Combined stent retriever angioplasty and continuous intra-arterial nimodipine infusion as salvage therapy for cerebral vasospasm and delayed cerebral ischemia after subarachnoid hemorrhage: illustrative case

Andreas Knoll Departments of Neurosurgery, and

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Gregor Durner Departments of Neurosurgery, and

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Michael Braun Neuroradiology, University of Ulm, Günzburg, Germany

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Bernd Schmitz Neuroradiology, University of Ulm, Günzburg, Germany

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Christian Rainer Wirtz Departments of Neurosurgery, and

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Ralph König Departments of Neurosurgery, and

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Andrej Pala Departments of Neurosurgery, and

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BACKGROUND

Delayed cerebral ischemia (DCI) and cerebral vasospasm (CV) are severe complications of spontaneous subarachnoid hemorrhage (SAH) contributing to an inferior outcome. Rescue therapies include intra-arterial balloon angioplasty and repetitive and finally continuous intra-arterial nimodipine infusion.

OBSERVATIONS

In the presented case, a young female patient with fulminant refractory DCI and CV, despite induced hypertension and nimodipine application, was treated with three-vessel continuous intra-arterial infusion and additional repetitive angioplasty of the basilar and middle cerebral arteries using a stent retriever, leading to a good clinical outcome. Additional stent retriever dilatation to continuous intra-arterial nimodipine application in three vessel territories may represent a further escalation step in the rescue therapy for severe CV and DCI after SAH. Montreal Cognitive Assessment and SF-36 testing showed satisfactory results 3 months after initial treatment with intra-arterial nimodipine catheters in three vessel territory circulations and additional stent retriever vasodilation of severe CV.

LESSONS

We report a unique rescue strategy involving implantation of an additional intra-arterial catheter into the vertebral artery and repetitive stent retriever dilatations of the middle cerebral and basilar arteries as an extra therapy for continuous intra-arterial nimodipine vaspospasmolytic therapy in three vessel territories, resulting in a very good clinical outcome.

ABBREVIATIONS

ACA = anterior cerebral artery; CT = computed tomography; CV = cerebral vasospasm; DCI = delayed cerebral ischemia; ICA = internal carotid artery; MCA = middle cerebral artery; MOCA = Montreal Cognitive Assessment; PICA = posterior inferior cerebellar artery; SAH = subarachnoid hemorrhage; TCD = transcranial Doppler ultrasonography

BACKGROUND

Delayed cerebral ischemia (DCI) and cerebral vasospasm (CV) are severe complications of spontaneous subarachnoid hemorrhage (SAH) contributing to an inferior outcome. Rescue therapies include intra-arterial balloon angioplasty and repetitive and finally continuous intra-arterial nimodipine infusion.

OBSERVATIONS

In the presented case, a young female patient with fulminant refractory DCI and CV, despite induced hypertension and nimodipine application, was treated with three-vessel continuous intra-arterial infusion and additional repetitive angioplasty of the basilar and middle cerebral arteries using a stent retriever, leading to a good clinical outcome. Additional stent retriever dilatation to continuous intra-arterial nimodipine application in three vessel territories may represent a further escalation step in the rescue therapy for severe CV and DCI after SAH. Montreal Cognitive Assessment and SF-36 testing showed satisfactory results 3 months after initial treatment with intra-arterial nimodipine catheters in three vessel territory circulations and additional stent retriever vasodilation of severe CV.

LESSONS

We report a unique rescue strategy involving implantation of an additional intra-arterial catheter into the vertebral artery and repetitive stent retriever dilatations of the middle cerebral and basilar arteries as an extra therapy for continuous intra-arterial nimodipine vaspospasmolytic therapy in three vessel territories, resulting in a very good clinical outcome.

