25.1 Case Description
25.1.1 Clinical Presentation
A 59-year-old female was transferred to our regional stroke center with a 90-minute history of sudden onset aphasia, right hemiplegia, and neglect. National Institutes of Health Stroke Scale (NIHSS) score was 28. She had known atrial fibrillation, and anticoagulation was on hold in view of a recent surgical procedure. In addition to the history of atrial fibrillation comorbidities included hypertension, which was controlled on medication. There were no other cardiovascular risk factors.
25.1.2 Imaging Workup and Investigations
Noncontrast enhanced computed tomography (NCCT) of the brain (Fig. 25.1a) demonstrated some loss of gray-white matter differentiation in the left lentiform nucleus and insular region. Elsewhere, the gray-white matter differentiation was preserved. There was hyperdensity which was consistent with thrombus in the left carotid termination and proximal middle cerebral artery (MCA; Fig. 25.1b).
Computed tomography angiography (CTA), single-phase study performed from the level of the aortic arch, showed filling of the left common carotid artery (CCA), and very proximal left internal carotid artery (ICA; Fig. 25.1c, d). There was, however, no contrast opacification of the left ICA beyond the level of the carotid bulb (Fig. 25.1e). The same applied to the left intracranial ICA, ICA termination, and M1 segment of MCA (Fig. 25.1f–h). The left A1 segment and more distal left anterior cerebral artery (ACA) appeared patent on CTA. Left MCA branches in the sylvian fissure filled through leptomeningeal collaterals (not shown). Subsequent catheter angiogram performed for purposes of endovascular stroke treatment showed that the left cervical and proximal intracranial ICA was, in fact, patent; injection of the left cervical ICA demonstrated slow filling of the ICA to the level of the supraclinoid segment where there was abrupt “cut-off” of contrast filling in keeping with left carotid terminus occlusion (Fig. 25.2a–d).
Left cervical and proximal intracranial ICA “pseudo-occlusion” in the setting of left carotid terminus occlusion.
Intravenous thrombolysis was contraindicated in view of the recent surgery and therefore not administered. The patient was transferred directly to the neurointerventional suite.
8-Fr short angiographic sheath.
8-Fr MERCI balloon guide catheter.
5-Fr VTK slip catheter.
0.035 Terumo angled guidewire.
Trevo 18 microcatheter.
Synchro 14 microguidewire.
Trevo ProVue 4 × 20 mm stent retriever.
8-Fr Angio-Seal closure device.
Endovascular treatment was performed with conscious sedation and local anesthetic. Heparin was not administered. A single-wall common femoral artery (CFA) puncture was performed, and an 8-Fr short vascular access sheath inserted. An 8-Fr balloon guide catheter was advanced to the cervical portion of the left ICA over a 5-Fr VTK slip catheter with the aid of an angled Terumo guidewire using roadmap guidance. Left ICA angiography showed slow filling of the left carotid artery to the level of the supraclinoid segment, where there was a sharp cut-off with meniscus sign at the proximal clot face (Fig. 25.2a–d). There was no anterograde flow and no opacification of the MCA or ACA. Contrast stagnation and layering was noted in the cervical and supraclinoid ICA. A Trevo 18 microcatheter was navigated across the occluded carotid terminus and left M1 segment of MCA and into the superior division of MCA. Microcatheter injection confirmed position distal to thrombus in a good caliber M2 branch. A Trevo ProVue 4 × 20 mm stent retriever device was then deployed from the proximal M2 segment back to the supraclinoid segment of the ICA (Fig. 25.2e).
Control angiography with the stent in situ showed some antegrade flow through the deployed stent with filling defect consistent with thrombus in the supraclinoid ICA and carotid terminus region (Fig. 25.2e). The stent was left in situ for 5 minutes to allow incorporation of thrombus and then retrieved using flow arrest and continuous aspiration. Clot fragments were retrieved in the stent, and on aspiration of the guide catheter. Control angiography showed complete recanalization of the left ICA, MCA, and the filling of the left ACA from the carotid injection (Fig. 25.2f, g). There was complete reperfusion of the distal territory (TICI 3), with no evidence of thromboembolic complication. Some mild vasospasm of the left cervical ICA was seen postretrieval which did not require treatment.
