510402

research-article2013

JDMXXX10.1177/8756479313510402Journal of Diagnostic Medical SonographyWhite and Chakraborty

Case Study

Common Carotid Artery Occlusion

With Retrograde Flow in the Internal
Carotid Artery: A Case Report

Journal of Diagnostic Medical Sonography

29(6) 269274
The Author(s) 2013
Reprints and permissions:
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DOI: 10.1177/8756479313510402
jdms.sagepub.com

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 case
presents 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
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 typically 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.25

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 demonstrated 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 therapeutic 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 frequency was used. Two-dimensional (B-mode) examination 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 demonstrated a high-pulsatility to-and-fro flow with low velocity, typical of a flow waveform proximal to an occlusion
(Figure 3). No flow was detected by color, power, or spectral 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
1

The 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: whitem8@rogers.com

270

Figure 1. Color and spectral Doppler evaluation of the left

internal carotid artery showing normal velocities and a normal
low-resistance antegrade flow pattern.

Journal of Diagnostic Medical Sonography 29(6)

Figure 3. Color and spectral Doppler evaluation of the

proximal right common carotid artery showing low velocities
with a pulsatile, to-and-fro flow waveform characteristic of a
more distal occlusion.

Figure 4. Color and spectral Doppler evaluation of the distal

right common carotid artery showing a complete absence
of flow. Note the increased sample volume size to maximize
sensitivity to any low flow signals.

Figure 2. (a) B-mode image of the right carotid artery

bifurcation region demonstrating evidence of a diffuse
atherosclerotic plaque with heterogeneous echogenicity. (b)
Transverse B-mode image of the distal right common carotid
artery showing a more homogeneous, somewhat hypoechoic
material characteristic of thrombus within the lumen of the
vessel.

ICA demonstrated retrograde blood flow. Spectral Doppler

analysis confirmed retrograde ICA flow with a peak systolic 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 confirmed by the presence of an arterial branch and visualization 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 angiography (CTA) of the neck and head with IV contrast.
The CT and CTA were performed using a General Electric

White and Chakraborty

271

Figure 5. Color and spectral Doppler evaluation of

the proximal right internal carotid artery (ICA) showing
low retrograde velocities with a blunted, damped flow
waveform. Note the antegrade flow direction shown by
color Doppler in the external carotid artery just superior
to the ICA in the image.
Figure 7. Computed tomography arteriogram of the right
common carotid artery and bifurcation in the sagittal plane
demonstrating the cutoff at the proximal common carotid
artery (black arrow) and the patency of the internal carotid
artery and external carotid artery (arrowheads).

Figure 6. Color and spectral Doppler image of the right

external carotid artery (ECA) confirming antegrade flow.
Note the branch vessel in the color Doppler image and the
temporal tap velocity fluctuations in the spectral display, both
characteristic of the ECA.

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

the departmental stroke protocol. The CT head scan demonstrated no acute abnormality of the parenchyma with
evidence of possible chronic ischemic microvascular disease. 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 supports the findings of delayed filling via the right ICA.
With this alternate collateral pathway for blood flow, the
contrast 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 diagnosis of atrial fibrillation, and an echocardiogram. The
echocardiogram showed severe left atrial dilation and left
ventricular systolic dysfunction; aortic atheromatous disease was also visualized.
Given that the patients right-sided symptoms were
slowly resolving and believed to be related to a thromboembolic event in the left cerebral hemisphere, with her
INR now at a therapeutic level, no significant changes
were 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 asymptomatic 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 physician to monitor her INR and adjust her warfarin dosage
appropriately.

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Journal of Diagnostic Medical Sonography 29(6)

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, parietal, temporal, and occipital lobes. There was no hemorrhagic 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 thromboembolic disease, and the right CCA occlusion was not a
source of the embolic event(s) that led to the patients
death.

Discussion

Figure 8. (a) Intracranial computed tomography arteriogram

(CTA) showing a patent anterior communicating artery
(AComA; black arrow), which is clearly visible and dilated
compared with its normal state. (b) Intracranial CTA showing
the circle of Willis, again demonstrating a patent, clearly
visible AComA, with nonvisualization of either posterior
communicating artery (PComA). The white arrows denote
the locations where the PComAs should be seen.

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 cranial nerves revealed no significant injury. The patient
remained on warfarin with a therapeutic INR.

