The Efficacy of Endovascular Stenting in the Treatment of Supraclinoid Internal Carotid Artery Blister Aneurysms Using a Stent-in-Stent Technique

Discussion

Ruptured blister aneurysms of the supraclinoid ICA present with SAH and are estimated to represent 0.9%–6.5% of ruptured intracranial aneurysms.⁹ Compared with saccular aneurysms, these lesions tend to have a more precipitous course, enlarging rapidly and rebleeding frequently. Morphologically, they appear as wide-necked, shallow outpouchings of nonbranching sites of the supraclinoid ICA. At surgery, they often contain a fragile, thin wall and a broad communication with the parent vessel, without an identifiable neck. Histologically, these lesions have been shown to represent focal wall defects covered with thin, fibrous tissue and adventitia, lacking the usual collagen layer, findings indicative of pseudoaneurysm.¹⁰ As such, these lesions have shown an association with arterial dissections.¹¹

Because of their broad-based, shallow profiles, these aneurysms often represent a diagnostic challenge, both with CTA and DSA. The imaging appearance of supraclinoid ICA blister aneurysms has been described in detail elsewhere.¹² In addition to an understanding of the morphology and distribution of these lesions, meticulous angiographic technique and a high index of suspicion are often both necessary to make this diagnosis. Any patient with SAH in an aneurysmal pattern and no detectable berry aneurysm should be carefully scrutinized for a blister aneurysm.

The 6 patients included in this study presented with acute SAH on unenhanced head CT and were diagnosed by CTA and/or DSA with blister aneurysms. In these patients, coil embolization was not performed at the initial treatment session because the operators deemed that the morphology of the aneurysms did not allow for safe coil deposition, even after stent placement. Instead, these patients were treated with a staged protocol: immediate treatment by using a stent-in-stent technique in an effort to temporize, preserve the artery, and redirect flow to prevent rehemorrhage. The second stage consisted of careful and rapid follow-up with coil embolization of the aneurysms that enlarged. Interestingly, in 3 patients, the aneurysms did not enlarge, and the stent-in-stent technique was curative.

Importantly, our patients also fell into 2 groups in terms of their initial imaging findings. In 1 group, we deemed the CTA and DSA to show definitive evidence of a blister aneurysm as the cause of the SAH. These patients were treated per our protocol as described. The second group of patients presented with suspicious but not definitive findings of blister aneurysms and were not treated immediately, but rather they were reevaluated with short-term follow-up DSA (within a few days). The reasoning for this decision stems from the concept that blister aneurysms tend to enlarge and change configuration rather rapidly. Three of our patients (50%) fell into the “suspicious but not definitive” category, all showing increase in the size and change in the configuration of the aneurysm on follow-up DSA. It should be noted that during DSA evaluation for endovascular treatment of blister aneurysms, consideration should be given to evaluating collateral flow to the affected circulation (cross-compression views, Alcock test) and possibly temporary balloon occlusion, as parent vessel occlusion remains the definitive endovascular treatment of ICA blister aneurysms, though the complications of parent vessel occlusion in the setting of acute subarachnoid hemorrhage are well documented.^13–16

Given the fragile nature of these aneurysms, they are associated with high surgical morbidity and mortality due to intraoperative rupture, regrowth, and rehemorrhage, even after the adequate aneurysm clip application.² Thus, the optimum treatment of these lesions remains uncertain, leading to attempts at numerous novel surgical^17–20 and endovascular^{2–7,9,12,17} treatment techniques.

Given the histopathology of these lesions (resembling pseudoaneurysms with an incomplete wall or fibrous capsule) and the hemodynamic stress these lesions experience, it is not surprising that these aneurysms react unfavorably after coil embolization or clipping or even after stent-assisted coil embolization. The small size and shallow, wide-necked morphology of these aneurysms makes safe deposition of coil material unlikely, due to the risk of further aneurysm rupture or coil migration. Additionally, the lack of a true aneurysm wall allows for frequent aneurysm regrowth.

Our treatment strategy in the acute setting, that is, endovascular treatment with a stent-in-stent approach, attempts to diminish the flow into and hemodynamic stresses placed upon these lesions through flow diversion. Theoretically, the overlapping stents at the aneurysm neck would create better flow diversion than a single stent. In fact, in our experience, overlapping stents markedly decrease the flow into these aneurysms, at least to visual inspection on the angiogram. Postprocedural DSA following overlapping stent placement demonstrated uniformly decreased flow within the aneurysm sacs of our cohort. Indeed, this treatment alone proved effective in 3 of our patients (50%), who have not needed further treatment or shown aneurysm regrowth at intermediate follow-up. Note that the stent-in-stent protocol should always include a plan for immediate follow-up and coiling of aneurysms that enlarge.

In our small cohort, 3 of 6 aneurysms enlarged (as expected) and underwent subsequent coil embolization as part of our planned staged procedure. In 1 patient, this goal was achieved with 1 coiling session, by using a single coil. In another patient, this entailed 3 coiling sessions and several coils. This treatment has proved effective in both of these patients, who have not shown aneurysm regrowth at intermediate follow-up.

Our final patient and only complication warrants some discussion. This patient had rebleeding from the blister aneurysm following overlapping stent deployment, necessitating eventual parent vessel occlusion. The treatment was complicated by initial maldeployment of 1 of the stents (the second stent in our stent-in-stent procedure). In retrospect, we think that this was an avoidable technical complication. As the second stent was being placed, the operator, in an effort to position it properly, maintained significant forward pressure on the stent, inadvertently forcing it forward in such a way that as it deployed, the distal end of the stent became trapped in 1 of the cells of the previously placed stent, preventing the second stent from opening properly, and resulting in poor apposition of the second stent to the wall of the vessel. We hypothesize that the poor treatment response at least partially related to abnormal flow alterations in the ICA and blister aneurysm. The second stent was at least ineffective at remodeling the artery and directing flow away from the aneurysm, and it may even have directed flow into the neck of the aneurysm, unfavorably altering the hemodynamic stresses on the wall of the aneurysm.

Park et al⁷ published a case series comparing coil embolization (with or without stent assistance or balloon remodeling) with aneurysm trapping and parent vessel occlusion, reporting much better clinical outcomes in patients undergoing parent vessel occlusion. The results of our study resemble those of their aneurysm trapping group. Given the similarity in clinical outcomes, we think that these treatment strategies should be considered as salvage procedures when initial treatments with endovascular stent placement with or without subsequent coiling have failed. This approach allows for parent vessel preservation, with concomitant reduction in the risk of subsequent stroke development. Proximal occlusion of the ICA as a definitive treatment for ruptured blister aneurysm, despite good collateral flow, has a potential of exaggerated short- and long-term cerebral ischemia, particularly in the event that these patients experience cerebral vasospasm. This point is illustrated in our patient treated with proximal ICA occlusion, who subsequently developed severe cerebral vasospasm, which severely diminished the flow to her occluded territory. This resulted in a large hemorrhagic middle cerebral artery infarction, despite aggressive medical management and intra-arterial infusion of verapamil.

The limitations of our study should be noted, including its retrospective evaluation, small study size, and lack of a comparative control group. Although our case series suggests a beneficial treatment outcome from the treatment algorithm studied, further investigation with larger patient populations and prospective evaluation (if possible) is clearly warranted to test the validity of these results.