ABBREVIATIONS

ACA = anterior cerebral artery; CT = computed tomography; CV = cerebral vasospasm; DCI = delayed cerebral ischemia; ICA = internal carotid artery; MCA = middle cerebral artery; MOCA = Montreal Cognitive Assessment; PICA = posterior inferior cerebellar artery; SAH = subarachnoid hemorrhage; TCD = transcranial Doppler ultrasonography

Cerebral vasospasm (CV) is a severe complication of spontaneous subarachnoid hemorrhage (SAH).1 Coherent delayed cerebral ischemia (DCI) with severe neurological deficits is still a limiting factor for a good functional outcome.2,3 Oral nimodipine therapy remains the only approved medical treatment related to a better functional outcome after SAH.4,5 Intravenous nimodipine application may be advantageous in patients fed by a nasogastric tube, as suggested by Isse et al.6 Improved bioavailability achieved by intravenous administration may reduce CV and DCI and improve the functional outcome. Further possible rescue therapies suggested in cases of severe and refractory CV and DCI are intra-arterial balloon angioplasty and repetitive and finally continuous intra-arterial nimodipine infusion.7–12 Nevertheless, despite these therapies and many scientific efforts, functional outcome in cases of severe CV and DCI remains unfavorable. The potential additional combination of intra-arterial continuous nimodipine infusion with local stent retriever dilatation and escalation of vasospasmolysis including the vertebral artery may be a further step in the rescue therapy for patients with severe, refractory DCI and CV.

Illustrative Case

History and Examination

A 44-year-old female patient presented to our neurosurgical department with severe SAH (Hunt and Hess grade IV, Fisher grade III) caused by a ruptured basilar aneurysm. Initially, during a woodland walk, the patient experienced a massive headache. An emergency service was called, and the patient was transferred to the nearest hospital. On admission to the primary hospital, no neurological deficits were detected. Based on her severe headache and progressive meningism, computed tomography (CT) was performed and showed a severe SAH with hydrocephalus (Fig. 1). Due to recurrent nausea and vigilance deterioration, mechanical ventilation and sedation were needed. On admission to our hospital, the patient presented with normal pupillary function. Hydrocephalus was immediately treated with two ventricular drains. The intracranial pressure measured intraoperatively reached 30 cm H2O. Subsequently, the ruptured basilar aneurysm and an incidental posterior inferior cerebellar artery (PICA) aneurysm were treated with interventional stent-assisted Woven Endobridge embolization of the basilar aneurysm and coiling of the PICA aneurysm. Afterward, sedation and mechanical ventilation were stopped and extubation was possible. The patient showed no neurological deficits in the intensive care unit. Because of the stent implantation, platelet aggregation inhibition with aspirin and clopidogrel (Plavix) was started.

FIG. 1
FIG. 1

Axial (left) and sagittal (right) CT scans acquired at admission, depicting severe spontaneous SAH (Fisher grade III) extending into the perimesencephalic and prepontine cisterns (white arrows) and in the sylvian fissure.

Transcranial Doppler ultrasonography (TCD) was performed daily under intravenous vasospasm therapy with nimodipine (2 mg/hr). TCD is performed daily as a screening method, and if we find a 30% increase of blood flow velocity or >120 cm/sec or neurological deterioration in patients without sedation and ventilation, CT, CT angiography, and perfusion are performed. In the case of CV and/or DCI confirmed by CT angiography, induced hypertension (mean arterial pressure 100–110 mm Hg) together with the intravenous application of nimodipine is routinely used in our department. If further progress of DCI is confirmed and results in a perfusion delay, salvage therapy with continuous intra-arterial nimodipine infusion is considered. The detailed management has been described in our previous publications.10,13

Therapeutic Intervention

Six days after SAH, the patient suddenly exhibited confusion despite ongoing intravenous nimodipine application. Although no significant increase in blood velocity of the middle cerebral artery (MCA; mean 100 cm/sec) and internal carotid artery (ICA; mean 80 cm/sec) was detected by TCD, a severe DCI due to CV in the MCA/anterior cerebral artery (ACA) territory of both sides was identified on CT angiography (Fig. 2). Consequently, intra-arterial microcatheters were placed into the petrosal part of both ICAs for continuous intra-arterial vasospasmolysis with nimodipine (0.8 mg/hr on each side). During intra-arterial catheter placement, therapeutic body weight-adapted anticoagulation using enoxaparin (Clexane) was performed. CT and CT angiography were performed the day after because of elevated blood flow detected with TCD, and persistent severe CV and hypoperfusion in the MCA territory as an expression of DCI on the right side were detected. Based on that, an additional temporary stent retriever-assisted dilatation of the MCA (Aperio Hybrid, preset LITE 4 × 20 mm, Acandis) was performed for 10 minutes on both sides (Fig. 3). In 2 days, progressive DCI and CV of the basilar artery was detected on CT angiography, so another intra-arterial microcatheter through the right brachial artery was placed in the right vertebral artery for continuous vasospasmolysis with nimodipine. The next day, additional basilar artery dilatation with a stent retriever (Solitaire 4/40) was performed (Fig. 4). On day 14, a further angioplasty using a stent retriever in the left MCA was needed because of severe recurrent CV. TCD showed only mild correlation to clinical and radiological progress of the CV during the treatment period.