Sonographic examination of the CCA and its major

branches, the ICA and ECA, has proven effective for the
assessment 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 manipulated to allow for detection of any low-velocity flow distal 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 luminal contents can be imaged, suggesting (but not definitively proving) a complete vessel occlusion.1 The
additional advantages of sonography in examining the
carotid arteries are those frequently referred to: it is noninvasive, 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 population with cerebrovascular disease.2,3,7,9,1013 There is little
information about the clinical features, neurologic symptoms, 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 associated with cerebral infarction or even measurable brain
dysfunction.3,1012 There are many potential causes of
CCA occlusion such as atherosclerosis, giant cell arteritis, fibromuscular dysplasia, thrombocytosis, dissection
of the CCA or aortic arch, aortic arch aneurysm, iatrogenic occlusion, mediastinal tumors, cardiac embolism,
irradiation, trauma, and idiopathic occlusion (of unknown

White and Chakraborty

origin).1,2,5,911 Of these, atherosclerosis has been shown
to be the most common cause.2,3,5,9,11 In the case presented, 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 proximal CCA, with antegrade propagation, or the occlusion
may begin at the carotid bifurcation with retrograde propagation 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.1012
CCA occlusion is most frequently associated with
ipsilateral 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 antegrade up the left ICA and through the carotid siphon into
the anterior cerebral artery, then across the AComA and
reversed through the right anterior cerebral artery, ultimately 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 incomplete 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 patients symptoms and ultimate death
secondary to severe stroke. With both anterior hemispheres
completely dependent on flow in the left carotid artery system, any disruption of that flow such as would occur with
a significant thromboembolic eventand with a right
CCA occlusion, any cerebral emboli would go through the
left carotid systemwould 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

273

Figure 9. Schematic drawing of the collateral pathway for

blood flow in the case presented. Coming off the aortic arch,
there is antegrade flow through the left common carotid
artery (CCA) and internal carotid artery (ICA) extracranially,
which flows through the intracranial ICA into the left anterior
cerebral artery (ACA). Blood flow crosses to the right
hemisphere via the anterior communicating artery (AComA),
with retrograde flows in the right ACA filling the intracranial
and extracranial ICA and ultimately leading to diminished but
antegrade flow in the right external carotid artery (ECA).
The vertebrobasilar system could not provide collateral
flows because of the functional absence of both posterior
communicating artery (PComAs) (dashed lines). BA, basilar
artery; MCA, middle cerebral artery; PCA, posterior cerebral
artery; VA, vertebral artery.

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

are significantly lower compared with the patent contralateral 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 presented, 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 ICA
after 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 circumstances might be considered a steal phenomenon where
blood is stolen from the intracranial circulation to perfuse an extracranial territory.13

274
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 transient ischemic attacks (TIAs) and stroke. Depending on
the source and the degree of the occlusion, appropriate
management can be provided and treatment plan developed. A treatment plan may be appropriate because
many of these patients are at risk for further TIAs or
stroke because of associated hemodynamic disturbances, 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 isolated 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 management 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 attention 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 Mnica A, Germano A, Biscoito L, Baptista
M: Common carotid artery occlusion Doppler ultrasound findings in two patients. J Diagn Med Sonography
2005;21(6):502508.

Journal of Diagnostic Medical Sonography 29(6)

2. Chang Y, Shin-Kuang L, Ryu S, Wai Y: Common carotid
artery occlusion: evaluation with duplex sonography. Am J
Neuroradiol 1995;16:10991105.
3. Tsai C, Jeng J, Lu C, Yip P: Clinical and ultrasound manifestation in major causes of common carotid artery occlusion. J Neuroimaging 2005;15(1):5056.
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):249252.
5. Riles T, Imparato A, Posner M, Bert MD, Eikelboom B:
Common carotid occlusion assessment of the distal vessels.
Ann Surg 1984;199(3):363366.
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):388391.
8. Dashefsky S, Cooperberg P, Harrison P, Reid J, Araki D:
Total occlusion of the common carotid artery with patent internal carotid artery identification with color flow
Doppler imaging. J Ultrasound Med 1991;10:417421.
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):7376.
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;82:219221.
11. Levine S, Welch KMA: Common carotid artery occlusion.
Neurology 1989;39:178186.
12. Belkin M, Mackey W, Pessin M, Caplan L, ODonnell T:
Common carotid artery occlusion with patent internal and
external carotid arteries: diagnosis and surgical management. J Vasc Surg 1993;17(6):10191028.
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;42:358360.
14. Zbornikova V, Lassvik C: Common carotid artery occlusion: haemodynamic features, duplex and transcranial
Doppler assessment and clinical correlation. Cerebrovasc
Dis 1991;1:136141.

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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 carotid
artery 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. <1%
b. 2%5%
c. 5%7%
d. >8%
3. The overall accuracy of duplex sonography in
diagnosing total CCA occlusion is
a. <80%
b. <90%
c. 90%95%
d. >95%
4. The typical clinical presentation of a total CCA
occlusion is
a. Stroke
b. Transient ischemic attack

276

Journal of Diagnostic Medical Sonography 29(6)

c. Amaurosis fugax
d. Any of a variety of symptoms, or may be
asymptomatic

5. The most common site of atherosclerotic disease in the extracranial cerebrovascular system
is the
a. 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 following 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 ECA
c. An occluded ipsilateral ICA
d. A patent ICA with collateral filling via proximal 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 occlusion 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