All devices were removed. An 8-Fr Angio-Seal was inserted for hemostasis at the femoral artery puncture site.
The patient demonstrated on-table improvement following clot retrieval with improved power in the right arm and leg, along with some improvement of aphasia and neglect. She was transferred to the neuro high-dependency unit (HDU) for further monitoring and care.
NCCT of the head performed 24 hours postprocedure (Fig. 25.2h) demonstrated infarction in the left lentiform nucleus, caudate, insula, and small volume patchy left frontal lobe infarction, with no evidence of hemorrhage.
Following CT, the patient was commenced on intravenous heparin infusion for anticoagulation. Anticoagulation with apixaban was later commenced.
On 3-month follow-up in clinic, the patient was well, with no residual significant symptoms or deficit (modified Rankin scale [mRS] of 0).
25.2 Companion Case
25.2.1 Clinical Presentation
A 58-year-old man was admitted through the emergency department with right-sided hemiparesis and expressive dysphasia. He was last seen well 4 hours previously. The NIHSS score was 23. Cardiovascular risk factors included a long history of cigarette smoking (0.5 pack/day for 38 years). There was also a positive family history of stroke, with his brother having experienced a stroke at the age of 60 years. In addition, the patient had a 10-month history of T4M1 goblet cell carcinoma of appendix, which was being treated with surgery and chemotherapy. The prestroke mRS score was 0.
25.2.2 Imaging Workup and Investigations
NCCT demonstrated subtle early ischemic changes with loss of gray–white matter differentiation in the region of the left caudate nucleus, insula, and left superior frontoparietal region with an Alberta Stroke Program Early CT (ASPECTS) score of 6 (Fig. 25.3a–c). No evidence of hemorrhage was seen. Hyperdense vessel sign was seen extending from the midportion of the left M1 to the proximal M2 (not shown).
CTA performed as single-phase study from the level of the aortic arch showed filling defects consistent with partially occlusive thrombus in the left distal M1 segment of MCA and proximal M2 branches (Fig. 25.3d). In the neck, there was filling of the left CCA and left external carotid artery (ECA); however, the left ICA appeared occluded (Fig. 25.3e). On correlation with axial source images, soft plaque/thrombus was noted at the origin of the left ICA, with only a small focus of contrast opacification of the left ICA in the region of the carotid bulb (Fig. 25.3f). More distally in the neck, there was no contrast opacification of the ICA (Fig. 25.3g, h). Distally, there was reconstitution of the distal ICA via the left posterior communicating artery (not shown).
Subsequent MRI and gadolinium-enhanced MRA on the day following presentation demonstrated that the left ICA was patent; however, there was severe, more than 90%, stenosis of the left ICA origin (Fig. 25.4a).
Partially occlusive left M1–M2 thrombus, with left cervical ICA “pseudo-occlusion” in the setting of severe left ICA origin stenosis.
As the patient was within the 4.5 hour window from onset of symptoms, intravenous tissue plasminogen activator (tPA) was administered. The NIHSS score decreased to 14 within 30 minutes of initiation of the tPA infusion.
Endovascular therapy was discussed; however, the decision was taken to not proceed in view of a combination of the following factors: already established early infarction with ASPECTS score of 6, the presence of partially occlusive thrombus with some contrast opacification around the thrombus, improvement with tPA to an NIHSS score that probably reflected the already established infarction, and the presence of an ICA pseudo-occlusion which would likely require acute intervention with angioplasty with or without stenting and acute initiation of antiplatelet therapy.
Follow-up imaging with MRI and gadolinium-enhanced MRA demonstrated patency of the left ICA with severe, more than 90%, stenosis of the left ICA origin and recanalization of the left MCA (Fig. 25.4a). Diffusion-weighted imaging (DWI) demonstrated diffusion restriction in keeping with infarction in the left caudate nucleus, insula, anterior temporal lobe, frontal and parietal lobes, as well as left posterior watershed territory (Fig. 25.4b–d). There was no evidence of hemorrhagic transformation.
Lipid lowering medication and antiplatelet therapy was commenced. The patient demonstrated further interval improvement to NIHSS score of 6 during his hospital stay. He was discharged to stroke rehabilitation center 5 days following admission. He subsequently underwent left carotid endarterectomy for the management of the left ICA stenosis.