Hamann, Gerhard F.

Milz, P.

Seelos, Klaus

Velden, J.

Winkler, F.

English

Open Access LMU ( Ludwig-Maximilians-Univ. München)

Short Reports 249Eur Neurol 2003;49:249–251DOI: 10.1159/000070198Nonionic Contrast Neurotoxicity afterCoronary Angiography Mimicking SubarachnoidHemorrhageJoachim Velden a, Petra Milzb, Frank Winkler a, Klaus Seelosb,Gerhard F. Hamann aaDepartment of Neurology and b Institute of Radiology,Division of Neuroradiology, Klinikum Grosshadern,Ludwig Maximilian University, Munich, GermanyIntroductionThe incidence of neurotoxic events due to intravascular applica-tion of iodinated x-ray contrast media (CM) has decreased markedlysince the introduction of nonionic CM [1]. Severe neurotoxic compli-cations are accompanied by disruption of the blood-brain barrier andCM extravasation [1–6]. Coronary angiography involving only non-ionic CM has been reported to cause transient cortical blindness,confusion and amnesia, but no focal deficits [3, 4], whereas coronaryangiography involving ionic CM was followed by more severe com-plications including seizures, motor and speech deficits [5, 6]. Herewe report on a patient who developed transient hemiparesis, aphasiaand confusion due to neurotoxicity of nonionic CM after coronaryangiography, and whose CT findings mimicked subarachnoid hem-orrhage (SAH).Case ReportAn 82-year-old right-handed Caucasian woman with progressiveangina underwent transfemoral coronary angioplasty with stentplacement. Her medical history included arterial hypertension andunilateral nephrectomy, but no neurological antecedents. Baselineserum creatinine levels were marginally elevated at 106 ÌM, reflect-ing F50% impairment in glomerular filtration. The angiographicintervention took 134 min and required the injection of 500 ml ofiomeprol (IomeronTM 350, Bracco SpA, Italy), a monomeric non-ionic CM. Additional treatment included 7,500 IU heparin, 300 mgclopidogrel and 100 mg aspirin. Before and during the intervention,the patient had no neurological deficits. However, 30 min after theFig. 1. Time series of brain CT scans from apatient with nonionic contrast neurotoxicityafter coronary angiography. Bihemisphericsulcal subarachnoid contrast enhancementsat 6 h (a) and 12 h (b), fading at 21 h (c), andcompletely cleared at 45 h (d). Note headrotation to the left (a) corresponding to righthemiparesis.250 Short ReportsFig. 2. Diffusion-weighted MRI with a b-value of 1,000 of the same anatomical region which displayed a contrastenhancement in the CCT. No sign of an acute or subacute stroke is visible.procedure she became increasingly disoriented and drowsy. Herblood pressure rose to 200/100 mm Hg. Within the following 4 h, shebecame aphasic and developed right hemiparesis. Cranial CT, per-formed first without and then with additional administration of80 ml Iomeron 300, revealed hyperdense material filling the sulci ofboth brain hemispheres, which was diagnosed as SAH (fig. 1a).At this time the patient was referred to our acute stroke unit. Onadmission, 9 h postintervention, she exhibited severe global aphasia,mild to moderate right hemiparesis, meningism, confusion and som-nolence. Blood pressure was 150/65 mm Hg. CT was repeated, con-firming bihemispheric hyperdense filling of the cerebral sulci, whichwas more prominent on the left hemisphere (fig. 1b). Cranial Dopp-ler ultrasonography detected no pathologic flow signals. Twenty-fourhours postevent, lumbar CSF analysis yielded normal standardresults concerning cell count and protein content; particularly neitherxanthochromia nor red blood cells were seen. Cerebral MRI compil-ing T1, T2, gradient echo, FLAIR, proton density, spin echo, diffu-sion-weighted sequences and MR angiography excluded hemorrhage,ischemia, or any other significant pathology besides mild hyperten-sive microangiopathy and dilative arteriopathy. There was no gadol-inium enhancement. Figure 2 shows the normal diffusion-weightedMRI images of the same regions displaying the CCT contrast en-hancement. There was no sign of cerebral ischemia.Spontaneous recovery was observed within 40 h postangiogra-phy. The patient fully regained consciousness, orientation, languageability, and muscular strength. In parallel, as observed with repeatCT scans, sulcal hyperdensities partly faded after 21 h (fig. 1c) andtotally disappeared within 45 h (fig. 1d). Serum creatinine, whichhad risen to 141 ÌM intermediately, returned to baseline levels(115 ÌM ). The patient was monitored 3 more