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Local thrombolytics via balloon-assisted intra-arterial infusion as rescue therapy for thromboembolism during endovascular coil embolisation
  1. Michiyasu Fuga1,
  2. Toshihide Tanaka1,2,
  3. Akihiko Teshigawara1 and
  4. Yuichi Murayama2
  1. 1Department of Neurosurgery, Jikei University School of Medicine Kashiwa Hospital, Kashiwa‑shi, Chiba, Japan
  2. 2Department of Neurosurgery, Jikei University School of Medicine, Minato-ku, Tokyo, Japan
  1. Correspondence to Dr. Michiyasu Fuga; fugamichiyasu{at}icloud.com

Abstract

Thromboembolism is the most frequent complication of coil embolisation for intracranial aneurysm. Complications of thromboembolism can lead to stroke and have a serious impact on sequelae and mortality, necessitating appropriate rescue therapy. Here, we succeeded in recanalisation of an occluded stent by balloon-assisted local infusion of a thrombolytic agent following stent-assisted coil embolisation of an unruptured posterior communicating artery aneurysm. This method involves inflating a microballoon just distal to the occluded vessel and then administering a thrombolytic agent through a microcatheter. This technique may increase the rate of vessel reopening by maximising the local drug concentration. This method can be applied to any type of thrombolytic agent and helps reduce the dose of systemic drugs, which might decrease the incidence of haemorrhagic complications. Balloon-assisted intra-arterial thrombolytic infusion for an occluded vessel during endovascular coil embolisation could offer an alternative rescue therapy when conventional thrombolytic agent administration fails to improve thromboembolism.

  • Neuroimaging
  • Radiology
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Background

Thromboembolism is the most frequent complication of coil embolisation for intracranial aneurysms, and 6.1% of patients who undergo embolisation receive rescue therapy using thrombolytic agents including glycoprotein (GP) IIb/IIIa inhibitors and fibrinolytic therapy.1 However, a meta-analysis showed a recanalisation rate for thromboembolism of 72.0% for GP IIb/IIIa inhibitors and 50.0% for fibrinolysis, meaning that some treatments fail to achieve recanalisation.1 Complications of thromboembolism can lead to stroke and have serious impacts on sequelae and mortality,2 so successful rescue therapy is crucial.

Here, we achieved successful recanalisation by balloon-assisted intra-arterial (IA) infusion of a thrombolytic agent following acute stent occlusion during stent-assisted coil embolisation of an unruptured posterior communicating artery (PcomA) aneurysm with placement of a stent in the PcomA. We propose balloon-assisted infusion for recanalisation of an occluded vessel as an alternative treatment option when conventional IA thrombolytic infusion fails to resolve thromboembolism.

Case presentation

A woman in her 80s with a history of hypertension, diabetes mellitus and dyslipidaemia who had undergone conservative treatment for brainstem infarction at another hospital 7 years earlier was referred to our institution for treatment of an unruptured intracranial aneurysm (UIA). Three-dimensional digital subtraction angiography identified an UIA (maximum diameter, 7.6 mm) at the fetal posterior cerebral artery (fPCA) bifurcation (figure 1A).

Figure 1

Right internal carotid angiography showing an unruptured intracranial aneurysm with a maximum diameter of 7.6 mm at the fetal posterior cerebral artery (fPCA) bifurcation (A) and occlusion of the fPCA after final coil insertion (B). Fluoroscopic view (C) showing microballoon guided and inflated just distal to the aneurysm, with blood flow blocked, and urokinase administered through the microcatheter. As a result, the occluded vessel was successfully recanalised (D). Arrow: occluded fPCA. Arrowhead: tip of microcatheter injecting urokinase.

Endovascular procedure

Since the broad-necked aneurysm showed the fPCA branching out from the dome, a stent was placed in the fPCA during coil embolisation for aneurysm to secure preservation of the fPCA. Dual antiplatelet therapy with aspirin (100 mg/day) and cilostazol (200 mg/day) was started 2 weeks before embolisation in preparation for stent placement. Thromboelastography 6s measurements demonstrated that arachidonic acid-induced platelet-fibrin clot strength and arachidonic acid inhibition rate during the procedure were 16.7 mm and 100%, respectively, showing no resistance to aspirin.

Coil embolisation was conducted under general anaesthesia. During treatment, heparin was given to maintain whole-blood activated clotting time (ACT)≥300 s. An 8-Fr guiding catheter (FUBUKI Dilator Kit; Asahi Intecc, Aichi, Japan) was guided via right transradial access into the cervical segment of the right internal carotid artery (ICA). The microcatheter (Excelsior SL10; Stryker, Kalamazoo, Michigan, USA) was then guided to the fPCA. Before stent deployment, the other microcatheter (Phenom 17; Medtronic, Dublin, Ireland) was directed into the aneurysm in advance and a framing coil was inserted to form a neckline. A low-profile open-cell stent (Neuroform Atlas 4.5 mm×30 mm; Stryker) was placed from fPCA to ICA. Coils were inserted into the aneurysm with the jailing technique under stent assistance. After insertion of the final coil, right ICA angiography was not able to visualise the fPCA (figure 1B). The fPCA was occluded due to thromboembolism in the stent placed in the fPCA.

