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Hyperacute Intracerebral Hemorrhage Complicating Carotid Stenting Should Be Distinguished from Hyperperfusion Syndrome

J.-H. Buhk, L. Cepek and M. Knauth
American Journal of Neuroradiology August 2006, 27 (7) 1508-1513;

Article Figures & Data

Figures

  • Fig. 1.
    Fig. 1.

    MR imaging before CAS.

    A–C, Lesion of focally restricted diffusion in the right-sided centrum semiovale, characteristic of acute hemodynamic infarction (A, diffusion-weighted MR imaging [DWI][; B, apparent diffusion coefficient [ADC]). In the FLAIR sequence, an incomplete demarcation can be seen (C).

    D–F, At the level of the basal ganglia there is no evidence of an acute ischemic lesion. The right occipital pole is part of the residual posterior territorial infarction. The FLAIR sequence demonstrates mild microangiopathic changes (F).

  • Fig. 2.
    Fig. 2.

    A maximum intensity projection (MIP) image reconstructed from CT-angiographic data shows the high-grade stenosis of the right ICA as well as associated calcified atherosclerotic plaques (A). Digital subtraction angiography of the right carotid bifurcation before and after the intervention shows a tight, short-segment, hemodynamically significant stenosis (B, closed arrow)—note the low attenuation of contrast medium in ICA distal to the stenosis (B, open arrow)—and a good hemodynamic result after stent-placement and dilation (C).

  • Fig. 3.
    Fig. 3.

    Unenhanced cranial CT from approximately 1 hour after the intervention demonstrates a large right basal ganglial hemorrhage with extension to intra-axial and extra-axial CSF spaces. The hematoma is ipsilateral to the treated stenosis. The uppermost section shows the residual lesion after previous infarction in the right PCA territory.

Tables

  • Characteristic features of cases reported with hyperacute ICH following CAS

    AuthorAge (y)/SexVessel Treated (NASCET)Other TerritoriesVascular Risk FactorsTime from Last SymptomRadiographic Pathologies before TreatmentBlood Pressure (mmHg)Anticoagulation (Procedural)Time between End of Procedure and Setup of Neurologic EventLocalization of ICHHPS Suspect Prodro-mataClinical Out-come
    EmbolicHemodynamicMicroangio-pathicDuring ProcedureAfter ProcedureDuring Neurologic EventHeparinOthers
    McCabe et al968/MLeft ICA (95%)No dataSmoking, alcohol5 mo, incomplete remissionCorticalNoneModerate periventricular160/90–175/105140–160/95150/855000 IUASA, dipyridamole7 hIpsilateral basal gangliaNoneFatal
    Moriet al1071/MLeft ICA (99%)No dataHypertensionNone, recurrent TIAsNoneNoneYes≤142 systolicNo data170–190 systolic10 000 IUWarfarin, ticlopidin4 hIpsilateral basal gangliaNoneFatal
    Morrishet al687/MLeft ICA (95%)No significant stenosis in contralateral ICANo data4 moNoneNoneSubcorticalNo data110/60125/807000 IUASA, ticlopidin10 hNo dataNoneFatal
    Morrishet al662/FRight ICA (95%)No significant stenosis in contralateral ICANo data6 wkLarge corticalNoneNoneNo data173/64173/649000 IUASA, ticlopidin15 minIpsilateral basal gangliaNoneFatal
    Chamorroet al1143/MRight ICA (95%)No stenosisHypertension7 dAcute embolicNoneLacunar135/75–180/80100/60–125/60180/755000 IUASA, clopidogrel, urokinase∼6 hContralateral basal gangliaNoneFatal
    Qureshiet al1266/FICA (99%)No dataHypertension, smoking, hyperlipidemia2 d after ischemic strokeNoneNoneLacunarNo dataMax. 165 systolicNo dataACT: 356 sASA, clopidogrel, abciximab1 hBasal gangliaNoneFatal
    Qureshiet al1256/MICA (90%)No dataHypertension, coronary and peripheral artery disease4 d after TIANoneNoneNoneNo dataMax. 199 systolicNo dataACT: 180 sASA, clopidogrel, abciximab8 hBasal gangliaNoneFatal
    Qureshiet al1261/MICA (90%)No dataCoronary and peripheral artery disease4 wk after ischemic strokeMultiple small infarcts ipsilateral to stenosisNoneNoneNo dataMax. 187 systolicNo dataACT: 320 sASA, clopidogrel, abciximab10 minLobarNoneFatal
    Qureshiet al1246/FICA (80%)No dataHypertension, smoking1 d after TIANoneNoneNoneNo dataMax. 260 systolicNo dataACT: 273 sASA, clopidogrel, abciximab1 hLobarNoneFatal
    Friedmanet al1382/MRight ICA (90%)Left ICA (60%), no collateralization from anterior or posterior communicating arteriesPositive family historyFew daysNoneYes, restricted diffusionNone∼140 systolic∼140 systolicNo data5000 IUASA, clopidogrel45 minIpsilateral basal gangliaNoneFatal
    Abou-Cheblet al14Not applicableLeft ICA (99%)Right ICA (80%)HypertensionNot applicable∼5000 IU (ACT > 250 s)ASA, clopidogrel1 hIpsilateral basal gangliaNoneFatal
    Case reported65/FRight ICA (95%)Left ICA (80%), proximal VA stenosis bilateralHypertension, smoking, alcohol, positive family historyMaximum 14 d, incomplete remissionCorticalYes, restricted diffusionMild140/70120/70Max. 160 systolic5000 IU (ACT: 278 s)ASA, clopidogrel30 minIpsilateral basal gangliaNoneFatal

    • Note:—NASCET indicates North American Symptomatic Carotid Endarterectomy Trial; ICA, internal carotid artery; VA, vertebral artery; TIA, transient ischemic attack; ASA, acetyl salicylic acid; ACT, activated clotting time.

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Hyperacute Intracerebral Hemorrhage Complicating Carotid Stenting Should Be Distinguished from Hyperperfusion Syndrome
J.-H. Buhk, L. Cepek, M. Knauth
American Journal of Neuroradiology Aug 2006, 27 (7) 1508-1513;
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