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Transient CT Hyperattenuation after Merci Clot Retrieval and Intraarterial Thrombolysis in Acute Stroke Mimicking Subarachnoid Hemorrhage Gyanendra Kumar, MD, Chetan Rasiklal Soni, MD, MS, and Pradeep Kumar Sahota, MD

Unenhanced computed tomography (CT) revealed hyperattenuating lesions in two patients with acute stroke immediately after clot retrieval with the Merci device in one patient and after intraarterial thrombolysis in the other. These areas of hyperattenuation were noted in the middle cerebral artery territory in the first patient and involving the brainstem, cerebellum, and tentorium in the second. Both were falsely interpreted as subarachnoid hemorrhage. The area of hyperattenuation resolved within a few hours in both patients, reflecting contrast medium extravasation/ leakage. This report highlights the need to improve physician skill in recognizing contrast medium extravasation that is common following neuroendovascular procedures, which are becoming commonplace in modern day medicine. J Vasc Interv Radiol 2010; 21:281–284 Abbreviations:

MCA ⫽ middle cerebral artery, SAH ⫽ subarachnoid hemorrhage

NEUROENDOVASCULAR procedures such as intraarterial thrombolysis, aneurysmal coiling, and mechanical clot retrieval require unenhanced head computed tomography (CT) to be performed immediately upon completion of the intervention to check for possible occurrence of hemorrhage and to evaluate progression of the initial lesion. Regardless of the success of the procedure, it is not uncommon to note hyperattenuating lesions on the postprocedure CT scans that simulate parenchymal and/or subarachnoid hemorrhage (SAH) (1– 4). These hyperattenuating lesions have been documented and described since 1977 as being either hemorrhage or the result of extravasation of the contrast media that is used during the angiography and intravascular in-

From the Department of Neurology, University of Missouri-Healthcare, CE-507 5 Hospital Dr, Columbia, MO 65212. Received March 19, 2009; final revision received October 21, 2009; accepted October 26, 2009. Address correspondence to G.K.; E-mail: [email protected] None of the authors have identified a conflict of interest. © SIR, 2010 DOI: 10.1016/j.jvir.2009.10.022

terventional procedures in either the anterior or posterior circulation territories (4 – 6). Some authors have shown that contrast medium enhancement and extravasation develop primarily in the region of the basal ganglia (most commonly the putamen and thalamus) in accordance with the specific vascular territory (6,7). Most of these highattenuation lesions resolve spontaneously (8) and reflect a mere leakage and/or extravasation of contrast medium across the blood-brain barrier (7). The difficulty that this epiphenomenon poses in distinguishing from intracerebral hemorrhage leads to false interpretation and erroneous management. Herein, we present two cases to highlight this point. A Health Insurance Portability and Accountability Act waiver was duly obtained from the institutional review board for this study.

CASE REPORTS Patient 1 A 60-year-old man developed leftsided hemiplegia, homonymous hemianopia, and hemianesthesia and presented within the 3-hour window of intravenous thrombolysis; however, he

did not qualify as he had a remote history of aneurysmal hemorrhage and subsequent ventriculoperitoneal shunt placement for hydrocephalus. The patient was taken to the angiography suite, where a right common carotid artery angiogram revealed an occlusion in the M1 segment of the right middle cerebral artery (MCA) (Fig 1a). An 8-F Merci balloon guide catheter (Concentric Medical Inc., Mountain View, California) was placed in the distal cervical segment of the right internal carotid artery. With use of an 18L Merci retriever device (Concentric Medical), two passes were made through the clot in the M1 segment of right MCA. Clot was noted in the retriever device after the second pass. Repeat right common carotid artery angiography revealed complete restoration of flow in the right anterior circulation (Fig 1b) without evidence of clot or distal emboli. The device was removed and the patient sent for unenhanced CT. The patient remained neurologically stable following the procedure and showed gradual improvement. Hemianopia resolved by day 2 and sensory deficit recovered significantly; however, severe motor deficit and cortical sensory loss persisted. The initial CT scan obtained 1

