Basilar Artery Bifurcation Aneurysm: Acute SAH, Ruptured Wide Neck Basilar Bifurcation Aneurysm, Coil Occlusion Assisted by Crossing Solitaire Stents, Symptomatic Vasospasm, Intra-arterial Nimodipine Infusion, Poor Clinical Outcome
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A medium-sized, wide-necked ruptured aneurysm of the basilar artery bifurcation was treated by endovascular coil occlusion assisted by crossing Solitaire stents (Medtronic). The initial clinical status of the patient was Hunt and Hess IV with a Fisher grade of IV. Three days after the subarachnoid hemorrhage, a routine CT examination showed an infarction of the left thalamus. Angiographic vasospasm was found 9 days after the subarachnoid hemorrhage and was treated by intra-arterial nimodipine (Nimotop S, Bayer Vital) infusion. Despite the angiographic improvement of the vasospasm, follow-up MRI showed bilateral frontal lobe infarcts. An attempted exchange of the external ventricular drainage 17 days after the subarachnoid hemorrhage and under dual platelet inhibition failed and caused a minor right basal ganglia hemorrhage. A ventricular-peritoneal shunt was installed 4 weeks after the subarachnoid hemorrhage. Follow-up angiography showed an asymptomatic reperfusion of the basilar bifurcation aneurysm, which prompted an uneventful recoiling 11 months after the subarachnoid hemorrhage. Bilateral small intradural aneurysms of the internal carotid arteries were treated by flow diversion using Pipeline (PED, Medtronic). Follow-up angiography examinations confirmed the complete exclusion of all three aneurysms from the brain circulation 17 months after the subarachnoid hemorrhage and 4 months after the last flow diverter treatment. Two years after the subarachnoid hemorrhage the patient was still suffering from severe cognitive deficits with amnesia. Thirty months after the subarachnoid hemorrhage an ischemic stroke with right hemianopia and dysarthria occurred and was due to emboli into the posterior circulation related to intermittent atrial fibrillation. The combination of a massive subarachnoid hemorrhage and the subsequent cerebral vasospasm left the patient with a minor hemiparesis and persistent cognitive deficits, which prevented him from his previously independent life (mRS 3). The main topics of this report are the crossing stent technique and the management of severe vasospasm.
KeywordsBasilar artery aneurysm Crossing Solitaires Aneurysm recurrence Vasospasm Antiaggregation
LA 49-year-old, male, spontaneous SAH, Hunt and Hess IV, Fisher IV
The primary goal of the treatment was the prevention of a recurrent SAH. Neither the clinical condition of the patient nor the location and size of the aneurysm appeared suitable for microsurgical clipping. Endovascular coil occlusion after reconstruction of the basilar artery bifurcation with crossing Solitaire (Medtronic) stents was preferred. During further course, the patient had endovascular treatment of cerebral vasospasm to prevent cerebral ischemia, a recurrent coil occlusion of the basilar bifurcation aneurysm to prevent rehemorrhage and a flow diverter treatment of incidental bilateral ICA aneurysms to prevent growth and possible rupture of the intradural aneurysms.
Procedure #1, 28.06.2010: stent-assisted coil occlusion of the basilar artery aneurysm
Anesthesia: general anesthesia; 5000 IU unfractionated heparin (Heparin Natrium, B. Braun) IV, 500 mg ASA (Aspirin i.v., Bayer Vital) IV, 600 mg clopidogrel (Plavix, Sanofi-Aventis) PO via a gastric tube
Access: right femoral artery, 6F sheath (Terumo); guide catheter: 6F Guider Softip (Boston Scientific); microcatheters: 2× Prowler Select Plus (Codman) for Solitaires, Excelsior SL10 (Stryker) for coils; microguidewires: Traxcess14 (MicroVention), Mirage 0.008″ (Medtronic), Radiofocus GT with Goldcoil 0.016″ (Terumo)
Implants: 2 stents: 2× Solitaire 4/20, (Medtronic); 25 coils (all Medtronic): 1× Morpheus 3D 4/10 (withdrawn), 1× 2D fibered (3/10), 1× 2D fibered (2/6), 3× 2D super soft (2/4), 1× 2D super soft (2/6), 14× 2D super soft (2/4), 4× 2D super soft (2/2)
Duration: 1st–35th DSA run: 285 min; fluoroscopy time: 99 min
Postmedication: 1× 100 mg ASA (Aspirin, Bayer Vital) PO daily lifelong, 1× 75 mg clopidogrel (Clopidogrel, Zentiva) PO daily for 6 weeks
The patient remained sedated and ventilated.
