The Aneurysm Casebook [1st ed.] 9783319778266, 9783319778273

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Hans Henkes Pedro Lylyk Oliver Ganslandt Editors

The Aneurysm Casebook

A Guide to Treatment Selection and Technique

The Aneurysm Casebook

Hans Henkes • Pedro Lylyk Oliver Ganslandt Editors

The Aneurysm Casebook A Guide to Treatment Selection and Technique

With 767 Figures and 9 Tables

Editors Hans Henkes Neuroradiologische Klinik Klinikum Stuttgart Stuttgart, Germany

Pedro Lylyk Interventional Neuroradiology Clinica La Sagrada Familia, ENERI Buenos Aires, Argentina

Oliver Ganslandt Neuroradiologische Klinik Neurozentrum, Klinikum Stuttgart Stuttgart, Germany

ISBN 978-3-319-77826-6 ISBN 978-3-319-77827-3 (eBook) ISBN 978-3-319-77828-0 (print and electronic bundle) https://doi.org/10.1007/978-3-319-77827-3 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG. The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Dedicated to our families with love our teachers with gratitude our patients with respect

Preface

Over 30 years ago, the professionalization of neurointerventional therapy began – with the 1986 publication of the textbook “Surgical Neuroangiography,” written by Pierre Lasjaunias and Alex Berenstein, by Springer-Verlag Berlin Heidelberg. In 1991, electrolytically detachable coils became the first dedicated neuroendovascular product to be developed and manufactured under industrial conditions. The use of coil occlusion techniques in the treatment of intracranial aneurysms was adopted rapidly after their safety, efficacy, and relative ease of use were understood. The practice of intracranial aneurysm coiling became a tremendous medical and economic success, supported by randomized trials such as ISAT. The success of aneurysm coiling continues today, with approximately 1,200,000 detachable coils implanted globally in 2018. The limitations of aneurysm coiling techniques became evident in the few first years after their introduction. Adjunctive methods, including balloonremodeling and stent-implantation, were developed, making wide-necked aneurysms amenable to coil occlusion. Other concepts, including the use of liquid embolic agents (e.g., Onyx), were introduced and subsequently withdrawn from the market, predominantly due to safety concerns. Today we have additional techniques and devices, including intra- and extra-aneurysmal flow diverters, neck bridging devices, and advanced coil derivatives available or under development. This technical evolution in endovascular therapy was genuinely disruptive, as demonstrated by a worldwide decline in the number of neurosurgical procedures for microsurgical clipping as the numbers of endovascular interventions rose. However, parallel to this process, the techniques and outcomes afforded by microsurgical clipping of intracranial aneurysms also improved considerably. The surgical treatment of aneurysms was challenged by the published results from endovascular centers and improved with advances in clip technology, intraoperative vessel imaging, and adjunctive measures such as bypass surgery. Today, many neurovascular centers offer dedicated teams of trained individuals to treat patients with endovascular and microsurgical aneurysm therapy. The future will show whether the concept of separated responsibilities or a “hybrid” model of technical skills and clinical work will prevail in clinical aneurysm practice. In 2019 an estimated number of 230,000 and 150,000 intracranial aneurysms were treated worldwide by endovascular and microsurgical means, respectively. vii

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Preface

In this book, the reader will find accounts of both approaches: surgical and endovascular concepts for the treatment of neurovascular aneurysms. The case-based presentation is structured by anatomic aneurysm location. The topics range from standard approaches to the treatment of frequently occurring aneurysms, through to procedures offering innovative solutions for the treatment of aneurysms in rarely described locations. The intention was to offer the entire spectrum of clinical presentation and possible therapy of neurovascular aneurysms from basic knowledge to unique cases, from stunning successes to epic failures. Parallel to the printed version, online access to the “living book” offers the opportunity to submit and read updated versions of the individual case presentations. This reference work is the first printed edition of “The Aneurysm Casebook,” which was written over a 2-year period and will hopefully be followed by future editions since many aspects of neurovascular aneurysm diagnosis and treatment have not been covered thus far. We cordially invite our readers and colleagues around the world to submit their experience to The Aneurysm Casebook and contribute to a better understanding and decision making in the highly demanding field of neurovascular pathology. July 2020

Hans Henkes Pedro Lylyk Oliver Ganslandt

Acknowledgments

The authors are grateful to Zoë Hall, Melissa Kuhnert, and Frances Colgan for tireless language revision of the manuscripts. James Lago encouraged and supported us with his experience and foresight.

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Contents

Volume 1 Part I 1

Cervical Internal Carotid Artery

Cervical Internal Carotid Artery Aneurysm: Spontaneous Dissection of the Cervical Internal Carotid Artery Resulting in Elongation and Pseudoaneurysm Formation Causing Hypoglossal Nerve Palsy; Endovascular Vessel Reconstruction with Stenting, Followed by Telescoping Flow Diversion, Achieving Straightening of the Artery, Aneurysm Occlusion, Hypoglossal Nerve Recovery, and Normalization of the Tongue . . . . . . . . . . . . . . . . . . . . . . . . . . Hosni Abu Elhasan, Pablo Albiña Palmarola, Marta Aguilar Pérez, Birgit Herting, Hansjörg Bäzner, and Hans Henkes

Part II 2

3

......................

Petrous Internal Carotid Artery . . . . . . . . . . . . . . . . . . . . . .

Petrous Internal Carotid Artery Aneurysm: A Giant Fusiform Aneurysm, Flow Diversion, Several Treatment Sessions, Metamizole Intake Five Years After the Initial Treatment, Thrombotic Internal Carotid Artery Occlusion, Thrombectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Marta Aguilar Pérez, Muhammad AlMatter, and Hans Henkes Petrous Internal Carotid Artery Aneurysm: Endovascular Treatment with Coils and Flow Diverter Stents of a Large Petrous Internal Carotid Artery Aneurysm Associated with Full-Blown Fibromuscular Dysplasia, and Flow Diverter Reconstruction of the Contralateral Internal Carotid Artery, Followed by the Coil Occlusion of an Aneurysm of the Anterior Communicating Artery, and Balloon Angioplasty of a Left Internal Carotid Artery In-Stent Stenosis, with Good Clinical Outcome . . . . . . . . . . . Pervinder Bhogal, Marta Aguilar Pèrez, Alexander Sirakov, Hansjörg Bäzner, and Hans Henkes

1

3

17

19

37

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Part III Cavernous Internal Carotid Artery . . . . . . . . . . . . . . . . . . . 4

5

6

7

Cavernous Internal Carotid Artery Aneurysm: Visual Disturbance Due to a Large Cavernous Aneurysm Presumably Causing Recurrent Retinal Ischemia; Coil Occlusion of the Aneurysm Together with the Parent Artery; Resolution of the Visual Disturbance and Clinical Recovery During Long-Term Follow-Up . . . . . . . . . . . . . . . . Frances Colgan, Marta Aguilar Pérez, Hansjörg Bäzner, and Hans Henkes Cavernous Internal Carotid Artery Aneurysm: Diplopia due to a Large Cavernous Aneurysm Causing Oculomotor Nerve Palsy; Partial Coil Occlusion and p64 Flow Diverter Implantation; Resolution of the Cranial Nerve Palsy and Complete Clinical Recovery . . . . . . . . . . . . . . . . . . . . . . . . . . Frances Colgan, Marta Aguilar Pérez, Hansjörg Bäzner, and Hans Henkes Cavernous Internal Carotid Artery Aneurysm: Rupture of a Presumably Traumatic Cavernous Internal Carotid Artery Pseudoaneurysm with Life-Threatening Epistaxis After Endonasal Pansinus Surgery . . . . . . . . . . . . . . . . . . . . . . . . . Cindy Richter, Helmut Steinhart, and Hans Henkes Cavernous Internal Carotid Artery Aneurysm: Exsanguinating Iatrogenic Internal Carotid Artery Injury During Transsphenoidal Surgery for Pituitary Macroadenoma – Packing, Transvenous Coil Occlusion of a Carotid Cavernous Sinus Fistula, and Repair of a Carotid Pseudoaneurysm with a Flow-Diverter Stent . . . . . . . . . . . . . José E. Cohen and Ronen R. Leker

57

59

69

81

87

8

Cavernous Internal Carotid Artery Aneurysm: Large Cavernous Carotid Artery Aneurysm Causing Compression of the Internal Carotid Artery in a Young Woman with EhlersDanlos Syndrome with Segmental Dissections of the Carotid and Vertebral Arteries; Complete Reconstruction of the Internal Carotid Artery with Five Pipeline Embolization Devices; Complete Aneurysm Resolution and Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95 Carlos Bleise, Rene Viso, Ivan Lylyk, Jorge Chudyk, and Pedro Lylyk

9

Cavernous Internal Carotid Artery Aneurysm: Giant Posttraumatic Carotid Cavernous Pseudoaneurysm, Presenting with Epistaxis; Treated in Two-Stage Strategy with Complete Occlusion and Delayed Coil Extrusion Through the Nostril . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107 Ivan Lylyk, Rene Viso, Esteban Scrivano, Javier Lundquist, and Pedro Lylyk

Contents

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Part IV

Paraophthalmic Internal Carotid Artery . . . . . . . . . . . . .

117

10

Paraophthalmic Internal Carotid Artery Aneurysm: Coil Occlusion Assisted by the Comaneci Device . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119 Sebastian Fischer

11

Paraophthalmic Internal Carotid Artery Aneurysm: Spontaneous Subarachnoid Hemorrhage, Blood Blister Aneurysm, Flow Diverter Treatment During the Acute Phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129 Victoria Hellstern, Marta Aguilar Pérez, Muhammad AlMatter, and Hans Henkes

12

Paraophthalmic Internal Carotid Artery Aneurysm: Incidental Paraophthalmic Aneurysm of the Right Internal Carotid Artery, Treated with Intra- and Extrasaccular Flow Diversion; Hyperresponse on Antiplatelet Medication with Sulcal Subarachnoid Hemorrhage; Reduction of the Antiplatelet Medication Dosage; Thromboembolic Occlusion of the p64 Flow Diverter Only 24 h After the Last Intake of Ticagrelor; Thrombectomy with Recanalization of the p64 and Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135 Marta Aguilar Pérez, Victoria Hellstern, Christof Klötzsch, Hansjörg Bäzner, and Hans Henkes

13

Paraophthalmic Internal Carotid Artery Aneurysm: Spontaneous Subarachnoid Hemorrhage Caused by the Rupture of a Paraophthalmic Aneurysm, Treated with Coils and Complicated by Severe Vasospasm, Treated with Pharmaceutical Vessel Dilatation and Proximal Balloon Angioplasty; Diffuse Distal Vasospasm Treated with the NeuroFlo Device with Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151 Ivan Lylyk, Carlos Bleise, Rene Viso, Esteban Scrivano, and Pedro Lylyk

14

Paraclinoid Internal Carotid Artery Aneurysm: TwoStage Treatment of a Giant Paraclinoid Internal Carotid Artery Aneurysm with Partial Clip Ligation, Followed by Flow Diverter Implantation; Late Thrombotic Flow Diverter Occlusion, Recanalized by Endovascular Means, with Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163 Amer Haj, Alexander Brawanski, Christina M. Wendl, and Karl-Michael Schebesch

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15

Paraophthalmic Internal Carotid Artery Aneurysm: Non-ischemic Cerebral Enhancing (NICE) Lesions After the Endovascular Treatment of an Incidental Paraophthalmic Aneurysm with Flow Diverters and Coils; Conservative Management, with Resolution of the Pathological Cerebral Findings and Clinical Recovery During Mid-Term Follow-Up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 183 Alex Sirakov, Marta Aguilar Pérez, Muhammad AlMatter, and Hans Henkes

16

Internal Carotid Artery Aneurysm: Multiple Internal Carotid Artery Aneurysms in a Patient Presenting with Subarachnoid Hemorrhage; Treatment with Flow Diverter Stents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195 José E. Cohen, Asaf Honig, and Gustavo Rajz

Part V

Ophthalmic Artery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

201

17

Ophthalmic Artery Aneurysm: Flow-Induced Intracranial and Intraorbital (“Peripheral”) Ophthalmic Artery Aneurysms, Associated with a Tentorial Dural Arteriovenous Fistula, Supplied by the Ophthalmic Artery; Endovascular Treatment of the Dural Arteriovenous Fistula and One Aneurysm; and Conservative Management of the Remaining Ophthalmic Artery Aneurysms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203 Victoria Hellstern, Marta Aguilar Pérez, Muhammad AlMatter, Hansjörg Bäzner, and Hans Henkes

18

Ophthalmic Artery Aneurysm: Subarachnoid Hemorrhage and Visual Disturbance due to a Ruptured Intracranial and Intracanalicular Ophthalmic Artery Aneurysm; Endovascular Remodeling of the Ophthalmic Artery via Flow Re-Direction Endoluminal Device (FRED Jr.); Resolution of the Visual Disturbance; Short-Term Clinical and Radiological Follow-Up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215 Stanimir Sirakov, Alexander Sirakov, and Hans Henkes

Part VI 19

Superior Hypophyseal Artery . . . . . . . . . . . . . . . . . . . . . . .

223

Superior Hypophyseal Artery Aneurysm; Giant Right Superior Hypophyseal Artery Aneurysm with Contralateral Carotid Artery Occlusion; Difficult Passage Through the Aneurysm Neck with Different Anchor Techniques, Treated by Telescoping Flow Diverter Deployment . . . . . . . . . . . . . . . . . 225 Jorge Chudyk, Ivan Lylyk, Carlos Bleise, Rene Viso, and Pedro Lylyk

Contents

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20

Superior Hypophyseal Artery Aneurysm: Nickel Allergy and Autoimmune Inflammatory Syndrome (ASIA) After Flow Diverter Implantation as a Treatment of an Internal Carotid Artery Aneurysm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237 Isabel Fragata, Catarina Perry, Rita Nogueira, Jaime Pamplona, and João Reis

Part VII

Supraclinoid Internal Carotid Artery . . . . . . . . . . . . . . . .

245

21

Supraclinoid Internal Carotid Artery Aneurysm: Incidental Aneurysm, Flow Diverter Deployment Practicing in an 1:1 3D-Printed Aneurysm Model, Complete Occlusion by Coil-Assisted p64 Flow Diversion . . . . . . . . . . . . . . . . . . . . . . 247 André Kemmling, Thomas Eckey, and Peter Schramm

22

Supraclinoid Internal Carotid Artery Aneurysm: Large Brain AVM of the Basal Ganglia, Intracranial Hemorrhage, Stereotactic Radiosurgery, Fusiform Aneurysm Formation with Optic Nerve Compression, Balloon Test Occlusion, and Parent Vessel Occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253 Franziska Dorn

23

Supraclinoid Internal Carotid Artery Aneurysm: Ruptured Dissecting ICA Pseudoaneurysm, Endovascular Treatment Using a FRED, Twisting with Thrombus Formation, Early Aneurysm Occlusion, Balloon Angioplasty and Telescoping Stenting, Transient In-Stent Stenosis . . . . . . . . . . . . . . . . . . . 261 Rosa Martinez Moreno, Ernesto García Bautista, Pablo Tomás Muñoz, and Pedro Pablo Alcázar Romero

24

Supraclinoid Internal Carotid Artery Aneurysm: Giant Supraclinoid Internal Carotid Artery Aneurysm, Treatment with Extra-Intracranial Bypass and Parent Artery Occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271 Yerbol Makhambetov and Assylbek Kaliyev

25

Supraclinoid Internal Carotid Artery Aneurysm: Acute Subarachnoid and Intraventricular Hemorrhage due to Aneurysm Rupture After Flow Diverter-Assisted Coil Occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283 Victoria Hellstern, Marta Aguilar Pérez, Muhammad AlMatter, Hansjörg Bäzner, and Hans Henkes

26

Supraclinoid Internal Carotid Artery Aneurysm: Giant Supraclinoid Aneurysm Treated with Telescoping p64 Flow Diverters with Complete Occlusion of the Aneurysm . . . . . . 293 Ivan Lylyk, Jorge Chudyk, Rene Viso, Carlos Bleise, Esteban Scrivano, and Pedro Lylyk

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27

Supraclinoid Internal Carotid Artery Aneurysm: Four Incidental Paraophthalmic and Supraclinoid Tandem Aneurysms, Treated with a Single Flow Diverter Stent . . . . 299 José E. Cohen, John Moshe Gomori, Sergey Spektor, and Yigal Shoshan

28

Supraclinoid Internal Carotid Artery Aneurysm: Iatrogenic Aneurysm of the Supraclinoid Internal Carotid Artery After Craniopharyngioma Resection; Treatment of an Unruptured Fusiform Aneurysm with a Cardiatis Flow Diversion Device; Technical Aspects, Follow-Up Results, and Literature Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305 D. Mauricio Alvarez, Rene Viso, Ivan Lylyk, Esteban Scrivano, and Pedro Lylyk

29

Internal Carotid Artery Aneurysm: Large Saccular Persistent Primitive Trigeminal Artery Aneurysm, with Mass Effect, Treated with Flow Diverter and Deconstructive Technique with Coils, Good Clinical Outcome, and Follow-Up Results . . . . . 317 Ivan Lylyk, Rene Viso, Rodrigo Muñoz, Jorge Chudyk, and Pedro Lylyk

Part VIII

Posterior Communicating Artery . . . . . . . . . . . . . . . . . . .

331

30

Posterior Communicating Artery Aneurysm: Subarachnoid Hemorrhage from a Small Aneurysm Located on an Infundibulum of the Posterior Communicating Artery; Partial Clipping of the Aneurysm, Followed by Endovascular Flow Diversion, with Good Clinical Outcome . . . . . . . . . . . . . . . . . 333 Erich Donauer, Farzaneh Jedi, Nirmal Jangid, Matthias Juergens, Klaus Terstegge, and Hans Henkes

31

Posterior Communicating Artery Aneurysm: Surgical Trapping of a Giant Posterior Communicating Artery Aneurysm – Balloon Test Occlusion and Clip Ligation for Trapping . . . . . . . . . . . . 347 Amer Haj, Alexander Brawanski, Christina M. Wendl, and Karl-Michael Schebesch

32

Posterior Communicating Artery Aneurysm: Giant Aneurysm of the Internal Carotid Artery, Acute SAH, Ruptured Wide Neck Aneurysm, Incorporation of the Fetal Origin of the Posterior Cerebral Artery, Coil Occlusion, Secondary Treatment of the Neck Remnant with a Single Derivo Flow Diverter, Intra-procedural Thrombosis, Intra-arterial Eptifibatide Infusion, Good Clinical Outcome . . . . . . . . . . . . 357 Michael Kirsch

33

Posterior Communicating Artery Aneurysm: Posttraumatic Pseudoaneurysm in a Child, Coil Occlusion and Flow Diverter Implantation, Hemorrhage Protection, Arterial Reconstruction with Relief of Mass Effect and Good Outcome . . . . . . . . . . . 363 José E. Cohen

Contents

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34

Posterior Communicating Artery Aneurysm: Unrecognized Previous Rupture, Recurrent Rupture During Angiography, Emergent Balloon-Assisted Coil Occlusion, Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 369 Christian Loehr, Jan Oliver Kuhnt, Muhammad AlMatter, and Hans Henkes

35

Posterior Communicating Artery Aneurysm: Unrecognized Previous Aneurysm Rupture, Acute Ischemic Stroke Symptoms Due to Post-Hemorrhagic Vasospasm, Emergent BalloonAssisted Coil Occlusion, and Repeated Intra-arterial Vasospasmolysis with Acceptable Clinical Outcome . . . . . . . 379 Christian Loehr and Jan Oliver Kuhnt

36

Posterior Communicating Artery Aneurysm: Multiple Aneurysms, Diagnosed in Mother and Daughter, the Increased Rupture Risk, Consequences for Diagnostic Protocols, and Treatment Decisions . . . . . . . . . . . . . . . . . . . . 385 Muhammad AlMatter, Marta Aguilar Pérez, and Hans Henkes

37

Posterior Communicating Artery Aneurysm: A Large Right Posterior Communicating Artery Aneurysm at a Sharp Angle to the Internal Carotid Artery, Treated with pCONUS2Assisted Coil Occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399 Rene Viso, Nicolas Perez, Ivan Lylyk, Javier Lundquist, Hans Henkes, and Pedro Lylyk

38

Posterior Communicating Artery Aneurysm: Ruptured Aneurysm with Contained Pseudoaneurysm; Clinical Deterioration due to a Massive Rehemorrhage After Insertion of Bilateral External Ventricular Drains . . . . . . . . . . . . . . . . 411 Muhammad AlMatter, Moritz Fass, Oliver Ganslandt, and Hans Henkes

39

Posterior Communicating Artery Aneurysm: Progressively Enlarging, Symptomatic, and Partially Thrombosed Fusiform True Posterior Communicating Artery Aneurysm, Treated by Coil Occlusion of the Parent Artery and Disconnection of the Posterior Communicating Artery by Parallel Flow Diversion in Two Treatment Sessions; Complete Aneurysm Occlusion, Aneurysm Shrinkage, and Good Clinical Recovery . . . . . . . 427 Alexander Sirakov, Hosni Abu Elhasan, Marta Aguilar Pérez, Hansjörg Bäzner, and Hans Henkes

Part IX 40

Anterior Choroidal Artery . . . . . . . . . . . . . . . . . . . . . . . . . . .

441

Anterior Choroidal Artery Aneurysm: Incidental Anterior Choroidal Artery Aneurysm, Treated by Flow Diversion Using a p64 with Preservation of the Anterior Choroidal Artery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 443 Muhammad AlMatter, Marta Aguilar Pérez, and Hans Henkes

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Contents

Anterior Choroidal Artery Aneurysm: Basal Ganglia AVM, Supplied by the Anterior Choroidal Artery, with an Intranidal Aneurysm; Targeted Embolization Prior to Radiosurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 453 Marta Aguilar Pérez, Muhammad AlMatter, Marcel Alfter, Marc Münter, and Hans Henkes

Part X

Internal Carotid Artery Bifurcation . . . . . . . . . . . . . . . . . . .

465

42

Internal Carotid Artery Bifurcation Aneurysm: Treatment with an Intrasaccular Flow Disruptor Contour Neurovascular System; Technical Aspects and Follow-Up Results . . . . . . . . 467 Carlos Bleise, Ivan Lylyk, Rene Viso, Rosana Ceratto, and Pedro Lylyk

43

Internal Carotid Artery Bifurcation Aneurysm: WEB Device Dislodging into the Middle Cerebral Artery Followed by Removal with an Alligator Retrieval Device and Subsequent Coiling of the Aneurysm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475 Isabel König, Anushe Weber, Werner Weber, and Sebastian Fischer

44

Internal Carotid Artery Bifurcation Aneurysm: Symptomatic Internal Carotid Artery Bifurcation Aneurysm in a Pediatric Patient Treated with Flow Diversion . . . . . . . . . . . . . . . . . . . 483 José E. Cohen, Hosni Abu Al-Hasan, Carlos Candanedo, Moatasim Shweiki, and Gustavo Rajz

45

Internal Carotid Artery Bifurcation Aneurysm: Spontaneous Thrombosis of an Incidental ICA Bifurcation Aneurysm Despite Dual Platelet Function Inhibition . . . . . . . . . . . . . . . 491 Georg Gihr, Stephan Felber, Hansjörg Bäzner, and Hans Henkes

46

Internal Carotid Artery Bifurcation Aneurysm: Large Wide-Necked Bifurcation Aneurysm; Stent-Assisted Coiling Technique Using a Barrel Vascular Reconstruction Device; Technical Aspects and Follow-Up Results . . . . . . . . . . . . . . . 499 Nicolas Perez, Ivan Lylyk, Rodolfo Nella Castro, Esteban Scrivano, and Pedro Lylyk

47

Internal Carotid Artery Bifurcation Aneurysm: Microsurgical Clipping of a Large Wide-Necked Internal Carotid Artery Bifurcation and Anterior Choroidal Artery Aneurysm After a Previous Failed Attempt at Flow Diverter Implantation . . . 507 Yerbol Makhambetov, Marat Kulmirzayev, and Assylbek Kaliyev

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48

Internal Carotid Artery Bifurcation Aneurysm: Ruptured Internal Carotid Artery Aneurysm in a Patient with Corrected Coarctation of the Aorta Treated with Balloon-Assisted Coiling, Exclusion of the Aneurysm, and Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 517 José E. Cohen, Yigal Shoshan, Haim Danenberg, David Planer, Asaf Honig, and Gustavo Rajz

Part XI Proximal Segment (A1) of the Anterior Cerebral Artery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

523

49

Anterior Cerebral Artery (A1 Segment) Aneurysm: Incidental, Giant, Partly Thrombosed Proximal Anterior Cerebral Artery Aneurysm with Stenosis of the A1 Segment, Treated with a p48 Flow Diverter with Angiographic Exclusion of the Aneurysm and Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . 525 Rene Viso, Nicolas Perez, Ivan Lylyk, Jorge Chudyk, and Pedro Lylyk

50

Anterior Cerebral Artery (A1 Segment) Aneurysm: A Very Small Incidental A1 Aneurysm Treated with p48 Flow Diverter with Good Clinical and Angiographic Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 535 Alvaro Valtorta, Ivan Lylyk, Rene Viso, Javier Lundquist, and Pedro Lylyk

51

Anterior Cerebral Artery (A1 Segment) Aneurysm: The eCLIPs Endovascular Clip System, a Novel Flow Diversion Approach to Managing Intracranial Aneurysms Arising from Arterial Bifurcations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 545 Ghouth Waggass, Saba Moghimi, Joost De Vries, and Thomas R. Marotta

52

Anterior Cerebral Artery (A1 Segment) Aneurysm: Abandoned Dual Platelet Inhibition Shortly After Endovascular Treatment with a Hydrophilic Polymer-Coated Flow Diverter p48MW HPC; Good Clinical Outcome and Early Aneurysm Occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . 555 Marie-Sophie Schüngel, Karl-Titus Hoffmann, Ulf Quäschling, and Stefan Schob

53

Anterior Cerebral Artery (A1 Segment) Aneurysm: Giant Partially Thrombosed A1 Aneurysm with Mass Effect, Treated with a Pipeline Embolization Device, Complete Resolution of the Mass Effect, and Modification of the Shape of the Implant During Long-Term Follow-Up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 563 Rene Viso, Ivan Lylyk, Nicolas Perez, Esteban Scrivano, and Pedro Lylyk

xx

Contents

Part XII

Azygos Anterior Cerebral Artery . . . . . . . . . . . . . . . . . . . .

575

54

Azygos Anterior Cerebral Artery Aneurysm: Ruptured Distal Azygos Anterior Cerebral Artery Aneurysm; Retractorless Clipping, Focused Interhemispheric Approach, Positioning of Head, Rationale for Open Surgery . . . . . . . . . . . . . . . . . . . . . 577 Hannes Rauter, Alexandra Resch, and Thomas Kretschmer

55

Azygos Anterior Cerebral Artery Aneurysm: Incidental Saccular Aneurysms of an Azygos Anterior Cerebral Artery and of the Right-Hand Fenestrated A1 Segment; Endovascular Treatment of Both Aneurysms with Stent- and pCONUS1-Assisted Coil Occlusion with Complete Occlusion During Long-Term Follow-Up and with a Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 585 Georg Gihr, Marta Aguilar Pérez, Alexander Sirakov, Hansjörg Bäzner, and Hans Henkes

Part XIII

Anterior Communicating Artery

...................

599

56

Anterior Communicating Artery Aneurysm: Subarachnoid and Intracerebral Hemorrhage from an Aneurysm on the Posterior Aspect of the Anterior Communicating Artery – Microsurgical Clipping with a Fenestrated and Angulated Clip Without Direct Visual Control During Clip Application . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 601 Athanasios K. Petridis, Jasper Hans van Lieshout, and Hans Jakob Steiger

57

Anterior Communicating Artery Aneurysm: Large Aneurysm, Mass Effect, Deconstructive Techniques and Coiling, Occlusion, Mass Effect Relief and Excellent Evolution . . . . . 609 José E. Cohen

58

Anterior Communicating Artery Aneurysm: Aneurysm Recurrence After Initial Coil Occlusion, Treated with a WEB Device . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 617 Werner Weber and Sebastian Fischer

59

Anterior Communicating Artery Aneurysm: Acute SAH Due to a Small Aneurysm, Coil Occlusion, the Issue of SAH from Small Aneurysms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 625 Muhammad AlMatter, Marta Aguilar Pérez, and Hans Henkes

60

Anterior Communicating Artery Aneurysm: Rupture with SAH, Endovascular Occlusion with Bare Coils, Early Re-rupture, Poor Clinical Outcome . . . . . . . . . . . . . . . 635 Muhammad AlMatter, Marta Aguilar Pérez, and Hans Henkes

Contents

xxi

61

Anterior Communicating Artery Aneurysm: Incidental AcomA Aneurysm, pCONUS-Assisted Coil Occlusion, Intracerebral Hematoma due to Hyper-Response on Aspirin and Clopidogrel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 647 Marta Aguilar Pérez, Muhammad AlMatter, Hansjörg Bäzner, and Hans Henkes

62

Anterior Communicating Artery Aneurysm: Incidental WideNecked Aneurysm and Stent-Assisted Coil Occlusion Using a Barrel Stent with Transient In-Stent Stenosis . . . . . . . . . . . . 657 Christian Loehr, Jan Oliver Kuhnt, and Hans Henkes

63

Anterior Communicating Artery Aneurysm: Procedural Aneurysmal Re-rupture During pCONUS1 Deployment, Device Thrombosis During Coil Occlusion of the Aneurysm, Recanalization of the pCONUS1 by Infusion of Eptifibatide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 665 Marta Aguilar Pérez, Muhammad AlMatter, Victoria Hellstern, and Hans Henkes

64

Anterior Communicating Artery Aneurysm: Blister-Like Aneurysm of the Anterior Communicating Artery Treated by Flow Diversion Two Weeks After Subarachnoid Hemorrhage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 673 Ivan Lylyk, Rene Viso, Carlos Bleise, Esteban Scrivano, and Pedro Lylyk

65

Anterior Communicating Artery Aneurysm: Multilobulated Aneurysm with SAH, Treatment with a Single WEB SL Device . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 683 Jan-Hendrik Buhk, Jens Fiehler, and Maxim Bester

66

Anterior Communicating Artery Aneurysm: Incidental Anterior Communicating Artery Aneurysm, Treated with X-Configured Stent-Assisted Coil Occlusion . . . . . . . . . . . . . 691 Ivan Lylyk, Esteban Scrivano, Rene Viso, Nicolas Perez, and Pedro Lylyk

67

Anterior Communicating Artery Aneurysm: SAH and Large Intracerebral Hematoma due to a Ruptured Anterior Communicating Artery Aneurysm, Initially Treated with a WEB Device, and Re-treatment of a Residual Aneurysm with Stent-Assisted Coiling . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 701 Christin Clajus, Joachim Klisch, and Donald Lobsien

xxii

Contents

68

Anterior Communicating Artery Aneurysm: Previously Ruptured and Clipped Anterior Communicating Artery Aneurysm; Incidental Aneurysm Recurrence or Remnant; Endovascular Treatment with a Pipeline Embolization Device and Long-Term Follow-Up . . . . . . . . . . . . . . . . . . . . . . . . . . . 711 Pablo Albiña Palmarola, Rene Viso, Ivan Lylyk, Jorge Chudyk, and Pedro Lylyk

69

Anterior Communicating Artery Aneurysm: Stent-Assisted Anterior Communicating Artery Aneurysm Coil Occlusion – A Duplicated AcomA as a Potentially Dangerous Cause of a Nonexpanding Stent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 725 Stephan Felber

70

Anterior Communicating Artery Aneurysm: Symptomatic Anterior Communicating Artery Aneurysms in a Patient with Autosomal Dominant Polycystic Kidney Disease, Treated with Flow Diversion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 735 José E. Cohen, John Moshe Gomori, Ronen R. Leker, Gustavo Rajz, Hans Henkes, and Samuel Moscovici

Part XIV

Pericallosal Artery

................................

743

71

Pericallosal Artery Aneurysm: Complex Wide-necked Aneurysm Located at a Pericallosal Artery Trifurcation; Microsurgical Clipping and Complete Obliteration of the Aneurysm with Preservation of the Efferent Vessels and with Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 745 Oliver Ganslandt, Marta Aguilar Pérez, and Alexander Sirakov

72

Pericallosal Artery Aneurysm: WEB Occlusion of a Ruptured Flow-Related Distal Aneurysm of the Pericallosal Artery in a Patient with a Parietal Arteriovenous Malformation and Intracerebral Hemorrhage . . . . . . . . . . . . . . . . . . . . . . . . . . . 753 Donald Lobsien, Joachim Klisch, Voitek Sychra, and Christin Clajus

Part XV

Proximal Segment (M1) of the Middle Cerebral Artery . . . 761

73

Middle Cerebral Artery Aneurysm: Multiple Intracranial Aneurysms Treated in Two Endovascular Sessions – Different Treatment Techniques in One Patient . . . . . . . . . . . . . . . . . . 763 Rene Viso, Ivan Lylyk, Carlos Bleise, Rosana Ceratto, and Pedro Lylyk

74

Middle Cerebral Artery Aneurysm: Dissecting Aneurysm in a Young Patient Treated with Three Flow Diverter Stents . . . 775 Nicolas Perez, Rene Viso, Ivan Lylyk, Angel Ferrario, and Pedro Lylyk

Contents

xxiii

75

Middle Cerebral Artery Aneurysm: Proximal Middle Cerebral Artery Aneurysm Treated with Telescoping Flow Diverter Implantation and Loose Coiling After Preparatory Implantation of a Braided Stent as a Scaffold . . . . . . . . . . . . 783 Sebastian Fischer, Volker Maus, and Werner Weber

76

Middle Cerebral Artery Aneurysm: Treatment of a Large Unruptured Partially Calcified and Thrombosed Dissecting Middle Cerebral Artery Aneurysm with a FRED Jr. Flow Diversion Device; Technical Aspects and Follow-Up Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 793 Noel P. Schechtman, Ivan Lylyk, Rodolfo Nella Castro, and Pedro Lylyk

Volume 2 Part XVI Lenticulostriate Artery . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77

803

Lenticulostriate Artery Aneurysm: Arterial Hypertension, Intracerebral Hemorrhage Associated with Lenticulostriate Artery (Charcot Bouchard) Aneurysms – Conservative Management, Spontaneous Aneurysm Resolution, and Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 805 Frances Colgan, Marta Aguilar Pérez, Guy Arnold, Hansjörg Bäzner, and Hans Henkes

Part XVII

Bifurcation of the Middle Cerebral Artery . . . . . . . . . .

813

78

Middle Cerebral Artery Bifurcation Aneurysm: Broad Neck Aneurysm, Incorporation of the Superior and Inferior MCA Trunk, Obliteration of the Aneurysm, and Reconstruction of the MCA Bifurcation with Four Clips . . . . . . . . . . . . . . . . . . 815 Oliver Ganslandt, Peter Kurucz, and Pervinder Bhogal

79

Middle Cerebral Artery Bifurcation Aneurysm: Incidental Aneurysm, Uneventful Microsurgical Clipping, Delayed Symptomatic Vasospasm, Treated with Short-Term Intraarterial Infusion of Milrinone, Followed by Continuous Local Intra-arterial Nimodipine Infusion, and Recurrent Generalized Epileptic Seizures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 823 Frances Colgan, Gottlieb Maier, Moritz Fass, and Hans Henkes

80

Middle Cerebral Artery Bifurcation Aneurysm: Wall Enhancement in MRI Vessel Wall Imaging Correlates with Histological Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 837 Charlotte Flüh, Naomi Larsen, and Michael Synowitz

xxiv

Contents

81

Middle Cerebral Artery Aneurysm: Incidental Small Saccular MCA Aneurysm with Complex Geometry in a Patient with Ischemic Pontine Stroke – Microsurgical Clipping of the Saccular Aneurysm and Wrapping of a Blister Aneurysm on the Inferior MCA Branch; Postoperative DSA Confirmed the Complete Occlusion of the Saccular Aneurysm and Patency of Both Efferent MCA Branches; Development of a High-Grade Stenosis of the Inferior Trunk of the MCA, Possibly Induced by Muslin Gauze, and Eventually Formation of a De Novo Aneurysm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 845 Muhammad AlMatter, Marta Aguilar Pérez, Oliver Ganslandt, and Hans Henkes

82

Middle Cerebral Artery Bifurcation Aneurysm: Ruptured Lobulated and Wide-Necked Aneurysm with Good Clinical Outcome After Treatment with a WEB-SL . . . . . . . . . . . . . . 855 Christin Clajus and Joachim Klisch

83

Middle Cerebral Artery Bifurcation Aneurysm: Acute SAH, Ruptured MCA Trifurcation Aneurysm, Coil Occlusion Using Dual Microcatheter Technique . . . . . . . . . . . . . . . . . . . . . . . . 863 Marta Aguilar Pérez, Muhammad AlMatter, and Hans Henkes

84

Middle Cerebral Artery Bifurcation Aneurysm: Incidental Wide-Necked Aneurysm, MCA Branch Incorporated in the Aneurysm Base, and Treatment with Stent-Assisted Coiling Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 873 Thomas Bonnet, Benjamin Mine, and Boris Lubicz

85

Middle Cerebral Artery Bifurcation Aneurysm: Recanalization of a Middle Cerebral Artery Bifurcation Aneurysm Following Treatment with a Woven EndoBridge (WEB) Device, Retreated with a pCONUS2 Device-Assisted Coil Occlusion with Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 879 Nicolas Perez, Ivan Lylyk, Rene Viso, Angel Ferrario, and Pedro Lylyk

86

Middle Cerebral Artery Bifurcation Aneurysm: A Ruptured Wide-Necked Aneurysm Treated with Comaneci-Assisted Coiling . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 889 Stanimir Sirakov, Alexander Sirakov, Ivan Lylyk, Carlos Bleise, Rene Viso, and Pedro Lylyk

87

Middle Cerebral Artery Bifurcation Aneurysm: WideNecked Incidental Middle Cerebral Artery Bifurcation Aneurysm – Endovascular Treatment with a WEB SingleLayer Device . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 897 Huu An Nguyen, Sébastien Soize, Matthias Gawlitza, and Laurent Pierot

Contents

xxv

88

Middle Cerebral Artery Bifurcation Aneurysm: Saccular Aneurysm of the Middle Cerebral Artery Bifurcation Treated with a Flow Diverter Stent . . . . . . . . . . . . . . . . . . . . 907 José E. Cohen, Hosni Abu Al-Hasan, and Samuel Moscovici

89

Middle Cerebral Artery Bifurcation Aneurysm: Incidental Tandem Aneurysms of the Middle Cerebral Artery; Periprocedural Rupture of a Temporal Artery Aneurysm During Coil Insertion; Sealing of the Rupture Site and Parent Vessel Occlusion with nBCA; Subsequent Coil Occlusion of an MCA Bifurcation Aneurysm Assisted by a pCONUS1 HPC Device Under Mono-antiaggregation with ASA Only . . . . . . 913 Marta Aguilar Pérez, Victoria Hellstern, Muhammad AlMatter, Hansjörg Bäzner, and Hans Henkes

90

Middle Cerebral Artery Bifurcation Aneurysm: Unruptured Wide-Necked Aneurysm of the Middle Cerebral Artery Bifurcation, Treatment with Intra-saccular Flow Disruptor (pCANVAS) Neck-Bridging Device, Technical Aspects and Follow-Up Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 927 Pablo Albiña Palmarola, Rene Viso, Ivan Lylyk, Rodolfo Nella Castro, and Pedro Lylyk

91

Middle Cerebral Artery Bifurcation Aneurysm: Wide-Necked Unruptured MCA Aneurysm Occlusion with Stent-Assisted WEB Implantation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 941 Donald Lobsien, Joachim Klisch, and Christin Clajus

92

Middle Cerebral Artery Bifurcation Aneurysm: Acute Subarachnoid Hemorrhage Secondary to a Saccular Aneurysm Arising from the Bifurcation of the Middle Cerebral Artery – Endovascular Treatment with the Woven EndoBridge Device . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 949 Ken Wong, William Crinnion, Levansri Makalanda, and Pervinder Bhogal

93

Middle Cerebral Artery Bifurcation Aneurysm: WideNecked Middle Cerebral Artery Bifurcation Aneurysm, Treated with the Woven EndoBridge (WEB), Assisted by pCONUS1 HPC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 957 Donald Lobsien, Joachim Klisch, and Christin Clajus

94

Middle Cerebral Artery Bifurcation Aneurysm: Incidental Aneurysm of the Middle Cerebral Artery Bifurcation, Treated with Crossing Solitaire Stent-Assisted Coil Occlusion; Aneurysm Growth with Partial Thrombosis and Perianeurysmal Edema During the Long-Term Course . . . . 965 Meike Dukiewicz, Muhammad AlMatter, Marta Aguilar Pérez, Hansjörg Bäzner, and Hans Henkes

xxvi

95

Contents

Middle Cerebral Artery Aneurysm: Complex Wide-Necked and Lobulated Aneurysm of the Middle Cerebral Artery Bifurcation, Treated by Stent-Assisted Coil Occlusion Using a pCONUS2 Aneurysm Bridging Device and p48MW Flow Modulation Device Deployed Through the pCONUS2 Device; Two Treatment Sessions, Complete Aneurysm Occlusion, and Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 981 Alexander Sirakov, Marta Aguilar Pérez, Muhammad AlMatter, and Hans Henkes

Part XVIII Distal Segments (M2 and Beyond) of the Middle Cerebral Artery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

993

96

Middle Cerebral Artery (M3) Aneurysm: Ruptured Mycotic Distal Aneurysm: Treatment by Deconstructive Technique Using a Liquid Embolic Agent . . . . . . . . . . . . . . . . . . . . . . . . 995 Jorge Chudyk, Esteban Scrivano, Nicolas Perez, Carlos Bleise, and Pedro Lylyk

97

Middle Cerebral Artery (M3) Aneurysm: Atypical Primary Morphology and Early Recurrence After Stent-Assisted Coil Occlusion During the Long-Term Left Ventricular Assist Device Treatment, Accompanied by Temporary Septicemia; Parent Vessel Occlusion as the Final Treatment with Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . 1001 Vera Reuschel, Matthias Groll, Ulf Quäschling, Karl-Titus Hoffmann, and Stefan Schob

98

Middle Cerebral Artery (M2) Aneurysm: Endovascular Treatment of a Ruptured Left MCA (M2) Aneurysm in an Elderly Patient with Good Clinical Outcome . . . . . . . . . . 1011 Muhammad AlMatter and Hans Henkes

99

Middle Cerebral Artery (M3) Aneurysm: Treatment of a Mycotic Aneurysm of the Distal Middle Cerebral Artery with Coil Occlusion of Both the Aneurysm and the Parent Vessel . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1019 Dominik F. Vollherbst and Markus A. Möhlenbruch

100

Middle Cerebral Artery (M3) Aneurysm: Two “Mycotic” Aneurysms of the Middle Cerebral Artery Due to Bacterial Endocarditis; Endovascular Treatment of One Aneurysm with Glue (nBCA) Injection During Adenosine-Induced Asystole; Spontaneous Resolution of the Second Aneurysm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1027 Alexander Sirakov, Hosni Abu Elhasan, Marta Aguilar Pérez, Carmen Serna Candel, Hansjörg Bäzner, and Hans Henkes

Contents

xxvii

Part XIX

Vertebral Artery (V4) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1039

101

Vertebral Artery Aneurysm: Incidental Large Vertebral Aneurysm with Medullary Compression, Incorporation of the PICA, Treatment with a Single p64 Flow Diverter, and Complete Aneurysm Occlusion . . . . . . . . . . . . . . . . . . . . . . . . 1041 André Kemmling, Thomas Eckey, Dirk Rasche, and Peter Schramm

102

Vertebral Artery Aneurysm: Acute Subarachnoid Hemorrhage Due to a Dissecting V4 Aneurysm, Treatment with a Flow Diverter Stent, and Complete Reconstruction of the Vessel Lumen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1049 Muhammad AlMatter, Marta Aguilar Pérez, and Hans Henkes

103

Vertebral Artery Aneurysm: Severe Subarachnoid Hemorrhage, Dissecting Pseudoaneurysm of the Vertebral Artery, and Reconstructive Treatment Using Telescoping Pipeline Flow Diverters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1057 Franziska Dorn

104

Vertebral Artery Aneurysm: Partially Thrombosed Dissecting Aneurysm, Symptomatic Through Brainstem Compression, Treatment with Telescoping Surpass Streamline Flow Diverters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1065 Marin Irizoiu, Andrik Aschoff, Christoph Schul, and Christian Taschner

105

Vertebral Artery Aneurysm: Stent-Assisted Coil Occlusion, Early Reperfusion, ASA/Metamizol Interaction with Poorly Controlled Platelet Function Inhibition, p64 Implantation, Aneurysm Reperfusion and Thrombus-Related Inflammation, Telescoping PED Implantation and Anti-Inflammatory Medication, Angiographic Exclusion of the Aneurysm, Regression of the Inflammation and Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1071 Cindy Richter, Karl-Titus Hoffmann, Katharina Köhlert, Ulf Quäschling, and Stefan Schob

106

Vertebral Artery Aneurysm: Ruptured Dissecting Aneurysm, Implantation of Telescoping p48MW HPC Flow Diverter Stents Under Antiaggregation with ASA Only . . . . . . . . . . . . . . . . . 1081 Frances Colgan, Marta Aguilar Pérez, Victoria Hellstern, Matthias Reinhard, Stefan Krämer, Hansjörg Bäzner, Oliver Ganslandt, and Hans Henkes

xxviii

Contents

107

Vertebral Artery Aneurysm: Unruptured Dissecting Intradural Right Vertebral Artery Aneurysm with Brainstem Compression; Coil Occlusion of the Aneurysm and the Parent Artery with Resolution of the Mass Effect; Good Clinical Outcome with Long-Term Follow-up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1097 Hegoda Levansri Dilrukshan Makalanda, Sundip D. Udani, Grainne McKenna, Ken Wong, and Pervinder Bhogal

108

Vertebral Artery Aneurysm: Endovascular Treatment of a Ruptured Left Vertebral Artery Aneurysm in a Patient Who Developed Takotsubo Cardiomyopathy . . . . . . . . . . . . . . . . . 1107 Muhammad AlMatter, Thomas Güthe, Hellen Wahler, Moritz Fass, Oliver Ganslandt, and Hans Henkes

109

Vertebral Artery Junction Aneurysm: Atherosclerotic Aneurysm of the Vertebrobasilar Junction, Treated with Coil Occlusion and Staged Flow Diversion . . . . . . . . . . . . . . . . . . 1119 Muhammad AlMatter, Christin Clajus, Hans Henkes, and Joachim Klisch

110

Vertebral Artery Aneurysm: A Ruptured Wide-Necked Distal Vertebral Artery Aneurysm, Treated with Cascade NetAssisted Coil Occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1131 Stanimir Sirakov, Alexander Sirakov, and Hans Henkes

111

Vertebral Artery Aneurysm: A Duplicated Vertebral Artery Dissecting Pseudoaneurysm; Successful Endovascular Treatment with the Pipeline Embolization Device of a Large, Unruptured Dissecting Pseudoaneurysm Located on a Fenestrated Limb of the Intracranial Vertebral Artery; Technical Aspects and FollowUp Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1139 Pablo Albiña Palmarola, Ivan Lylyk, Rene Viso, Esteban Scrivano, and Pedro Lylyk

Part XX 112

Vertebral Artery Junction . . . . . . . . . . . . . . . . . . . . . . . . . . 1151

Vertebral Artery Junction Aneurysm: Ruptured Aneurysm at a Fenestrated Vertebrobasilar Junction, Treated with Stent-Assisted Coil Occlusion and Telescoping Flow Diverters . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1153 Nicolas Perez, Ivan Lylyk, Rene Viso, Jorge Chudyk, and Pedro Lylyk

Contents

xxix

113

Vertebral Artery Junction Aneurysm: Brain Stem Compression due to a Giant Dolichoectatic and Partially Thrombosed Aneurysm Involving the Intradural Segments of Both Vertebral Arteries and the Proximal Trunk of the Basilar Artery; Asymptomatic Thrombosis of the Vertebral Artery Junction After Ventricle Shunting; Endovascular Disconnection of the Vertebrobasilar Junction Using Coil Occlusion of Both V4 Segments and Flow Diverter Stent Deployment from Both Posterior Inferior Cerebellar Arteries to the Afferent V4 Segments; Long-Term Follow-Up Showing Aneurysm Shrinkage and Good Clinical Outcome . . . . . . . . 1159 Alexander Sirakov, Marta Aguilar Pérez, Klaus Terstegge, Erich Donauer, and Hans Henkes

Part XXI

Basilar Artery Trunk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1175

114

Basilar Artery Trunk Aneurysm: Giant Transitional Aneurysm, Mass Effect, Balloon Test Occlusion, Occlusion of Both Vertebral Arteries with Relief of Mass Effect and Good Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1177 José E. Cohen

115

Basilar Artery Trunk Aneurysm: Concomitant Retroperitoneal and Subarachnoid Hemorrhage, Segmental Arterial Mediolysis (SAM), Dissecting Aneurysm, Treatment by Partial Coil Occlusion and Flow Diversion . . . . . . . . . . . . . . . . . . . . . . . . . 1187 Victoria Hellstern, Marta Aguilar Pérez, Patricia Kohlhof-Meinecke, Hansjörg Bäzner, Oliver Ganslandt, and Hans Henkes

116

Basilar Trunk Aneurysm: Blunt Head Trauma, Dissecting Aneurysm of the Proximal Basilar Trunk Causing a Subarachnoid Hemorrhage, Reconstruction of the Basilar Artery with Three Telescoping Flow Diverters Anchored in the Left Vertebral Artery, Followed by Coil Occlusion of the Right V4 Segment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1195 Christina M. Wendl, Marta Aguilar Pérez, Gerhard Schuierer, and Hans Henkes

117

Basilar Artery Trunk Aneurysm: Large Transitional Vertebrobasilar Artery Aneurysm Causing Severe Ischemic Cerebellar Stroke; Treatment with a Surpass Flow Diverter with Growing Thrombus, Increasing Mass Effect and Continued Contrast Medium Pooling in the Thrombus Despite Angiographic Remodeling . . . . . . . . . . . . . . . . . . . . . 1203 Ivan Lylyk, Rene Viso, Carlos Bleise, and Pedro Lylyk

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Basilar Artery Trunk Aneurysm: Spontaneous Subarachnoid Hemorrhage due to an Aneurysm Associated with a Fenestration of the Basilar Artery, Endovascular Coil Occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1211 Muhammad AlMatter, Marta Aguilar Pérez, Oliver Ganslandt, and Hans Henkes

119

Basilar Artery Trunk Aneurysm: Incidental Aneurysm of the Basilar Artery Trunk, Incorporating Cerebellar Arteries; Documented Growth, Implantation of Two Telescoping p64 Flow Diverter Stents Under Combined Dual Antiaggregation and Anticoagulation; Complete Aneurysm Occlusion; and Collateral Supply of the Cerebellar Arteries . . . . . . . . . . . . . 1229 Marta Aguilar Pérez, Muhammad AlMatter, Ulrike Ernemann, Hansjörg Bäzner, and Hans Henkes

120

Basilar Artery Trunk Aneurysm: A Complex Aneurysm at a Basilar Artery Trunk Fenestration, Treated with ComaneciAssisted Coil Occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1243 Stanimir Sirakov and Alexander Sirakov

121

Basilar Artery Trunk Aneurysm: Unruptured Saccular Aneurysm of the Distal Basilar Artery Trunk at the Origin of the Left Superior Cerebellar Artery with Brainstem Compression, LEO Stent-Induced Flow Diversion of the Aneurysm with Resolution of the Mass Effect and No Perforator Occlusion, and Good Clinical Outcome with Midterm Follow-Up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1251 Hegoda Levansri Dilrukshan Makalanda, Geoffrey Lie, Ken Wong, and Pervinder Bhogal

122

Basilar Artery Trunk Aneurysm: Symptomatic Basilar Artery Trunk Dissecting Aneurysm with Critical Vasospasm Treated by Blind Deconstructive Coiling, Angioplasty, Embolectomy, and Flow Diversion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1259 José E. Cohen, Samuel Moscovici, Andrew H. Kaye, and Gustavo Rajz

Part XXII Pontine Perforator Artery . . . . . . . . . . . . . . . . . . . . . . . . . 1269 123

Basilar Perforator Artery Aneurysm: Spontaneous Subarachnoid Hemorrhage Caused by the Rupture of a Small Aneurysm of a Pontine Perforating Vessel Originating from the Upper Basilar Artery Trunk; Conservative Management, with Fatal Outcome After Recurrent Hemorrhages and due to Severe Vasospasm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1271 Victoria Hellstern, Marta Aguilar Pérez, Muhammad AlMatter, Patricia Kohlhof-Meinecke, Hansjörg Bäzner, and Hans Henkes

Contents

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Part XXIII

Basilar Artery Bifurcation

. . . . . . . . . . . . . . . . . . . . . . . . 1281

124

Basilar Artery Bifurcation Aneurysm: Giant Basilar Bifurcation Aneurysm, Mass Effect, Stent-Assisted Coil Occlusion with a Single Enterprise Stent, Complete Long-Term Occlusion, Good Clinical Outcome . . . . . . . . . . . 1283 Michael Kirsch

125

Basilar Artery Bifurcation Aneurysm: Acute SAH, Ruptured Wide Neck Basilar Bifurcation Aneurysm, Medina and Coil Occlusion Assisted by pCONUS2, Early Interruption of Antiaggregation Without Sequelae . . . . . . . . . . . . . . . . . . . . . 1289 Harald Sahl and Hans Henkes

126

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 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1297 Marta Aguilar Pérez, Muhammad AlMatter, and Hans Henkes

127

Basilar Artery Bifurcation Aneurysm: Recurrence and Significant Growth After Stent-Assisted Coil Occlusion, Hemodynamic Treatment Using pCANVAS and Medina Embolization Devices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1309 Franziska Dorn and Hans Henkes

128

Basilar Artery Bifurcation Aneurysm: Spontaneous SAH, Endovascular Coil Occlusion, Recurrent SAH, Multiple Retreatments, and Continued Recanalizations of a Growing Aneurysm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1319 Muhammad AlMatter, Marta Aguilar Pérez, and Hans Henkes

129

Basilar Artery Bifurcation Aneurysm: Spontaneous SAH and Recurrent Aneurysm Rupture During Computed Tomography Angiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1335 Georg Gihr, Franziska Dorn, and Hans Henkes

130

Basilar Artery Bifurcation Aneurysm: Retrograde Access via the Posterior Communicating Artery to the Basilar Artery Bifurcation for Stent-Assisted Recoiling of a Wide-Necked Aneurysm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1345 Christian Roth and Stefan Pfleiderer

131

Basilar Artery Bifurcation Aneurysm: Ruptured Wide-Necked Basilar Bifurcation Aneurysm Presenting with Atypical Clinical Signs and Symptoms, Treated with a WEB Device After a Failed Attempt at Coil Occlusion . . . . . . . . . . . . . . . . 1351 Maxim Bester, Jens Fiehler, and Jan-Hendrik Buhk

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Basilar Artery Bifurcation Aneurysm: A Ruptured WideNecked Basilar Bifurcation Aneurysm, Treated by Dual Comaneci-Assisted Coil Occlusion . . . . . . . . . . . . . . . . . . . . . 1361 Stanimir Sirakov, Alexander Sirakov, Ivan Lylyk, Carlos Bleise, Rene Viso, and Pedro Lylyk

133

Basilar Artery Bifurcation Aneurysm: Giant Incidental Basilar Artery Bifurcation Aneurysm, Treated by Stent-Assisted Coil Occlusion Using Two Crossing pCONUS1 Aneurysm Bridging Devices and Two Crossing Solitaire Stents Deployed in Telescoping Fashion; Four Treatment Sessions, Resulting in Permanent Aneurysm Occlusion and Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1369 Marta Aguilar Pérez, Muhammad AlMatter, and Hans Henkes

134

Basilar Artery Bifurcation Aneurysm: Incidental Flow-Related Wide-Necked Basilar Bifurcation Aneurysm in a Ruptured Arteriovenous Malformation, Treated with PulseRiderAssisted Coil Occlusion with Angiographic Exclusion of the Aneurysm and Good Clinical Outcome . . . . . . . . . . . . . . . . . 1391 Ivan Lylyk, Rodolfo Nella Castro, Rene Viso, and Pedro Lylyk

135

Basilar Artery Bifurcation Aneurysm: Small Wide-Necked Incidental Basilar Artery Bifurcation Aneurysm, Treated with Staged pCONUS1 HPC Implantation and Coil Occlusion; Protrusion of a Coil Loop into the Basilar Artery Bifurcation, Which Prompted the Removal of That Coil Using an Alligator Device . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1401 Alexander Sirakov, Muhamad Elhalal, Klaus Terstegge, Erich Donauer, and Hans Henkes

Part XXIV

Posterior Inferior Cerebellar Artery Aneurysm

. . . . 1411

136

Posterior Inferior Cerebellar Artery Aneurysm: Microsurgical Clipping of a Ruptured Posterior Inferior Cerebellar Artery (PICA) Aneurysm Not Well Suited to Endovascular Treatment, Far-Lateral Transcondylar Approach to the Anterior Medullary Segment of the PICA, Complete Exclusion of the Aneurysm with Preservation of the Parent Artery . . . . . . . . 1413 Silvia Hernández-Durán and Veit Rohde

137

Posterior Inferior Cerebellar Artery Aneurysm: Incidental Aneurysm, Trapping by Microsurgical Clipping, and Resection of the Aneurysm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1421 Marvin Darkwah Oppong and Ulrich Sure

138

Posterior Inferior Cerebellar Artery Aneurysm: Subarachnoid Hemorrhage after a Minor Trauma, Fusiform Dissecting Aneurysm, Treatment with a p64 Flow Diverter . . . . . . . . . . 1427 Stephan Felber and Ali Daoun

Contents

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139

Posterior Inferior Cerebellar Artery Aneurysm: Incidental Wide-Neck Aneurysm, Incorporation of the PICA, and Treatment with a Single 3D Coil and a p64 Flow Diverter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1433 Marta Aguilar Pérez, Muhammad AlMatter, and Hans Henkes

140

Posterior Inferior Cerebellar Artery Aneurysm: Multiple Incidental Aneurysms of Both MCAs and the Left Vertebral Artery, Surgical Clipping of two Right MCA Aneurysms, and Flow Diversion Using the Slipstream Effect of the Left PICA and Left M1 Aneurysm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1439 Marta Aguilar Pérez, Muhammad AlMatter, Oliver Ganslandt, and Hans Henkes

141

Posterior Inferior Cerebellar Artery Aneurysm: Dissecting Aneurysm Treated in Multiple Sessions and Multiple Endovascular Modalities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1449 Rene Viso, Ivan Lylyk, Nicolas Perez, and Pedro Lylyk

142

Posterior Inferior Cerebellar Artery Aneurysm: Spontaneous Subarachnoid Hemorrhage Secondary to a Dissecting Aneurysm of a Double Origin PICA . . . . . . . . . . . . . . . . . . . 1463 Ken Wong, Sundip D. Udani, Hegoda Levansri Dilrukshan Makalanda, and Pervinder Bhogal

143

Posterior Inferior Cerebellar Artery Aneurysm: Ruptured Dissecting Small Aneurysm, Treated with Pipeline Embolization Device in the Acute Phase . . . . . . . . . . . . . . . . 1469 Rene Viso, Ivan Lylyk, Carlos Bleise, Esteban Scrivano, and Pedro Lylyk

144

Posterior Inferior Cerebellar Artery Aneurysm: Acute SAH due to a Ruptured Dissecting Aneurysm of the Left PICA, Treated with Coil Occlusion of the Aneurysm and of the Dissected Vessel Segment with No Resulting PICA Infarct . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1475 Muhammad AlMatter, Moritz Fass, Bernd Tomandl, Frances Colgan, and Hans Henkes

Part XXV 145

Anterior Inferior Cerebellar Artery . . . . . . . . . . . . . . . . 1485

Anterior Inferior Cerebellar Artery Aneurysm: Saccular NonRuptured Aneurysm of the Premeatal Segment of the Anterior Inferior Cerebellar Artery, Treated with Flow Diverter Implantation into the Basilar Artery, with Complete Aneurysm Occlusion, Preservation of the Parent Artery, and Good Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1487 Rene Viso, Ivan Lylyk, Javier Lundquist, and Pedro Lylyk

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Contents

Part XXVI

Superior Cerebellar Artery . . . . . . . . . . . . . . . . . . . . . . . 1501

146

Superior Cerebellar Artery Aneurysm: A Small Ruptured Superior Cerebellar Artery Aneurysm Detected by Repeated Angiography and Successfully Treated by Microsurgical Clipping After a Failed Attempt at Coil Occlusion . . . . . . . . 1503 Maria Wostrack and Kornelia Kreiser

147

Superior Cerebellar Artery Aneurysm: Spontaneous SAH, Occlusion of a Mid-sized, Wide-Necked Superior Cerebellar Artery Aneurysm with a Medina Device and Coils; Subsequent Coil Compaction, Treated with Flow Diversion Using a p64 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1513 Marcel Kalman, Muhammad AlMatter, Marta Aguilar Pérez, Ludwig Niehaus, and Hans Henkes

148

Superior Cerebellar Artery Aneurysm: Spontaneous Subarachnoid Hemorrhage and Stent-Assisted Coil Occlusion of a Ruptured Aneurysm at the Superior Cerebellar Artery Origin and of an Unruptured Small Basilar Artery Bifurcation Aneurysm, Bacterial Endocarditis, Early Major Aneurysm Recurrence with Oculomotor Palsy, and Treatment of the “Mycotic” Aneurysm by Flow Diverter Implantation, with Resolution of the Aneurysm and Good Clinical Recovery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1523 Anna Hartmann, Karl-Titus Hoffmann, Caroline Sander, Ulf Quäschling, and Stefan Schob

149

Superior Cerebellar Artery Aneurysm: Ruptured Blister Aneurysm Treated with Balloon-Assisted Coil Occlusion with Good Angiographic and Clinical Outcome . . . . . . . . . . . . . . 1533 Alvaro Valtorta, Esteban Scrivano, Ivan Lylyk, Rene Viso, and Pedro Lylyk

Part XXVII Posterior Cerebral Artery . . . . . . . . . . . . . . . . . . . . . . . . 1543 150

Posterior Cerebral Artery Aneurysm: A Dissecting, Partially Thrombosed Fusiform Aneurysm of the Left Posterior Cerebral Artery, Treated with a p64 Flow Diverter . . . . . . . 1545 Stanimir Sirakov and Alexander Sirakov

151

Posterior Cerebral Artery Aneurysm: Unruptured, Large, Dissecting, and Partially Thrombosed Aneurysm of the Posterior Cerebral Artery, Treated with a p64 Flow Diverter, with Reconstruction of the Parent Artery . . . . . . . 1553 Ketevan Mikeladze and Evgeni Bucharin

Contents

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152

Posterior Cerebral Artery Aneurysm: Endovascular Treatment of a Fusiform, Partially Thrombosed P2-Aneurysm with a Dual-Layer Flow-Diverting Stent (FRED) in a Young Patient with Good Clinical Outcome . . . 1561 Dominik F. Vollherbst and Markus A. Möhlenbruch

Part XXVIII 153

Middle Meningeal Artery Aneurysm: Non-traumatic Incidental Aneurysm of a Middle Meningeal Artery Supplying a Pial Arteriovenous Malformation; Endovascular Occlusion of the Aneurysm Using nBCA During the Preoperative Embolization of the AVM . . . . . . . . . . . . . . . . . 1571 Pervinder Bhogal, Marta Aguilar Pérez, Marcel Alfter, Oliver Ganslandt, and Hans Henkes

Part XXIX 154

Dural Artery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1569

Spinal Cord Artery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1585

Sulco-commissural Artery Aneurysm: Spontaneous Cervical Intramedullary and Subarachnoid Hemorrhage, Cervical Intradural Arteriovenous Fistula, Aneurysm of a Cervical Sulco-commissural Artery, Failed Attempt to Occlude the Aneurysm by Endovascular Means, Surgical Resection of the Aneurysm with Preservation of the Anterior Spinal Artery, and Partial Resection of the Intradural Arteriovenous Fistula . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1587 Erich Donauer, Marta Aguilar Pérez, Nirmal Jangid, Bernd Tomandl, Oliver Ganslandt, and Hans Henkes

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1603

About the Editors

Hans Henkes M.D. Ph.D., studied medicine and psychology at the Freie Universität Berlin and graduated in 1985. After residencies in neurophysiology and general radiology in Berlin, and in diagnostic neuroradiology in Homburg/Saar, he worked under Dietmar Kühne as an interventional neuroradiologist for 15 years at the Alfried Krupp Krankenhaus (Essen, Germany). In 2006 Dr. Henkes became an Extraordinary Professor for Neuroradiology at the University Duisburg-Essen, Germany. Since 2007 he has been the Medical Director of the Neuroradiological Clinic at the Klinikum Stuttgart, Germany. Dr. Henkes has co-authored more than 225 peerreviewed publications and serves as a reviewer for several journals including Stroke, AJNR, JNIS, Neurosurgery, Clinical Neuroradiology, Interventional Neuroradiology, and Neuroradiology. In 2013, he was awarded an honorary doctorate by the Dnipro State Medical Academy (Ukraine). In 2017, Dr. Henkes received the CIRSE Award for Excellence and Innovation in Interventional Radiology for the invention of stent-retriever thrombectomy in acute ischemic stroke.