days before release.Follow-up interviews 1 and 4 weeks later confirmed that the patienthad no sequelae other than persistent amnesia obscuring the 24-hourperiod immediately following angiography. Seizures were never ob-served.Chemical assessment of iomeprol concentrations (kindly per-formed by Dr Lorusso, Bracco SpA) revealed a strong enrichment ofiomeprol in the lumbar CSF (547 Ìg/ml) as compared to the simulta-neous serum sample (129 Ìg/ml) 24 h after coronary angiography.Voxel density measurements within the initial CT scan showed thatthe subarachnoidal hyperdensities reached up to 96 Hounsfieldunits.DiscussionTo our knowledge, this is the first case illustrating the occurrenceof focal deficits such as hemiparesis and aphasia following coronaryangiographic application of nonionic CM. Furthermore, our caseshows that CT findings due to CM extravasation can be indistin-guishable from SAH, so that the correct diagnosis requires furtherinvestigations. As presented here, routine CSF analysis and MRIexcluded SAH. Special CSF analysis confirmed iomeprol enrichmentin the CSF as the cause of subarachnoid contrast enhancement. Thiswas also consistent with voxel densities reaching as much as 96Hounsfield units, clearly exceeding blood density ranging from 40 to60 units [5]. CM enrichment in the CSF is a consequence of CM-toxic blood-brain/blood-CSF barrier disruption followed by CMextravasation [1]. A subacute stroke as the source of a disturbedblood-brain barrier could be excluded by the MRI findings with anormal diffusion-weighted image of the same anatomical regionwhich displayed contrast enhancement in the sulci in the CCTAlthough the administration of 500 ml Iomeron 350 was justbelow the maximum recommended dose for coronary angiography asindicated by the manufacturer, it may be regarded as a relative over-dosage in our patient with underlying chronic renal function impair-ment. Taking this into account, an additional dose, as given here forcontrast CT, should have been avoided.In conclusion, apparent SAH following any intravascular applica-tion of any CM has to be clarified by lumbar puncture and/or MRI,even if CT strongly suggests SAH, in order to avoid additional CMShort Reports 251administration and toxicity as well as further risks associated withcerebral angiography, which is required in the case of true SAH.References1 Torvik A, Walday P: Neurotoxicity of water-soluble contrast media. ActaRadiol Suppl 1995;399:221–229.2 Lantos G: Cortical blindness due to osmotic disruption of the blood-brainbarrier by angiographic contrast material: CT and MRI studies. Neurology1989;39:567–571.3 Sticherling C, Berkefeld J, Auch-Schwelk W, Lanfermann H: Transientbilateral cortical blindness after coronary angiography. Lancet 1998;351:570.4 Parry R, Rees JR, Wilde P: Transient cortical blindness after coronaryangiography. Br Heart J 1993;70:563–564.5 Sharp S, Stone J, Beach R: Contrast agent neurotoxicity presenting as sub-arachnoid hemorrhage. Neurology 1999;52:1503–1505.6 May EF, Ling GSF, Geyer CA, Jabbari B: Contrast agent overdose causingbrain retention of contrast, seizures, and parkinsonism. Neurology 1993;43:836–838.Prof. Gerhard Hamann, Department of NeurologyKlinikum Grosshadern, Ludwig Maximilian UniversityMarchioninistrasse 15, D–81377 Munich (Germany)Tel. +49 89 70 95 36 70, Fax +49 89 70 95 36 77E-Mail hamann@brain.nefo.med.uni-muenchen.de

Contrast agent neurotoxicity presenting as subarachnoid hemorrhage.

Contrast agent overdose causing brain retention of contrast, seizures, and parkinsonism. Neurology

Cortical blindness due to osmotic disruption of the blood-brain barrier by angiographic contrast material: CT and MRI studies.

Lanfermann H: Transient bilateral cortical blindness after coronary angiography.

Transient cortical blindness after coronary angiography.

Walday P: Neurotoxicity of water-soluble contrast media. Acta Radiol Suppl

Nonionic contrast neurotoxicity after coronary angiography mimicking subarachnoid hemorrhage

Universität München: Elektronischen Publikationen

Joachim Velden

Petra Milz

Frank Winkler

Klaus Seelos

Gerhard F. Hamann

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Nonionic Contrast Neurotoxicity after Coronary Angiography Mimicking Subarachnoid Hemorrhage

http://epub.ub.uni-muenchen.de/16807/1/10_1159_000070198.pdf

Nonionic contrast neurotoxicity after coronary angiography mimicking subarachnoid hemorrhage

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