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| REVIEW ARTICLE |
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| Year : 2019 | Volume
: 67
| Issue : 5 | Page : 1194-1199 |
Rupture of Intradural Giant Aneurysms: The Mode of Treatment, Anatomical, and Mechanical Factors
Xianli Lv1, Zhiyong Chen2, Liguo Liu3, Chuhan Jiang1, Guihuai Wang1, Jin Wang1
1 Department of Neurosurgery, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing, China
2 Department of Neurosurgery, Qinhunangdao Jungong Hospital, Qinhuangdao, China
3 Department of Neurosurgery, Jikuang Hospital, Jixi, Heilongjiang, China
| Date of Web Publication | 19-Nov-2019 |
Correspondence Address:
Dr. Jin Wang
Neurosurgical Department, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Litang Road 168, Beijing - 102218
China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.271250
Objective: Aneurysm rupture is often a fatal complication of giant intradural aneurysm (GIA) treatments. The purpose of this study was to review aneurysm rupture in GIA treatment.
Materials and Methods: We performed a systematic review on aneurysm rupture related to GIA treatment. For each reported case, we collected the following information: aneurysm location, size and rupture status, the mode of treatment, timing of the hemorrhage, anatomical, and hemodynamic factors.
Results: We identified 56 aneurysm ruptures related to treatment in 38 published studies. Of the nine intraoperative ruptures, eight occurred during endovascular procedures and one in surgical treatment. Of the 47 delayed ruptures, 72.3% occurred within 2 weeks. The prognosis of intraoperative and delayed ruptures was poor, with 83.9% experiencing death. Of these aneurysms, 75% were initially unruptured. Of the delayed ruptured aneurysms, 21.3% had prior surgical treatment, 74.4% had prior endovascular treatment, and 4.3% had prior combined surgical and endovascular treatments. Vertebrobasilar artery (VBA) location was significantly associated with aneurysm rupture after treatment, occurring at 57.2%. Flow diverter (FD) treatment seemed to elevate the delayed rupture proportion of giant paraclinoid internal carotid artery (ICA) aneurysms from 22.0% to 42.9%. FD treatment did not lower the rupture risk of giant VBA aneurysms and the corresponding death rate.
Conclusion: Intraoperative and delayed aneurysm ruptures were the most challenging in endovascular treatment of GIAs. Giant VBA aneurysm had the highest rupture risk after treatment. FD seemed to elevate the delayed rupture proportion of giant paraclinoid aneurysms.
Keywords: Giant aneurysm, intradural, rupture, treatment
Key Message: Intraoperative and delayed aneurysm ruptures are the most challenging in endovascular treatment of GIAs. Giant VBA aneurysm has the highest rupture risk after treatment. The prognosis of intraoperative and delayed ruptures is poor. VBA location was significantly associated with aneurysm rupture after treatment.FD seemed to elevate the delayed rupture proportion of giant paraclinoid aneurysms and did not lower the rupture risk of giant VBA aneurysms. New strategies for GIA treatment need to be explored.
How to cite this article:
Lv X, Chen Z, Liu L, Jiang C, Wang G, Wang J. Rupture of Intradural Giant Aneurysms: The Mode of Treatment, Anatomical, and Mechanical Factors. Neurol India 2019;67:1194-9 |
How to cite this URL:
Lv X, Chen Z, Liu L, Jiang C, Wang G, Wang J. Rupture of Intradural Giant Aneurysms: The Mode of Treatment, Anatomical, and Mechanical Factors. Neurol India [serial online] 2019 [cited 2019 Dec 7];67:1194-9. Available from: http://www.neurologyindia.com/text.asp?2019/67/5/1194/271250 |
Lv X and Chen Z contributed equally in this article.
