95

REVIEW

Complete occlusion of extracranial internal carotid artery:

clinical features, pathophysiology, diagnosis and
management
Bhomraj Thanvi, Tom Robinson
...................................................................................................................................

Postgrad Med J 2007;83:9599. doi: 10.1136/pgmj.2006.048041

A complete occlusion of the internal carotid artery (ICA) is an of ICA disease proximal to the ophthalmic branch.
ICA occlusion is an independent predictor of
important cause of cerebrovascular disease. A never- neurological worsening in stroke.4
symptomatic ICA occlusion has a relatively benign course, A thorough history may disclose a haemody-
whereas symptomatic occlusion increases future risk of strokes. namic basis of symptoms in some patients. Any
Ultrasonography, magnetic resonance imaging and contrast condition that further reduces cerebral perfusion
for example, rising from a sitting or lying position
angiography are useful diagnostic tests, and functional imaging (orthostatic TIAs), postprandial hypotension, fluid
of the brain (eg, with positron emission tomography) helps to or blood loss, exercise (cerebral claudication) or
understand haemodynamic factors involved in the cardiac failuremay precipitate ischaemic symp-
toms in these patients. A rare manifestation of
pathophysiology of brain ischaemia. Recently, there has been a haemodynamic compromise in patients with ICA
resurgence of interest in the role of extracranialintracranial occlusion is limb shaking.5 The patients complain
bypass surgery for the treatment of completely occluded ICA. of repetitive involuntary movements of one or both
With advances in the measurement of cerebral limbs on one side. This is often misdiagnosed as
partial seizures. An electroencephalogram during
haemodynamics, it may be possible to identify high-risk patients such episodes does not show any epileptiform
who could benefit from the bypass surgery. activity and cerebral blood flow (CBF) is
............................................................................. reduced.6 7 Even rarer are the symptoms of retinal
ischaemia (spells of monocular reduced vision)
that occur on looking into bright light (retinal

T
he accurate prevalence and incidence rates of claudication),8 presumably resulting from an
internal carotid artery (ICA) occlusion are increase in metabolic demand in the retina on
difficult to ascertain as ICA occlusion can the background of an already reduced perfusion.
remain asymptomatic. In a retrospective, popula- Importantly, limb shaking and retinal claudication
tion-based study on patients with symptomatic occur in only a minority of patients,9 and have a
ICA occlusion, an incidence rate of 6/100 000 was high positive predictive value but a poor negative
reported.1 The authors of the study consider it to be value for diagnosing ICA occlusion.
an underestimation as many patients with tran- Some patients develop unaccustomed headaches
sient ischaemic attack (TIA) do not seek medical in chronic ICA occlusion as a result of the
attention and some patients with stroke or TIA do development of collateral circulation. In ICA
not undergo carotid imaging. The same study occlusion, collateral flow from the branches of
suggests that about 15% of large-vessel infarctions external carotid artery (ECA) may cause ipsilateral
may be caused by ICA occlusion. In a study in brisk pulsations at the angle of the jaw, brow and
Manchester, UK, Mead et al2 reported ICA occlu- cheek, the so-called ABC pulsations of Fisher.10
sion in 50 of 380 patients with ischaemic stroke However, collateralisation may predominantly
consecutively over a 1-year period. In a study on occur through the circle of Willis and, therefore,
the correlation of arteriographic findings and ABC pulsations may not be brisk.
symptoms in patients with cerebrovascular dis- Although amaurosis fugax is a symptom of
ease, 25% of patients with ischaemic stroke had acute retinal ischaemia most often caused by
ICA occlusion.3 The prevalence of asymptomatic embolism from the ICA, in 418% of patients with
See end of article for ICA occlusion is unknown.
authors affiliations occlusion or severe stenosis of the ICA, a syndrome
........................ of chronic ocular ischaemia may develop.11
CLINICAL FEATURES OF ICA OCCLUSION Patients complain of progressive loss of visual
Correspondence to: The clinical spectrum of ICA occlusion ranges from acuity. Venous stasis retinopathy is the term used
Dr Bhomraj Thanvi, being a completely asymptomatic occlusion (often
Department of Integrated to describe ophthalmoscopic appearance in the
Medicine, Glenfield noted on the wrong side during investigation of syndrome of chronic ocular ischaemia and is
General Hospital, University a TIA or stroke) to a devastating stroke or death. It characterised by mid-peripheral microaneurysms
Hospitals of Leicester NHS is possible that in patients with adequate collateral
Trust, Leicester LE3 9QP, flow, ICA occlusion may remain asymptomatic.
UK; bthanvi@hotmail.com Abbreviations: CBF, cerebral blood flow; CTA, computed
TIA or stroke caused by ICA occlusion can present tomographyangiography; ECA, external carotid artery;
Received 29 March 2006 with clinical features similar to those due to any ICA, internal carotid artery; MCA, middle cerebral artery;
Accepted 28 April 2006 other aetiology. An episode of transient monocular MRA, magnetic resonance angiography; OEF, oxygen
........................ blindness (amaurosis fugax) is highly suggestive extraction fraction; TIA, transient ischaemic attack