Treatment

Balloon-assisted thrombolytics infusion

After the onset of thromboembolism, ACT was remeasured and remained >300 s, so no additional heparin was administered. Urokinase (120 000 units) was injected by IA infusion through a microcatheter, but the occluded vessel did not recanalise. A microballoon (Shouryu HR 7 mm×7 mm; Kaneka Medix, Osaka, Japan) was then guided just distal to the aneurysm and inflated. With blood flow blocked, urokinase (60 000 units) was administered through the microcatheter (figure 1C), achieving successful recanalisation of the occluded vessel (figure 1D). Argatroban (60 mg/day) was then started to prevent reocclusion. After reopening the fPCA, the procedure was terminated after confirming that no reocclusion of the fPCA or delay in blood flow was observed for 30 min.

Outcome and follow-up

Postoperative neurological findings did not deteriorate, and MRI the day after the procedure did not show cerebral infarction or haemorrhage. Two days after treatment, the patient was discharged with a modified Rankin Scale score of 0.

Discussion

In the present case, thromboembolic occlusion of a stent placed in a fPCA was successfully recanalised by guiding a microballoon just distal to the aneurysm, inflating the balloon to block blood flow, and administering urokinase through a microcatheter. Urokinase was infused for thromboembolism because GP IIb/IIIa inhibitors, which have been shown to offer significantly lower short-term and long-term morbidity rates compared with fibrinolytic therapy,1 are not currently approved by insurance in Japan. A meta-analysis of rescue therapy for intraoperative thromboembolism in aneurysm coiling showed that fibrinolytic therapy did not significantly differ in vessel revascularisation rates, postoperative clinical stroke or haemorrhage, mortality or long-term good neurological outcomes compared with GP IIb/IIIa inhibitors.1

Advantages of balloon-assisted thrombolytic infusion

The therapeutic concept of balloon-assisted thrombolytic infusion is that a microballoon is inflated just distal to the occluded vessel, followed by administration of the thrombolytic agent through a microcatheter to raise local concentrations of thrombolytic agent, in anticipation of recanalisation of the occluded vessel (figure 2).

Figure 2

Schematic image showing microballoon guided and inflated just distal to the aneurysm, with blood flow blocked, and urokinase administered through the microcatheter. This illustration was prepared for this report by coauthor, AT, who has given permission for its inclusion in this report. Arrowhead: tip of microcatheter injecting urokinase.

This method can also be applied to any type of thrombolytic agent, including GP IIb/IIIa inhibitors, and contributes to reducing the dose of systemic drugs, which may also contribute to a decreased incidence of haemorrhagic complications. The time of blood flow interruption by microballoon inflation itself raises a risk of ischaemia and should be kept to a minimum.3 In the present patient, blood flow was interrupted for a total of 5 min by the microballoon during urokinase infusion. In addition, the placement of microballoons increases the risk of thromboembolism due to the increased number of devices, complicates the procedure, and may even cause vascular injury from microballoon inflation.4 We decided that the Shouryu HR (Kaneka Medix), providing the lightest vascular load among microballoons, should be used for the treatment of the present patient.5 Because of the potential for complications with this procedure, as described above, we propose strict application of this technique only when conventional thrombolytic therapy fails. Despite the above limitations, balloon-assisted IA thrombolytic infusion for an occluded vessel during endovascular coil embolisation of the UIA may represent an alternative rescue therapy when conventional thrombolytic agent administration fails to improve thromboembolism. Further studies are warranted in a clinical trial setting in the future.

Learning points

  • Inflating a microballoon just distal to the occluded vessel and then administering a thrombolytic agent through a microcatheter may maximise the local drug concentration and thus increase the rate of vessel reopening.

  • Intra-arterial thrombolytic infusion under balloon assistance can be applied to any type of thrombolytic agent and helps reduce the dose of systemic drugs, which might decrease the incidence of haemorrhagic complications.

  • Balloon-assisted intra-arterial thrombolytic infusion for an occluded vessel during endovascular coil embolisation could offer an alternative rescue therapy when conventional thrombolytic agent administration fails to improve thromboembolism.

Ethics statements

Patient consent for publication

References

Footnotes

  • Twitter @ttanaka@jikei.ac.jp

  • Contributors The following authors were responsible for drafting of the text, sourcing and editing of clinical images, investigation results, drawing original diagrams and algorithms, and critical revision for important intellectual content: MF, AT, TT and YM. The following authors gave final approval of the manuscript: MF, AT, TT and YM.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.