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distal, middle, and proximal portions. An additional 6 mg of alteplase was laced into the clot in two additional passes with repeat angiography. Increased incremental filling of the basilar artery was seen with successive alteplase treatments. Finally, a microcatheter was placed in the P1 segments of the left and right posterior cerebral arteries, where each side was injected with 1 mg of alteplase. The microcatheter was removed and a final angiogram obtained in anteroposterior and lateral projections. The angiogram showed recanalization of the basilar artery with restoration of flow in bilateral superior cerebellar arteries and posterior cerebral arteries (Fig 2b). Head CT performed immediately after recanalization (Fig 2c) revealed hyperattenuation along the tentorium and transverse venous sinuses, the superior vermis, bilateral cerebellar hemispheres, the upper brainstem, the floor of the 4th ventricle, and the medial occipital lobes. This was reported as SAH. Follow-up head CT performed 10 hours later revealed resolution of the ‘SAH’ (Fig 2d). Despite successful intraarterial recanalization of the basilar artery, the patient continued to deteriorate and developed acute obstructive hydrocephalus due to compression of the 4th ventricle from cerebellar swelling. He eventually died after his family refused surgical decompression and chose palliative care. Figure 1. (a) Four-vessel angiogram reveals blockage of the M1 segment of the right MCA (arrow). (b) The patency of the MCA is reestablished immediately following clot retrieval with the Merci device. (c) Head CT scan obtained immediately following clot retrieval reveals a heterogeneous area of sulcal hyperattenuation on the right side conforming to the right MCA territory. (d) Unenhanced head CT scan obtained 7 hours after retrieval of the Merci device reveals resolution of the area of hyperattenuation seen in c. It does, however, show the evolving right MCA territory infarct.

hour after the onset of stroke, before the Merci procedure, did not reveal any infarct. Head CT performed immediately after retrieval with the Merci device (Fig 1c) showed a heterogeneous area of hyperattenuation in the right MCA territory that was reported as SAH. A repeat CT scan obtained 7 hours after the procedure revealed resolution of the ‘SAH’ but did show the evolving MCA territory infarct (Fig 1d). Patient 2 An 81-year-old man developed vertigo and collapsed to the floor uncon-

scious. An unenhanced head CT scan revealed a hyperattenuating basilar artery lumen in its distal course. Magnetic resonance (MR) imaging of the brain revealed an acute infarct in the bilateral cerebellar hemispheres and upper brainstem. The patient was taken to the angiography suite because he was beyond 6 hours from the onset of stroke; right vertebral catheterization was performed, confirming the absence of anterograde flow through the distal basilar artery (Fig 2a). A microcatheter/microwire combination was advanced into the distal basilar artery and 5 mg of alteplase delivered into the clot in its

DISCUSSION Neurointerventional procedures have become a part of everyday clinical practice in modern medicine. This underscores the need to improve physician skill across all specialties to recognize the complications and epiphenomena that result as a consequence of these procedures. Contrast medium extravasation following angiographic procedures is one such epiphenomenon that gets falsely interpreted as SAH or parenchymal hemorrhage. The major premise for explaining that extravasation is disruption of the blood-brain barrier (7). Contrast medium extravasation occurs in 77% of patients who undergo angiographic thrombolysis and resolves within a few hours (9). In addition, from a prognostic perspective, contrast medium extravasation has been perceived as an endangering event following aneurysm embolization; however, neurologic outcome was unaffected (10).

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Figure 2. (a) Initial angiogram shows filling of the distal right vertebral artery and the middle to proximal basilar artery. The distal basilar artery and posterior cerebral arteries are occluded (arrow). Bilateral anterior and posterior inferior cerebellar arteries (AICA and PICA) fill. Minimal retrograde flow is seen in the distal left vertebral artery. (b) Angiogram obtained immediately after thrombolysis shows restoration of flow in the basilar artery as well as in the bilateral superior cerebellar arteries and the bilateral posterior cerebral arteries. However, the bilateral posterior cerebral arteries are severely stenotic in the distal P1 segments. (c) CT scan of the head obtained after intraarterial thrombolysis shows a new area of hyperattenuation along the tentorium and transverse venous sinuses, superior cerebellar vermis, bilateral cerebellar hemispheres, upper brainstem, cerebellar parenchyma, and floor of the 4th ventricle. (d) Follow-up unenhanced CT scan obtained after 10 hours shows resolution of the hyperattenuation and a large infarct involving the posterior fossa structures (cerebellum and upper brainstem).