FIG. 2
FIG. 2

CT angiography (upper) and perfusion CT (lower) at the time of initial bleeding (left) and at the beginning of the vasospasm (right). Perfusion CT showed severe reduction of brain perfusion. CT angiography depicted vasospasm of the MCA and ACA on both sides (white arrows).

FIG. 3
FIG. 3

Vasospasm of the MCA immediately before (left) and after (right) additional mechanical vasodilatation with a stent retriever for 10 minutes. The M1/M2 segments are indicated by white arrows.

FIG. 4
FIG. 4

Vasospasm of the basilar artery immediately before (left) and after (right) additional mechanical vasodilatation with stent retriever for 10 minutes.

After 17 days, intra-arterial catheters could be removed and nimodipine medication was administered intravenously and finally orally for an additional 2 weeks. After successful reduction of sedation, mechanical ventilation was not necessary anymore. The patient was finally transferred to a rehabilitation unit and recovered almost entirely after 3 months. Her Montreal Cognitive Assessment (MOCA) score was 27/30 and SF-36 was 75% 3 months after treatment.

To our knowledge, we present the first case of combined continuous intra-arterial nimodipine application in both ICAs and in the vertebral artery as well as stent retriever angioplasty of the MCA and basilar artery in severe and refractory diffuse vasospasm of the anterior and posterior circulation, resulting in a good clinical outcome.

Patient Informed Consent

The necessary patient informed consent was obtained in this study.

Discussion

DCI and CV remain severe complications of SAH, limiting patients’ functional outcome given the lack of therapeutic options.1,14,15

Observations

We report on a 44-year-old female with severe diffuse CV and DCI despite maximal therapy using continuous intra-arterial infusion in three vessel territories including the vertebral artery with simultaneous dilation of the MCA and basilar artery with a stent retriever. Finally, a very good functional outcome was confirmed by MOCA and SF-36 at 3 months after discharge. Despite extensive research of DCI, detailed pathophysiological mechanisms remain unclear.15 Nimodipine is still the only approved medication resulting in a better clinical outcome after CV and DCI.4,16 The potential advantages of intravenous or intra-arterial application are the subject of intensive discussion and ongoing research.17–19 Continuous intra-arterial nimodipine has been proposed as a salvage therapy for refractory CV and DCI.7,8,18 However, the clinical benefit must be considered because of the potential serious complications.20 Nevertheless, patients with severe and refractory DCI and CV without further therapeutic options may profit from this therapy.10,19,21 A question arises: is there a possible escalation in patients who exhibit a further increase of DCI and CV despite continuous intra-arterial vasospasmolytic therapy.

In the presented case, CV and DCI increased within 24 hours of intra-arterial vasospasmolysis according to CT angiography. Hypotension, increased intraventricular pressure, or other factors possibly reasonable for reduction of brain perfusion were excluded. Especially the basilar artery was severely affected. After interdisciplinary discussion, an additional intra-arterial catheter in the MCA and vertebral artery was implanted, and further treatment escalation with additional temporary stent retriever dilation (Aperio Hybrid) of both MCAs (M1 and M2) was performed for 10 minutes on each side (left side twice). Additionally, stent retriever angioplasty of the basilar artery was done for 10 minutes. The synergistic effect of mechanical dilatation during ongoing intra-arterial nimodipine application and reduction of CV was detected during conventional angiography, after the stent retriever was removed and the microcatheter was again implanted for continuous intra-arterial nimodipine application.

