Neuroradiology (2007) 49:265–269
DOI 10.1007/s00234-006-0172-2

INTERVENTIONAL NEURORADIOLOGY

The use of intraoperative monitoring and treatment
of symptomatic microemboli in carotid artery stenting:
case report and discussion
P. S. Rangi & H. S. Markus & M. N. M. Punter & A. Clifton

Received: 18 July 2006 / Accepted: 6 October 2006 / Published online: 24 November 2006
# Springer-Verlag 2006

Abstract Carotid artery stenting is a recently introduced
treatment in symptomatic atherosclerotic carotid artery
disease with acceptable complication rates. The major risk
is perioperative embolic stroke. Transcranial Doppler
ultrasonography (TCD) can be used to identify embolic
signals and guide therapy. We present a case of symptomatic embolization in a 72-year-old female following carotid
stent deployment complicated by haemodynamic changes.
Despite concurrent dual antiplatelet medication significant
symptomatic embolization occurred even after restoration
of the blood pressure, and modulation of the rate of
embolization was achieved using dextran-40 guided by
TCD monitoring. The patient recovered from an initially
profound hemiparesis and dysphasia to minor sensory
changes. Microemboli are common following carotid artery
stenting and there appears to be a threshold phenomenon
associated with prolonged embolization and progression to
cerebral infarction. TCD can be used to detect particulate
microemboli and therefore may be useful in guiding
antithrombotic therapy in this setting. Dextran-40 has been
shown to reduce the embolic load following carotid
endarterectomy and was used to good effect in this patient
in terms of both embolic load and clinical outcome. This is
the first case of embolization following carotid stenting
successfully treated with dextran-40, and offers a further
P. S. Rangi (*) : A. Clifton
Department of Neuroradiology, Atkinson Morley Wing,
St Georges Hospital,
Blackshaw Road,
Tooting, London, UK
e-mail: permrangi@hotmail.com
H. S. Markus : M. N. M. Punter
Centre for Clinical Neuroscience,
St Georges University of London,
Cranmer Terrace, London SW17 ORE, UK

option for therapeutic intervention in microembolism detected
by TCD and stresses the importance of perioperative
monitoring of embolic load for postoperative stroke risk.
Keywords Dextran . Carotid . Stent . Stroke

Introduction
Until recently, the only means beyond medical intervention
for secondary stroke prevention in patients with symptomatic atherosclerotic carotid artery stenosis has been carotid
endarterectomy (CEA). Interventional radiology offers a
recently introduced means of secondary stroke prevention
with endovascular carotid artery stenting (CAS), with or
without adjuvant angioplasty. This new strategy is becoming increasingly accepted as its advantages and efficacy are
being recognized. There have been several large multicentre
trials, which have demonstrated the role for intervention in
selected patients with significant symptomatic extracranial
atherosclerotic carotid disease [1, 2], with acceptable
complication rates and durable efficacy. It is increasingly
accepted that endovascular interventional radiology provides an alternative strategy for treating such patients. The
current evidence would suggest that the level of efficacy of
the endovascular approach is at least of the same order,
with comparable primary clinical end-points, namely death
or stroke [3–5]. In addition, the endovascular approach has
several immediate advantages that are well established and
documented.
The endovascular route has the same major complication
as CEA, that of causing perioperative stroke within the
carotid territory [5, 6] despite intraprocedural antiplatelet
and anticoagulation agents. Stroke in the periprocedural
phase is thought to be due to one of two mechanisms, either

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Neuroradiology (2007) 49:265–269

singly or in combination. The commonest mechanism is
due to thromboembolism, from either rupture/fragmentation
of the atherosclerotic plaque at the time of balloon or stent
deployment or from secondary thrombus formation which
can occur either during the procedure or afterwards for up
to 48 hours. These risks might be reduced by intraprocedural deployment of a cerebral protective device [7,
8] and appropriate antiplatelet agents, with aspirin in
combination with clopidogrel and intraprocedural heparinization. The second mechanism for perioperative ischaemia/
stroke is from mechanical haemodynamic occlusion or
compromise in antegrade flow. Patients treated by CEA
are also prone, particularly in the first 6 hours postoperatively, to thromboembolism with consequential graft
failure. Transcranial Doppler ultrasonography (TCD) is
well established in CEA-treated patients for the detection
of microemboli [9, 10] and subsequent progression to
thromboembolic stroke in patients with sustained embolization, and thus can be utilized to guide management of
such a complication. The role of dextran-40 after CEA in
patients with microembolic complications is equally well
documented [11]. We present a case of significant symptomatic microembolism after CAS, detected with periprocedural TCD, and subsequent effective reversal of
ischaemic symptoms with administration of intravenous
dextran-40.