Pedro Lylyk M.D. Ph.D., graduated from the Faculty of Medicine of the University of Buenos Aires (UBA). He completed his residency program in pediatric neurosurgery with Professor Raúl Carrea at the Ricardo Gutiérrez Children’s Hospital of Buenos Aires. After that, Dr. Lylyk completed fellowships in diagnostic neuroradiology and therapeutic and endovascular neurosurgery at the University Hospital of London of the University of Western Ontario, Canada, and at the University of California, Los Angeles, USA. xxxvii

xxxviii

About the Editors

Among his extensive academic background, he is Chair of Neurosurgery and Hemodynamics at the University of Buenos Aires (UBA), Professor and Chair of the Department of Vascular Medicine at the Universidad del Salvador (USAL), Professor and Chair of Endovascular Surgery at the Universidad de Ciencias Sociales y Empresariales (UCES), and Director of Master Degrees in Neuroradiology and Hemodynamics Neurology, Diagnostic Imaging, and Kinesiology at the University of Buenos Aires (UBA). Dr. Lylyk is the founder and president of the FENERI Foundation (Fundación para el Estudio de las Neurociencias y la Radiología Intervencionista) and co-founder of the Cerebrovascular Research and Education Foundation (CREF) and the Intracranial Stent Meeting and Society (ICS). He is a member of the SwissNeuroFoundation and a founding member and former president of SILAN (Sociedad Iberolatinoamericana de Neurorradiología Diagnóstica y Terapéutica), AANDIT (Asociación Argentina de Neurorradiología Diagnóstica y Terapéutica), and CANI (Colegio Argentino de Neurointervencionistas). The endovascular lab at Clinica La Sagrada Familia is one of the training centers for SILAN fellows, which has allowed the training of more than 90 neuroendovascular professionals since 1995. Since 1986 Dr. Lylyk has been dedicated to the development and improvement of devices and therapeutic options to enhance the endovascular neurosurgical field and represents an international reference for the medical device industry.

Oliver Ganslandt M.D. Ph.D., studied medicine at the Friedrich-Alexander-Universität Erlangen, Germany. He completed his doctoral thesis in 1992 on magnetoencephalography and gained his Ph.D. (“Habilitation” grade) in 2002 in the subject of functional neuronavigation. His training as a neurosurgeon began in 1991 under Professor Fahlbusch at the Department of Neurosurgery Erlangen and later continued under Professor Buchfelder, where he worked as Vice Chairman of the department until January 2014. Dr. Ganslandt was then elected as Medical Director of the Neurosurgical Clinic of the Klinikum

About the Editors

xxxix

Stuttgart, Germany, where he works today. His clinical and scientific interests are functional imaging, neuro-oncology, and radiosurgery. Dr. Ganslandt has given numerous presentations at national and international meetings, serves as reviewer for many peer-reviewed journals (including Neurosurgery and Journal of Neurosurgery) as well as for national and international scientific organizations (Deutsche Forschungsgemeinschaft, Canada Foundation for Innovation, Dutch Cancer Society), and he is a member of the advisory board of the journal Strahlentherapie und Onkologie.

Contributors

Hosni Abu Al-Hasan Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Marta Aguilar Pérez Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany Pablo Albiña Palmarola Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Neurosurgery Division, Hospital Barros Luco Trudeau, Santiago, Chile Pedro Pablo Alcázar Romero Hospital Universitario Virgen de las Nieves, Granada, Spain Marcel Alfter Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany Muhammad AlMatter Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany Guy Arnold Klinik für Neurologie mit Neurophysiologie und Schlaganfalleinheit, Klinikum Sindelfingen-Böblingen, Sindelfingen, Germany Andrik Aschoff Klinik für diagnostische und interventionelle Radiologie und Neuroradiologie, Klinikum Kempten, Kempten, Germany Hansjörg Bäzner Neurologische Klinik, Klinikum Stuttgart, Stuttgart, Germany Maxim Bester Klinik und Poliklinik für Neuroradiologische Diagnostik und Intervention, Universitätsklinikum Hamburg Eppendorf, Hamburg, Germany Neuroradiology, UKE, Hamburg, Germany Pervinder Bhogal Department of Interventional Neuroradiology, The Royal London Hospital, London, UK Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany Carlos Bleise Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina xli

xlii

Thomas Bonnet Department of Interventional Neuroradiology, ERASME University Hospital, Brussels, Belgium Alexander Brawanski Department of Neurosurgery, University Medical Center Regensburg, Regensburg, Germany Evgeni Bucharin Department of Vascular Surgery, Burdenko Neurosurgery Institute, Moscow, Russia Jan-Hendrik Buhk Klinik und Poliklinik für Neuroradiologische Diagnostik und Intervention, Universitätsklinikum Hamburg Eppendorf, Hamburg, Germany Neuroradiology, UKE, Hamburg, Germany Rosana Ceratto Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Carlos Candanedo Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Jorge Chudyk Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Christin Clajus Institut für diagnostische und interventionelle Radiologie und Neuroradiologie, HELIOS Klinikum Erfurt, Erfurt, Germany José E. Cohen Hadassah-Hebrew University Medical Center, Jerusalem, Israel Frances Colgan Department of Radiology, University of Otago, Christchurch Hospital, Christchurch, New Zealand William Crinnion Department of Interventional Neuroradiology, The Royal London Hospital, London, UK Haim Danenberg Department of Cardiology, Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Ali Daoun Institut für Diagnostische und Interventionelle Radiologie, Neuroradiologie, Gemeinschaftsklinikum Mittelrhein, Koblenz, Germany Marvin Darkwah Oppong Department of Neurosurgery, University Hospital, University of Duisburg-Essen, Essen, Germany Joost De Vries Radboud University, Nijmegen, The Netherlands Erich Donauer Klinik für Neurochirurgie und Stereotaxie, MediClin Krankenhaus Plau am See, Plau am See, Germany Franziska Dorn Department of Neuroradiology, University Hospital of Munich, Campus Grosshadern, Munich, Germany Meike Dukiewicz Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany

Contributors

Contributors

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Thomas Eckey Institut für Neuroradiologie, Universitätsklinikum Schleswig-Holstein, Lübeck, Germany Muhamad Elhalal Klinik für Radiologie und Neuroradiologie, MediClin Krankenhaus Plau am See, Plau am See, Germany Hosni Abu Elhasan Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Ulrike Ernemann Abteilung Diagnostische und Interventionelle Neuroradiologie, Universitätsklinikum Tübingen, Tübingen, Germany Moritz Fass Neurochirurgische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany Stephan Felber Institut für Diagnostische und Interventionelle Radiologie, Neuroradiologie, Gemeinschaftsklinikum Mittelrhein, Koblenz, Germany Angel Ferrario Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Jens Fiehler Klinik und Poliklinik für Neuroradiologische Diagnostik und Intervention, Universitätsklinikum Hamburg Eppendorf, Hamburg, Germany Neuroradiology, UKE, Hamburg, Germany Sebastian Fischer Institut für Diagnostische und Interventionelle Radiologie, Neuroradiologie und Nuklearmedizin, Universitätsklinikum Bochum, Bochum, Germany Charlotte Flüh Klinik für Neurochirurgie, Universitätsklinikum SchleswigHolstein, Campus Kiel, Kiel, Germany Isabel Fragata Departamento de Neurorradiologia, Centro Hospitalar Universitário de Lisboa Central, Lisbon, Portugal Oliver Ganslandt Neurochirurgische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany Ernesto García Bautista Hospital Universitario Virgen de las Nieves, Granada, Spain Matthias Gawlitza Hôpital Maison-Blanche, Université Reims-Champagne-Ardenne, Reims, France Georg Gihr Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany John Moshe Gomori Department of Medical Imaging, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Matthias Groll Klinik und Poliklinik für Neurochirurgie, Universitätsklinik Leipzig AöR, Leipzig, Germany Thomas Güthe Klinik für Herz- und Gefäßkrankheiten, Klinikum Stuttgart, Stuttgart, Germany

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Contributors

Amer Haj Department of Neurosurgery, University Medical Center Regensburg, Regensburg, Germany Anna Hartmann Abteilung für Neuroradiologie, Universitätsklinikum Leipzig, Leipzig, Germany Victoria Hellstern Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany Hans Henkes Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany Silvia Hernández-Durán Department of Neurological Universitätsmedizin Göttingen, Göttingen, Germany

Surgery,

Birgit Herting Klinik für Neurologie und Gerontoneurologie, DiakonieKlinikum Schwäbisch Hall, Schwäbisch Hall, Germany Karl-Titus Hoffmann Abteilung für Neuroradiologie, Universitätsklinikum Leipzig, Leipzig, Germany Asaf Honig Department of Neurology, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Marin Irizoiu Klinik für diagnostische und interventionelle Radiologie und Neuroradiologie, Klinikum Kempten, Kempten, Germany Nirmal Jangid Klinik für Neurochirurgie und Frührehabilitation, MediClin Krankenhaus Plau am See, Plau am See, Germany Farzaneh Jedi Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany Matthias Juergens Klinik für Radiologie und Neuroradiologie, MediClin Krankenhaus Plau am See, Plau am See, Germany Assylbek Kaliyev Department of Cerebrovascular Neurosurgery, National Center of Neurosurgery, Nur-Sultan, Kazakhstan Marcel Kalman Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany Andrew H. Kaye Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Department of Surgery, University of Melbourne, Melbourne, Australia André Kemmling Institut für Neuroradiologie, Universitätsklinikum Schleswig-Holstein, Lübeck, Germany Michael Kirsch Institut für Diagnostische Radiologie und Neuroradiologie, Universitätsmedizin Greifswald, Greifswald, Germany Joachim Klisch Institut für diagnostische und interventionelle Radiologie und Neuroradiologie, HELIOS Klinikum Erfurt, Erfurt, Germany

Contributors

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Christof Klötzsch Neurologische Klinik, Hegau-Bodensee- Klinikum Singen, Singen, Germany Patricia Kohlhof-Meinecke Institut für Pathologie, Klinikum Stuttgart, Stuttgart, Germany Katharina Köhlert Klinik für Neurochirurgie, Universitätsklinikum Leipzig, Leipzig, Germany Isabel König Institut für Diagnostische und Interventionelle Radiologie, Neuroradiologie und Nuklearmedizin, Universitätsklinikum Bochum, Bochum, Germany Stefan Krämer Klinik für Radiologie und Nuklearmedizin, Klinikum Esslingen, Esslingen, Germany Kornelia Kreiser Department of Neuroradiology, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany Thomas Kretschmer Department of Neurosurgery, Klinikum Klagenfurt, Klagenfurt, Austria Jan Oliver Kuhnt Klinik für Radiologie, Neuroradiologie und Nuklearmedizin, Knappschaftskrankenhaus Recklinghausen, Klinikum Vest, Recklinghausen, Germany Marat Kulmirzayev Department of Cerebrovascular National Center of Neurosurgery, Nur-Sultan, Kazakhstan

Neurosurgery,

Peter Kurucz Neurochirurgische Klinik, Klinikum Stuttgart, Stuttgart, Germany Naomi Larsen Klinik für Neurochirurgie, Universitätsklinikum SchleswigHolstein, Campus Kiel, Kiel, Germany Ronen R. Leker Department of Neurology, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Geoffrey Lie Department of Interventional Neuroradiology, The Royal London Hospital, London, UK Donald Lobsien Institut für diagnostische und interventionelle Radiologie und Neuroradiologie, HELIOS Klinikum Erfurt, Erfurt, Germany Christian Loehr Klinik für Radiologie, Neuroradiologie und Nuklearmedizin, Knappschaftskrankenhaus Recklinghausen, Klinikum Vest, Recklinghausen, Germany Boris Lubicz Department of Interventional Neuroradiology, ERASME University Hospital, Brussels, Belgium Javier Lundquist Interventional Neuroradiology, Clínica La Sagrada Familia, ENERI, Buenos Aires, Argentina

xlvi

Ivan Lylyk Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Pedro Lylyk Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Gottlieb Maier Neurochirurgische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany Hegoda Levansri Dilrukshan Makalanda Department of Interventional Neuroradiology, The Royal London Hospital, London, UK Levansri Makalanda Department of Interventional Neuroradiology, The Royal London Hospital, London, UK Yerbol Makhambetov Department of Cerebrovascular Neurosurgery, National Center of Neurosurgery, Nur-Sultan, Kazakhstan Thomas R. Marotta Department of Medical Imaging, Diagnostic and Therapeutic Neuroradiology, St. Michael’s Hospital University of Toronto, Toronto, ON, Canada Rosa Martinez Moreno Hospital Universitario Virgen de las Nieves, Granada, Spain D. Mauricio Alvarez Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Volker Maus Institut für Diagnostische und Interventionelle Radiologie, Neuroradiologie und Nuklearmedizin, Universitätsklinikum Bochum, Bochum, Germany Grainne McKenna Department of Neurosurgery, The Royal London Hospital, London, UK Ketevan Mikeladze Department of Vascular Surgery, Burdenko Neurosurgery Institute, Moscow, Russia Benjamin Mine Department of Interventional Neuroradiology, ERASME University Hospital, Brussels, Belgium Saba Moghimi Faculty of Medicine, University of Toronto, Toronto, ON, Canada Markus A. Möhlenbruch Department of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany Samuel Moscovici Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Rodrigo Muñoz Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Marc Münter Klinik für Strahlentherapie und Radioonkologie, Klinikum Stuttgart, Stuttgart, Germany

Contributors

Contributors

xlvii

Rodolfo Nella Castro Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Huu An Nguyen Hôpital Maison-Blanche, Université Reims-ChampagneArdenne, Reims, France Bach Mai Hospital, Hanoi, Vietnam Ludwig Niehaus Neurologische Klinik, Rems-Murr-Klinikum Winnenden, Winnenden, Germany Rita Nogueira Departamento de Medicina, Centro Hospitalar Universitário de Coimbra, Coimbra, Portugal Jaime Pamplona Departamento de Neurorradiologia, Centro Hospitalar Universitário de Lisboa Central, Lisbon, Portugal Nicolas Perez Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Catarina Perry Departamento de Neurorradiologia, Centro Hospitalar Universitário de Lisboa Central, Lisbon, Portugal Athanasios K. Petridis Department of Neurosurgery, Heinrich Heine University, Düsseldorf, Germany Stefan Pfleiderer Institut für Diagnostische und Interventionelle Radiologie, Klinikum Reinkenheide, Bremerhaven, Germany Laurent Pierot Hôpital Maison-Blanche, Université Reims-ChampagneArdenne, Reims, France David Planer Department of Cardiology, Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Ulf Quäschling Abteilung für Neuroradiologie, Universitätsklinikum Leipzig, Leipzig, Germany Gustavo Rajz Department of Neurosurgery, Shaare Zedek Medical Center, Jerusalem, Israel Dirk Rasche Klinik für Neurochirurgie, Universitätsklinikum SchleswigHolstein, Lübeck, Germany Hannes Rauter Department of Neurosurgery, Klinikum Klagenfurt, Klagenfurt, Austria Matthias Reinhard Klinik für Neurologie und klinische Neurophysiologie, Klinikum Esslingen, Esslingen, Germany João Reis Departamento de Neurorradiologia, Universitário de Lisboa Central, Lisbon, Portugal

Centro

Hospitalar

Alexandra Resch Department of Neurosurgery, Klinikum Klagenfurt, Klagenfurt, Austria

xlviii

Contributors

Vera Reuschel Abteilung für Neuroradiologie, Universitätsklinikum Leipzig AöR, Leipzig, Germany Cindy Richter Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany Abteilung für Neuroradiologie, Universitätsklinikum Leipzig, Leipzig, Germany Veit Rohde Department of Neurological Surgery, Universitätsmedizin Göttingen, Göttingen, Germany Christian Roth Klinik für Diagnostische und Interventionelle Neuroradiologie, Klinikum Bremen-Mitte, Bremen, Germany Harald Sahl Institut für Nuklearmedizin und Radiologie, Klinikum Braunschweig, Braunschweig, Germany Caroline Sander Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Leipzig, Leipzig, Germany Karl-Michael Schebesch Department of Neurosurgery, University Medical Center Regensburg, Regensburg, Germany Noel P. Schechtman Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Stefan Schob Abteilung für Neuroradiologie, Universitätsklinikum Leipzig, Leipzig, Germany Peter Schramm Institut für Neuroradiologie, Universitätsklinikum Schleswig-Holstein, Lübeck, Germany Gerhard Schuierer Zentrum für Neuroradiologie, Universitätsklinikum und Bezirksklinikum Regensburg, Regensburg, Germany Christoph Schul Klinik für Neurochirurgie, Klinikum Kempten, Kempten, Germany Marie-Sophie Schüngel Abteilung für itätsklinikum Leipzig, Leipzig, Germany

Neuroradiologie,

Univers-

Esteban Scrivano Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Carmen Serna Candel Neuroradiologische Klinikum Stuttgart, Stuttgart, Germany

Klinik,

Neurozentrum,

Yigal Shoshan Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Moatasim Shweiki Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Alexander Sirakov Neuroradiology, University Hospital St. Ivan Rilski, Sofia, Bulgaria Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany

Contributors

xlix

Stanimir Sirakov Neuroradiology, University Hospital St. Ivan Rilski, Sofia, Bulgaria Sébastien Soize Hôpital Maison-Blanche, Université Reims-ChampagneArdenne, Reims, France Sergey Spektor Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel Hans Jakob Steiger Department of Neurosurgery, Heinrich Heine University, Düsseldorf, Germany Helmut Steinhart Klinik für Hals-Nasen-Ohren-Heilkunde, Kopf- und Halschirurgie, Marienhospital Stuttgart, Stuttgart, Germany Ulrich Sure Department of Neurosurgery, University Hospital, University of Duisburg-Essen, Essen, Germany Voitek Sychra Institut für diagnostische und interventionelle Radiologie und Neuroradiologie, HELIOS Klinikum Erfurt, Erfurt, Germany Michael Synowitz Klinik für Neurochirurgie, Universitätsklinikum Schleswig-Holstein, Campus Kiel, Kiel, Germany Christian Taschner Klinik für Neuroradiologie, Universitätsklinikum Freiburg, Freiburg, Germany Klaus Terstegge Klinik für Radiologie und Neuroradiologie, MediClin Krankenhaus Plau am See, Plau am See, Germany Bernd Tomandl Klinik für Radiologie und Neuroradiologie, Klinikum Christophsbad, Göppingen, Germany Pablo Tomás Muñoz Hospital Universitario Virgen de las Nieves, Granada, Spain Sundip D. Udani Department of Interventional Neuroradiology, The Royal London Hospital, London, UK Alvaro Valtorta Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Jasper Hans van Lieshout Department of Neurosurgery, Heinrich Heine University, Düsseldorf, Germany Rene Viso Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Dominik F. Vollherbst Department of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany Ghouth Waggass Faculty of Medicine, University of Toronto, Toronto, ON, Canada Hellen Wahler Neurochirurgische Klinik, Klinikum Stuttgart, Stuttgart, Germany

l

Anushe Weber Institut für Diagnostische und Interventionelle Radiologie, Neuroradiologie und Nuklearmedizin, Universitätsklinikum Bochum, Bochum, Germany Werner Weber Institut für Diagnostische und Interventionelle Radiologie, Neuroradiologie und Nuklearmedizin, Universitätsklinikum Bochum, Bochum, Germany Christina M. Wendl Zentrum für Neuroradiologie, Universitätsklinikum und Bezirksklinikum Regensburg, Regensburg, Germany Ken Wong Department of Interventional Neuroradiology, The Royal London Hospital, London, UK Maria Wostrack Department of Neurosurgery, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany

Contributors

Part I Cervical Internal Carotid Artery

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Cervical Internal Carotid Artery Aneurysm: Spontaneous Dissection of the Cervical Internal Carotid Artery Resulting in Elongation and Pseudoaneurysm Formation Causing Hypoglossal Nerve Palsy; Endovascular Vessel Reconstruction with Stenting, Followed by Telescoping Flow Diversion, Achieving Straightening of the Artery, Aneurysm Occlusion, Hypoglossal Nerve Recovery, and Normalization of the Tongue Hosni Abu Elhasan, Pablo Albiña Palmarola, Marta Aguilar Pérez, Birgit Herting, Hansjörg Bäzner, and Hans Henkes Abstract

H. Abu Elhasan Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel e-mail: [email protected] P. Albiña Palmarola Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina Neurosurgery Division, Hospital Barros Luco Trudeau, Santiago, Chile e-mail: [email protected] M. Aguilar Pérez · H. Henkes (*) Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; [email protected] B. Herting Klinik für Neurologie und Gerontoneurologie, DiakonieKlinikum Schwäbisch Hall, Schwäbisch Hall, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_154

A 48-year-old male patient, with a history of intermittent atrial fibrillation, endogenous depression, and Meulengracht syndrome, presented 2 days after the acute onset of a paralysis of the right-hand side of his tongue, causing dysarthria and difficulty swallowing. When he stuck out his tongue, it deviated to the right. Otherwise, his neurological condition was within normal limits, and the diagnosis of an acute hypoglossal nerve palsy was made. Magnetic resonance imaging and angiography (MRI, MRA), followed by diagnostic digital subtraction angiography (DSA), showed a 360
loop and a dissecting aneurysm in his right cervical internal carotid artery (ICA) just proximal to the petrous segment. The maximum neck and fundus diameters were 6 mm and 11 mm, respectively. Endovascular treatment was carried out, starting with balloon 3

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straightening of the ICA followed by deploying a self-expanding Carotid Wallstent (Boston Scientific) into the affected ICA segment. Followup examinations after 2 months showed a straightened ICA with persistent perfusion of the false ICA lumen and the dissecting aneurysm. A p64 flow diverter (phenox) was implanted inside the Carotid Wallstent. DSA 3 months later confirmed the occlusion of the pseudoaneurysm and the false lumen. The hypoglossal nerve palsy disappeared within 2 months after the first treatment in which the ICA had been straightened. Hypoglossal nerve palsy due to ICA dissection with pseudoaneurysm formation, including management of this condition, is the main topic of this chapter.

diameter was 11 mm. The cervical ICA was elongated forming a 360
loop. There was high-grade stenosis in a small segment of the ICA, level with the pseudoaneurysm (Fig. 1).

Treatment Strategy The symptoms displayed by the patient were due to the hypoglossal nerve being compressed by the aneurysm and the elongated ICA. The primary treatment goal was to recover the function of the hypoglossal nerve. Dissecting pseudoaneurysms of the ICA are a potential source of emboli to the dependent vasculature. The secondary treatment goal was to exclude the dissecting pseudoaneurysm from blood circulation.

Keywords

Cervical internal carotid artery · Hypoglossal nerve palsy · Dissecting pseudoaneurysm · Carotid Wallstent · Flow diversion · p64

Patient A 48-year-old male patient presented 2 days after the acute onset of a paralysis of the right-hand side of his tongue, causing dysarthria and difficult swallowing. His medical history was, apart from intermittent atrial fibrillation, endogenous depression, and Meulengracht syndrome, otherwise inconspicuous. Neurological examination showed that his tongue lolled to the right when stuck out, in line with an acute hypoglossal nerve palsy.

Diagnostic Imaging MRI, MRA, and DSA showed a presumably dissecting pseudoaneurysm of the distal cervical ICA proximal to the petrous segment of said artery. The neck width was 6 mm, and the fundus

H. Bäzner Neurologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]

Treatment Procedure #1, 25.01.2013: endovascular treatment of a dissected right-hand cervical ICA by means of balloon angioplasty and stent implantation Anesthesia: general anesthesia; 1 500 mg ASA (Aspirin i.v. 500 mg, Bayer Vital) IV, 1 5,000 IU unfractionated heparin (1 HeparinNatrium, B. Braun) IV, 7 1 mg glyceryl trinitrate (Nitrolingual, G. Pohl Boskamp) IA Premedication: 1 500 mg ASA PO and 1 600 mg clopidogrel (Plavix, Sanofi-Aventis) PO 1 day before the procedure; 1 100 mg ASA PO and 1 75 mg clopidogrel PO on the morning of the treatment day, 4 h before the procedure; response testing immediately before the procedure: Multiplate (Roche Diagnostic), area under curve (ARU): ADP 24, ASPI 9, TRAP 108, indicating that the Aspirin and clopidogrel were, as desired, significantly inhibiting dual platelet function Access: right femoral 8F, puncture site later occluded with Angio-Seal (Terumo); diagnostic catheter: Tempo4 vertebral (Cordis); guide catheter: 8F Brite Tip 90 cm (Cordis); microcatheters: 1 Marathon, 2 Echelon14 45
, 1 Rebar27 (all then Covidien, now Medtronic); microguidewires: 1 Mirage 0.00800 (then Covidien, now Medtronic), 1 Traxcess 14 (MicroVention),

1

Cervical Internal Carotid Artery Aneurysm: Spontaneous Dissection of the Cervical. . .

Fig. 1 (continued)

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H. Abu Elhasan et al.

Fig. 1 Diagnostic imaging in a patient with acute onset of a hemiparalysis on the right-hand side of his tongue. MRA (a), CTA (axial reformation (b), coronal reformation (c)), and DSA (d, e) showed the elongation of the tortuous right cervical ICA, with an aneurysm proximal to the petrous

segment. The size of the aneurysm was measured as 6 mm (neck), 6 mm (depth), and 11 mm (cranio-caudal). An ICA stenosis of 80% was found at the level of the aneurysm (magnified view, arrow (e))

1 Traxcess 14 EX (MicroVention), 1 X-celerator-10 (Covidien), X-celerator-14 (Covidien); 3x Hi-Torque All Star (Abbott Vascular) Balloon catheters: 2 Ryujin Plus (Terumo) 4/40 mm; manometer (Medflator II, Smiths Medical) Stents: 1 Carotid Wallstent (Boston Scientific) 5/30 mm (implanted); Coroflex Please (B. Braun) 4/28 mm (not insertable) Course of treatment: an 8F guide catheter was inserted into the straight proximal segment of the right ICA; the 360
loop of said vessel was catheterized using an exchange maneuver. After inserting a Marathon/Mirage combination, the Mirage wire was replaced by an X-celerator-10 wire. This wire was then used to replace the Marathon microcatheter with an Echelon-14 microcatheter through which an X-celerator-14 microguidewire was then inserted. The Echelon14 microcatheter was replaced by a Rebar-027 microcatheter, through which an All-Star 0.01400 coronary microguidewire was inserted. The tip of

this microguidewire was never further distal than the paraclinoid segment of the ICA but did not straighten the 360
ICA loop. Several attempts to introduce a Coroflex Please stent failed. Eventually, on the second attempt, we managed to insert a 4/40 mm coronary balloon catheter. The balloon was slowly inflated to 12 atm using a manometer. Inflating the balloon straightened the 360
ICA loop, and the vessel remained straight after the balloon catheter was withdrawn. Subsequently, a Carotid Wallstent was inserted and deployed. The previously used coronary stent was replaced by a Carotid Wallstent since a better wall apposition was expected from this implant. It had not been used beforehand as prior to straightening of the ICA loop, inserting a Carotid Wallstent had simply appeared impossible. The deployed Carotid Wallstent fully opened and kept the ICA straight. When contrast medium was injected into the ICA, the newly created lumen inside the stent as well as the vessel loop and the pseudoaneurysm were opacified synchronously. We assumed that the balloon inflation and vessel straightening had caused

1

Cervical Internal Carotid Artery Aneurysm: Spontaneous Dissection of the Cervical. . .

another ICA dissection, creating a new false lumen, which was prevented from collapsing by the Wallstent. The DSA of the dependent intracranial vasculature was within normal limits (Fig. 2). Complications: none Duration: 1st–28th DSA run: 274 min; fluoroscopy time: 154 min Postmedication: 1 100 mg ASA PO daily for life, 1 75 mg clopidogrel PO daily for 1 year; prolonged prescription of dual antiplatelet medication was chosen on the assumption that the “false lumen” created by the balloon angioplasty and stent implantation would need several months for complete endothelialization

Follow-Up Examinations MRI on day 3 after the procedure showed a single small lesion adjacent to the right-hand lateral ventricle. DSA 2 months after the treatment confirmed the straightening of the cervical ICA and the formation of a new vessel lumen. The previous, presumably false, lumen and the dissecting aneurysm were, however, not excluded from the blood circulation due to the large cell size of the Carotid Wallstent, exerting no significant flow diversion effect (Fig. 3).

Treatment Strategy The first treatment session had been partially successful. While the vessel had now been straightened, the false lumen and the pseudoaneurysm, both remnants of a previous dissection, were still perfused and considered a potential source of future emboli to the distal vasculature. The hypoglossal nerve palsy had resolved within 2 months after the first treatment. A much denser coverage of the false lumen was considered crucial. An offer to implant dedicated flow-diverting stents inside the Carotid Wallstent was accepted by the patient.

7

implanting flow diverters inside a previously deployed Carotid Wallstent Anesthesia: general anesthesia; 1 500 mg ASA (Aspirin i.v. 500 mg, Bayer Vital) IV, 1 5,000 IU unfractionated heparin (1 Heparin-Natrium, B. Braun) IV, 1 1 mg glyceryl trinitrate (Nitrolingual, Pohl Boskamp) IA Premedication: 1 100 mg ASA PO daily and 1 75 mg clopidogrel PO daily for the last 2 months; Multiplate (Roche Diagnostic), area under curve (ARU): ADP 7, ASPI 10, TRAP 93, indicating significant dual platelet function inhibition by the ASA and clopidogrel Access: right femoral 6F, puncture site later occluded with Angio-Seal (Terumo); guide catheter: 6F Brite Tip 90 cm (Cordis); microcatheter: 1 Excelsior XT-27 (Stryker); microguidewire: 1 Traxcess14 (MicroVention) Flow diverter: 1x p64 (phenox) 5/24 (diameter too large, did not open properly and was therefore withdrawn); 1x p64 (phenox) 4.5/24 (implanted) Course of treatment: a 6F guide catheter was navigated into the proximal segment of the righthand ICA. The previously deployed Carotid Wallstent was catheterized with an Excelsior XT-27 microcatheter. A p64 5/24 flow diverter was inserted through this microcatheter. Despite the straight course of the Carotid Wallstent, this p64 did not open properly. The 5 mm diameter appeared to be too large. This first p64 was replaced by a p64 4.5/24, which was deployed and eventually detached without further difficulty. The final DSA run already showed significant contrast medium stasis inside the false lumen of the ICA (Fig. 4). Complications: none Duration: 1st–7th DSA run: 37 min; fluoroscopy time: 25 min Postmedication: 1 100 mg ASA PO daily for life, 1 75 mg clopidogrel PO daily for 1 year

Follow-Up Examinations Treatment Procedure #2, 20.03.2013: endovascular treatment of a false lumen of the right-hand cervical ICA (a remnant of an earlier dissection) by

Follow-up DSA 5 months after the first treatment (Carotid Wallstent) and 3 months after the second treatment session (p64 flow diverter) confirmed the obliteration of the false lumen and of the

8

Fig. 2 (continued)

H. Abu Elhasan et al.

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Cervical Internal Carotid Artery Aneurysm: Spontaneous Dissection of the Cervical. . .

Fig. 2 Endovascular treatment of a dissecting pseudoaneurysm of the right-hand cervical ICA. DSA confirmed the 360
loop of the cervical ICA with the dissecting pseudoaneurysm (a, b). Using a complex exchange maneuver, a robust coronary guidewire (All Star) was inserted with its tip at the paraclinoid ICA segment. The attempt to introduce a balloon-expandable coronary stent (Coroflex Please) failed. A coronary balloon catheter (Ryujin Plus) was inserted instead into said loop (c).

dissecting pseudoaneurysm. Further follow-up examinations were carried out 8 months, 20 months, 4 years, and 6.5 years after the treatment and confirmed the stable reconstruction of the right-hand cervical ICA (Fig. 5).

Clinical Outcome The hemiatrophy of the tongue resolved within 2 months after the first treatment. At the last consultation, 6.5 years after the first stent procedure, the patient was neurologically asymptomatic.

9

Slowly inflating this balloon catheter eventually straightened the artery as intended (d). The microguidewire was kept in its position, while the balloon catheter was withdrawn. A 5/30 mm Carotid Wallstent was inserted (e) and deployed (f, g, h). The balloon dilatation had most likely again dissected the ICA, and the course of the deployed Wallstent was out of the previous vessel lumen and the aneurysm (i). The previous ICA lumen with the aneurysm was winding around the stent

Discussion Internal carotid artery dissection is a recognized cause of ischemic stroke and cranial nerve palsy among young and middle-aged patients, accounting for up to 25% of all ischemic stroke cases in patients under age 45 (Bogousslavsky and Pierre 1992; Schievink 2001). Most ICA dissections occur spontaneously or are related to a minor trauma such as straining, sneezing, coughing, hiccups, or chiropractic manipulation of the neck. Less frequently, major trauma, such as a motor vehicle accident, is the cause. Other etiologies

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Fig. 3 Follow-up imaging after the first treatment session of a dissecting pseudoaneurysm of the right-hand cervical ICA. Coronal DWI MRI 3 days after the procedure showed a single small lesion of restricted diffusion (a). DSA 2 months after the straightening of the dissected ICA

showed that the Wallstent was still straight and had created a new vessel lumen. The false ICA lumen and the dissecting pseudoaneurysm were still perfused through the stent struts (b, c)

include arterial hypertension, connective tissue disorders like fibromuscular dysplasia, Marfan syndrome, type IV Ehlers-Danlos syndrome, alpha-1 antitrypsin deficiency, autosomal dominant polycystic kidney disease, osteogenesis imperfecta, internal carotid artery redundancy, estrogen-progesterone treatment, and infectious diseases (Campos-Herrera et al. 2008; Fusco and Harrigan 2011). In most cases, the extradural ICA is affected; however, rarely a dissection of the ICA may extend further distally and reach the intradural segment (Fusco and Harrigan 2011). There are two types of arterial wall dissections. The first is the subintimal type, which is more common and typically leads to arterial lumen narrowing causing the risk of a cerebrovascular ischemic event. The second type is subadventitial dissection, where the lumen and thus the flow rate as examined by ultrasound may remain normal. The pathophysiology of the ICA dissection is thought to be due to a sequence of insults which lead to a compromise of the structural integrity of the arterial wall due to a tear in the tunica intima

and secondary intramural hematoma formation and creation of a false lumen, often resulting in stenosis, occlusion, and intramural thrombus formation and distal emboli that may lead to ischemic stroke. The dissection may separate the tunica media from the tunica adventitia, resulting in aneurysmal dilatation of the affected vessel (Schievink 2001). Such a dilatation may result in compression of adjacent structures, including the hypoglossal nerve. The motor innervation of the tongue comes from the hypoglossal nerve. The radicular strands of the hypoglossal nerve exit the medulla oblongata at the preolivary sulcus. Two trunks enter the hypoglossal canal. The further course runs through the retrostyloid, carotid, submandibular, and sublingual regions, eventually reaching the genioglossus muscle. The hypoglossal nerve travels as part of the cervical sympathetic chain between the ICA and the internal jugular vein. Therefore, a pseudoaneurysm of the upper cervical portion of the ICA can exert pressure and mass effect onto the hypoglossal nerve on this peripheral course (Leblanc 1992) (Fig. 6).

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Cervical Internal Carotid Artery Aneurysm: Spontaneous Dissection of the Cervical. . .

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Fig. 4 Second treatment session of a chronic dissection of the right-hand cervical ICA, which had caused an acute hypoglossal nerve palsy. The previous 360
loop of the ICA had been straightened with balloon dilatation and implanting a Carotid Wallstent 2 months earlier. Blood

flow through the struts of the Carotid Wallstent prevented the thrombosis of the false lumen and the pseudoaneurysm (a). After the implantation of a p64 flow diverter (b) significant contrast stagnation inside the false lumen and the pseudoaneurysm was observed (c)

Spontaneous ICA dissections usually occur unilaterally; however, occasionally they may also occur synchronously on both sides (Woll et al. 2001) and even in combination with vertebral artery dissections. Patients with ICA dissection usually present with headaches, ipsilateral facial pain, neck pain, ipsilateral Horner’s syndrome (when sympathetic fibers are affected), cerebral ischemia, TIA, amaurosis fugax, or even hemiparesis or hemiplegia. Less common presentations include bruit, which may be audible for the patient as pulsatile tinnitus and cranial nerve palsies. These symptoms are caused by different mechanisms following the dissection. They include ischemic events secondary to arterial stenosis, embolic events, antegrade propagation of the thrombus, or mass effect and pressure on the cranial nerves or the sympathetic chain.

Cranial nerve palsies as a clinical presentation of ICA dissection occur in 10–20% of cases (Baumgartner et al. 2001; Desfontaines and Despland 1995; Gobert et al. 1996; Mokri et al. 1996). The lower cranial nerves are those most often affected because of their vicinity to the ICA. ICA dissection was reported in 1.2% of the patients with hypoglossal nerve palsy (Stino et al. 2016). A large series involving 190 patients found that cranial nerve palsy was present in 12% of the patients of extracranial ICA dissection (Mokri et al. 1996). The lower four cranial nerves were affected in 5% of the patients with hypoglossal nerve involvement. The hypoglossal nerve was the only cranial nerve involved in just three patients in this study 1.5% (Mokri et al. 1996; Olzowy et al. 2006).

12

Fig. 5 (continued)

H. Abu Elhasan et al.

1

Cervical Internal Carotid Artery Aneurysm: Spontaneous Dissection of the Cervical. . .

Fig. 6 Illustration of the course of the hypoglossal nerve and its relation to the dissected ICA. The elongated and dilated ICA is stretching and compressing the hypoglossal nerve on its peripheral course. This drawing illustrates why treating the aneurysm alone (e.g., with flow diversion) without straightening the ICA would most likely not have resulted in an improvement of the function of the hypoglossal nerve. (Artwork by Pablo Albiña Palmarola)

Hypoglossal nerve palsy may cause mild dysphagia, difficulty in chewing, dysarthria, difficulty or inability to move the tongue, and tongue numbness and swelling. The clinical findings include fasciculation, atrophy, diminished mobility, and deviation toward the affected side when the tongue is protruded. On fiber-optic and mirror examination as well as on imaging, the tongue base may be prominent (Keane 1996). While an isolated hypoglossal nerve palsy is a rare manifestation of a cervical ICA dissection, it may be the only manifestation of this disorder, like in our case.

13

The imaging appearance of a hypoglossal nerve palsy depends on the clinical phase. In the acute and early subacute phases, the side of the tongue affected may be edematous and swollen with “geographical” T1 hypointensity and T2 hyperintensity on MRI. There is often contrast enhancement, while in the late subacute and early chronic phase, the base of the tongue protrudes into the oropharyngeal lumen, potentially mimicking a tumor. In the late chronic phase, there is volume loss and fatty infiltration of the affected tongue side. On imaging, an extracranial ICA dissection is characterized by mural hematoma with associated luminal narrowing. When the tunica media and tunica adventitia become separated, a pseudoaneurysm may develop at the site of the intimal tear. The characteristic appearance on MRI is seen on T1-weighted images with fat suppression as a crescentic T1 high signal within the vessel wall, representing the mural hematoma, with luminal narrowing. Cranial CT scan is frequently the first-line imaging modality requested in patients with a suspected stroke. However, it is unlikely to detect an ICA dissection with CT. The diagnosis of an ICA dissection largely depends on the imaging techniques. A carotid Doppler test is frequently also requested for patients with a suspected stroke, and this may detect abnormal flow patterns in patients with ICA dissection (Schievink 2001). In patients with suspected ICA dissection, CTA/MRA should be considered (Olzowy et al. 2006). Digital subtraction angiography (DSA) has long been considered the gold standard for diagnosing ICA dissections. On DSA, the dissected artery frequently exhibits a beaded and threadlike appearance, irregular fan-shaped stenosis, and indirect signs such as pseudoaneurysm and venous phase contrast agent retention and direct signs like dual lumen appearance of two-way blood flow (Freilinger et al. 2010). In cases of

ä Fig. 5 Long-term follow-up imaging after the endovascular reconstruction of a symptomatic dissection of the right-hand cervical ICA. DSA 5 months (a), 8 months (b), 20 months (c), and 4 years (d) and contrast-enhanced

MRA 6.5 years (e) after the first treatment confirmed the stable straightening of the ICA and the obliteration of the false lumen and dissecting pseudoaneurysm

14

suspected ICA dissection, CTA or MRA should be considered as these tests are noninvasive modalities and the combination of non-contrast non fatsuppression T1-weighted and fat-suppressed T1-weighted and T2-weighted MRI is the imaging modality of choice for identifying an intramural hematoma (Schievink 2001). The natural history of ICA dissections is not completely understood and difficult to predict. Most cases have a benign course. Two-thirds of occlusions recanalize, and one-third of resulting aneurysms spontaneously decrease in size (Cohen et al. 2003; Houser et al. 1984). The healing process may take 2–3 months following the event. Anticoagulation or antiaggregation over 3–6 months is the recommended treatment for patients with acute extracranial carotid artery dissections (Lyrer and Engelter 2004; Schievink 2000; Schievink et al. 1993) although no randomized controlled trial exists for the management of ICA dissections and the benefits of this treatment are unknown (Lyrer and Engelter 2004, 2010). Most ICA dissections heal spontaneously, and endovascular or surgical management is usually reserved for patients who have not responded appropriately to medical therapy. Endovascular treatment should be considered for patients with recurrent acute cerebral ischemia or progressive symptoms under adequate medical treatment. Cervical artery stenosis or occlusion caused by an intramural hematoma with poor collaterals, an expanding dissection and contraindications for anticoagulation might be arguments in favor of endovascular treatment (Biggs et al. 2004; Moon et al. 2017; Schievink 2001). Although conservative medical therapy is often used for pseudoaneurysms, occasionally, these pseudoaneurysms do not obliterate spontaneously and may instead cause symptoms due to thromboembolism or dilatation or blood flow compression (Chen et al. 2016). The Royal College of Physicians Stroke Guidelines support the use of anticoagulant or antiplatelet therapy in the treatment of ICA dissection (National Collaborating Centre for Chronic Conditions (UK) 2008), and the final decision is usually made by the attending physician. However, there is no evidence of any

H. Abu Elhasan et al.

superiority of anticoagulant or antiplatelet therapy in preventing strokes after carotid and vertebral artery dissections (CADISS trial investigators et al. 2015). According to the literature, about 15–20% of the patients who receive appropriate medical therapy will suffer from a persisting neurological deficit (Anson and Crowell 1991). Surgery has been recommended for patients after the failure of medical treatment, should neurological symptoms worsen and the pseudoaneurysm progress. The surgical options include vessel ligature, resection with revascularization, or extra-intracranial bypass (Biggs et al. 2004; Gonzales-Portillo et al. 2002). Endovascular treatment has been recommended during the past few years for the management of extracranial ICA dissections and pseudoaneurysms with promising results. Although there is no general consensus, endovascular therapy includes aneurysm coiling, stent-assisted coiling, and, more recently, flowdiverting stents for complex cases involving large pseudoaneurysms, especially after the failure of conservative medical management or a worsening of symptoms under adequate medical therapy. An early patient was treated with endovascular stent-mediated repair for an acute ICA dissection by Matsuura et al. (1997). Recently, flow diverters have been used for the treatment of ICA dissections, especially for wide-necked and large pseudoaneurysms where straight coiling or stentassisted coiling may fail to achieve complete occlusion or to decrease the mass effect of the pseudoaneurysm. The use of flow diverters for extracranial carotid artery dissections was recently suggested by several authors (Chen et al. 2016; Kurre et al. 2016). The mode of action of these implants in treating pseudoaneurysms of the ICA is the same as in treating intracranial aneurysms. They allow the reconstruction of the damaged artery segment and divert the blood flow from the pseudoaneurysm toward the main blood vessel, leading to aneurysm thrombosis and shrinkage, as the clot becomes organized and reduces, thus resolving the mass effect caused by the aneurysm.

1

Cervical Internal Carotid Artery Aneurysm: Spontaneous Dissection of the Cervical. . .

15

Fig. 7 Straightening of a dissected ICA in order to reduce the compression of the adjacent hypoglossal nerve. A coronary balloon catheter was inserted (a). Inflation of the balloon resulted in straightening of balloon and

surrounding ICA (b). Elastic recoiling of the straightened vessel was prevented by implanting a self-expanding Carotid Wallstent (c). (Artwork by Pablo Albiña Palmarola)

In the case presented here, covering the dissecting pseudoaneurysm with a flow diverter would not have addressed the compression of the hypoglossal nerve. In order to reduce the compressive effect of the dissected ICA, which was elongated and enlarged, it was crucial that the vessel be straightened (Fig. 7). The removal of the 360
loop of the cervical ICA required a more complex maneuver and eventually was only possible by an iatrogenic dissection of the ICA with a coronary balloon catheter. The subsequently implanted Wallstent helped to stabilize and straighten the vessel and to avoid an elastic recoiling after withdrawing the balloon catheter. The effectiveness of this concept was confirmed by the rapid restitution of the hypoglossal nerve function.

Therapeutic Alternatives Parent Vessel Occlusion Surgical Carotid Shortening

References Anson J, Crowell RM. Cervicocranial arterial dissection. Neurosurgery. 1991;29(1):89–96. https://doi.org/ 10.1097/00006123-199107000-00015. Baumgartner RW, Arnold M, Baumgartner I, Mosso M, Gönner F, Studer A, Schroth G, Schuknecht B, Sturzenegger M. Carotid dissection with and without ischemic events: local symptoms and cerebral artery findings. Neurology. 2001;57(5):827–32. https://doi. org/10.1212/wnl.57.5.827. Biggs KL, Chiou AC, Hagino RT, Klucznik RP. Endovascular repair of a spontaneous carotid artery

16 dissection with carotid stent and coils. J Vasc Surg. 2004;40(1):170–3. https://doi.org/10.1016/j. jvs.2004.03.018. Bogousslavsky J, Pierre P. Ischemic stroke in patients under age 45. Neurol Clin. 1992;10(1):113–24. CADISS trial investigators, Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015;14(4):361–7. https://doi. org/10.1016/S1474-4422(15)70018-9. Campos-Herrera CR, Scaff M, Yamamoto FI, Conforto AB. Spontaneous cervical artery dissection: an update on clinical and diagnostic aspects. Arq Neuropsiquiatr. 2008;66(4):922–7. https://doi. org/10.1590/s0004-282x2008000600036. Chen PR, Edwards NJ, Sanzgiri A, Day AL. Efficacy of a self-expandable porous stent as the sole curative treatment for extracranial carotid pseudoaneurysms. World Neurosurg. 2016;88:333–41. https://doi.org/10.1016/j. wneu.2015.12.023. Cohen JE, Leker RR, Gotkine M, Gomori M, Ben-Hur T. Emergent stenting to treat patients with carotid artery dissection: clinically and radiologically directed therapeutic decision making. Stroke. 2003;34(12):e254–7. https://doi.org/10.1161/01. STR.0000101915.11128.3D. Desfontaines P, Despland PA. Dissection of the internal carotid artery: aetiology, symptomatology, clinical and neurosonological follow-up, and treatment in 60 consecutive cases. Acta Neurol Belg. 1995;95(4): 226–34. Freilinger T, Heuck A, Strupp M, Jund R. Images in vascular medicine: hypoglossal nerve palsy due to internal carotid artery dissection. Vasc Med. 2010;15(5):435–6. https://doi.org/10.1177/1358863X10378789. Fusco MR, Harrigan MR. Cerebrovascular dissections – a review part I: spontaneous dissections. Neurosurgery. 2011;68(1):242–57.; discussion 257. https://doi.org/ 10.1227/NEU.0b013e3182012323. Gobert M, Mounier-Vehier F, Lucas C, Leclerc X, Leys D. Cranial nerve palsies due to internal carotid artery dissection: seven cases. Acta Neurol Belg. 1996;96(1):55–61. Gonzales-Portillo F, Bruno A, Biller J. Outcome of extracranial cervicocephalic arterial dissections: a follow-up study. Neurol Res. 2002;24(4):395–8. https://doi.org/ 10.1179/016164102101200087. Houser OW, Mokri B, Sundt TM Jr, Baker HL Jr, Reese DF. Spontaneous cervical cephalic arterial dissection and its residuum: angiographic spectrum. AJNR Am J Neuroradiol. 1984;5(1):27–34. Keane JR. Twelfth-nerve palsy. Analysis of 100 cases. Arch Neurol. 1996;53(6):561–6. https://doi.org/ 10.1001/archneur.1996.00550060105023. Kurre W, Bansemir K, Aguilar Pérez M, Martinez Moreno R, Schmid E, Bäzner H, Henkes H. Endovascular treatment of acute internal

H. Abu Elhasan et al. carotid artery dissections: technical considerations, clinical and angiographic outcome. Neuroradiology. 2016;58(12):1167–79. https://doi.org/10.1007/ s00234-016-1757-z. Leblanc A. Anatomy and imaging of the cranial nerves. Berlin/Heidelberg/New York: Springer-Verlag; 1992. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Stroke. 2004;35(2):613–4. https://doi.org/ 10.1161/01.STR.0000112970.63735.FC. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev. 2010;10:CD000255. https://doi.org/10.1002/ 14651858.CD000255.pub2. Matsuura JH, Rosenthal D, Jerius H, Clark MD, Owens DS. Traumatic carotid artery dissection and pseudoaneurysm treated with endovascular coils and stent. Endovasc Surg. 1997;4(4):339–43. https://doi. org/10.1583/1074-6218(1997)0042.0.CO;2. Mokri B, Silbert PL, Schievink WI, Piepgras DG. Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery. Neurology. 1996;46 (2):356–9. https://doi.org/10.1212/wnl.46.2.356. Moon K, Albuquerque FC, Cole T, Gross BA, McDougall CG. Stroke prevention by endovascular treatment of carotid and vertebral artery dissections. J Neurointerv Surg. 2017;9(10):952–7. https://doi.org/ 10.1136/neurintsurg-2016-012565. National Collaborating Centre for Chronic Conditions (UK). Stroke: national clinical guideline for diagnosis and initial management of acute stroke and transient ischaemic attack (TIA). London: Royal College of Physicians (UK); 2008. Olzowy B, Lorenzl S, Guerkov R. Bilateral and unilateral internal carotid artery dissection causing isolated hypoglossal nerve palsy: a case report and review of the literature. Eur Arch Otorhinolaryngol. 2006;263(4):390–3. https://doi.org/10.1007/s00405005-1005-3. Schievink WI. The treatment of spontaneous carotid and vertebral artery dissections. Curr Opin Cardiol. 2000;15(5):316–21. https://doi.org/10.1097/ 00001573-200009000-00002. Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med. 2001;344(12):898–906. https://doi.org/10.1056/ NEJM200103223441206. Schievink WI, Mokri B, Whisnant JP. Internal carotid artery dissection in a community. Rochester, Minnesota, 1987–1992. Stroke. 1993;24(11):1678–80. https://doi. org/10.1161/01.str.24.11.1678. Stino AM, Smith BE, Temkit M, Reddy SN. Hypoglossal nerve palsy: 245 cases. Muscle Nerve. 2016;54 (6):1050–4. https://doi.org/10.1002/mus.25197. Woll MM, Goff JM Jr, Gillespie DL, Minken SL. Bilateral spontaneous dissection of the internal carotid arteries–a case report. Vasc Surg. 2001;35(3):221–4. https://doi. org/10.1177/153857440103500310.