www.postgradmedj.com
96 Thanvi, Robinson

and small dot-and-blot intraretinal haemorrhages, arterial ICA, where it flows in the usual anterograde fashion. Less
narrowing and venous dilatation, and in advanced stages, commonly, collateral circulation may come from the vertebro-
cotton-wool exudates and neovascularisation of the optic disc, basilar systems or the cortical surface branches.
retina and iris. Nearly one third of patients with symptomatic If collateralisation is inadequate, CBF can be maintained
ICA occlusion show evidence of venous stasis retinopathy, despite reduced cerebral perfusion pressure by dilatation of the
although clinical manifestations are rare.11 Venous stasis resistance vessels (cerebral autoregulation). This autoregulatory
retinopathy can be distinguished from diabetic retinopathy by vasodilatation can be diagnosed by reduced or absent CBF
its unilaterality, mid-peripheral location and low retinal artery response to vasodilative stimuli such as hypercapnia or
pressure. It is important to recognise this condition in order to acetazolamidecerebrovascular reactivity. In patients with
start secondary prevention strategies. ICA occlusion, a vasodilative stimulus does not increase CBF,
ICA occlusion can also manifest as syncopal episodes.12 as autoregulation has already caused maximal vasodilatation in
It is suggested that chronic cerebral ischaemia caused by ICA response to a reduced cerebral perfusion pressure. When
occlusion could cause dementia.13 Improvement in cognitive autoregulatory vasodilatation fails to maintain normal CBF,
function after external carotidinternal carotid bypass surgery oxygen extraction fraction (OEF) of the affected brain tissue
has been reported by some13 but not by others.14 increases to maintain normal cerebral metabolism, the so-
called stage II haemodynamic failure or misery perfusion.21 An
increased OEF has shown to be a powerful independent risk
PATHOGENESIS OF CEREBRAL AND RETINAL
factor for subsequent ischaemic strokes in patients with
ISCHAEMIA IN ICA OCCLUSION
symptomatic ICA occlusion.18 The combined annual stroke risk
ICA occlusion can produce brain or retinal ischaemia by the
in the subgroups with impaired haemodynamic measurements
following mechanisms:
of any severity was 12.5% for all strokes and 9.5% for ipsilateral
1. Embolism from the distal or proximal stump or from strokes, suggesting a definitely worse prognosis in patients with
atherosclerotic plaques in the common carotid artery or impaired cerebral perfusion than in those without.16
ECA, which traverse through the collateral pathways
involving the ECA. Arguments in favour of this hypothesis DIAGNOSIS OF ICA OCCLUSION
are the cessation of symptoms after excision or clipping of It is technically challenging to accurately differentiate total
the proximal stump, and with antithrombotic treatment.15 occlusion from a near-total occlusion (also termed preocclusive
In addition, some pathological evidence is consistent with stenosis). This is important from the points of view of
embolism from the distal tail of the occluded ICA.16 treatment and prognosis. The patients with symptomatic
Embolism is probably the most common mechanism, near-occlusion are considered to be at a high risk of future
accounting for nearly two thirds of strokes in ICA embolisation and can derive benefit from carotid endarter-
occlusion.17 ectomy. However, carotid endarterectomy is not an option in
2. A compromised CBF, the so-called perfusion failure with complete ICA occlusion. Therefore, missing a residual lumen
distal insufficiency or misery perfusion syndrome, may have may deprive a patient of a potentially beneficial surgery, and
a role in the pathogenesis of ischaemia in patients with ICA misdiagnosing a complete occlusion as near-occlusion has the