Case report
A 72-year-old female patient, with a previous history of
angina and percutaneous transluminal coronary angioplasty,
presented with a single transient ischaemic attack referable
to the left internal carotid artery (ICA) territory. MR
imaging showed no evidence of an acute ischaemic lesion.
Extracranial MR angiography demonstrated an ipsilateral
severe (>90%) stenosis of the proximal left ICA. CAS was
planned for her symptomatic carotid artery stenosis.
The patient was treated prior to the procedure with oral
aspirin 75 mg daily and enrolled into a study comparing
optimal methods for preventing thromboembolism during
stent deployment. This was a double-blind randomized trial
of antiplatelet therapy comparing the additional efficacy of
intravenous S-nitrosoglutathione (GSNO) or oral clopidogrel
with placebo. Conventional catheter angiography via a right
femoral artery puncture at the time of stenting confirmed the
proximal high-grade left ICA stenosis (Fig. 1). The patient
received intraoperative full heparinization (to more than
twice baseline activated clotting time) prior to commencement of stent deployment. A cerebral protection device
(Boston Scientific) was deployed approximately 4 cm
superior to the level of the carotid stenosis within the high
cervical ICA, and predilatation with a 3-mm balloon was

Fig. 1 Digital subtraction angiogram of the left common carotid
artery, confirming >90% stenosis of the proximal left common carotid
artery (arrows)

performed uneventfully. A carotid wall stent (Boston
Scientific) was deployed across the stenosis, during which
the patient became mildly hypotensive with accompanying
mild reduced mean flow in the left middle cerebral artery,
demonstrated on TCD, but remained clinically asymptomatic.
The stent was dilated to the ICA diameter of 5 mm with
accompanying marked reduction in mean middle cerebral
artery velocity as illustrated on TCD, and reduced blood
pressure to 84/36 mmHg, from a preinterventional reading of
135/65 mmHg, presumably related to distension of the carotid
bulb. The patient clinically deteriorated, developing a right
hemiparesis and dysphasia. Intravenous atropine (300 μg) was
administered, with a prompt increment in blood pressure. A
left common carotid artery angiogram at this stage demonstrated cessation of flow within the left ICA. The filter was

Neuroradiology (2007) 49:265–269

rapidly removed and found to contain thrombus, following
which flow within the left ICA was restored with accompanying clinical recovery of the patient. A subsequent angiogram at this point showed several filling defects within the
stent, presumed to represent acute thrombus (Fig. 2).
The patient was transferred to the ICU. Shortly after
arrival her blood pressure dropped to 88/32 mmHg, and she
once more became symptomatic, developing dysphasia,
dysarthria and a grade 2–3/5 paresis of the right arm and
hand. At this stage it was unclear if the primary mechanism

267

for her neurological symptoms was hypotension or cerebral
embolism, or a combination of the two mechanisms.
Breaking the trial randomization code revealed the patient
was on GSNO and due to the potential hypotensive effect
of GSNO, this infusion was stopped and 300 mg of
clopidogrel given orally. The patient was additionally
infused with volume expanders and noradrenaline in an
effort to increase her systolic blood pressure and reduce any
watershed ischaemic events. The blood pressure was
rapidly stabilized towards her baseline level. TCD showed
numerous microembolic signals (MES) per screen (Fig. 3)
with the rate rising to a peak of seven per minute and a total
of 31 recorded in the first 20 minutes of the second hour
after stent deployment. Carotid duplex examination
revealed that there was good flow in the stent and left
ICA. In view of the numerous MES the patient was
commenced on dextran-40, titrated at 20 ml over 1 hour
for 2 hours. This was subsequently accompanied by a rapid
reduction in the number of MES to 20 over 1 hour. The
patient’s condition continued to resolve, with only residual
slight paresis and reduced sensation involving the right
ulnar three fingers at 1 hour after the commencement of
dextran. By 24 hours after the commencement of the
dextran infusion the patient showed further improvement
with residual mild reduced sensation over the ulnar three
fingers, which persisted at discharge. MR imaging 48 hours
after intervention showed two tiny focal cortical infarcts
(Fig. 4).