Although only small series have reported on such matters, complications after intra-arterial balloon dilatation in the treatment of CV are relatively high. As reported by Higashida et al.,22 vessel rupture occurred in up to 7.1% of cases. Based on that, we decided to use a stent retriever for this procedure to decrease potential complications. The device has already been used for the treatment of CV after SAH, and nowadays it has been used routinely in thromboembolic stroke and may have a lower traumatic impact on vessels.23,24

This invasive therapy resulted in a very good clinical outcome, confirmed by functional tests. Based only on this case, we surely cannot compare the treatment results with those of large cohort studies. However, in selected cases in young patients with no history of other comorbidities, this invasive therapy may be an option in desperate cases of CV and DCI. Conscious study has shown that CV is not the only reason for a bad outcome, and intensive research is dealing with DCI and its consequences for SAH patients.25 Nevertheless, nimodipine may have further beneficial impact on microcirculation and reduction of severe CV as in presented case; it seems to be reasonable for improvement of cerebral perfusion and oxygenation, especially if both anterior and posterior circulations are affected. Complications resulting from nimodipine are one potential limitation; however, as reported by our study group earlier, the negative effects are difficult to predict and must be considered individually since many patients may profit from this therapy even despite an excessive vasopressor dose.21 In the presented case, despite a considerable nimodipine dose, we did not note any additional severe complications. Nevertheless, this additional therapy escalation must be considered individually. In some reports, a very bad outcome was reported after continuous intra-arterial therapy.26 According to our experience published in previous studies, these patients may achieve a good outcome.10,21 However, patients and time point selection for this treatment is surely crucial, and better characterization of these aspects is necessary for the success of this treatment.

Additionally, another aspect of and potential players are antiplatelet or nonsteroidal anti-inflammatory agents.27,28 Their role in DCI therapy is a matter of extensive research. It has been shown that antiplatelet agents may have a beneficial effect on patient outcome.28 In the presented case, dual antiplatelet therapy with aspirin and clopidogrel was performed from the beginning of aneurysm treatment, and we cannot exactly define the impact of this medication on clinical outcome, but there may be a synergistic effect to intra-arterial vasospasmolysis. Furthermore, the benefit for CV seems to be limited, so there could be a potential benefit of all three therapeutic approaches. In our opinion, the sweeping effect of the treatment path in our case was a combination of systemic and mechanical treatment in the acute phase of vasospasm. The combination of stent retriever vessel dilation and continuous intra-arterial nimodipine infusion even in the basilar artery is feasible and may be an effective treatment option in cases of persistent and severe CV and DCI.

Limitations

Further clinical studies must confirm the potential benefit of the proposed therapy. Given the single case, surely our aim is not to provide general recommendations but to suggest a possible solution in desperate cases of CV and DCI affecting young and healthy patients without large primary cerebral injuries. Patient selection is still unclear, and further potential risks, as discussed above, must be considered.

Lessons

Stent retriever dilatation in severe and refractory vasospasm in addition to ongoing continuous intra-arterial vasospasmolysis therapy may be an optional rescue treatment strategy. Furthermore, placement of an intra-arterial catheter in the vertebral artery is feasible and may be considered in patients with fulminant basilar vasospasm without causing further side effects, such as the dislocation or thrombosis of small brainstem vessels in our case.

Author Contributions

Conception and design: Pala. Acquisition of data: Pala, Knoll, Schmitz. Analysis and interpretation of data: Pala, Knoll. Drafting the article: Pala, Knoll. Critically revising the article: Knoll, Durner, Braun, Schmitz, Wirtz. Reviewed submitted version of manuscript: König. Approved the final version of the manuscript on behalf of all authors: Pala. Administrative/technical/material support: Schmitz, König. Study supervision: Wirtz, König.

References

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  • Collapse
  • Expand
  • FIG. 1

    Axial (left) and sagittal (right) CT scans acquired at admission, depicting severe spontaneous SAH (Fisher grade III) extending into the perimesencephalic and prepontine cisterns (white arrows) and in the sylvian fissure.

  • FIG. 2

    CT angiography (upper) and perfusion CT (lower) at the time of initial bleeding (left) and at the beginning of the vasospasm (right). Perfusion CT showed severe reduction of brain perfusion. CT angiography depicted vasospasm of the MCA and ACA on both sides (white arrows).

  • FIG. 3

    Vasospasm of the MCA immediately before (left) and after (right) additional mechanical vasodilatation with a stent retriever for 10 minutes. The M1/M2 segments are indicated by white arrows.

