Case Reports

Extravasating Contrast Material on Angiography FollowingCarotid Angioplasty and Stenting: Not NecessarilySubarachnoid Hemorrhage

Pranshu Sharma, MD, Alexandre Y. Poppe, MD, FRCPC, Muneer Eesa, MD, Nikolai Steffanhagan, MD,Mark Hudon, MD, FRCPC, William Morrish, MD, FRCPCFrom the Department of Diagnostic Imaging, Foothills Medical Centre, Calgary, Alberta, Canada (PS, ME, MH, WM); Calgary Stroke Program, Department of ClinicalNeurosciences, University of Calgary, Calgary, Alberta, Canada (AYP, NS).

[Correction added after online publication 17-March-2010: Received date corrected.]

Keywords: Carotid angioplasty andstenting, extravasation, sub-arachnoidhemorrhage.

Acceptance: Received March 19, 2008,and in revised form August 11, 2008. Ac-cepted for publication August 29, 2008.

Correspondence: Address corre-spondence to Pranshu Sharma, MD,Department of Diagnostic Imaging,Foothills Medical Centre, 1403-29 St NWCalgary, Alberta, Canada T2N2T9. E-mail: pranshu.sharma@calgaryhealthregion.ca.

Disclosure: The authors report noconflicts of interest.

J Neuroimaging 2010;20:180-182.DOI: 10.1111/j.1552-6569.2008.00316.x

A B S T R A C TWe describe a case of asymptomatic extravasation of iodinated contrast material intothe sulci on digital subtraction angiography following carotid angioplasty and stentingresulting in sulcal hyperdensity on computed tomography (CT). We believe the mechanismfor this observation is hyperperfusion injury and that in the absence of any associatedclinical signs, it should not be considered alarming for subarachnoid hemorrhage.

IntroductionAtherosclerotic carotid stenosis is responsible for approxi-mately 20-30% of ischemic strokes in North America.1 TheNorth American Symptomatic Carotid Endarterectomy Trial(NASCET)2 and Asymptomatic Carotid Atherosclerosis Study(ACAS)3 have shown benefit of carotid endarterectomy insymptomatic and asymptomatic patients with moderate-to-severe stenoses for reducing the risk of stroke. Carotid angio-plasty and stenting (CAS) is an alternative to endarterectomybut is not without its risks, with stroke and hyperperfusion syn-drome chief among them.

We report a case of asymptomatic sulcal hyperdensity onCT following ipsilateral CAS with evidence of extravasation ofiodinated contrast material during digital subtraction angiog-raphy, the likely mechanism being hyperperfusion injury.

Case ReportA 65-year-old man presented several days after acute onset ofmild right-sided weakness and aphasia. Computed tomogra-phy (CT) of the head showed infarcts in the left parasagittaldeep hemispheric white matter. CT angiography (CTA) re-

vealed >90% stenosis of the left internal carotid artery (ICA).The right ICA was normal. Furthermore, the CTA of the headshowed absence of the anterior communicating artery and afetal posterior cerebral artery on the left side with a hypoplasticleft P1 segment isolating the left cerebral hemispheric circula-tion. It was decided to perform CAS of the left ICA. The patientwas started on aspirin and clopidogrel 72 hours before the pro-cedure. CAS was performed 4 weeks after the onset of symp-toms under local anesthesia and vital signs were monitored.The blood pressure before the procedure was 160/70 mmHg.Through a right transfemoral route a 6F guiding sheath wasplaced in the left common carotid artery. Heparin was admin-istered intravenously for maintaining an activated coagulationtime of >250 seconds. Angiogram of the left common carotidartery revealed >90% stenosis of the left ICA at the bulb. Distalflow appeared adequate. Anteroposterior and lateral views werealso obtained. The intracranial vessels showed normal courseand caliber with no stenosis or occlusion of any vessel. Therewas no opacification of contralateral ICA branches.

A protection device (FilterWire, Boston Scientific Corp.,Mountain View, CA) was used to cross the stenotic lesionand placed at C1 vertebral level. Using a monorail system,

180 Copyright ◦C 2008 by the American Society of Neuroimaging

Fig 1. (A) and (B). Lateral view of the left ICA cerebral angiogram following CAS shows extravasation of contrast in the frontal region (arrows).

pre-dilatation was performed with a low-profile, compliant, 4-mm angioplasty balloon. A self-expanding stent (Carotid Wall-stent Monorail; Boston Scientific Corp., Natick, MA) was thenplaced across the lesion. Post-dilatation was performed witha 5-mm angioplasty balloon. The blood pressure during theprocedure ranged from 120 to 170 mmHg (systolic) and from50 to 70 mmHg (diastolic). Check angiogram of the commoncarotid artery at this stage revealed successful treatment of thestenosis with no residual stenosis. Check angiogram of the headshowed good flow into the intracranial branches with no throm-boembolic complication. However, there was a small area ofextravasation of contrast material in the left frontal region(Fig 1). There was concern about subarachnoid hemorrhage butthe patient’s condition was stable with no change in blood pres-sure, heart rate, or complaints of headache. The blood pressure

Fig 2. Plain CT head immediately post-CAS shows marked sulcalhyperdensity (143 HU) in left frontal region.

post-procedure was 120/50 mmHg. Immediate CT of the headrevealed sulcal hyperdensity in the left frontal, parietal, andtemporal regions (Fig 2). No new lesions were seen in the brainparenchyma. Two days later, follow-up non-contrast CT of thehead revealed partial resolution of the previously described sul-cal hyperdensity. There was, however, an asymptomatic smallhematoma in the left temporal lobe (Fig 3) without associatedmass effect. The blood pressure ranged from 83/52 mmHg inthe 2 days following stenting to 140/70 mmHg at dischargefrom hospital. The patient had an otherwise uneventful courseand was discharged in stable condition on anti-hypertensives,aspirin, and clopidogrel.