Giant cerebral aneurysms (measuring greater than 25 mm) represent 5% of intracranial aneurysms and become symptomatic between 40 and 70 years of age with a female predominance.[1],[2] Giant aneurysms are found mostly in the cavernous and paraclinoid segments, and within the internal carotid artery (ICA) and the vertebrobasilar artery (VBA). They often present with mass effect, intracerebral hemorrhage, cranial neuropathies, and thromboembolism. Classified as saccular, fusiform, and serpentine, the natural history of giant cerebral aneurysms is characterized by thrombosis, growth, and rupture.[1],[2] Five-year cumulative rupture rates for patients with a giant aneurysm were 40% for those located on the anterior part of circle of Willis and 50% for those with the aneurysm located on the posterior part.[2],[3] The poor outcome of untreated patients justifies the therapeutic risks. The study of Zhang et al.[4] includded 39 patients with a giant aneurysm and pointed out that untreated giant aneurysms have a higher morbidity and mortality compared to patients treated with the endovascular technique. Although surgical therapy has evolved with refinement of microsurgical technique, combined surgical morbidity and mortality have remained in the 20–30% range for many years.[5] Persistent morbidity with surgical therapy and steady advances in endovascular therapy have encouraged attempts at coiling of giant aneurysms, with or without the assistance of stents.[6] Although coil embolization has been successful at aneurysm obliteration with improved patient outcomes compared with clip ligation, endovascular treatments yielded a dramatic decline in perioperative mortality for treatment of giant aneurysms.[5] Incomplete obliteration and aneurysm recanalization remain a problematic event in coil embolization (with or without stenting) of giant aneurysms frequently resulting rupture. In addition to coiling techniques, flow diversion and endoluminal reconstruction with devices like covered stents (Jostent and Willis stent graft) have been utilized with promising early results, particularly with giant aneurysms located along petrocavernous and paraclinoid segments of ICA, and along VBA.[7],[8],[9],[10] In the previous case reports, delayed aneurysm rupture was reported as a fatal complication in surgical carotid ligation and extracranial–intracranial (EC–IC) bypass, parent vessel occlusion (PVO), stent-assisted coiling, and flow diverter (FD) treatment.[3],[7],[11],[12],[13] The purpose of this study was to review aneurysm rupture in giant intradural aneurysms (GIAs) related to their treatment.
| » Materials and Methods | |  |
We conducted a PubMed search to review all studies on the treatment of giant aneurysms before December 22, 2016. We used the keywords “giant aneurysm,” “cerebral,” “intracranial,” “rupture,” “hemorrhage,” and “bleeding.” Inclusion criteria were as follows: English language and the presence of data on aneurysmal rupture postoperatively. The exclusion criteria were as follows: only a subset of patients of the total number of GIA was analyzed. We also searched the reference lists of all eligible studies and pertinent publications for additional studies. In the case of overlapping study populations, we tried to exclude the possibility of individual patients being described twice. Abstracts, methods, results, figures, and tables of the full studies were searched for data on aneurysmal rupture after treatment.
Data on GIA had to be distinguishable from those on non-GIA. Treatment outcome had to be reported insufficient detail for a clear interpretation. If relevant data, for example, treatment outcome or giant aneurysm location, were missing for a case, the entire case was excluded from the analysis.
| » Data Extraction | | |
Standardized forms were used by reviewers to extract the following data: name of study author, year of publication, patient age and sex, location, type of treatment. GIA location was categorized as paraclinoid ICA, middle cerebral artery (MCA), and VBA (including the vertebral, basilar, and posterior cerebral arteries). The type of treatment was divided into non-FD (surgical, endovascular, and combined surgical/endovascular) and FD.
