and spectral Doppler evaluation of the leftinternal carotid artery showing normal velocities and a normallow-resistance antegrade flow pattern.


3/8

White and Chakraborty 271

(GE, Piscataway, New Jersey) 64-slice scanner following

the departmental stroke protocol. The CT head scan dem-

onstrated no acute abnormality of the parenchyma with

evidence of possible chronic ischemic microvascular dis-ease. The CTA of the neck showed left-sided patency

with no significant narrowing. Occlusion of the right

CCA in the mid and distal segments was demonstrated

with the cutoff of IV contrast; more distally, the patency

of the ICA and ECA was demonstrated by the presence of

IV contrast (Figure 7). The intracranial portion of the

CTA showed patency of the anterior communicating

artery (AComA); the posterior communicating arteries

(PComA) were not seen (Figure 8a,b). While the CTA did

not provide direction of flow information, it can be seen

that in the right ECA and its branches, the contrast is not

as concentrated and is less dense, which indirectly sup-

ports the findings of delayed filling via the right ICA.

With this alternate collateral pathway for blood flow, thecontrast media required additional time to reach the ECA,

causing the contrast to be less dense compared with the

ICA and contralateral arteries.

Additional diagnostic studies for the patient included

an electrocardiogram (ECG), which confirmed the diag-

nosis of atrial fibrillation, and an echocardiogram. The

echocardiogram showed severe left atrial dilation and left

ventricular systolic dysfunction; aortic atheromatous dis-

ease was also visualized.

Given that the patient’s right-sided symptoms were

slowly resolving and believed to be related to a thrombo-

embolic event in the left cerebral hemisphere, with her

INR now at a therapeutic level, no significant changeswere made in her treatment plan from her previous visit

to the Stroke Prevention Clinic. The impression of the

Neuro Sonography Unit staff was that she was asymp-

tomatic with regard to the right CCA occlusion, and no

interventions were warranted at this time. The patient

was scheduled for follow-up with the Stroke Prevention

Clinic and advised to follow up with her family physi-

cian to monitor her INR and adjust her warfarin dosage

appropriately.

Figure 6. Color and spectral Doppler image of the rightexternal carotid artery (ECA) confirming antegrade flow.Note the branch vessel in the color Doppler image and thetemporal tap velocity fluctuations in the spectral display, bothcharacteristic of the ECA.

Figure 5. Color and spectral Doppler evaluation ofthe proximal right internal carotid artery (ICA) showinglow retrograde velocities with a blunted, damped flowwaveform. Note the antegrade flow direction shown bycolor Doppler in the external carotid artery just superiorto the ICA in the image.

Figure 7. Computed tomography arteriogram of the rightcommon carotid artery and bifurcation in the sagittal planedemonstrating the cutoff at the proximal common carotidartery (black arrow) and the patency of the internal carotidartery and external carotid artery (arrowheads).


4/8


The patient returned two months later to the Stroke

Prevention Clinic. In that time interval, there had been

no recurrence of the transient right arm weakness. Aside

from the mild left facial flattening attributed to the prior

remote (2004) ischemic event, examination of the cra-

nial nerves revealed no significant injury. The patient

remained on warfarin with a therapeutic INR.

In the following months, however, this patient had

multiple ischemic events and ultimately presented with

delirium and dementia, with a subtherapeutic INR of 1.3.

She underwent a CT head scan, which demonstrated an

acute infarction of the left middle cerebral and posterior

cerebral arterial territories involving the left frontal, pari-

etal, temporal, and occipital lobes. There was no hemor-rhagic transformation or midline shift, but the patient did

succumb to her ischemic events. All diagnostic studies

indicated that the final stroke the patient had occurred in

the left cerebral hemisphere secondary to thromboem-

bolic disease, and the right CCA occlusion was not a

source of the embolic event(s) that led to the patient’s

death.

