Staged endovascular treatment of ruptured vertebral artery dissection involving the posterior inferior cerebellar artery

In the treatment of vertebral artery (VA) dissection involving the origin of the posterior inferior cerebellar artery (PICA), the prevention of rebleeding and the preservation of VA and PICA patency are challenging. We report a case with ruptured VA dissection involving the origin of the PICA. In the acute stage, the fusiform dilatation of the dissection was first treated by means of stent-assisted coil embolization. Dual-antiplatelet therapy was administered just before stent placement. Seven days after the first treatment, two additional stents without coils were added. Rebleeding did not occur, and the lesion was thrombosed successfully 4 days after the second treatment, with the preservation of VA and PICA patency. This staged therapy appears to be beneficial in preventing rebleeding and in preserving VA and PICA patency.

Key-words:

Antiplatelet therapy - endovascular treatment - stent-assisted coil embolization - vertebral artery dissection

Introduction

Ruptured vertebral artery (VA) dissection has a high risk of rapid rebleeding and must be treated quickly.[[1]] In the treatment of VA, dissection involving the origin of the posterior inferior cerebellar artery (PICA), the prevention of rebleeding, and the preservation of VA and PICA patency are challenging. Herein, we first report a staged therapy of ruptured VA dissection involving PICA, with the preservation of the patency of VA and PICA without cerebral infarction.

Case Report

A 48-year-old male patient presenting with sudden headache and disturbance of consciousness was referred. A computed tomography scan revealed subarachnoid hemorrhage (SAH) with acute hydrocephalus, the World Federation of Neurosurgical Societies Grade IV [[Figure 1]]a. Emergency digital subtraction angiography (DSA) under general anesthesia demonstrated stenosis and fusiform dilatation of left VA [[Figure 1]]b and [[Figure 1]]c and double origin of PICA[[2]],[[3]] [[[Figure 1]]c,[[Figure 1]]d,[[Figure 1]]e, white arrow]. The diameter of the left VA was 4.2 mm and the diameter of the main branch of the PICA was 1.2 mm. A diagnosis of ruptured VA dissection involving PICA was made.

Figure 1: (a) A computed tomography scan on admission shows a massive subarachnoid hemorrhage. (b) Right vertebral angiography. (c) Left vertebral angiography demonstrates the stenosis and fusiform dilation of the left vertebral artery. (d) Three-dimensional digital subtraction angiography reveals double origin of the posterior inferior cerebellar artery: one from the dilatation itself, and the other from the stenosis proximal to the dilatation. (e) Coil embolization of the fusiform dilatation with stenting is performed (arrow; flared ends of the stent). Vertebral artery and posterior inferior cerebellar artery patency was preserved. (f) Postoperative digital subtraction angiography (venous phase) showed contrast medium stagnated in the fusiform dilatation. White arrows (c-e) show double origin of posterior inferior cerebellar artery

First, ventricular drainage was performed on day 0. Endovascular therapy was performed on day 1 under general anesthesia. For stenting, a Prowler Select Plus microcatheter (Codman and Shurtleff, Inc., Raynham, MA) was placed into the left VA, using a contralateral approach. For coil embolization, two Excelsior SL-10 microcatheters (Stryker, Kalamazoo, MI) were placed into the fusiform dilatation of left VA, using an ipsilateral approach. Immediately after the two coils were placed, loading doses of aspirin (200 mg) and clopidogrel (300 mg) were administered. An Enterprise 2 4.0 mm × 30 mm stent (Codman and Shurtleff, Inc.) was placed over the whole lesion of left VA. Then, coil embolization was added. Postoperative DSA (venous phase) showed contrast medium stagnated at the fusiform dilatation [[Figure 1]]f, white arrowhead].

VA and PICA patency was preserved and a postoperative magnetic resonance imaging scan showed no infarction at the medulla oblongata or PICA territory. After the first treatment, to monitor the neurological condition, the patient was kept with the awake condition, under strict control of blood pressure. Dual-antiplatelet therapy (DAPT) continued with aspirin 100 mg/day and clopidogrel 75 mg/day.

Although rebleeding did not occur, follow-up DSA performed 2 days after the first treatment showed enlargement just proximal to the coil mass [[[Figure 2]]a, double arrows], but contrast medium still stagnated in the fusiform dilatation [[[Figure 2]]b, double white arrowheads]. After a plateau of inhibition of platelet aggregation achieved, a second endovascular therapy was performed 7 days after the first treatment. Under local anesthesia, an Enterprise 2 4.0 mm × 30 mm stent was placed at the enlargement of the dissection, and an Enterprise 2 4.0 mm × 39 mm stent was placed to overlap the two former stents [[Figure 2]]c. We expected a flow-diversion effect with the additional stent placement; thus, no coils were added.