| » Results | | |
Study selection
Our search strategy revealed a total number of 144 different studies, 107 of which were excluded by title and abstract screening. Of the 37 remaining studies, full texts were accessed, and 16 studies met our predefined inclusion criteria. Twenty-two additional studies were found by considering the reference lists of the previously mentioned studies. [Figure 1] presents a flow chart illustrating the above search process.[1],[2],[3],[5],[6],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35],[36],[37],[38],[39],[40],[41]
Aneurysm and patient characteristics
A total of 56 ruptured GIAs from 38 studies were included in the analysis [Table 1]. Thirty-nine patients were female and 17 were male. Patients' age were 4 months to 83 years old and mean was 54.9 years old. Mean aneurysm size was 30.5 mm (range, 25–60 mm). There were 14 ruptured GIAs and 42 unruptured GIAs. Of the 42 unruptured patients, 36 presented with massive effect, and the other 6 presented with ischemic symptoms. The location distribution of the aneurysms was 15 paraclinoid ICA, 8 MCA, 32 (58.2) VBA, and 1 PCA. Thirty-eight patients were saccular aneurysms, and 18 were fusiform. We included 14 GIAs with FD treatment and 42 non-FD treatments (29 endovascular, 11 surgical, and 2 combined). | Table 1: Studies reporting on ruptured giant intradural aneurysm related to treatment
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Study outcomes
Nine bleedings occurred intraoperatively eight related to endovascular procedures and one related to surgical treatment. Forty-seven bleedings developed several hours to 10 years post-treatment and the median delayed rupture time was 6 days. Of all 56 ruptured GIAs, 9 patients survived and 47 patients died [Table 2]. The mortality rate after GIA rupture was 83.9%. Initial SAH presentation was not associated with aneurysm rupture related to treatment. VBA location was significantly associated with aneurysm rupture after treatment and and occurred at 57.2%. FD seemed to elevate the delayed rupture proportion of giant paraclinoid ICA aneurysms from 22.0% to 42.9%. FD treatment did not affect the proportion of intraoperative aneurysm rupture. FD treatment did not lower the rupture risk of giant VBA aneurysms and the death rate caused by the aneurysm ruptured. | Table 2: Clinical data of ruptured giant aneurysms treated with non-flow-diverter and flow diverter
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| » Discussion | | |
It is known that GIAs have a high rupture and mortality rate.[4],[42] Furthermore, their optimal treatment method is not straightforward. While traditionally they have been managed with surgical clipping, this is not always possible. PVO either surgically or by the endovascular means using coils with or without bypass is still the best option and is more likely to yield permanent results.[4] However, rupture of giant aneurysm after parent vessel ligation is a rare complication and has been reported as a complication when performed in conjunction with EC–IC bypass.[30],[37],[39] This complication has also been reported after EC–IC bypass before a planned parent vessel ligation.[12],[14],[40],[41] Recently, Pandey et al.[43] have also reported that a giant ophthalmic aneurysm continued to grow on follow-up angiogram after EC–IC bypass.[44] Endovascular coiling (with or without stenting) still transforms a significant number of giant aneurysms into a chronic disease leading to recurrent aneurysm, multiple retreatments, occasional rehemorrhages, and neurological deterioration from progressive aneurysm enlargement.[28] In one of the largest endovascular experiences with 39 giant aneurysms, Jahromi et al.[27] reported a complete occlusion rate of 36%, stent-assistance in 66%, and an average of 2 sessions to treat each aneurysm. Cumulative treatment morbidity occurred in 12 patients (32%), and treatment mortality occurred in 6 patients (16%). Overall, 11 patients died at late follow-up (29%). Their follow-up was short (mean duration, 25 months), which can result in underestimates of rates of recurrence, retreatment, and complications. In the Dumont et al. series[5] of patients with giant aneurysms treated with endovascular techniques between December 2001 and July 2007, they performed a mean follow-up in excess of 2 years. The study stands as among the worst in terms of long-term mortality (at 29%) after endovascular treatment of giant aneurysms. They found that the introduction of next-generation intracranial stents and FD stents has not resulted in a dramatic decline in the incidence of complications after treatment of giant aneurysms. Their single-institution experience since then (between August 2007 and December 2012; mean follow-up ± SD, 9.4 ± 18 months) included 8 mortalities among 26 patients treated (31%), including 12 patients with perioperative complications and 12 patients with permanent neurological morbidity or death (46%) at last follow-up. Aneurysms located at the VBA junction or mid-basilar artery all resulted in permanent neurological morbidity or death.
