Choroid artery occlusion after treatment of ICA termination aneurysm: was it caused by stent induced vasospasm?

Abstract

Dear Sirs: Endovascular occlusion has become the main treatment for cerebral aneurysms in the last decade. This development was much facilitated by the ISAT trial [1] for ruptured aneurysms, but coiling, stenting and flow diversion are now also widely used for unruptured cases. While endovascular treatment is usually less invasive than surgical aneurysm clipping, coil occlusion of an aneurysm seems less durable. This has led to the increasing use of stents to reconstruct the vessel wall for the prevention of recurrences. If an elective stent placement is performed under appropriate antiplatelet medication, stentrelated complications such as thrombotic stent occlusion and embolic events are infrequent [2, 3]. We report on a rare complication after placement of a selfexpanding endovascular stent, leading to a disabling stroke in a young patient with an unruptured internal carotid artery (ICA) aneurysm. A 27-year-old female patient, who had delivered a healthy daughter 6 weeks previously, presented to her local hospital with transient left-sided weakness. Vascular risk factors included obesity (BMI=35 kg/m) and smoking. A probable transient ischaemic attack (TIA) was diagnosed, and the patient was investigated accordingly. While no obvious aetiologywas found for the TIA, her brain imaging had shown an incidental lesion, which was suggestive of a left ICA aneurysm with a diameter of around 10 mm. A subsequent CT angiogram (CTA) done at the local neurosciences centre confirmed the presence of a broad-based left ICA termination aneurysm with a maximum diameter of 12 mm, mostly extending on to the left M1 segment, but also slightly affecting the A1. No other aneurysm was seen. Given the size of the aneurysm, the patient was offered endovascular treatment. She was quoted a risk of permanent neurological deficit of 3 % or less. Because of the large neck size, a stent-assisted coil embolisation was planned, and the patient was asked to take 75 mg of aspirin and clopidogrel each starting 5 days before the planned procedure. The patient was admitted on the morning of the intervention and clerked by the clinical team. She confirmed having taken her dual antiplatelet therapy as prescribed. She also stated that she was only smoking occasionally, but her frequent absences from the ward suggested higher nicotine consumption on that morning. The procedure was performed under general anaesthetic (GA). However, bronchospasm and a sudden severe drop in blood saturation levels complicated the induction of the anaesthesia. The patient had no background of respiratory problems, and according to the anaesthetist, heavy smoking prior to the GAwas the most likely explanation. A diagnostic angiogram after intubation confirmed the presence of a large left carotid terminus aneurysm (Fig. 1a). No other abnormalities were seen. The patient received IV heparin under ACT monitoring (>250 s), but platelet function inhibition was not tested. Over an exchange wire, a 6-F 90-cm Terumo Destination sheath was placed into the left proximal ICA, and a Fargomax distal access catheter was advanced into the petrous segment of the ICA. This was complicated by vasospasm at the tip of the long sheath, and therefore, 2 mg of nimodipine was added to the saline flush. W. Kuker (*) Department of Neuroradiology, West Wing, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK e-mail: wilhelm.kuker@ndcn.ox.ac.uk