Treatment of giant posterior circulation aneurysms, via endovascular or microsurgical approaches, carries a high risk of morbidity and mortality. While flow-diverting stents (FDSs) represent a potent therapy for endovascular reconstruction of complex aneurysms, they are also associated with novel complications for which effective salvage techniques are lacking. We present a unique complication from failed treatment with a FDS. A 51 year-old male presented with increasing headaches secondary to a giant, fusiform aneurysm of the left posterior cerebral artery, which was largely thrombosed. Due to progressive enlargement of the aneurysm corresponding to worsening clinical symptoms, the lesion was treated with two Pipeline embolization devices (ev3, Plymouth, MN, United States). Three months after Pipeline embolization device treatment, complete posterior cerebral artery occlusion was observed at the origin of the proximal stent. Despite the lack of arterial inflow, the aneurysm dome continued to grow, resulting in obstructive hydrocephalus. Therefore microsurgical intervention was undertaken to trap and excise the aneurysm. The patient's postoperative course was complicated by multiple venous infarcts, ultimately resulting in death. Successful microsurgical obliteration of aneurysms previously treated with FDSs is extremely difficult. A combination of judicious preoperative planning and meticulous intraoperative surgical technique are requisite for effective management of these complicated cases.
Giant intracranial aneurysms, defined as those greater than 25 mm in diameter, rank among the most complex neurosurgical pathologies to safely and effectively manage.
A 51 year-old male presented to an outside institution seven years prior with chronic headaches, which began following a motor vehicle accident. He had decreased visual acuity in the left eye from a previous gunshot wound to the face. The patient was diagnosed at initial presentation with a giant, fusiform left PCA aneurysm which was partially thrombosed. It was decided at the time of diagnosis that the risk of morbidity associated with either endovascular or microsurgical treatment of the aneurysm exceeded that of conservative management. Over time, the patient's headaches progressively worsened to an average visual analog scale (VAS) score of 7/10 despite maximal medical management, and the aneurysm gradually enlarged over serial angiographic imaging. The decision was made at this time to treat the lesion via an endovascular approach with the PED (
The patient presented three months post-PED with progressively worsening headaches to an average VAS score of 9/10, new gait ataxia, and new temporal hemianopsia of the right eye. While the stents remained patent at six weeks, by the follow-up angiography at three months, the diseased segment of the left PCA had progressed to complete occlusion at the origin of the proximal PED (
The patient was repositioned for aneurysm excision through an infratemporal, post-auricular, presigmoid skull base approach. Electrophysiological monitoring, including motor and somatosensory evoked potentials (motor evoked potential (MEP) and somatosensory evoked potential (SSEP), respectively), was utilized. A standard temporal craniotomy and partial mastoidectomy were performed. During the craniotomy, the sigmoid sinus was breached, requiring hemostatic control with gelfoam tamponade. After dural opening, 50 mL of cerebrospinal fluid was drained from the external ventricular drain to facilitate brain relaxation. After opening the arachnoid of the ambient cistern, the PCA and superior cerebellar artery were identified along with the fundus of the aneurysm dome posteriorly.
Due to the high degree of thrombosis, the aneurysm was firm and immobile. Therefore the aneurysm dome was opened so that the intrasaccular thrombus could be debulked. Decompression of the fundus facilitated dissection of the aneurysm from the surrounding cortex and brainstem. The proximally placed PED was identified in the lumen of the diseased PCA without evidence of endothelialization and was removed cautiously. After PED extraction from the inflow segment of the parent artery, there was brisk bleeding from the proximal PCA which controlled by clipping the P2 segment. After further debulking of the thrombus, the distal PED placed in the aneurysm outflow was identified and a clip was placed on the outflow portion of the PCA, effectively trapping the aneurysm. The entirety of the aneurysm was then excised from the PCA (
The patient's postoperative course was complicated by an extradural hematoma requiring surgical evacuation and thrombosis of the left transverse and sigmoid sinuses, resulting in multiple large territory venous infarcts requiring decompressive craniectomy. The extent of the postoperative infarcts was neurologically devastating, and the patient expired two weeks following the initial surgical intervention.
PCA aneurysms are rare, tend to affect a relatively younger patient population, and are more likely to be non-saccular than those located at more common sites.
FDSs are a potent therapeutic option for complex aneurysms, but their applicability to aneurysms located distal to the supraclinoid internal carotid artery and those located in the posterior circulation remains controversial. Pistocchi et al. reported FDS treatment of 30 distally located aneurysms at or beyond the circle of Willis.