Although FDs show promise as the simplest and most effective endovascular modalities available at present, ruptures following placement of FDs for GIAs have been previously reported.[8] In our recent review of pipeline device (PED) in giant aneurysms,[7] we showed a 16.6% mortality rate of intradural anterior and posterior circulation giant aneurysms, respectively, after postoperative hemorrhage. Seven patients (17.5%) developed intracranial hemorrhages 5 developed ischemic attacks (12.5%), and 13 (32.5%) developed mass effect after PED treatment. The complication rate of PED for giant VBA aneurysms was 77.8%. The cumulative mortality rate for giant paraclinoid ICA and MCA aneurysms was 13.3% and high up to 50% for giant VBA aneurysms. The high mortality rate of giant VBA aneurysm was contributed by hemorrhage (3/9) and mass effect (6/9). Mass effect is the most common mechanism of complications. Adjunctive coiling does not eliminate aneurysm rupture following PED therapy. The rate of complete obliteration of these giant aneurysms was only 60% among cases with follow-up. Subacute or delayed aneurysm rupture following FD therapy is not specific to PED and has also been described following placement of the Silk FD (Balt Extrusion, Montmorency, France). Efficacy after off-label use of FD and covered stents for giant aneurysms remains unclear. Our exemplary experience to date with Silk FD device and Willis covered stent has encountered hemorrhagic complications; ruptures took place in the subacute phase 2 and 4 days following treatment.
Multiple theories have been proposed to explain aneurysm rupture following therapy. Previously, it has been hypothesized that pressure changes and an inflammatory or mural destabilization after EC–IC bypass and FD therapy were responsible for aneurysm rupture.[14],[20],[22],[24] Although these were likely contributing factors, pathology at postmortem examination has supported the theory that intra-aneurysmal thrombi may result in aneurysm rupture through mechanical stretching.[16] The persistence of intra-aneurysmal flow preserves the potential for the continued accumulation of an intra-aneurysmal thrombus and aneurysm growth. Thrombus formation within the aneurysm can result in aneurysm enlargement by aggregating platelets and continuously entrapping circulating white blood cells and absorbing plasma components. The temporary swelling and increased volume of a thrombosed aneurysm following FD treatment, PVO, or EC–IC bypass might also be explained by a similar mechanism, though following gradual rather than rapid thrombosis (the latter favoring rupture). This was also documented both on a CT scan (which showed a high-density or equal-density thrombus within the aneurysm) and on angiography (which showed a much smaller aneurysm lumen compared with the pre-embolization angiogram). It has been well documented that increases in giant aneurysm size may occur after thrombosis, resulting in temporary exacerbation of symptoms.[7],[15],[25]
It is conceivable that the partially thrombosed aneurysm was enlarged by the acute luminal clot and that this led to stretching of the aneurysm wall and other morphological changes, which in turn resulted in rupture. On autopsy, the site of aneurysm rupture was directly opposite of the PED and parent vessel and had a linear appearance as if the thrombus outgrew the aneurysm and split the aneurysm wall.[16] Histopathological evaluation of the aneurysm wall at the site of rupture revealed no significant inflammatory response. It is not attributable to an inflammatory or mural destabilization process since this is likely to take days to weeks to occur. Therefore, steroid medical management may not reduce the risk of delayed aneurysm rupture. The pattern of aneurysm rupture supports the idea that flow diversion can result in aneurysm rupture through mechanical stretching, although it is highly unlikely that the aneurysm rupture in this patient was part of the natural history of the disease and unrelated to the embolization. Another unlikely possibility is that the hemorrhage occurred not from the residual lumen but from the vascularized wall. Enlargement of thrombosed giant aneurysms has been attributed to such a mechanism,[7],[21] but the partially patent lumen would be a far more likely source. It seems that conventional coil embolization has an entirely different implication than flow diversion does. While coiling has a well-described generally benign natural history, the same is not likely true for aneurysms treated with flow diversion. In the Standhardt et al. observation,[42] three (37.5%) of the eight giant aneurysms of the posterior circulation ruptured after coiling. Rupture of the aneurysms occurred between 18 and 52 months after initial treatment. The calculated annual risk of rupture is 11.5% per year. In contrast to giant aneurysms of the posterior circulation, none of the giant aneurysms of the anterior circulation ruptured.