Part II Petrous Internal Carotid Artery

2

Petrous Internal Carotid Artery Aneurysm: A Giant Fusiform Aneurysm, Flow Diversion, Several Treatment Sessions, Metamizole Intake Five Years After the Initial Treatment, Thrombotic Internal Carotid Artery Occlusion, Thrombectomy Marta Aguilar Pérez, Muhammad AlMatter, and Hans Henkes Abstract

A giant fusiform aneurysm of the petrous segment of the right internal carotid (ICA) artery was diagnosed in a 52-year-old woman, who presented with headache. Balloon test occlusion of the right ICA was clinically tolerated, yet the venous phase of the right anterior circulation after injection of the left ICA opacified with delay. The continuity of the right ICA was reconstructed with three Pipeline flow diverters (Medtronic) in September 2012. From there on, the patient was under dual platelet function inhibition by a medication with 1
100 mg acetylsalicylic acid (Aspirin, Bayer Vital) and 2
90 mg ticagrelor (Brilique, AstraZeneca) daily. Subsequent examinations showed that the aneurysm was not completely isolated from the blood circulation. A balloon expandable drug-eluting stent and an additional 12 flow diverters (10
p64 (phenox), 2
PEDs) were implanted into the petrous segment of the right ICA in the subsequent treatment sessions. In October 2015, a de novo stenosis of the proximal right ICA was

treated by stent angioplasty. The patient had been asymptomatic for the last 5 years, when she then presented with an episode of headache, visual disturbance of her right eye, and fatigue on September 10, 2017. MRI showed an occlusion of the right ICA at the level of the implanted stents and flow diverters. CT perfusion (CTP) revealed an exhausted reserve capacity of the right anterior circulation. The Multiplate test (Roche) confirmed that the ASA effect was insufficient. The patient had taken the prescribed medication as usual, however, on September 5, 2017, she had a tooth extraction; on the following 5 days she had consumed a cumulative dosage of 10 g of metamizole. The onset of her neurological symptoms was on September 9, 2017. The recanalization of the right ICA was achieved by combining aspiration and mechanical thrombectomy on September 13, 2017. MRI showed minor ischemic lesions of the dependent right hemisphere. Follow-up DSA 1 week later confirmed the patency of the right ICA and on CTP the concerning reserve capacity was restituted. The flow diverter treatment of

M. Aguilar Pérez (*) · M. AlMatter · H. Henkes Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_27

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M. Aguilar Pérez et al.

fusiform aneurysms and the interaction between metamizole and ASA are the main topics of this chapter. Keywords

Petrous internal carotid artery · Fusiform aneurysm · Giant aneurysm · Flow diversion · Endoleak · Reserve capacity · Thrombectomy · ASA interaction · Metamizole

delay of the venous phase of the right anterior circulation (Fig. 2). An extra-intracranial bypass surgery for the right anterior circulation, followed by a right ICA PVO, or the endovascular reconstruction of the right ICA using flow-diverting stents, were the alternative options. After a thorough discussion with the patient, her family and our neurosurgical colleagues, the decision was made to attempt the endovascular reconstruction of the parent artery by means of flow diversion.

Patient Treatment 52-year-old, female, presenting with severe headache since months, with a medical history of arterial hypertension, diabetes mellitus type 2, smoking, and obesity, with a giant aneurysm of the petrous segment of the right ICA.

Diagnostic Imaging In August 2012, this female patient presented with severe headache, having resided weeks in the referring hospital. MRI and MRA, CTA and DSA (September 7, 2012) showed a giant fusiform aneurysm of the petrous segment of the right ICA (Fig. 1).

Treatment Strategy The goals of the treatment were the prevention of a further growth of the giant aneurysm. In addition, the aneurysm was considered to be the likely cause of the headache and as a potential source of future emboli to the right anterior circulation. Size and location made the aneurysm unsuitable for a surgical approach. An endovascular parent vessel occlusion (PVO) would have been the technically most straightforward and aneurysmwise the most efficient treatment concept. A balloon test occlusion was performed on September 12, 2012. It was tolerated clinically; however, the contrast injection of the left ICA with balloon occlusion of the right ICA showed a significant

Procedure #1, 18.09.2012: implantation of three flow diverters into the petrous segment of the right ICA Anesthesia: general anesthesia; 5000 IU unfractionated heparin (Heparin Natrium, B. Braun) IV, 500 mg ASA (Aspirin i.v., Bayer Vital) IV, 2 mg glycerol trinitrate (Nitrolingual infus., G. Pohl-Boskamp) IV, 0.5 mg atropine (Atropinsulfat, B. Braun) IV Premedication: 500 mg ASA PO and 600 mg clopidogrel (Plavix, Sanofi-Aventis) PO on 17.09.2012 Access: right femoral artery; guide catheters: 8F Brite tip (Codman), Navien Aþ 058 115 cm (Medtronic); microcatheters: Marathon (Medtronic) (for catheterization of the ICA beyond the aneurysm), Marksman (Medtronic) (for the implantation of the flow diverters); microguidewires: Mirage (Medtronic), X-celerator-10 (Medtronic), Silverspeed 16 (Medtronic) Implants, flow diverters: 3
Pipeline Embolization Device (PED, Medtronic) 5/30 mm Course of treatment: DSA confirmed the giant fusiform aneurysm of the petrous segment of the right ICA. Difficulty to catheterize the efferent course of the right ICA beyond the aneurysm was anticipated, though this was eventually possible with a Marathon/Mirage combination. Once the right M1 segment was catheterized, the Mirage guidewire was exchanged for an Xcelerator-10 guidewire. The Marathon was over this wire exchanged for a Marksman

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Petrous Internal Carotid Artery Aneurysm: A Giant Fusiform Aneurysm, Flow Diversion. . .

21

Fig. 1 MRA (TOF) (a) contrast-enhanced CT (b) and DSA (right ICA, lateral view) (c) of a 52-year-old woman, presenting with headache on the right side. The

images show a giant fusiform aneurysm of the petrous segment of the right ICA

microcatheter. Via the Marksman catheter, three PEDs 5/30 were implanted from distal to proximal in a telescoping fashion with about 1 cm overlap between consecutive devices. The final DSA run showed significant contrast stagnation within the aneurysm. The key images of this procedure can be found in Fig. 3. Duration: 1st–7th DSA run: 61 min; fluoroscopy time: 29 min Complications: none Postmedication: 1
100 mg ASA PO daily lifelong; 1
75 mg clopidogrel PO daily lifelong; dexamethasone (Fortecortin, Merck Pharma) 3
8 mg PO daily for 10 days, 2


4 mg PO daily for 10 days, 1
4 mg PO daily for 10 days, 1
2 mg PO daily for 10 days; 2
150 mg ranitidine (Ranitidin, ratiopharm) PO daily for 40 days; 1
8000 U certoparin (Mono-Embolex, Aspen) SC daily for 3 days, 2
3000 U certoparin (Mono-Embolex, Aspen) SC daily for 4 weeks

Clinical Outcome The headache improved after the treatment; otherwise, the condition of the patient was unchanged.

22

Fig. 2 Balloon test occlusion (BTO) of the right ICA as a part of the therapeutic decision making. In an awake patient, the right ICA was occluded with a balloon catheter and the left ICA was injected. The arterial phase (a) showed cross flow from the left to the right anterior circulation via the anterior communication artery (AcomA). The venous

Follow-Up and Subsequent Treatments The first follow-up DSA was performed 3 months after the initial treatment and showed an endoleak through the PEDs and a distal mal-apposition of the PEDs to the vessel wall (Fig. 4a, b). Two days later the distal end of the PEDs underwent balloon dilatation. Procedure #2, 13.12.2012: balloon angioplasty of flow diverters in the petrous segment of the right ICA Premedication: 1
100 mg ASA PO daily since September 2012, 1
75 mg clopidogrel PO daily since September 2012, 1
300 mg clopidogrel on December 12, 2012 Anesthesia: general anesthesia; 1
5000 IU unfractionated heparin IV, 1
500 mg ASA IV, 1
1000 mg thiopental (Trapanal, Nycomed) IV Access: right femoral artery (Terumo); guide catheter: 6F Brite Tip MPC (Codman); microcatheter: Echelon-14 45 (Medtronic); microguidewire: Traxcess 14 EX with docking wire (MicroVention) Balloons: Ryujin Plus (Terumo) 3/20 8 atm, Ryujin Plus (Terumo) 2.75/10 8 atm

M. Aguilar Pérez et al.

phase of the right anterior circulation was, however, delayed (b). The BTO was clinically tolerated, yet the venous delay was considered as a hint that the right ICA occlusion might have compromised the blood supply of the right hemisphere

Course of treatment: DSA confirmed the endoleak and the partial collapse of the PEDs in the petrous segment of the right ICA. The ICA distal to the PEDs was catheterized with a Traxess 14 EX with docking wire using a microcatheter. Once the microcatheter was withdrawn, the attempt to introduce a Ryujin Plus 3/20 balloon catheter failed. It was, however, possible to introduce a Ryujin Plus 2.75/10 balloon catheter and dilate the PEDs, which resulted in their improved wall apposition. The key images of this procedure can be found in Fig. 4. Duration: 1st–5th DSA run: 125 min; fluoroscopy time: 23 min Complications: none Postmedication: 1
100 mg ASA PO daily lifelong; 1
75 mg clopidogrel PO daily lifelong The second follow-up DSA and the third treatment were performed 10 weeks later. Since the DSA showed a persistent malapposition of the distal end of the PEDs, a drug-eluting coronary stent was implanted (Fig. 5). Procedure #3, 01.03.2013: balloon expandable stent angioplasty of flow diverters in the petrous segment of the right ICA

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Petrous Internal Carotid Artery Aneurysm: A Giant Fusiform Aneurysm, Flow Diversion. . .

23

Fig. 3 DSA with injection of the right ICA showed the giant fusiform aneurysm of the petrous segment (a, lateral view). The right M1 segment was catheterized

Premedication: 1
100 mg ASA PO daily since September 2012, 1
75 mg clopidogrel PO daily since September 2012 Anesthesia: general anesthesia; 1
5000 U unfractionated heparin IV, 1
500 mg ASA IV, 1
1 mg glyceroltrinitrate IA Access: right femoral artery 8F; guide catheter: 8F Brite Tip; intermediate catheter: Navien Aþ 058 115 cm; microcatheter: none; microguidewire: X-celerator-14 (Medtronic) Implant, stent: Resolute Integrity (Medtronic) 4/9, 9 atm (drug-eluting stent, DES) Course of treatment: DSA confirmed the persistent partial collapse of the PEDs in the petrous

segment of the right ICA, despite the previous balloon angioplasty. The ICA distal to the PEDs was again catheterized, now with an X-celerator14 microwire without using a microcatheter. A drugeluting coronary stent was implanted and resulted in a complete expansion of the PEDs. The key images of this procedure can be found in Fig. 5. Duration: 1st–9th DSA run: 67 min; fluoroscopy time: 18 min Complications: none Postmedication: 1
100 mg ASA PO daily lifelong; 1
75 mg clopidogrel PO daily lifelong DSA follow-up examinations 7 weeks, 14 weeks and 27 weeks later showed the complete

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M. Aguilar Pérez et al.

Fig. 4 The DSA follow-up and second treatment session 3 months after the initial treatment. An endoleak with a distal collapse of the flow diverters (“fish mouth phenomenon”) can be seen (a, b). The distal part of the PEDs was

dilated with a Ryujin plus 2.75/10 balloon catheter with 8 atm (c), which improved the wall apposition of the PEDs with persistent endoleak (circle, d)

Fig. 5 DSA follow-up and third treatment 20 weeks after the first and 10 weeks after the second treatment. The persistent collapse of the distal end of the PEDs (a) was

removed by the implantation of a 4/9 mm coronary drugeluting stent (b), which now resulted in the complete expansion of the PEDs (c)

expansion of the PEDs without intimal hyperplasia and with a persistent minor endoleak. One year after the implantation of the DES, the endoleak through the PEDs was still there. Previous experience had shown to us that even minor endoleaks can prevent the regression of fusiform aneurysms. Since telescopic implantation of flow diverters with non-matching braiding patterns is supposed to enhance their hemodynamic effect, p64 was chosen.

Procedure #4, 10.04.2014: telescopic implantation of two flow diverters into the petrous segment of the right ICA Premedication: 1
100 mg ASA PO daily since September 2012, 1
75 mg clopidogrel PO daily since September 2012; since the Multiplate test showed an insufficient platelet function inhibition in the ADP test, 2
90 mg ticagrelor (Brilique, AstraZeneca) were given to replace the previous medication with clopidogrel.

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Petrous Internal Carotid Artery Aneurysm: A Giant Fusiform Aneurysm, Flow Diversion. . .

25

Fig. 6 Persistent endoleak is seen, approximately 1.5 years after the implantation of three PEDs into a giant fusiform aneurysm of the petrous segment of the right ICA (a, circle). Two additional p64 flow diverters were

coaxially implanted (b, arrows point at the proximal markers of the p64). The final DSA run (c) shows, as expected, the unchanged endoleak (c)

Anesthesia: general anesthesia; 1
5000 IU unfractionated heparin IV, 1
500 mg ASA IV, 1
1 mg glycerol trinitrate IA, 500 mg thiopental IV Access: right femoral artery 6F (Terumo) guide catheter: 6F Heartrail II (Terumo); microcatheter: Excelsior XT-27 (Stryker); microguidewire: Synchro2 0,01400 200 cm (Stryker) Implants, flow diverters: 2
p64 (phenox) 4/ 21, 4/18 Course of treatment: DSA confirmed the persistent endoleak through the PEDs in the petrous segment of the right ICA. Two p64 flow diverters were implanted in a telescopic fashion without difficulty. The key images of this procedure can be found in Fig. 6. Duration: 1st–8th DSA run: 56 min; fluoroscopy time: 6 min Complications: none Postmedication: 1
100 mg ASA PO daily lifelong; 2
90 mg ticagrelor PO daily lifelong DSA follow-up examinations 3 months and 9 months later showed the endoleak unchanged. With the assumption that an endothelialization of the already implanted flow diverters will not occur and a mechanical flow interruption has to be achieved, another seven p64 flow diverters were implanted. We again combined PED and p64 with the expectation that the non-matching

pattern of the two different devices would enhance the hemodynamic effect. Procedure #5, 26.02.2015: telescopic implantation of additional seven flow diverters into the petrous segment of the right ICA Premedication: 1
100 mg ASA PO daily since September 2012, 2
90 mg ticagrelor PO daily since April 2014; the Multiplate test showed a sufficient dual platelet function inhibition Anesthesia: general anesthesia; 1
5000 IU unfractionated heparin IV, 1
500 mg ASA IV, 1
1 mg glycerol trinitrate IA Access: right femoral artery 6F (Terumo) guide catheter: 6F Heartrail II; microcatheter: Excelsior XT-27; microguidewire: Synchro2 0,01400 200 cm Implants, flow diverter: PED 4/20, p64 4/24, p64 4/24, PED 4.25/20, p64 3.5/18, p64 3.5/18, p64 3.5/18 Balloon: 1
SeQuent Neo (B.Braun) 4/20, 8 atm Course of treatment: DSA confirmed the persistent endoleak through the flow diverters in the petrous segment of the right ICA. Seven additional flow diverters were implanted in a telescopic fashion without difficulty. In order to achieve a better wall apposition, a balloon angioplasty using a non-compliant balloon was performed after the 4th and the 7th flow diverter

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Fig. 7 Still persistent endoleak about 2.5 years after the implantation of three PEDs and 10 months after the implantation of additional two p64 into a giant fusiform aneurysm of the petrous segment of the right ICA (a,

circle). Seven additional flow diverters (2 PED, 5 p64) were now coaxially implanted. The final DSA run (b) shows, again as expected, the unchanged endoleak. Again 5 months later, the endoleak was still visible (c)

was deployed. The key images of this procedure can be found in Fig. 7. Duration: 1st–14th DSA run: 73 min; fluoroscopy time: 30 min Complications: none Postmedication: 1
100 mg ASA PO daily lifelong; 2
90 mg ticagrelor PO daily lifelong The DSA follow-up examination 5 months later showed the persistent endoleak (Fig. 7c). Procedure #6, 15.10.2015: stent-PTA of a de novo stenosis in the proximal course of the right ICA, telescopic implantation of additional three flow diverters into the petrous segment of the right ICA Premedication: 1
100 mg ASA PO daily since September 2012, 1
90 mg ticagrelor PO daily since April 2014; the Multiplate test showed a sufficient dual platelet function inhibition. Anesthesia: general anesthesia; 1
5000 IU unfractionated heparin IV, 1
0.5 mg glyceroltrinitrate IA, 1
0.5 mg atropine IV Access: right femoral artery 8F; guide catheter: 8F Guider Softip (Boston Scientific); microcatheter: Excelsior XT-27; microguidewire: Synchro2 0,01400 200 cm, X-celerator-14 Ballons: Ryujin Plus 7/40 8 atm (predilatation of the proximal ICA), SeQuent Neo 3.5/20 8 atm (adaptation of the flow diverters)

Implant, stent: Carotid Wallstent (Boston Scientific) 7/40 Implants, flow diverters: p64 3.5/21, p64 3.5/ 18, p64 4/15 Balloon: 1
SeQuent Neo 4/20, 8 atm Course of treatment: DSA showed a de novo stenosis of the proximal segment of the right ICA as well as the previously known endoleak through the flow diverters in the petrous segment of the right ICA. The proximal right ICA stenosis was treated by predilatation followed by stent deployment. Three additional flow diverters were implanted in a telescopic fashion into the petrous segment of the right ICA without difficulty. In order to achieve a better wall apposition, a balloon angioplasty using a non-compliant balloon was performed after the 3rd flow diverter has been deployed. The key images of this procedure can be found in Fig. 8. Duration: 1st–8th DSA run: 58 min; fluoroscopy time: 29 min Complications: none Postmedication: 1
100 mg ASA PO daily lifelong; 2
90 mg ticagrelor PO daily lifelong The DSA follow-up 6 months later showed a high-grade in-stent stenosis of the Wallstent in the proximal segment of the right ICA, which underwent balloon angioplasty.

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Petrous Internal Carotid Artery Aneurysm: A Giant Fusiform Aneurysm, Flow Diversion. . .

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Fig. 8 Endovascular treatment of an atherosclerotic de novo stenosis of the proximal right ICA (a) by stent angioplasty (b). The continued endoleak through the flow

diverters in the petrous segment of the right ICA (c) was addressed by the deployment of additional three p64 flow diverters (d)

Procedure #7, 03.05.2016: re-PTA of an instent stenosis in the proximal course of the right ICA Premedication: 1
100 mg ASA PO daily since September 2012, 1
90 mg ticagrelor PO daily since April 2014; the multiplate test confirmed a sufficient dual platelet function inhibition. Anesthesia: general anesthesia; 1
3000 IU unfractionated heparin IV, 1
0.5 mg atropine IV

Access: right femoral artery 8F; guide catheter: 8F Guider Softip; microguidewire: ChoICE PT extra support 0.01400 300 cm (Boston Scientific) Ballons: SeQuent Please NEO (B.Braun) 4/10, 8 atm, 1 min inflation (coronary drug-eluting balloon, DEB); Falcon Grande (Invatec) 5/40 5 atm (secondary dilatation after the DEB) Course of treatment: DSA showed an in-stent stenosis inside the Wallstent, which had been deployed 6 months before into the distal CCA and

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the proximal ICA on the right side. After insertion of the ChoICE PT guide wire, a 4/10 mm DEB was inflated in several overlapping levels of the stent, followed by a secondary dilatation using a 5/40 mm conventional balloon catheter, which entirely removed the in-stent stenosis. The key images of this procedure can be found in Fig. 9. Duration: 1st–16th DSA run: 46 min; fluoroscopy time: 16 min Complications: none Postmedication: 1
100 mg ASA PO daily lifelong; 2
90 mg ticagrelor PO daily lifelong The endoleak through the flow diverter construct in the petrous segment of the right ICA was no longer visible during this examination (Fig. 10). At this point, the plan was to proceed with a follow-up DSA in 1 year’s time. On September 10, 2017, the patient presented with a sudden headache and visual disturbance, both on the right side. The MRI examination was interrupted by the patient’s claustrophobia but showed DWI lesions on the right parietal lobe and an occlusion of the right ICA. The patient and her family confirmed that she had been taken 1
100 mg ASA

Fig. 9 In-stent stenosis 31 months after the initial flowdiverter treatment of a giant aneurysm of the right petrous ICA and 6 months after the treatment of a de novo stenosis of the right proximal ICA (a). The in-stent stenosis was removed by endovascular angioplasty using a coronary drug-eluting balloon and secondary dilatation using a conventional balloon (b)

M. Aguilar Pérez et al.

and 2
90 mg ticagrelor daily. DSA on September 11, 2017, showed the thrombotic occlusion of the right ICA affecting both the cervical Wallstent as well as the flow diverters in the petrous segment. The collaterals to the right anterior circulation appeared insufficient (Fig. 11). The Multiplate test on September 11, 2017, at 00:20 a.m. showed no platelet function inhibition, neither in the ADP test nor in the ASPI test. Therefore 1
500 mg ASA and 1
180 mg ticagrelor were given immediately. At 11 and 34 h later, the repeated Multiplate tests confirmed dual platelet function inhibition. During a discussion with the patient and her husband, it was reported that after a tooth extraction on September 5, 2017, she consumed a total of 20 ml metamizole (novaminsulfon) with 500 mg/ml within 5 days, until September 10, 2017. Since September 9, 2017, she suffered from headache on the right side, visual disturbance of her right eye and unusual fatigue. The interference between ASA and metamizole, resulting in an interruption of the required dual platelet function inhibition with subsequent thrombotic occlusion of the stents and flow diverters in the right ICA, was considered the most likely explanation for the patient’s condition. CT perfusion (CTP) on September 11, 2017, in resting state and after diamox challenge showed a reduced perfusion and an exhausted reserve capacity of the right anterior circulation (Fig. 12). This was in line with the finding of poor collaterals for the right anterior circulation observed on angiography. The patient continued to complain about rightsided headache with a recent onset but had no focal neurological deficit. After an extensive discussion of the situation with the patient and her family, the decision was made to attempt the recanalization of the right ICA. Procedure #8, 13.09.2017: aspiration and mechanical thrombectomy of the thrombosed right ICA Premedication: 1
100 mg ASA PO daily since September 2012, 2
90 mg ticagrelor PO daily since April 2014; body weight adapted bolus followed by infusion of eptifibatide (Integrilin, GlaxoSmithKline) since September 12, 2017, 3:30 p.m.

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Fig. 10 Follow-up examinations concerning the endoleak through the flow diverters in the petrous segment of the right ICA. On April 29, 2016, no endoleak was visible (a).

Following DSA examinations on August 26, 2016, (b) and on February 17, 2017 (c), however, once again revealed the endoleak (circles)

Anesthesia: general anesthesia Access: right femoral artery 8F; guide catheter: 8F Cello (Medtronic); microguidewire: Synchro2 0.01400 300 cm, microcatheter: Trevo Pro 18 Microcatheter (Stryker) Thrombectomy: aspiration thrombectomy: SOFIA (MicroVention); mechanical thrombectomy: pRESET 6/30 (phenox) Balloon: Ryujin plus 3/40

Course of treatment: The balloon guide catheter was inserted into the proximal segment of the right ICA and was inflated there. Under proximal flow arrest, aspiration thrombectomy using the SOFIA catheter was not successful. The thrombus was catheterized and a pRESET 6/30 stent retriever was deployed. After an incubation time of 5 minutes, a large thrombus was withdrawn from the right ICA using a

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Fig. 11 Acute thrombotic occlusion of the right ICA (a), 5 years after the initial treatment of a giant aneurysm of the petrous segment of the right ICA using flow diverters. There is collateral flow to the right anterior circulation through the right ophthalmic artery (b), from

the left anterior circulation via the anterior communicating artery (c); however, showing a significant delay of the right anterior circulation venous phase (d). The right posterior communicating artery (arrow(e)) had a small caliber

combination of aspiration and mechanical thrombectomy. Remaining thrombus adhering to the vessel wall could not be removed by thrombectomy. A combination of balloon angioplasty and direct aspiration eventually allowed the removal of said thrombus. Significant emboli into the dependent intracranial vasculature were not observed. The key images of this procedure can be found in Fig. 13. Duration: 1st–15th DSA run: 57 min; fluoroscopy time: 16 min Complications: none

Postmedication: 2
100 mg ASA PO daily lifelong; 2
90 mg ticagrelor PO daily lifelong, body-weight-adapted infusion of eptifibatide for the 2 following days Follow-up examinations revealed a few DWI lesions related to the right anterior circulation. The concerning reserve capacity was back to normal (Fig. 14.) Follow-up DSA on September 20, 2017, revealed residual thrombus adherent to the stents and flow diverters in the right ICA with normal perfusion of the right cerebral hemisphere.

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Petrous Internal Carotid Artery Aneurysm: A Giant Fusiform Aneurysm, Flow Diversion. . .

Fig. 12 CTP from September 11, 2017, in the subacute phase after the thrombotic occlusion of the right ICA in resting state (a) and after diamox challenge (b) with a delayed time to drain and mean transit time (a) and an exhausted reserve capacity (b) of the right anterior circulation

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Fig. 13 Endovascular recanalization after thrombotic occlusion of the right ICA. A balloon guide catheter was inserted into the proximal segment of the right ICA and the balloon was inflated inside the Wallstent with a SOFIA aspiration catheter inside (arrow(a)). After the failure of

aspiration alone, a combination of mechanical thrombectomy using a pRESET 9/30 and the SOFIA aspiration catheter was used (b), followed by balloon angioplasty, and allowed the recanalization of the right ICA (c) without significant distal emboli (d)

Clinical Outcome

Discussion

On September 21, 2017, the patient was discharged home without a neurological deficit.

The petrous segment (C2) of the ICA is distal to the cervical (C1) and proximal to the lacerum (C3) segments and runs through the petrous

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Petrous Internal Carotid Artery Aneurysm: A Giant Fusiform Aneurysm, Flow Diversion. . .

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Fig. 14 Early follow-up examinations after the endovascular recanalization of the right ICA, required after the thrombotic occlusion of this artery. MRI 3 days after the thrombectomy showed several small DWI lesions (a). CTP

with diamox challenge confirmed now the normalization of the previously exhausted reserve capacity of the right anterior circulation (b)

temporal bone. Aneurysms of the petrous ICA are infrequent, mostly fusiform, large and partially thrombosed. True congenital aneurysms are to be differentiated from pseudo-aneurysms that have an interruption of the vessel wall, as a result of inflammation (“mycotic”), trauma, dissection, and irradiation. “Mycotic” petrous aneurysms are rather due to infections adjacent to the petrous bone than of cardioembolic origin. The petrous ICA is susceptible to dissections, both traumatic and spontaneous. The vast majority of these aneurysms, however, have no apparent cause. Petrous aneurysms can remain asymptomatic and have been found in patients presenting with headache. Related symptoms include Horner syndrome, diplopia, facial palsy, tinnitus, hearing loss, vertigo, epistaxis, otorrhagia, but not subarachnoid hemorrhage (Liu et al. 2004). The indication for treatment is, as always, a balance between the current and potential risks of the aneurysm and the anticipated risks of the treatment. Apart from conservative management with imaging-based follow-up, endovascular

parent vessel occlusion (PVO) or reconstruction of the ICA are further options. Balloon test occlusion is required prior to the PVO in order to make sure that the collateral circulation is sufficient to prevent ischemia of the hemisphere dependent on the concerning ICA. The clinical tolerance of balloon test occlusion is a prerequisite but does not exclude cerebral hypoperfusion after PVO. In our experience, the angiographic evaluation of the opacification of the cerebral veins and venous sinuses of both anterior circulations during BTO reliably predicts the future tolerance of an ICA PVO. A venous delay on the occluded side, despite clinical tolerance, is a strong argument against an ICA occlusion (Abud et al. 2005). A temporal extra-intracranial bypass may improve the supply but adds surgical risks to those of the PVO (Gratzl et al. 1976; Gelber and Sundt 1980). Aneurysm obliteration without sacrifice of the ICA can be achieved by endovascular coil occlusion, in the majority of cases as a stent-assisted procedure (Hauck et al. 2009). In large and giant aneurysms, however, the procedure per se can be a challenge and recurrent perfusion due to coil

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compaction is rather the rule than the exception. Covered stents (stent grafts) are theoretically the ideal solution for fusiform aneurysms (Saatci et al. 2004). The major drawback of the currently available stent grafts is their stiffness, making their implantation in curved vessels both difficult and dangerous. Flow-diverting stents, alone or combined with coil insertion, offer a viable alternative (Puffer et al. 2014; Gross et al. 2017). In fusiform aneurysms without wall apposition of the implant, the telescoping deployment of several stents is required (Bhogal et al. 2017). Persistent blood flow through the cells of the flow diverters (“endoleak”) cannot only prevent the thrombosis of the aneurysm, yet they may also become the cause of continued aneurysm growth. Endothelialization of telescoping flow diverters in a fusiform aneurysm is unlikely to occur. Thus, an endoleak calls for the implantation of further flow diverters in order to create more coverage. The use of stents and flow diverters requires dual platelet function inhibition followed by mono-medication, according to different regimens, which depend on the individual circumstances. In the case of multiple telescoping flow diverters, without expected complete endothelialization of the implants, lifelong dual anti-aggregation is needed to prevent embolic events and thrombotic occlusion. Late ischemic complications have been encountered in patients after flow diversion (Klisch et al. 2011; Skukalek et al. 2016). Dual platelet function inhibition is usually maintained by a medication, which combines ASA and a P2Y12 inhibitor. The required action of ASA becomes an issue in patients who also take ibuprofen, naproxen or metamizole. ASA and several non-steroidal anti-inflammatory drugs (NSAID) including the aforementioned, compete in binding to the same platelet COX1. Taking these NSAIDs together with ASA has been shown to nullify the platelet inhibition effect of ASA, as demonstrated in the patient reported here (Meek et al. 2013; Polzin et al. 2015). The acute thrombotic occlusion of intracranial stents and flow diverters is a serious event (Briganti et al. 2012). Mechanical and aspiration thrombectomy have been shown to be efficacious

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options to remove thrombus from the lumen of these implants (Klisch et al. 2011). The indication for this procedure is based either on a hemodynamic compromise or on recurrent emboli to the distal vasculature.

Therapeutic Alternatives Extra-Intracranial Bypass Parent Vessel Occlusion Stent Assisted Coil Occlusion Telescoping Flow Diverters

References Abud DG, Spelle L, Piotin M, Mounayer C, Vanzin JR, Moret J. Venous phase timing during balloon test occlusion as a criterion for permanent internal carotid artery sacrifice. AJNR Am J Neuroradiol. 2005;26 (10):2602–9. Bhogal P, Pérez MA, Ganslandt O, Bäzner H, Henkes H, Fischer S. Treatment of posterior circulation non-saccular aneurysms with flow diverters: a single-centerexperience and review of 56 patients. J Neurointerv Surg. 2017 9(5):471-481. https://doi.org/10.1136/neurintsurg2016-012781. Briganti F, Napoli M, Tortora F, Solari D, Bergui M, Boccardi E, Cagliari E, Castellan L, Causin F, Ciceri E, Cirillo L, De Blasi R, Delehaye L, Di Paola F, Fontana A, Gasparotti R, Guidetti G, Divenuto I, Iannucci G, Isalberti M, Leonardi M, Lupo F, Mangiafico S, Manto A, Menozzi R, Muto M, Nuzzi NP, Papa R, Petralia B, Piano M, Resta M, Padolecchia R, Saletti A, Sirabella G, Bolgè LP. Italian multicenter experience with flowdiverter devices for intracranialunruptured aneurysm treatment with periprocedural complications–a retrospective data analysis. Neuroradiology. 2012 54(10):1145-52. https://doi.org/10.1007/s00234-012-1047-3. Gelber BR, Sundt TM Jr. Treatment of intracavernous and giant carotid aneurysms by combined internal carotid ligation and extra- to intracranial bypass. J Neurosurg. 1980;52(1):1–10. Gratzl O, Schmiedek P, Spetzler R, Steinhoff H, Marguth F. Clinical experience with extra-intracranial arterial anastomosis in 65 cases. J Neurosurg. 1976;44(3):313–24. Gross BA, Moon K, Ducruet AF, Albuquerque FC. A rare but morbid neurosurgical target: petrous aneurysms and their endovascular management in the stent/flow diverter era. J Neurointerv Surg. 2017;9(4):381-383. https://doi.org/10.1136/neurintsurg-2016-012668. Hauck EF, Welch BG, White JA, Replogle RE, Purdy PD, Pride LG, Samson D. Stent/coil treatment of very

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large and giant unruptured ophthalmic and cavernous aneurysms. Surg Neurol. 2009;71(1):19-24; discussion 24. https://doi.org/10.1016/j.surneu.2008. 01.025. Klisch J, Turk A, Turner R, Woo HH, Fiorella D. Very late thrombosis of flow-diverting constructs after the treatment of large fusiform posterior circulation aneurysms. AJNR Am J Neuroradiol. 2011;32(4):627-32. https:// doi.org/10.3174/ajnr.A2571. Liu JK, Gottfried ON, Amini A, Couldwell WT. Aneurysms of the petrous internal carotid artery: anatomy, origins, and treatment. Neurosurg Focus. 2004;17(5): E13. Meek IL, Vonkeman HE, Kasemier J, Movig KL, van de Laar MA. Interference of NSAIDs with the thrombocyte inhibitory effect of aspirin: a placebo-controlled, ex vivo, serial placebo-controlled serial crossover study. Eur J Clin Pharmacol. 2013;69(3):365-71. https://doi. org/10.1007/s00228-012-1370-y. Polzin A, Hohlfeld T, Kelm M, Zeus T. Impairment of aspirin antiplateleteffects by non-opioid analgesic

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medication. World J Cardiol. 2015;7(7):383-91. https://doi.org/10.4330/wjc.v7.i7.383. Puffer RC, Piano M, Lanzino G, Valvassori L, Kallmes DF, Quilici L, Cloft HJ, Boccardi E. Treatment of cavernous sinus aneurysms with flow diversion: results in 44 patients. AJNR Am J Neuroradiol. 2014;35(5):948-51. https://doi.org/10.3174/ajnr.A3826. Saatci I, Cekirge HS, Ozturk MH, Arat A, Ergungor F, Sekerci Z, Senveli E, Er U, Turkoglu S, Ozcan OE, Ozgen T. Treatment of internal carotid artery aneurysms with a covered stent: experience in 24 patients with mid-term follow-up results. AJNR Am J Neuroradiol. 2004;25(10):1742–9. Skukalek SL, Winkler AM, Kang J, Dion JE, Cawley CM, Webb A, Dannenbaum MJ, Schuette AJ, Asbury B, Tong FC. Effect of antiplatelet therapy and platelet function testing on hemorrhagic and thrombotic complications in patients with cerebral aneurysms treated with the pipeline embolization device: a review and meta-analysis. J Neurointerv Surg. 2016;8(1):58-65. https://doi.org/ 10.1136/neurintsurg-2014-011145.

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Petrous Internal Carotid Artery Aneurysm: Endovascular Treatment with Coils and Flow Diverter Stents of a Large Petrous Internal Carotid Artery Aneurysm Associated with Full-Blown Fibromuscular Dysplasia, and Flow Diverter Reconstruction of the Contralateral Internal Carotid Artery, Followed by the Coil Occlusion of an Aneurysm of the Anterior Communicating Artery, and Balloon Angioplasty of a Left Internal Carotid Artery In-Stent Stenosis, with Good Clinical Outcome Pervinder Bhogal, Marta Aguilar Pèrez, Alexander Sirakov, Hansjörg Bäzner, and Hans Henkes Abstract

A 63-year-old female patient was diagnosed with a large saccular aneurysm of the petrous segment

P. Bhogal (*) Department of Interventional Neuroradiology, The Royal London Hospital, London, UK Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; [email protected] M. Aguilar Pèrez · H. Henkes Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; [email protected]

of the right internal carotid artery (ICA) and a severe manifestation of fibromuscular dysplasia (FMD) on the left ICA. The saccular aneurysm was partially coiled and covered with flow diverting stents. The left ICA was reconstructed with balloon angioplasty and flow diverter implantation. An incidental de novo aneurysm of the anterior communicating artery (AcomA) underwent coil occlusion. In-stent stenosis of the reconstructed left ICA prompted balloon angioplasty with a drug-coated balloon. The significance of FMD-associated aneurysms and their management and the significance and management of FMD-related arterial vessel wall pathology are the main topics of this chapter.

A. Sirakov Neuroradiology, University Hospital St. Ivan Rilski, Sofia, Bulgaria Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_163

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Keywords

Petrous internal carotid artery · Fibromuscular dysplasia, FMD · Flow diverter · Vessel wall dissection · Vessel wall reconstruction

Patient A 63-year-old female patient with a background history of fibromuscular dysplasia (FMD), bipolar disease, and previous abdominal aortic aneurysm was found to have an aneurysm of the right ICA after imaging for memory disturbances, tremor, and cognitive decline.

Diagnostic Imaging An MRI of the brain and contrast-enhanced MRA revealed evidence of small vessel ischemic disease of the brain with several foci of micro-hemorrhage but no features of amyloid angiopathy. Imaging of the cervical vessels demonstrated a large aneurysm of the petrosal portion of the right ICA at the level of the skull base. This measured approximately 1.9
2.5 cm in maximal dimension. There was a high-grade stenosis of the left ICA due to FMD-related arterial vessel wall pathology (Fig. 1).

Treatment Strategy The goal of the treatment was to reconstruct the right ICA as the parent vessel and prevent potential embolic phenomenon from the large aneurysm. Given the severe stenosis of the contralateral ICA, it was necessary to preserve the flow within the right ICA, and therefore a surgical ligation or endovascular parent vessel occlusion was not felt to be appropriate. The left ICA was considered a potential source of emboli to the

H. Bäzner Neurologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]

dependent vasculature, and the reconstruction of said artery was a secondary treatment goal.

Treatment Procedure #1, 22.10.2013: stent- and flow diverter-assisted coil occlusion of a large aneurysm of the petrous segment of the right ICA Anesthesia: general anesthesia, 5,000 IU unfractionated heparin (Heparin Natrium, B. Braun) IV to double the baseline activated clotting time (ACT) Premedication: 1
500 mg ASA (Aspirin, Bayer Vital) PO and 1
600 mg clopidogrel (Plavix, Sanofi-Aventis) PO 1 day prior to the procedure; Multiplate analyzer (Roche Diagnostics), area under curve (AUC): ADP 17, ASPI 6, TRAP 109 (dual platelet function inhibition) Access: puncture of the right-hand common femoral artery; 1
8F short sheath (Cordis); guide catheter: 1
8F Guider Softip (Boston Scientific), 1
Tempo 4 Vertebral catheter (Cordis); microcatheters: 1
Excelsior XT-27 (Stryker Neurovascular); 1
Prowler Select Plus (Cordis); 1
Echelon-10 (Stryker); microguidewires: 1
SilverSpeed-16 (ev3/Covidien), 1
GT Gold 0.016 (Terumo) Implants: 1
p64 4.5/21 (phenox); Solitaire AB 4/20 (ev3/Covidien) 5
Nexus Morpheus 3D 10/30 coils (ev3/Covidien), 2
Deltamaxx18 24/60 Cerecyte coils, 3
Deltamaxx18 Cerecyte 22/60 coils (Codman) Course of treatment: selective angiography of the right ICA revealed the large aneurysm and evidence of underlying FMD. Direct passage across the aneurysm neck was not possible, and therefore, the XT-27 microcatheter and microwire were initially looped inside the aneurysm prior to tracking into the intracranial circulation. In order to straighten the microcatheter a Solitaire AB was tracked through the microcatheter and temporarily placed in the intracranial ICA after gentle manipulation of the microcatheter allowed it to be straightened at the level of the aneurysm. The aneurysm was then catheterized using the Echelon-10 microcatheter, and several coils were placed within the aneurysm. Following

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Petrous Internal Carotid Artery Aneurysm: Endovascular Treatment with Coils and Flow. . .

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Fig. 1 (continued)

implantation of the coils, a p64 flow diverter was deployed across the neck of the aneurysm. To ensure good apposition of the p64 flow diverter, the Solitaire device was deployed within the flow diverter (Fig. 2).

Duration: 1st–44th DSA run: 206 min; fluoroscopy time: 59 min Complications: there was bleeding and pseudoaneurysm formation at the site of the right common femoral artery puncture

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Fig. 1 Diagnostic imaging in a 63-year-old woman with the incidental finding of a large aneurysm of the petrous segment of the right ICA (MRI FLAIR (a)). Contrastenhanced MRA (b) confirmed the size and location of the aneurysm and revealed severe FMD-related arterial pathology of the cervical left ICA. Both findings were confirmed

Postmedication: 1
100 mg ASA PO daily for life and 1
75 mg clopidogrel PO daily for at least 1 year

Clinical Outcome The neurological status of the patient remained unchanged. However, a massive hemorrhage into the right-hand abdominal wall occurred, which was managed conservatively but required an extended stay in the hospital (Fig. 3).

Follow-Up Examination Angiography performed 2 months later demonstrated significant continued inflow into the aneurysm.

Treatment Strategy The aneurysm was not excluded from the blood circulation, and therefore a repeated procedure was undertaken to reconstruct the parent vessel.

P. Bhogal et al.

by DSA (right ICA (c), left ICA (d)). The anterior and posterior intracranial vasculature was, apart from vessel elongation, within normal limits (right anterior circulation, posterior-anterior view (e), left anterior circulation, posterior-anterior view (f), posterior circulation, lateral view (g))

Treatment Procedure #2, 12.12.2013: endovascular removal of a previously implanted Solitaire stent from the right ICA, coverage of the pre-treated large petrous ICA aneurysm with another 5 p64 flow diverters Anesthesia: general anesthesia, 3,000 IU unfractionated heparin (Heparin Natrium, B. Braun) IV to double the baseline activated clotting time (ACT) Premedication: 1
100 mg ASA PO daily and 1
75 mg clopidogrel PO daily since the previous 2 months Access: puncture of the right-hand common femoral artery; 1
8F short sheath (Cordis); guide catheter: 2
8F Envoy MPA (Codman), 1
Tempo 4 Vertebral catheter (Cordis); microcatheters: 2
Excelsior XT-27 (Stryker Neurovascular); 1
Prowler Select Plus (Codman) microguidewires: 2
Synchro2 0.01400 (Stryker), 1
X-Celerator-14 (ev3), 1
Traxcess 14 (MicroVention), balloons: 1
Ryujin Plus 2.5/20 (Terumo), 1
Ryujin Plus 4/20 (Terumo), 1
SeQuent Neo 4/20 (B. Braun)

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Petrous Internal Carotid Artery Aneurysm: Endovascular Treatment with Coils and Flow. . .

Fig. 2 Flow diverter- and stent-assisted coil occlusion of a large aneurysm of the petrous segment of the right-hand ICA. DSA showed an intimal fold at the entrance level of the aneurysm (arrow (a)). Direct access to the ICA distal to the aneurysm was not possible. The Excelsior XT-27 microcatheter was therefore looped inside the aneurysm (b), from there inserted into the distal ICA and then straightened with a Solitaire, which was temporarily deployed in the ICA and used as a distal anchor. Thereafter the aneurysm was

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catheterized with an Echelon-10 microcatheter and loosely filled with 10 coils (c, d). The aneurysm neck was then covered with a p64 4.5/21 flow diverter. The wall apposition of said implant was poor due to the intimal fold and the vessel bend at the neck level of the aneurysm. Therefore, the Solitaire stent, which had been previously used, was deployed into the already detached p64 and electrolytically detached. The procedure was finished with a partial occlusion of the petrous ICA aneurysm (e, f)

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Postmedication: 1
100 mg ASA PO daily for life and 1
75 mg clopidogrel PO daily for at least 1 year

Clinical Outcome

Fig. 3 Massive hemorrhage in the abdominal wall after the endovascular treatment of an ICA aneurysm in a patient with full-blown FMD. The due to the FMD fragile vasculature may have contributed to the development of this hemorrhagic complication, which was managed conservatively

Stent: Coroflex Please 4/28 (B. Braun) Snare: 1
4 mm Gooseneck Snare (Amplatz) Implants: 5
p64: 2
4.5
21, 1
5
30, 2
5
18 (phenox) Course of treatment: There was continued filling of the aneurysm, particularly at the neck, following the previous treatment. The purpose of implanting the Solitaire stent previously had been to straighten the vessel at the origin of the aneurysm; however, this had not occurred, and it was believed that the Solitaire was kinked at this point. Initially, two balloon catheters were passed across the site of the kink and inflated; however, this did not result in an improvement in the kinking. Further treatment of the parent vessel with flow diversion with the Solitaire in this position would have proven impossible. The Solitaire was removed using a Gooseneck snare; however, a large piece of intimal tissue could be seen attached to the extracted Solitaire stent. There was no evidence of acute contrast extravasation. In order to cover the damaged vessel, five telescoped p64 flow diverters were implanted at the neck of the aneurysm and more proximally (Fig. 4). Duration: 1st–57th DSA run: 282 min; fluoroscopy time: 184 min Complications: left ACA-MCA border zone infarction

After the procedure the patient was slow to wake from the general anesthetic, the cause of which was unknown as there were no intraoperative complications. Therefore, a CT head and CT with contrast was performed. This did not demonstrate any evidence of acute hemorrhage or large vessel occlusion; however, there was evidence to suggest new watershed infarction in the left cerebral hemisphere with cortical enhancement and swelling (Fig. 5). The patient made a good recovery and was back at baseline neurology prior to discharge.

Follow-Up Examinations A follow-up DSA 10 weeks later showed the complete obliteration of the aneurysm of the petrous ICA and the reconstruction of the parent artery. There was spontaneous cross flow to the left-hand anterior circulation via the anterior communicating artery (AcomA), indicating the hemodynamic relevance of the FMD-related pathology of the left ICA (Fig. 6). There were no complications following the angiogram. Treatment of the left ICA was planned due to the finding of the cross-flow and previously known infarctions within the left cerebral hemisphere.

Treatment Strategy The FMD-related pathology of the left ICA with high-grade stenosis, dissections, and small “aneurysms” was considered the reason for an impaired supply to the left anterior circulation. Even more important were these vessel wall changes considered a possibly lifelong source of distal emboli.

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Fig. 4 (continued)

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Fig. 4 Completion of the treatment of a large right-hand ICA petrous aneurysm, 2 months after partial coil occlusion and flow diverter implantation. The course of the ICA in front of the aneurysm orifice was bent (a). The Solitaire stent had not, as expected, straightened the vessel. Passage and inflation of two balloon catheters was possible, but did not improve the shape of the obviously collapsed Solitaire (b, c). The Solitaire in this shape and position would have

Treatment Procedure #3, 26.02.2014: endovascular reconstruction of the left ICA, affected by FMD, with balloon angioplasty and implantation of two stents and two p64 flow diverters Anesthesia: general anesthesia, 3,000 IU unfractionated heparin (Heparin Natrium, B. Braun) IV to double the baseline activated clotting time (ACT) Premedication: 1
100 mg ASA PO daily and 1
75 mg clopidogrel PO daily since October 2013 Access: puncture of the left common femoral artery; 1
8F short sheath (Cordis); guide

P. Bhogal et al.

prevented the successful implantation of flow diverters. The Solitaire was therefore withdrawn with a 2 mm snare (d). A long piece of vessel wall tissue was attached to the extracted stent. Assuming a significant damage to the intima rather proximal than distal to the aneurysm orifice, the parent artery was covered with five flow diverter stents at the neck level of the aneurysm and proximal to it (e, f, g, h)

catheter: 1
8F Guider Softip (Boston Scientific), 1
Tempo 4 Vertebral catheter (Cordis); microcatheters: 1
Excelsior XT-27 (Stryker Neurovascular); 1
Echelon-10 (Medtronic), 1
Marathon (Medtronic); microguidewires: 2
X-Celerator-14 (ev3), 1
X-Celerator-10 (ev3), 1
Hybrid 0.00700 (Balt); Angioplasty balloons: 1
Ryujin plus 3/30 (Terumo), 1
Ryujin plus 3.5/40 (Terumo), 1
Ryujin plus 4/20 (Terumo) Implants: 2
Wallstent 7/40 (Boston Scientific), 2
p64 4/21 (phenox) Course of treatment: the severely affected left cervical ICA was thought to pose a persistent risk of thromboembolic complications and resulted in flow restriction as demonstrated by the cross-

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Petrous Internal Carotid Artery Aneurysm: Endovascular Treatment with Coils and Flow. . .

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Fig. 5 Post-procedure the patient was slow to wake, and therefore imaging of the brain pre and post contrast was performed. This showed an area of swelling in the left

frontal lobe that showed cortical enhancement and was thought to represent a new area of watershed ischemia

flow from the right ICA across the AcomA. Therefore, the purpose of the treatment was to improve the caliber of the left ICA. The cavernous ICA was accessed using a combination of different microwires and microcatheters starting with the Hybrid 00700 microguidewire and Marathon microcatheter and then exchanging up to a X-Celerator-14 microguidewire. Gentle balloon angioplasty was then performed from distal to proximal with slow inflations to minimize the chance of dissection after which two Wallstents were placed in the cervical ICA from distal to proximal. Following the implantation of the Wallstents, two p64 flow diverters were implanted into the petrous ICA and upper cervical ICA which resulted in a complete reconstruction of the ICA. There were no intraoperative complications with no evidence of either arterial injury or distal thromboembolic complication (Fig. 7). Duration: 1st–42nd DSA run: 142 min; fluoroscopy time: 94 min Complications: none

Postmedication: 1
100 mg ASA PO daily for life and 1
75 mg clopidogrel PO daily for at least 1 year

Follow-Up Examinations Follow-up DSA examinations 7 months and 10 months after the last treatment session confirmed the occlusion of the right ICA aneurysm and the reconstruction of the left cervical ICA with in-stent stenosis. The injection of the right ICA demonstrated a previously not recognized AcomA aneurysm (Fig. 8).

Treatment Strategy The de novo AcomA aneurysm was possibly a sequel of the long-term increased flow from the right ICA to the left anterior circulation via the AcomA, while the left ICA was highly stenotic. This aneurysm was associated with a potential

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Fig. 6 Follow-up DSA 10 weeks after the reconstruction of the right-hand ICA with five flow diverter stents. The large aneurysm is occluded, and the parent vessel is

reconstructed (a). There is spontaneous cross flow to the left anterior circulation via the AcomA due to the impaired supply via the left ICA (b)

risk of rupture, and the goal of treatment was to eliminate this risk.

guide catheter: 1
8F Guider Softip (Boston Scientific), 1
Tempo 4 Vertebral catheter (Cordis); microcatheters: 1
Excelsior SL 10 (Stryker Neurovascular), 1
Echelon-10 (ev3); microguidewires: 1
Synchro2 0.01400 (Stryker) Implants: 4 coils: 1
Target 360 Nano 3/6 (Stryker), 1
Target 360 Nano 5/4, 1
Microplex 10 2/6 (MicroVention), 1
Microplex 10 2/4 (MicoVention) Course of treatment: the aim of the treatment of the AcomA aneurysm was to prevent rupture. Although both surgical and endovascular options were available, the patient opted for endovascular coil occlusion. After puncture of the right common femoral artery and catheterization of the right ICA rotational angiography were performed, and working projections for coil occlusion selected.

Treatment Procedure #4, 12.02.2015: endovascular coil occlusion of an unruptured de novo AcomA aneurysm Anesthesia: general anesthesia, 3,000 IU unfractionated heparin (Heparin Natrium, B. Braun) IV to double the baseline activated clotting time (ACT) Premedication: 1
100 mg ASA PO daily and 1
75 mg clopidogrel PO daily since October 2013 Access: puncture of the right-hand common femoral artery; 1
8F short sheath (Cordis);

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Fig. 7 (continued)

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Fig. 7 Endovascular reconstruction of the left cervical ICA, affected by severe FMD-related vessel wall pathology (a). Under road map guidance, a microguidewire was inserted into the petrous segment of the left ICA (b). Gentle balloon angioplasty was performed from distal to proximal (c, d, e). The cervical segment was supported

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with 2 Wallstents (f). The petrous segment was again dilated before (g) and after (i) the implantation of a p64 flow diverter (h). The final DSA run showed that the FMD-related vessel wall changes were removed; the vessel contour and diameter were now within normal limits (j)

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Fig. 8 Follow-up DSA 7 months (a, b) and 10 months (c, d) after the last treatment session (concerning the left ICA). The petrous aneurysm of the right ICA was occluded, the left ICA was straightened, and the lumen was essentially

49

normalized, but there was an in-stent stenosis developing. Contrast medium injection of the right ICA revealed a previously not recognized AcomA aneurysm (e)

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Fig. 9 Endovascular coil occlusion of an unruptured de novo AcomA aneurysm 1 year after the reconstruction of a previously stenotic left ICA. The right petrous ICA aneurysm was occluded (a). 2D DSA (b) and rotational DSA

Initially the aneurysm was catheterized using an Excelsior SL10 microcatheter and a 3/6 coil implanted into the aneurysm but not detached. Subsequently an Echelon microcatheter was used to catheterize the aneurysm and a second coil placed inside the aneurysm after which both coils were detached. Two further coils were then placed into the aneurysm resulting in exclusion of the dome of the aneurysm and a small neck remnant (Fig. 9). Duration: 1st–24th DSA: 104 min; fluoroscopy time: 63 min Complications: none Postmedication: 1
100 mg ASA PO daily for life and 1
75 mg clopidogrel PO daily for at least 1 year

P. Bhogal et al.

with 3D reconstruction (c) confirmed the previously diagnosed aneurysm, which was catheterized (arrow (d)) and occluded with coils (arrow (e))

Follow-Up Examination Follow-up DSA 6 months after the coil occlusion of the AcomA aneurysm revealed a minor reperfusion of the neck region of the previously coiled aneurysm and a progressive in-stent stenosis of the left cervical ICA (Fig. 10).

Treatment Strategy The left ICA in-stent stenosis was slowly progressive, which prompted us to propose a balloon angioplasty in order to avoid an occlusion of the said stent.

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Fig. 10 Follow-up DSA 20 months after the second session for the reconstruction of the right ICA, 18 months after the endovascular reconstruction of the left ICA, and 6 months after the coil occlusion of an unruptured

Treatment Procedure #5, 19.08.2015: endovascular balloon angioplasty of an in-stent stenosis of the left cervical ICA Anesthesia: general anesthesia, 3,000 IU unfractionated heparin (Heparin Natrium, B. Braun) IV to double the baseline activated clotting time (ACT) Premedication: 1
100 mg ASA PO daily and 1
75 mg clopidogrel PO daily since October 2013; Multiplate analyzer (Roche Diagnostics), area under curve (AUC): ADP

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de novo AcomA aneurysm. The right ICA (a) was essentially as expected with a minor neck remnant of the coiled AcomA aneurysm. The left cervical ICA (b) showed a progressive in-stent stenosis

1, ASPI 3, TRAP 62 (dual platelet function inhibition) Access: puncture of the right-hand common femoral artery: 1
8F short sheath (Cordis); guide catheter: 1
8F Guider Softip (Boston Scientific), 1
Tempo 4 Vertebral catheter (Cordis); microguidewire, 1
Choice PT 0.014 300 cm extra support (Boston Scientific); paclitaxel-coated balloon: 1
SeQuent Please 4/15 (B. Braun) Course of treatment: routine angiography had previously demonstrated a progressive in-stent stenosis on the left-hand ICA that measured approximately 70%. In order to preserve flow

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and prevent progressive stenosis and potential infarction, balloon angioplasty of the localized stenosis was performed (Fig. 11). Duration: 1st–6th DSA run: 17 min; fluoroscopy time: 14 min

P. Bhogal et al.

Complications: none Postmedication: 1
100 mg ASA PO daily for life and 1
75 mg clopidogrel PO daily for at least 1 year

Fig. 11 Balloon angioplasty of an in-stent stenosis of the left ICA, 18 months after the reconstruction of this artery. The inflation of a 4/15 mm drug-coated balloon (a) removed the in-stent stenosis (b)

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Follow-Up Examinations Further follow-up examinations were carried out 3 months and 30 months after the last treatment session. They demonstrated both ICAs are well reconstructed and both aneurysms sufficiently occluded (Fig. 12).