Furthermore, there were no endovascular options at this point since occlusion of the parent artery rendered the aneurysm inaccessible from a transarterial route. Therefore, the only feasible strategy was microsurgical excavation of the aneurysm dome, given the patient's deteriorating neurological function and the obstructive hydrocephalus caused by the expanding aneurysm dome. Since there was no distal PCA flow on preoperative angiography, surgical reconstruction of the diseased parent vessel or distal bypass were not considered in our case. Unfortunately, due to poor collateral venous drainage, injury to the sigmoid sinus during the approach ultimately proved to be lethal. The patient's preoperative angiography showed limited collateral venous drainage. Therefore, we believe that sigmoid sinus occlusion by gelfoam tamponade was the principal cause of the venous infarctions. Another potential, although less likely, cause was prolonged temporal lobe retraction during surgery, which may have resulted in impaired cortical venous return or venous occlusion.
For giant and fusiform aneurysms such as the one we presented, traditional endovascular coiling treatments are ineffective.
Based on our experience with the PED and the treatment of giant aneurysms, we believe that the use of FDSs should be very limited in perforator-rich arteries, such as the arteries comprising the circle of Willis, cerebral arteries distal to the circle of Willis, and arteries of the posterior circulation. In agreement with the literature, we found that the use of FDSs in perforator-rich arteries is associated with a significantly increased risk of thromboembolic complications. Therefore, alternative endovascular or surgical approaches should be considered for aneurysms arising from these locations before resorting to the use of FDSs. If surgery is undertaken, important countermeasures for undesirable intraoperative situations, such as major arterial or venous injury, include arterial re-anastomosis or bypass and repair or reconstruction of major venous sinuses.
This is the first reported case of PED extraction from a posterior circulation aneurysm and of microsurgical intervention following failed endovascular occlusion with a FDS. These cases are exceedingly difficult to manage successfully. Further experience and reports are necessary to define the optimal management of these patients.
Non-contrast brain computed tomography (CT), axial view, (A) shows no evidence of obstructive hydrocephalus and (B) demonstrates a round, hyperdense structure (circle) in the region of the left thalamus compatible with the partially thrombosed aneurysm sac arising from the left posterior cerebral artery (PCA) previously diagnosed. The intra-aneurysmal thrombotic mass measures 21×21 mm, increased from 17×18 mm 10 weeks prior and from 14×14 mm eight months prior. Brain CT angiography (CTA), (C) axial, (D) coronal, and (E) sagittal views, demonstrates an irregular, fusiform dilatation of the left PCA P2 and P3 segments (arrow) with a largely thrombosed aneurysm sac arising medially. Cerebral angiography, lateral (F) and anteroposterior (G) views, demonstrates a giant, fusiform aneurysm of the left distal PCA P2 and P3 segments with a similar serpentine morphology (arrow) compared to prior angiography 10 months prior. The aneurysm measures approximately 40 mm in length and its proximal dilatation has increased in size to 4.5 mm from 3.7 mm on previous angiography. Arterial flow through the diseased segment of the parent artery is mildly delayed, and the majority of the aneurysm sac known to be thrombosed from non-invasive imaging (B-E). The diameter of the parent PCA vessel is 1.3 mm. The aneurysm was treated with two telescoping pipeline embolization devices, 2.5×20 mm and 3.0×35 mm in size, without complications. The proximal (+) and distal (*) ends of the dual PED construct are marked (F, G).
Non-contrast brain computed tomography (CT), axial view, performed six weeks after pipeline embolization device (PED) treatment demonstrates (A) interval development of obstructive hydrocephalus due to (B) enlargement of the hyperdense intra-aneurysmal thrombus (circle) to 24×24 mm from 21×21 mm previously, resulting in increased mass effect upon the posterior aspect of the third ventricle. The previously deployed PEDs (arrow) are visualized within the diseased parent artery (A, B). Cerebral angiography, lateral (C) and anteroposterior (D) views, performed three months after PED treatment demonstrates thrombosis of the left PCA at the P2 segment (arrow). The origin of the thrombosis corresponds to the origin of the proximal PED.
Following an infratemporal, post-auricular, presigmoid skull base approach to the middle fossa, the (A) aneurysm dome (asterisk) was visualized superior to the tentorial incisura through a subtemporal corridor. After the aneurysm dome was excised, the pipeline embolization device (arrow) was identified within the lumen of the diseased parent posterior cerebral artery. (B) Gross examination of the debulked thrombus removed from the aneurysm sac.