Discussion

Sonographic examination of the CCA and its major

branches, the ICA and ECA, has proven effective for theassessment of stenosis and flow.2,7 For cases of CCA

occlusion, color Doppler and spectral Doppler analysis

have a reported 97% accuracy, 91% sensitivity, and 99%

specificity.7 Sonography not only demonstrates patency,

or lack thereof, in the ICA distal to a CCA occlusion but

also allows determination of the direction of flow.8 The

anatomical location of the CCA makes it a relatively easy

vessel to access, and if an occlusion is visualized, the

Doppler pulse repetition frequency (PRF) can be manipu-

lated to allow for detection of any low-velocity flow dis-

tal to the occlusion.2,9 It is not only color and spectral

Doppler analysis that contributes to the diagnosis of CCA

occlusion. Using B-mode ultrasound imaging, the lumi-nal contents can be imaged, suggesting (but not defini-

tively proving) a complete vessel occlusion.1 The

additional advantages of sonography in examining the

carotid arteries are those frequently referred to: it is non-

invasive, is relatively easy to use (especially in unstable

patients), provides hemodynamic as well as anatomic

data, and uses no ionizing radiation or intraluminal

contrast.1,10

CCA occlusion is detected in 2% to 5% of the popula-

tion with cerebrovascular disease.2,3,7,9,10–13

There is little

information about the clinical features, neurologic symp-

toms, etiologies, and pathogenesis of CCA occlusion.

3

Patients who have CCA occlusion can present clinically

with a wide range of symptoms, from asymptomatic to

severe stroke, and CCA occlusion is not necessarily asso-

ciated with cerebral infarction or even measurable brain

dysfunction.3,10–12 There are many potential causes of

CCA occlusion such as atherosclerosis, giant cell arteri-

tis, fibromuscular dysplasia, thrombocytosis, dissection

of the CCA or aortic arch, aortic arch aneurysm, iatro-

genic occlusion, mediastinal tumors, cardiac embolism,

irradiation, trauma, and idiopathic occlusion (of unknown

Figure 8. (a) Intracranial computed tomography arteriogram(CTA) showing a patent anterior communicating artery(AComA; black arrow), which is clearly visible and dilatedcompared with its normal state. (b) Intracranial CTA showingthe circle of Willis, again demonstrating a patent, clearlyvisible AComA, with nonvisualization of either posteriorcommunicating artery (PComA). The white arrows denotethe locations where the PComAs should be seen.


5/8

White and Chakraborty 273

origin).1,2,5,9–11

Of these, atherosclerosis has been shown

to be the most common cause.2,3,5,9,11

In the case pre-

sented, the presence of atrial fibrillation significantly

raises the likelihood of a cardiac embolus, a diagnosis

supported by the sonographic evidence of thrombus

throughout the vessel with very little or no evidence of

any atherosclerotic disease on either side.3

The triggering or initial site of the origin of the CCA

occlusion can vary. The occlusion may begin in the proxi-

mal CCA, with antegrade propagation, or the occlusion

may begin at the carotid bifurcation with retrograde prop-

agation back to the vessel origin.3,4,7,11

The thrombus

typically will extend to the level of the next large vessel

reentry point.3,4,7

The prevalence of CCA occlusion tends

to be slightly higher on the left side compared with the

right, possibly attributable to the differences in arterial

length or the direct relationship the left CCA has to the

aortic arch.10–12

CCA occlusion is most frequently associated withipsilateral ICA and/or ECA occlusion. Infrequently,

patency is maintained in the distal vessels.1,9

Most often

in these cases, ICA perfusion is maintained by flow from

collateral circulation through proximal branches filling

the ECA.1,8,13

In the least common scenario, rarely seen,

retrograde flow can be found in the ICA, being perfused

from cerebral circulation, and then into the ECA.1,3,8

Combining the results from the carotid duplex study

and the CTA, a blood flow pathway for the case presented

can be suggested. Given the complete occlusion of the

right CCA, it is likely that the blood flow pathway is ante-

grade up the left ICA and through the carotid siphon into

the anterior cerebral artery, then across the AComA andreversed through the right anterior cerebral artery, ulti-

mately reversing through the right carotid siphon and ICA

to supply the right ECA (Figure 9). A potential alternate

pathway is retrograde collateral filling of the intracranial

ICA via the basilar artery and PComAs7,8; however, in the

case presented, the posterior circulation was seen to be

noncontributory due to an apparent functionally incom-

plete circle of Willis, with very small or hypoplastic

PComAs, forcing the remaining patent anterior circulation

to be the source for collateral flow. This would also explain

the severity of the patient’s symptoms and ultimate death

secondary to severe stroke. With both anterior hemispherescompletely dependent on flow in the left carotid artery sys-

tem, any disruption of that flow such as would occur with

a significant thromboembolic event—and with a right

CCA occlusion, any cerebral emboli would go through the

left carotid system—would severely impair flow to the

entire anterior cerebral circulation.