Discussion
The role and potential advantages of endovascular treatment of symptomatic atherosclerotic carotid disease is
increasingly recognised. The endovascular route is becom-

Fig. 2 After stent deployment and EPI filter removal digital
subtraction angiogram of the left common carotid artery illustrates
good resultant effective calibre at the level of the stent with good
patency. However, there are filling defects on the surface of the stent
indicating thrombus (arrows)

Fig. 3 TCD spectral display representing 5–seconds of cerebral blood
flow in the middle cerebral artery. Demonstrates baseline artefact
(double-headed arrows) and three high-intensity MES (single arrows)

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Fig. 4 Axial FLAIR image (a; TR 1100 ms, TE 140 ms) and DW
image (b; TR 4430 ms, TE 90 ms) show several foci of cortical high
signal, consistent with recent microembolic cortical infarcts (arrows)

ing not only a viable treatment option; it is not infrequently
the only option, particularly in patients with coexisting
morbidity. The major clinical end-points of endovascular
stenting are comparable with those of CEA [3]. The Carotid
and Vertebral Artery Transluminal Angioplasty Study
(CAVATAS) [12] gives the greatest information regarding
efficacy of endovascular treatment to date. The recurrence
of significant stenosis (≥70%) for treated carotid artery
disease with angioplasty alone is in the order of threefold
higher compared with CEA at 1 year. However, of these
patients only a small percentage (15%) are symptomatic at
1 year, and none of these in CAVATAS went on to have a

Neuroradiology (2007) 49:265–269

significant cerebrovascular event, defined as a reduction in
life-style or death. Early data suggest that stenting either
alone or in combination with angioplasty in the first month
after the intervention is associated with a lower incidence of
significant stenosis. A number of trials are currently
evaluating the efficacy of carotid stenting in the medium
and long term including the International Carotid Stenting
Study (ICSS) [13]. Results of the recent SPACE (Stenting
Protected Angioplasty versus Carotid Endarterectomy) trial
were presented at the European Stroke Conference (May
2006). Although it showed a small trend towards benefit of
CEA, the trial was unable to show any clear benefit of one
treatment option over the other.
The major complication from the treatment of atherosclerotic extracranial carotid artery disease, whether by CEA or
CAS, is thromboembolism. This is a relatively frequent
occurrence during such treatments, with a significantly higher
incidence during CAS, in the order of fourfold [9]. Microemboli can be detected using TCD and there is a threshold
phenomenon associated with particulate microemboli within
the cerebral circulation and consequential progression to
symptomatic ischaemia/infarction, which is preceded by a 1to 2-hour phase of sustained increased embolization. This
can be an effective surrogate marker for eventual progression to ischaemic stroke, thus highlighting the potential for
prophylactic intervention [10, 11]. Levi et al. [10] demonstrated that TCD can be used to evaluate the number of MES
events in a given time interval after CEA. MES detected
using TCD can be effectively used to guide treatment in
conjunction with the clinical status. Vulnerable patients can
be identified perioperatively, and appropriate intervention
initiated. The role of dextran-40 in reducing the frequency of
MES is supported by the work of Lennard et al. [11]. The
role for both monitoring with TCD and subsequent
intervention with dextran is well established in patients
treated with CEA but not in patients treated with CAS.
We present a symptomatic patient treated by CAS with
perioperative clinical deterioration from microembolic
showering, confirmed using TCD. Hypotension could have
been a compounding event in our patient. However, the
neurological deficit persisted despite prompt management
of the patient’s hypotension, and ultimately was not felt to
be the main factor contributing to the patient’s symptoms.
This is the first case of embolization following CAS
documented to have been successfully treated with
intravenously administrated dextran-40, with near complete resolution of ischaemic symptoms and prevention
of progression to a major stroke. The mechanism by
which dextran-40 is believed to reduce microemboli is
threefold. Firstly, it reduces platelet adhesiveness [14,
15]. Secondly, it reduces factor VIII activity [16]. Thirdly,
it increases clot lysability with resultant prevention of
stent thrombus formation, possibly by creating a coating

Neuroradiology (2007) 49:265–269

effect on both the artery and/or the stent causing decreased
electronegativity.
This case offers a further option in the management of
patients treated for atherosclerotic carotid artery disease
with microembolic complications. On a cautionary note, the
blanket use of dextran-40 has been demonstrated to
increase haemorrhagic complications in CEA-treated
patients [17]. This case demonstrates the value of periprocedural TCD and complimentary successful treatment of
symptomatic postprocedural microemboli with intravenous
dextran-40. Moreover, this case illustrates the need for
further research of the adjuvant role of both periprocedural
TCD and dextran-40, to evaluate its potential role in stroke
prevention in patients managed by stenting of symptomatic
extracranial carotid artery stenosis.
Acknowledgements Martin Punter is supported by a British Heart
Foundation project grant (PG 03/067).
Conflict of interest statement
of interest.

We declare that we have no conflict

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