Limitations
The major limitation of this study is the lack of exact data on the incidences of aneurysm rupture after treatment. No scientifically reliable registry data are available to address the exact incidence. We suggest that for delayed rupture to occur, a complex interaction of multiple factors is required. As of yet, these factors and interactions have been only partially unraveled for intracranial aneurysms.
| » Conclusion | | |
Intraoperative and delayed aneurysm ruptures are the most challenging in the endovascular treatment of GIAs. Giant VBA aneurysms had the highest rupture risk after treatment. FD seemed to elevate the rupture proportion of giant paraclinoid aneurysms. GIA therapy can result in aneurysm enlargement and rupture through mechanical stretching; the use of FDs is associated with a higher proportion of rupture of giant aneurysms.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| » References | | |
| 1. | Ponce FA, Spetzler RF, Han PP, Wait SD, Killory BD, Nakaji P, et al. Cardiac standstill for cerebral aneurysms in 103 patients: An update on the experience at the Barrow Neurological Institute. J Neurosurg 2011;114:877-84.  |
| 2. | Lv X, Jiang C, Li Y, Yang X, Wu Z. Treatment of giant intracranial aneurysms. Interv Neuroradiol 2009;15:135-144. |
| 3. | Ge H, Li Y, Lv X. A challenging entity of unruptured giant saccular aneurysms of vertebrobasilar artery. Neurol Neurochir Pol 2016;50:236-40. |
| 4. | Zhang Z, Lv X, Yang X, Shiqing Mu, Wu Z, Shen C, et al. Endovascular management of giant aneurysms: An introspection. Neurol India 2015;63:184-9. [ PUBMED] [Full text] |
| 5. | Dumont TM, Levy EI, Siddiqui AH, Snyder KV, Hopkins LN 3 rd. Endovascular treatment of giant intracranial aneurysms: A work in progress. World Neurosurg 2014;81:671-5. |
| 6. | Gruber A, Killer M, Bavinzski G, Richling B. Clinical and angiographic results of endosaccular coiling treatment of giant and very large intracranial aneurysms: A 7-year, single-center experience. Neurosurgery 1999;45:793-803; discussion 803-4. |
| 7. | Lv X, Ge H, He H, Jiang C, Li Y. A systematic review of pipeline embolization device for giant intracranial aneurysms. Neurol India 2017;65:35-8. [ PUBMED] [Full text] |
| 8. | Lv X, Yang H, Liu P, Li Y. Flow-diverter devices in treatment of intracranial aneurysms: A Meta-analysis and systematic review. Neuroradiol J 2016;29:66-71. |
| 9. | Lv X, Jiang C, Li Y, Lv M, Zhang J, Wu Z. Intracranial pseudoaneurysms, dissections and carotid-cavernous fistulas: Repair with percutaneous implantation of endovascular covered stents. Interv Neuroradiol 2008;14:435-40. |
| 10. | Li MH, Li YD, Fang C, Gu BX, Cheng YS, Wang YL, et al. Endovascular treatment of giant or very large intracranial aneurysms with different modalities: An analysis of 20 cases. Neuroradiology 2007;49:819-28. |
| 11. | Gentric JC, Fahed R, Darsaut TE, Salazkin I, Roy D, Raymond J. Fatal arterial rupture during angioplasty of a flow diverter in a recurrent, previously Y-stented giant MCA bifurcation aneurysm. Interv Neuroradiol 2016;22:278-86. |
| 12. | Eom KS, Kim DW, Kang SD. Intracerebral hemorrhage caused by rupture of a giant aneurysm complicating superficial temporal artery-middle cerebral artery anastomosis for moyamoya disease. Acta Neurochir (Wien) 2010;152:1069-73; discussion 1073. |