Follow-Up and Subsequent Treatments
Nine days after the SAH, vasospasm of both ACAs and the left MCA was suspected, based on transcranial Doppler sonography; thus confirmed by DSA (Fig. 3d, e). Despite a short-term IA infusion of 10 ml nimodipine over 20 min giving some resolution of the vasospasm, bilateral frontal lobe ischemic lesions were shown by CT the next day (Fig. 3f).
In order to avoid further ischemic brain damage, the patient was brought to the angio suite immediately after the CT examination. DSA now showed a significant worsening of the vasospasm (Fig. 3g, h). Via bilateral 4F sheaths, two Marathon (Medtronic) catheters were introduced into each ICA (Fig. 3i). The patient received 1× 8000 U certoparin (Mono-Embolex, Aspen) SC daily. Via each microcatheter, 5 ml nimodipine (Nimotop S, Bayer Vital) per hour was infused.
DSA after 3 days with continued IA infusion of nimodipine confirmed a significant improvement in the diameters of both ICAs and the left MCA (Fig. 3j, k). CT 2 days later showed no new ischemic lesions. A further 2 days later, an attempt to insert a new external ventricular drainage failed; CT revealed now a small hemorrhage of the basal ganglia (Fig. 3l).
Four weeks after the SAH a ventriculo-peritoneal shunt operation was performed. The patient was transferred for further rehabilitation 2 days later, still intubated and ventilated. The left leg was plegic and the left arm was paretic. The hemiparesis improved gradually. During the following months severe cognitive deficits with anterograde amnesia persisted. The patient improved considerably, becoming able to walk again without assistance; however, he did require close supervision and was never again able to return to his previous profession as a gardener.
DSA follow-up seven and 55 months after the retreatment (Fig. 5a, b) confirmed the persistent occlusion of the aneurysm. Small incidental aneurysms of both ICAs, each at the origin of the superior hypophyseal artery, were treated 12 months (right) and 14 months (left) after the SAH by flow diversion using PEDs. A first DSA follow-up 4 months after the second PED implantation showed both aneurysms still perfused. A subsequent DSA follow-up 10 months after the second flow diversion treatment confirmed the complete obliteration of both ICA aneurysms. At 30 months after the SAH the patient presented with a left visual field cut, ataxia, dysarthria, and nausea. MRI showed ischemic lesions in the supply territories of both AICAs and the left PCA (Fig. 5c), most likely related to an embolic event. The hemianopia persisted, the other symptoms resolved within 3 months. Neither DSA examinations nor a cardiological work-up showed other reasons for these embolic lesions than intermittent atrial fibrillation.
Basilar artery bifurcation aneurysms carry an increased rupture risk (Murayama et al. 2016; Wermer et al. 2007). The prognosis after SAH from aneurysms in this location is worse compared to others (Abla et al. 2014; Osawa et al. 2001). In general, endovascular coil occlusion of ruptured intracranial aneurysms yields better results than microsurgical clipping (Nagashima et al. 2004). Good results of the endovascular treatment of basilar bifurcation aneurysms in particular have been reported for both incidental and ruptured aneurysms (Henkes et al. 2005). The use of stent-assisted coiling for ruptured aneurysms in the acute phase after SAH may be associated with an increased risk of both ischemic and hemorrhagic complications (Piotin et al. 2010). This is the reason while we were hesitant for several years to use intracranial stents in the acute phase SAH setting. Meanwhile, good safety margins have been reported for acute phase stent deployment despite dual antiaggregation (Qian et al. 2017). The use of crossing stents became an accepted technical option (Fargen et al. 2013). Since 2010, when the treatment of this report took place, several modifications have become part of our clinical practice. We replaced the loading dose from 1× 500 mg ASA IC and 1× 600 mg clopidogrel PO to 1× 500 mg