Introduction
An increasing number of patients with subarachnoid hemorrhage (SAH) caused by vertebral artery dissecting aneurysms (VADAs) are being reported.1-7) Recent reports have suggested that recurrent bleeding from an unsecured VADA is extremely high (50%~70%) and usually occurs within 24 hours of the initial rupture.1)5)8) These reports had indicated that very early treatment of the ruptured VADA is required to prevent fatal rebleeding.1)3)5) Although many surgical and endovascular treatments for ruptured VADAs have been reported, the question of optimum treatment remains controversial. We have reported our experience with endovascular treatment in two patients with ruptured VADAs. We have reviewed these cases and have discussed the treatment and outcome of dissecting vertebral aneurysms.
Case Descriptrion
Case 1
A 36-year-old woman presented with the sudden onset of headache, vomiting, and disturbance of consciousness. A computed tomography (CT) scan showed a suba- rachnoid hemorrhage (SAH; Fig. 1 A). Subsequent cerebral angiography delineated a dissecting aneurysm of the left vertebral artery (VA), with a typical pearl-and-string sign (Fig. 1 B). The posterior inferior cerebellar artery (PICA) was not visualized, which was consistent with a type IV (non-PICA) VADA according to the Mizutani classification.5) Because the blood supply through the right VA had been sufficient and PICA had not been definite, we believed that the left VA could be sacrificed without any neurologic consequences.
Prior to occlusion of the left VA, a preliminary test occlusion of the left VA was performed using a 4 x 20 mm Savvy balloon (Cordis Corporation, Miami Lakes, FL, USA). The test balloon was positioned at the extracranial portion of the VA and inflated for 40 minutes. For the first 20 minutes, the patient had neurologic monitoring. Then, hypotension was provoked using a calcium channel blocker for another 20 minutes. The patient tolerated balloon test occlusion, and did not present with any neurologic symptoms. Following a successful test occlusion, the parent vessel, including the dissecting aneurysm, was completely occluded with 13 Guglielmi detachable coils (GDCs; two 5 mm x 15 cm, two 5 mm x 9 cm, two 4 mm x 8 cm, two 3 mm x 8 cm, three 3 mm x 6 cm, 2 mm x 6 cm, and 2 mm x 4 cm coils) introduced through an Excelsior SL-10 microcatheter (Boston Scientific, USA) (Fig. 1 C and D). The procedure was successful and free from complications. A post-operative right vertebral angiogram revealed good flow to the basilar artery (E).
Six months after the embolization, follow-up angiography was performed, which revealed preservation of the total occlusion state in the left VA (Fig. 1 D). It was determined that no further intervention was needed. At the last clinical follow-up, 12 months after the emboli- zation, the patient had recovered fully.
Case 2
A 39-year-old woman was transferred to our hospital after having a sudden, severe headache and loss of consciousness. At the time of admission, the neurologic status was classified as grade 2 according to the Hunt-Hess grading system. A CT scan revealed SAH, and cerebral angiography demonstrated a dissecting aneurysm of the dominant, right VA (Fig. 2 A). The dissection was located at the intradural segment of the right VA distal to the PICA, which was consistent with a type I (post-PICA) VADA according to the Mizutani classification.5) The left vertebral angiogram revealed that the left VA ended in the PICA (Fig. 2 B).
The patient tolerated a balloon test occlusion using a Hyper Form balloon (Microtherapeutics, USA; Fig. 2 C). The aneurysmal sac and the right VA were completely occluded with 6 GDCs (one 4 mm x 8 cm, two 2 mm x 6 cm, one 2 mm x 4 cm, and one 2 mm x 2 cm coils) under general anesthesia (Figs. 2 D and E). The right PICA was preserved and the flow to the vertebrobasilar system was preserved through the right internal carotid artery via the posterior communicating artery (Fig. 2 F). The patient had a full neurologic recovery the next day and an uneventful post-operative course. The patient was discharged and has remained well for the last 6 months.
Discussion
Recently, VADAs have been recognized with increasing frequency as a cause of stroke, which often leads to SAH. Further, VADAs have been demonstrated to have a high rate of rebleeding associated with a grim prognosis.1-3)7) Recurrent hemorrhage has generally occurred during the acute stage, usually within several hours after the initial SAH5)8). Therefore, urgent treatment for preventing fatal recurrent hemorrhage is needed.9)
The mechanism of arterial dissection has been thought to be a sudden disruption of the internal elastic lamina and subsequent penetration of circulating blood into the media. Depending on the depth of the vessel wall dissection, clinical presentation can be defined. If the internal elastic lamina has been disrupted by the dissection, SAH has been shown to occur.10)
Common methods of surgical management have included proximal occlusion of the VA, trapping, direct clipping, and vertebral arterial reconstruction. However, several authors have reported that some surgical strategies for ruptured VADAs are unsuitable in the acute stage because of a high incidence of complications.5)11) For example, Kitanaka, et al.12) reported that 29% of patients treated surgically for ruptured VADAs exhibited new post-operative deficits.12) Further, Mizutani, et al.5) reported a complication rate of 31.3% for the early surgical treatment of ruptured VADAs.5)
With the development of endovascular treatment, especially with the introduction of the GDC, end- ovascular treatment has become safer and more effective because most coils are soft and easily controlled1)4)6-7) Thus, endovascular treatment has shifted from proximal occlusion to internal trapping, in which the dissected site is completely occluded with detachable coils.7) Recently, a number of reports have demonstrated the efficacy of endovascular coil embolization for ruptured VADAs. On the basis of data culled from the literature, the endovascular approach is the best for treating ruptured VADAs in the acute stage.1)4)6-7) However, many neurosurgeons continue to render surgical treatment, thus the need for early treatment of ruptured VADAs is recognized; however, the optimal treatment has not been determined.
Because the endovascular approach using detachable coils has included the sacrifice of the affected VA, there are several limitations to this treatment, as follows: (1) bilateral lesions; (2) a hypoplastic contralateral VA; (3) PICA involved type (type II); and (4) a dissecting aneurysm that includes the basilar artery. In patients with VADAs, the best treatment may be surgical or endovascular trapping of the lesion, combined with bypass surgery, such as an occipital artery–PICA anastomosis, or using new endovascular techniques, including stent technology.2-3)13-15)
In our cases, the dissecting aneurysms were located at the dominant VAs. However, the contralateral VAs were not hypoplastic and collateral flow to the vertebrobasilar circulation was sufficient, as confirmed by the balloon test occlusion. Therefore, both cases were treated uneventfully with standard endovascular occlusion sacrificing the parent arteries. Thus, as in our cases, when dissections involve the dominant VA, a balloon test occlusion may be useful in evaluating the collateral circulation via the contralateral VA or posterior communicating arteries to the vertebrobasilar circulation.16)
Conclusion
Based on our results, and the results of previous studies, we suggest that immediate internal coil trapping is the preferred therapy in the acute phase of SAH after vertebral dissection. Even in cases of ruptured VADAs on dominant VAs, if a balloon test occlusion is tolerable, internal trapping using detachable coils may be a desirable treatment in select cases.
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