Clinical Outcome The neurological status of the patient upon the last follow-up examination was rated mRS 0.

Discussion In 1958 McCormack et al. reported a pathological description of “fibromuscular hyperplasia,” one of the original used names, in four patients with renovascular hypertension (McCormack et al. 1958). It was subsequently discovered that the disease was heterogenous and not necessarily associated with hyperplasia (Hunt et al. 1965). Fibromuscular dysplasia is currently defined as an idiopathic, segmental, noninflammatory and non-atherosclerotic disease of the musculature of arterial walls that leads to stenosis of small- and medium-sized arteries. Three main types of FMD have been described – intimal, medial, and peri-medial – (Harrison and McCormack 1971) with each of these types being seen in the extra-renal arteries also (Lüscher et al. 1987). The most common sub-type, at least in the renal vasculature, which is most extensively examined, is the medial sub-type accounting for 85% of all cases. It is not uncommon for more than one arterial layer to be involved, and multilayer involvement is seen in 66% of cases (Alimi et al. 1992). Kincaid et al. (1968) described the radiographic appearances in 125 patients, 60 of whom had surgical tissue removed that was available for pathological correlation. Based on the imaging findings, four different vascular patterns of FMD were proposed:

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1. Multifocal with multiple stenoses and “string of beads” appearance 2. Tubular type with a long concentric stenosis 3. Focal type with a focal stenosis less than 1 cm in length 4. Mixed type Interestingly all of the 38 patients that had multifocal stenoses were found to have the medial histological sub-type of FMD, and this radiological sign is the most suggestive and most frequent imaging feature of FMD. The renal and carotid arteries are the most commonly affected although involvement of the axillary, iliac, basilar, hepatic, and intracranial arteries has also been described. In an analysis of 1197 patient, the renal arteries were involved in 58%, and the carotid arteries were involved in 32% with other arterial beds involved in only 10% (Mettinger 1982). Unlike atherosclerotic stenoses, those due to FMD rarely affect the ostia or proximal segments of arteries. Most carotid artery FMD lesions occur adjacent to the C1-2 interspace (Osborn and Anderson 1977). Intracranial aneurysms have been reported to be associated with FMD. In the meta-analysis of Cloft et al. (1998) that used data from 17 studies and included 498 patients the authors showed a prevalence of 7.6  2.5% for incidental, asymptomatic aneurysms in patients with FMD of the internal carotid artery (ICA) or vertebral artery (VA). After the authors included their own patients (n = 117), the prevalence was found to be 7.3 +/ 2.2%. More recently, Lather et al. (2017) issued a report from the US registry for fibromuscular dysplasia. Of 1112 female patients in the registry, 669 (60.2%) had undergone intracranial imaging at the time of enrollment (age 55.6  10.9 years). Inclusion criteria included aneurysms measuring at least 2 mm as well as extradural but intracranial location (e.g., the petrous segment of the ICA). Of the 669 patients included in the analysis, 86 (12.9%; 95% CI, 10.3%–15.9%) had at least one intracranial aneurysm with 25 of these patients (53.8%) harboring more than one aneurysm. Intracranial aneurysms

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Fig. 12 Follow-up DSA 3 months (a, b) and 30 months (c, d, e) after the last treatment session demonstrated the

stable reconstruction of both ICAs and the sufficient occlusion of both aneurysms

5 mm or larger occurred in 32 of 74 patients (43.2%), and 24 of 128 intracranial aneurysms (18.8%) were located in the posterior communicating or posterior arteries. The mean size of UIAs in the current study of women with FMD was at

least 5.0 mm, and the largest UIA in 22.0% of patients was 7 mm or larger. The larger size and higher incidence of aneurysms in the posterior circulation may confer a higher risk of rupture on these aneurysms compared to those found in

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Petrous Internal Carotid Artery Aneurysm: Endovascular Treatment with Coils and Flow. . .

screening studies of health volunteers. However, confounding factors such as differences in age make comparison if these results with other studies looking at the incidence of aneurysms in healthy volunteers difficult. Interestingly, the presence of intracranial aneurysm did not vary with location of extracranial FMD involvement. A history of smoking was significantly associated with intracranial aneurysm: 42 of 78 patients with intracranial aneurysm (53.8%) had a smoking history versus 163 of 564 patients without intracranial aneurysm (28.9%; p < 0.001), and it is possible that smoking may trigger aneurysm formation intracranially. There are few reports detailing the treatment of aneurysms in patients with FMD. The largest series that we are aware of was recently published by Bender et al. (2018). In this retrospective series, 31 patients, from a screened sample of 1025, were diagnosed with FMD. These patients underwent a total of 43 embolization procedures. The vast majority of patients (n = 30) were female and the average age was 62 years. The multifocal stenosis with string of beads sign was the commonest radiological appearance, and the vast majority of patients had more than one vessel affected (n = 30). The average size of the aneurysms was 7.1  3.6 mm, and the aneurysms were saccular in 93% (n = 40/42). The majority of aneurysms were located in the anterior circulation (n = 37, 86%). The commonest locations for the aneurysms were the ophthalmic (n = 9) and paraophthalmic (n = 9) locations. Flow diversion was the most commonly performed treatment (n = 29, 67%). Coiling (19%), stent-assisted coiling (12%), and intrasaccular flow diversion (2%) were also used. There were no major complications such as stroke, intracranial hemorrhage, or subarachnoid hemorrhage. There were no cases of death. No iatrogenic dissections were seen. Minor complications included a transient ischemic attack with negative cerebral imaging and a groin hematoma. At follow-up imaging 79% of the flow-diverted aneurysms were completely occluded (n = 22/28). In this large series, there

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were no major complications associated with endovascular procedures performed through vessels affected by FMD; however, the authors state that caution must be used when navigating catheters given previous reports of iatrogenic dissection and subsequent aneurysm formation (Fuse et al. 2006).

Therapeutic Alternatives Balloon Remodeling Parent Vessel Occlusion Stent Graft

References Alimi Y, Mercier C, Péllissier JF, Piquet P, Tournigand P. Fibromuscular disease of the renal artery: a new histopathologic classification. Ann Vasc Surg. 1992;6(3):220–4. https://doi.org/10.1007/BF0 2000266. Bender MT, Hurtado C, Jiang B, Campos JK, Huang J, Tamargo RJ, Lin LM, Coon AL, Colby GP. Safety assessment of endovascular treatment of cerebral aneurysms in patients with fibromuscular dysplasia. Interv Neurol. 2018;7(1-2):110–7. https:// doi.org/10.1159/000485133. Cloft HJ, Kallmes DF, Kallmes MH, Goldstein JH, Jensen ME, Dion JE. Prevalence of cerebral aneurysms in patients with fibromuscular dysplasia: a reassessment. J Neurosurg. 1998;88(3):436–40. https://doi.org/10.3171/jns.1998.88.3.0436. Fuse T, Umezu M, Yamamoto M, Demura K, Nishikawa Y, Niwa Y. External carotid artery aneurysm developing after embolization of a ruptured posterior inferior cerebellar artery aneurysm in a patient with cervicocephalic fibromuscular dysplasia – case report. Neurol Med Chir (Tokyo). 2006;46(6):290–3. https://doi.org/10.2176/ nmc.46.290. Harrison EG Jr, McCormack LJ. Pathologic classification of renal arterial disease in renovascular hypertension. Mayo Clin Proc. 1971;46(3):161–7. Hunt JC, Harrison EG, Sheps SG, Bernatz PE, Davis GD, Bulbulian AH. Hypertension caused by fibromuscular dysplasia of the renal arteries. Postgrad Med. 1965;38:53–63. https://doi.org/10.1080/ 00325481.1965.11695580. Kincaid OW, Davis GD, Hallermann FJ, Hunt JC. Fibromuscular dysplasia of the renal arteries. Arteriographic features, classification, and observations on natural history of the disease. Am J Roentgenol Radium Therapy, Nucl Med. 1968;104(2):271–82.

56 Lather HD, Gornik HL, Olin JW, Gu X, Heidt ST, Kim ESH, Kadian-Dodov D, Sharma A, Gray B, Jaff MR, Chi YW, Mace P, Kline-Rogers E, Froehlich JB. Prevalence of intracranial aneurysm in women with fibromuscular dysplasia: a report from the US Registry for Fibromuscular Dysplasia. JAMA Neurol. 2017;74(9):1081–7. https://doi.org/10.1001/ jamaneurol.2017.1333. Erratum in: JAMA Neurol. 2018;75(3):384 Lüscher TF, Lie JT, Stanson AW, Houser OW, Hollier LH, Sheps SG. Arterial fibromuscular dysplasia. Mayo Clin

P. Bhogal et al. Proc. 1987;62(10):931–52. https://doi.org/10.1016/ s0025-6196(12)65051-4. McCormack LJ, Hazard JB, Poutasse EF. Obstructive lesions of renal artery associated with remediable hypertension. Am J Pathol. 1958;38:582. Mettinger KL. Fibromuscular dysplasia and the brain. II. Current concept of the disease. Stroke. 1982;13 (1):53–8. https://doi.org/10.1161/01.str.13.1.53. Osborn AG, Anderson RE. Angiographic spectrum of cervical and intracranial fibromuscular dysplasia. Stroke. 1977;8 (5):617–26. https://doi.org/10.1161/01.str.8.5.617.

Part III Cavernous Internal Carotid Artery

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Cavernous Internal Carotid Artery Aneurysm: Visual Disturbance Due to a Large Cavernous Aneurysm Presumably Causing Recurrent Retinal Ischemia; Coil Occlusion of the Aneurysm Together with the Parent Artery; Resolution of the Visual Disturbance and Clinical Recovery During Long-Term Follow-Up Frances Colgan, Marta Aguilar Pérez, Hansjörg Bäzner, and Hans Henkes Abstract

A 44-year-old male patient presented with recurrent episodes of visual disturbance. CT, MRI/MRA, followed by DSA, demonstrated a large aneurysm of the cavernous segment of the left internal carotid artery (ICA). The left A1 segment was absent and a large caliber left posterior communicating artery (PcomA) with a patent P1 segment was present. The left anterior cerebral artery (ACA) was exclusively supplied by the right ICA via the anterior communicating artery (AcomA). A balloon test

occlusion of the left ICA was tolerated without any neurological deficit. The aneurysm was treated endovascularly with coil occlusion of both the aneurysm and the parent artery (parent vessel occlusion, PVO). The episodes of visual disturbance did not recur and the PVO of the left ICA was tolerated without neurological deficit. During the following 6 years, the patient complained of dizziness, memory disturbance, and episodes of amnestic aphasia. Further examinations during this time failed to demonstrate any impairment of the cerebral perfusion. The treatment of large cavernous ICA aneurysms by PVO is the main topic of this chapter. Keywords

F. Colgan (*) Department of Radiology, University of Otago, Christchurch Hospital, Christchurch, New Zealand e-mail: [email protected] M. Aguilar Pérez · H. Henkes Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; [email protected]

Cavernous internal carotid artery · Saccular aneurysm · Retinal ischemia · Balloon test occlusion · Parent vessel occlusion · Collateral supply

H. Bäzner Neurologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_93

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Patient

Treatment

A 44-year-old male patient presenting with recurrent episodes of visual disturbance in the left eye. The medical history of the patient was otherwise unremarkable.

Procedure #1, 27.09.2011: BTO of the left ICA Anesthesia: local anesthesia, 1 5000 IU non-fractionated heparin (Heparin Natrium, B. Braun) IV Premedication: none Access: right common femoral artery, 6F sheath (Terumo); left common femoral artery, 4F sheath (Terumo); guide catheter: 6F Guider Softip (Boston Scientific); diagnostic catheter: 4F Tempo 4 vertebral (Cordis); microguidewire: SilverSpeed-14 (Medtronic) Compliant balloon catheter: Ascent 4/10 (Micrus), inflated for 20 min Course of treatment: A 6F guide catheter was inserted into the left ICA. A compliant balloon catheter was then inserted to the petrous segment of the left ICA and inflated under fluoroscopy until occlusion was achieved. From the left groin access, the right ICA was catheterized and angiography demonstrated opacification of the left ACA from the right ICA via the AcomA. The left A1 segment was not opacified. Contrast injection from the left vertebral artery (VA) showed collateral supply of the left MCA through the left P1 segment and the left PcomA (Fig. 2). Duration: 1st–6th run: 31 min; fluoroscopy time: 6 min Complications: none Postmedication: none The result of this examination was discussed with the patient the following day and he consented to the proposed aneurysm treatment with PVO. Procedure #2, 29.09.2011: parent vessel occlusion of an aneurysm of the cavernous segment of the left ICA together with the parent artery Anesthesia: general anesthesia, 1 3000 IU nonfractionated heparin IV Premedication: none Access: right common femoral artery, 6F sheath (Terumo); guide catheter: 6F Guider Softip; microcatheter: Echelon-14 45 (Medtronic); microguidewire: Traxcess 14 (MicroVention)

Diagnostic Imaging Diagnostic CT, MRI/MRA, and DSA examinations in September 2011 demonstrated a large aneurysm of the cavernous segment of the left ICA. The left A1 segment was not demonstrated on angiography. Collateral supply to the left middle cerebral artery (MCA) was visible via the left P1 segment and the left posterior communicating artery (PcomA) (Fig. 1).

Treatment Strategy The aim of the treatment was to prevent recurrent emboli from the aneurysm to the ipsilateral retinal circulation or the dependent cerebral vasculature and to avoid further growth of the aneurysm with the risk of cranial nerve compression. The risk of intracranial hemorrhage was considered to be very low due to the extradural location of the aneurysm. The location made the aneurysm unsuitable for microsurgical clipping. Attempted endosaccular coil occlusion with a view to preservation of the parent vessel was considered unpredictable since the lumen of the left cavernous ICA at the level of the aneurysm was no longer visible. Stent-assisted coiling was also considered, as was flow diverter stent (FDS) insertion, but PVO was the treatment of choice in this case. The advantages of PVO were the instantaneous occlusion of the aneurysm and also avoiding the need for antiplatelet medication. In 2011, which was early in our flow diversion experience, the reconstruction of the ICA with a Pipeline Embolization Device (PED) would have been our second choice had carotid balloon test occlusion (BTO) not been tolerated.

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Cavernous Internal Carotid Artery Aneurysm: Visual Disturbance Due to a Large Cavernous. . .

Fig. 1 Diagnostic imaging of a large left cavernous ICA aneurysm. CT (a) and CTA (b, c) demonstrated the aneurysm at the left cavernous sinus (arrows). Due to the slow flow within the aneurysm, the signal intensity on TOF

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MRA (d) is low (arrow), with a high signal intensity on contrast enhanced T1WI (arrow, (e)). TOF MRA demonstrated the absent A1 segment on the left (arrow, (f) and the large caliber left PcomA (arrow, (g)). DSA confirmed these

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Fig. 2 Balloon test occlusion in a left cavernous ICA aneurysm in preparation for the potential PVO. A compliant balloon is inflated in the petrous segment of the left ICA (posterior-anterior view, arrow (a)). Injection of the left VA with left ICA occlusion shows the collateral supply of the left MCA via the left PcomA (posterior-anterior projection (b); lateral projection (c)). Contrast injection of the right

ICA, also with balloon occlusion, demonstrates perfusion of the left ACA via the AcomA but no leptomeningeal collaterals to the left MCA territory (posterior-anterior view, arrow (d)). The BTO was tolerated without any neurological symptoms for 20 min at a systemic blood pressure of 120/75 mmHg. A hypotensive challenge was not considered necessary

Implants: 22 coils: 1 Morpheus 3D 9/28, 1 Morpheus 3D 9/18, 1 Helix Standard 5/20, 19 Helix Standard Fiber 3/10 (ev3) Course of treatment: Via a 6F guide catheter positioned in the left ICA, the cavernous aneurysm was catheterized with an Echelon-14 microcatheter. Using two long 3D coils, a mesh was created in the aneurysm sac in order to avoid an

inadvertent distal migration of the small fibered coils used during this procedure to densely obliterate the ICA proximal to the aneurysm. An occlusion distal to the aneurysm sac was avoided since compromise of the ophthalmic artery or the PcomA origins might have resulted. The fibered coils, which are no longer available, were used because their enhanced thrombogenicity allowed

ä Fig. 1 (continued) findings. Contrast injection of the left ICA showed the dilution of the contrast medium distal to the aneurysm through nonopacified blood from the PcomA (posterior-anterior projection, (h)), the origin of the ophthalmic artery distal to the aneurysm (lateral view, arrow

(i), the supply of the left ACA via the AcomA from the right ICA (posterior-anterior view, (j)), and the spontaneous supply of the left MCA via the left P1/PcomA (lateral view (k))

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Cavernous Internal Carotid Artery Aneurysm: Visual Disturbance Due to a Large Cavernous. . .

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Fig. 3 Endovascular coil occlusion of a wide-necked cavernous ICA aneurysm and the parent artery. Contrast injection from the left ICA demonstrates the 20 mm diameter cavernous aneurysm (posterior-anterior view, (a); lateral view, (b)). Under roadmap conditions, the aneurysm is catheterized (lateral view, (c)). Aneurysm and ICA are occluded with coils (lateral view, (d)). Despite the thrombogenic fibered coils used in this patient, several

centimeters of the artery had to be filled with coils in order to interrupt the flow. The final DSA run showed the collateral supply of the left MCA via the left PcomA (lateral projection with contrast injection from the left VA (e)). Since the left ICA is proximally occluded, the left ophthalmic artery now shows retrograde flow with supply through the left external carotid artery (arrows (f))

a faster parent vessel occlusion with fewer coils. Detachable balloons were no longer used by us owing to the potential risk of distal embolization from balloon deflation or shrinkage. Alternative implants to achieve complete vessel occlusion today would include the Amplatzer Vascular Plug (St. Jude Medical/Abbott) and the UNO (Medtronic). Once the left ICA was considered occluded, the left VA was injected to confirm collateral supply via the left PcomA (Fig. 3). Duration: 1st–8th run: 106 min; fluoroscopy time: 32 min Complications: none Post medication: 100 mg ASS PO daily for 1 year, 2 8000 U Certoparin (MonoEmbolex, Novartis, Pharma) SC daily for 3 days, during the following 3 days the patient was continuously monitored on the intensive care unit with a target systolic blood pressure > 140 mmHg

Clinical Outcome The patient tolerated PVO of the left ICA well. The patient was discharged home 6 days later without any new neurological deficit. In the following year, he presented to another hospital with dizziness, memory disturbance, and episodes of amnestic aphasia, requesting a bypass procedure. Perfusion CT (CTP) and transcranial Doppler investigation (TCD) failed to show any compromise of the anterior circulation.

Follow-Up Examinations Follow-up MRI/MRA, DSA, and CTP examinations were carried out after the left ICA PVO. Both aneurysm and parent vessel remained occluded. Despite nonspecific complaints and the perception of reduced cerebral perfusion by the patient,

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Fig. 4 (continued)

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Fig. 4 MRI/MRA 5 days after left ICA PVO. No ischemic lesion is visible and the left PcomA now supplies the left MCA (DWI, (a); T2WI, (b); ToF MRA, (c)). DSA 5 months (d) and 6 years (e) after left ICA PVO. The ophthalmic artery is not visible after injection of the vertebral arteries due to the retrograde flow in this artery. A

comparison of the caliber of the left PcomA immediately after PVO (f) and 6 years later (g) shows a slight increase in the vessel diameter (arrows). T2WI MRI 6 years after treatment did not show any parenchymal lesions (h). The ventricular asymmetry was longstanding. CTP did not show any perfusion abnormality or asymmetry (i)

perfusion abnormality in the left anterior circulation was not confirmed (Fig. 4).

or adjacent cranial nerve compression, including visual symptoms (diplopia, retro-orbital pain, and visual disturbance) and headaches (Hahn et al. 2000). Clinical examination may reveal visual deficits, ophthalmoplegia, and trigeminal neuropathy. In the event of aneurysm rupture, usually only occurring after the aneurysm has achieved a significant size, carotid-cavernous sinus fistula (CCF), subdural hemorrhage, subarachnoid hemorrhage (SAH), and epistaxis can also occur (Starke et al. 2014; Wiebers et al. 2003). As the use of diagnostic imaging is increasing, a significant proportion of cavernous carotid aneurysms, like many other intracranial aneurysms, are now detected incidentally, and agreement regarding the optimum management of these incidentally detected lesions has not been reached.

Discussion Aneurysms of the cavernous portion of the internal carotid artery have a varied etiology and comprise approximately 2% of all intracranial aneurysms and up to 6% of all ICA aneurysms (International Study of Unruptured Intracranial Aneurysms Investigators 1998). On account of their extradural location, the most common presentation is not of rupture, as for many other intracranial aneurysms, but more usually from the compressive effects of the aneurysm on surrounding structures. Patients most frequently present with symptoms of distal embolization

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The skull base location of the cavernous ICA makes microsurgical clipping techniques difficult and most operative interventions in this area are associated with significant perioperative risks of cerebral ischemia and cranial nerve damage (Abe et al. 2011; Sriamornrattanakul et al. 2017). In cavernous ICA aneurysms presenting without CCF, surgical treatment of the aneurysm might include proximal ICA occlusion with or without the creation of an extra-intracranial bypass. Surgical intervention for cavernous ICA aneurysm presenting with CCF aims to obliterate the fistula and may require aneurysm trapping, again, with or without bypass. To allow safe ICA ligation and aneurysm trapping without surgical bypass, the presence of sufficient collateral supply to the cerebral parenchyma should be proven, usually via carotid occlusion testing (Koebbe et al. 2006). Delayed complications of the surgical management of these aneurysms include late aneurysm reperfusion, with the recurrent risk of rupture and distal embolization (Abe et al. 2011; Sriamornrattanakul et al. 2017). The advent of interventional neurovascular techniques has enabled aneurysms in these locations to be treated with a higher success and lower complication rates (Koebbe et al. 2006). Strategies can broadly be divided into aneurysm obliteration with preservation of the parent vessel lumen and parent vessel occlusion (PVO) with or without prior surgical bypass, and more recently, flow-diverter stenting (van Rooij and Sluzewski 2009). Many operators report preferring coiling techniques in smaller aneurysms and PVO in large or giant cavernous ICA aneurysms, owing to the smaller perceived risks of significant periprocedural cerebral ischemia (Labeyrie et al. 2015; Morita et al. 2011). Parent vessel occlusion techniques prevent flow to the aneurysm and facilitate thrombosis of the aneurysm sac. This approach has the advantage of instantaneous aneurysm occlusion and subsequent reduction in the local mass effect exerted by the aneurysm sac as the thrombus within it starts to resorb. Lower aneurysm reperfusion rates occur than with coiling, meaning fewer secondary re-interventions (Labeyrie et al. 2015; Morita et al. 2011). If performed after

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satisfactory carotid occlusion testing or after successful extracranial-intracranial bypass surgery, significant ischemic complications occur rarely. There exists some debate, however, as to the interpretation of satisfactory and unsatisfactory carotid occlusion test results. In this case, aneurysm coiling without ICA stenting was not possible owing to the aneurysm configuration, and while stent-assisted coiling may have been possible, it would not have achieved instantaneous aneurysm occlusion. Flow diverter stent (FDS) insertion was also considered, having the advantage of preserving the parent vessel lumen, but the disadvantage of delayed aneurysm occlusion. This case occurred before the widespread use of FDS, and at this time PVO was chosen for its advantage of immediate isolation of the aneurysm from the circulation. Several longitudinal studies report good results from PVO in the treatment of giant cavernous ICA aneurysms, but owing to the low incidence of this condition, case numbers are relatively small. A large meta-analysis compared procedural success and clinical outcomes of 509 patients with 515 large or giant cavernous aneurysms across 20 retrospective series (Turfe et al. 2015). In this series, 77% of the treated patients presented with cranial nerve symptoms and approximately 7% each with SAH and CCF. A total of 176 aneurysms were treated with PVO without bypass and 339 with aneurysm coiling and preservation of the parent vessel lumen. The meta-analysis demonstrated a higher rate of persistent aneurysm occlusion at 3 months in the PVO group (93% vs. 67% in the coiling group) as well as a lower rate of reintervention (6% vs. 18% in the coiling group). However, a higher incidence of perioperative morbidity (ischemia or hemorrhage) was demonstrated in the PVO group (7% vs. 3% in the coiling group). A large single-center series demonstrated good results with low complication and reintervention rates after treatment of 86 CCA aneurysms in 85 patients with both endosaccular coiling (in smaller lesions) and PVO in large and giant aneurysms (van Rooij 2012). The authors describe a treatment preference for coiling in asymptomatic aneurysms and PVO in those

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lesions presenting with cranial neuropathies owing to the differential effect on aneurysm mass effect. PVO has the advantages of effective aneurysm exclusion and a low rate of aneurysm reperfusion, over endosaccular coiling. It also offers some advantage over the newer FDS technology as it does not require ongoing treatment with dual antiplatelet therapy (Raper et al. 2017; Starke et al. 2014). Shimizu et al. (2017) report low morbidity and mortality in their series of 28 patients with cavernous carotid aneurysms treated with PVO, after judicious use of surgical bypass depending on the results of the BTO. The most frequently occurring complications in this series were perioperative ischemic complications and cranial nerve palsies. Perioperative ischemia was observed more frequently in patients with preexisting cardiovascular risk factors and a venous phase delay of 1–2 s on BTO and the authors attribute this phenomenon to coverage of the perforating arteries. Temporary cranial nerve palsies occurred in four patients, all of which resolved completely. Similar findings have been reported in other case series (Labeyrie et al. 2015; Ganesh Kumar et al. 2017). In conclusion, owing to the low incidence of this condition, robust data on the safety and efficacy of PVO in the treatment of ICA aneurysms compared with other treatment options are not available. If competent collateral supply is confirmed or created through bypass-surgery, PVO is thought to be a safe and effective strategy in the management of a symptomatic nonruptured cavernous ICA aneurysm with low periprocedural morbidity and unlike treatment with FDS, does not require treatment with dual antiplatelet medication.

Therapeutic Alternatives Conservative Management FRED Pipeline Embolization Device, PED Stent Graft Stent-Assisted Coil Occlusion Telescoping Stents UNO for Parent Vessel Occlusion

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References Abe H, Takemoto K, Higashi T, Inoue T. Surgical treatment for aneurysms in the cavernous-petrous portion of the internal carotid artery. Acta Neurochir Suppl. 2011;112:77–83. https://doi.org/10.1007/978-3-70910661-7_14. Ganesh Kumar N, Ladner TR, Kahn IS, Zuckerman SL, Baker CB, Skaletsky M, Cushing D, Sanborn MR, Mocco J, Ecker RD. Parent vessel occlusion for treatment of cerebral aneurysms: Is there still an indication? A series of 17 patients. J Neurol Sci. 2017;372:250–5. https://doi.org/10.1016/j.jns.2016.11.057. Hahn CD, Nicolle DA, Lownie SP, Drake CG. Giant cavernous carotid aneurysms: clinical presentation in fiftyseven cases. J Neuroophthalmol. 2000;20(4):253–8. International Study of Unruptured Intracranial Aneurysms Investigators. Unruptured intracranial aneurysms – risk of rupture and risks of surgical intervention. N Engl J Med. 1998;339(24):1725–33. https://doi.org/10.1056/ NEJM199812103392401. Koebbe CJ, Veznedaroglu E, Jabbour P, Rosenwasser RH. Endovascular management of intracranial aneurysms: current experience and future advances. Neurosurgery. 2006;59(5 Suppl 3):93–102.; discussion S3–13. https://doi.org/10.1227/01.NEU.0000237512 .10529.58. Labeyrie MA, Lenck S, Bresson D, Desilles JP, Bisdorff A, Saint-Maurice JP, Houdart E. Parent artery occlusion in large, giant, or fusiform aneurysms of the carotid siphon: clinical and imaging results. AJNR Am J Neuroradiol. 2015;36(1):140–5. https://doi.org/ 10.3174/ajnr.A4064. Morita K, Sorimachi T, Ito Y, Nishino K, Jimbo Y, Kumagai T, Fujii Y. Intra-aneurysmal coil embolization for large or giant carotid artery aneurysms in the cavernous sinus. Neurol Med Chir (Tokyo). 2011;51 (11):762–6. Raper DM, Ding D, Peterson EC, Crowley RW, Liu KC, Chalouhi N, Hasan DM, Dumont AS, Jabbour P, Starke RM. Cavernous carotid aneurysms: a new treatment paradigm in the era of flow diversion. Expert Rev Neurother. 2017;17(2):155–63. https://doi.org/ 10.1080/14737175.2016.1212661. Shimizu K, Imamura H, Mineharu Y, Adachi H, Sakai C, Tani S, Arimura K, Beppu M, Sakai N. Endovascular parent-artery occlusion of large or giant unruptured internal carotid artery aneurysms. A long-term singlecenter experience. J Clin Neurosci. 2017;37:73–8. https://doi.org/10.1016/j.jocn.2016.11.009. Sriamornrattanakul K, Sakarunchai I, Yamashiro K, Yamada Y, Suyama D, Kawase T, Kato Y. Surgical treatment of large and giant cavernous carotid aneurysms. Asian J Neurosurg. 2017;12(3):382–8. https:// doi.org/10.4103/1793-5482.180930. Starke RM, Chalouhi N, Ali MS, Tjoumakaris SI, Jabbour PM, Fernando Gonzalez L, Rosenwasser RH, Dumont AS. Endovascular treatment of carotid cavernous aneurysms: complications, outcomes and comparison of

68 interventional strategies. J Clin Neurosci. 2014;21 (1):40–6. https://doi.org/10.1016/j.jocn.2013.03.003. Turfe ZA, Brinjikji W, Murad MH, Lanzino G, Cloft HJ, Kallmes DF. Endovascular coiling versus parent artery occlusion for treatment of cavernous carotid aneurysms: a meta-analysis. J Neurointerv Surg. 2015;7 (4):250–5. https://doi.org/10.1136/neurintsurg-2014011102. van Rooij WJ. Endovascular treatment of cavernous sinus aneurysms. AJNR Am J Neuroradiol. 2012;33 (2):323–6. https://doi.org/10.3174/ajnr.A2759.

F. Colgan et al. van Rooij WJ, Sluzewski M. Endovascular treatment of large and giant aneurysms. AJNR Am J Neuroradiol. 2009;30(1):12–8. https://doi.org/10.3174/ajnr.A1267. Wiebers DO, Whisnant JP, Huston J 3rd, Meissner I, Brown RD Jr, Piepgras DG, Forbes GS, Thielen K, Nichols D, O’Fallon WM, Peacock J, Jaeger L, Kassell NF, Kongable-Beckman GL, Torner JC, International Study of Unruptured Intracranial Aneurysms Investigators. Unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet. 2003;362(9378):103–10.

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Cavernous Internal Carotid Artery Aneurysm: Diplopia due to a Large Cavernous Aneurysm Causing Oculomotor Nerve Palsy; Partial Coil Occlusion and p64 Flow Diverter Implantation; Resolution of the Cranial Nerve Palsy and Complete Clinical Recovery Frances Colgan, Marta Aguilar Pérez, Hansjörg Bäzner, and Hans Henkes Abstract

A 48-year-old female patient presented with a sudden onset of diplopia. MRI/MRA and DSA demonstrated a large aneurysm of the cavernous segment of the right internal carotid artery (ICA). This aneurysm was treated with partial endovascular coil occlusion and implantation of three flow diverters, two p64, and one Pipeline Embolic Device (PED). The patient demonstrated hyper-response to dual antiplatelet therapy (aspirin and ticagrelor) which was managed by a monitored dosage reduction. The diplopia resolved 4 months after the endovascular treatment and DSA at 4 and 11 months and MRI/MRA at 5 months

postprocedure confirmed the complete occlusion of the aneurysm with significant reduction in size. Extrasaccular flow diversion treatment for cavernous ICA aneurysms causing cranial neuropathy is the main topic of this chapter. Keywords

Cavernous internal carotid artery · Saccular aneurysm · Diplopia · Oculomotor nerve palsy · Partial coil occlusion · p64 flow diversion · Dual anti-aggregation · Hyperresponse on platelet function inhibition medication

Patient F. Colgan (*) Department of Radiology, University of Otago, Christchurch Hospital, Christchurch, New Zealand e-mail: [email protected] M. Aguilar Pérez · H. Henkes Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; [email protected]; [email protected] H. Bäzner Neurologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_92

A 48-year-old female patient presenting after a sudden onset of diplopia. The patient’s medical history was unremarkable.

Diagnostic Imaging Diagnostic MRI/MRA and DSA examinations in January 2018 demonstrated a large, partially thrombosed aneurysm originating from the cavernous segment of the right ICA. Collateral 69

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supply to the right anterior circulation via the anterior communicating artery (AcomA) was present but not fully tested (Fig. 1).

Treatment Strategy The goal of the treatment was to reduce the cranial nerve compression from the mass effect of the aneurysm. Due to the extradural location of the aneurysm, intracranial hemorrhage was not a concern. The aneurysm’s size and location made it unsuitable for open surgery. Endovascular treatment options comprised coil occlusion, including stent-assisted coiling, parent vessel occlusion (PVO), and flow diverter stent (FDS) insertion. When aneurysms are treated with FDS, partial coil occlusion with loose coil packing is known to enhance the hemodynamic effect of the implanted FDS. The final treatment concept was a combination of FDS insertion with partial aneurysm coiling, as we expected this to result in rapid relief of the cranial nerve compression.

Treatment Procedure, 12.01.2018: endovascular treatment of a cavernous ICA aneurysm causing cranial nerve compression with FDS insertion and loose coiling Anesthesia: general anesthesia, 1
3000 IU unfractionated heparin (Heparin Natrium, B. Braun) IV, 1
500 mg thiopental (Trapanal, Nycomed) IV, 1
40 mg dexamethasone (Fortecortin, Merck Serono) IV Premedication: 1
500 mg ASA (Aspirin, Bayer Vital) PO and 2
90 mg ticagrelor (Brilique, AstraZeneca) PO on the day prior to the procedure; on the morning prior to the procedure 1
100 mg ASA PO and 1
90 mg ticagrelor PO; Multiplate (AUC: ADP 35, ASPI 18) and VerifyNow (ARU 381, P2Y12 86% inhibition) on the morning prior the procedure confirmed the dual platelet function inhibition Access: right common femoral artery, 8F sheath (Terumo); guide catheter: 8F Guider Softip XF (Boston Scientific); microcatheters:1


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Excelsior XT-27 (Stryker) for the flow diverters, 1
Excelsior SL-10 (Stryker) for the coils; microguidewire:1
Synchro2 0.01400 200 cm (Stryker) Implants: 10 coils: 1
Target 360 soft 9/20 (Stryker), 1
Morpheus 3D 10/30, 7
Morpheus 3D 9/18,1
Tetris 3D 7/15 (all Medtronic); 3 flow diverters: 1
p64 4/24, 1
4/21 (both phenox), 1
PED 4/20 (Medtronic) Balloon catheter: pITA 3.5/20 (phenox), 8 atm Course of treatment: An 8F guide catheter was inserted into the right ICA. Under road map conditions, a microcatheter was advanced into the aneurysm sac. Care was taken not to penetrate the intra-aneurysmal thrombus (i.e., the tip of the microcatheter remained within the lumen of the aneurysm sac, demonstrated by contrast injection). Balloon remodeling was not considered necessary. A total of 10 coils were deployed into the aneurysm sac. The stenotic segment of the ICA proximal to the aneurysm origin was dilated using a 3.5 mm non-compliant balloon, after which a 0.02700 inner diameter microcatheter was inserted into the right middle cerebral artery. A 4/24 p64 flow diverter was introduced and deployed. To facilitate safe deployment of the device, the road map function was switched off and high frequency, high intensity pulsed fluoroscopy (30 frames/second) was used, with intermittent storage of digital radiographic images. During the deployment of the p64, the radiopaque distal marker of the inner wire of the flow diverter moved distally. The expansion of the flow diverter was completed as expected and mechanical detachment of the stent from the insertion device was performed without difficulty. In order to avoid a proximal endoleak, a second p64 flow diverter (4/21) was added proximally, with an overlap of about 30% with the first flow diverter. The second flow diverter showed a proximal “fish mouth” phenomenon with incomplete apposition of the radiopaque markers to the vessel wall. Since this phenomenon is recognized as a potential precursor of device collapse and can result in the occlusion of the parent artery, a third flow diverter was implanted. The hemodynamic effect of flow diverting stents is enhanced if stents with nonmatching braiding patterns are combined in a telescoping

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Cavernous Internal Carotid Artery Aneurysm: Diplopia due to a Large Cavernous Aneurysm. . .

Fig. 1 T2WI MRI (arrow, (a)) and ToF MRA (b) of a large, partially thrombosed aneurysm of the cavernous segment of the right ICA. DSA (lateral view, (c); posterior-anterior view, (d); left anterior oblique view,

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(e)) demonstrated the origin of the aneurysm from the cavernous segment of the right ICA (c) with a largest diameter of 2 cm. The uneven, irregular contour of the aneurysm was due to the intra-aneurysmal thrombus (c, d).

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fashion. For this reason, a 4/20 PED was chosen as the third flow diverter. The final DSA runs demonstrated significant contrast stasis within the aneurysm, and the dependent intracranial arteries remained within normal limits (Fig. 2). Duration: 1st -15th run:133 min; fluoroscopy time: 35 min Complications: none Post medication: 1
100 mg ASA PO daily for life, 2
90 mg ticagrelor PO daily for 1 year, 3
4 mg dexamethasone (Fortecortin, Merck Serono) PO daily for 7 days, followed by a tapering steroid dose regime

Clinical Outcome The endovascular treatment was tolerated without significant complication. The patient was discharged home 4 days later with an oculomotor palsy and without new neurological deficit. Eight weeks after the treatment the patient complained of recurrent epistaxis, increased bruising, and menorrhagia. A hyper-response on ASA and/or ticagrelor was suspected. Based on the results of Multiplate and VerifyNow tests the dosage was gradually reduced to 1
50 mg ASA and 2
45 mg ticagrelor PO daily, resulting in an improvement in both platelet aggregation results and clinical symptoms. Multiplate, VerifyNow, and PFA tests confirmed the dual platelet function inhibition with this adjusted dosage. Four months and 11 months after the procedure, the patient attended for follow-up and the diplopia had completely resolved.

Follow-Up Examinations Follow-up MRI/MRA examinations were carried out after the procedure, demonstrating progressive shrinkage of the aneurysm sac within

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5 months. DSA after 4 and 11 months confirmed the complete obliteration of the aneurysm (Fig. 3). Final follow-up examinations are scheduled at 24 months after the treatment.

Discussion Cavernous ICA aneurysms comprise approximately 2–12% of all intracranial aneurysms and occur most commonly in female patients (Stiebel-Kalish et al. 2005; Wiebers et al. 2003). Owing in part to their extra-dural location, their clinical presentation is different to that of other intracranial aneurysms. Mass effect on the surrounding structures leads to symptoms of visual disturbance, ophthalmoplegia, and oculomotor nerve palsy as well as headaches (Wiebers et al. 2003). Large aneurysms may present with carotid-cavernous fistula (CCF), extra-dural hemorrhage, or epistaxis, but subarachnoid hemorrhage (SAH) is rare. As these lesions occur relatively infrequently, data on their optimal management are limited. Treatment of these lesions carries potential significant neurological morbidity and death, and there is no consensus on the optimum management of unruptured, asymptomatic lesions. Treatment options for symptomatic lesions vary with the clinical presentation and include both surgical and endovascular techniques. Surgical access to this anatomical space is complex and options include aneurysm trapping or ICA ligation, with bypass performed if appropriate, usually depending on the results of a carotid balloon test occlusion (BTO) (Linskey et al. 1991). In the early part of this century, endovascular techniques had developed to include endosaccular aneurysm coiling, with or without adjunctive techniques, and endovascular parent vessel occlusion (PVO) (Raper et al. 2017; Starke et al. 2014). Both aneurysm coiling and PVO have demonstrated good

ä Fig. 1 (continued) Proximal to the aneurysm origin a stenotic vessel segment was visualized on an oblique projection (e). Contrast injection from the left ICA during

manual compression of the right common carotid artery (CCA) shows the cross flow from the left to the right via the AcomA (f)

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Cavernous Internal Carotid Artery Aneurysm: Diplopia due to a Large Cavernous Aneurysm. . .

Fig. 2 (continued)

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Fig. 2 Endovascular treatment of a large, partially thrombosed right cavernous ICA aneurysm. The aneurysm sac was catheterized with a microcatheter under road map conditions (a). A total of 10 coils were inserted into the

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aneurysm (b). The stenotic segment of the right ICA proximal to the aneurysm was dilated with a 3.5 mm noncompliant balloon (arrow (c)). A 0.02700 inner diameter microcatheter (arrow (d) was used to deploy a 4/24 mm

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Cavernous Internal Carotid Artery Aneurysm: Diplopia due to a Large Cavernous Aneurysm. . .

periprocedural and intermediate-term outcomes in the treatment of these lesions (Turfe et al. 2015). The advent of Flow Diverter Stents (FDS) allowed significant advances in the treatment of intracranial aneurysms. Their structure alters flow through the aneurysm and reduces wall shear stress while providing a scaffold for endothelization across the aneurysm neck. Their braided design allows continued flow through the parent vessel and perforators while facilitating exclusion of the aneurysm from the circulation. Although excellent results have been demonstrated with this technique, aneurysm thrombosis is delayed, and thus, in the immediate postoperative period, compressive symptoms will persist and the risk of rupture remains (Starke et al. 2014; Zanaty et al. 2014). Additionally, patients treated with FDS also have a requirement for antiplatelet medication to reduce the risk of stent thrombosis. Two large meta-analyses by the same group have evaluated the efficacy and complication rates of intracranial aneurysm treatment with FDS. Treatment of 2493 aneurysms in 2263 patients reported in 59 studies demonstrated a 97.4% technical success rate of FDS in the treatment of all intracranial aneurysms, resulting in an overall occlusion rate of 82.5% (83.3% in the treatment of anterior circulation aneurysms) (Zhou et al. 2016). A second large meta-analysis of 66 retrospective studies involving 3125 patients reported an overall complication rate of 17% and a mortality rate of 2.8% for FDS treatment of intracranial aneurysms in all locations. No significant difference was identified in success or complication rates in treatment with the two most commonly reported devices, PED and SILK (Zhou et al. 2017).

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Outcomes after carotid aneurysm treatment with PED have been compared with those of other treatments including coiling, with and without stent assistance, and carotid vessel deconstruction (CVD), with or without bypass (Zanaty et al. 2014). The authors performed a retrospective review of a prospectively maintained database and identified 167 cavernous ICA aneurysms treated in 157 patients, of which 142 were symptomatic. The authors report a complication rate of FDS treatment with PED of 3.4%, lower than stent-assisted coiling (5.6%) and significantly lower than with CVD (13.3%). Complete or near-complete occlusion of the aneurysms treated with PED was demonstrated in 89.8%, similar to that achieved by CVD in the same series (86.7%). The rate of symptom improvement was highest in patients treated with FDS, with 92% experiencing an improvement in symptoms; however, the follow-up interval was not specified. This improvement was significantly more than that seen in patients treated with CVD (79%) and stent and stent-assisted coiling (50 and 51%, respectively). The highest reintervention rate was in the groups treated with stent-assisted coiling. Predictors of clinically apparent worsening mass effect included treatment with methods other than PED or CVD and a pretreatment aneurysm size > 15 mm. The authors conclude that FDS treatment for symptomatic cavernous ICA aneurysms is safe and effective, and associated with a high rate of aneurysm occlusion, a significant reduction in mass symptoms and a lower reintervention rate when compared with traditional endovascular techniques. While the PED is the most frequently used device, and thus the one with the largest published

ä Fig. 2 (continued) p64 flow diverter into the cavernous ICA, covering the aneurysm orifice (arrow (e)). A second flow diverter (4/21 p64) was inserted and deployed more proximally, with the intention of enhancing the hemodynamic effect on the aneurysm perfusion and to avoid a proximal endoleak. The proximal end of this second flow diverter showed a “fish mouth” phenomenon immediately after deployment (f). A 4/20 PED was deployed inside the

p64 flow diverters with an estimated 50% overlap, removing the “fish mouth” and enhancing the hemodynamic impact on the aneurysm perfusion (arrow (g)). The perfusion of the aneurysm was reduced (h), the dependent intracranial vessels were normal (i, j), and a typical contrast pattern within the aneurysm sac was observed (k). Completion imaging showed the complete expansion of the flow diverters (l)

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Fig. 3 (continued)

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Cavernous Internal Carotid Artery Aneurysm: Diplopia due to a Large Cavernous Aneurysm. . .

data series, other FDS are available. A large retrospective multicenter Italian study has reported early outcomes on 273 patients with 295 nonruptured intracranial aneurysms, of which 76 involved the cavernous segment of the ICA, treated across 25 centers with both PED and SILK FDS (Briganti et al. 2012). Periprocedural outcomes and the incidence of major adverse events were similar between the two devices. Favorable initial technical experience in the cavernous segment with the Surpass device (Stryker) has been described (Colby et al. 2016). This device has shown comparable outcomes to other available FDS and traditional coiling techniques in a large multicenter prospective study involving 186 intracranial aneurysms in 161 patients (Wakhloo et al. 2015). Longer-term outcome data for this device are still awaited (Kan et al. 2018). The safe and effective treatment of cavernous ICA aneurysms has also been demonstrated with the Flow Re-direction Endoluminal Device, FRED (MicroVention), another FDS, in the SAFE study (Safety and Efficacy of FRED Embolic Device in Aneurysm Management), a prospective multicenter study with core-lab analysis, conducted in France. A total of 103 patients with anterior circulation aneurysms were treated in 13 centers with a 95% success rate, 2% morbidity, and 1% mortality rate at 6 months (Pierot et al. 2018). As discussed above, a frequent indication for the treatment of cavernous aneurysms is cranial neuropathy, usually secondary to the compression of adjacent structures by the aneurysm sac. Occasionally such symptoms are attributed to aneurysm pulsation. As aneurysm occlusion with FDS is not instantaneous, as may be the case in PVO or surgical ligation, compressive symptoms including cranial neuropathy can persist after the exclusion of the aneurysm from the circulation. Limited data are available on the natural history of

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cranial neuropathy after the treatment of these aneurysms with flow diversion. Moon et al. (2014) identified 22 patients presenting with cranial neuropathies from 127 patients treated with PED, of which 20 had sufficient clinical follow-up for analysis and of which 13 lesions were in the cavernous ICA. The authors report that 75% patients had resolution or significant improvement in their symptoms 9 months postprocedure, and this correlated with the rate of complete or near complete aneurysm occlusion. An analysis of cranial neuropathy in patients in the PUFS trial (The Pipeline for Uncoilable or Failed Aneurysms) demonstrated clinical improvement in 25 (64%) of the 39 patients presenting with neuro-ophthalmic symptoms attributable to the aneurysm, after FDS treatment with the PED. Symptoms worsened in one patient and new symptoms developed in five. Aneurysm size was noted to be a risk factor for failure to improve or worsening of symptoms (Sahlein et al. 2015). Brown et al. (2016) report a series of 45 patients treated with FDS for ICA aneurysms in the cavernous, clinoid, and ophthalmic segments and compared the outcomes with those from surgical and endovascular PVO in the available literature. They describe similar rates of improvement in ophthalmic and oculomotor nerve palsies; however, they also highlight a worsening of the presenting cranial neuropathy in the short term, falling to 4.8% at 12 months post-FDS treatment. The p64 device, used in this case, has the advantage of being both repositionable and removable and has shown promising initial results in small series (Fischer et al. 2015; Morais et al. 2017). Further prospective evaluation is awaited. In the case presented in this chapter, the treatment goal was to reduce compressive symptoms from the cavernous ICA aneurysm. It is known that combining partial coil occlusion of aneurysms with FDS insertion leads to an enhanced hemodynamic effect. This patient demonstrated complete clinical

ä Fig. 3 Sequential follow-up T2WI MRI examinations on the day of treatment (a), 2 days later (b), and 5 months later (c) confirmed the progressive shrinkage of the aneurysm (arrows). DSA 4 months after the procedure demonstrated

the unchanged configuration of the implanted flow diverters (d) and the complete occlusion of the aneurysm sac (e) without in-stent stenosis

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and radiographic success with a resolution of the diplopia and complete obliteration of the aneurysm on imaging at 4 months postprocedure. A symptomatic hyper-response to the dual antiplatelet treatment necessitated by FDS implantation was managed with dose reduction.

Therapeutic Alternatives Conservative Management Parent Vessel Occlusion Pipeline Embolization Device, PED Stent Graft Stent-Assisted Coil Occlusion Telescoping Stents

References Briganti F, Napoli M, Tortora F, Solari D, Bergui M, Boccardi E, Cagliari E, Castellan L, Causin F, Ciceri E, Cirillo L, De Blasi R, Delehaye L, Di Paola F, Fontana A, Gasparotti R, Guidetti G, Divenuto I, Iannucci G, Isalberti M, Leonardi M, Lupo F, Mangiafico S, Manto A, Menozzi R, Muto M, Nuzzi NP, Papa R, Petralia B, Piano M, Resta M, Padolecchia R, Saletti A, Sirabella G, Bolgè LP. Italian multicenter experience with flowdiverter devices for intracranial unruptured aneurysm treatment with periprocedural complications – a retrospective data analysis. Neuroradiology. 2012;54 (10):1145–52. https://doi.org/10.1007/s00234-0121047-3. Brown BL, Lopes D, Miller DA, Tawk RG, Brasiliense LB, Ringer A, Sauvageau E, Powers CJ, Arthur A, Hoit D, Snyder K, Siddiqui A, Levy E, Hopkins LN, Cuellar H, Rodriguez-Mercado R, Veznedaroglu E, Binning M, Mocco J, Aguilar-Salinas P, Boulos A, Yamamoto J, Hanel RA. The fate of cranial neuropathy after flow diversion for carotid aneurysms. J Neurosurg. 2016;124(4):1107–13. https://doi.org/ 10.3171/2015.4.JNS142790. Colby GP, Lin LM, Caplan JM, Jiang B, Michniewicz B, Huang J, Tamargo RJ, Coon AL. Flow diversion of large internal carotid artery aneurysms with the surpass device: impressions and technical nuance from the initial North American experience. J Neurointerv Surg. 2016;8(3):279–86. https://doi.org/10.1136/ neurintsurg-2015-011769. Fischer S, Aguilar-Pérez M, Henkes E, Kurre W, Ganslandt O, Bäzner H, Henkes H. Initial experience with p64: a novel mechanically detachable flow diverter for the treatment of intracranial saccular

F. Colgan et al. sidewall aneurysms. AJNR Am J Neuroradiol. 2015;36(11):2082–9. https://doi.org/10.3174/ajnr. A4420. Kan P, Meyers PM, Hanel R. E-022 The Surpass™ IntraCranial Aneurysm Embolization System pivotal trial to treat large or giant wide neck aneurysms (SCENT Trial). J Neurointerv Surg. 2018;8(Suppl 1): A56.2–A57. https://doi.org/10.1136/neurintsurg-2016012589.94. https://clinicaltrials.gov/ct2/show/NCT01 716117 Linskey ME, Sekhar LN, Horton JA, Hirsch WL Jr, Yonas H. Aneurysms of the intracavernous carotid artery: a multidisciplinary approach to treatment. J Neurosurg. 1991;75(4):525–34. https://doi.org/10.3171/jns.1991. 75.4.0525. Moon K, Albuquerque FC, Ducruet AF, Crowley RW, McDougall CG. Resolution of cranial neuropathies following treatment of intracranial aneurysms with the pipeline embolization device. J Neurosurg. 2014;121(5):1085–92. https://doi.org/10.3171/2014.7. JNS132677. Morais R, Mine B, Bruyère PJ, Naeije G, Lubicz B. Endovascular treatment of intracranial aneurysms with the p64 flow diverter stent: mid-term results in 35 patients with 41 intracranial aneurysms. Neuroradiology. 2017;59(3):263–9. https://doi.org/10.1007/s002 34-017-1786-2. Pierot L, Spelle L, Berge J, Januel AC, Herbreteau D, Aggour M, Piotin M, Biondi A, Barreau X, Mounayer C, Papagiannaki C, Lejeune JP, Gauvrit JY, Costalat V. Feasibility, complications, morbidity, and mortality results at 6 months for aneurysm treatment with the Flow Re-Direction Endoluminal Device: report of SAFE study. J Neurointerv Surg. 2018;10 (8):765–70. https://doi.org/10.1136/neurintsurg-2017013559. Raper DM, Ding D, Peterson EC, Crowley RW, Liu KC, Chalouhi N, Hasan DM, Dumont AS, Jabbour P, Starke RM. Cavernous carotid aneurysms: a new treatment paradigm in the era of flow diversion. Expert Rev Neurother. 2017;17(2):155–63. https://doi.org/ 10.1080/14737175.2016.1212661. Sahlein DH, Fouladvand M, Becske T, 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, Marosfoi M, Cekirge SH, Kallmes DF, Nelson PK. Neuroophthalmological outcomes associated with use of the pipeline embolization device: analysis of the PUFS trial results. J Neurosurg. 2015;123(4):897–905. https://doi.org/ 10.3171/2014.12.JNS141777. Starke RM, Chalouhi N, Ali MS, Tjoumakaris SI, Jabbour PM, Fernando Gonzalez L, Rosenwasser RH, Dumont AS. Endovascular treatment of carotid cavernous aneurysms: complications, outcomes and comparison of interventional strategies. J Clin Neurosci. 2014;21 (1):40–6. https://doi.org/10.1016/j.jocn.2013.03.003. Stiebel-Kalish H, Kalish Y, Bar-On RH, Setton A, Niimi Y, Berenstein A, Kupersmith MJ. Presentation, natural

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Cavernous Internal Carotid Artery Aneurysm: Diplopia due to a Large Cavernous Aneurysm. . .

history, and management of carotid cavernous aneurysms. Neurosurgery. 2005;57(5):850–7.. discussion 850–7 Turfe ZA, Brinjikji W, Murad MH, Lanzino G, Cloft HJ, Kallmes DF. Endovascular coiling versus parent artery occlusion for treatment of cavernous carotid aneurysms: a meta-analysis. J Neurointerv Surg. 2015;7(4):250–5. https://doi.org/10.1136/neurintsurg-2014-011102. Wakhloo AK, Lylyk P, de Vries J, Taschner C, Lundquist J, Biondi A, Hartmann M, Szikora I, Pierot L, Sakai N, Imamura H, Sourour N, Rennie I, Skalej M, Beuing O, Bonafé A, Mery F, Turjman F, Brouwer P, Boccardi E, Valvassori L, Derakhshani S, Litzenberg MW, Gounis MJ, Surpass Study Group. Surpass flow diverter in the treatment of intracranial aneurysms: a prospective multicenter study. AJNR Am J Neuroradiol. 2015;36 (1):98–107. https://doi.org/10.3174/ajnr.A4078. Wiebers DO, Whisnant JP, Huston J 3rd, Meissner I, Brown RD Jr, Piepgras DG, Forbes GS, Thielen K, Nichols D, O’Fallon WM, Peacock J, Jaeger L, Kassell NF,

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Kongable-Beckman GL, Torner JC, International Study of Unruptured Intracranial Aneurysms Investigators. Unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet. 2003;362(9378):103–10. Zanaty M, Chalouhi N, Starke RM, Barros G, Saigh MP, Schwartz EW, Ajiboye N, Tjoumakaris SI, Hasan D, Rosenwasser RH, Jabbour P. Flow diversion versus conventional treatment for carotid cavernous aneurysms. Stroke. 2014;45(9):2656–61. https://doi.org/ 10.1161/STROKEAHA.114.006247. Zhou G, Su M, Zhu YQ, Li MH. Efficacy of flow-diverting devices for cerebral aneurysms: a systematic review and meta-analysis. World Neurosurg. 2016;85: 252–62. https://doi.org/10.1016/j.wneu.2015.09.088. Zhou G, Su M, Yin YL, Li MH. Complications associated with the use of flow-diverting devices for cerebral aneurysms: a systematic review and meta-analysis. Neurosurg Focus. 2017;42(6):E17. https://doi.org/ 10.3171/2017.3.FOCUS16450.