  • FIG. 4

    Vasospasm of the basilar artery immediately before (left) and after (right) additional mechanical vasodilatation with stent retriever for 10 minutes.

  • 1

    Miller BA, Turan N, Chau M, Pradilla G. Inflammation, vasospasm, and brain injury after subarachnoid hemorrhage. BioMed Res Int. 2014;2014(2):384342.

  • 2

    Macdonald RL, Schweizer TA. Spontaneous subarachnoid haemorrhage. Lancet. 2017;389(10069):655666.

  • 3

    AlMatter M, Aguilar Péreza M, Bhogal P, Hellstern V, Ganslandt O, Henkes H. Results of interdisciplinary management of 693 patients with aneurysmal subarachnoid hemorrhage: clinical outcome and relevant prognostic factors. Clin Neurol Neurosurg. 2018;167:106111.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 4

    Pickard JD, Murray GD, Illingworth R, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ. 1989;298(6674):636642.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Mees SD, Rinkel GJ, Feigin VL, et al. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev. 2007;2007(3):CD000277.

  • 6

    Isse FA, Abdallah YEH, Mahmoud SH. The impact of nimodipine administration through feeding tube on outcomes in patients with aneurysmal subarachnoid hemorrhage. J Pharm Pharm Sci. 2020;23(1):100108.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 7

    Ott S, Jedlicka S, Wolf S, et al. Continuous selective intra-arterial application of nimodipine in refractory cerebral vasospasm due to aneurysmal subarachnoid hemorrhage. BioMed Res Int. 2014;2014(2):970741.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 8

    Hänggi D, Turowski B, Beseoglu K, Yong M, Steiger HJ. Intra-arterial nimodipine for severe cerebral vasospasm after aneurysmal subarachnoid hemorrhage: influence on clinical course and cerebral perfusion. AJNR Am J Neuroradiol. 2008;29(6):10531060.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 9

    Bashir A, Andresen M, Bartek J Jr, Cortsen M, Eskesen V, Wagner A. Intra-arterial nimodipine for cerebral vasospasm after subarachnoid haemorrhage: Influence on clinical course and predictors of clinical outcome. Neuroradiol J. 2016;29(1):7281.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 10

    Pala A, Schneider M, Brand C, et al. The evolution of invasive cerebral vasospasm treatment in patients with spontaneous subarachnoid hemorrhage and delayed cerebral ischemia—continuous selective intracarotid nimodipine therapy in awake patients without sedation. Neurosurg Rev. 2019;42(2):463469.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 11

    Eskridge JM, McAuliffe W, Song JK, et al. Balloon angioplasty for the treatment of vasospasm: results of first 50 cases. Neurosurgery. 1998;42(3):510517.

  • 12

    Bejjani GK, Bank WO, Olan WJ, Sekhar LN. The efficacy and safety of angioplasty for cerebral vasospasm after subarachnoid hemorrhage. Neurosurgery. 1998;42(5):979987.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13

    Pala A, Durner G, Braun M, Schmitz B, Wirtz CR, Coburger J. The impact of an ultra-early postoperative mri on treatment of lower grade glioma. Cancers (Basel). 2021;13(12):2914.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 14

    Al-Khindi T, Macdonald RL, Schweizer TA. Cognitive and functional outcome after aneurysmal subarachnoid hemorrhage. Stroke. 2010;41(8):e519e536.

  • 15

    Dodd WS, Laurent D, Dumont AS, et al. Pathophysiology of delayed cerebral ischemia after subarachnoid hemorrhage: a review. J Am Heart Assoc. 2021;10(15):e021845.

  • 16

    Allen GS, Ahn HS, Preziosi TJ, et al. Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med. 1983;308(11):619624.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 17

    Mayer TE, Dichgans M, Straube A, et al. Continuous intra-arterial nimodipine for the treatment of cerebral vasospasm. Cardiovasc Intervent Radiol. 2008;31(6):12001204.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 18

    Bele S, Proescholdt MA, Hochreiter A, et al. Continuous intra-arterial nimodipine infusion in patients with severe refractory cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a feasibility study and outcome results. Acta Neurochir (Wien). 2015;157(12):20412050.

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 19

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