Figure 2: (a and b) Digital subtraction angiography 2 days after the first treatment demonstrates the enlargement of the fusiform dilatation (a, double arrows), but contrast medium remained stagnated (b, double white arrowheads). (c) Two stents were added at the fusiform dilatation (the second stent) and the left vertebral artery over the two stents (the third stent) 7 days after the first treatment. (d) Digital subtraction angiography 4 days after the second treatment demonstrates thrombosis. (e) Digital subtraction angiography 6 months after the onset shows no regrowth (arrow, flared ends of the first stent; arrowhead, those of the second stent; and white arrowhead, those of the third stent). (f) Magnetic resonance angiography 2 years after procedure shows preservation of left posterior inferior cerebellar artery and no dilatation of the right vertebral artery

Follow-up DSA on day 12 (4 days after the second treatment) showed thrombosis of the lesion [[Figure 2]]d. After it was confirmed that repeated DSA performed before the shunt operation did not show regrowth, DAPT was changed to single-antiplatelet therapy about 1 month after second treatment due to a lumboperitoneal shunt operation for hydrocephalus. DSA performed 6 months after the onset did not show regrowth [[Figure 2]]e. Single-antiplatelet therapy has been administered, and the patient has displayed no neurological deficits over 3 years after the onset [[Figure 2]]f.

Discussion

VA dissection is normally idiopathic and is an uncommon cause of SAH. The rebleeding rate of ruptured VA dissection has been reported to be as high as 71.4% of cases; moreover, rebleeding has led to a high mortality rate.[[1]],[[4]] All possible endovascular treatment options for ruptured VA dissection involving PICA were listed as follows: parent artery occlusion with/without bypass, stent-assisted coiling, and stenting. Internal trapping or proximal/distal occlusion of parent VA by coil embolization has become the first-line treatment for ruptured VA dissection; however, parent artery occlusion for VA dissection involving PICA carries a risk of severe ischemic complications, even if occipital artery-PICA anastomosis is performed.[[5]],[[6]] In addition, de novo VA dissecting aneurysms after trapping or occlusion of a dissecting aneurysm in contralateral VA have been reported, likely due to excessive hemodynamic stress, even if the occlusion side was not the dominant side.[[7]],[[8]] Therefore, preservation of VA and PICA patency in treatment for VA dissection involving PICA is necessary. To preserve PICA patency, it was reported that an Enterprise stent was deployed from the PICA to the proximal VA and the segment of dissection was completely occluded by coils.[[9]] However, evidence detailing the feasibility, use, or safety of Enterprise stents in small cerebral vessels (<2 mm in diameter) is lacking. We did not use this strategy in this case, as the diameter of the PICA was 1.2 mm and the PICA had two origins.

We selected the strategy of stent-assisted coiling in the acute stage to prevent rebleeding. In a review of ruptured and unruptured VA dissection,[[10]] rebleeding was found to occur in 6.9% of ruptured VA dissection treated using stent placement and coils. This suggests that stent-assisted coiling alone does not completely eliminate the risk of rebleeding or enlargement of dissection.[[11]] Careful follow-up study is required to check for enlargement of residual dissection after stent-assisted coiling. On the contrary, due to a delay in aneurysmal occlusion and high complication rate, treatment using flow diverter stents without coil embolization may not be suitable for ruptured aneurysms in the acute stage.[[12]],[[13]] In addition, patients with ruptured VA dissection cannot receive premedication with antiplatelet agents, resulting in more frequent thromboembolic complications.[[11]] Placement of multiple stents or flow diverter stents in the acute stage potentially risks inducing thromboembolic complications.[[13]] In this case, DAPT continued after the first stent placement. After clopidogrel achieved a plateau of inhibition of platelet aggregation after 3–7 days,[[14]] two additional Enterprise stents were added to achieve a “flow diversion” effect because a low-profile visualized intraluminal support (LVIS) stent (MicroVention/Terumo, Aliso Veijo, CA) was not available in Japan at that time. In an aneurysm model study,[[15]] reduction in the velocity within the aneurysm sac using two Enterprise stents was not as significant as that achieved using flow diverter stents. Consistent with this finding, treatment using one Enterprise stent with coil embolization resulted in the enlargement of the fusiform dilatation, and 4 days after two additional Enterprise stents were deployed (three Enterprise stents in total), the lesion was thrombosed. Therefore, at least three Enterprise stents might be needed to achieve the flow diversion effect.

No protocol has been established for the management of antiplatelet therapy in cases of stent-assisted coil embolization for ruptured VA dissection. In this case, DAPT was changed to single-antiplatelet therapy about 1 month after the procedure due to a shunt operation, since DAPT was a significant risk factor for hemorrhagic complications associated with ventriculoperitoneal shunt placement.[[16]] In previous studies for unruptured aneurysms, the stent-containing vessel with incomplete aneurysm occlusion is a risk factor for a delayed thromboembolic event,[[17]] and long-term DAPT did not prevent the incidence of delayed thromboembolic events.[[18]] In this case, due to confirmation of thrombosis of the lesion, single-antiplatelet therapy has been administered without delayed thromboembolic event, but further studies are warranted to determine the optimal antiplatelet therapy for ruptured aneurysms.

Conclusion

Preventing rebleeding and preserving VA and PICA patency can be challenging in treatment of PICA-involved VA dissection. The reported therapy might be a treatment option.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Conflict of Interest

There are no conflicts of interest.

Financial support and sponsorship

Nil.

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Publication History

Article published online:
09 September 2022