ASA IV, 1× 180 mg ticagrelor (Brilique) PO and the body weight adapted bolus dose of eptifibatide (Integrilin) IV. The use of crossing self-expanding stents has been replaced by the implantation of an intra-extra saccular bifurcation device (pCONus) (Pérez et al. 2017). The amount of metal within the vessel bifurcation is at least a theoretical concern. The main issue is related to the need to catheterize both efferent arteries of the aneurysms. Depending on the bifurcation angle, this can be anything from difficult to simply impossible. Posthemorrhagic vasospasm, as encountered in this patient, remains the main cause of handicap or death after SAH and after survived acute phase treatment. If IV and short-term IA infusion of nimodipine fails, the intra-arterial infusion of nimodipine for three to 4 days is worth to try (Musahl et al. 2011). The mechanical dilatation using stent-retrievers like Solitaire or pREset is an alternative, which was only recently proposed (Bhogal et al. 2017). The initial results with this treatment modification are quite promising. The recurrent perfusion of a previously completely coiled aneurysm is more frequent if the coil treatment was carried out in the acute phase after SAH (Nguyen et al. 2007; Pandey et al. 2007; Raymond et al. 2003). Recoiling, as was done in this patient, is the accepted mode of treatment (Henkes et al. 2006). Concomitant aneurysms in other locations may carry a higher risk of hemorrhage after an aneurysmal SAH from another aneurysm (Murayama et al. 2016; White and Wardlaw 2003). For aneurysms of the ICA, flow diversion has meanwhile become the treatment of choice (Becske et al. 2017). In this patient, the endovascular treatment was able to prevent a recurrent SAH from any of the three intracranial aneurysms. His poor clinical outcome is within the range of expectations (Henkes et al. 2005). The underlying reasons are most likely related to the initial SAH, a temporarily elevated ICP and the ischemic brain injury due to vasospasm. The statistical risk of poor clinical outcome after aneurysmal SAH with an initial clinical condition equivalent to Hunt and Hess IV in a 49-year-old patient is in the range of two-thirds of patients (de Oliveira Manoel et al. 2016). The emboli into the posterior circulation about 5 years after the SAH were most likely related to an intermittent atrial fibrillation.
- Abla AA, Wilson DA, Williamson RW, Nakaji P, McDougall CG, Zabramski JM, Albuquerque FC, Spetzler RF. The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial. J Neurosurg. 2014;120(2):391–7. https://doi.org/10.3171/2013.10.JNS13419.CrossRefPubMedGoogle Scholar
- Becske T, Potts MB, Shapiro M, Kallmes DF, Brinjikji W, Saatci I, McDougall CG, Szikora I, Lanzino G, Moran CJ, Woo HH, Lopes DK, Berez AL, Cher DJ, Siddiqui AH, Levy EI, Albuquerque FC, Fiorella DJ, Berentei Z, Marosföi M, Cekirge SH, Nelson PK. Pipeline for uncoilable or failed aneurysms: 3-year follow-up results. J Neurosurg. 2017;127(1):81–8. https://doi.org/10.3171/2015.6.JNS15311.CrossRefPubMedGoogle Scholar
- de Oliveira Manoel AL, Mansur A, Silva GS, Germans MR, Jaja BN, Kouzmina E, Marotta TR, Abrahamson S, Schweizer TA, Spears J, Macdonald RL. Functional outcome after poor-grade subarachnoid hemorrhage: a single-center study and systematic literature review. Neurocrit Care. 2016;25(3):338–50.CrossRefPubMedGoogle Scholar
- Fargen KM, Mocco J, Neal D, Dewan MC, Reavey-Cantwell J, Woo HH, Fiorella DJ, Mokin M, Siddiqui AH, Turk AS, Turner RD, Chaudry I, Kalani MY, Albuquerque F, Hoh BLA. Multicenter study of stent-assisted coiling of cerebral aneurysms with a Y configuration. Neurosurgery. 2013;73(3):466–72. https://doi.org/10.1227/NEU.0000000000000015.CrossRefPubMedGoogle Scholar
- Osawa M, Hongo K, Tanaka Y, Nakamura Y, Kitazawa K, Kobayashi S. Results of direct surgery for aneurysmal subarachnoid haemorrhage: outcome of 2055 patients who underwent direct aneurysm surgery and profile of ruptured intracranial aneurysms. Acta Neurochir. 2001;143(7):655–63. Discussion 663–4.CrossRefPubMedGoogle Scholar