occlusion. In chronic ICA occlusion, collateral circulation risk of subjecting the patient to unnecessary angiography or
may maintain cerebral perfusion. Failure of collateralisation surgery. However, a recent article reported lesser benefits of
may contribute to the haemodynamic compromise. Recent surgery in near-occlusion.22
studies using functional brain imaging with positron emis- Ultrasonography is usually the initial imaging modality for
sion tomography or single-photon emission computed the evaluation of symptomatic ICA disease. B-mode (brightness
tomography showed haemodynamic compromise as an modulation) ultrasonography is quite accurate for assessing
independent risk factor for future strokes or TIAs.18 ICA luminal narrowing and for differentiating normal artery or
occlusion is frequently associated with borderzone infarcts,19 artery with non-significant plaque disease from a severely
implicating haemodynamic failure. stenotic lesion (stenosis .70%). However, it may be difficult to
3. Both embolic and haemodynamic factors may act syner- differentiate near-occlusion from a complete occlusion.
gistically in the same patient.17 Animal studies have shown Addition of continuous and pulsed Doppler techniques to
that for a given embolic event, the size of the infarct is B-mode in duplex systems provides qualitative and quantitative
markedly increased in presence of a pre-existing hemody- information about the haemodynamic variables (eg, velocity
namic impairment.20 changes, post-stenotic turbulence). ICA occlusion is charac-
terised by the absence of any signal along the extracranial
Compensatory mechanisms can prevent ischaemia in ICA course of the ICA (fig 1). Sometimes, a low-velocity signal with
occlusion. Development of collateral circulation is one of them. a marked reversed signal and absent diastolic flow can be
The most important source of collateral flow is provided by the recorded at the origin of the ICAthe stump flow. The accuracy
contralateral ICA via the circle of Willis. The blood flows in an of carotid duplex ultrasonography in diagnosing total carotid
anterograde manner up the contralateral ICA and then across occlusion is reported as 97%, with a positive predictive value of
the circle of Willis to the anterior communicating artery. From 96%, a negative predictive value of 98%, a sensitivity of 91% and
here, it goes in an anterograde manner along the cortical a specificity of 99%.23 Newer techniques including power and
branches of the anterior cerebral artery and in a retrograde colour Doppler ultrasonography improve detection of near-
manner along the anterior cerebral artery to the middle cerebral occlusions.24 The use of a contrast agent with duplex ultrasound
artery (MCA), and then distally into the MCA territory in the imaging techniques has improved reliability in distinguishing
usual anterograde manner. The other important source of total occlusions from near-total occlusions.25 Ultrasonography
collateral flow is from the orbital branches of the ipsilateral may not reliably depict high-up occlusions (beyond the
ECA. Anterograde flow up in the ECA to the orbit (mainly via available sonographic window). Low-velocity flow with a high
its maxillary branches, but also via facial, frontal branches or resistance pattern when measured in a patent cervical ICA may
leptomeningeal branches) allows links with the ophthalmic suggest such a lesion, but similar waveforms could be found in
branch (OA) of the ICA. Blood flows in a retrograde manner in a severe high-grade distal stenosis. Transoral ultrasonography
the ophthalmic branch to join the supraophthalmic part of the may help in detecting distal ICA occlusion.26