| 13. | Wu Z, Lv X, Li Y, Jiang C, Yang X. Endovascular treatment for complex intracranial aneurysms: Lessons learnt in five patients. Neuroradiol J 2010;23:459-66. |
| 14. | Anson JA, Stone JL, Crowell RM. Rupture of a giant carotid aneurysm after extracranial-to-intracranial bypass surgery. Neurosurgery 1991;28:142-7. |
| 15. | Hongo K, Morota N, Watabe T, Isobe M, Nakagawa H. Giant basilar bifurcation aneurysm presenting as a third ventricular mass with unilateral obstructive hydrocephalus: Case report. J Clin Neurosci 2001;8:51-4. |
| 16. | Fox B, Humphries WE, Doss VT, Hoit D, Elijovich L, Arthur AS. Rupture of giant vertebrobasilar aneurysm following flow diversion: Mechanical stretch as a potential mechanism for early aneurysm rupture. J Neurointerv Surg 2015;7:e37. |
| 17. | Velat GJ, Fargen KM, Lawson MF, Hoh BL, Fiorella D, Mocco J. Delayed intraparenchymal hemorrhage following pipeline embolization device treatment for a giant recanalized ophthalmic aneurysm. J Neurointerv Surg 2012;4:e24. |
| 18. | Darsaut TE, Rayner-Hartley E, Makoyeva A, Salazkin I, Berthelet F, Raymond J. Aneurysm rupture after endovascular flow diversion: The possible role of persistent flows through the transition zone associated with device deformation. Interv Neuroradiol 2013;19:180-5. |
| 19. | Fujita K, Kondo T, Matsumoto S. Experience with electrothrombosis of a giant aneurysm with copper wire. No Shinkei Geka 1987;15:75-9. [Article in Japanese] |
| 20. | Siddiqui AH, Abla AA, Kan P, Dumont TM, Jahshan S, Britz GW, et al. Panacea or problem: Flow diverters in the treatment of symptomatic large or giant fusiform vertebrobasilar aneurysms. J Neurosurg 2012;116:1258-66. |
| 21. | Chen Z, Yang Y, Miao H, Tang W, Chen J, Niu Y, et al. Endovascular treatment for large and giant fusiform aneurysms of the vertebrobasilar arteries. Clin Imaging 2013;37:227-31. |
| 22. | Hampton T, Walsh D, Tolias C, Fiorella D. Mural destabilization after aneurysm treatment with a flow-diverting device: A report of two cases. J Neurointerv Surg 2011;3:167-71. |
| 23. | Plowman RS, Clarke A, Clarke M, Byrne JV. Sixteen-year single-surgeon experience with coil embolization for ruptured intracranial aneurysms: Recurrence rates and incidence of late rebleeding. J Neurosurg 2011;114:863-74. |
| 24. | Cirillo L, Leonardi M, Dall'olio M, Princiotta C, Stafa A, Simonetti L, et al. Complications in the treatment of intracranial aneurysms with silk stents: An analysis of 30 consecutive patients. Interv Neuroradiol 2012;18:413-25. |
| 25. | van Oel LI, van Rooij WJ, Sluzewski M, Beute GN, Lohle PN, Peluso JP. Reconstructive endovascular treatment of fusiform and dissecting basilar trunk aneurysms with flow diverters, stents, and coils. AJNR Am J Neuroradiol 2013;34:589-95. |
| 26. | Pavlisa G, Ozretic D, Murselovic T, Pavlisa G, Rados M. Sole stenting of large and giant intracranial aneurysms with self-expanding intracranial stents-limits and complications. Acta Neurochir (Wien) 2010;152:763-9. |
| 27. | Jahromi BS, Mocco J, Bang JA, Gologorsky Y, Siddiqui AH, Horowitz MB, et al. Clinical and angiographic outcome after endovascular management of giant intracranial aneurysms. Neurosurgery 2008;63:662-75. |
| 28. | Sluzewski M, Menovsky T, van Rooij WJ, Wijnalda D. Coiling of very large or giant cerebral aneurysms: Long-term clinical and serial angiographic results. AJNR Am J Neuroradiol 2003;24:257-62. |