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Cavernous Internal Carotid Artery Aneurysm: Rupture of a Presumably Traumatic Cavernous Internal Carotid Artery Pseudoaneurysm with Life-Threatening Epistaxis After Endonasal Pansinus Surgery Cindy Richter, Helmut Steinhart, and Hans Henkes Abstract

An 85-year-old female patient was referred to our institution by the ENT department of another hospital with nonarresting epistaxis and severe blood loss caused by a ruptured cavernous internal carotid artery (ICA) pseudoaneurysm extending into the sphenoid sinus. Preceding transnasal pansinus surgeries had presumably perforated the bone wall of the sphenoid sinus and affected the arterial wall, which had allowed a traumatic pseudoaneurysm to develop. Emergent DSA with endovascular coil occlusion of the aneurysm was performed which in turn revealed a mechanically caused high-grade stenosis with thrombotic plaques in the distal ICA. Although no ischemic infarct occurred, due to the effect

C. Richter (*) Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany Abteilung für Neuroradiologie, Universitätsklinikum Leipzig, Leipzig, Germany e-mail: [email protected] H. Steinhart Klinik für Hals-Nasen-Ohren-Heilkunde, Kopf- und Halschirurgie, Marienhospital Stuttgart, Stuttgart, Germany e-mail: [email protected] H. Henkes Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_68

of earlier epistaxis on hemodynamic stability, the patient died of cardiac failure 2 weeks later. Epistaxis in the context of cavernous ICA pseudoaneurysms is the main topic of this chapter. Keywords

Internal carotid artery aneurysm · Coiling · Pansinus surgery · Sphenoid sinus · Epistaxis

Patient A female 85-year-old patient was admitted to the ENT department of the referring hospital with nonsuppressible epistaxis from the left nostril. Her past medical history included hypertension, intermittent absolute arrhythmia, one-vessel coronary artery disease with myocardial infarction and cardiopulmonary resuscitation in 2006, anamnestic apoplexy, and incipient dementia.

Diagnostic Imaging The emergency thin-layer CT of the paranasal sinuses showed the sphenoid sinus with an intact bone wall. Postsurgical CT angiography (CTA) after initial pansinus surgery and nasal packing revealed an enlarged sphenoethmoidal recess as well as missing posterolateral bone wall between the left-hand sphenoid sinus and the carotid sulcus 81

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Fig. 1 Thin-layer CT and CT angiography (CTA) examination of a patient with nonsuppressible nasal bleeding. The presurgery emergency CT of the paranasal sinuses showed an intact sphenoid sinus boundary bone (a, b). Postsurgical CTA was obtained after the first endonasal pansinus surgery in which the sphenoid sinus was opened (c, d). Bone wall imaging had already shown the enlarged sphenoethmoidal recess and the missing posterolateral

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bone boundary between the left sphenoid sinus and the carotid sulcus with minor contrast leakage. Eleven days later following a third endonasal surgery in which the sphenoid sinus was occluded with a muscle seal, followup CTA revealed a new traumatic left-hand saccular pseudoaneurysm of the cavernous ICA. Now, there is a false aneurysm in the sphenoid sinus (e, f)

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Cavernous Internal Carotid Artery Aneurysm: Rupture of a Presumably Traumatic Cavernous. . .

with contrast leakage. Despite repeated nasal packing, epistaxis continued for another 11 days. During the third transnasal surgery, the patient suffered hemodynamic cardiopulmonary arrest due to severe blood loss. As a last ditch attempt to stem the bleeding, a quadriceps femoris muscle seal was harvested to occlude the sphenoid sinus. Repeated postinterventional computer tomography with angiography (CTA) finally showed a de novo pseudoaneurysm of the left internal carotid artery (ICA) extending into the sphenoid sinus. The patient was immediately referred to our center for endovascular treatment and further management (Figs. 1 and 2).

Treatment Strategy The aim of the treatment was to prevent recurrent epistaxis. It was decided to pack coils as densely as possible in the aneurysmal fundus. To prevent having to use stents in the acute phase, the neck was saved with coils. This set the stage for a later, second intervention in which a complete exclusion of the pseudoaneurysm with patency of the ICA might have been obtained (e.g., by stent-assisted coiling, depending on clinical outcome).

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Treatment Procedure, 30.03.2007: endovascular coil occlusion of a ruptured left cavernous ICA pseudoaneurysm Anesthesia: general anesthesia; 5000 IU unfractionated heparin (Heparin-Natrium, B. Braun) after securing the femoral sheath, 0.5 mg atropine IV, rinsing solution with 1000 IU unfractionated heparin per liter IA Premedication: none Access: right common femoral artery, 1 6F sheath (Terumo); guide catheter: 1 6F Guider Softip (Boston Scientific); microcatheter: 1 Echelon-10 90 (then ev3, now Medtronic); microguidewire: 1 Silverspeed-14 200 cm (then ev3, now Medtronic) Implants: 6 coils: 2 Morpheus 3D CS 5/15; 1 Helix Standard fibered coil 3/10; 3 Helix Standard fibered coil 2/6 (then ev3, now Medtronic) Course of treatment: Under general anesthesia a catheter angiography of both ICAs was performed prior to intervention. The injection of the right ICA did not show any spontaneous cross flow to the left side. The injection of the left ICA showed an elongated cervical course of this artery with the expected cavernous pseudoaneurysm.

Fig. 2 Subsequently performed DSA confirmed a wide-necked, elongated and partially thrombosed pseudoaneurysm of the left cavernous ICA (a). The distal ICA was stenotic due to recent dissection (a, b)

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The fundus height was 8 mm, the fundus width was 8  10 mm, and the neck width was measured at 5.8 mm. The pseudoaneurysm was frontally directed, at the level of the sphenoid sinus and proximal to the origin of the ophthalmic artery. Furthermore, high-grade stenosis with intraluminal thrombus could be seen in the left paraclinoid segment of the ICA, presumably caused by the previous tamponade of the sphenoid sinus. The guide catheter was placed into the cervical segment of left ICA. A working projection showing the entire length of the aneurysm sac including the neck plane was selected. An Echelon10 90

shaped microcatheter was used to selectively catheterize said aneurysm. The aneurysm was occluded with six detachable coils in a single session under fluoroscopic control and roadmap conditions. The final angiogram showed a subtotal aneurysm exclusion with residual opacification of the proximal aneurysmal sac and the aneurysm neck adjacent to the ICA (Fig. 3). Epistaxis ceased and the posterior nasal packing was removed 2 days later. There were no procedure-related complications. Duration: 1st–25th DSA run: 60 min; fluoroscopy time: 14 min Complications: none

Fig. 3 The working projection (63 left anterior oblique/  0 craniocaudal) of a pretreatment injection (a) shows the frontally oriented left ICA pseudoaneurysm proximal to the origin of the ophthalmic artery. Straightforward catheterization of the aneurysm fundus (b). Insertion of six

detachable microcoils (c). The postprocedural injection demonstrates the sufficient yet subtotal aneurysm occlusion with residual opacification of the proximal sac near the ICA orifice (d)

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Cavernous Internal Carotid Artery Aneurysm: Rupture of a Presumably Traumatic Cavernous. . .

Postmedication: low-dose low-molecularweight heparin SC during bedrest, antibiotic coverage (Fig. 4)

Clinical Outcome Postintervention, the patient was able to breathe independently and had stable circulation. However, she was poorly responsive on request. A subsequent bilateral pleural effusion led to her being newly intubated with an intercostal drain. She was referred back in a stabilized condition. Unfortunately, the patient died of cardiac failure in the night of the 10th of April 2007 (mRS 6, GOS 1).

Discussion This case impressively demonstrates a rare complication of transnasal pansinus surgery in which a traumatic, life-threatening pseudoaneurysm develops in the cavernous portion of the ICA. Cavernous ICA aneurysms constitute 1–2% of all intracranial aneurysms and are divided into traumatic or nontraumatic types (Chaboki et al. 2004). True, nontraumatic ICA aneurysms

Fig. 4 Follow-up CT 3 days after the endovascular procedure showed chronic postischemic lesions in both middle cerebral artery supply territories without acute

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extending into the sphenoid sinus are rare and the overall incidence of bleeding (i.e., epistaxis) is low. In contrast, traumatic pseudoaneurysms can cause severe and even fatal epistaxis due to a rupture into the sphenoid sinus, which is associated with high mortality of up to 50% (Holmes and Harbaugh 1993; Larson et al. 2000; Cohen et al. 2008; Dubey et al. 2008). Their optimal treatment remains a matter of controversy (Ronchetti et al. 2013). The thin bony coverage of the cavernous ICA makes it especially vulnerable to surgical and traumatic injury. Studying cadavers, Renn and Rhoton (1975) found that the bony coverage of the cavernous ICA within the sphenoid sinus was thinner than 1 mm in 66% of the cases and not present at all in 4%. Pseudo- or false aneurysms result from a disruption of all three vessel wall layers with the wall of the aneurysm being formed by surrounding structures, particularly hematoma (Chambers et al. 1981; Larson et al. 2000; Dubey et al. 2008). Later on, a fibrous capsule develops from the perivascular connective tissue and surrounds the extravasated blood (Garg et al. 2016). The vulnerable boundary easily ruptures, causing a massive epistaxis. Therefore, patients with a posttraumatically or postsurgically opened sphenoid sinus – whether or not massive epistaxis has

infarction due to thrombosis of left ICA (a). Coil artifact in left sphenoid sinus (b)

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been present – should be evaluated for the possible development of a traumatic ICA pseudoaneurysm as soon as possible. If the initial DSA was negative, a second follow-up DSA should be obtained if there is recurring epistaxis. Furthermore, it should be remembered that pseudoaneurysms do not consist of the normal vessel wall. Owing to the fragility of a pseudoaneurysm, direct tight coiling is always much more difficult than in a true aneurysm (Lempert et al. 1998). Occluding the parent artery is possible with open and endovascular access but carries a high ischemic risk. The first choice of treatment should be an endovascular, less invasive procedure, especially if the patient is older. In the end, life-saving therapeutic success can be hard to achieve in such cases.

Therapeutic Alternatives Coil Occlusion Flow Diverters Parent Vessel Occlusion Stent Assisted Coil Occlusion Stent Graft

References Chaboki H, Patel AB, Freifeld S, Urken ML, Som PM. Cavernous carotid aneurysm presenting with epistaxis. Head Neck. 2004;26(8):741–6. https:// doi.org/10.1002/hed.20081.

C. Richter et al. Chambers EF, Rosenbaum AE, Norman D, Newton TH. Traumatic aneurysms of cavernous internal carotid artery with secondary epistaxis. AJNR Am J Neuroradiol. 1981;2(5):405–9. Cohen JE, Gomori JM, Segal R, Spivak A, Margolin E, Sviri G, Rajz G, Fraifeld S, Spektor S. Results of endovascular treatment of traumatic intracranial aneurysms. Neurosurgery. 2008;63(3):476–85 ; discussion 485–6. https://doi.org/10.1227/01.NEU.000032499 5.57376.79. Dubey A, Sung WS, Chen YY, Amato D, Mujic A, Waites P, Erasmus A, Hunn A. Traumatic intracranial aneurysm: a brief review. J Clin Neurosci. 2008;15(6):609–12. https://doi.org/10.1016/j.jocn.2 007.11.006. Garg K, Gurjar HK, Singh PK, Singh M, Chandra PS, Sharma BS. Internal carotid artery aneurysms presenting with epistaxis – our experience and review of literature. Turk Neurosurg. 2016;26(3):357–63. https:// doi.org/10.5137/1019-5149.JTN.12598-14.1. Holmes B, Harbaugh RE. Traumatic intracranial aneurysms: a contemporary review. J Trauma. 1993;35(6):855–60. Review Larson PS, Reisner A, Morassutti DJ, Abdulhadi B, Harpring JE. Traumatic intracranial aneurysms. Neurosurg Focus. 2000;8(1):e4. Review Lempert TE, Halbach VV, Higashida RT, Dowd CF, Urwin RW, Balousek PA, Hieshima GB. Endovascular treatment of pseudoaneurysms with electrolytically detachable coils. AJNR Am J Neuroradiol. 1998;19(5):907–11. Renn WH, Rhoton AL Jr. Microsurgical anatomy of the sellar region. J Neurosurg. 1975;43(3):288–98. https:// doi.org/10.3171/jns.1975.43.3.0288. Ronchetti G, Panciani PP, Cornali C, Mardighian D, Villaret AB, Stefini R, Fontanella MM, Gasparotti R. Ruptured aneurysm in sphenoid sinus: which is the best treatment? Case Rep Neurol. 2013;5(1):1–5. https:// doi.org/10.1159/000346347.

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Cavernous Internal Carotid Artery Aneurysm: Exsanguinating Iatrogenic Internal Carotid Artery Injury During Transsphenoidal Surgery for Pituitary Macroadenoma – Packing, Transvenous Coil Occlusion of a Carotid Cavernous Sinus Fistula, and Repair of a Carotid Pseudoaneurysm with a Flow-Diverter Stent José E. Cohen and Ronen R. Leker

Abstract

Transsphenoidal surgery for pituitary adenoma is associated with low rates of morbidity and mortality; however, complications from internal carotid artery (ICA) injury can lead to disability or even death. Patient outcome depends primarily on the ability to recognize and manage these complications promptly. A 22-year-old patient was transferred to our center after massive epistaxis that began during the early stages of a transsphenoidal intervention for a non-secreting pituitary macroadenoma. She presented with headaches, visual disturbance, and moderate hyperprolactinemia (pituitary stalk compression syndrome). Intraoperative hemorrhage was massive and partially controlled with gauze tampons and a nasal Foley catheter. Despite these measures, proptosis

J. E. Cohen (*) Hadassah-Hebrew University Medical Center, Jerusalem, Israel e-mail: [email protected] R. R. Leker Department of Neurology, Hadassah-Hebrew University Medical Center, Jerusalem, Israel e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_75

developed and active epistaxis persisted. After a 30-minute transfer process, the patient was admitted directly to our interventional angiography room. Under general anesthesia, angiography of both ICAs and vertebral arteries (VA) demonstrated a right ICA cavernous pseudoaneurysm, a direct high-flow carotid cavernous sinus fistula (CCF), and a complete circle of Willis. The patient underwent emergent transient balloon occlusion of the injured ICA segment to achieve hemorrhage control, followed by transvenous endovascular coil occlusion of the CCF through the superior and inferior petrosal sinuses with coils and Onyx under intermittent carotid occlusion/protection. She stabilized rapidly and was discharged after 7 days without ophthalmological signs of carotid cavernous sinus fistula. Angiographic follow-up was obtained after 3 weeks, and the right ICA pseudoaneurysm was treated with implantation of a flow-diverter stent. Angiographic follow-up obtained 3 months later confirmed reconstruction of the injured artery with complete exclusion of the pseudoaneurysm. One month later, she underwent further uneventful transsphenoidal surgery for removal of the pituitary tumor. The staged strategy of emergent 87

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hemorrhage control followed by delayed definitive arterial reconstruction with flow-diverter stents as the endovascular management of iatrogenic carotid pseudoaneurysms is the main topic of this chapter. Keywords

Carotid cavernous sinus fistula · Flow-diverter stent · Iatrogenic internal carotid artery dissection · Transvenous route · Pseudoaneurysm

Patient A 22-year-old female patient presented with headaches, progressive visual alterations, and bitemporal hemianopia due to a pituitary macroadenoma. She was transferred from another center after massive hemorrhage due to internal carotid artery (ICA) injury during the early stages of transsphenoidal surgery for macroadenoma resection. Gauze packing and nasal Foley catheter placement partially controlled the active hemorrhage and allowed for emergent patient transfer to a neuroendovascular center.

Diagnostic Imaging Preoperative coronal MR image demonstrates the pituitary macroadenoma (Fig. 1). Our admission head CT-CTA examination showed engorgement of the right cavernous sinus (CS) and associated venous channels (Fig. 2). Bone-windowed images showed the surgical sphenoid sinus access and a metallic clip at the arterial injury site. On diagnostic cerebral angiogram, a carotid cavernous sinus fistula draining primarily through the superior ophthalmic vein, the petrosal sinus, and the pterygoid sinus was seen (Fig. 3).

Treatment Strategy The first goals of treatment were to control the active hemorrhage, preserve the ICA, and occlude the CCF. This was accomplished with balloon

Fig. 1 Preoperative coronal MR image shows a pituitary macroadenoma displacing the optic chiasm

occlusion of the ICA (compliant balloon) and transvenous transpetrosal cavernous sinus occlusion with coils and Onyx. A second intervention was carried out 3 weeks later to reconstruct the injured ICA and exclude the pseudoaneurysm that resulted from the initial injury. This was achieved by flow-diverter stent implantation.

Treatment Procedure #1, 17.09.2015: diagnostic cerebral angiography and transvenous endovascular coil occlusion of a direct CCF with ICA protection Anesthesia: general anesthesia; 4000 IU heparin IV, bolus dose 80–100 IU/kg, target activated coagulation time (ACT) 250–320 s Premedication: none Access: (A) right femoral artery; 6F sheath (Terumo); guiding catheter: Envoy 6F (Cordis); balloon catheter: Hyperglide (Medtronic); microguidewire: Transend 0.01400 (Stryker). (B) right femoral vein; 8F sheath (Terumo); guiding catheter: Guider 8F (Stryker); intermediate catheter: Navien A+ 058 (Medtronic); microcatheter: Echelon-10 (Medtronic) for coils and Onyx Implants: 29 coils: 2 Cosmos18 12/43, 2 Cosmos18 10/36, 2 Cosmos10 8/25, 5 Cosmos10 5/22, 5 Hydrosoft10 5/10, 5 Hydrosoft10 4/10, 8 Hypersoft helical 4/8 (MicroVention); Liquid embolic agent 0.5 cc ethylene vinyl alcohol copolymer (Onyx 18, Medtronic)

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Cavernous Internal Carotid Artery Aneurysm: Exsanguinating Iatrogenic Internal Carotid. . .

Fig. 2 Admission head CT-CTA shows engorgement of the right cavernous sinus and associated venous channels. Sagittal and coronal bone-windowed images show the

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sphenoid sinus surgical access and a metallic clip at the arterial injury site

Fig. 3 Diagnostic angiography of the right internal carotid artery, lateral view, confirmed a carotid cavernous sinus fistula mainly draining through the superior ophthalmic vein, the petrosal sinus, and the pterygoid sinus (source of active nasal hemorrhage)

Course of treatment: the right ICA was catheterized with a 6F guiding catheter. A Hyperglide 415 mm compliant balloon catheter (Medtronic) was placed at the cavernousparaclinoid segment of the ICA, centered on the arterial laceration, and inflated to control the hemorrhage. Heparin was given after balloon inflation when the hemorrhage was controlled. Coaxial guiding and intermediate catheters were telescopically placed at the internal jugular vein, and the intermediate catheter was navigated across the jugular bulb. The microcatheter was navigated through the inferior petrosal sinus (Fig. 4a), and coils were placed at the anterior most aspect of the CS (junction with superior orbital vein). Thereafter, 0.5 cc Onyx 18 was injected. The microcatheter was then navigated through the superior

petrosal sinus (Fig. 4b–c) and placed in a more posterior CS compartment, and Onyx was injected following the same principles. The balloon catheter in the ICA accomplished a double role: rapid control of the hemorrhage at an early stage of the intervention and protection of the ICA lumen during transvenous embolization. The balloon was intermittently inflated and deflated during coiling, and especially during Onyx injection. A total of 29 detachable coils (MicroVention) were implanted. At the end of the intervention, the active hemorrhage was completely controlled, and the high-flow CCF was occluded (Fig. 5). Duration: 1st–31st DSA run: 71 min; fluoroscopy time: 48 min Complications: none Postmedication: analgesics, eye drops

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Fig. 4 Intraprocedural road map image showing anterior CS embolization via the inferior petrosal sinus (a) and posterior CS embolization via the superior petrosal sinus

(b). Radiographic image of trans-superior petrosal sinus embolization during right ICA balloon inflation (c)

Procedure #2, 29.10.2015: cavernous right ICA reconstruction by flow diverter implantation Anesthesia: general anesthesia; 4000 IU heparin IV; target ACT 250–270 s Premedication: 1 100 mg ASA PO, 1 75 mg clopidogrel PO starting 5 days before the intervention Access: right femoral artery; 6F arrow sheath (Arrow); guide catheter: Navien A+ 058 (Medtronic); microcatheter: Excelsior XT-27 (Stryker) for flow diverter and stent implant (Pipeline Flex, Medtronic); microguidewire: Transend 14 (Stryker)

Implant: Pipeline Embolization Device 3.25/ 20 mm (PED, Medtronic) Course of treatment: the microcatheter was placed coaxially at the origin of the right MCA with the aid of a guidewire in the M2 segment (Fig. 6a), and a Pipeline flow diverter stent was initially deployed. The catheters were then repositioned more proximally, and the Pipeline was completely deployed at the right cavernous ICA, centered on the site of the arterial injury and covering the ostium of the pseudoaneurysm. The microcatheter was then navigated through the implanted stent to improve wall apposition. No

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Cavernous Internal Carotid Artery Aneurysm: Exsanguinating Iatrogenic Internal Carotid. . .

significant changes were detected in the opacification of the pseudoaneurysm immediately. Duration: 1st–9th DSA run: 22 min; fluoroscopy time: 15 min

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Complications: none Postmedication: 1 100 mg ASA PO daily for 1 year, 1 75/37.5 mg clopidogrel on alternating days for 4 months

Clinical Outcome

Fig. 5 Immediate post-embolization angiography confirmed occlusion of the CCF, achieving clinical control of hemorrhage as well as the anterior cavernous ICA pseudoaneurysm. Antegrade hemispheric supply was regained

Fig. 6 Angiographic control (right ICA, oblique view) obtained 3 weeks after embolization of the carotid cavernous fistula, showing persistent occlusion of the fistula and the cavernous right ICA pseudoaneurysm (a). The angiographic image was taken immediately after gaining distal

Immediately after the first endovascular procedure, the patient was extubated and was noted to have normal conjunctiva and sclera, without injection or chemosis. There was no palpable thrill or bruit on auscultation over either eye. Her visual acuity and extraocular movements were unchanged. She was discharged home after 7 days. She was readmitted 3 weeks later for follow-up angiography and then underwent a second interventional procedure for ICA reconstruction by means of flow diverter implantation. She was discharged home 4 days after the second procedure and was able to return to teaching on her normal schedule. Neurological and neuro-ophthalmological examinations were unremarkable.

guidewire positioning at M2 and before navigation of the Excelsior XT-27 microcatheter. Immediate angiographic image (right ICA, lateral view) obtained after flow diverter stent implantation (b)

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Fig. 7 Angiograms obtained 3 months after flow diverter stent implantation (a). Right ICA on magnified oblique view, lateral view (b), and magnified lateral view (c). The

reconstructed artery showed no signs of residual arterial pseudoaneurysm, arterial defect, or in-stent stenosis

Follow-Up Examinations

Discussion

NCCT and angiography 3 months later confirmed arterial reconstruction with no residual pseudoaneurysm or carotid cavernous fistula (Fig. 7). One month later, the patient underwent uneventful transsphenoidal removal of the pituitary macroadenoma while on aspirin. Follow-up angiography 18 months later showed stable angiographic findings and no signs of in-stent stenosis.

Iatrogenic injury of the ICA leading to hemorrhage is one of the most severe complications associated with transsphenoidal pituitary surgery. Raymond et al. (1997) reported that arterial injuries during or after such surgery occurred in about 1% of cases and were associated with significant morbidity (24%) and mortality (14%). Injury to the vessel wall may lead to epistaxis and

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Cavernous Internal Carotid Artery Aneurysm: Exsanguinating Iatrogenic Internal Carotid. . .

intracranial hemorrhage, including SAH and/or intraventricular hemorrhage. This potentially fatal complication can result in severe peri- or postoperative bleeding, the development of a false aneurysm of the ICA, and carotid cavernous sinus fistula (CCF). Immediate diagnosis and prompt treatment of these complications is essential to prevent a poor outcome. Emergent measures include carotid manual compression (e.g., by the anesthesiologist), hemostatic maneuvers, and mechanical tamponade. The endovascular options described in the literature include deconstructive techniques (i.e., carotid sacrifice in patients with adequate collaterals). Parent artery occlusion with detachable balloons or coils is traditionally considered the safest and most durable treatment for arterial injuries. However, a functionally incomplete circle of Willis may not allow carotid sacrifice, particularly in the acute phase. Transient balloon occlusion is generally performed with clinical and angiographic assessment, with or without hypotensive challenge and EEG recording. However, delayed ischemic events have been reported in 5–20% of patients who initially tolerated transient balloon occlusion (Kadyrov et al. 2002) and after reconstructive techniques based on cavernous sinus embolization (balloons, coils, Onyx) and arterial reconstruction by means different stents, or both. For cavernous sinus obliteration, coils and Onyx (Medtronic) are frequently used (Barry et al. 2011; Benndorf et al. 2000). To avoid compartmentalization, embolization with coils was started in the most anterior compartment while moving the microcatheter gradually posteriorly, thus allowing complete obliteration of the cavernous sinus. Onyx permeates and occludes the sinus and the coil interstices. In our case, the emergent goal was to control the active hemorrhage, to seal the communication between the ICA and the cavernous sinus, and subsequently to repair the injured artery using a flow diverter. Flow diverter stents are a new class of low-porosity, self-expanding, stent-like devices, specifically designed for the

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endovascular management of select intracranial aneurysms previously considered untreatable by conventional techniques. The use of flow diverter stents as a treatment option for carotid injuries and direct carotid cavernous fistulas in general and post-transsphenoidal surgery has been described infrequently (Iancu et al. 2015; Wendl et al. 2017).

Therapeutic Alternatives Parent Vessel Occlusion Stent Graft Telescoping Stents

References Barry RC, Wilkinson M, Ahmed RM, Lim CS, Parker GD, McCluskey PJ, Halmagyi GM. Interventional treatment of carotid cavernous fistula. J Clin Neurosci. 2011;18(8):1072–9. https://doi.org/10.1016/ j.jocn.2010.12.026. Benndorf G, Bender A, Lehmann R, Lanksch W. Transvenous occlusion of dural cavernous sinus fistulas through the thrombosed inferior petrosal sinus: report of four cases and review of the literature. Surg Neurol. 2000;54(1):42–54. Iancu D, Lum C, Ahmed ME, Glikstein R, Dos Santos MP, Lesiuk H, Labib M, Kassam AB. Flow diversion in the treatment of carotid injury and carotid-cavernous fistula after transsphenoidal surgery. Interv Neuroradiol. 2015;21(3):346–50. https://doi.org/10. 1177/1591019915582367. Kadyrov NA, Friedman JA, Nichols DA, Cohen-Gadol AA, Link MJ, Piepgras DG. Endovascular treatment of an internal carotid artery pseudoaneurysm following transsphenoidal surgery. Case report. J Neurosurg. 2002;96(3):624–7. https://doi.org/10. 3171/jns.2002.96.3.0624. Raymond J, Hardy J, Czepko R, Roy D. Arterial injuries in transsphenoidal surgery for pituitary adenoma; the role of angiography and endovascular treatment. AJNR Am J Neuroradiol. 1997;18(4):655–65. Wendl CM, Henkes H, Martinez Moreno R, Ganslandt O, Bäzner H, Aguilar Pérez M. Direct carotid cavernous sinus fistulae: vessel reconstruction using flowdiverting implants. Clin Neuroradiol. 2017;27 (4):493–501. https://doi.org/10.1007/s00062-0160511-6.

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Cavernous Internal Carotid Artery Aneurysm: Large Cavernous Carotid Artery Aneurysm Causing Compression of the Internal Carotid Artery in a Young Woman with EhlersDanlos Syndrome with Segmental Dissections of the Carotid and Vertebral Arteries; Complete Reconstruction of the Internal Carotid Artery with Five Pipeline Embolization Devices; Complete Aneurysm Resolution and Good Clinical Outcome Carlos Bleise, Rene Viso, Ivan Lylyk, Jorge Chudyk, and Pedro Lylyk

Abstract

A 47-year-old female presented with intense headaches and oculomotor, trochlear, and abducens nerve palsy. A dissecting internal carotid artery (ICA) cavernous aneurysm associated with a dissection of the left proximal M1 segment from the proximal segment of the left ICA as well as segmental dissections of the right-hand ICA and both vertebral arteries was found. The cavernous ICA aneurysm associated with the dissection of the left ICA was treated by the endovascular implantation of

five Pipeline Embolization Device (PED) flow diverters with good angiographic and clinical outcome. Placing flow diverter stents in a dissected artery allows the lacerated vessel segment to reconstruct. Vascular EhlersDanlos syndrome and its cerebrovascular complications is the main topic of this chapter, together with using flow diversion to treat dissected vessel segments in an acute setting. Keywords

Internal carotid artery · Flow diverter · EhlersDanlos syndrome · Telescoping flow diverters · Carotid cavernous aneurysm · Carotid artery dissection

C. Bleise · R. Viso · I. Lylyk · J. Chudyk · P. Lylyk (*) Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina e-mail: [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_129

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Patient

Treatment

A 47-year-old female patient with a family history of cerebral aneurysms, who presented with thunderclap headache and oculomotor, trochlear, and abducens nerve palsy during a vacation abroad.

Procedure, 15.10.2017: endovascular reconstruction of the left intracranial internal carotid artery with telescoping flow diverters and endovascular treatment of a dissecting carotid cavernous aneurysm Anesthesia: general anesthesia; 10,000 IU unfractionated heparin (Riveparin, Ribero) IV Premedication: 1
100 mg ASA (Aspirin, Bayer Vital) daily for 3 days prior intervention Access: right femoral artery, 8F sheath (Terumo); guide catheter: 6F Shuttle (Cook) and Navien A+ 058 (Medtronic); microcatheters: Excelsior SL-10 (Stryker), Marksman 0.02700 (Medtronic); microguidewire: Synchro2 0.01400 (Stryker), Chikai Black 0.01400 (Asahi Intecc), Transend 0.01400 300 cm (Stryker) Implants: 5
Pipeline Embolization Device (PED) – 3.25/20 mm, 3.5/20 mm, 4.5/20 mm, 4/30 mm, 5/35 mm (Medtronic) Balloon: Minitrek 1.5/12 mm (Abbott) Course of treatment: After the diagnostic DSA, the left ICA was catheterized with a 6F Shuttle catheter. The ICA was then catheterized with an Excelsior SL-10 microcatheter over a Synchro2 0.01400 microguidewire. After several failed attempts to pass the aneurysm neck, the Synchro2 microguidewire was replaced by a Chikai Black 0.01400 microguidewire. The aneurysm neck was crossed, and the microcatheter was placed into the left MCA (M1 segment). The Excelsior SL-10 was removed over a Transend 0.01400 300 cm microguidewire, and a Marksman 0.02700 microcatheter was placed in the first third of the M1 segment. After the placement of said microcatheter, a DSA with contrast medium injection through the microcatheter was done to confirm the patency of the MCA. A Pipeline Embolization Device (PED) 3.5/ 20 mm was inserted and deployed from the left proximal M1 segment to the distal supraclinoid segment of the ICA. After deploying the first PED, the reconstruction of the ICA was carried out by telescopically placing another four PEDs from distal to proximal (3.5/20 mm, 4.5/20 mm, 4/30 mm, 5/35 mm). The subsequent DSA revealed a partial opening of the distal PED. A Mini Trek balloon catheter was inserted into the

Diagnostic Imaging On a non-contrast CT (NCCT), a hyperdense mass with erosion of the sphenoidal bone and the dorsum sellae was seen. On CT angiography (CTA), a partially thrombosed carotid cavernous aneurysm was diagnosed. Subsequent evaluation of the aneurysm by MRI and MRA was done. On axial T2WI and contrast-enhanced T1WI MRI, the thrombosed portion of the aneurysm was better visible. On the TOF MRA, slow blood flow from the left ICA could be seen, although the supraclinoid carotid artery was not shown. In the subsequent DSA examination, poor filling of the left ICA beyond the cavernous segment was seen, attributed to both compression from the partially thrombosed aneurysm to the left ICA and segmental dissection (similar to fibromuscular dysplasia) of the left cervical and supraclinoid ICA. Injecting contrast medium into the right-hand ICA revealed similar segmental dissections in the cervical segment of said artery. The right-hand intracranial ICA was supplying the left anterior circulation via the anterior communicating artery (AcomA). However, a significant delay of the arterial phase of the left anterior circulation was obvious. Injecting contrast into both vertebral arteries also revealed segmental dissections (Fig. 1).

Treatment Strategy The aims of the treatment were to prevent further growth of the cavernous aneurysm and to reduce the mass effect of the cavernous ICA aneurysm on the adjacent cranial nerves. Given the segmental dissections of the right ICA and of both VAs, preserving the patency of left ICA was deemed crucial in order to maintain the brain supply and to avoid future ischemic events. Both ICAs and VAs appeared fragile as well as thrombogenic.

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Fig. 1 (continued)

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Fig. 1 Diagnostic imaging in a female patient presenting with sudden-onset severe headache and oculomotor, trochlear, and abducens nerve palsy. NCCT shows a hyperdense mass with erosion of the sphenoidal bone and the dorsum sellae (a). On CTA a partially thrombosed carotid cavernous aneurysm becomes visible (b). T2WI axial MRI shows the intra-aneurysmal thrombus with heterogeneous signal intensity (c) with contrast enhancement of the aneurysm wall on the axial post-gadolinium T1WI (red arrow (d)). No arterial blood flow is visible on TOF MRA in the left ICA distal to the aneurysm, with preserved flow in the left ACA and MCA (e). DSA in posterior-anterior (f) and

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lateral (g) projection showing dysplasia of the left ICA with a partially thrombosed carotid cavernous aneurysm and reduced flow in the supraclinoid ICA and the MCA. The cervical segment of the right ICA shows multiple focal dissections, similar to “fibromuscular dysplasia” (lateral projection (h)). The left anterior circulation has some collateral supply from the right ICA via the anterior communicating artery (i) as well as through the posterior communicating artery (not shown). Both vertebral arteries share similar features to both the ICAs with multiple segmental dissections

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Cavernous Internal Carotid Artery Aneurysm: Large Cavernous Carotid Artery Aneurysm. . .

distal ICA, and angioplasty of the most distal PED was carried out. DSA then confirmed that the reconstruction of the ICA was complete and that there were both reduced flow inside the aneurysm and significant improvement of the distal flow in the left ICA and MCA (Fig. 2). Duration: 1st–30th DSA run: 130 min; fluoroscopy time: 60 min Complications: none Postmedication: 1
100 mg ASA PO daily for life and 1
10 mg prasugrel PO daily for 1 year

Clinical Outcome The procedure was well tolerated, and the patient was discharged home 5 days later. The cranial nerve palsies partially resolved during the following months although diplopia persisted.

Follow-Up Examinations Cranial MRI performed 6 months after the endovascular procedure showed shrinkage of the cavernous aneurysm and a change of the signal characteristics of the intra-aneurysmal thrombus. Follow-up DSA at 12 months showed a complete reconstruction of the left ICA with a minor neck remnant of the cavernous aneurysm and normalized distal flow in the left MCA and the ACA. Genetic studies for connective tissue disorders were carried out. A mutation in the COL3A1 coordinates NM_000090.3:c.952G > T Cp.(Gly318Cys) was detected, in line with the diagnosis of the vascular type of the Ehlers-Danlos syndrome. This genetic disorder causes a generalized fragility of arteries and is notorious for a high rate of vascular complications in catheter angiography. Therefore, no further follow-up DSA examinations were carried out. The 1-year follow-up MRI in October 2018 did not show any other manifestations of this

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disease, and the patient is scheduled for annual follow-up MRI/MRA examinations (Fig. 3).

Discussion Ehlers-Danlos Syndrome (EDS) is a clinically and genetically heterogeneous group of disorders secondary to alteration in collagen metabolism, with an estimated prevalence of 1:500 to 1:250.000 births (Germain 2007). This alteration is characterized by friable soft connective tissues manifesting with alteration in the skin, ligaments, joints, blood vessels, and organs. Clinical manifestations include hyperextensibility of the skin, hypermobility of joints, atrophic scar formation after superficial injury, and premature rupture of membrane during pregnancy; however the clinical findings depend on the subtype of EDS (Eagleton 2016). EDS classification is based on the clinical characteristics and the genetic defect (Malfait et al. 2017) and summarized in Table 1. The main clinical characteristics of the classic EDS are present in varying degrees in each subtype of EDS, and the most common feature is skin hyperextensibility. However, this is not seen in the vascular type. Vascular EDS is an autosomal dominant defect in type III collagen synthesis and represents about 5% of all EDS cases (Bergqvist et al. 2013). The patients are at risk of arterial dissection, rupture, and aneurysm formation with a reduced median life expectancy of 40–50 years only due to the vascular complication (Pepin et al. 2000). In patients with vascular complications associated with the EDS, several technical considerations have to be taken into account. The extreme fragility of the vessels is the underlying reason for further damage from medical procedures. In general, vascular clamps should be avoided because they may induce vessel transection. The use of endovascular balloon catheters can cause a vessel rupture. Bergqvist et al. (2013) reported on a total of 231 EDS patients. Half of

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Fig. 2 (continued)

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Fig. 2 Treatment of a dissecting carotid cavernous aneurysm attributed to an ICA dissection in a patient with Ehlers-Danlos syndrome with endovascular reconstruction of the left ICA. After inserting the microcatheter into the left M1 segment, contrast medium injection confirmed the position of this microcatheter in the true lumen of the left MCA/M1 (a). The first PED 3.5/20 mm was deployed from the M1 segment to the distal supraclinoid ICA (b).

The endovascular reconstruction of the left ICA was continued toward the cervical segment, finishing with a PED 5/35 mm (c). A DSA run showed the complete reconstruction of the ICA (d). VasoCT confirmed the complete opening and correct wall apposition of the five PEDs (e). DSA eventually showed the improved blood flow to the left MCA and the dependent vessels (posterior-anterior projection (f)

these patients had aneurysms, and one third presented with spontaneous arterial rupture in the absence of an aneurysm. Open surgical repair was done in 44 patients with a mortality of 30%. Endovascular procedures were performed in 33 patients with a mortality rate of 24%. The complications in the surgical group were caused by intra- or postoperative bleedings. The complications of the endovascular group occurred at sites remote from the intervention. Oderich et al. (2005) reported on 31 patients with vascular EDS, observed during 30 years (1971–2001). An angiography was performed in 42% of these patients (in 70% performed on an

emergency basis), with a complication rate of 23% and with a mortality rate of 20%. In the series of Brooke et al. (2010), 40 patients with EDS had a total of 45 endovascular procedures, and 18 underwent open surgical procedures. The 5and 10-year survival rate free of complications was 54% and 42%, respectively. However, only three of these patients had a vascular type of EDS. In the report by Cikrit et al. (1987), complications associated with angiographic procedures caused a morbidity of 67% and a mortality of 10%. The disease frequently involves the proximal branches of the aortic arch, the descending thoracic aorta, and the abdominal aorta (Germain

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Fig. 3 (continued)

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Fig. 3 Follow-up MRI 6 months after the treatment of a dissecting aneurysm of the left cavernous ICA with 5 PEDs. Axial T2WI showed an increase of the signal intensity of the aneurysm (a). On post-contrast T1WI, no contrast medium accumulation of the aneurysm was seen (b). The image quality of TOF MRA was impaired due to an artifact, but no supraclinoid mass was seen, with normal signal intensity in the MCA and ACA (c). At the 12-month follow-up MRI (d), the axial T2WI showed a decreased thrombus signal with normal signal intensity in the TOF

MRA (e). A 1-year follow-up DSA showed adequate distal flow in the MCA with complete reconstruction of the supraclinoid ICA and a small neck remnant of the cavernous aneurysm (f). The left cervical, petrous, and cavernous ICA was well reconstructed (g). VasoCT showed adequate apposition of the PEDs to the left ICA (h, i). 3D DSA showed the adequate vascular diameter of the complete ICA with a small neck remnant of the cavernous aneurysm (j)

2007). Possible cerebrovascular manifestations include carotid cavernous sinus fistulae, dissections of the vertebral and the carotid arteries in their extra- and intracranial segments, and intracranial aneurysms (Schievink 2004). In a report by Pepin et al. (2000), 11% of patients with EDS type IV presented with cerebrovascular complications (six carotid cavernous sinus fistulae, four intracranial aneurysms, four intracranial hemorrhages suspected to be due to intracranial aneurysms, four spontaneous internal carotid artery or vertebral artery dissections, and one suspected vertebral artery dissection). The most frequent location of the intracranial aneurysm formation is the cavernous segment of the ICA (Kim et al. 2016). North et al. (1995) reviewed the clinical data of 202 individuals with EDS type IV. A total of 19 patients presented with neurovascular complications, including 6 patients with carotid cavernous sinus fistulae, 4 ruptured intracranial

aneurysms, and 4 intracranial hemorrhage of uncertain etiology. Incidentally discovered, unruptured intracranial aneurysms are generally managed conservatively because of the extremely fragile arteries. Sultan et al. (2002) reported the case of a 46-year-old patient with an extracranial vertebral artery aneurysm, treated with a common carotid artery to V3 bypass, using reversed saphenous vein graft with incidental avulsion of the V2 segment of the vertebral artery. Since no proximal flow control was achieved, endovascular coil occlusion of the vertebral artery was required to control the bleeding with complete postoperative recovery of the patient. Schievink et al. (2002) reported on four patients with EDS who underwent open surgery. One patient died as a direct result of the operation. The incidence of cervical carotid and vertebral artery dissection in EDS patients has been

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Table 1 Classification of the EDS EDS type Classic (I/II)

Genetic defect COL5A1/COL5A2

Protein affect Procollagen type V

Hypermobility (III)

Not known

Not known

Vascular (IV)

COL3A1

Procollagen type III

Kyphoscoliosis (VI)

PLOD1

Lysyl-hydroxylase-1

Arthrochalasia (VII a,b) Dermatosparaxis (VIIc)

COL1A1/COL1A2 COL1A1/COL1A2

Familial joint hypermobility syndrome Tenascin X deficiency

Not known

Procollagen type I Procollagen N-peptidase Not known

TNX-B

Tenascin-X

EDS progeroid form

4GALT

Galactosyltransferase I

EDS cardiac valvular form

COL1A2

Deficiency of a2

Vascular like

COL1A1

Procollagen type I

addressed in only a few studies. Brandt et al. (2001) reported on 65 patients with non-traumatic spontaneous cervical artery dissection. Skin biopsies were done on a total of 36 patients with connective tissue alterations found compatible with EDS type II or III. In a previous report on 25 patients with non-traumatic cervical dissection, 68% of the abnormalities were associated with EDS type II or III (Brandt et al. 1998). An internal carotid artery occlusion due to a giant cavernous carotid artery aneurysm is infrequently reported in the literature. Whittle et al. (1982) reported on a patient with ophthalmoplegia and proptosis with unilateral headache due to a thrombosed cavernous ICA aneurysm and occlusion of the same ICA. The patient underwent microsurgery. Opening the aneurysm and removing the clot resulted in no improvement in the ophthalmoplegia. In a review by Sastri et al. (2013), two patients with ICA occlusion due to cavernous ICA aneurysms were presented, and a

Clinical manifestation Skin and joint hypermobility, atrophic scars, easy bruising Joint hypermobility and dislocations Joint pain Thin skin. Arterial, hollow organ, and uterine rupture, small joint hyperextensibility Hypotonia, joint laxity, congenital scoliosis, and ocular fragility Severe joint hypermobility and scoliosis Severe skin fragility, cutis laxa, and easy bruising Joint hypermobility with the absence of skin hyperextensibility and atrophic scarring, excluding type I EDS Joint hypermobility and skin hyperextensibility; increased risk of postpartum hemorrhage Progeroid appearance, curly and fine hair, and periodontitis Joint hypermobility, skin hyperextensibility, and cardiac valvular defects Classic EDS presentation with propensity for arterial rupture in adulthood

total of 15 cases from the literature were reviewed. The majority had ophthalmoparesis, facial pain, or hypoesthesia. Several pathomechanisms have been proposed in order to explain the ICA occlusion: (1) direct stretching and compression of the ICA by the giant aneurysm (Whittle et al. 1982), (2) a proximal propagation of the intramural thrombus (Inagawa 1991), or (3) compression of the ICA against the anterior clinoid process (Perrini et al. 2005). In the report of Sastri et al. (2013), the authors recommended the clinical and radiological follow-up in patients who are not acutely or severely symptomatic. The risk of ischemia is below 1% per patient year (Kupersmith et al. 2002). The term matricidal carotid artery aneurysm refers to carotid cavernous aneurysms that cause external compression and stenosis of the adjacent ICA. In a multicenter retrospective case series of Dacus et al. (2019), flow diversion was the most commonly attempted single treatment modality used to treat those aneurysms (20/40 patients) with a treatment failure rate

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of 30%. The parent vessel occlusion in 12 patients (4 with bypass and 8 without bypass) had a failure rate of 17%. Coil occlusion was carried out in seven patients with a failure rate of 29%. Three patients died, and two patients clinically deteriorated. The morbidity and mortality rates were 5.4% and 7.5%, respectively. The medical management of traumatic cervical ICA dissections with anticoagulation or antiplatelet therapy yields good clinical outcomes in 75% of cases with a complete recanalization rate of 50%. In a subset of patients, however, the dissection will progress despite the medical therapy (Amuluru et al. 2017). Endovascular treatment is indicated after failure of conservative management (e.g., progressive pseudoaneurysm enlargement, acute hemodynamic infarcts). A wide variety of stents have been used to open and reconstruct the dissected segment of the ICA. The usage of dedicated carotid stents for that purpose can be technically challenging due to the rigidity of the stent delivery system. These stents can be used for proximal ICA dissections. For the petrous segment of the ICA and beyond, self- expanding stents for assisted coiling (e.g., Neuroform; Stryker) have been used prior to the availability of flow diverters (Ecker et al. 2007). Both the radial force and the hemodynamic effect of these stents may be insufficient to both keep the dissected vessel patent and to obliterate the aneurysm. Coronary balloon expandable stents have been used successfully to prevent vessel occlusion. Their wall apposition in dissected arteries is, however, poor after the resolution of the intramural hematoma. Flow diverter stents (e.g., PED, Medtronic; p64, phenox) combine advantageous flexibility, sufficient radial force, good wall apposition, and high coverage. They have become the preferred device for the endovascular treatment of dissecting ICA aneurysms (Brzezicki et al. 2016). When a flow diverter is implanted into an acutely dissected artery, the vessel is narrow due to the intramural hematoma. The resulting vessel diameter once this hematoma is resolved is impossible to predict. A potential issue in the treatment of ICA dissections with flow diverter stents is the migration of the implanted device (Amuluru et al. 2017). Brzezicki et al. (2016) treated 11 patients

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with 9 traumatic and 4 spontaneous high cervical and skull base ICA dissections with the PED. They achieved complete revascularization in 91% of the treated vessels, and 75% of the aneurysms were completely obliterated at follow-up. One PED was found partially collapsed without neurological sequelae.

Therapeutic Alternatives Extra-Intracranial Bypass Parent Vessel Occlusion Telescoping Stents

References Amuluru K, Al-Mufti F, Roth W, Prestigiacomo CJ, Gandhi CD. Anchoring pipeline flow diverter construct in the treatment of traumatic distal cervical carotid artery injury. Interv Neurol. 2017;6(3–4):153–62. https://doi. org/10.1159/000457836. Bergqvist D, Björck M, Wanhainen A. Treatment of vascular Ehlers-Danlos syndrome: a systematic review. Ann Surg. 2013;258(2):257–61. https://doi.org/ 10.1097/SLA.0b013e31829c7a59. Brandt T, Hausser I, Orberk E, Grau A, Hartschuh W, Anton-Lamprecht I, Hacke W. Ultrastructural connective tissue abnormalities in patients with spontaneous cervicocerebral artery dissections. Ann Neurol. 1998;44(2):281–5. https://doi.org/10.1002/ana.41044 0224. Brandt T, Orberk E, Weber R, Werner I, Busse O, Müller BT, Wigger F, Grau A, Grond-Ginsbach C, Hausser I. Pathogenesis of cervical artery dissections: association with connective tissue abnormalities. Neurology. 2001;57(1):24–30. Brooke BS, Arnaoutakis G, McDonnell NB, Black JH 3rd. Contemporary management of vascular complications associated with Ehlers-Danlos syndrome. J Vasc Surg. 2010;51(1):131–8; discussion 138–9. https://doi.org/ 10.1016/j.jvs.2009.08.019. Brzezicki G, Rivet DJ, Reavey-Cantwell J. Pipeline embolization device for treatment of high cervical and skull base carotid artery dissections: clinical case series. J Neurointerv Surg. 2016;8(7):722–8. https://doi.org/ 10.1136/neurintsurg-2015-011653. Cikrit DF, Miles JH, Silver D. Spontaneous arterial perforation: the Ehlers-Danlos specter. J Vasc Surg. 1987; 5(2):248–55. Dacus MR, Nickele C, Welch BG, Ban VS, Ringer AJ, Kim LJ, Levitt MR, Lanzino G, Kan P, Arthur AS; Endovascular Neurosurgery Research Group (ENRG). Matricidal cavernous aneurysms: a multicenter case

106 series. J Neurointerv Surg. 2019; pii: neurintsurg-2018014562. https://doi.org/10.1136/neurintsurg-2018014562. Eagleton MJ. Arterial complications of vascular EhlersDanlos syndrome. J Vasc Surg. 2016;64(6):1869–80. https://doi.org/10.1016/j.jvs.2016.06.120. Ecker RD, Levy EI, Hopkins LN. Acute Neuroform stenting of a symptomatic petrous dissection. J Invasive Cardiol. 2007;19(5):E137–8. Germain DP. Ehlers-Danlos syndrome type IV. Orphanet J Rare Dis. 2007;2:32. https://doi.org/10.1186/17501172-2-32. Review. PubMed PMID: 17640391 Inagawa T. Follow-up study of unruptured aneurysms arising from the C3 and C4 segments of the internal carotid artery. Surg Neurol. 1991;36(2):99–105. Kim ST, Brinjikji W, Lanzino G, Kallmes DF. Neurovascular manifestations of connective-tissue diseases: a review. Interv Neuroradiol. 2016;22(6): 624–37. https://doi.org/10.1177/1591019916659262. Kupersmith MJ, Stiebel-Kalish H, Huna-Baron R, Setton A, Niimi Y, Langer D, Berenstein A. Cavernous carotid aneurysms rarely cause subarachnoid hemorrhage or major neurologic morbidity. J Stroke Cerebrovasc Dis. 2002;11(1):9–14. https://doi.org/ 10.1053/jscd.2002.123969. Malfait F, Francomano C, Byers P, Belmont J, Berglund B, Black J, Bloom L, Bowen JM, Brady AF, Burrows NP, Castori M, Cohen H, Colombi M, Demirdas S, De Backer J, De Paepe A, FournelGigleux S, Frank M, Ghali N, Giunta C, Grahame R, Hakim A, Jeunemaitre X, Johnson D, JuulKristensen B, Kapferer-Seebacher I, Kazkaz H, Kosho T, Lavallee ME, Levy H, Mendoza-Londono R, Pepin M, Pope FM, Reinstein E, Robert L, Rohrbach M, Sanders L, Sobey GJ, Van Damme T, Vandersteen A, van Mourik C, Voermans N, Wheeldon N, Zschocke J, Tinkle B. The 2017 international classification of the Ehlers-Danlos syndromes. Am J Med Genet C Semin Med Genet. 2017;175(1):8–26. https://doi.org/ 10.1002/ajmg.c.31552.

C. Bleise et al. North KN, Whiteman DA, Pepin MG, Byers PH. Cerebrovascular complications in Ehlers-Danlos syndrome type IV. Ann Neurol. 1995;38(6):960–4. https://doi.org/10.1002/ana.410380620. Oderich GS, Panneton JM, Bower TC, Lindor NM, Cherry KJ, Noel AA, Kalra M, Sullivan T, Gloviczki P. The spectrum, management and clinical outcome of EhlersDanlos syndrome type IV: a 30-year experience. J Vasc Surg. 2005; https://doi.org/10.1016/j.jvs.2005.03.053. Pepin M, Schwarze U, Superti-Furga A, Byers PH. Clinical and genetic features of Ehlers-Danlos syndrome type IV, the vascular type. N Engl J Med. 2000;342(10): 673–80. Erratum in: N Engl J Med 2001 Feb 1;344 (5):392. https://doi.org/10.1056/NEJM200003093421001. Perrini P, Bortolotti C, Wang H, Fraser K, Lanzino G. Thrombosed giant intracavernous aneurysm with subsequent spontaneous ipsilateral carotid artery occlusion. Acta Neurochir. 2005;147(2):215–6; discussion 216–7. https://doi.org/10.1007/s00701-004-0403-4. Sastri SB, Sadasiva N, Pandey P. Giant cavernous carotid aneurysm with spontaneous ipsilateral ICA occlusion: report of 2 cases and review of literature. J Neurosci Rural Pract. 2013;4(Suppl 1):S113–6. https://doi.org/ 10.4103/0976-3147.116439. Schievink WI, Link MJ, Piepgras DG, Spetzler RF. Intracranial aneurysm surgery in Ehlers-Danlos syndrome type IV. Neurosurgery. 2002;51(3):607–11; discussion 611–3. Schievink WI. Cerebrovascular involvement in EhlersDanlos syndrome. Curr Treat Options Cardiovasc Med. 2004;6(3):231–6. Sultan S, Morasch M, Colgan MP, Madhavan P, Moore D, Shanik G. Operative and endovascular management of extracranial vertebral artery aneurysm in Ehlers-Danlos syndrome: a clinical dilemma–case report and literature review. Vasc Endovasc Surg. 2002;36(5):389–92. https://doi.org/10.1177/153857440203600510. Whittle IR, Williams DB, Halmagyi GM, Besser M. Spontaneous thrombosis of a giant intracranial aneurysm and ipsilateral internal carotid artery. Case report. J Neurosurg. 1982;56(2):287–9. https://doi.org/10. 3171/jns.1982.56.2.0287.

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Cavernous Internal Carotid Artery Aneurysm: Giant Posttraumatic Carotid Cavernous Pseudoaneurysm, Presenting with Epistaxis; Treated in Two-Stage Strategy with Complete Occlusion and Delayed Coil Extrusion Through the Nostril Ivan Lylyk, Rene Viso, Esteban Scrivano, Javier Lundquist, and Pedro Lylyk Abstract

Keywords

A giant, wide-necked pseudoaneurysm of the cavernous internal carotid artery (ICA) was found in a 17-year-old male patient who had suffered a high impact car accident. Four months after the accident, he presented with diplopia and facial pain associated with severe epistaxis. Coil occlusion of the aneurysm was performed and stopped the bleeding. One week later, a control DSA was carried out. Recanalization of the aneurysm due to coil compaction was observed, for which a Pipeline Embolization Device was implanted. The patient had a complete clinical recovery, and follow-up examinations confirmed aneurysm occlusion. Two years later, he presented to the emergency department with a coil protruding through his nostril. The actions taken following this event are explained below. The management of posttraumatic cavernous ICA aneurysms is the main topic of this chapter.

Cavernous internal carotid artery · Posttraumatic aneurysm · Epistaxis · Coil occlusion · Coil compaction · Flow diversion

I. Lylyk (*) · R. Viso · E. Scrivano · J. Lundquist · P. Lylyk Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina e-mail: [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_167

Patient A 17-year-old male patient with no relevant medical history suffered a car accident with severe head trauma and multiple skull fractures. Four months after the car accident, the patient presented with diplopia and facial pain. Severe epistaxis appeared 24 h before the arrival to the emergency department.

Diagnostic Imaging A noncontrast cranial computed tomography (NCCT) showed a giant erosive dense mass in the skull base with the destruction of the sphenoidal sinus, ethmoidal cells, and the internal wall of the orbit. Mass effect was being exerted on the medial rectus muscle. On the NCCT, the superior wall of the frontal sinus and orbit floor were fractured. Digital subtraction angiography (DSA) was carried out, showing a giant carotidcavernous pseudoaneurysm of 27
25 mm diameter with a wide neck of 8 mm (Fig. 1). 107

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Fig. 1 Diagnostic imaging in a young male patient 4 months after severe head trauma. NCCT with coronal (a, b), sagittal (c), and axial (d, e) reconstructions showed fractures of the left orbital floor, the superior wall of the left frontal sinus (red circles), erosion of the sphenoidal sinus and ethmoidal cells with a dense mass, and compression of

the medial components of the orbit (d, e). DSA showed a giant carotid-cavernous pseudoaneurysm with 27
25 mm diameter with a wide neck of 8 mm (posterior-anterior view (f), lateral view (g), 3D reconstruction of a rotational DSA (h))

Treatment Strategy

Treatment

The primary goal of the treatment was to stop the epistaxis and decrease the mass effect. Due to the acute bleeding from the pseudoaneurysm, initial coil occlusion was performed, and endovascular repair of the carotid artery was planned for a second treatment session using flow diversion.

Procedure #1, 23.08.2010: endovascular coil occlusion of the carotid-cavernous pseudoaneurysm with coil occlusion Anesthesia: general anesthesia: 10,000 IU unfractionated heparin (Riveparin, Rivero) IV Premedication: none

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Cavernous Internal Carotid Artery Aneurysm: Giant Posttraumatic Carotid Cavernous. . .

Access: right femoral artery, 7F sheath (Terumo); guide catheter: 6F Envoy (Codman); microcatheter: Tracker Excel-14 (Boston Scientific); microguidewire: Transend 0.01400 (Stryker) Implants: 18 coils: 3
Microcoil GDC -18 360 Standard 24/40, 3
Microcoil GDC -18 360 Standard 22/40, 7
Microcoil GDC -18 360 Standard 20/33, 2
Microcoil GDC -18 360 Standard 18/40, 1
Microcoil GDC -18 2D 18/30, 1
Microcoil GDC -18 2D 16/30, 1
Microcoil GDC -18 360 Standard 14/30 (then Boston Scientific, now Stryker) Course of treatment: The left internal carotid artery was catheterized with a 6F Envoy catheter. A Tracker Excel-14 microcatheter with a 0.01400 microwire was navigated inside the pseudoaneurysm sac. Then, conventional coil occlusion was successfully carried out (Fig. 2). Duration: 1st – 14th DSA run: 79 min; fluoroscopy time: 51 min. Complications: none Postmedication: none

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Follow-Up Examinations Follow-up MRI and DSA examinations were done 7 days after the first treatment session and showed early aneurysm recanalization (Fig. 3).