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Complete occlusion of extracranial ICA 97

Figure 1 Occlusion of the right internal

carotid artery with no evidence of flow using
pulsed Doppler imaging.

Magnetic resonance angiography (MRA), with or without lumen with a high degree of accuracy.28 Multislice CTA showed
gadolinium enhancement, is increasingly used in the evalua- an excellent correlation with catheter angiography in diagnos-
tion of stroke. Unlike conventional angiography, MRA does not ing total versus near-ICA occlusion.29 When used in combina-
show the vessel anatomy but creates an image of flow in the tion with duplex ultrasonography, CTA may obviate the need
vessels. Time-of-flight MRA depends on the movement of for catheter angiography.30
blood. The magnetisation of protons in the moving tissue Digital subtraction angiography is the gold standard
appears bright. Total occlusion is defined as a flow signal imaging modality for the evaluation of carotid occlusive
termination on all sequences at any point along the intracranial disease. However, it is an invasive procedure and therefore
or extracranial ICA with no flow signal intensity distally (fig 2). should be used only when ultrasonography or MRA fail to
In case of near-occlusion, a focal flow gap is noted. provide a definitive distinction between a near-occlusion and a
Gadolinium-enhanced MRA is at least as sensitive as ultra- complete occlusion. Angiography may be the best imaging
sonography in diagnosing total occlusions in the neck, and technique for making appropriate therapeutic decisions in
probably better than ultrasonography at diagnosing near- patients with diffuse narrowing (string lesions) on MRA and
occlusions.27 However, supraclinoid occlusions may not be those with low-velocity high-resistance flow in the ICA on
reliably diagnosed. ultrasonography.27
Recently, computed tomographyangiography (CTA) has
been used to diagnose ICA disease. Single-row detector CTA
TREATMENT OF SYMPTOMATIC ICA OCCLUSION
can distinguish total ICA occlusion from hairline residual
Acute ICA occlusion is a therapeutic challenge as a result of
poor neurological outcome and paucity of effective therapeutic
options available. Patients presenting with stroke should be
admitted to a stroke unit. Hypertension should not be corrected
in the acute phase unless in a malignant range. Hypotension
should be avoided in view of its potential to severely
compromise cerebral perfusion in ICA occlusion. Some clin-
icians use short-term (about 6 weeks) anticoagulation with
heparin and warfarin to reduce embolisation from the fresh clot
followed by antiplatelet drugs, although evidence for this
strategy is unavailable. In patients presenting soon (,3 h) after
the onset of stroke with no evidence of cerebral haemorrhage or
a large infarction on brain imaging, intravenous thrombolysis
using recombinant tissue plasminogen activator may be
considered. However, a large clot usually fails to lyse. In a
retrospective study, most patients did not recanalise their ICA
occlusion after intravenous recombinant tissue plasminogen
activator treatment.31 The recanalisation rate of an associated
proximal MCA clot, found in 45% of patients, was good and
accounted for a good outcome.
Thrombolytic treatment using a combination of intravenous
and intra-arterial routes or using the intra-arterial only route
has been reported to be effective in distal ICA occlusion,
particularly when given soon after the onset of stroke.32
Figure 2 Magnetic resonance angiography showing occluded right In a small study on 21 patients with strokes due to major
proximal internal carotid artery (arrow). The collateral flow to the right arterial occlusions, an intravenous bolus of tirofiban and
hemisphere from the circle of Willis can be seen. heparin followed by intra-arterial administration of urokinase

www.postgradmedj.com
98 Thanvi, Robinson

coupled with mechanical thrombolysis was shown to be emission tomography.44 An increased OEF distal to a sympto-
successful in re-establishing vessel patency with a good matic ICA occlusion is a requirement for randomisation to
functional outcome.33 surgery or medical treatment. A newer technique using a
A high revascularisation rate has been reported with venous transplant for a bypass between the proximal super-
angioplasty and stenting (endovascular treatment) for acute ficial temporal artery and the most distal, intracranial part of
carotid occlusions. Sugg et al34 reported a 64% immediate the ICA or the proximal MCA results in a larger increase in
recanalisation rate with endovascular treatment in patients blood flow (high-flow external carotidinternal carotid
with ICA occlusion treated within 3 h of onset of stroke. bypass) and may be more effective at restoring CBF.45
However, as yet, there are no large controlled trials showing
efficacy of any of these approaches, and an acute ICA occlusion
is mostly managed conservatively. Indirect procedures