| 29. | Desai K, Nadkarni T, Muzumdar D, Goel A. Rupture of a giant posterior inferior cerebellar artery aneurysm in an infant following a ventriculoperitoneal shunt--Case report. Neurol Med Chir (Tokyo) 2001;41:127-30. |
| 30. | Chang SD, Marks MP, Steinberg GK. Recanalization and rupture of a giant vertebral artery aneurysm after Hunterian ligation: Case report. Neurosurgery 1999;44:1117-21. |
| 31. | Piepgras DG, Khurana VG, Nichols DA. Occult rupture of a giant vertebral artery aneurysm following proximal occlusion and intrasaccular thrombosis. Case report. J Neurosurg 2001;95:132-7. |
| 32. | Lubicz B, Leclerc X, Gauvrit JY, Lejeune JP, Pruvo JP. Giant vertebrobasilar aneurysms: Endovascular treatment and long-term follow-up. Neurosurgery 2004;55:316-23; discussion 323-6. |
| 33. | Hodes JE, Aymard A, Gobin YP, Rüfenacht D, Bien S, Reizine D, et al. Endovascular occlusion of intracranial vessels for curative treatment of unclippable aneurysms: Report of 16 cases. J Neurosurg 1991;75:694-701. |
| 34. | Nakajima N, Nagahiro S, Matsubara S, Satoh K. Ruptured de novo thrombotic giant aneurysm induced by ethyl 2-cyanoacrylate: Case report. Surg Neurol 2004;62:346-52. |
| 35. | Iwamuro Y, Miyake H, Ito T, Kumai J, Kuroda T, Sugino T. Recurrence of a giant fusiform aneurysm after neck clipping: Case report. No Shinkei Geka 1996;24:357-61. [Article in Japanese] |
| 36. | Civit T, Auque J, Marchal JC, Bracard S, Picard L, Hepner H. Aneurysm clipping after endovascular treatment with coils: A report of eight patients. Neurosurgery 1996;38:955-61. |
| 37. | Scott RM, Liu HC, Yuan R, Adelman L. Rupture of a previously unruptured giant middle cerebral artery aneurysm after extracranial-intracranial bypass surgery. Neurosurgery 1982;10:600-3. |
| 38. | Gurian JH, Viñuela F, Gobin YP, Waston VE, Duckwiler GR, Gulielmi G. Aneurysm rupture after parent vessel sacrifice: Treatment with Guglielmi detachable coil embolization via retrograde catheterization: Case report. Neurosurgery 1995;37:1216-21. |
| 39. | Matsuda M, Shiino A, Handa J. Rupture of previously unruptured giant carotid aneurysm after superficial temporal-middle cerebral artery bypass and internal carotid occlusion. Neurosurgery 1985;16:177-84. |
| 40. | Plangger CA, Mohsenipour I, Grunert V, Twerdy K. Rupture of a giant aneurysm of the inferior wall of the internal carotid artery after saphenous vein interposition graft to the middle cerebral artery. Zentralbl Neurochir 1989;50:61-3. |
| 41. | Heros RC, Ameri AM. Rupture of a giant basilar aneurysm after saphenous vein interposition graft to the posterior cerebral artery. Case report. J Neurosurg 1984;61:387-90. |
| 42. | Standhardt H, Boecher-Schwarz H, Gruber A, Benesch T, Knosp E, Bavinzski G. Endovascular treatment of unruptured intracranial aneurysms with Guglielmi detachable coils: Short- and long-term results of a single-centre series. Stroke 2008;39:899-904. |
| 43. | Pandey P, Rayes M, Hong D, Guthikonda M, Xavier A. Endovascular management of a giant aneurysm through saphenous vein graft after extracranial-intracranial bypass: Case report and literature review. J Neurointerv Surg 2011;3:361-3. |
| 44. | Limaye US, Baheti A, Saraf R, Shrivastava M, Siddhartha W. Endovascular management of giant intracranial aneurysms of the posterior circulation. Neurol India 2012;60:597-603. [ PUBMED] [Full text] |
[Figure 1]
[Table 1], [Table 2]
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