Treatment Strategy A second treatment appeared necessary in order to avoid further growth of the pseudoaneurysm, which might have resulted in recurrent episodes of epistaxis or emboli into the dependent vasculature. Coil occlusion alongside flow diversion was considered the most appropriate treatment strategy.

Treatment

The procedure was well tolerated, and the epistaxis stopped after the procedure. The patient remained in the ICU for 5 days.

Procedure #2, 01.09.2010: repeated endovascular coil occlusion of a cavernous ICA pseudoaneurysm remnant and endovascular reconstruction of the ICA with a flow diverter stent Anesthesia: general anesthesia; 10,000 IU unfractionated heparin (Riveparin, Rivero) IV Premedication: 1
100 mg ASA (Aspirin, Bayer Vital) PO daily and 1
75 mg clopidogrel (Troken, Laboratio Bagó) PO daily, both starting 2 days before the intervention

Fig. 2 Endovascular treatment of a posttraumatic lefthand cavernous ICA aneurysm causing epistaxis. The aneurysm was catheterized (arrow, the tip of the

microcatheter, posterior-anterior view (a)) and occluded with 18 GDC platinum microcoils (posterior-anterior view (b), lateral view (c))

Clinical Outcome

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Fig. 3 Follow-up imaging only 7 days after the endovascular coil occlusion of a posttraumatic left-hand cavernous ICA aneurysm. MRI/MRA including sagittal T2WI

(a), sagittal TOF MRA (b), and DSA (c) showed the early recanalization of the pseudoaneurysm

Access: right femoral artery, 7F sheath (Terumo); guide catheter: 6F Envoy (Codman); microcatheter: Tracker Excel-14 (Boston Scientific) for coil insertion and Marksman 27 (Medtronic) for the flow diverter deployment; microguidewire: Transend 0.01400 (Stryker) Implants: 11 coils: 1
Microcoil GDC -18 360 Standard 24/40, 1
Microcoil GDC -18 360 Standard 22/40, 2
Microcoil GDC -18 360 Standard 22/33, 2
Microcoil 360 GDC -18 20/33, 2
Microcoil GDC -18 360 Standard 18/40, 1
Microcoil 360 GDC -18 18/40, 2
Microcoil GDC -18 360 Standard 16/40 (Boston Scientific); 2 flow diverters: Pipeline Embolization Device (Medtronic) 2
4/20 Course of treatment: The left internal carotid artery was catheterized with a 6F Envoy guide catheter. A Tracker Excel-14 microcatheter with a 0.01400 microguidewire was navigated into the pseudoaneurysm. The pseudoaneurysm was occluded with 11 coils, after which the endovascular reconstruction of the cavernous ICA segment was achieved using two PEDs. A Marksman 27 microcatheter was placed into the left MCA, and a PED 4/20 was deployed. Due to the continuous filling of the pseudoaneurysm, a second PED 4/20 was added in a telescoping fashion. Adequate apposition of the two devices with a reconstruction of the cavernous segment and a

significantly reduced flow in the pseudoaneurysm were accomplished (Fig. 4). Duration: 1st – 16th DSA run: 72 min; fluoroscopy time: 43 min Complications: none Postmedication: 1
100 mg ASA PO daily for life and 1
75 mg clopidogrel PO daily for 6 months

Clinical Outcome The second procedure was well tolerated. The patient remained in the ICU for 2 days and was discharged home after another 2 days. Cavernous sinus syndrome progressively improved. After 3 months, his diplopia and facial pain had ceased.

Follow-Up Examinations Follow-up MRI/MRA exams at 6 and 15 months showed progressive shrinkage and thrombosis of the aneurysm. DSA at 6 and 15 months confirmed the complete occlusion of the aneurysm (Fig. 5). Two years later, the patient consulted the medical department because metallic material was extruding through his nose. An NCCT was done, showing a coil protruding through the left nostril.

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Fig. 4 (continued)

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Fig. 4 Endovascular management of early reperfusion of a traumatic cavernous ICA pseudoaneurysm after initial coil occlusion. The second treatment session was carried out 1 week after the coil occlusion of a posttraumatic lefthand cavernous ICA pseudoaneurysm with early reperfusion. Coil occlusion of the pseudoaneurysm remnant with

11 coils (a). A first PED 4/20 was deployed covering the aneurysm neck (b, c). A second PED 4/20 was inserted in a telescoping fashion into the first PED (d, e). Adequate apposition of the two PED devices with a reconstruction of the cavernous segment was achieved (f) with a significant reduction of the flow into the pseudoaneurysm (g, h)

The coil was gently pulled out and cut off without being completely removed. Subsequent DSA showed a fully occluded aneurysm (Fig. 6).

is characterized by repeated episodes, with bleeding increasing over time (Sridharan et al. 2014). Mauner’s triad

Discussion

• Unilateral blindness • Orbital fracture and • Massive epistaxis

Direct ICA injuries are rare yet potentially lethal conditions. The resulting pseudoaneurysms or “false aneurysms” by definition consist of a hematoma surrounded by a fibrous layer, rather than a “true” arterial wall (Wang et al. 2018). Due to the influence of continuous, pulsatile arterial forces, these expand to a more spherical shape (Sirakov et al. 2019). They are extremely prone to rupture and may cause life-threatening epistaxis resulting from the disruption through the sphenoid sinus (Chaboki et al. 2004). Cadaveric dissection has revealed that 71% of cavernous carotid arteries project into the lateral sphenoid sinus, 66% have a bony covering of less than 1 mm, and 4% are dehiscent (Chaboki et al. 2004). Although rare, aneurysmal rupture may result due to the anteromedial expansion of the pseudoaneurysm sac directly into the ethmoid sinus or into the petrous bone. In such cases, the epistaxis

has been observed in some cases and is considered pathognomonic for ICA pseudoaneurysms. ICA pseudoaneurysms may result from several conditions and events, including sphenoidal and transsphenoidal surgery, a neoplastic process, local intracranial pyogenic or “mycotic” infections, and congenital collagen vascular diseases. While severe hemorrhage due to an ICA pseudoaneurysm is a dreadful condition, direct microsurgical management of such lesions usually proves to be complicated. The constant need for hemostasis and an extensive skull base exploration when attempting direct arterial repair are sometimes considered obstacles. Definitive microsurgical treatment may often require parent vessel sacrifice or microvascular arterial reconstruction with bypass grafting. These techniques often bear some limitations, in that the patient

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Cavernous Internal Carotid Artery Aneurysm: Giant Posttraumatic Carotid Cavernous. . .

might not fully tolerate the procedure, resulting in a significant stroke unless there is patent and adequate collateral circulation. As a result, the management of these unique entities has shifted towards endovascular methods. However, treating a cavernous ICA pseudoaneurysm by endovascular means is more complicated than for regular true cerebral aneurysms. Endovascular reconstruction of the parent vessel is considered a safe and effective procedure with a complication rate of up to approximately 10% (Mohan et al. 2017). Moreover, the endovascular coil embolization of cerebral pseudoaneurysms is commonly associated with some unusual and rare complications in terms of delayed coil extrusion and migration. According to a report by Struffert

Fig. 5 (continued)

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et al. (2009), pseudoaneurysms within the sphenoid sinus are most likely to have arisen secondary to previous surgical intervention. Coil extrusion into the nostril and oropharynx up to 26 months after neurointerventional therapy was reported in two cases (Struffert et al. 2009). Nasi et al. (2019) reported on a case in which coil extrusion had actually happened 10 years after the treatment was conducted. The absence of a real arterial wall combined with a perianeurysmal hematoma- and thrombus resolving, thus causing coils to loosen and migrate via preexisting fractures, is a possible mechanism behind coil herniation hypothesized by Singh et al. (2018). Pseudoaneurysmal walls are inherently unstable, and metallic coils have the

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Fig. 5 Follow-up imaging after the endovascular management of a posttraumatic cavernous ICA aneurysm. MRI/MRA at 6 months (a, b, c) and 15 months (d, e, f) including axial T1WI (a), axial T2WI (b), and sagittal T2WI (c) showed a modification in the signal intensity of the thrombus. No evidence of any growth of the aneurysm was seen, and a decrease in mass effect was also noted on

the 6-month follow-up. The mass effect and the pseudoaneurysm size had decreased by the 15-month follow-up (T1WI (d), axial T2WI (e), FLAIR image (f)). Note the disappearance of the mass effect of the aneurysm on the adjacent orbit (e). Follow-up DSA at 6 months confirmed the complete occlusion of the aneurysm and the reconstruction of the cavernous ICA segment (g)

potential to dislodge and escape out of the confines of the pseudoaneurysm (Chen et al. 1998). Some authors reported iatrogenic perforation of the aneurysmal wall during coiling (Aoun et al. 2013) or the force of blood flow compressing the coils against the aneurysmal dome resulting in coil extrusion either through an already vulnerable site or by creating a new tear in the aneurysm wall (Wilseck et al. 2018). The mechanics and

process described above usually take time and reflect the fact that the extrusion is reported from several months to years after the endovascular coiling procedure (Nasi et al. 2019). Extruded coils have the potential to destabilize prior arterial embolization, and they should be managed emergently. It is crucial in such cases to take a multidisciplinary approach, and intraoperative angiography and endovascular procedures must

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Fig. 6 Long-term follow-up after coil occlusion and flow diverter treatment of a posttraumatic aneurysm of the lefthand cavernous ICA. The patient presented with a coil loop protruding from his left nostril. Axial NCCT (a) and volume rendering NCCT reconstruction (b) confirmed the coil

extrusion. The coil material was cut off (c). Subsequent DSA (d) and VasoCT (e) confirmed the persistent occlusion of the pseudoaneurysm with the migration of the coil cast through the sphenoid sinus

be in place in case of hemorrhage occur (Dedmon et al. 2014). The extruded coil loop should be treated by trimming at the level of the defect, while the embedded portions of the coil wire must be left in place in order to minimize the risk of possibly destabilizing the occlusive matrix (Nasi et al. 2019). Other cases of coil extrusion have been reported in the literature. Chow et al. (2004) reported on the case of a 70-year-old male patient with a medical history of nasopharyngeal carcinoma treated with radiotherapy 7 years previously, which had resulted in temporal bone radionecrosis. He presented with bleeding from the ear due to a pseudoaneurysm of the proximal petrous left internal carotid artery, complicated by a foreign body sensation in the left ear. Upon examining the patient with an otoscope, a

tympanic membrane perforation was found, with a coil wire protruding through. The wire was cut flush to the tympanic membrane, and the patient was discharged home. The fibred steel coils used before the GDC coils carry a very low uncoiling rate because steel has a strong coiling memory. In contrast, a GDC has a much finer caliber and is softer; it is made of platinum and has a relatively poor coiling memory. It also lacks fibers and is less thrombogenic (Chow et al. 2004).

Therapeutic Alternatives Parent Vessel Occlusion Stent Graft Stent-Assisted Coiling

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References Aoun SG, Rahme RJ, El Ahmadieh TY, Bendok BR, Hunt Batjer H. Incorporation of extruded coils into the third nerve in association with third nerve palsy. J Clin Neurosci. 2013;20(9):1299–302. https://doi.org/ 10.1016/j.jocn.2012.10.040. Chaboki H, Patel AB, Freifeld S, Urken ML, Som PM. Cavernous carotid aneurysm presenting with epistaxis. Head Neck. 2004;26(8):741–6. https://doi.org/ 10.1002/hed.20081. Chen D, Concus AP, Halbach VV, Cheung SW. Epistaxis originating from traumatic pseudoaneurysm of the internal carotid artery: diagnosis and endovascular therapy. Laryngoscope. 1998;108(3):326–31. Chow MW, Chan DT, Boet R, Poon WS, Sung JK, Yu SC. Extrusion of a coil from the internal carotid artery through the middle ear. Hong Kong Med J. 2004; 10(3):215–6. Dedmon M, Meier J, Chambers K, Remenschneider A, Mehta B, Lin D, Yoo AJ, Curry W, Gray S. Delayed endovascular coil extrusion following internal carotid artery embolization. J Neurol Surg Rep. 2014;75(2): e255–8. https://doi.org/10.1055/s-0034-1387193. Mohan B, Singal S, Bawa AS, Mahindra P, Yamin M. Endovascular management of traumatic pseudoaneurysm: short & long term outcomes. J Clin Orthop Trauma. 2017;8(3):276–80. https://doi.org/10.1016/j. jcot.2017.05.010. Nasi D, Dobran M , di Somma L, Di Rienzo A, De Nicola M, lacaangeli M. Coil extrusion into the naso- and oropharynx ten years after internal carotid artery

I. Lylyk et al. pseudoaneurysm embolization: a case report. Case Rep Neurol. 2019;11(1):4–9. https://doi.org/10.1159/ 000496283. Singh A, Sikka K, Jain N, Devarajan LJ. Delayed endovascular coil extrusion presenting as a foreign body of the throat: a case report. Neurointervention. 2018;13 (1):66–9. https://doi.org/10.5469/neuroint.2018.13.1.66. Sirakov S, Panayotova A, Sirakov A, Minkin K, Hristov H. Delayed intranasal coil extrusion after internal carotid artery pseudoaneurysm embolization. Interv Neuroradiol. 2019;25(2):139–43. https://doi.org/ 10.1177/1591019918805151. Sridharan R, Low SF, Mohd MR, Kew TY. Intracavernous internal carotid artery pseudoaneurysm. Singap Med J. 2014;55(10):e165–8. https://doi.org/10.11622/smed j.2014148. Struffert T, Buhk JH, Buchfelder M, Rohde V, Doerfler A, Knauth M. Coil migration after endovascular coil occlusion of internal carotid artery pseudoaneurysms within the sphenoid sinus. Minim Invasive Neurosurg. 2009;52(2):89–92. https://doi.org/10.1055/s-00291215579. Wang T, Zhang C, Xie X. Delayed coil migration after treatment of traumatic pseudoaneurysm. World Neurosurg. 2018;113:206–7. https://doi.org/10.1016/j. wneu.2017.12.040. Wilseck Z, Savastano L, Chaudhary N, Pandey AS, Griauzde J, Sankaran S, Wilkinson D, Gemmete JJ. Delayed extrusion of embolic coils into the airway after embolization of an external carotid artery pseudoaneurysm. J Neurointerv Surg. 2018;10(7):e18. https:// doi.org/10.1136/neurintsurg-2017-013178.rep.

Part IV Paraophthalmic Internal Carotid Artery

Paraophthalmic Internal Carotid Artery Aneurysm: Coil Occlusion Assisted by the Comaneci Device

10

Sebastian Fischer

Abstract

This 45-year-old female experienced an episode of severe headache. Diagnostic work-up including a clinical examination performed at the initially consulted hospital revealed a neurologically asymptomatic patient at the time of admission. CT showed no evidence of a subarachnoid hemorrhage (SAH) or other findings potentially causative for the episode of headache but did reveal a hyper dense rounded lesion located in the left-sided subarachnoid space involved in the paraophthalmic segment of the internal carotid artery (ICA). The diagnosis of a wide-necked paraophthalmic ICA aneurysm was confirmed by MRI including contrast enhanced angiographic imaging. The patient was then referred to the author’s institution for endovascular occlusion of the aneurysm. A diagnostic angiography confirmed the diagnosis of a wide-necked aneurysm at the paraophthalmic segment of the ICA. Further to the initial investigation, a small aneurysm originating directly at the ophthalmic artery was found.

S. Fischer (*) Institut für Diagnostische und Interventionelle Radiologie, Neuroradiologie und Nuklearmedizin, Universitätsklinikum Bochum, Bochum, Germany e-mail: [email protected]; sebastian.fi[email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_16

The aneurysm was treated by coil occlusion assisted by a temporary neck-bridging device (Comaneci, Rapid Medical). This technique allows for a coil occlusion of wide-necked aneurysms, avoiding use of a permanent implant in the parent artery and therefore use of concomitant anti-aggregation. The difference in the neck-bridging remodeling technique compared to that of a compliant balloon is the avoidance of flow arrest during the expansion of the device in the parent artery (i.e., the Comaneci Device can be left deployed throughout the entire procedure without a need of repeated deflations). The procedure was carried out under general anesthesia without clinical or technical complication. The patient was discharged 2 days later in a neurologically asymptomatic condition. Follow-up angiography performed 3 months later revealed a stable and complete occlusion of the large aneurysm in the clinically unchanged asymptomatic patient. The main topic of this presentation is to demonstrate a novel technique for the endovascular treatment of widenecked aneurysms, without placing a permanent implant in the parent artery, offering a promising approach particularly for acutely ruptured aneurysms.

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Keywords

ICA aneurysm · Paraophthalmic aneurysm · Wide-necked aneurysm · Comaneci Device · Coil occlusion

Patient 45-year-old, female, incidental finding of a widenecked paraophthalmic ICA aneurysm

Diagnostic Imaging A non-enhanced computer tomography was performed at the referring hospital after an episode of severe headaches. There was no evidence of a subarachnoid hemorrhage (SAH) but a large paraophthalmic aneurysm of the left ICA (Fig. 1a) was suspected. A contrast enhanced MRA of the intracranial vasculature confirmed the diagnosis of a broad-based aneurysm at the paraophthalmic segment of the left ICA (Fig. 1b). The patient was referred to our institution for further diagnostic evaluation and the endovascular occlusion of the aneurysm. The diagnostic angiography of both ICAs and the left vertebral artery (VA) was performed with a rotational 3D angiography to

Fig. 1 Non-contrastenhanced CT and contrastenhanced MRI of a 45-yearold woman, presenting with an initial episode of severe headaches. Non-enhanced CT (a) showed the absence of a SAH, with an incidental finding of a rounded, hyperdense lesion that indicates an aneurysm of the left ICA. Contrast-enhanced MRI (b) confirmed the diagnosis of a broad-based left ICA aneurysm originating from the paraophthalmic segment

S. Fischer

attain better visualization of the aneurysm morphology (Fig. 2). Additionally, the diagnostic angiography showed a small aneurysm at the origin of the ophthalmic artery opposite to the primary aneurysm. The fundus size of said aneurysm was approximately 10 mm in both height and width. The neck width of the aneurysm was around 7 mm referring to an aspect ratio (dometo-neck ratio) of 1:4. Simultaneous injection of the right ICA under manual compression of the left cervical ICA proved the absence of cross-flow via the small anterior communicating artery (AcomA), thus indicating the imperative of a reconstructive treatment strategy for the left-sided paraophthalmic aneurysm.

Treatment Strategy The case was discussed in our institutional neurovascular meeting resulting in a consensus for an endovascular treatment of this young patient’s large intradural aneurysm. The anatomic location of the aneurysm appeared unsuitable for a microsurgical clipping, the group decided against permanent implant in the ICA (flow diverter alone or stent-assisted coiling) in order to avoid longterm anti-aggregation medication. Therefore, a

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Fig. 2 DSA with injection of the left ICA shows the broad-based paraophthalmic aneurysm in an oblique view (a). Rotational angiographic visualization of the aneurysm in the ‘seethrough’ reconstruction mode (b)

coil occlusion of the aneurysm assisted by the Comaneci device as a compliant remodeling mesh temporarily placed inside the ICA (Fig. 3) was planned.

Treatment Procedure, 04.09.2015: Comaneci-assisted coil occlusion of a paraophthalmic aneurysm of the left ICA Anesthesia: general anesthesia; 5000 IU unfractionated heparin (Heparin-Natrium, B. Braun) IV Premedication: single dose of 600 mg clopidogrel (Plavix, Sanofi-Aventis) and 500 mg ASA (Aspirin, Bayer Vital) PO 5 days prior to the procedure followed by 75 mg clopidogrel PO and 100 mg ASA PO, both daily Access: right femoral artery 8F sheath; guide catheter: Neuron MAX 6F (Penumbra); intermediate catheter: Navien Aþ 072 (Medtronic); microcatheters: Vasco 21 (Balt) (for the Comaneci Device), Excelsior SL-10 45 (Stryker) (for coils); microguidewires: SilverSpeed-16 (Medtronic) (for the navigation of Vasco 21); Synchro2 0.01400 200 cm (for the navigation of the Excelsior SL-10) Implants: 13 coils: Target XL 360 SOFT 12/ 45, Target XL 360 SOFT 10/40, Target 360 SOFT 8/20 (Stryker), MicroPlex VFC 6–10/20

Fig. 3 Expansion of the Comaneci device in an aneurysm model

(2), MicroPlex VFC 3–6/15, MicroPlex VFC 3–6/10, MicroPlex VFC 3–6/6 (4), HydroCoil 10 5/10, HydroCoil 10 5/8 (MicroVention) Course of treatment: A coaxial guiding catheter system consisting of a Neuron MAX 6F sheath and a Navien Aþ 072 intermediate catheter was placed in the cervical segment of the left ICA. DSA runs including standard and oblique

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projections visualized the broad-based aneurysm without superimposed imaging of surrounding branches. The aneurysm diameters were as described above. The Vasco 21 microcatheter was placed in the M1 segment of the left-middle cerebral artery (MCA) navigated by a SilverSpeed-16 microwire (Fig. 4a). An Excelsior SL-10 microcatheter was advanced into the aneurysm supported by a Synchro2 0.01400 microguidewire (Fig. 4b). A standard Comaneci device (32 mm length when undeployed, shortening to 12 mm in a 4.5 mm vessel) was placed at the orifice of the aneurysm by continuous backwards pulling of the previously placed microcatheter, technically comparable to the placement of a self-expanding stent. Once the Comaneci reached the correct position, centered at the broad-based neck of the aneurysm, it was slowly unfolded operated by the slider at the handle of the device (Fig. 4c). The Comaneci device was left expanded with complete coverage of the broad-based aneurysm during the insertion of the first two large framing coils (Fig. 5a). The coil occlusion of the aneurysm was then finalized with the above coils and the aneurysm neck was protected by the Comaneci device (Fig. 5b, c). The stable position of the coils at the aneurysm base was documented by several ‘deflations’ of the Comaneci device under continuous fluoroscopy. The final angiographic run demonstrated a near complete occlusion of the aneurysm with a minor filling at the neck. The Excelsior SL10 microcatheter was withdrawn, leaving the Comaneci device unfolded so as to protect the coils from dislocating into the parent artery. Thereafter, the final “deflation” of the Comaneci device again proved the stable positioning of the coils (Fig. 6a). Lastly, the Vasco 21 microcatheter was advanced up, into the distal ICA in order to recapture and withdraw the deflated Comaneci device. Any adverse events that could potentially have occurred (e.g., a dissection of the ICA or peripheral emboli within the dependent vasculature) were ruled out by the final

S. Fischer

angiographic run in two standard projections (Fig. 7a, b). Duration: 1st –14th DSA run: 73 min; fluoroscopy time: 49 min Complications: none Postmedication: 100 mg ASA PO daily ongoing for 4 weeks

Clinical Outcome The general anesthesia was completed in the angiography suite, the clinical condition of the patient remained unchanged.

Follow-Up Examinations and Subsequent Procedures A post procedure routine MRI performed before discharge 2 days later showed a minor asymptomatic ischemic lesion in the dependent frontal parenchyma (not shown). An angiographic follow-up was carried out 3 months after the procedure, which confirmed a complete and stable occlusion of the paraophthalmic ICA aneurysm (Fig. 8). The patient remained clinically asymptomatic in regards to the treated aneurysm. The episodic headaches were treated by specific drug therapy.

Discussion Intracranial aneurysms can be described by the relation of the maximum dome height to the diameter of their neck. This measure, known as the aspect ratio, is a helpful tool to identify the need for adjunctive devices in the preparation of endovascular treatment strategies for intracranial aneurysms (Brinjikji et al. 2009). An aspect ratio 7 mm) and location (vertebrobasilar, AcomA, and PcomA) were predictors of rupture (Greving et al. 2014; Nehls et al. 1985). Another study comparing the features of ruptured and unruptured aneurysms found that an irregular aneurysm shape and an aspect ratio of 1.3 are associated with increased risk of rupture

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Fig. 2 Intraprocedural angiogram of the left ICA (a), contra-oblique view, obtained after gaining microcatheter access to the proximal middle cerebral artery (MCA). Radiographic image, lateral view (b), of the implanted

telescoping flow diverter stents. Angiographic image, late arterial phase, lateral view (c), obtained immediately after flow diverter stent implantation, shows contrast stagnation in the covered ophthalmic and PcomA aneurysms

(Backes et al. 2014). Computational fluid dynamics (CFD) has recently become a popular tool for studying intracranial aneurysm hemodynamics and assessing the likelihood of previous or future rupture (Valen-Sendstad and Steinman 2014), and contrast-enhanced MR vessel wall imaging may be helpful in identifying the site of rupture in patients with multiple aneurysms (Omodaka et al. 2018). However, neither the classical nor more recent approaches are currently accurate enough to identify the ruptured lesion in patients with multiple aneurysms, especially when they are located in close proximity.

According to previous reports, surgical clipping of multiple aneurysms can lead to poorer outcomes (Mizoi et al. 1989) and endovascular therapy of multiple aneurysms has usually been performed in staged procedures. Thus, patients with SAH and multiple intracranial aneurysms present a unique challenge to the neurosurgeon as well as to the neurointerventionalist. Unless all aneurysms can be treated during a single intervention, the physician must accurately determine which aneurysm has ruptured. Misjudgment may result in disastrous postoperative rebleeding from the untreated lesion responsible for the initial bleeding.

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Internal Carotid Artery Aneurysm: Multiple Internal Carotid Artery Aneurysms in a Patient. . .

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Fig. 3 Angiographic image of the left ICA, oblique view (a), and 3D reconstruction images of a rotational angiogram of the left ICA (b) obtained 3 months after stent

deployment. All ICA aneurysms are completely excluded and the parent vessels are preserved

Our patient presented with SAH and three aneurysms, each of which could have been the origin of the hemorrhage. All supraclinoid aneurysms were treated by means of telescoping implantation of two flow diverter stents in a single intervention during the acute phase of hemorrhage. The case illustrates the management of multiple aneurysms by means of flow diverter stents and the use of these devices during the acute phase of SAH, a controversial strategy that is slowly gaining acceptance. Stenting devices have greatly expanded the therapeutic spectrum of endovascular techniques for the management of intracranial aneurysms; however, they have largely been reserved for patients with unruptured aneurysms because of concerns regarding the use of antiplatelet therapy in cases of SAH. Several authors have nevertheless presented their experience with the use of stents in patients with ruptured aneurysms, and a systematic review of stent-assisted coiling in ruptured aneurysms concluded that the technique can be performed with a high degree of technical success, although adverse events appear more common (Bodily et al. 2011). In recent reports, we found many variations in the strategies for managing these patients (Amenta et al. 2012; Bodily et al. 2011; Cai

et al. 2017; Chalouhi et al. 2013; Chung et al. 2014; Lessne et al. 2011; Tähtinen et al. 2009). Early external ventricular drain (EVD) placement was not frequently discussed, suggesting there are no special considerations in this population. There were many approaches to antiplatelet type, dose, and timing, and assessment of the effects of antiplatelet medications was rare. Given the relatively high rates of hemorrhage, thrombotic complications, and mortality that have been reported, guidelines in these areas are urgently needed. One recent publication (Cohen et al. 2018) presented a protocol for stent-based treatment of acutely ruptured aneurysms based on a low threshold for EVD placement prior to stenting and preprocedure administration of antiplatelet agents with platelet response testing to ensure that the response falls within a safe range. This protocol aims to limit the risks of both hemorrhage and stent-related thrombus formation. In this series of 47 patients with acutely ruptured aneurysms, including 46 with aneurysmal SAH, immediate total or near-total aneurysm occlusion was achieved in 97% of patients treated with a combination of stents and coils, and there were even higher delayed occlusion rates in patients treated with flow diverter stents for the 45 surviving patients. Despite the routine administration of

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dual antiplatelet therapy and heparin, there were no episodes of intra- or post-procedural hemorrhage. Isolated intraprocedural thromboembolic events in 8.5% of patients were managed conservatively without long-term sequelae. We believe this illustrative case contributes to the growing body of evidence supporting the use of flow diverter stent techniques in the management of multiple ICA aneurysms, even in acute cases, with judicious placement of pre-procedure ventriculostomy and strict adherence to a carefully designed policy for antiplatelet therapy in these patients.

Therapeutic Alternatives Balloon Remodeling Microsurgical Clipping Stent-Assisted Coiling Telescoping Stenting

References Amenta PS, Dalyai RT, Kung D, Toporowski A, Chandela S, Hasan D, Gonzalez LF, Dumont AS, Tjoumakaris SI, Rosenwasser RH, Maltenfort MG, Jabbour PM. Stent-assisted coiling of wide-necked aneurysms in the setting of acute subarachnoid hemorrhage: experience in 65 patients. Neurosurgery. 2012;70(6):1415–29; discussion 1429. https://doi.org/ 10.1227/NEU.0b013e318246a4b1. Backes D, Vergouwen MD, Velthuis BK, van der Schaaf IC, Bor AS, Algra A, Rinkel GJ. Difference in aneurysm characteristics between ruptured and unruptured aneurysms in patients with multiple intracranial aneurysms. Stroke. 2014;45(5):1299–303. https://doi.org/ 10.1161/STROKEAHA.113.004421. Bodily KD, Cloft HJ, Lanzino G, Fiorella DJ, White PM, Kallmes DF. Stent-assisted coiling in acutely ruptured intracranial aneurysms: a qualitative, systematic review of the literature. AJNR Am J Neuroradiol. 2011; 32(7):1232–6. https://doi.org/10.3174/ajnr.A2478. Cai K, Ji Q, Cao M, Shen L, Xu T, Zhang Y. Association of different stenting procedures with symptomatic thromboembolic complications in stent-assisted coiling of ruptured wide-necked intracranial aneurysms. World Neurosurg. 2017;104:824–30. https://doi.org/10.1016/ j.wneu.2017.05.093. Chalouhi N, Jabbour P, Singhal S, Drueding R, Starke RM, Dalyai RT, Tjoumakaris S, Gonzalez LF, Dumont AS, Rosenwasser R, Randazzo CG. Stent-assisted coiling of intracranial aneurysms: predictors of complications,

J. E. Cohen et al. recanalization, and outcome in 508 cases. Stroke. 2013;44(5):1348–53. https://doi.org/10.1161/ STROKEAHA.111.000641. Chung J, Lim YC, Suh SH, Shim YS, Kim YB, Joo JY, Kim BS, Shin YS. Stent-assisted coil embolization of ruptured wide-necked aneurysms in the acute period: incidence of and risk factors for periprocedural complications. J Neurosurg. 2014;121(1):4–11. https://doi. org/10.3171/2014.4.JNS131662. Cohen JE, Gomori JM, Leker RR, Spektor S, Abu El Hassan H, Itshayek E. Stent and flow diverter assisted treatment of acutely ruptured brain aneurysms. J Neurointerv Surg. 2018;10(9):851–8. https://doi.org/ 10.1136/neurintsurg-2017-013742. Greving JP, Wermer MJ, Brown RD Jr, Morita A, Juvela S, Yonekura M, Ishibashi T, Torner JC, Nakayama T, Rinkel GJ, Algra A. Development of the PHASES score for prediction of risk of rupture of intracranial aneurysms: a pooled analysis of six prospective cohort studies. Lancet Neurol. 2014;13(1):59–66. https://doi. org/10.1016/S1474-4422(13)70263-1. Juvela S. Risk factors for multiple intracranial aneurysms. Stroke. 2000;31(2):392–7. Lessne ML, Shah P, Alexander MJ, Barnhart HX, Powers CJ, Golshani K, Ferrell A, Enterline D, Zomorodi A, Smith T, Britz GW. Thromboembolic complications after Neuroform stent-assisted treatment of cerebral aneurysms: the Duke Cerebrovascular Center experience in 235 patients with 274 stents. Neurosurgery. 2011;69(2):369–75. https://doi.org/10.1227/ NEU.0b013e31821bc49c. Mizoi K, Suzuki J, Yoshimoto T. Surgical treatment of multiple aneurysms. Review of experience with 372 cases. Acta Neurochir. 1989;96(1–2):8–14. Nehls DG, Flom RA, Carter LP, Spetzler RF. Multiple intracranial aneurysms: determining the site of rupture. J Neurosurg. 1985;63(3):342–8. Omodaka S, Endo H, Niizuma K, Fujimura M, Endo T, Sato K, Sugiyama SI, Inoue T, Tominaga T. Circumferential wall enhancement on magnetic resonance imaging is useful to identify rupture site in patients with multiple cerebral aneurysms. Neurosurgery. 2018;82(5):638–44. https://doi.org/10.1093/ neuros/nyx267. Rinne J, Hernesniemi J, Puranen M, Saari T. Multiple intracranial aneurysms in a defined population: prospective angiographic and clinical study. Neurosurgery. 1994;35(5):803–8. Tähtinen OI, Vanninen RL, Manninen HI, Rautio R, Haapanen A, Niskakangas T, Rinne J, Keski-Nisula L. Wide-necked intracranial aneurysms: treatment with stent-assisted coil embolization during acute (1.6, and detrimental effects on the intraaneurysmal flow pattern induced by the implanted flow diverter. Aneurysm rupture after flow diversion usually occurs within 6 weeks, but late rupture up to 5 months after the procedure has also been observed (Kulcsár et al. 2011). The aneurysm rupture seems related to a rapid intraaneurysmal thrombus formation and thrombus organization mediated by inflammatory cells and fibrocytes releasing lytic enzymes. The rupture risk is higher in red thrombi as compared to white thrombi due to the higher concentration of erythrocytes and proteolytic enzymes (Turowski et al. 2011; Weisel and Litvinov 2008). Coil occlusion before or together with flow diverter implantation has been thought to reduce the risk of early postinterventional aneurysm rupture after flow diversion in large aneurysm. The underlying

ä Fig. 2 Endovascular treatment of a large left-side supraclinoid ICA aneurysm (a) with PED-assisted coil occlusion using the “jailed catheter” technique. The aneurysm was partially occluded with six coils, and the parent vessel was reconstructed with three PEDs. In order to avoid bulging of coil loops into the parent vessel, the coiling catheter was inserted into the aneurysm. This catheter was then covered

by a PED and coil insertion was started (b). Coil occlusion and PED implantation were completed in steps (c, d, e). The final DSA run (f) showed a partial obliteration of the aneurysm by the coils and that the parent vessel was patent, protected by the three PEDs. At this time, there was perfusion around the coil mass inside the aneurysm

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Fig. 3 (continued)

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Supraclinoid Internal Carotid Artery Aneurysm: Acute Subarachnoid and Intraventricular. . .

Fig. 3 (continued)

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Fig. 3 MRI 6 h after the treatment of a large supraclinoid aneurysm of the left ICA was within normal limits (T2WI (a), DWI (b)). On day 3, after a clinical deterioration of the patient, T2WI MRI (c) and FLAIR images (d, e) showed a hematoma adjacent to the medial and cephalad aspect of the treated aneurysm and a massive ventricular hemorrhage, confirmed by CT (i). DSA was performed immediately thereafter (f, g, h). The dome of the aneurysm fundus, which had still been perfused at the end of the previous treatment, was now thrombosed. Outside the contour of the

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aneurysm, a circumscribed extravascular pooling of contrast medium was found, indicating the presumable rupture site. CT scan after DSA confirmed a further increase in the ventricular hemorrhage. (i) Therefore, a second ventricular drain was put in place. A second DSA was performed a day later. The extravasation was not seen anymore. (j) NCCT prior to transfer of the rehabilitation showed complete resolution of the hemorrhage. No hydrocephalus was observed (k)

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Supraclinoid Internal Carotid Artery Aneurysm: Acute Subarachnoid and Intraventricular. . .

assumption here is that the additional coiling increases the probability of forming a white thrombus with a larger portion of fibrin and a lower amount of lytic enzymes (Turowski et al. 2011). However, aneurysm rupture has been observed even after coil-assisted flow diversion. In our patient we hypothesize that the cleft between the aneurysm wall and the coil package visible in the final DSA run might have been responsible for or at least contributed to the aneurysm rupture. Hemodynamic changes after the flow diverter was implanted and the subsequent thrombus formation combined with the local effect of proteolytic enzymes may have caused the aneurysm wall to break down. In the case above, it is remarkable that the rupture site was shown on DSA. It was located at the dome of the aneurysm fundus and adjacent to that part of the aneurysm which was filled with coils and fresh thrombus. Furthermore it has been described in various publications that inflammation plays an important role in the pathophysiology of aneurysm rupture (Chyatte et al. 1999; Makino et al. 2012), especially for large and giant aneurysms.Several treatment strategies have been developed since the early encounters with flow diverter-induced aneurysm rupture. Staggered treatment starting with at least partial coil occlusion of the aneurysm might offer better protection than coiling at the same time as implanting a flow diverter. In the case presented above, the very wide neck of the aneurysm would have required a stent in order to prevent coil herniation inside the parent artery. The speed of thrombus formation induced by flow diversion apparently plays a role. Dual platelet function inhibition is required to prevent thrombus formation induced by the foreign body (i.e., the flow diverter). The thrombus formation inside the aneurysm sac can be delayed by concomitant anticoagulation. Both heparin and direct thrombin inhibitors (e.g., dabigatran) have been used for this purpose. This would be an off-label use of direct oral anticoagulants. The inflammatory aspect of the underlying pathophysiology of flow diversion- and thrombus-induced aneurysm rupture is usually addressed by prescribing anti-inflammatory

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medication (Sirakov et al. 2019). Metamizole (or dipyrone) and ibuprofen should be avoided since both drugs interfere with the platelet inhibition effect of aspirin (Martinez-Moreno et al. 2016). According to our institutional protocol, patients receive a bolus of 40 mg dexamethasone IV immediately after the procedure followed by 3 4 mg dexamethasone PO daily for 4–10 days (with subsequent tapering of the dosage) as well as 60 mg etoricoxib (Arcoxia; MSD Sharp & Dohme) PO over 6 weeks to suppress the inflammatory response and reduce the risk of early aneurysm rupture.

Therapeutic Alternatives Microsurgical Clipping Parent Vessel Occlusion Stent Assisted Coiling Telescoping Stenting

References Chyatte D, Bruno G, Desai S, Todor DR. Inflammation and intracranial aneurysms. Neurosurgery. 1999;45(5):1137–46; discussion 1146-7. https://doi. org/10.1097/00006123-199911000-00024. Kallmes DF, Hanel R, Lopes D, Boccardi E, Bonafé A, Cekirge S, Fiorella D, Jabbour P, Levy E, McDougall C, Siddiqui A, Szikora I, Woo H, Albuquerque F, Bozorgchami H, Dashti SR, Delgado Almandoz JE, Kelly ME, Turner R 4th, Woodward BK, Brinjikji W, Lanzino G, Lylyk P. International retrospective study of the pipeline embolization device: a multicenter aneurysm treatment study. AJNR Am J Neuroradiol. 2015;36 (1):108–15. https://doi.org/10.3174/ajnr.A4111. Kulcsár Z, Houdart E, Bonafé A, Parker G, Millar J, Goddard AJ, Renowden S, Gál G, Turowski B, Mitchell K, Gray F, Rodriguez M, van den Berg R, Gruber A, Desal H, Wanke I, Rüfenacht DA. Intraaneurysmal thrombosis as a possible cause of delayed aneurysm rupture after flow-diversion treatment. AJNR Am J Neuroradiol. 2011;32(1):20–5. https://doi.org/ 10.3174/ajnr.A2370. Makino H, Tada Y, Wada K, Liang EI, Chang M, Mobashery S, Kanematsu Y, Kurihara C, Palova E, Kanematsu M, Kitazato K, Hashimoto T. Pharmacological stabilization of intracranial aneurysms in mice: a feasibility study. Stroke. 2012;43(9):2450–6. https:// doi.org/10.1161/STROKEAHA.112.659821.

292 Martinez-Moreno R, Aguilar M, Wendl C, Bäzner H, Ganslandt O, Henkes H. Fatal thrombosis of a flow diverter due to ibuprofen-related antagonization of acetylsalicylic acid. Clin Neuroradiol. 2016;26(3):355–8. https://doi.org/10.1007/s00062015-0487-7. Rouchaud A, Brinjikji W, Lanzino G, Cloft HJ, Kadirvel R, Kallmes DF. Delayed hemorrhagic complications after flow diversion for intracranial aneurysms: a literature overview. Neuroradiology. 2016;58(2):171–7. https:// doi.org/10.1007/s00234-015-1615-4. Sirakov S, Sirakov A, Bhogal P, Penkov M, Minkin K, Ninov K, Hristov H, Karakostov V, Raychev R. The p64 flow diverter – mid-term and long-term results from a single center. Clin Neuroradiol 2019. https:// doi.org/10.1007/s00062-019-00823-y. Turowski B, Macht S, Kulcsár Z, Hänggi D, Stummer W. Early fatal hemorrhage after endovascular

V. Hellstern et al. cerebral aneurysm treatment with a flow diverter (SILK-Stent): do we need to rethink our concepts? Neuroradiology. 2011;53(1):37–41. https://doi.org/ 10.1007/s00234-010-0676-7. Weisel JW, Litvinov RI. The biochemical and physical process of fibrinolysis and effects of clot structure and stability on the lysis rate. Cardiovasc Hematol Agents Med Chem. 2008;6(3):161–80. Ye G, Zhang M, Deng L, Chen X, Wang Y. Meta-analysis of the efficiency and prognosis of intracranial aneurysm treated with flow diverter devices. J Mol Neurosci. 2016;59(1):158–67. https://doi.org/10.1007/s12031016-0723-x. Zhou G, Su M, Yin YL, Li MH. Complications associated with the use of flow-diverting devices for cerebral aneurysms: a systematic review and meta-analysis. Neurosurg Focus. 2017;42(6):E17. https://doi.org/ 10.3171/2017.3.FOCUS16450.

Supraclinoid Internal Carotid Artery Aneurysm: Giant Supraclinoid Aneurysm Treated with Telescoping p64 Flow Diverters with Complete Occlusion of the Aneurysm

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Ivan Lylyk, Jorge Chudyk, Rene Viso, Carlos Bleise, Esteban Scrivano, and Pedro Lylyk

Abstract

A symptomatic giant supraclinoid aneurysm was found in a 68-year-old female patient who had a history of mild hypertension. She presented with episodes of severe headache and visual disturbance of the right eye. The aneurysm was treated with a telescoping technique using two p64 flow-diverter stents (phenox). The patient was prepared for the stent implants with a course of dual-platelet function inhibition using acetylsalicylic acid (ASA) and clopidogrel 5 days prior to the procedure. The original plan for the procedure was to use a single flow-diverter device, but in the immediate DSA after the deployment of the first device, there was still a considerable amount of flow entering into the aneurysm sac. Therefore, a second device was placed, overlapping the first p64 at the aneurysm neck in order to further increase the flow diversion effect. The procedure was completed without any complications, and the patient was discharged after 3 days. The patient

I. Lylyk · J. Chudyk · R. Viso · C. Bleise · E. Scrivano · P. Lylyk (*) Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina e-mail: [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_21

showed rapid clinical improvement. In the follow-up DSA performed 1 year after the procedure, the aneurysm was angiographically completely occluded, and the flow diverters as well as the parent vessel remained patent. On MRI no significant shrinkage of the meanwhile thrombosed aneurysm sac was encountered. The use of flow diverters to treat aneurysms located in the supraclinoid segment of the ICA is the main topic of this chapter. Keywords

Supraclinoid ICA · Flow diversion · Complete angiographic occlusion · Telescoping flowdiverter stents · Space-occupying effect · Giant aneurysm

Patient A 68-year-old female patient presenting with a severe headache and visual disturbance of the right eye. Her medical history was unremarkable apart from high arterial blood pressure.

Diagnostic Imaging MRI/MRA showed a giant aneurysm of the supraclinoid segment of the right ICA with minor wall adherent thrombus. Running a DSA essentially 293

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confirmed the size and location of the aneurysm (width 26 mm, height 28 mm, neck 11 mm). The origin of the aneurysm was about 5 mm distal to the origin of the ophthalmic artery. A manual cross-compression test failed to show a collateral supply of the right anterior circulation via the anterior communicating artery (AcomA) or the right posterior communicating artery (PcomA) (Fig. 1).t

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device for coiling in order to prevent coil protrusion into the parent artery. Therefore, endovascular reconstruction with a flow diverter was chosen to induce a progressive thrombosis of the aneurysm and hopefully a reduction in size.

Treatment

The goal of the treatment of this aneurysm was to reduce the mass effect and to avoid an aneurysm rupture, which could lead to subarachnoid and/or intracerebral hemorrhage. The rupture risk was considered high, given the size of the aneurysm. Microsurgical clipping was anticipated to be associated with an increased level of difficulty. Coil occlusion would have had the disadvantage of preventing possible shrinking of the aneurysm. The wide neck would have required an assistance

Procedure, 06.07.2016: endovascular treatment of a giant aneurysm of the right ICA by parent artery reconstruction with flow diverters. Anesthesia: general anesthesia, 10,000 IU unfractionated heparin (Riveparin Ribero) IV Premedication: 1
100 mg ASA (Aspirin, Bayer Vital) PO daily and 1
75 mg clopidogrel (Troken, Laboratories Bagó) PO daily, starting 5 days before the intervention Access: right femoral artery, 8F sheath (Terumo); guide catheter: Shuttle 8F (Cook); intermediate catheter: Navien A+ 072 (Medtronic); microcatheters: Excelsior SL-10 (Stryker) and Marksman 0.02700 (Medtronic);

Fig. 1 Diagnostic imaging of a patient with a symptomatic giant aneurysm located in the right ICA. T2WI MRI/MRA shows the giant supraclinoid aneurysm with

mass effect and midline shift (a, b, c). Diagnostic DSA confirms the giant right supraclinoid aneurysm. The aneurysm size is 26
28 mm with a neck width of 11 mm

Treatment Strategy

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microguidewires: Transend 0.01400 200 cm (Stryker) and Synchro2 0.01400 300 cm (Stryker) Implants: 1
p64 5/30 mm and 1
p64 4.5/21 mm (phenox) Course of treatment: The right ICA was catheterized with an 8 F. Shuttle guide catheter and a Navien A+ 072 intermediate catheter were placed in the internal carotid artery. An Excelsior SL-10 microcatheter over a Transend 0.01400 microwire was placed in the M2 segment of the right middle cerebral artery (MCA). A Synchro2 0.01400 300 cm was used to swap the Excelsior SL-10 for a Marksman microcatheter. A p64 flow diverter 5/30 mm was implanted. After the p64 was deployed, DSA showed a significant flow entering the aneurysm sac, with contrast stagnation. The effect of a single flow diverter was therefore considered to be

insufficient. As a result, a second p64 flow diverter 4.5
21 mm was deployed inside the first device, with both implants covering the aneurysm neck (Fig. 2). Duration: 1st–10th DSA run: 70 min; fluoroscopy time: 30 mines Complications: none Post medication: 1
100 mg ASA PO daily for life and 1
75 mg of clopidogrel PO daily for at least 6 months

Fig. 2 DSA showing the implantation of two p64 flowdiverting devices in a patient with a giant symptomatic supraclinoid aneurysm. Manual compression of the right CCA with injection of the left ICA did not show any cross flow to the right (a). DSA run after the first (a) and second

(b, c) p64 device had been deployed. VasoCT (e) shows that both telescoping flow diverters have opened up fully; there is a correct wall apposition of the devices and significant contrast stagnation inside the aneurysm (e, f)

Clinical Outcome During the first 24 h after the procedure, the patient suffered from a mild headache and a right retro-ocular pain. She was discharged home asymptomatic after 3 days.

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Follow-Up Examinations

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The use of flow diverters has been increasing in recent years. The principle of flow diversion consists of redirecting the blood flow away from the aneurysm into the parent vessel, inducing blood stasis and aneurysm thrombosis with complete exclusion of the aneurysm from the

circulation and causing endothelial proliferation in the struts of the device. In practice, flow diverters have shown an aneurysm occlusion rate of 70–94% in the first 6 months and 86%–95% in the first year (Lylyk et al. 2009; Szikora et al. 2010). Aneurysms of the ophthalmic segment of the ICA have been shown to have a high angiographic occlusion rate with a low incidence of permanent clinically adverse effects. Some authors claim flow diversion to be the treatment of choice for the aneurysms of this vessel segment (Dai et al. 2012). In a subgroup analysis of the “Pipeline for Uncoilable or Failed Aneurysm” (PUFS) trial, a total of 30 paraophthalmic aneurysms were treated, 8 of those patients presented with a visual field deficit and 7 of them improved in this regard after flow diversion (Sahlein et al.

Fig. 3 One year follow-up MRI/MRA and DSA in a patient with a giant symptomatic aneurysm after two p64 devices had been implanted. The size of the thrombosed aneurysm is essentially unchanged; a significant modification of the intra-aneurysmal thrombus intensity is shown

on axial, coronal, and sagittal T2WI TSE (a, b, c). There is no edema around the aneurysm, and the midline shift has partially resolved. On the 1-year follow-up DSA, a complete occlusion of the aneurysm with patency of both p64s can be seen. There is no in-stent stenosis (d, e, f)

MRI performed 1 year after the procedure showed the thrombosed aneurysm was still of a similar size, with changes in the MRI being characteristics indicative of a thrombus (Fig. 3). The previous visual disturbance had completely resolved, and there was no evidence of neurological complications.

Discussion

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Supraclinoid Internal Carotid Artery Aneurysm: Giant Supraclinoid Aneurysm Treated with. . .

2015). Due to the technical challenge of some aneurysms in this location, the use of flow diverters can lead to serious complications such as ischemic or hemorrhagic events. The most common complications are thromboembolic events. Despite the low incidence of hemorrhagic events, their high mortality causes a need for the understanding and prevention of the factors that may lead to aneurysm rupture after flow diversion. In the case described in this chapter, no evidence of rupture was seen, and the patient remains asymptomatic. However, during the procedure, due to the hemodynamic characteristic of the inflow after the deployment of the first device, a second device was implanted to further increase the flow diversion effect and to hopefully diminish the hemodynamic stress on the aneurysm wall. There are four risk factors, which might increase the probability of hemorrhagic events after the deployment of a flow-diverting stent, as described by Kulcsar et al. (2011) in a report of ruptured aneurysm after flow diversion. The most important factors to consider are: 1. The size of the aneurysm: large and giant aneurysms can accumulate a large amount of thrombus. 2. Aneurysm-related symptoms, since they may indicate wall instability. 3. Morphology: an aspect ratio (i.e., height/neck) of >1.6, which means long aneurysms. 4. Morphology: a predisposition to an inertiadriven inflow, not addressed by the implanted flow diverter(s). This describes the situation in which the plane of the aneurysm orifice is perpendicular to the direction of the blood flow in the parent artery (Shojima 2017). A similar report has been published by Kallmes et al. (2015). In a retrospective study of 793 patients treated with flow-diverter stents, the incidence of post-procedural rupture was 0.5% (5/793), and they were more common in the posterior circulation and in aneurysms with a fundus diameter of >10 mm. The case described above presents all the risk factors described by Kulcsar

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et al. (2011), and one of the two as described by Kallmes et al. (2015). In about 80% of the patients concerned, aneurysm rupture after implanting a flow diverter occurs within the first 30 days after the procedure. This carries a mortality rate of 70–80% (Rouchaud et al. 2016). The underlying mechanism is not fully understood and needs further investigation. Some authors recommend the use of coils before implanting a flow diverter. The theory behind this is that coiling would stabilize the thrombus. Multiple reports, however, have shown that 20% of aneurysms treated with flow diverters had been previously coiled and still showed similar rupture rates (Rouchaud et al. 2016). After deploying a flow diverter, it is useful to differentiate between the proximal and distal landing zones, the compaction zone in the middle, and the transition zones between these three. Despite the compression maneuver used to compact the flow diverter in order to decrease the porosity, the transition zone remains relatively unchanged with a higher porosity (Darsaut et al. 2013; Makoyeva et al. 2013). Damiano et al. (2017) compared three types of aneurysm (fusiform, large, and medium saccular aneurysm) and compared flow reduction after compacting the device as opposed to telescoping with a second flow diverter. In this report, compacting induced greater flow reduction in fusiform aneurysms than in saccular aneurysms. In the patient reported in this chapter, the risk of an aneurysm rupture after the flow diversion procedure was considered high. The hemodynamic effect of a single p64 flow diverter did not appear sufficient to the operator. Therefore, he decided to deploy a second device inside the first flow diverter to completely cover the aneurysm neck, which would reduce the porosity of the implant.

Therapeutic Alternatives Extra-Intracranial Bypass Medina Microsurgical Clipping Parent Vessel Occlusion

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References Dai D, Ding YH, Kadirvel R, Rad AE, Lewis DA, Kallmes DF. Patency of branches after coverage with multiple telescoping flow-diverter devices: an in vivo study in rabbits. AJNR Am J Neuroradiol. 2012;33(1):171–4. https://doi.org/10.3174/ajnr.A2879. Damiano RJ, Tutino VM, Paliwal N, Ma D, Davies JM, Siddiqui AH, Meng H. Compacting a single flow diverter versus overlapping flow diverters for intracranial aneurysms: a computational study. AJNR Am J Neuroradiol. 2017;38(3):603–10. https://doi.org/ 10.3174/ajnr.A5062. Darsaut TE, Rayner-Hartley E, Makoyeva A, Salazkin I, Berthelet F, Raymond J. Aneurysm rupture after endovascular flow diversion: the possible role of persistent flows through the transition zone associated with device deformation. Interv Neuroradiol. 2013;19(2): 180–5. Kallmes DF, Hanel R, Lopes D, Boccardi E, Bonafé A, Cekirge S, Fiorella D, Jabbour P, Levy E, McDougall C, Siddiqui A, Szikora I, Woo H, Albuquerque F, Bozorgchami H, Dashti SR, Delgado Almandoz JE, Kelly ME, Turner R 4th, Woodward BK, Brinjikji W, Lanzino G, Lylyk P. International retrospective study of the pipeline embolization device: a multicenter aneurysm treatment study. AJNR Am J Neuroradiol. 2015;36(1):108–15. https://doi.org/ 10.3174/ajnr.A4111. Kulcsár Z, Houdart E, Bonafé A, Parker G, Millar J, Goddard AJ, Renowden S, Gál G, Turowski B, Mitchell K, Gray F, Rodriguez M, van den Berg R, Gruber A, Desal H, Wanke I, Rüfenacht DA. Intraaneurysmal thrombosis as a possible cause of delayed aneurysm rupture after flow-diversion treatment. AJNR Am J Neuroradiol. 2011;32(1):20–5. https://doi.org/ 10.3174/ajnr.A2370.

I. Lylyk et al. Lylyk P, Miranda C, Ceratto R, Ferrario A, Scrivano E, Luna HR, Berez AL, Tran Q, Nelson PK, Fiorella D. Curative endovascular reconstruction of cerebral aneurysms with the Pipeline embolization device: the Buenos Aires experience. Neurosurgery. 2009;64(4): 632–42; discussion 642–3; quiz N6. https://doi.org/ 10.1227/01.NEU.0000339109.98070.65. Makoyeva A, Bing F, Darsaut TE, Salazkin I, Raymond J. The varying porosity of braided self-expanding stents and flow diverters: an experimental study. AJNR Am J Neuroradiol. 2013;34(3):596–602. https://doi.org/ 10.3174/ajnr.A3234. Rouchaud A, Brinjikji W, Lanzino G, Cloft HJ, Kadirvel R, Kallmes DF. Delayed hemorrhagic complications after flow diversion for intracranial aneurysms: a literature overview. Neuroradiology. 2016;58(2):171–7. https:// doi.org/10.1007/s00234-015-1615-4. Sahlein DH, Fouladvand M, Becske T, 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, Marosfoi M, Cekirge SH, Kallmes DF, Nelson PK. Neuroophthalmological outcomes associated with use of the pipeline embolization device: analysis of the PUFS trial results. J Neurosurg. 2015;123(4):897–905. https://doi.org/10.3171/ 2014.12.JNS141777. Shojima M. Basic fluid dynamics and tribia related to flow diverter. J Neuroendovasc Ther. 2017;11(3):109–16. https://doi.org/10.5797/jnet.ra-diverter.2016-0012. Szikora I, Berentei Z, Kulcsar Z, Marosfoi M, Vajda ZS, Lee W, Berez A, Nelson PK. Treatment of intracranial aneurysms by functional reconstruction of the parent artery: the Budapest experience with the pipeline embolization device. AJNR Am J Neuroradiol. 2010;31(6):1139–47. https://doi.org/10.3174/ajnr. A2023.