ESTABLISHED ICA OCCLUSION

N Endarterectomy or angioplasty stenting of a haemodynamically
relevant stenosis of the contralateral ICA: the contralateral ICA is
As it is technically difficult to open a chronically occluded ICA, often the most important source of collateral flow in ICA
the management of a chronic ICA occlusion mainly includes occlusion. In patients with ICA occlusion and a severe
strategies to reduce the risk of future strokes and other stenosis of the contralateral ICA, carotid endarterectomy of
cardiovascular events. This usually means treatments to reduce the contralateral ICA resulted in a long-term cerebral
embolic risk, but in some cases also to improve cerebral haemodynamic improvement not only on the side of surgery
perfusion. but also on the side of the ICA occlusion.46 Gonzalez et al47
have recently reported endovascular treatment (angioplasty
Modification of risk factors and stenting) of contralateral ICA to be safe and effective in
As with other cardiovascular diseases, modifications of risk patients with a symptomatic ICA occlusion and a severe
factorsfor example, hypertension, diabetes, hyperlipidaemia stenosis of the contralateral ICA.47 However, no large,
and smokingare vital secondary prevention measures. controlled studies have evaluated the efficacy and safety of
However, aggressively correcting hypertension should be these therapeutic approaches in ICA occlusion.
avoided when clinical features (eg, limb shaking, orthostatic
TIAs, syndrome of chronic ocular ischaemia) and investigations
N Endarterectomy of the ipsilateral ECA: in some patients with ICA
occlusion, collateral flow may predominantly be provided by
suggest a haemodynamic origin for the symptoms. This is in the branches of ECA. A stenotic lesion in ECA may lead to
view of the fact that a relatively slight decrease in blood ischaemic symptoms in these patients.15 In a collective
pressure can precipitate cerebral ischaemia. A recent study review of case series, Gertler et al48 reported safety and
showed adverse outcome of correcting hypertension in bilateral efficacy of endarterectomy of ipsilateral ECA in a subgroup
but not in unilateral ICA occlusion.35 of patients with symptomatic ICA occlusion. Resolution of
symptoms was seen in 83% of patients, with another 7%
ANTITHROMBOTIC AND ANTICOAGULANT AGENTS showing marked improvement. The overall neurological
In patients with previous stroke or TIA, antiplatelet treatment complication rate was 5%, with more recent reports being
leads to a 22% reduction in the risk of future non-fatal stroke, associated with improved mortality and morbidity, implying
non-fatal myocardial infarction or a vascular death per 1000 a learning curve.
patients treated.36 Aspirin has shown to reduce risk of future
cardiovascular events by about 13% (95% confidence interval
4% to 21%) in patients with TIAs or non-disabling ischaemic OUTCOME OF ICA OCCLUSION
stroke from any cause.37 On this basis, aspirin is also used in The subject of future risk of stroke or TIA in patients with ICA
patients with symptomatic ICA occlusion. Addition of dipyr- occlusion is complex. A never-symptomatic ICA occlusion is
idamole may further reduce the risk of strokes.38 In genuinely considered to have a benign course.49 However, symptomatic
aspirin-intolerant people, clopidogrel may be considered.39 ICA occlusion increases the risk of future cerebrovascular
Addition of clopidogrel to aspirin probably increases the risk events. In a study on angiographically proved ICA occlusion,
of bleeding, with no major additional benefit.40 No studies have the rate of recurrent stroke was 4.8% at 1 year, 12.2% at 3 years
compared aspirin with oral anticoagulants in ICA occlusion. and 17.1% at 5 years.50 In a meta-analysis of 20 follow-up
Although anticoagulants are often used in ICA occlusion caused studies on patients with symptomatic ICA occlusion, the annual
by dissection, the evidence base for this is poor. Similarly, it is risk of stroke was 5.5% and that of ipsilateral stroke was 2.1%.16
unclear whether antithrombotic agents reduce the risk of future Those with evidence of haemodynamic compromise on func-
strokes in the subset of patients with a haemodynamic basis for tional imaging are at an even higher risk (all strokes, 12.5%;
the cerebral ischaemia. and ipsilateral stroke, 9.5%). Patients with bilateral carotid
occlusion have a high risk of stroke.
Revascularisation procedures in ICA occlusion
Direct procedure for revascularisation
CONCLUSION
N External carotidinternal carotid bypass surgery: the superficial
temporal artery to middle cerebral artery bypass can improve
ICA occlusion is an important cause of cerebral or retinal
ischaemia. The clinical course of ICA occlusion is variable, from
CBF in patients with symptomatic unilateral carotid occlu-
being a completely asymptomatic to one leading to devastating
sion.41 However, a large, randomised clinical trial failed to strokes. Our understanding of the role of embolism and
show any benefit of this bypass over contemporary medical haemodynamic factors in the pathogenesis has greatly improved
treatment in preventing stroke in patients with symptomatic in recent years, largely due to advances in morphological and
ICA occlusion.42 One of the criticisms of this study is that it did functional imaging techniques. This will hopefully help in
not identify patients with compromised CBF who could have developing treatments targeted to the underlying mechanism.
derived greater benefit from the operation.43 Therefore, an
ongoing Carotid Occlusion Surgery Study is aiming to re- .......................
examine its effectiveness in reducing subsequent ipsilateral Authors affiliations
ischaemic stroke in patients with recent cerebral ischaemic Bhomraj Thanvi, Department of Integrated Medicine, Glenfield General
symptoms and increased OEF as measured by positron Hospital, University Hospitals of Leicester NHS Trust, Leicester, UK

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Complete occlusion of extracranial ICA 99

Tom Robinson, Department of Ageing and Cerebrovascular Medicine, 26 Isa K, Yasaka M, Kimura K, et al. Transoral carotid ultrasonography for
Leicester General Hospital, University Hospitals of Leicester NHS Trust, evaluating internal carotid artery occlusion. Intern Med 2005;44:56771.
27 El-Saden SM, Grant EG, Hathout GM, et al. Imaging of the internal carotid
Leicester, UK
artery: the dilemma of total versus near total occlusion. Radiology
Competing interests: None declared. 2001;221:3018.
28 Lev MH, Romero JM, Goodman DN, et al. Total occlusion versus hairline residual
lumen of the internal carotid arteries: accuracy of single section helical CT
angiography. AJNR Am J Neuroradiol 2003;24:11239.
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