Basilar Artery Trunk Aneurysm: Spontaneous Subarachnoid Hemorrhage Due to an Aneurysm Associated with a Fenestration of the Basilar Artery, Endovascular Coil Occlusion
- 85 Downloads
The following case concerns a young female patient with spontaneous subarachnoid hemorrhage (SAH) due to a ruptured aneurysm originating at a non-fused, fenestrated proximal segment of the basilar artery. The aneurysm was treated with endovascular coil embolization which resulted in complete exclusion, and the patient showed a complete clinical recovery. A second aneurysm originating from the left internal carotid artery (ICA) was diagnosed during the follow-up and was treated in a separate session using a flow diverter stent. Three additional cases of ruptured aneurysms of non-fused basilar arteries are presented at the end of the discussion. Basilar artery fenestration with associated aneurysm formation is the main topic of this chapter.
KeywordsBasilar artery trunk Fenestration Subarachnoid hemorrhage Coiling pCONus
A previously healthy 28-year-old female patient presenting with spontaneous subarachnoid hemorrhage resulting in a severe headache of sudden onset (Hunt and Hess grade I). The physical examination was unremarkable.
Due to the distribution of the SAH, the BA trunk aneurysm was presumed to be the most likely cause of the SAH. As the fundus-to-neck ratio was favorable, the decision was made to treat with endovascular coil occlusion. In anticipation of a possible coil dislocation and the emergent need for an adjunctive device (i.e., a stent), the patient was pretreated with dual antiplatelets the evening before the treatment.
Procedure #1, 12.06.2014: endovascular coil occlusion of a ruptured aneurysm at the proximal third of the BA trunk
Anesthesia: general anesthesia; intraprocedural medications, 1000 mg thiopental (Trapanal, Nycomed) IV, 1 mg glyceroltrinitrate (Nitrolingual infus., Pohl - Boskamp) IA
Premedication: 1× 500 mg ASA (Aspirin, Bayer Vital) and 1× 180 mg ticagrelor (Brilique, AstraZeneca) both PO the evening prior to the endovascular treatment
Access: right common femoral artery; 1× 6F sheath (Terumo); guide catheter, 1× 6F Heartrail II (Terumo); microcatheter, 1× Echelon-14 (Medtronic); microguidewire, 1× Synchro2 0.014″ 200 cm (Stryker)
Coils: 1× GDC 360° 6/11 (Stryker), 1× HydroCoil 5/15, 1× MicroPlex10 4/8; 3× MicroPlex10 3/8; 1× MicroPlex10 2/6 (MicroVention)
Duration: 1st–35th DSA run, 105 min; fluoroscopy time, 44 min
Post medication: standard posthemorrhagic vasospasm prophylaxis; ASA and ticagrelor were discontinued
Follow-Up and Subsequent Treatment
The patient had an uneventful recovery after the first endovascular treatment. Although the BA trunk aneurysm was the most likely cause of the hemorrhage, rupture of the left ICA aneurysm could not be completely ruled out. The patient was thus offered and accepted endovascular treatment of the left ICA aneurysm during the same hospitalization. As this was a side-wall wide-necked aneurysm, covering with a flow diverter was deemed to be the most suitable treatment.
Procedure #2, 17.06.2014: endovascular treatment of a wide-necked left ICA aneurysm at the level of the PcomA using flow diversion
Anesthesia: general anesthesia; 5000 U unfractionated heparin IV, 500 mg ASA IV, 600 mg clopidogrel PO, 1 mg glyceroltrinitrate (Nitrolingual infus., pohl - Boskamp) IA
Access: right common femoral artery, 1× 6F sheath (Terumo); guide catheter, 1× 6F Heartrail II (Terumo); microcatheter, 1× Excelsior XT-27 (Stryker); microguidewire, 1× Synchro2 0.014″ (Stryker)
Implant: 1× p64 flow modulation device 3.5/15 mm (phenox)
Duration: 1st–10th DSA run, 20 min; fluoroscopy time, 14 min
Post medication: 1× 100 mg ASA PO daily for life, 1× 75 mg clopidogrel PO daily for 1 year
The postprocedural course was uneventful, and the patient was discharged home 12 days after the hemorrhage with no neurological or cognitive deficit (modified Rankin Scale 0, Glasgow Outcome Score 5).
Follow-Up and Subsequent Treatment
Normal variants and anomalies of the cerebral vasculature are frequent (Van Den Bergh and Van Der Eecken 1968; Puchades-Orts et al. 1976). Some of these variants are very common and readily apparent on imaging; others, however, are less frequent and require special attention to identify. Both normal variants and anomalies can be associated with an increased frequency to aneurysm formation and rupture.
Some of anatomic variants of the cerebral vasculature are best understood based on the embryonic development of the cerebral vessels. The anterior and posterior cerebral circulation develops separately and differently during embryonic life. While the internal carotid arteries and their branches are formed through serial changes to the pharyngeal arches connecting the ventral and dorsal aortae, the posterior circulation develops from longitudinal anastomoses between the cervical segmental arteries known as the longitudinal neural system. The basilar artery is formed through midline fusion of the posterior longitudinal system. Incomplete fusion to some extent leads to a fenestration or segmental non-fusion of the basilar artery (Padget 1948). Another possible explanation for duplicated segments of the vertebrobasilar system is persistence of the primitive lateral basilovertebral anastomosis (Gregg and Gailloud 2017). The basilar artery and the vertebral arteries are common locations for intracranial arterial fenestration (Sanders et al. 1993). One review of 2280 cranial MR angiographies detected fenestration of the basilar artery in 23 (1%) cases with the majority of detected fenestrations occurring proximal to the origin of the AICA (Tanaka et al. 2006). The incidence of BA fenestration is even higher in postmortem series (Wollschlaeger et al. 1967). Double and multiple concurrent fenestrations of the vertebrobasilar system have also been reported (Fujimura et al. 1997; Stark et al. 2013).
Intracranial arterial fenestration is reported to be associated with higher incidence of intracranial aneurysms of over 30% (Miyazaki et al. 1981; Campos et al. 1987; Picard et al. 1993; Tasker and Byrne 1997; Tanaka et al. 2006). A series of 103 posterior circulation aneurysms reported fenestration of the basilar artery in nine cases, and the aneurysm was located at the site of fenestration in 6 of them (Tasker and Byrne 1997). Possible explanation of the high frequency of aneurysms associated with arterial fenestration is defects in the medial layers at the proximal and distal edges of the fenestration (Finlay and Canham 1994). Hemodynamic stress from two separate inflows from both vertebral arteries has been suggested as a possible explanation for the formation of kissing aneurysms at the site of fenestration (Tsuei et al. 2009).
Like the majority of posterior circulation aneurysms, these lesions are frequently best treated via an endovascular approach. Simple coil occlusion can be safely performed if the anatomy is favorable (Nakstad et al. 1998). In the case of a wide-necked aneurysm, an adjunctive device may become necessary (Stark et al. 2013).
- Padget DH. The development of the cranial arteries in the human embryo. Contrib Embryol. 1948;32:205–61.Google Scholar
- Stark MM, Skeik N, Delgado Almandoz JE, Crandall BM, Tubman DE. Concurrent basilar artery double fenestration with aneurysm and vertebral artery dissection: case report and literature review of rare cerebrovascular abnormalities. Ann Vasc Surg. 2013;27(4):497.e15–21. https://doi.org/10.1016/j.avsg.2012.06.017.CrossRefGoogle Scholar