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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

  • Marta Aguilar Pérez
  • Muhammad AlMatter
  • Hans HenkesEmail author
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Abstract

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.

Keywords

Basilar artery aneurysm Crossing Solitaires Aneurysm recurrence Vasospasm Antiaggregation 

Patient

LA 49-year-old, male, spontaneous SAH, Hunt and Hess IV, Fisher IV

Diagnostic Imaging

The patient was in his usual condition and, apart from poorly controlled arterial hypertension, healthy when he presented with severe headache and lost consciousness. Emergency CT and CTA in the referring hospital showed a massive SAH and a wide-necked aneurysm of the basilar artery bifurcation (Fig. 1). The clinical condition of admission was Hunt and Hess IV, the SAH grading was Fisher IV. An external ventricular drainage was inserted.
Fig. 1

CT (a, b) and CTA (c) of a 49-year-old patient with spontaneous SAH. The basal cisterns (a) and the ventricles (b) are filled with fresh clot, the lateral ventricles are enlarged. CTA (c) reveals a wide-necked aneurysm of the basilar artery bifurcation with a longitudinal diameter of about 10 mm

Treatment Strategy

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.

Treatment

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

Premedication: none

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)

Course of treatment: The right VA was catheterized with a 6F guide catheter. DSA confirmed the aneurysm of the basilar artery bifurcation with a neck width of 4 mm and a longitudinal diameter of 10 mm. The origin of the left PCA was incorporated in the aneurysm neck. The left PCA was catheterized with a 0.021″ ID microcatheter (Fig. 2d), and a Solitaire 4/20 stent was deployed from the left P1 segment to the distal segment of the basilar artery (Fig. 2e). Thereafter the right PCA was catheterized through the shaft of the first Solitaire stent. A second Solitaire 4/20 stent was deployed in a crossing fashion from the right PCA to the distal segment of the basilar artery (Fig. 2f). After the electrolytic detachment of the Solitaire stents was the aneurysm catheterized (Fig. 2g, h) and densely occluded with coils (Fig. 2i, j).
Fig. 2

DSA with injection of the right VA shows the ruptured aneurysm of the basilar artery bifurcation (a, pa view; b, lateral view, c, rotational DSA with 3D reconstruction). Catheterization of the left PCA (d) and Solitaire stent deployment (e, circle around distal markers of the stent in the left PCA), followed by crossing deployment of a second Solitaire into the right PCA (f, circle around distal markers of the stent in the right PCA). Catheterization (g, h) and coil occlusion (i) of the aneurysm. The unsubtracted image shows the position of the crossing stents and the intra-aneurysmal coils (j)

Duration: 1st–35th DSA run: 285 min; fluoroscopy time: 99 min

Complications: none

Postmedication: 1× 100 mg ASA (Aspirin, Bayer Vital) PO daily lifelong, 1× 75 mg clopidogrel (Clopidogrel, Zentiva) PO daily for 6 weeks

Clinical Outcome

The patient remained sedated and ventilated.

Follow-Up and Subsequent Treatments

CT 3 days after the endovascular treatment (01.07.2010) showed a partial infarct of the anterior and medial part of the left thalamus (Fig. 3a). DSA on the same day was within normal limits (Fig. 3b, c).
Fig. 3

CT 3 days after spontaneous SAH and coil occlusion assisted by crossing Solitaire stents of the ruptured basilar artery bifurcation aneurysm shows an infarct of the anterior and medial part of the left thalamus (a). DSA of the posterior circulation is essentially within normal limits (b, pa view; c, lateral view). DSA of the right (d) and left (e) anterior circulation shows vasospasm of both ACAs and the left MCA. Short-term IA infusion of 10 ml nimodipine could not prevent bilateral frontal lobe infarctions, seen on the CT examination the next day (f, circle indicates bilateral frontal lobe infarcts). DSA 1 day after the examination shown in (d), (e). The vasospasm on the right (g) and left (h) side has increased. Microcatheters were introduced in both ICAs to allow continuous IA infusion of nimodipine (i, see circles around distal markers of the microcatheters). DSA after 3 days with IA infusion of nimodipine into both ICAs. The vessel diameter of the right (j) and the left (k) ACA has improved; the left MCA is almost back to normal. Four days later, after the failed attempt to replace the external ventricular drainage, a small hemorrhage of the right basal ganglia is observed on CT (l)

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.

Routine follow-up DSA 9 months after the initial treatment showed a significant reperfusion of the previously ruptured and coiled aneurysm (Fig. 4a, b), which was reoccluded 7 weeks later by inserting another eight coils (Fig. 4c).
Fig. 4

DSA follow-up of a ruptured basilar bifurcation aneurysm 9 months after coil-occlusion assisted by crossing Solitaire stents (a, pa view; b, lateral view) with significant aneurysm reperfusion. The aneurysm was again occluded by insertion of eight coils 11 months after the initial treatment (c)

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.

Clinical Outcome

The final outcome of the patient was equivalent to mRS 3. His handicap was related to the massive SAH and the poorly controlled vasospasm in the aftermath.
Fig. 5

DSA follow-up 7 months (a) and 55 months (b) after the retreatment confirmed the persistent complete occlusion of the ruptured and coiled basilar artery bifurcation aneurysm. At 30 months after the SAH, the patient suffered an embolic stroke with ischemic lesions in the posterior circulation, including a left partial PCA infarct causing an incomplete right hemianopia. Atrial fibrillation was the most likely reason

Discussion

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.

Cross-References

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Copyright information

© Springer Nature Switzerland AG 2018

Authors and Affiliations

  • Marta Aguilar Pérez
    • 1
  • Muhammad AlMatter
    • 1
  • Hans Henkes
    • 1
    Email author
  1. 1.Neuroradiologische KlinikNeurozentrum, Klinikum StuttgartStuttgartGermany

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