Supraclinoid Internal Carotid Artery Aneurysm: Four Incidental Paraophthalmic and Supraclinoid Tandem Aneurysms, Treated with a Single Flow Diverter Stent

27

José E. Cohen, John Moshe Gomori, Sergey Spektor, and Yigal Shoshan Abstract

Tandem aneurysms are rare vascular lesions that denote the presence of two or more aneurysms in close proximity to each other on the same parent vessel. This condition presents unique challenges for treatment, whether via a surgical or an endovascular strategy. The occurrence of a posterior communicating artery aneurysm together with an ophthalmic segment or a paraclinoid aneurysm is among the most frequently observed combinations of tandem internal carotid artery (ICA) aneurysms. Each lesion requires a different surgical technique, and the mere presence of multiple aneurysms complicates the therapy for each one. This is also partially true for endovascular strategies, where the presence of tandem aneurysms requires additional precautions and probably a longer flow diverter stent. Traditionally, endovascular management of tandem aneurysms

was based on embolization tailored to each aneurysm and requiring multiple catheterizations for the treatment of each one. With this approach, procedural risks are multiplied by the number of aneurysm to be treated. More recent studies have presented encouraging results with the use of a single flow diverter for the treatment of tandem ICA aneurysms with a high rate of aneurysm exclusion and an acceptable risk profile. This approach also seems to compare favorably with the multistage approach in terms of cost, procedure time, fluoroscopy time, and radiation exposure. The presented case supports previous observations on the safety and effectiveness of the implantation of single flow diverter stent for the management tandem ICA aneurysms. Keywords

Internal carotid artery · Tandem aneurysms · Flow diverter stent · Stent-assisted coiling

J. E. Cohen (*) Hadassah-Hebrew University Medical Center, Jerusalem, Israel e-mail: [email protected] J. M. Gomori Department of Medical Imaging, Hadassah-Hebrew University Medical Center, Jerusalem, Israel e-mail: [email protected] S. Spektor · Y. Shoshan Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel e-mail: [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_94

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Patient A 65-year-old female patient with new-onset intermittent left-sided fronto-orbital headaches.

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segment measuring 7.5
8
4.5 mm and 4
2.5
2 mm, a small PcomA aneurysm measuring 3
3
2 mm, and a 1.5
1.5
1.5 mm aneurysm at the anterior choroidal artery (AchoA) segment (Fig. 1).

Diagnostic Imaging Treatment Strategy Preoperative brain MRI revealed a left internal carotid artery aneurysm. Diagnostic cerebral angiography confirmed the presence of multiple tandem left internal carotid artery aneurysms: two aneurysms in the carotid ophthalmic

The primary treatment goal was exclusion of all four left ICA aneurysms with a single flow diverter stent. We attributed the clinical complaint of orbital headaches to the largest

Fig. 1 Diagnostic imaging demonstrating tandem paraophthalmic and supraclinoid aneurysms of the left ICA. An axial T2WI MR image shows a midsized left ICA paraophthalmic aneurysm medial to the optic nerve [arrow (a)]. Three-dimensional reconstruction images of

rotational diagnostic angiography of the left ICA performed for workup revealed two carotid ophthalmic aneurysms. One PcomA and one AchoA aneurysm are shown. Working projections (b, c) were selected to adequately depict the four aneurysms

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Supraclinoid Internal Carotid Artery Aneurysm: Four Incidental Paraophthalmic and. . .

ophthalmic aneurysm but considered all the aneurysms as equal targets for effective treatment.

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Postmedication: 1
100 mg aspirin PO daily, 1
75 mg clopidogrel PO daily for 6 months; clopidogrel was then discontinued and ASA was continued indefinitely.

Treatment Clinical Outcome Procedure, 30.11.2015: flow diverter stent implantation into the left ICA from the left proximal M1 segment to the cavernous segment Anesthesia: general anesthesia; 4,000 IU heparin IV, bolus dose 80–100 IU/kg; target activated clotting time (ACT) 250–320 ses. Premedication: 1
100 mg ASA PO daily, 1
75 mg clopidogrel PO daily, 1
40 mg atorvastatin PO daily starting 5 days before the intervention; platelet reactivity to clopidogrel based on VerifyNow (Accumetrics) Access: right femoral artery, 6F Arrowsheath (Arrow); guide catheter: Navien A+ 058 (Medtronic); microcatheter: Excelsior XT27 (Stryker) for flow diverter stent implantation; microguidewire: Synchro2 0.01400 200 cm (Stryker) Implant: Pipeline Shield 3.75/20 (Medtronic) Stent apposition: Hyperglide 4/20 (Medtronic) Course of treatment: the Arrowsheath was placed into the left cervical ICA after catheter exchange in the left external carotid artery (ECA). The Navien intermediate catheter was positioned coaxially in the petrous left ICA segment, allowing the sheath to be further advanced into the mid-cervical left ICA. An Excelsior XT-27 microcatheter was then navigated along the distal half of the M1 segment. The flow diverter was deployed from the proximal M1 segment so that it covered the supraclinoid ICA, the paraclinoid ICA, and the horizontal cavernous portion of the ICA, and landed proximally at the posterior cavernous bend. Under-expansion of the deployed flow diverter at the paraclinoid and cavernous segments required gentle balloon angioplasty with a Hyperglide 4/20 compliant balloon (Medtronic) (Fig. 2). Duration: 1st–8th DSA run: 102 min; fluoroscopy time: 35 min Complications: none

Immediately after the endovascular procedure, the patient was transferred to the neurosurgical intensive care unit. The introducer sheath was removed 1 h later after ACT reevaluation. The patient was then extubated and her status returned to baseline. She did not complain of pain or discomfort and head CT performed 24 h later was unremarkable. The patient was discharged home 2 days later and was able to return to her regular activities. She was readmitted twice through the emergency room for left orbital pain; however, no hemorrhage was detected on head CT, and she was discharged on both occasions with regular analgesia.

Follow-Up Examinations Follow-up MRI 2 months after flow diverter implant did not show any lenticulostriate infarction in relation to the implanted stent. Follow-up angiography after 6 months confirmed complete exclusion of all four treated aneurysms and complete angiographic reconstruction of the left ICA (Fig. 3).

Discussion Multiple strategies exist for the treatment of tandem intracranial aneurysms. Among the endovascular options, flow diverter stents may offer distinct advantages compared with other methods. From a technical point of view, coiling techniques allow for focal arterial reconstruction and intra-aneurysmal maneuvering, while flow diverter stents allow for segmental arterial reconstruction without the need for intra-aneurysmal maneuvering.

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Fig. 2 Treatment of four aneurysms of the left intradural ICA with a single flow diverter. Angiography of the left ICA from the contralateral oblique projection was chosen for guidewire navigation up to the PcomA segment (a). Road map in the contralateral oblique projection allowed safe, albeit challenging navigation of the microcatheter

across the left ICA to reach the distal M1 segment (b). The radiographic image (contralateral oblique view), shows balloon angioplasty of the proximal half of the deployed flow diverter (c). Radiographic image (lateral view) confirms full expansion of the flow diverter stent (d)

One of the first reported experiences treating tandem aneurysms with flow diverter stents (John et al. 2017) included a series of 20 female patients with a total of 47 aneurysms treated with the Pipeline Embolization Device (PED). All aneurysms were located along the ICA: 15 patients had two aneurysms, three patients

had three aneurysms, and two patients had two aneurysms on bilateral ICAs. The average size of the largest aneurysms was 6.6  5.5 mm and the smaller second aneurysms averaged 3.0  1.4 mm. The average distance between the 33 aneurysms that were not on opposite sides of the vessel wall was 9.1  2.5 mm. An average of

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Supraclinoid Internal Carotid Artery Aneurysm: Four Incidental Paraophthalmic and. . .

Fig. 3 Follow-up imaging after flow diversion of four intradural ICA tandem aneurysms. MRI (axial FLAIR image (a)) performed 2 months after the intervention did not show any area of lenticulostriate infarction in relation to the implanted stent. Angiography of the left ICA

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(posterior–anterior view (b), lateral view (c)) obtained after 6 months demonstrates complete exclusion of all four ICA aneurysms and arterial reconstruction. The flow diverter stent is fully patent with no features of in-stent stenosis

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1.3 Pipeline devices (range 1–4) were used to treat the aneurysms, while a single flow diverter stent was placed in over 80% of cases (18/22). None of the aneurysms were adjunctively coiled. The authors reported no technical intraprocedural complications. Three patients (15%) had mild transient neurological symptoms but none suffered permanent neurological deficits. There were no cases of aneurysmal rupture or hemorrhage and no deaths. Follow-up imaging was available for 40 aneurysms, 34 of which showed complete occlusion (85%) and six showing residual filling (15%). Similar results have recently been presented by other groups (Bhogal et al. 2018) in a multicenter study enrolling a total of 69 patients (62 female, 89.8%). Overall, there were 169 aneurysms, and 47 patients (68.1%) presented with tandem aneurysms. The largest aneurysms measured 7.69  5.3 mm (range 1.5–26 mm) in height and 6.64  4.71 mm (range 1.5–23 mm) in width, while the smaller aneurysms measured 2.61  1.32 mm (range 0.8–9.5 mm) in height and 2.32  1.12 mm (range 0.7–8 mm) in width. The p64 was used in 36 patients, the Pipeline device in 28 patients, and the Surpass device (Stryker) in five patients. Follow-up information was available for 130 aneurysms in 54 patients. At initial follow-up (mean 7.2  4.2 months), 45 (83.3%) of the larger aneurysms and 66 (86.8%) of the smaller aneurysms were satisfactorily occluded. At delayed follow-up (18  4.6 months), 48 of the larger aneurysms (88.9%) and 71 of the smaller aneurysms (93.4%) were occluded. There were three complications, including one death. The authors concluded that a single flow diverter stent can be used to successfully treat multiple tandem

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aneurysms of the ICA with a high rate of aneurysm exclusion and an acceptable risk profile. Tandem aneurysms of the ICA can be often be managed successfully with flow diverter stent implantation, and this approach is likely to become the therapy of choice for this condition. From a technical point of view, the presence of multiple aneurysms requires more careful endovascular micronavigation, and the need to protect longer arterial segments requires judicious use of longer or multiple flow diverter stents, as seen in 20% of the cases presented by John et al. (2017). Our case demonstrates the effective simultaneous treatment of four ICA aneurysms with a single flow diverter, and contributes to the available body of evidence supporting the use of flow diverters in the management of tandem aneurysms of the ICA.

Therapeutic Alternatives Microsurgical Clipping Stent-Assisted Coil Occlusion Telescoping Stenting

References Bhogal P, Chudyk J, Bleise C, Lylyk I, Perez N, Henkes H, Lylyk P. Treatment of unruptured, tandem aneurysms of the ICA with a single flow diverter. Clin Neuroradiol. 2018. https://doi.org/10.1007/ s00062-018-0723-z. John S, Bain M, Cerejo R, Bauer A, Masaryk T, Hussain MS, Rasmussen P, Toth G. Flow diverter treatment of tandem intracranial aneurysms. World Neurosurg. 2017;107:142–7. https://doi.org/10.1016/j. wneu.2017.07.146.

Supraclinoid Internal Carotid Artery Aneurysm: Iatrogenic Aneurysm of the Supraclinoid Internal Carotid Artery After Craniopharyngioma Resection; Treatment of an Unruptured Fusiform Aneurysm with a Cardiatis Flow Diversion Device; Technical Aspects, Follow-Up Results, and Literature Review

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D. Mauricio Alvarez, Rene Viso, Ivan Lylyk, Esteban Scrivano, and Pedro Lylyk Abstract

At the age of 21, 13 years after a successful total gross resection of a craniopharyngioma (CP) had been performed using a right transcranial approach, a male patient presented with a fusiform aneurysm of the right supraclinoid internal carotid artery (ICA). This was manifesting through cluster headaches and amaurosis in the right eye, and magnetic resonance angiography (MRA) was immediately carried out. Although there are plentiful references to this complication following craniopharyngioma treatment in literature, there is still discussion regarding how to treat it, with endovascular treatment generally considered a safer option in respect to the aneurysm’s anatomy. It is thought that flow diverter devices carry the fewest complications as well as offering unique advantages over other devices currently available. The management of

D. M. Alvarez · R. Viso · I. Lylyk · E. Scrivano · P. Lylyk (*) Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina e-mail: [email protected]; reneviso@lylyk. com.ar; [email protected]; [email protected]; [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_140

fusiform supraclinoid ICA aneurysms following CP surgery is the main topic of this chapter. Keywords

Supraclinoid internal carotid artery · Cardiatis · Flow diverter · Fusiform aneurysm · Craniopharyngioma

Patient Thirteen years after the successful total gross resection (TGR) of a craniopharyngioma (CP) via a right transcranial approach, a 21-year-old male patient presented with cluster headaches and right eye amaurosis. After the surgery, the patient had become obese and developed panhypopituitarism, and he was still under the care of a nutritionist and taking hormone replacement therapy. Magnetic resonance imaging (MRI) of the brain did not show any recurrence of the CP; however, magnetic resonance angiography (MRA) revealed a fusiform aneurysm of the right supraclinoid internal carotid artery (ICA).

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Diagnostic Imaging

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The main treatment objectives of this case were not only to prevent the aneurysm rupturing but also to stop the mass effect from increasing, which

would have happened had the aneurysm continued to grow. Another equally important treatment objective was to alleviate the existing mass effect, which had actually led to the aneurysm being discovered. Many times, fusiform aneurysms are considered to be a benign lesion; however, they can exhibit characteristics alongside their size and morphology, which translate into risks such as those evident in the clinical history of our patient and described in current literature. The treatment plan was to deploy a flow diverter device from the distal segment of the ICA to the proximal ophthalmic segment, thus preserving the parent artery

Fig. 1 DSA showing a fusiform aneurysm of the right ICA starting distal to the ophthalmic artery origin up to the ICA bifurcation; posterior-anterior (a) and lateral

projection (b), and rotational DSA with 3D reconstruction (c) with a fusiform aneurysm with a vessel diameter of 6.5 mm maximum and a length of almost 20 mm

A digital subtraction angiography (DSA) was performed, confirming a fusiform aneurysm of the right supraclinoid ICA (Fig. 1).

Treatment Strategy

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Supraclinoid Internal Carotid Artery Aneurysm: Iatrogenic Aneurysm of the Supraclinoid. . .

and its branches while letting the mass effect symptoms decrease as the aneurysm thrombosed and gradually reduced.

Treatment Procedure, 21.09.2011: endovascular treatment of a fusiform aneurysm of the right supraclinoid ICA with a flow diverter stent Anesthesia: general anesthesia, 10,000 IU unfractionated heparin (Riveparin, Rivero) IV Premedication: 1
100 mg ASA (Aspirin, Bayer Vital) PO daily and 1
75 mg clopidogrel (Troken, Laboratorio Bagó) PO daily, both starting 5 days before the procedure Access, right femoral artery, 8F sheath (Terumo); guide catheter: 8F Brite Tip (Cordis) and 6F Envoy (Cordis); microcatheter: Marksman 0.02700 (Medtronic); microguidewire: Transend 0.01400 (Stryker) Implant: 1
Multilayer Flow Modulator (MFM) 4.25/20 mm (Cardiatis) Course of treatment: after an 8F vascular sheath was placed in the right common femoral artery and the right ICA was catheterized. Standard posterior-anterior, lateral and Towne’s angiographic images were taken for all vessels involved in the procedure. Rotational angiography with 3D reconstruction was also done in order to determine the most suitable working projection. The aneurysm was measured using standard methods and included the height and width of the aneurysm. The angles of flow and connecting branches were also calculated. After a diagnostic DSA was carried out, an 8F Brite Tip catheter was placed into the right common carotid artery, and an Envoy 6F catheter was placed into the petrous segment of the ICA. A Marksman 0.02700 microcatheter was maneuvered into the distal M1 segment of the right-hand middle cerebral artery (MCA). A Cardiatis MFM device was deployed and positioned from the distal segment of the ICA to the proximal ophthalmic segment, entirely covering the fusiform aneurysm segment. The final angiogram confirmed the correct position of the device as well as showing significant contrast

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stagnation inside the dome. An Xpert CT was performed right after the procedure, in which no ischemic or hemorrhagic lesions were observed (Fig. 2). Duration: 1st–11th DSA run: 85 min; fluoroscopy time: 43 min Complications: none Post medication: 1
100 mg ASA PO daily for life and 1
75 mg clopidogrel for 6 months

Clinical Outcome The endovascular treatment was well tolerated and no ischemic or hemorrhagic events were observed. After the procedure, the patient went to an inpatient unit for recovery, where an inguinal ultrasound was performed that showed no local complications. A physical examination showed no new neurological deficits and the patient was discharged 2 days later with a mRS score of 1.The cluster headaches eventually ceased some time after the procedure.

Follow-Up Examinations The first follow-up DSA was performed the day after the procedure and showed no change. The second DSA follow-up was done 6 months after the treatment and showed complete occlusion of the aneurysm with a discrete in-stent stenosis that had neither clinical nor hemodynamic relevance. The third follow-up DSA was done 13 months after the procedure and confirmed that the aneurysm had been completely occluded, and the in-stent stenosis was remaining stable and still clinically irrelevant. The final follow-up DSA was performed 28 months after the treatment, confirming both the complete occlusion of the aneurysm and the patency of the flow diverter device, with no in-stent stenosis. Finally, a follow-up MRI/MRA was performed 50 months after the procedure, which highlighted how the MR intensity signal of the thrombus had changed over time and that this was commensurate with the aneurysm occluding (Fig. 3).

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Fig. 2 Treatment of a symptomatic right fusiform aneurysm of the right supraclinoid ICA. DSA images in working positions during (a) and after (b, c) deployment of a Cardiatis MFM device, this confirmed the correct opening of the proximal and distal ends of the device (b). After deployment,

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a stagnation of contrast material was clearly seen inside the aneurysm (d). VasoCT high resolution images at maximum intensity (e, f) confirmed that the stent to wall apposition was good and that the aneurysm had been fully covered

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Supraclinoid Internal Carotid Artery Aneurysm: Iatrogenic Aneurysm of the Supraclinoid. . .

Discussion Intracranial aneurysms are classified according to their shape into saccular and non-saccular types. “Fusiform” describes non-saccular arterial vessel dilatations involving the entire vessel wall (Nakayama et al. 1999). It is a morphological term with no reference to the origin or clinical significance of the lesion (Horie et al. 2003). It is defined as a circumferential arterial dilatation resulting from pathological involvement of the entire artery, giving it a spindle shape when viewed externally (Day et al. 2003; Findlay et al. 2002). Fusiform aneurysms may be caused by dissection or atherosclerosis (Day et al. 2003), by collagen or elastin metabolism disorders, by infections, or (very rarely) by neoplastic invasion of the arterial wall (Selviaridis et al. 2002). They represent about 3–13% of all intracranial aneurysms (Al-Yamany and Ross 1998) and tend to be located in the vertebrobasilar system. They are only infrequently found in the anterior circulation, in which case they tend to be seen in either the middle cerebral artery or internal carotid artery (Day et al. 2003; Findlay et al. 2002; Horie et al. 2003). The age and sex distribution of patients with fusiform aneurysms differs from that of patients with saccular aneurysms, with the former being more frequent in men (Park et al. 2008). The most frequent clinical manifestations are subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), neurological deficits caused by either ischemia or mass effect exerted by the aneurysm, nonspecific symptoms such as dizziness with or without headache, and incidental findings (Park et al. 2008). Treatment of fusiform aneurysms should be based on the presence and type of symptoms, the lesion size and location, and the anticipated risk of the possible intervention(s) (Park et al. 2008). Given the fact that fusiform aneurysms of the MCA are the most frequent, Day, Lanzino, and Nikawa (Day et al. 2003; Lanzino et al. 1997; Niikawa et al. 2002) have suggested that most small and some large focal dilatations, especially those that are asymptomatic, should be treated conservatively unless serial neuroimaging assessment indicates significant enlargement over time.

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However, once symptoms manifest, strong intervention is called for. Dilations occurring as a side effect of intercranial tumors (generally CP tumors) could be added to the pathophysiology of fusiform aneurysms of the right supraclinoid carotid artery, whether they are surgically treated or not. This has been mentioned several times in the literature, in which aneurysms found intraoperatively but physiopathologically related to the presence of the tumor are treated as a subsection of fusiform aneurysms. One such example is the case reported on by Qian et al. (2019) where they describe a patient with an intraoperative finding of a previous communicating artery blister-like aneurysm during a primary CP resection. According to the literature, its formation could have been due to several potential factors. These include dissemination of the tumor tissue and degeneration of the vascular wall which could be secondary to the rupture of the cysts characteristic of a CP. The pus which comes out of a ruptured cyst contains inflammatory mediators such as Interleukin-6 (IL-6), a2HS-glycoprotein, a1-antichymotrypsin, and apolipoproteins, all of which are capable of producing inflammatory and cytotoxic reactions, including lipid oxidative damage, reactive gliosis, and chemical meningitis. These ultimately end up changing the internal environment around the tumor (Hakizimana et al. 2018; Massimi et al. 2017; Mori et al. 2004). Equally, aneurysms can form following surgical trauma during a resection. CPs are rare embryonic malformations of the sellar and parasellar areas with a low histological grade (WHO Io), even though they can arise anywhere along the craniopharyngeal canal (Müller 2014). They are considered to be benign tumors and are typically treated with both surgery and radiation, an approach that offers 5-year progression-free survival (PFS) rates exceeding 90%. However, CPs present a surgical challenge because of their central location and close proximity to sensitive structures such as the optic apparatus, pituitary gland, hypothalamus, circle of Willis, brain stem, and temporal lobes. As a result, CPs carry high morbidity and mortality, including endocrinopathy, hypothalamic

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Fig. 3 Follow-up DSA on day 1 (a) after the flow diverter implantation confirmed the patency of the device. DSA at 6 months (b) and at 28 months (c) confirmed the complete occlusion of the aneurysm with discrete in-stent stenosis

dysfunction, visual field deficits, cerebrovascular sequelae, secondary malignancies, and neurocognitive decline, all of which significantly impact the quality of life among this mostly

pediatric population (O’steen and Indelicato 2018). CP represents 1.2–4% of all childhood intracranial tumors with a bimodal age distribution

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Supraclinoid Internal Carotid Artery Aneurysm: Iatrogenic Aneurysm of the Supraclinoid. . .

with peak incidence rates in children of ages 5 to 14 years and adults of ages 50 to 74 years. From an anatomopathological point of view, there are two types of CP: adamantinomatous and papillary, the former being most frequent in childhood and adolescence (Larkin and Ansorge 2013). Within the differential diagnoses of suprasellar tumors are included hypothalamic glioma and optic glioma, Langerhans cell histiocytosis, Rathke’s cleft cyst, xanthogranuloma, intracranial germinoma, epidermoid tumor, arachnoid cysts, colloidal cyst of the third ventricle, pituitary adenoma, aneurysm (Fig. 4), and rare inflammatory variations (Warmuth-Metz et al. 2004). Treatment strategies vary depending on the location of the tumor. For favorably localized CPs, the preferred treatment of choice is an attempt at complete resection while preserving both visual and hypothalamic function. For unfavorably localized tumors (e.g., too close to or too entangled with the optic nerve and/or the hypothalamus), controversy exists over whether complete resection should still be attempted or whether a planned limited resection should be performed. Taking into account the above, the treatment guidelines include the surgical approach. This could involve a transcranial approach, a transsphenoidal approach, a less invasive surgical technique such as the application of sclerosing substances for cystic tumors that show recurrence. The guidelines also include adjuvant therapy, including radiosurgery, stereotactic radiotherapy and intracavitary beta irradiation. Therapeutic consequences of surgery and irradiation also remain a matter of debate (Buchfelder et al. 2013; Müller 2014). The short and long-term prognosis depends on the treatment modality and success. The range of possibilities varies between cases of pituitary deficiencies, hypothalamic dysfunction, obesity and eating disorders, visual disturbances, and cerebrovascular morbidity. The latter also includes fusiform aneurysms of the right supraclinoid carotid artery on postoperative MRI (Müller 2014; Reynolds et al. 2018). It is this last morbidity on which this chapter is based. Fusiform aneurysms of the right supraclinoid carotid artery are not infrequent complications following radical CP resection (Li et al. 2015)

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taking either a transcranial or transsphenoidal approach. These lesions appear as a supraclinoid fusiform widening of the ICA, often with distal extension (Reynolds et al. 2018). The incidence is about 9–29%, with a mean time to onset of 6.8 months, and tends to stabilize in the pediatric population in an average time of 15.4 months. Its course is often asymptomatic, and this is why several authors suggest observation and conservative treatment (Elliott and Wisoff 2010). Nagata et al. (2010) found in their study that fusiform dilatations of the ICA are due to damage to either the adventitia or the vasa vasorum. Following this damage, which usually occurs during manipulation or surgical traction, a natural healing process would ensue, involving adventitial hyperplasia and elastic fiber deposition in the adventitia-like tissue and thus a more stable diameter and lower risk of rupture. This hyperplasia theory may best explain the pathogenesis of fusiform dilations of the ICA in pediatric patients. However, the elastic fibers of the ICA are markedly reduced in adult patients, offering better tolerance to vessel manipulation. This might partially explain why fusiform aneurysms of the supraclinoid ICA are rare in adult patients (Gomes and Chopard 2003). Among the histological findings were neogenesis of the vasa vasorum and an increase of collagen fibers in the adventitia. In the media, collagen fibers became rougher and the elastic fibers shortened. The smooth muscle was also damaged in the media. These findings strongly indicate that the surgical manipulation of the ICA can be an important cause of these fusiform dilatations (Nagata et al. 2010). Sutton (1994) postulates that because of the mechanical disruption of muscle, collagen, and elastic fibers within the aneurysm wall, these lesions represent dissecting pseudoaneurysms. There are many factors that must be considered to prevent the formation of FASICA during surgery as adopting a surgical approach, minimizing bipolar cauterization, and a generally piecemeal tumor treatment strategy strongly adhered to vascular structures (Li et al. 2015). The treatment of patients with CP includes adjuvant radiotherapy (RT), which has been the

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Fig. 4 Diagnostic DSA showing a large superior hypophyseal artery aneurysm in a 41-year-old male patient discovered as an incidental finding during pituitary surgery in which no pituitary adenoma was found (a, b, c), images

in working position during treatment in which a Pipeline Embolization Device (PED) (d, e) was placed, and followup MRA of the patient 4 years later showing complete occlusion of the aneurysm

subject of much discussion (Abla et al. 2014; Kamide et al. 2016; Wang et al. 2018; Wu et al. 2014). The natural history of RT-induced aneurysms is different to that of spontaneous aneurysms. These aneurysms are more often saccular than fusiform; they develop at a mean

time of 10 years following treatment and present with subarachnoid hemorrhage in more than 60% of cases. The putative pathogenesis of RT-induced aneurysms is endothelial damage from the ionizing radiation, and smaller vessels and capillaries are usually more greatly affected than larger-caliber vessels. Another

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important difference is that an RT-induced aneurysm does not necessarily have to be ipsilateral to the surgical approach as in traumatic aneurysms during neurosurgery (Elliott and Wisoff 2010). This kind of fusiform dilatation of carotid artery represents a benign entity that should be radiographically observed. Despite the anxiety naturally felt by patients, their families, and practitioners with the growth of an aneurysm, a conservative approach may be appropriate as long as the progressive dilation remains asymptomatic. However, some specific scenarios have been proposed in which one should try to actively prevent rupture: persistent or severe headaches around the lesion location and side, neurological deficits from mass effect, and thromboembolic events or focal change in morphological characteristics (development of a significant asymmetry along one wall or saccular component), all of which make rupture a concern (Elliott and Wisoff 2010; Reynolds et al. 2018). If conservative management is chosen, the patient should be evaluated annually by MRI/MRA to assess shape and size of the aneurysm (Egemen et al. 2012).

Apart from conservative management, surgery and endovascular treatment can also be considered. Despite successful surgical interventions having been described, including cases of clipping, trapping, wrapping, resection, primary reconstruction, or arterial graft interposition, dissecting pseudoaneurysms in particular are not always suitable for surgical occlusion because of the absence of a true neck or aneurysm wall. They may be difficult to treat surgically without sacrificing the parent vessels (Reynolds et al. 2018; Tirakotai et al. 2002; Tokunaga et al. 2001). Endovascular techniques, which are considered less invasive than open microsurgery, have been widely shown to be associated with successful results. These techniques have also been increasingly utilized to treat these aneurysms with acceptable morbidity and mortality rates. Several publications have been published by different authors concerning endovascular treatment techniques. These include Kim et al. (2018) with a selective coil embolization of a ruptured fusiform aneurysm involving the anterior choroidal artery and posterior communicating artery and Ogilvy et al. (2011) who reported on an asymptomatic,

Fig. 5 Diagnostic DSA showing a dissecting pseudoaneurysm on the lateral aspect of the distal segment of the right ICA in a 7-year-old male patient, found during follow-up MRI (images not available) after the second resection for hypothalamic tumor (a). VasoCT acquisition

(b) with maximum intense projection (MIP) demonstrates the post-treatment result after coil occlusion of the aneurysm and covering of the aneurysm and the concerning vessel segment with a flow diverter stent

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enlarging fusiform dilatation of carotid artery in a child after CP resection. The child subsequently underwent stent-assisted coiling without complications and with complete obliteration of the lesion at 6 months. Flow diverter devices allow the parent artery to be preserved by altering flow and promoting intraaneurysmal thrombus formation. They have a high rate of aneurysm occlusion and may nullify the need for additional endovascular treatments, as sometimes required after coiling. Since the entire length of the diseased artery is treated, the likelihood of a local recurrence from an adjacent portion of the aneurysm is low. Furthermore, it removes the need to catheterize the fragile pseudoaneurysm fundus, relying instead on the appropriate sizing of the device to the arterial segments proximal and distal to the aneurysm and addressing symptoms due to mass effect via gradual thrombosis and involution of the treated aneurysm. For the above reasons, these devices should be a tool to be taken into consideration for the endovascular treatment of traumatic dissections and dissecting aneurysms (Reynolds et al. 2018) (Fig. 5). To conclude, cases of fusiform aneurysms of the right supraclinoid ICA after a surgical trauma during the resection of a CP are widely reported in the literature. Although they are benign in most cases, the treatment guidelines and the best approach should be individualized for each patient. In patients who experience tumor recurrence and significant mass effect, open surgical treatment with tumor resection and vessel reconstruction with clips is a possible option. Several reports have described the benefits of endovascular therapy. Flow diverter devices in particular allow for safe and efficacious treatment of these vessel injuries.

Therapeutic Alternatives Conservative Management Microsurgical Clipping Microsurgical Wrapping Telescoping Stenting

D. M. Alvarez et al.

References Abla AA, Lawton MT, McDermott MW. Intracranial aneurysm formation following radiation. World Neurosurg. 2014;81(3–4):492–3. https://doi.org/10.1016/j.wneu.2014. 01.007. Al-Yamany M, Ross IB. Giant fusiform aneurysm of the middle cerebral artery: successful Hunterian ligation without distal bypass. Br J Neurosurg. 1998;12(6): 572–5. Buchfelder M, Schlaffer SM, Lin F, Kleindienst A. Surgery for craniopharyngioma. Pituitary. 2013;16(1):18–25. https://doi.org/10.1007/s11102-012-0414-8. Day AL, Gaposchkin CG, Yu CJ, Rivet DJ, Dacey RG Jr. Spontaneous fusiform middle cerebral artery aneurysms: characteristics and a proposed mechanism of formation. J Neurosurg. 2003;99(2):228–40. https:// doi.org/10.3171/jns.2003.99.2.0228. Egemen E, Massimi L, Di Rocco C. Iatrogenic intracranial aneurysms in childhood: case-based update. Childs Nerv Syst. 2012;28(12):1997–2004. https://doi.org/ 10.1007/s00381-012-1907-5. Elliott RE, Wisoff JH. Fusiform dilation of the carotid artery following radical resection of pediatric craniopharyngiomas: natural history and management. Neurosurg Focus. 2010;28(4):E14. https://doi.org/ 10.3171/2010.1.FOCUS09296. Findlay JM, Hao C, Emery D. Non-atherosclerotic fusiform cerebral aneurysms. Can J Neurol Sci. 2002; 29(1):41–8. https://doi.org/10.3171/2010.1.FOCUS 09296. Gomes CR, Chopard RP. A morphometric study of age-related changes in the elastic systems of the common carotid artery and internal carotid artery in humans. Eur J Morphol. 2003;41(3–4):131–7. Hakizimana D, Poulsgaard L, Fugleholm K. Chemical meningitis from a leaking craniopharyngioma: a case report. Acta Neurochir. 2018;160(6):1203–6. https:// doi.org/10.1007/s00701-018-3530-z. Horie N, Takahashi N, Furuichi S, Mori K, Onizuka M, Tsutsumi K, Shibata S. Giant fusiform aneurysms in the middle cerebral artery presenting with hemorrhages of different origins. Report of three cases and review of the literature. J Neurosurg. 2003;99 (2):391–6. Kamide T, Mohri M, Misaki K, Uchiyama N, Nakada M. Intracranial aneurysm formation after radiotherapy for medulloblastoma. Surg Neurol Int. 2016;7(Suppl 37): S880–2. https://doi.org/10.4103/2152-7806.194501. Kim J, Chang C, Jung Y. Selective coil embolization of ruptured fusiform aneurysm involving anterior choroidal artery and posterior communicating artery. World Neurosurg. 2018;118:274–8. https://doi.org/10.1016/j. wneu.2018.07.135. Lanzino G, Kaptain G, Kallmes DF, Dix JE, Kassell NF. Intracranial dissecting aneurysm causing subarachnoid hemorrhage: the role of computerized tomographic angiography and magnetic resonance

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angiography. Surg Neurol. 1997;48(5):477–81. https:// doi.org/10.1016/s0090-3019(97)00178-x. Larkin SJ, Ansorge O. Pathology and pathogenesis of craniopharyngiomas. Pituitary. 2013;16(1):9–17. https://doi.org/10.1007/s11102-012-0418-4. Li Q, Wang C, Xu J, You C. Endovascular treatment for fusiform dilation of internal carotid artery following craniopharyngioma resection: a case illustration. J Child Neurol. 2015;30(10):1354–6. https://doi.org/ 10.1177/0883073814552105. Massimi L, Martelli C, Caldarelli M, Castagnola M, Desiderio C. Proteomics in pediatric cystic craniopharyngioma. Brain Pathol. 2017;27(3):370–6. https://doi.org/10.1111/bpa.12502. Mori M, Takeshima H, Kuratsu J. Expression of interleukin-6 in human craniopharyngiomas: a possible inducer of tumor-associated inflammation. Int J Mol Med. 2004;14(4):505–9. Müller HL. Craniopharyngioma. Endocr Rev. 2014;35(3): 513–43. https://doi.org/10.1210/er.2013-1115. Nagata T, Goto T, Ichinose T, Mitsuhashi Y, Tsuyuguchi N, Ohata K. Pathological findings of fusiform dilation of the internal carotid artery following radical dissection of a craniopharyngioma. J Neurosurg Pediatr. 2010; 6(6):567–71. https://doi.org/10.3171/2010.9.PEDS10280. Nakayama Y, Tanaka A, Kumate S, Tomonaga M, Takebayashi S. Giant fusiform aneurysm of the basilar artery: consideration of its pathogenesis. Surg Neurol. 1999;51(2):140–5. Niikawa S, Yamada J, Sumi Y, Yamakawa H. Dissecting aneurysm of the middle cerebral artery manifesting as subarachnoid hemorrhage and hemorrhagic infarctions–case report. Neurol Med Chir (Tokyo). 2002;42(2):62–6. https://doi.org/10.2176/nmc.42.62. O’steen L, Indelicato DJ. Advances in the management of craniopharyngioma. F1000Res. 2018;7:F1000. Faculty Rev-1632. https://doi.org/10.12688/f1000research. 15834.1. Ogilvy CS, Tawk RG, Mokin M, Yang X, Levy EI, Hopkins LN, Siddiqui AH. Stent-assisted coiling treatment of pediatric traumatic pseudoaneurysm resulting from tumor surgery. Pediatr Neurosurg. 2011;47(6):442–8. https://doi.org/10.1159/000339353. Park SH, Yim MB, Lee CY, Kim E, Son EI. Intracranial fusiform aneurysms: it’s pathogenesis, clinical characteristics and managements. J Korean Neurosurg Soc.

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2008;44(3):116–23. https://doi.org/10.3340/jkns.2008. 44.3.116. Qian H, Wang L, Brooks KS, Zhao X, Liu F, Sun Y, Shi X, Lei T. Intraoperative finding of an anterior communicating artery blister-like aneurysm during a primary craniopharyngioma resection: accidental or incidental? World Neurosurg. 2019;127:514–7. https://doi.org/10. 1016/j.wneu.2019.04.067. Reynolds MR, Heiferman DM, Boucher AB, Serrone JC, Barrow DL, Dion JE. Fusiform dilatation of the internal carotid artery following childhood craniopharyngioma resection treated by endovascular flow diversion-a case report and literature review. J Clin Neurosci. 2018; 54:143–5. https://doi.org/10.1016/j.jocn.2018.05.006. Selviaridis P, Spiliotopoulos A, Antoniadis C, Kontopoulos V, Foroglou G. Fusiform aneurysm of the posterior cerebral artery: report of two cases. Acta Neurochir. 2002;144(3):295–9. Discussion 299. https://doi.org/10.1007/s007010200039. Sutton LN. Vascular complications of surgery for craniopharyngioma and hypothalamic glioma. Pediatr Neurosurg. 1994;21(Suppl 1):124–8. https://doi.org/ 10.1159/000120874. Tirakotai W, Sure U, Benes L, Aboul-Enein H, Schulte DM, Riegel T, Bertalanffy H. Successful management of a symptomatic fusiform dilatation of the internal carotid artery following surgery of childhood craniopharyngioma. Childs Nerv Syst. 2002;18(12): 717–21. https://doi.org/10.1007/s00381-002-0666-0. Tokunaga K, Kusaka N, Nakashima H, Date I, Ohmoto T. Coil embolization of intradural pseudoaneurysms caused by arterial injury during surgery: report of two cases. AJNR Am J Neuroradiol. 2001;22(1):35–9. Wang G, Zhang X, Feng M, Guo F. Comparing survival outcomes of gross total resection and subtotal resection with radiotherapy for craniopharyngioma: a metaanalysis. J Surg Res. 2018;226:131–9. https://doi.org/ 10.1016/j.jss.2018.01.029. Warmuth-Metz M, Gnekow AK, Müller H, Solymosi L. Differential diagnosis of suprasellar tumors in children. Klin Padiatr. 2004;216(6):323–30. https://doi. org/10.1055/s-2004-832358. Wu H, Guo L, Qiu Y, Yuan X. Cavernous internal carotid artery aneurysm after radiotherapy presenting with external ophthalmoplegia. J Craniofac Surg. 2014;25(4): e380–2. https://doi.org/10.1097/SCS.0000000000000930.

Internal Carotid Artery Aneurysm: Large Saccular Persistent Primitive Trigeminal Artery Aneurysm, with Mass Effect, Treated with Flow Diverter and Deconstructive Technique with Coils, Good Clinical Outcome, and Follow-Up Results

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Ivan Lylyk, Rene Viso, Rodrigo Muñoz, Jorge Chudyk, and Pedro Lylyk Abstract

A 60-year-old female patient presented with diplopia, facial pain, and recurrent episodes of headaches. A large symptomatic aneurysm of the left internal carotid artery (ICA) at the origin of a persistent primitive trigeminal artery (PPTA) was treated using a combined endovascular deconstructive technique with coils and a reconstructive technique with a flow diverter stent. DSA after 3 months showed a remnant of the aneurysm still present, and the patient was indeed still symptomatic. A second flow diverter stent was placed, which then led to a good clinical and angiographic result. This case illustrates the benefit of combining different endovascular techniques. Flow diversion is a treatment method

used for large saccular sidewall aneurysms. However, if a flow diverter stent covers an aneurysm at the origin of an artery with high flow requirements, the aneurysm may take longer to completely occlude or even not occlude at all if only one flow diverter stent is implanted. Combining the techniques of coil occlusion and extrasaccular flow diversion is the main topic of this report, alongside an analysis of the association of this particular anatomic variant with more frequent presentations of cerebrovascular malformations. Keywords

Internal carotid artery · Persistent primitive trigeminal artery · Aneurysm · Cranial nerve palsy · Flow diverter · Endovascular treatment · Deconstructive endovascular treatment

I. Lylyk (*) · R. Viso · R. Muñoz · J. Chudyk · P. Lylyk Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina e-mail: [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_145

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Patient A 60-year-old female patient with a known medical history of high arterial blood pressure and hypothyroidism, who presented with diplopia, facial pain probably due to a compression of the

Fig. 1 (continued)

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V1 or V2 root of the 5th cranial nerve, and recurrent episodes of headaches, which had started 1 month before admission. The physical examination revealed a 6th cranial nerve palsy on the left-hand side.

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Fig. 1 Diagnostic DSA of a patient with a symptomatic, large saccular left ICA aneurysm at the origin of a Saltzman type II PPTA (posterior-anterior projection (a) and lateral projection (b)). Rotational DSA with 3D reconstruction (c) showed the neck of the aneurysm in relation to the ICA and the PPTA trunk with an aneurysm height of 18 mm, a fundus width of 18 mm, and a neck diameter of 9 mm. Contrast medium injection and posterior-anterior projection of the right-hand (d) and left-hand (e) vertebral arteries and lateral projection of the left-hand vertebral

Diagnostic Imaging Diagnostic MRI/MRA revealed a large saccular aneurysm, related to the carotid-cavernous segment of the left ICA (not shown). A subsequent DSA was carried out, showing a left-hand large saccular aneurysm at the origin of a persistent primitive trigeminal artery (PPTA) (Fig. 1).

Treatment Strategy The main treatment goal for this patient was to diminish the mass effect, which would relieve the symptoms arising from the cranial nerve palsy. Considering the size of the aneurysm, its location, and the mass effect, flow diversion therapy was chosen to induce progressive thrombosis of the aneurysm and decrease the transmitted pulsation on the adjacent cranial nerves. Due to the diameter of the PPTA and the presence of a persistent fetal

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artery (f), showing a lack of spontaneous PPTA filling (d, e). Lateral projection with contrast medium injection of the left vertebral artery with manual compression of the left common carotid artery (CCA) (so-called Allcock maneuver) demonstrated the filling of the PTA and its aneurysm (f). Note the complete filling of the basilar trunk during the compression of the left CCA. Both posterior cerebral arteries filled through the posterior communicating artery (PcomA)

predecessor to the PcomA, it was intended to use an adjuvant deconstruction therapy with coil occlusion of the PPTA to decrease the flow demand into the PPTA and therefore indirectly into the aneurysm.

Treatment Procedure #1, 01.07.2009: endovascular coil packing of a large, unruptured saccular aneurysm of the left ICA at the origin of a PPTA and occlusion of the PPTA Anesthesia: general anesthesia; 10,000 IU unfractionated heparin (Riveparin, Rivero) IV. Premedication: 1
100 mg ASA (Aspirin, Bayer Vital) PO daily and 1
75 mg clopidogrel (Troken, Laboratorio Bagó) PO daily, both starting 5 days before the intervention Access: left femoral artery, 7F sheath (Terumo); guide catheter: 6F Envoy (Cordis);

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microcatheter: Renegade 0.02700 (Boston Scientific); microguidewire: Transend 0.01400 (Stryker) Implants: 1
Pipeline Embolization Device 4.5/22 mm (Medtronic); 3 coils, 1
microcoil Matrix Ultra Soft SR 3/60 mm, 1
microcoil Matrix Soft SR 2/80 mm, and 1
microcoil Matrix Soft SR 2/60 mm (then Boston Scientific, now Stryker) Course of treatment: a 7F vascular sheath was placed in the left common femoral artery, and the left ICA was catheterized. Standard posterioranterior, lateral, and oblique angiographic images were gathered for all vessels involved. Rotational angiography with 3D reconstruction was obtained in order to determine the most suitable working projection. The aneurysm measurements were made using standard methods and included aneurysm height, width, and neck diameter (18
18
9 mm). A 6F Envoy guide catheter was placed in the cervical segment of the left ICA. A Renegade 0.02700 microcatheter was navigated over the Transend 0.01400 200 cm microguidewire and placed in the proximal M1 segment of the left MCA. The Pipeline Embolization Device was deployed and positioned from the distal cavernous segment to the proximal cavernous segment of the left ICA, covering the PPTA ostium. Angiography confirmed both the correct position of the device and significant contrast stagnation inside the aneurysm fundus. The left VA was catheterized with a coaxial system, using the 6F Envoy guide catheter and placed in the V2 segment. The left PPTA was catheterized with an Excelsior SL10 microcatheter over a Transend 0.01400 200 cm microguidewire, and coil occlusion of the PPTA was carried out. The final angiogram confirmed the occlusion of the left PPTA and complete filling of the basilar trunk, while all posterior circulation vessels remained patent. XperCT was performed immediately after the procedure, and no hemorrhagic or ischemic complications were encountered (Fig. 2).

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Duration: 1st–23rd DSA run: 60 min; fluoroscopy time, 41 min Complications: none Post medication: 1
100 mg ASA PO daily for life and 1
75 mg clopidogrel for 6 months

Clinical Outcome Procedure #1 was well tolerated, and the patient was discharged home 3 days later, with no change in clinical condition. At the 3-month clinical follow-up, an improvement in the left-hand trigeminal neuralgia and headache was seen; however, the 6th cranial nerve palsy was still persisting on the left-hand side.

Follow-Up Examinations DSA follow-up was performed at 3 months, showing partial thrombosis of the PPTA aneurysm with an aneurysm remnant (Raymond-Roy III). The flow diverter device was well positioned, and no in-stent stenosis was seen (Fig. 3).

Treatment Strategy The hemodynamic effect of the single implanted flow diverter was considered insufficient to induce complete aneurysm occlusion, especially since the 6th cranial nerve palsy had only partially improved. For this reason, the patient underwent a second endovascular procedure.

Treatment Procedure #2, 03.10.2009: telescopic deployment of a second flow diverter to occlude an aneurysm remnant of the PPTA Anesthesia: general anesthesia; 10,000 IU unfractionated heparin (Riveparin, Rivero) IV

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Fig. 2 (continued)

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Fig. 2 (continued)

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Internal Carotid Artery Aneurysm: Large Saccular Persistent Primitive Trigeminal Artery. . .

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Fig. 2 Treatment of an unruptured, symptomatic, large saccular ICA aneurysm at the origin of a Saltzman type II PPTA. DSA immediately after deployment of the PED in the early arterial phase (a) and the late parenchymal angiographic phase (b) revealed contrast stagnation inside the aneurysm. Occlusion of the PPTA with road map visualization of the posterior circulation (c) showed the

catheterization of the PPTA. DSA after the coil occlusion of the left-hand PPTA with injection of the left VA in frontal (d) and lateral projection (e) with complete occlusion of the PPTA distal to the BA (cast of coils (f)). Final follow-up DSA of the left ICA (g, h) and VasoCT (i) confirmed the adequate opening and position of the PED in the ICA

Fig. 3 Follow-up DSA 3 months after the treatment of a left ICA/PPTA aneurysm with flow diversion (left ICA) and parent vessel occlusion with coils (left PPTA) (posterior-anterior view (a), lateral view (b)) showed a

small aneurysm remnant of the PTA aneurysm. The flow diverter stent was patent and well positioned with good wall apposition, and there was no in-stent stenosis

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Medication: 1
100 mg ASA (Aspirin, Bayer Vital) PO daily and 1
75 mg clopidogrel (Troken, Bagó) PO daily; the patient had been taking this medication for the last 3 months Access: left femoral artery, 7F sheath (Terumo); guide catheter: 6F Envoy (Cordis); microcatheter: Renegade 0.02700 (Boston Scientific); microguidewire: Transend 0.01400 200 cm (Stryker). Implant: 1
Pipeline Embolization Device 4.5/18 mm (Medtronic). Course of treatment: a 7F vascular sheath was placed in the left common femoral artery, and the left ICA was catheterized. Standard posterioranterior, lateral, and oblique angiographic images were gathered for all vessels involved. Rotational angiography with 3D reconstruction was obtained in order to determine the most suitable working projection. The aneurysm remnant measurements were made using standard methods and included aneurysm height, width, and neck diameter (10
7
5 mm). After the diagnostic DSA, a 6F Envoy guide catheter was placed in the cervical portion of the left ICA. A Renegade 0.02700 microcatheter was navigated over a Transend 0.14 microguidewire through the first flow diverter device and placed in the proximal M1 segment of the left MCA. The second Pipeline Embolization Device was positioned from the distal cavernous segment to the proximal cavernous segment of the left ICA and overlapped with the first flow diverter, covering the PPTA ostium. DSA confirmed the correct position of the device and the contrast medium stagnation inside the aneurysm remnant. All access devices were retrieved (Fig. 4). XperCT was performed immediately after the procedure, and no hemorrhagic or ischemic lesions were observed. Duration: 1st–20th DSA run: 44 min; fluoroscopy time, 32 min Complications: none Post medication: 11
100 mg ASA PO daily for life and 11
75 mg clopidogrel PO daily for 6 months

Clinical Outcome Procedure #2 was also well tolerated, and no hemorrhagic or ischemic complications occurred.

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Three days later the patient was discharged home with no change in her clinical condition. The clinical follow-up at 6 months after the procedure showed an improvement in the left trigeminal neuralgia and the headaches, and it was ascertained that the left-hand 6th cranial nerve palsy had resolved. The patient’s mRS score was now 0, without any other procedure-related complications.

Follow-Up Examinations Follow-up DSA was performed at 6 months after the second procedure and MRI at 4 and 10 years, showing complete occlusion of the PPTA aneurysm (Raymond-Roy I). The Pipeline Embolization Devices were patent and well positioned, and there was no evidence of in-stent stenosis. The coil cast in the left PPTA was stable, and there was no recanalization of the left PPTA. In the 4- and 10-year follow-up MRIs, no ischemic or hemorrhagic lesions were found (Fig. 5).

Discussion A persistent primitive trigeminal artery (PPTA) is an embryonic remnant of fetal circulation still present in adulthood and is one of the most common vertebrobasilar anastomoses, with an incidence of 0.06–0.6%, more frequent in women (Vasović et al. 2012). Most of the time, a PPTA is an incidental finding, but it may be associated with other cerebrovascular abnormalities, of which aneurysms are the most common. Other cerebrovascular disorders possibly related are arteriovenous malformations and carotid-cavernous fistulas (Weon et al. 2011). The PPTA originates from the pre-cavernous ICA, just proximal to the meningohypophyseal trunk. Its course can run medially (sphenoidal) or laterally (petrosal) between the ICA and basilar artery; the laterally variant course runs through the cavernous sinus, just next to the 5th and 6th cranial nerves. The 6th cranial nerve is superior and medial to the 5th cranial nerve and does not have a dural cover. Therefore, 6th cranial nerve palsy is more frequent in aneurysmal dilatations of the lateral PPTA variant due to their close proximity (Luh et al. 1999).

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Fig. 4 Deployment of a second PED inside the first PED to treat an aneurysm remnant of the PPTA. A digital radiograph showed the flow-diverter position and that it had expanded (a). DSA in the working projection after the

deployment of the PED during the early arterial (b) and late parenchymal (c) angiographic phases demonstrated the contrast stagnation inside the aneurysm remnant, which was now covered by two flow diverters

The PPTA is anatomically classified according to Saltzman in three different variants. Type I encompasses 67% of all PPTAs. In this type, the anastomosis between the PPTA and the basilar trunk is below the superior cerebellar

artery (SCA) and above the anterior inferior cerebellar artery (AICA). In this vascular disposition, the distal part of the basilar trunk is mainly supplied by the PPTA and is associated with either a hypoplastic or missing PcomA.

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Fig. 5 (continued)

Type II is found in 20% of all PPTA cases, and the anastomosis on the BA is above the SCA, and the posterior cerebral arteries (PCA) are supplied by the PcomA. Type III represents about 13% of all PPTA cases and is a

combination of the two previously described configurations. In this configuration, both SCAs and the contralateral PCA receive flow through the PPTA; the ipsilateral PCA is supplied by the PcomA. There are some variations,

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Internal Carotid Artery Aneurysm: Large Saccular Persistent Primitive Trigeminal Artery. . .

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Fig. 5 Follow-up examinations after staged endovascular treatment of a large left-hand ICA aneurysm at a PPTA origin. DSA with contrast medium injection of the left ICA 6 months after the second procedure (posterior-anterior view (a), lateral views (b, c)) confirmed the complete occlusion of the aneurysm. Injections of the left VA (lateral

views, without (d) and with (e) simultaneous compression of the left CCA) confirmed the occlusion of the PPTA. MRI was carried out 10 years after the first treatment and showed that the previously large left-hand ICA aneurysm had disappeared

as anastomosis of PPTA to the SCA (IIIa), to the AICA (IIIb), or to the PICA (IIIb) (AlonsoVanegas et al. 2017; Weon et al. 2011). Aneurysms arising from the PPTA are not frequent. Aneurysm formation is thought to be due to the turbulent flow near the bifurcation of the PPTA and ICA. Approximately 15–29% of cases of PPTA have an associated aneurysm (Ajeet and

John 2016; O’uchi and O’uchi 2010), with the most common location being the bifurcation of the cavernous segment of the ICA and the PPTA. Aneurysms that originate from the PPTA trunk are exceptionally rare and have been reported in 1–2% of cases (Ajeet and John 2016; Tubbs et al. 2011). The pathogenesis of the PPTA aneurysm could be related to hemodynamic stress and

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structural dysfunction of the vessel wall (Kwon et al. 2007). PPTA aneurysms are often asymptomatic. When they become symptomatic, the first cause is subarachnoid hemorrhage, as these aneurysms have a high propensity to rupture. Furthermore, mass effect on the adjacent cranial nerves often calls for urgent treatment (Ladner et al. 2014). Most commonly, it is the 3rd, 4th, and 5th cranial nerves which are compromised, a situation which manifests through nerve palsy and – more rarely – the trigeminal neuralgia (V1 and V2) (Meckel et al. 2013). If these aneurysms rupture, they may cause a carotid-cavernous sinus fistula (Kim et al. 2010; Yoshida et al. 2011). Open surgery is difficult in these aneurysms because the cavernous segment of the ICA is too deeply located. The cavernous segment of the ICA is located in front of the brainstem and in close proximity to the cranial nerves and perforating vessels (Kwon et al. 2007; Mohammed et al. 2002). Endovascular ICA occlusion is another therapeutic option; however, this technique may cause ischemic injury to the brain stem by occluding the perforator vessels. Furthermore, the patient needs to have developed communicating arteries (Ajeet and John 2016; Ladner et al. 2014). Aneurysm coil occlusion through the PPTA is an option; however, there are reports of embolus migration to the anterior and posterior circulation by thrombus formation at the afferent and efferent stumps of the trunk related to the aneurysm. It is important to develop an appropriate treatment strategy. In the above case, the aneurysm had a wide neck. An elevated risk of coil protrusion into the anterior or posterior circulation was anticipated (Onizuka et al. 2006). Coiling of the aneurysm does not immediately decrease the mass effect like surgical clipping would do. Rather, coiling eliminates high-velocity pulsatile flow through the aneurysm across the surface of the compressed nerve and can quickly relieve symptoms. Stent-assisted coil embolization has been widely used for wide-necked aneurysms. This technique is safer and more effective in the occlusion of the carotid-basilar anastomosis aneurysms (Ajeet and John 2016; Zenteno et al. 2018).

I. Lylyk et al.

Endovascular flow diverter treatment of lateral ICA aneurysms has been widely studied, with a reported occlusion rate of 96.3% with an mRS 4 mm or dome to neck ratio < 1.5) and 44 aneurysms measured less than 4 mm. This cohort of small aneurysms, a considerable proportion of which had a narrow neck, may have contributed to the favorable occlusion rates at follow-up. More prospective data is needed with controlled subjects to assess the difference between therapies; however, current data suggests the WEB is capable of stable long-term occlusion in ruptured aneurysms. During follow-up, only one patient from any of the studies had a further hemorrhage from the treated aneurysm (Liebig et al. 2015). Among the 168 patients followed up, this gives a re-rupture rate of 0.6%. This is much lower than large-scale trials of alternative therapies: ISAT found a rebleeding rate of 1.82% at 1 year of follow-up in those treated with coils and surgical clipping (Molyneux et al. 2005), and a series of ruptured wide-neck aneurysms treated with stentassisted coiling showed a rebleeding rate of 4.5% (Alurkar et al. 2012). Retreatment rates in survivors have been reported at between 6.8% and 8%, and survivors at follow-up had an mRS  2 in 81–91% of cases (Da Ros et al. 2019; Liebig et al. 2015; Raj et al. 2019; van Rooij et al. 2017). Data so far suggests that if the initial WEB placement is without complication, there is a good prognosis for surviving patients and an extremely low rate of repeat hemorrhage.

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In conclusion, the WEB device is a potentially safe and effective treatment for suitable ruptured intracranial aneurysms. The first prospective trial (CLARYS) of 58 patients has completed enrollment, and the 1-month follow-up has shown the WEB device to be effective in preventing repeat hemorrhage in all 58 patients (Spelle et al. 2018). Further follow-up and analysis will potentially answer some of the uncertainties posited here.