When analyzing the vessels distal to a CCA occlusion,

it is important to note not only the presence but also the

direction and velocity of flow. It will be found that distal to

the occlusion, the velocities of the ICA and ECA, if patent,

are significantly lower compared with the patent contralat-

eral side.14

This does not necessarily indicate that the there

is insufficient collateral flow but reflects that blood flow

velocity is dependent not only on the arterial pressure but

also on the degree of peripheral resistance. In the case pre-

sented, the velocity in the retrograde ICA was significantly

lowered, with a peak systolic velocity of only 14 cm/s and

a blunted, damped waveform. As explained by Dermitzakis

et al,

7

who observed flow reversal in the contralateral ICAafter endarterectomy, the blood flow to the brain from the

contralateral side is unobstructed and creates a pressure

difference via the collateral pathway of the circle of Willis

that would be sufficient to overcome the resistance of the

ipsilateral side and produce retrograde flow in the ICA,

similar to a subclavian steal syndrome.11,13

Both circum-

stances might be considered a steal phenomenon where

blood is “stolen” from the intracranial circulation to per-

fuse an extracranial territory.13

Figure 9. Schematic drawing of the collateral pathway forblood flow in the case presented. Coming off the aortic arch,there is antegrade flow through the left common carotidartery (CCA) and internal carotid artery (ICA) extracranially,which flows through the intracranial ICA into the left anteriorcerebral artery (ACA). Blood flow crosses to the righthemisphere via the anterior communicating artery (AComA),with retrograde flows in the right ACA filling the intracranialand extracranial ICA and ultimately leading to diminished butantegrade flow in the right external carotid artery (ECA).The vertebrobasilar system could not provide collateralflows because of the functional absence of both posteriorcommunicating artery (PComAs) (dashed lines). BA, basilarartery; MCA, middle cerebral artery; PCA, posterior cerebral

artery; VA, vertebral artery.


6/8


With CCA occlusion being a relative rarity, treatment

typically is planned on an individual case basis.13

Most

of the signs and symptoms are related to those of tran-

sient ischemic attacks (TIAs) and stroke. Depending on

the source and the degree of the occlusion, appropriate

management can be provided and treatment plan devel-

oped. A treatment plan may be appropriate becausemany of these patients are at risk for further TIAs or

stroke because of associated hemodynamic distur-

bances, cerebral or ocular hypoperfusion, or emboli

from the stump of the occlusion.7,13

It is imperative to

note the patency and flow direction of the distal vessels

for treatment planning, as patients who present with iso-

lated CCA occlusion typically have a better outcome

than those with an associated ICA occlusion.2,3

Depending on the circumstances, the treatment plan

may vary from a surgical approach, revascularization

from a bypass graft or thrombectomy, or medical man-

agement with anticoagulation.

3,9

Conclusion

Sonography is a very valuable tool to assess the carotid

arteries, especially due to its ability to provide functional,

hemodynamic information as well as anatomic data.13

In

the event of a CCA occlusion, it is particularly important

to note the patency of the more distal vessels, with atten-

tion to the analysis of any distal flow patterns.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect

to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research,

authorship, and/or publication of this article.

References

1. Nassauer Mónica A, Germano A, Biscoito L, Baptista

M: Common carotid artery occlusion Doppler ultra-

sound findings in two patients. J Diagn Med Sonography

2005;21(6):502–508.

2. Chang Y, Shin-Kuang L, Ryu S, Wai Y: Common carotid

artery occlusion: evaluation with duplex sonography. Am J

Neuroradiol 1995;16:1099–1105.

3. Tsai C, Jeng J, Lu C, Yip P: Clinical and ultrasound mani-

festation in major causes of common carotid artery occlu-

sion. J Neuroimaging 2005;15(1):50–56.

4. Blackshear WM, Phillips DJ, Bodily KC, Strandness DE:Ultrasonic demonstration of external and internal carotid

patency with common carotid occlusion: a preliminary

report. J Am Heart Assoc 1980;11(3):249–252.

5. Riles T, Imparato A, Posner M, Bert MD, Eikelboom B:

Common carotid occlusion assessment of the distal vessels.

Ann Surg 1984;199(3):363–366.

6. American Association of Clinical Chemistry: PT and INR.

http://labtestsonline.org/understanding/analytes/pt/tab/test.

Accessed July 21, 2013.