Fig 3. Plain CT head 2 days post-CAS shows left temporalhematoma.

Sharma et al: Contrast-material extravasation following CAS 181

DiscussionSulcal hyperdensity after CAS may occur in subarachnoid hem-orrhage, extravasation of contrast material, or leptomeningealenhancement.4,5 Subarachnoid hemorrhage following CAS isassociated with rise in blood pressure, severe headache, and isoften fatal.6,7 In our patient extravasation of contrast materialon angiogram and sulcal hyperdensity on CT were unlikely tobe due to subarachnoid hemorrhage as there were no accompa-nying clinical symptoms and the course in hospital was unevent-ful. Leptomeningeal enhancement is not likely to be visualizedon angiograms as extravasating contrast material. Previouslyreported instances of asymptomatic sulcal hyperdensity/hyperintensity following carotid stenting did not unequivocallydemonstrate extravasation of contrast material and thereforeleptomeningeal enhancement could not be entirely excludedas the cause.4,5 However, in our case observation of contrast-material extravasating during angiography in an asymptomaticpatient suggests leakage of contrast material without accompa-nying subarachnoid hemorrhage.

In our opinion the underlying pathophysiology of thiscontrast-material extravasation and sulcal hyperdensity is likelyhyperperfusion injury. It is unlikely to represent an enhancingsubacute infarct as the hyperdensity was sulcal and not gy-ral, as would be seen in enhancing infarcts. Also, we did notidentify any cortical infarcts on the CT. Hyperperfusion syn-drome has been defined as hemispheric neurological deficit (orseizure) occurring after cerebral revascularization, localized ip-silateral to the treated artery, not related to thromboembolism,and without evidence of new infarction on diffusion weightedMRI.8 Chronic underperfusion due to severe ICA stenosis leadsto maximal dilatation of cerebral arterioles and loss of auto-regulation. Sudden restoration of cerebral blood flow followingangioplasty and stenting overwhelms the cerebral autoregula-tion, disrupts the blood-brain barrier, and leads to edema and/or hemorrhage.8 The intracranial hemorrhage may be intra-parenchymal or subarachnoid and can be fatal.

Our patient had several predisposing factors for a hyperper-fusion injury, including severe ipsilateral carotid stenosis andpoor cross-circulation due to an incomplete circle of Willis.The left temporal hematoma noted a few days later in our casealso suggests an underlying hyperperfusion injury. Thus, it islikely that the sulcal hyperdensity occurred due to the sameunderlying pathophysiology and we have been able to demon-strate early angiographic evidence of hyperperfusion injury inthe form of contrast-material extravasation.

In summary, we describe a case of sulcal hyperdensity dueto contrast-material extravasation into the subarachnoid space,following CAS. We believe the mechanism for this observationis hyperperfusion injury and that in the absence of any clinicalsigns, it need not be alarming for subarachnoid hemorrhage.

References1. Morrish W, Grahovac S, Douen A, et al. Intracranial hemorrhage

after stenting and angioplasty of extra-cranial carotid stenosis. Am JNeuroradiol 2000;21:1911-1916.

2. North American Symptomatic Carotid Endarterectomy Trial Col-laborators. Beneficial effect of carotid endearterectomy in symp-tomatic patients with high grade carotid stenosis. N Engl J Med1991;325:445-453.

3. Executive Committee for the Asymptomatic Carotid Atherosclero-sis Study. Endarterectomy for asymptomatic carotid artery stenosis.JAMA 1995;273:1421-1428.

4. Wilkinson ID, Griffiths PD, Hoggard N, et al. Unilateral lep-tomeningeal enhancement after carotid stent insertion detected bymagnetic resonance imaging. Stroke 2000;31:848-851.

5. Lu C-J, Sun Y, Huang K-M. Leptomeningeal enhancement aftercarotid stenting (Letter). Stroke 2000;31(9):2274-2275.

6. Al-Mubarak N, Roubin GS, Vitek JJ, et al. Subarachnoidal hemor-rhage following carotid stenting with the distal-balloon protection.Catheter Cardiovasc Interv 2001;54:521-523.

7. Hartmann M, Weber R, Zoubaa S, et al. Fatal subarachnoid hem-orrhage after carotid stenting. J Neuroradiol 2004;31:63-66.

8. Coutts SB, Hill MD, Hu WY, et al. Hyperperfusion syndrome:toward a stricter definition. Neurosurgery 2003;53:1053-1057.

182 Journal of Neuroimaging Vol 20 No 2 April 2010