Abstract 097: Un‐stumped by Carotid Stump Syndrome: Use of External Carotid Stenting in Preventing Ischemic Stroke

Abstract

Introduction Recurrent infarcts to the internal carotid artery territory in the setting of a corresponding occlusion raises concern for carotid stump syndrome. Over time, robust anastomoses may develop between the patent ipsilateral external carotid artery and the anterior circulation distal to the site of occlusion. A carotid stump’s disturbance of flow uncommonly can form emboli that travel via retrograde flow from the occluded internal carotid artery to the ipsilateral external carotid artery and its collaterals. Stenosis of the external carotid artery in such patients can be a source of atheroembolism or hypoperfusion. We describe a case of external carotid stenting with carotid stump coil occlusion. Methods We present a case report. Verbal consent to share this information was obtained directly from the patient. Results A 75‐year‐old man with aortic stenosis, atrial arrhythmia, multiple prior bi‐hemispheric strokes, on aspirin and clopidogrel, presented with left facial droop, arm weakness, and slurred speech. Magnetic resonance imaging revealed embolic appearing strokes in the right middle cerebral artery territory (Figure 1A). Cerebral angiography revealed complete occlusion of the right internal carotid artery with perfusion of the right middle cerebral artery by external carotid artery anastomoses, and the external carotid was found to be stenosed proximally. Digital subtraction angiography revealed right external carotid – middle cerebral artery anastomoses via the right sphenopalatine artery, middle meningeal artery, internal maxillary artery, and ophthalmic collaterals (Figure 1B). The patient underwent coiling of the right internal carotid artery stump (Figure 1C) followed by stenting of the right external carotid using a 9 mm x 40 mm Cordis precise Pro stent. Post‐stenting angiogram demonstrated good apposition of the stent to the parent vessel walls and improvement of flow into the right external carotid and intracranial circulation (Figure 1D). The patient was treated with aspirin and ticagrelor for 3 months. Repeat imaging at follow up did not show further embolic episodes, with improvement in the patient’s deficits. After three months, he was continued on aspirin alone. Conclusion In patients with an occluded internal carotid artery and recurrent embolic infarcts ipsilateral to the side of the occlusion, carotid stump syndrome may be considered. In this case, we believe the patient’s carotid occlusion served as a nidus for emboli formation, or that there was atheroembolism from the stenosed external carotid artery despite adherence to dual antiplatelet therapy. By coiling the stump, we addressed a possible source of emboli, and stenting of the proximal external carotid optimized anterograde flow and prevented further atheroembolism. Our case showcases an interventional neuroradiology approach to carotid stump emboli and external carotid artery stenosis.