7. Dermitzakis I, Minardos I, Kampanarou M, Mitakou D:

Color duplex sonography of occlusion of the common

carotid artery with reversed flow in the extracranial internal

carotid artery. J Clin Ultrasound 2002;30(6):388–391.

8. Dashefsky S, Cooperberg P, Harrison P, Reid J, Araki D:Total occlusion of the common carotid artery with pat-

ent internal carotid artery identification with color flow

Doppler imaging. J Ultrasound Med 1991;10:417–421.

9. Cull D, Hansen J, Taylor S, Langan E, Snyder B, Coffey C:

Internal carotid artery patency following common carotid

artery occlusion: management of the asymptomatic patient.

Ann Vasc Surg 1999;13(1):73–76.

10. Verbeeck NY, Vazquez Rodriguez C: Patent internal and

external carotid arteries beyond an occluded common

carotid artery: report of a case diagnosed by color Doppler.

Belgian J Radiol 1999;82:219–221.

11. Levine S, Welch KMA: Common carotid artery occlusion.

Neurology 1989;39:178–186.

12. Belkin M, Mackey W, Pessin M, Caplan L, O’Donnell T:

Common carotid artery occlusion with patent internal and

external carotid arteries: diagnosis and surgical manage-

ment. J Vasc Surg 1993;17(6):1019–1028.

13. Pretre R, Kalangos A, Bednarkiewica I, Faidutti B:

Reversed flow in the internal carotid artery after occlusion

of the common carotid artery. Thorac Cardiovasc Surg

1994;42:358–360.

14. Zbornikova V, Lassvik C: Common carotid artery occlu-

sion: haemodynamic features, duplex and transcranial

Doppler assessment and clinical correlation. Cerebrovasc

Dis 1991;1:136–141.


7/8

Article: Common Carotid Artery Occlusion With

Retrograde Flow in the Internal Carotid Artery

Authors: Megan A. White, BMRSc, RVT, CRGS, CRVS,

Santanu Chakraborty, MD, MRCP

Category: Vascular

Credit: 1.0 SDMS CME Credit

Objectives: After studying the article entitled “Common

Carotid Artery Occlusion With Retrograde Flow in the

Internal Carotid Artery,” you will be able to:

1. Optimize machine settings for detection of carotidartery occlusion

2. Apply diagnostic criteria for total carotid artery

occlusions

3. Appropriately document hemodynamics distal to a

common carotid artery (CCA) occlusion

1. The most common cause of CCA occlusion is

a. Dissection

b. Cardiac embolism

c. Atherosclerosis

d. Giant cell arteritis

2. The prevalence of CCA occlusion in patients with

carotid artery atherosclerotic disease is

a. 8%

3. The overall accuracy of duplex sonography in

diagnosing total CCA occlusion isa.


8/8


c. Amaurosis fugax

d. Any of a variety of symptoms, or may be

asymptomatic

5. The most common site of atherosclerotic dis-

ease in the extracranial cerebrovascular system

is thea. Origin of the CCA

b. Origin of the ICA

c. Distal ICA

d. Proximal ECA

6. Duplex sonographic criteria to diagnose a total

CCA occlusion typically include all of the follow-

ing except

a. An anechoic vessel lumen

b. Absence of color Doppler filling

c. Absence of a spectral Doppler signal

d. Lack of radial pulsatility of the vessel

7. To document the absence of a spectral Doppler

signal in an occluded CCA, machine settings

should be made for all of the following except

a. Increased Doppler gain

b. Decreased pulse repetition frequency

c. Decreased sample volume size

d. Increased probe transmit frequency

8. An occluded CCA is most frequently associated

with

a. A disease-free contralateral CCA

b. A widely patent ipsilateral ICA and ECAc. An occluded ipsilateral ICA

d. A patent ICA with collateral filling via proxi-

mal ECA branches

9. To-and-fro flow in a proximal common carotid

artery is usually characteristic of

a. Aortic stenosis

b. More distal CCA occlusion

c. Isolated ipsilateral ECA occlusion

d. Severe contralateral CCA obstruction

10. Clinical outcomes for patients with a CCA occlu-sion are usually better when

a. The ipsilateral ICA is patent

b. The ipsilateral ICA is occluded, preventing

emboli

c. The ipsilateral ECA is occluded

d. The contralateral CCA is also occluded

Documents

Common Carotid Artery Occlusion and Retrograde Flow