There is also suggestion that it may severely worsen prognosis (11). Extravasation of contrast medium has been defined in the literature as an area of hyperattenuation with a maximal Hounsfield unit measurement of more than 90 and/or the disappearance of the hyperattenuation on a repeat CT scan obtained within 24 hours, as seen in both our patients (5). Yoon et al (7) formally distinguished contrast medium extravasation from contrast deposition and/or enhancement by using Hounsfield units and found that extravasation portended a higher symptomatic intracerebral hemorrhage rate and poorer

outcome than did enhancement. They proposed that contrast medium extravasation may be due to degradation of the basal lamina, whereas contrast enhancement may be due to increased bloodbrain barrier permeability (7). The former disruption would likely be required for hemorrhagic transformation (12). In the series by Yoon et al (6,7), contrast medium extravasation was found to occur primarily in the basal ganglia in accordance with the vascular territory being studied. Investigators have also shown that microcatheter contrast medium injections may increase the risk of intrace-



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rebral hemorrhage in the setting of combined intravenous/intraarterial recombinant tissue-type plasminogen activator therapy, possibly due to contrast medium toxicity or pressure transmission by injections (13). In our patients, extravasation of contrast medium and sulcal hyperattenuation on CT were unlikely to be due to SAH as there were no accompanying clinical symptoms (patient 1) and the area of hyperattenuation seen had resolved within a few hours (both patients). The underlying pathophysiology of this contrast medium extravasation and sulcal hyperattenuation is likely one end of the spectrum of hyperperfusion injury (13). It is unlikely to represent enhancing acute infarct because the area of hyperattenuation is sulcal and not gyral, as would be seen in an enhancing acute infarct. Hyperperfusion syndrome is conventionally defined as hemispheric neurologic deficit or seizure occurring after cerebral revascularization that is localized ipsilateral to the treated artery, not related to thromboembolism, and without evidence of new infarction on diffusion-weighted MR images (14). It is estimated to occur in 1.1%– 6.8% of patients after endovascular cerebral revascularization, with mortality rates ranging from 3% to 26% when intracerebral hemorrhage is present (15). It is not unlikely, given the poor outcome that our second patient developed hyperperfusion syndrome, although cerebellar swelling and compression leading to noncommunicating hydrocephalus would occur in an extensive posterior circulation infarct as well; thus making the distinction between the two difficult. In the day and age of neuroendovascular surgery when neurointerventional procedures have become commonplace, the phenomenon of contrast medium extravasation should be promptly recognized to avoid misdiagnosis and untoward management decisions. Its prognostic implications are still debated and need further study. References 1. Wildenhain SL, Jungreis CA, Barr J, Mathis J, Wechsler L, Horton JA. CT after intracranial intraarterial thrombolysis for acute stroke. AJNR Am J Neuroradiol 1994; 15:487– 492. 2. Nakano S, Iseda T, Kawano H, Yoneyama T, Ikeda T, Wakisaka S. Parenchymal hyperdensity on computed tomography after intra-arterial reperfusion therapy for acute

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contrast extravasation on computed tomography after intra-arterial thrombolysis in patients with acute ischemic stroke. Stroke 2004; 35:876–881. 8. Jang YM, Lee DH, Kim HS, et al. The fate of high-density lesions on the noncontrast CT obtained immediately after intra-arterial thrombolysis in ischemic stroke patients. Korean J Radiol 2006; 7: 221–228. 9. Yokogami K, Nakano S, Ohta H, Goya T, Wakisaka S. Prediction of hemorrhagic complications after thrombolytic therapy for middle cerebral artery occlusion: value of pre- and post-therapeutic computed tomographic findings and angiographic occlusive site. Neurosurgery 1996; 39:1102–1107. 10. Hue YH, Yi HJ, Kim YJ. Extravasation during aneurysm embolization without neurologic consequences: lessons learned from complications of pseudoaneurysm coiling–- report of 2 cases. J Korean Neurosurg Soc 2008; 44:178–181.

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