Therapeutic Alternatives Balloon Remodeling Coil Occlusion Contour Device Microsurgical Clipping pCANVAS pCONUS-Assisted Coiling PulseRider Y-Stenting-Assisted Coiling

References Alurkar A, Karanam LS, Nayak S, Oak S. Stent-assisted coiling in ruptured wide-necked aneurysms: a singlecenter analysis. Surg Neurol Int. 2012;3:131. https://doi.org/10.4103/2152-7806.102946. Arthur AS, Molyneux A, Coon AL, Saatci I, Szikora I, Baltacioglu F, Sultan A, Hoit D, Delgado Almandoz JE, Elijovich L, Cekirge S, Byrne JV, Fiorella D, WEB-IT Study Investigators. The safety and effectiveness of the Woven EndoBridge (WEB) system for the treatment of wide-necked bifurcation aneurysms: final 12-month results of the pivotal WEB Intrasaccular Therapy (WEB-IT) study. J Neurointerv Surg. 2019; pii: neurintsurg-2019014815. https://doi.org/10.1136/neurintsurg-2019014815 Bechan RS, Sprengers ME, Majoie CB, Peluso JP, Sluzewski M, van Rooij WJ. Stent-assisted coil embolization of intracranial aneurysms: complications in acutely ruptured versus unruptured aneurysms. AJNR Am J Neuroradiol. 2016;37(3):502–7. https://doi.org/ 10.3174/ajnr.A4542. Caroff J, Mihalea C, Dargento F, Neki H, Ikka L, Benachour N, Moret J, Spelle L. Woven Endobridge (WEB) device for endovascular treatment of ruptured intracranial wide-neck aneurysms: a single-center experience. Neuroradiology. 2014;56(9):755–61. https://doi.org/10.1007/s00234-014-1390-7.

K. Wong et al. Cognard C, Pierot L, Anxionnat R, Ricolfi F, Clarity Study Group. Results of embolization used as the first treatment choice in a consecutive nonselected population of ruptured aneurysms: clinical results of the Clarity GDC study. Neurosurgery. 2011;69(4):837–41; discussion 842. https://doi.org/ 10.1227/NEU.0b013e3182257b30. Da Ros V, Bozzi A, Comelli C, Semeraro V, Comelli S, Lucarelli N, Burdi N, Gandini R. Ruptured intracranial aneurysms treated with Woven Endobridge intrasaccular flow disruptor: a multicenter experience. World Neurosurg. 2019;122:e498–505. https://doi.org/ 10.1016/j.wneu.2018.10.088. Itoyama Y, Fujioka S, Takaki S, Morioka M, Hide T, Ushio Y. Significance of elevated thrombinantithrombin III complex and plasmin-alpha 2-plasmin inhibitor complex in the acute stage of nontraumatic subarachnoid hemorrhage. Neurosurgery. 1994;35(6):1055–60. https://doi.org/10.1227/ 00006123-199412000-00006. Liebig T, Kabbasch C, Strasilla C, Berlis A, Weber W, Pierot L, Patankar T, Barreau X, Dervin J, Kuršumović A, Rath S, Lubicz B, Klisch J. Intrasaccular flow disruption in acutely ruptured aneurysms: a multicenter retrospective review of the use of the WEB. AJNR Am J Neuroradiol. 2015;36(9):1721–7. https://doi.org/ 10.3174/ajnr.A4347. Molyneux AJ, Kerr RS, Yu LM, Clarke M, Sneade M, Yarnold JA, Sandercock P, International Subarachnoid Aneurysm Trial (ISAT) Collaborative Group. International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet. 2005;366 (9488):809–17. https://doi.org/10.1016/S0140-6736 (05)67214-5. Pierot L, Cognard C, Anxionnat R, Ricolfi F, CLARITY Investigators. Ruptured intracranial aneurysms: factors affecting the rate and outcome of endovascular treatment complications in a series of 782 patients (CLARITY study). Radiology. 2010;256(3):916–23. https://doi.org/10.1148/radiol.10092209. Pierot L, Moret J, Barreau X, Szikora I, Herbreteau D, Turjman F, Holtmannspötter M, Januel AC, Costalat V, Fiehler J, Klisch J, Gauvrit JY, Weber W, Desal H, Velasco S, Liebig T, Stockx L, Berkefeld J, Molyneux A, Byrne J, Spelle L. Safety and efficacy of aneurysm treatment with WEB in the cumulative population of three prospective, multicenter series. J Neurointerv Surg. 2018;10(6):553–9. https://doi.org/ 10.1136/neurintsurg-2017-013448. Popielski J, Berlis A, Weber W, Fischer S. Two-center experience in the endovascular treatment of ruptured and unruptured intracranial aneurysms using the WEB device: a retrospective analysis. AJNR Am J Neuroradiol. 2018;39(1):111–7. https://doi.org/ 10.3174/ajnr.A5413.

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Middle Cerebral Artery Bifurcation Aneurysm: Acute Subarachnoid Hemorrhage Secondary to a. . .

Raj R, Rautio R, Pekkola J, Rahi M, Sillanpää M, Numminen J. Treatment of ruptured intracranial aneurysms using the Woven EndoBridge device: a two-center experience. World Neurosurg. 2019;123:e709–16. https://doi.org/10.1016/j.wneu. 2018.12.010. Spelle L, Herbreteau D, Barreau X, Ferré JC, Fiehler J, Pierot L, pour les investigateurs CLARYS. CLARYS: clinical assessment of WEB ® device in ruptured

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aneurysms : résultats préliminaires. /data/revues/ 01509861/v45i2/S0150986117305655/, July 3, 2018. https://www.em-consulte.com/en/article/1202396. van Rooij SBT, van Rooij WJ, Peluso JP, Sluzewski M, Bechan RS, Kortman HG, Beute GN, van der Pol B, Majoie CB. WEB treatment of ruptured intracranial aneurysms: a single-center cohort of 100 patients. AJNR Am J Neuroradiol. 2017;38(12):2282–7. https://doi.org/10.3174/ajnr.A5371.

Middle Cerebral Artery Bifurcation Aneurysm: Wide-Necked Middle Cerebral Artery Bifurcation Aneurysm, Treated with the Woven EndoBridge (WEB), Assisted by pCONUS1 HPC

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Donald Lobsien, Joachim Klisch, and Christin Clajus

Abstract

We report on a 63-year-old female patient with an incidentally detected complex aneurysm of the right middle cerebral artery (MCA) bifurcation. The aneurysm was treated with endosaccular flow disruption using a Woven EndoBridge (WEB; MicroVention) supported by a pCONUS1 (phenox) bifurcation stent with hydrophilic coating, to stabilize the WEB. The combined use of the WEB and pCONUS1 is the main topic of this chapter. Keywords

Middle cerebral artery · Woven EndoBridge (WEB) · MCA aneurysm · pCONUS1 · pHPC coating

Patient We report on a 63-year-old female patient with non-specific headaches, for which she underwent brain MRI at another institution. This

D. Lobsien (*) · J. Klisch · C. Clajus Institut für diagnostische und interventionelle Radiologie und Neuroradiologie, HELIOS Klinikum Erfurt, Erfurt, Germany e-mail: [email protected]; [email protected]; [email protected]; [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_136

demonstrated an incidental right MCA bifurcation aneurysm but was otherwise unremarkable. The patient presented to our outpatient clinic for advice regarding management of the aneurysm. The physical examination revealed no neurological deficit, she had no relevant medical history, and the routine laboratory findings were normal. The treatment options were discussed in an interdisciplinary meeting between neurosurgeons and neuroradiologists and subsequently with the patient. After careful consideration of all treatment options, the team and the patient opted for endovascular treatment of the aneurysm.

Diagnostic Imaging The initial MRI/MRA showed a 4
3 mm berrylike aneurysm of the right MCA bifurcation, with a lobulated irregular aspect and partial fusiform involvement of the MCA bifurcation. On review of the 3D reconstructions of the TOF MRA, the aneurysm seemed to predominantly involve the inferior trunk of the MCA bifurcation and partially involve the duplicated superior trunk. The decision to treat was based on these images, and

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after deciding in favor of endovascular treatment, the patient was informed and prepared for all possible treatment options (stent-assisted coiling, WEB, flow diverter). The initial procedural DSA

Fig. 1 (continued)

D. Lobsien et al.

images showed a broad-based aneurysm arising from the right MCA bifurcation and involving both the inferior trunk and the duplicated superior trunk (Fig. 1).

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Middle Cerebral Artery Bifurcation Aneurysm: Wide-Necked Middle Cerebral Artery. . .

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Fig. 1 Diagnostic imaging of an incidental aneurysm of the right-hand side MCA bifurcation. 2D TOF MRA (a, b) and 3D TOF MRA (c, d) demonstrated a small, shallow aneurysm with an irregular surface and wide neck arising from the right MCA bifurcation. The superior branch of the right MCA shows a bifurcation adjacent to the aneurysm. Five months after the TOF MRA, 2D DSA with contrast medium injection of the right ICA (e, f) essentially confirmed these features. The saccular component of the

aneurysm, however, appeared more pronounced than on MRA. 3D reconstruction of the rotational angiography (g, h) gave improved visualization of the aneurysm anatomy: the wide neck, the irregular shape, and the absence of separation of the efferent MCA branches, particularly of the inferior trunk. The aneurysm measured 2.4
2 mm in height. A WEB SL 4.5
2 was chosen, being slightly oversized for the aneurysm height according to the size selection chart

Treatment Strategy

Treatment

The aim of treatment was to prevent aneurysm growth and subsequent rupture. After reviewing and discussing the initial diagnostic DSA images, the decision was made to implant a WEB into the aneurysm sac. If the WEB position appeared unstable, or if the device was not well-placed, an additional implantation of a pCONUS1 HPC was planned, in order to stabilize the WEB.

Procedure, 11.07.2019: treatment of a broadbased bifurcation aneurysm of the right MCA with a WEB, stabilized by a pCONUS1 HPC bifurcation stent Anesthesia: general anesthesia Premedication: 1
100 mg ASA (Aspirin, Bayer Vital) PO and 1
75 mg clopidogrel (Plavix, Sanofi-Aventis) PO daily, starting 7 days

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before the procedure. The patient was admitted the day before the procedure, and platelet function was tested (Multiplate, Roche Diagnostics), confirming adequate platelet inhibition. Access: right common femoral artery, 1
6F sheath (Terumo); guide catheter: 6F Envoy (Codman); intermediate catheter: SOFIA 5F (MicroVention); microcatheters: VIA 17 (MicroVention), Rebar-18 (Medtronic); microguidewire: Synchro2 0.01400 200 cm (Stryker) Implants: WEB SL W5-4.5-2 (MicroVention), pCONUS1 HPC 20-3-4 (i.e., 20 mm shaft length, 3 mm shaft diameter, 4 mm petal diameter) (phenox) Course of treatment: arterial access was established from the right common femoral artery. The right ICA was selectively catheterized with the guide catheter. Due to the moderate vasospasm in the right ICA, the guide catheter was placed in the proximal cervical ICA. A diagnostic DSA run and subsequent rotational angiography with 3D reconstruction were performed and reviewed to determine the optimal treatment strategy. It was decided first to place a WEB followed by, if necessary, a pCONUS1 to stabilize the WEB. The distal ICA was selectively catheterized with the VIA 17, the microguidewire, and the intermediate catheter. The intermediate catheter was placed in the terminal ICA close to the carotid bifurcation. A working projection was chosen, and the aneurysm was catheterized with the VIA 17 and the microguidewire. The WEB was placed and detached after confirmation of correct positioning. Due to the small height of the aneurysm and its broad base, a slight stenosis of the superior trunk of the right MCA at the base of the WEB was noticed, and it was decided to stabilize the WEB with a pCONUS1 bifurcation stent. The VIA 17 was withdrawn, and a Rebar-18 microcatheter was introduced into the MCA via the intermediate catheter, through which the pCONUS1 was introduced. The petals of the crown of the pCONUS1 were opened outside the aneurysm directly in front of the WEB and moved forward against the WEB. This maneuver led to further distal migration of the WEB into the aneurysm. The petals of the crown of the pCONUS1 were

D. Lobsien et al.

finally placed partly within the aneurysm sac and partly in the superior trunk of the MCA, stabilizing the WEB in this position. The final DSA run confirmed the patency of the three efferent branches, the previous narrowing of the superior MCA trunk had been resolved, and moderate stasis of contrast medium was seen inside the WEB (Fig. 2). Duration: 1st–11th DSA run: 72 min; fluoroscopy time: 27 min Complications: none Postmedication: 2
40 mg enoxaparin (Clexane, Sanofi) SC daily for 3 days, 1
100 mg ASA PO daily for life, and 1
75 mg clopidogrel PO daily for 6 months

Clinical Outcome The patient woke up from anesthesia immediately following the procedure and was discharged 2 days later with no neurological deficit.

Follow-Up Examinations None. A first angiographic follow-up is planned in 6 months.

Discussion We have reported on a case of endovascular therapy for a broad-based MCA bifurcation aneurysm with the WEB, assisted by a pCONUS1 bifurcation stent. The WEB device is an endosaccular flow disruptor. Among the available endosaccular flow disruptors, it is the most widely used and best-studied device on the market and recently obtained approval by the US Food and Drug Administration for the US market. This has led to a further increase in interest in the WEB and to an increase of published studies evaluating the device (Gawlitza et al. 2019) In meta-analyses and studies, the device was shown to yield reasonable occlusion rates in

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Middle Cerebral Artery Bifurcation Aneurysm: Wide-Necked Middle Cerebral Artery. . .

broad-based aneurysms, with complete or acceptable occlusion rates up to 81% and relatively low morbidity rates (3–5%), predominantly with the use of newer versions of the

Fig. 2 (continued)

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device (Asnafi et al. 2016; Clajus et al. 2017; Lv et al. 2018). Although the WEB is mostly used as a solitary device, recent studies reported promising results

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D. Lobsien et al.

Fig. 2 Endovascular treatment of an incidentally detected wide-necked, shallow aneurysm of the right MCA bifurcation with pCONUS1-assisted WEB implantation. The chosen working projection showed the broad base of the aneurysm with the efferent superior and inferior MCA branches (left anterior oblique, LAO (a). A WEB was implanted inside the aneurysm sac (solid arrowhead, the distal tip of the intermediate catheter; solid arrow, a distal marker of the WEB; transparent arrow, a proximal marker of the WEB (b)). A second projection (right anterior oblique, RAO) was used to better control the process of device implantation (solid arrow, the distal tip of the intermediate catheter; solid arrowhead, a proximal marker of the WEB; transparent arrows, border of the open WEB inside the aneurysm (c)). The WEB was detached, and the WEB delivery wire was withdrawn. The proximal marker of the WEB indicated that the WEB reached proximal to the base of the aneurysm, being oversized for the height of the aneurysm dome (d). This assumption was confirmed in the second working projection (e). The arrowheads indicate the border of the WEB and the vessel wall of the superior MCA trunk, appearing relatively stenosed. The VIA microcatheter was exchanged for a

Rebar 18 microcatheter, and the pCONUS1 was introduced. Shown is the opened but not yet detached pCONUS1 (solid arrow, the marker of the crown of the pCONUS1, partly within the aneurysm, partly in the base of the superior trunk, outside the aneurysm; arrows, distal and proximal markers of the WEB (f)). The situation after detachment of the WEB (on the left) and after opening and gentle forward pressure on the pCONUS1 (on the right) is shown (transparent arrowheads, borders of the WEB; solid arrowheads, pCONUS1 markers; RAO (g)). The pCONUS1 is clearly shown supporting the WEB and opening up the lumen of the superior MCA trunk. Maximum intensity projection reconstruction from a 3D angiogram after the implantation of the WEB and the pCONUS1 demonstrated the anatomy and the positioning of the devices (h). The pCONUS1 was supporting the WEB, partially inside and partially outside the aneurysm, and the superior and inferior trunks are patent. A final DSA run (i) confirmed the patency of all branches of the MCA. Contrast medium stasis can be seen inside the WEB, placed inside the MCA aneurysm, and stabilized in position with a pCONUS1

in conjunction with other implants, typically used to further stabilize the WEB while treating complex aneurysms. In a small series recently

published by Mihalea et al. (2019), the authors showed that the WEB performed well when used with a remodeling balloon as an adjunctive

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Middle Cerebral Artery Bifurcation Aneurysm: Wide-Necked Middle Cerebral Artery. . .

device. In the ten patients studied, the WEB was successfully deployed in all cases, supported by a balloon in a remodeling fashion. No thromboembolic or hemorrhagic complications occurred. Cagnazzo et al. (2019) published a study in which they used the WEB together with selfexpandable micro-stents for the management of broad-based aneurysms. Seventeen patients, most undergoing treatment for MCA bifurcation aneurysms, were treated with a stent to protect the branch of the bifurcation at risk for stenosis. Two aneurysms were treated in the acute phase after rupture. The authors reported no permanent or significant complications and achieved complete or near-complete occlusion at angiographic follow-up in 81.5%. Mihalea et al. (2018) describe the treatment of a large, broad-based basilar bifurcation aneurysm with a technique they called “WEB device waffle-cone technique,” supporting the WEB with a Solitaire stent. The solitaire was placed with the distal end of the stent protruding into the base of the aneurysm opening. The WEB was then deployed through the lumen of the stent into the aneurysm sac, which kept it within the aneurysm. This procedure is a variation of a procedure described earlier in conjunction with coil occlusion of aneurysms together with various stents, called the “waffle-cone technique” (Pierot and Biondi 2016). The technique was further developed by the introduction of dedicated stents which were designed to be placed into the base of widenecked aneurysms and provide a platform to carry coil constructs and avoid more sophisticated techniques such as y-stenting. The pCONUS1 and the newer version, pCONUS2, are stent-like devices consisting of a so-called crown, designed to be placed inside the aneurysm sac and create a platform for coil retention. The crown is connected to a shaft that stabilizes the device in the parent vessel to keep it in position. In a study by Gory et al. (2015), 40 patients with wide-necked aneurysms of the MCA (90% unruptured) were treated with pCONUS1-assisted coiling, and adequate aneurysm occlusion was obtained in 79%. To date and to the best of our knowledge, the use of a pCONUS1 device to stabilize a WEB has not been reported. We chose this approach as a

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further modification of the “WEB waffle-cone technique” mentioned above, placing the WEB first, as opposed to deploying the stent first, as described by Mihalea et al. (2018). This strategy leaves the operator to decide whether the aneurysm can be treated with WEB alone, if the WEB device position is stable enough, avoiding placement of the stent. Avoiding dual microcatheter techniques reduces the complexity of the procedure and obviates the need for large caliber distal access. However, because the WEB is already in place, there is the possibility of encountering difficulties with the pCONUS placement. In our case, the pCONUS implantation resulted in a stable position of the WEB while preserving the patency of the efferent branches of the MCA bifurcation. In conclusion, in selected cases, this novel technique is, in our opinion, a promising approach to the safe treatment of complex bifurcation aneurysms that would otherwise be difficult to manage.

Therapeutic Alternatives eCLIPs Assisted Coiling Flow Diversion Microsurgical Clipping pCONUS-Assisted Coiling PulseRider-Assisted Coiling Stent-Assisted Coiling

References Asnafi S, Rouchaud A, Pierot L, Brinjikji W, Murad MH, Kallmes DF. Efficacy and safety of the woven EndoBridge (WEB) device for the treatment of intracranial aneurysms: a systematic review and meta-analysis. AJNR Am J Neuroradiol. 2016;37(12):2287–92. https://doi.org/10.3174/ajnr.A4900. Cagnazzo F, Ahmed R, Dargazanli C, Lefevre PH, Gascou G, Derraz I, Kalmanovich SA, Riquelme C, Bonafe A, Costalat V. Treatment of wide-neck intracranial aneurysms with the Woven EndoBridge device associated with stenting: a single-center experience. AJNR Am J Neuroradiol. 2019;40(5):820–6. https:// doi.org/10.3174/ajnr.A6032. Clajus C, Strasilla C, Fiebig T, Sychra V, Fiorella D, Klisch J. Initial and mid-term results from 108 consecutive patients with cerebral aneurysms treated with the

964 WEB device. J Neurointerv Surg. 2017;9(4):411–7. https://doi.org/10.1136/neurintsurg-2016-012276. Gawlitza M, Soize S, Manceau PF, Pierot L. An update on intrasaccular flow disruption for the treatment of intracranial aneurysms. Expert Rev Med Devices. 2019;16(3):229–36. https://doi.org/10.1080/ 17434440.2019.1584035. Gory B, Aguilar-Pérez M, Pomero E, Turjman F, Weber W, Fischer S, Henkes H, Biondi A. pCONus device for the endovascular treatment of wide-neck middle cerebral artery aneurysms. AJNR Am J Neuroradiol. 2015;36(9):1735–40. https://doi.org/10.3174/ajnr.A4392. Lv X, Zhang Y, Jiang W. Systematic review of woven EndoBridge for wide-necked bifurcation aneurysms: complications, adequate occlusion rate, morbidity, and mortality. World Neurosurg. 2018;110:20–5. https://doi.org/10.1016/j.wneu.2017.10.113.

D. Lobsien et al. Mihalea C, Caroff J, Rouchaud A, Pescariu S, Moret J, Spelle L. Treatment of wide-neck bifurcation aneurysm using “WEB device waffle cone technique”. World Neurosurg. 2018;113:73–7. https://doi.org/10.1016/j. wneu.2018.02.020. Mihalea C, Escalard S, Caroff J, Ikka L, Rouchaud A, Da Ros V, Pagiola I, de la Torre JJ M, Yasuda T, Popa BV, Ples H, Benachour N, Ozanne A, Moret J, Spelle L. Balloon remodeling-assisted woven EndoBridge technique: description and feasibility for complex bifurcation aneurysms. J Neurointerv Surg. 2019;11(4):386–9. https://doi.org/10.1136/neurintsurg-2018-014104. Pierot L, Biondi A. Endovascular techniques for the management of wide-neck intracranial bifurcation aneurysms: a critical review of the literature. J Neuroradiol. 2016;43(3):167–75. https://doi.org/ 10.1016/j.neurad.2016.02.001.

Middle Cerebral Artery Bifurcation Aneurysm: Incidental Aneurysm of the Middle Cerebral Artery Bifurcation, Treated with Crossing Solitaire Stent-Assisted Coil Occlusion; Aneurysm Growth with Partial Thrombosis and Perianeurysmal Edema During the Long-Term Course

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Meike Dukiewicz, Muhammad AlMatter, Marta Aguilar Pérez, Hansjörg Bäzner, and Hans Henkes

Abstract

A 75-year-old female patient received endovascular treatment for a left middle cerebral artery (MCA) bifurcation aneurysm. Crossing Solitaire stents were implanted to reconstruct the MCA bifurcation and allow for a dense coil occlusion of the aneurysm. The patient remained in a structured follow-up program including recurrent treatment sessions. She presented to the referring hospital 7.5 years after the initial treatment. A CT examination as work-up for an episode of disturbed consciousness and impaired articulation showed massive edema in the left temporal lobe. DSA showed a partial reperfusion of the coiled aneurysm. Only 2 months later, MRI revealed significant growth in the

previously treated aneurysm, which now contained a newly formed intraaneurysmal thrombus and a massive perianeurysmal edema. The coils had migrated into the intraaneurysmal thrombus. After repacking the aneurysm and administering steroids as anti-edematous medication, the patient was discharged. Perianeurysmal edema formation is the main topic of this chapter. Keywords

Middle cerebral artery · Perianeurysmal edema · Partially thrombosed cerebral aneurysm · Coil embolization · Aneurysm recurrence

Patient M. Dukiewicz · M. AlMatter · M. Aguilar Pérez · H. Henkes (*) Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; [email protected]; [email protected]; [email protected]; [email protected]

A 75-year-old female patient with an anxiety disorder but with an otherwise insignificant medical history underwent an MRI examination as work-up for recurrent headaches. A large aneurysm

H. Bäzner Neurologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_153

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of the left middle cerebral artery (MCA) bifurcation was found. The said aneurysm was treated by endovascular means. Her headaches did not improve after the aneurysm treatment; however, they disappeared after a course of high-dosage steroids was begun, supporting the diagnosis of a giant cell arteritis. During the following long-term course, repeated coil treatment sessions were carried out on the aneurysm. At the age of 82 years, she presented after a short episode of impaired consciousness and poor articulation, which might well have been the expression of an epileptic seizure. These symptoms were considered indirectly related to a recurrence of the previously coiled aneurysm.

Diagnostic Imaging CT/CTA and MRI/MRA were carried out in December 2011 and showed a large wide-necked aneurysm of the left MCA bifurcation (neck width 5.5 mm, fundus width 13 mm, fundus depth 7 mm). Further aneurysms were ruled out. The left internal carotid artery (ICA) was not particularly elongated (Fig. 1).

Treatment Strategy The main goal of the treatment was to prevent further growth of the aneurysm and possible aneurysm rupture. The following options were explained to the patient and her daughter in a balanced way: • Conservative management with annual followup imaging and treatment once growth and/or a change of shape has been observed • Microsurgical clipping • Endovascular coil occlusion, most likely with stent assistance After thinking through these possibilities, the patient and her family opted for endovascular

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treatment. It was decided to implant the stents and occlude the aneurysm with coils in separate sessions.

Treatment Procedure #1, 07.12.2011: endovascular implantation of crossing stents as preparation for assisted coil occlusion of an incidental, wide-necked left MCA bifurcation aneurysm Anesthesia: general anesthesia, 1
5,000 IU non-fractionated heparin (Heparin-Natrium, B. Braun) IV, 1
500 mg ASA (Aspirin I.V. 500 mg, Bayer Vital) IV, 2
2 mg glyceryl trinitrate (Nitrolingual, G. Pohl-Boskamp) IA Premedication: 1
100 mg ASA (Aspirin, Bayer Vital) PO daily and 1
75 mg clopidogrel (Plavix, Sanofi-Aventis) PO given 5 days before the procedure; Multiplate (Roche Diagnostics) (ARU): ADP 39, ASPI 56 (dual platelet function inhibition) Access: right common femoral artery, long 8F sheath (St. Jude); guide catheter: 8F Guider Softip (Boston Scientific); intermediate catheter: DAC (Concentric); microcatheter: 1
Prowler Select Plus J (Cerenovus); microguidewire: 0.016” Radifocus Guidewire GT (Terumo) Implants: 2
Solitaire SAB 3/30 (Medtronic) Course of treatment: an 8F guiding catheter and an intermediate catheter were inserted into the left ICA. The inferior trunk of the left MCA was catheterized without difficulty, and a Solitaire stent was implanted from this vessel to the left M1 segment. After the stent had been detached, the same microcatheter was used to catheterize the superior trunk of the left MCA. From there, a second Solitaire stent was implanted into the left M1 segment, crossing the first stent (Fig. 2). Duration: 1st–10th run: 56 min; fluoroscopy time: 25 min Complications: none Postmedication: 1
100 mg ASA PO for life and 1
75 mg clopidogrel PO daily for at least 3 months

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Fig. 1 (continued)

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Fig. 1 Diagnostic imaging in an incidental, large, widenecked aneurysm of the left MCA bifurcation. Non-contrast cranial CT (a), axial (b) and sagittal (c) contrast-enhanced CT images, DSA in a straight lateral

projection (d), and 3D reconstructions of a rotational DSA showing the anterior (e) and posterior aspect (f) of said aneurysm

Fig. 2 Preparation for coil occlusion of a wide-necked left MCA bifurcation aneurysm by implanting two Solitaire stents. The first stent was implanted from the inferior trunk (distal markers, yellow arrow (a)); the second stent

was deployed from the superior trunk (distal markers, blue arrow (b)). Both stents cross each other in front of the aneurysm and the proximal ends are deployed into one another in the left M1 segment

Procedure #2, 13.01.2012: endovascular coil occlusion of a wide-necked left MCA bifurcation aneurysm after preparatory implantation of crossing stents 5 weeks previously Anesthesia: general anesthesia, 1
5,000 IU non-fractionated heparin (Heparin-Natrium, B. Braun) IV, 1
500 mg ASA (Aspirin

i.v. 500 mg, Bayer Vital) IV, 1
2 mg glycerol trinitrate (Nitrolingual, G. Pohl-Boskamp) IA Premedication: 1
100 mg ASA PO daily and 1
75 mg clopidogrel PO daily for the last 6 weeks Access: right common femoral artery, long 8F sheath (St. Jude); guide catheter: 8F Guider Softip

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Middle Cerebral Artery Bifurcation Aneurysm: Incidental Aneurysm of the Middle Cerebral. . .

(Boston Scientific); intermediate catheter: ReFlex 058 (Reverse Medical); microcatheter: 1
Echelon-10 90 , 1
Echelon-10 straight (Medtronic); microguidewire: Transend 0.01400 ex (Stryker) Implants: 18 coils: 1
Nexus Helix Soft 10/30 (ev3), DeltaPlush Cerecyte 1
4/8, 6
4/6, 5
3/6, 1
3/4, 4
2/6 (Codman) Course of treatment: after access to the left ICA, the MCA aneurysm was catheterized with an Echelon-10 microcatheter through the crossed Solitaire stents. Despite these stents, coil retention inside the aneurysm was not particularly stable. A partial coil occlusion was achieved, and the decision was made to wait for several weeks for the necessary completion of the coil occlusion (Fig. 3). Duration: 1st–37th run: 201 min; fluoroscopy time: 107 min Complications: transient right-hand hemiparesis and aphasia, which resolved within 2 days and was considered to be a sequel of contrast medium toxicity Postmedication: 1
100 mg ASA PO for life and 1
75 mg clopidogrel PO daily for at least 1 year Procedure #3, 01.03.2012: completion of the endovascular coil occlusion of a wide-necked left MCA bifurcation aneurysm after preparatory implantation of crossing stents and after previous partial coil occlusion Anesthesia: general anesthesia, 1
5,000 IU non-fractionated heparin (Heparin-Natrium, B. Braun) IV, 1
2 mg glycerol trinitrate (Nitrolingual, G. Pohl-Boskamp) IA Premedication: 1
100 mg ASA PO daily and 1
75 mg clopidogrel PO daily since December 2011 Access: right common femoral artery, long 8F sheath (St. Jude); guide catheter: 8F Guider Softip (Boston Scientific); intermediate catheter: ReFlex 058 (Reverse Medical); microcatheter: 1
Excelsior SL-10 straight (Stryker); microguidewire: Traxcess 14 (MicroVention) Implants: 15 coils: 5
Standard Fiber 3/10 (ev3), 1
Standard Fiber 2/6, not insertable (ev3), DeltaPlush Cerecyte 2
2/6, 7
2.4/4 (Codman) Course of treatment: after access to the left ICA, the left MCA aneurysm was catheterized.

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Coil insertion was much easier than during the previous session, and the 14 coils implanted allowed for a sufficiently occluded aneurysm with a neck remnant (Fig. 4). Duration: 1st–12th run: 143 min; fluoroscopy time: 105 min Complications: none Postmedication: 1
100 mg ASA PO for life and 1
75 mg clopidogrel PO daily for 1 year Procedure #4, 14.06.2012: completion of endovascular coil occlusion of a wide-necked left MCA bifurcation aneurysm after preparatory procedures where crossing stents were implanted and after two previous coiling sessions Anesthesia: general anesthesia, 1
5,000 IU non-fractionated heparin (Heparin Natrium, B. Braun) IV Premedication: 1
100 mg ASA PO daily and 1
75 mg clopidogrel PO daily since December 2011 Access: right common femoral artery, long 8F sheath (St. Jude); guide catheter: 8F Guider Softip (Boston Scientific); intermediate catheter: ReFlex 058 (Reverse Medical); microcatheter: 1
Excelsior SL-10 straight (Stryker); microguidewire: Traxcess 14 (MicroVention) Implants: 8 coils: DeltaPlush Cerecyte 6
3/6, 2
2/4 (Codman) Course of treatment: the left MCA aneurysm was catheterized again. A total of eight coils were implanted (Fig. 5). Duration: 1st–9th run: 62 min; fluoroscopy time: 31 min Complications: none Postmedication: 1
100 mg ASA PO for life and 1
75 mg clopidogrel PO daily for 1 year

Clinical Outcome After the second procedure, the patient developed temporary aphasia and hemiparesis of the right side, which both resolved within 2 days. CT right after the patient woke up from general anesthesia showed swelling and contrast medium accumulation in the left MCA supply territory, which resolved alongside the clinical symptoms within 2 days (Fig. 6).

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Fig. 3 Partial coil occlusion of a wide-necked left MCA aneurysm after preparatory implantation of crossing stents. A working projection was chosen which showed the aneurysm neck free from the superimposition of the efferent MCA branches (a). A microcatheter with a 90 angled tip

was inserted (b). Inserting the coils was more difficult than expected, and the poor coil retention exerted by the crossing stents did not allow for a complete occlusion of the aneurysm (c, d)

Follow-Up Examinations

Treatment Strategy

Follow-up DSA 17 months after the first and 12 months after the third coiling session confirmed complete aneurysm occlusion. However, just 1 year later, DSA once again showed a reperfusion of the aneurysm (Fig. 7).

A continuation of the treatment was considered crucial. The surgical creation of an extracranialintracranial bypass between the superficial temporal artery and the left-hand MCA, followed by the parent vessel occlusion at the level of the MCA

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Fig. 4 Completion of the coil occlusion of a wide-necked left MCA bifurcation aneurysm. A previous treatment session 6 weeks earlier resulted in a partial coil occlusion (a).

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Inserting a further 14 coils resulted in a densely packed aneurysm with a non-occluded neck (b). This neck was most likely the reason for the reperfusion of the aneurysm

Fig. 5 Fourth treatment session with coil occlusion of a partially recanalized wide-necked left MCA bifurcation aneurysm, pre (a) and post (b) recoiling, required 5 months after the first coiling session

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Fig. 6 NCCT after the coil occlusion of a left MCA bifurcation aneurysm. The patient woke up from anesthesia with aphasia and hemiparesis on the right side. NCCT showed a swelling and contrast medium accumulation of

the left MCA supply territory (a), which resolved within 2 days (b). Contrast medium toxicity and relative hypoperfusion during coil insertion were considered the most likely reasons for the transient neurological deficit

bifurcation, was discussed with the patient. She did not want to have any open surgery. We therefore offered another endovascular treatment session.

Implants: 9 coils: DeltaPlush Cerecyte 1
6/ 25 (Codman), HydroCoils 2
5/15, 2
4/10, 1
3/10, 1
3/6, MicroPlex10 1
3/8, 1
2/6 (MicroVention) Course of treatment: the left MCA aneurysm was catheterized, and a total of nine coils were implanted (Fig. 8). Duration: 1st–9th run: 109 min; fluoroscopy time: 60 min Complications: none Postmedication: 1
100 mg ASA PO for life and 1
75 mg clopidogrel PO daily for 1 year

Treatment Procedure #5, 20.06.2014: completion of the endovascular coil occlusion of a wide-necked left MCA bifurcation aneurysm after preparatory implantation of crossing stents and after three previous coiling sessions Anesthesia: general anesthesia, 1
3,000 IU non-fractionated heparin (Heparin-Natrium, B. Braun) IV, 1 mg glycerol trinitrate IA Premedication: 1
100 mg ASA PO daily and 1
75 mg clopidogrel PO daily since December 2011 Access: right common femoral artery, 6F sheath (Terumo); guide catheter: 6F Guider Softip (Boston Scientific); microcatheter: 1
Excelsior SL-10 straight (Stryker); microguidewire: Synchro2 14 (Stryker)

Follow-Up Examinations Follow-up DSA 1 year later or 3.5 years after the first coiling session again showed a reperfusion of the aneurysm. The patient did, however, not accept the proposal of new treatment (Fig. 9). The next follow-up examinations were carried out 4 years later, when the patient presented after a short episode of disturbed consciousness and poor

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Fig. 7 Follow-up DSA 1 year after the so far last coiling session showed a complete occlusion of the aneurysm (a). Only 1 year later, the aneurysm was once again partially recanalized (arrows (b, c))

articulation. CT showed massive edema of the white matter of the left temporal lobe. DSA revealed a recanalization of the aneurysm between the coil loops. The maximum diameter of the aneurysm had increased if compared to the initial diameter, but the coil mass was still compact. MRI and DSA only 2 months later showed a rapid further increase in the size of the aneurysm. The perfused part of the aneurysm was embedded in a huge aneurysm sac filled with thrombus and with

intense contrast enhancement of the aneurysm wall (Fig. 10).

Treatment Strategy The failure of the endovascular treatments to prevent this aneurysm from growing was obvious. Conservative management would have been associated with a foreseeable risk of

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Fig. 8 Fifth treatment session with repeated coil occlusion of a partially recanalized wide-necked left MCA bifurcation aneurysm, pre (a), during (b), and after (c) recoiling, required 23 months after the first coiling session

further growth. Microsurgical clipping or the creation of an extra-intracranial bypass, followed by occluding the left MCA bifurcation, was again discussed. The anticipated risks were considered high, and the patient was not willing to undergo open surgery. Knowing the presumably limited efficacy further coil occlusion was offered to and accepted by the patient.

Treatment Procedure #6, 07.10.2019: repeated endovascular stent-assisted coil occlusion of an incidental, widenecked left MCA bifurcation aneurysm Anesthesia: general anesthesia, 3,000 IU unfractionated heparin (Heparin-Natrium, B. Braun) IV

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Complications: none Postmedication: 1
100 mg ASA PO daily, 3
4 mg dexamethasone (Fortecortin, Merck Serono) PO daily for 10 days, 60 mg etoricoxib (Arcoxia, MSD Sharp & Dohme) for 6 weeks

Follow-Up Examinations Immediate postprocedural MRI showed that the size of the aneurysm and the edema remained unchanged (Fig. 12).

Clinical Outcome Fig. 9 Partial reperfusion of a wide-necked left MCA bifurcation aneurysm after five previous procedures. The recanalization has reached the aneurysm wall (arrow)

Premedication: the patient had been under dual platelet function inhibition since December 2011 but had stopped this medication in mid-2018; dual platelet inhibition was reinstituted 5 days before this treatment by a medication of 1
100 mg ASA PO daily and 2
90 mg ticagrelor PO daily. A Multiplate Analyzer test (Roche Diagnostics) confirmed significant dual platelet function inhibition. Access: right common femoral artery, 1
6F sheath (Terumo); guide catheter: 1
6F Heartrail II (Terumo); microcatheter: 1
Excelsior SL10 45 (Stryker); microguidewire: 1
pORTAL 0.01400 200 cm (phenox) Implants: 10 coils: 5
Target XL 360 Soft 5/10, 2
Target XL 360 Soft 2/6, 3
Target XL 360 Soft 2/3 (Stryker) Course of treatment: the guiding catheter was placed in the midcervical segment of the left ICA, followed by an atraumatic navigation of the Excelsior microcatheter into the reperfused coil mass. The aforementioned coils were placed one by one into the aneurysm. A final DSA run confirmed the complete occlusion of the perfused part of the aneurysm (Fig. 11). Duration: 1st–12th DSA run: 63 min; fluoroscopy time: 32 min

The patient tolerated the endovascular treatment sessions well. Her clinical condition at the latest discharge was mRS 1 with mild chronic cognitive impairment.

Discussion This failure of endovascular coil occlusion to permanently exclude an intracranial aneurysm from the blood circulation is the rare exception. This may not only result in the rupture of said aneurysm. Further aneurysm growth and perianeurysmal edema are also possible sequelae. Perianeurysmal edema is a not very well-understood phenomenon and has been described with both treated and untreated cerebral aneurysms (Fanning et al. 2008; Su et al. 2014). The reported incidence varies from about 1% in the total population of endovascular-treated patients (Sim et al. 2015) up to 95% in highly selected cases (Krings et al. 2007), where almost all (17 of 18) of untreated, large or giant, partially thrombosed aneurysms showed perianeurysmal edema. Luckily, the majority of the patients is asymptomatic for the perianeurysmal edema. Only a few cases have been published where patients have suffered from seizures, hydrocephalus, or neurological deterioration due to the edema.

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It is still unknown which aneurysm is more likely to show perianeurysmal edema, because there is no favored location. However, if the aneurysm is large or partially thrombosed, perianeurysmal edema is more likely. Aneurysms with edema are often embedded in the brain parenchyma, although it seems that direct contact between the aneurysm wall and the brain

Fig. 10 (continued)

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parenchyma is needed, as shown by Dengler et al. (2015). In their series, giant cavernous ICA aneurysms which were separated from the brain by dura mater did not cause any perianeurysmal edema, even though they exerted mass effect and brain indentation. Since perianeurysmal edema is found in different cases, there might be more than one

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Fig. 10 Long-term follow-up 7.5 years after the initial endovascular treatment of a wide-necked left MCA bifurcation aneurysm. The patient was symptomatic with a transient episode of disturbed consciousness and impaired articulation. CT (a) showed a massive edema of the left temporal lobe and DSA (b) revealed an increased reperfusion of the coiled aneurysm between the coil loops. Only

2 months later, the aneurysm sac had increased to a maximum diameter of 36 mm (c), the edema had also increased (d), and there was an intense contrast enhancement of the aneurysm wall (e). The coil loops had migrated into the thrombus within a short period and a lumen with a spherical shape had reperfused (f, g)

underlying mechanism (e.g., arterial hypertension, Lukic et al. 2015). Mass effect is one, as in large or giant aneurysms perianeurysmal edema is seen more frequently. A water hammer effect has also been proposed. Partially (re)perfused aneurysms (Tomokiyo et al. 2007) and intraaneurysmal thrombus (Roccatagliata et al. 2010) or recurrent hemorrhage in the aneurysm wall, especially giant or partially thrombosed aneurysms, may play a role

(Krings et al. 2007). With its inflammatory mediators, cytokines and pro-inflammatory substances (Frösen et al. 2012; Sim et al. 2015) may contribute. In aneurysms with perianeurysmal edema, contrast enhancement of the aneurysm wall can almost always be observed (Su et al. 2014). This may suggest that there is an underlying inflammatory process. Perianeurysmal edema is usually vasogenic, not cytotoxic.

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Fig. 11 Retreatment of a recurrent perfusion of a left MCA bifurcation aneurysm. The previously implanted coils have separated due to coil migration into the

intraaneurysmal thrombus (arrow (a, b). Another ten coils were inserted to obliterate this compartment of the aneurysm (c)

As several studies have shown, aneurysmal wall enhancement is associated with a higher risk of aneurysm instability (Vergouwen et al. 2019), meaning growth, rupture (Sato et al. 2019; Frösen et al. 2012), or recurrence after treatment (Fanning et al. 2008). Partially thrombosed aneurysms show not only a higher risk of treatment-related complications but also a higher risk of growth and rupture if left untreated (Sano et al. 1998).

Like in the case presented above, Hasan et al. (2012) showed in a case series of eight major recurrences after coil embolization that aneurysm sac growth rather than coil compaction was the primary mechanism associated with aneurysm recurrence. In our patient, coil migration into the intraaneurysmal thrombus occurred in addition. Although per se asymptomatic in the majority of cases, perianeurysmal edema around treated aneurysms is considered a warning sign,

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Fig. 12 FLAIR MRI after the coil treatment of a retreated, partially thrombosed left MCA aneurysm with significant edema of the adjacent left temporal and occipital lobe

possibly indicating recurrent aneurysm perfusion with the risk of further aneurysm growth and rupture.

Therapeutic Alternatives Bypass Surgery and Parent Vessel Occlusion Conservative Management Flow Diversion Microsurgical Clipping

References Dengler J, Maldaner N, Bijlenga P, Burkhardt JK, Graewe A, Guhl S, Hong B, Hohaus C, Kursumovic A, Mielke D, Schebesch KM, Wostrack M, Rufenacht D, Vajkoczy P, Schmidt NO, Giant Intracranial Aneurysm Study Group. Perianeurysmal edema in giant intracranial aneurysms in relation to aneurysm location, size, and partial thrombosis. J Neurosurg. 2015;123(2): 446–52. https://doi.org/10.3171/2014.10.JNS141560. Fanning NF, Willinsky RA, ter Brugge KG. Wall enhancement, edema, and hydrocephalus after

980 endovascular coil occlusion of intradural cerebral aneurysms. J Neurosurg. 2008;108(6):1074–86. https://doi.org/10.3171/JNS/2008/108/6/1074. Frösen J, Tulamo R, Paetau A, Laaksamo E, Korja M, Laakso A, Niemelä M, Hernesniemi J. Saccular intracranial aneurysm: pathology and mechanisms. Acta Neuropathol. 2012;123(6):773–86. https://doi.org/ 10.1007/s00401-011-0939-3. Hasan DM, Nadareyshvili AI, Hoppe AL, Mahaney KB, Kung DK, Raghavan ML. Cerebral aneurysm sac growth as the etiology of recurrence after successful coil embolization. Stroke. 2012;43(3):866–8. https://doi.org/10.1161/STROKEAHA.111.637827. Krings T, Alvarez H, Reinacher P, Ozanne A, Baccin CE, Gandolfo C, Zhao WY, Reinges MH, Lasjaunias P. Growth and rupture mechanism of partially thrombosed aneurysms. Interv Neuroradiol. 2007;13(2):117–26. https://doi.org/ 10.1177/159101990701300201. Lukic S, Jankovic S, Popovic KS, Bankovic D, Popovic P, Mijailovic M. Analysis of risk factors for perifocal oedema after endovascular embolization of unruptured intracranial arterial aneurysms. Radiol Oncol. 2015;49 (4):341–6. https://doi.org/10.1515/raon-2015-0044. Roccatagliata L, Guédin P, Condette-Auliac S, Gaillard S, Colas F, Boulin A, Wang A, Guieu S, Rodesch G. Partially thrombosed intracranial aneurysms: symptoms, evolution, and therapeutic management. Acta Neurochir. 2010;152(12):2133–42. https://doi. org/10.1007/s00701-010-0772-9. Sano H, Kato Y, Shankar K, Kanaoka N, Hayakawa M, Katada K, Kanno T. Treatment and results of

M. Dukiewicz et al. partially thrombosed giant aneurysms. Neurol Med Chir (Tokyo). 1998;38(Suppl):58–61. https://doi.org/ 10.2176/nmc.38.suppl_58. Sato T, Matsushige T, Chen B, Gembruch O, Dammann P, Jabbarli R, Forsting M, Junker A, Maderwald S, Quick HH, Ladd ME, Sure U, Wrede KH. Wall contrast enhancement of thrombosed intracranial aneurysms at 7T MRI. AJNR Am J Neuroradiol. 2019;40 (7):1106–11. https://doi.org/10.3174/ajnr.A6084. Sim KJ, Yan B, Dowling RJ, Mitchell PJ. Intracranial aneurysms with perianeurysmal edema: long-term outcomes post-endovascular treatment. J Neuroradiol. 2015;42(2):72–9. https://doi. org/10.1016/j.neurad.2014.05.001. Su IC, Willinsky RA, Fanning NF, Agid R. Aneurysmal wall enhancement and perianeurysmal edema after endovascular treatment of unruptured cerebral aneurysms. Neuroradiology. 2014;56(6):487–95. https://doi.org/10.1007/s00234-014-1355-x. Tomokiyo M, Kazekawa K, Onizuka M, Aikawa H, Tsutsumi M, Ikoh M, Kodama T, Nii K, Matsubara S, Tanaka A. Mechanisms of perianeurysmal edema following endovascular embolization of aneurysms. Interv Neuroradiol. 2007;13(Suppl 1):145–50. https://doi.org/10.1177/15910199070130S122. Vergouwen MDI, Backes D, van der Schaaf IC, Hendrikse J, Kleinloog R, Algra A, Rinkel GJE. Gadolinium enhancement of the aneurysm wall in unruptured intracranial aneurysms is associated with an increased risk of aneurysm instability: a follow-up study. AJNR Am J Neuroradiol. 2019;40(7):1112–6. https://doi.org/10.3174/ajnr.A6105.

Middle Cerebral Artery Aneurysm: Complex Wide-Necked and Lobulated Aneurysm of the Middle Cerebral Artery Bifurcation, Treated by Stent-Assisted Coil Occlusion Using a pCONUS2 Aneurysm Bridging Device and p48MW Flow Modulation Device Deployed Through the pCONUS2 Device; Two Treatment Sessions, Complete Aneurysm Occlusion, and Good Clinical Outcome

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Alexander Sirakov, Marta Aguilar Pérez, Muhammad AlMatter, and Hans Henkes Abstract

A 72-year-old female patient was admitted to another hospital due to an upper respiratory tract infection. While carrying out a noncontrast-enhanced cranial CT (NCCT) to

This case report has been previously published in part in an Open Access article in the journal Clinical Neuroradiology: Sirakov et al. (2019): Complex widenecked and lobulated aneurysm of the middle cerebral artery bifurcation, treated with a pCONUS2 neck bridging device and p48 flow modulation device deployed through the pCONUS2. https://doi.org/10.1007/s00062-019-00862-5 A. Sirakov (*) Neuroradiology, University Hospital St. Ivan Rilski, Sofia, Bulgaria Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] M. Aguilar Pérez · M. AlMatter · H. Henkes Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_161

investigate recurrent headaches and dizziness, a hyperdense Sylvian lesion was incidentally found on the right-hand side. An MRI examination was then performed, which revealed a lobulated wide-necked saccular aneurysm located on the bifurcation of the right-hand middle cerebral artery (MCA). The aneurysm neck was close to the origins of both efferent M2 branches. During the first endovascular treatment session, we were able to completely reconstruct the aneurysmal neck by implanting a pCONUS2 device into the aneurysm sac. This device is crowned with six petals, which prevented any coil loops from protruding into the parent vessel of the wide-necked aneurysm during coil occlusion. The attempt to electively coil the secondary lobule of the aneurysm failed due to the coils repeatedly compacting in the main aneurysmal sac. During a second treatment session, two p48MW flow modulation devices were telescopically deployed from the inferior trunk of the MCA through to the

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M1 segment, crossing the pCONUS2 stent. Both procedures were well tolerated, and the patient’s postoperative neurological condition remained unchanged from baseline. This combined treatment strategy, which involved implanting both a pCONUS2 bifurcation stent and a low-profile flow modulation device in order to treat a complex middle cerebral artery aneurysm, is the main topic of this chapter. Keywords

Middle cerebral artery · Stent-assisted coil occlusion · pCONUS2 bifurcation stent · Flow diversion · p48MW flow modulation device · pCONUS2/p48MW combination

Patient A 72-year-old female patient was admitted to another hospital with flu-like symptoms. An upper respiratory tract infection was diagnosed based on her clinical signs and symptoms, laboratory findings, and a CT scan of the thorax. Despite being prescribed antibiotics and nonsteroid anti-inflammatory drugs, the patient persistently complained of recurrent headaches and dizziness. An MRI scan revealed a complex saccular aneurysm located on the bifurcation of the right-hand middle cerebral artery. The patient had a medical history of hypothyroidism on optimal dose substitution therapy and a 10-year history of controlled arterial hypertension.

Diagnostic Imaging Initial MRI workup revealed the presence of a complex lobulated aneurysm of the right middle cerebral artery (MCA). The DSA examination showed that this aneurysm had a wide neck, with the fundus measuring 5.5
5 mm, and the neck is 5.7 mm wide open to the lumen of the right MCA bifurcation. The diameter of the inferior trunk of the righthand MCAwas measured at 2.6 mm. 3D reconstructions made from rotational angiography also revealed an aneurysmal irregularity of the presence

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of a secondary lobule adjacent to the aneurysm neck and the inferior trunk of the MCA (Fig. 1).

Treatment Strategy The goal of the treatment was to prevent this aneurysm from potentially rupturing at a future date. The lobulated irregularities of the aneurysmal sac and the width of the neck were both identified as potential issues. Microsurgical clip ligation was recommended to and declined by the patient. pCONUS2-assisted coil embolization was considered feasible. The treatment concept involved deploying a pCONUS2 stent under dual antiplatelet medication from the aneurysm sac to the M1 segment to protect the neck during subsequent coil occlusion. The intended treatment, together with the potential alternatives and their respective risks and likelihood of success, was explained to the patient. Informed consent was obtained in written form.

Treatment Procedure #1, 04.06.2018: stent-assisted coil occlusion of an unruptured wide-necked saccular aneurysm located at the bifurcation of the right MCA using a pCONUS2 stent and detachable coils Anesthesia: general anesthesia, 1
3,000 IU non-fractionated heparin (Heparin Natrium, B. Braun) IV, 1
500 mg thiopental (Trapanal, Nycomed) IV Premedication: 1
100 mg ASA (Aspirin, Bayer Vital) PO daily and 1
10 mg prasugrel (Efient, Daiichi Sankyo/Lilly) PO given 5 days before the procedure; Multiplate (Roche Diagnostics) and VerifyNow (Accriva) tests confirmed dual platelet function inhibition Access, right common femoral artery, 8F sheath (Terumo); guide catheter: 8F Guider Softip (Boston Scientific); intermediate catheter: Syphontrak (InNeuroCo/Cerenovus); microcatheter: 1
Prowler Select Plus 90 (Cerenovus) used for pCONUS2 deployment and 1
Excelsior SL-10 (Stryker) for coil insertion; microguidewire: Synchro2 0.01400 300 cm (Stryker)

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Middle Cerebral Artery Aneurysm: Complex Wide-Necked and Lobulated Aneurysm of the Middle. . .

Fig. 1 Diagnostic imaging in a patient with an unruptured MCA bifurcation aneurysm. Contrast-enhanced T1WI MRI (a) and TOF MRA (b) unveiled a wide-necked saccular aneurysm of the right-hand MCA bifurcation. The diagnostic DSA examination in which contrast medium was injected into the right internal carotid artery (ICA) showed a complex lobulated aneurysm arising from the right-hand MCA bifurcation with two M2 branches incorporated into the neck

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(posterior-anterior view (c), left anterior oblique view (d)). Rotational DSA with 3D reconstruction (e, f) confirmed the presence of focal irregularities (arrow) and a secondary lobule (arrow) arising from the main aneurysmal sac, together with an unfavorable dome-to-neck ratio. The separated lobule of the main aneurysm sac adjacent to the inferior MCA branch was of significant concern, both as a potential rupture site and as a challenge for the forthcoming treatment

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Implants: 1
bifurcation stent pCONUS2 4/15/6 (phenox); 4 coils: 1
Target 360 XL soft 4/8, 1
Target 360 ultra 3/10, 1
Target Helical Nano 3/8, 1
Target Helical Nano 2/4 (Stryker) Course of treatment: an 8F guiding catheter was inserted into the right ICA. Under road map guidance, the Syphontrak intermediate catheter was navigated into the petrous segment of the right ICA. DSA, including standard and oblique projections, was performed to enable a better understanding of the aneurysm geometry without any superimposition of the surrounding structures. A Prowler Select Plus microcatheter was navigated over a microguidewire and positioned inside the aneurysm sac, and a pCONUS2 was then successfully introduced into the sac with the device petals carefully positioned across the aneurysm neck. A DSA run was performed to confirm both the optimal position of the device and the location of the aneurysm’s artificial metal neck. Once an Excelsior SL-10 microcatheter had been guided distally through the shaft and petals of the pCONUS2, the aneurysm was packed with the coils as mentioned earlier and occluded. The microcatheter remained in a stable position inside the aneurysm dome, while the coils were being inserted; however, due to the dense coil structure inside the main sac of the aneurysm, the secondary lobule adjacent to the inferior trunk of the MCA remained non-occluded. Final angiography showed no evidence of either coil protrusion into the MCA bifurcation, thrombus formation, or distal emboli. No device-related spasm, vessel perforation, or coil entanglement was detected. After the aneurysm had been successfully packed and occluded, the pCONUS2 was electrolytically detached in 82 s. The procedure was finished as intended (Fig. 2). Duration: 1st–17th DSA run: 119 min; fluoroscopy time: 52 min Complications: none Postmedication: 1
100 mg ASA PO daily for life and 1
10 mg prasugrel PO daily for 3 months, 2
3000 IU certoparin (MonoEmbolex, Aspen) SC daily for 1 week

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Follow-Up Examinations MRI on the second postoperative day did not show any foci of diffusion restriction in either cerebral hemisphere, nor did it reveal any FLAIR hyperintensities of clinical relevance. The diagnostic angiography performed on the second month after the initial treatment showed that the pCONUS2 stent shaft was patent and that the residual lobule of the aneurysm sac adjacent to the inferior trunk was being filled with contrast medium. No in-stent stenosis or vascular changes of the distal MCA branches were noted (Fig. 3).

Treatment Strategy As mentioned above, the patent lobule of the aneurysm sac was considered to be a potential rupture site. There was little reason to assume that the first treatment had eliminated the rupture risk of this aneurysm, and conservative management might have exposed the patient to a significant rupture risk over time. Neither endovascular-endosaccular (e.g., coil occlusion) nor microsurgical (e.g., clipping) options were appealing. Instead, based on previous experience, we felt that flow diversion offered the best risk/benefit ratio.

Treatment Procedure #2, 06.08.2018: low-profile flow diverter implantation from the right inferior MCA trunk to the right M1 segment as a part of the final and conclusive treatment of a complex wide-necked aneurysm of the right MCA bifurcation Anesthesia: general anesthesia, 1
3,000 IU non-fractionated heparin (Heparin Natrium, B. Braun) IV, 1
500 mg thiopental (Trapanal, Nycomed) IV Premedication: 1
500 mg ASA (Aspirin, Bayer Vital) PO and 1
10 mg prasugrel (Efient, Daiichi Sankyo/Lilly) PO on the day prior to the

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Fig. 2 (continued)

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Fig. 2 The first stage in staggered endovascular treatment of a complex right-hand MCA bifurcation aneurysm. The angiographic working projection (left anterior oblique view (a)) showed the anatomical details of the aneurysm. The aneurysm sac was catheterized under road map guidance (b). The crown of the pCONUS2 implant was deployed with the petals placed across the aneurysm neck (c, d, e). Note the radiopacity of the device (the crown with six petals; the distal marker at the articulation, connecting shaft and crown; the proximal marker, indicating the

detachment zone), as shown in the fluoroscopic snapshot images (e, f). The petals of the device and the aneurysm’s new artificial neck (g) aided coil retention and protected both the neck and the efferent branches while coiling the aneurysm (h, i). A final DSA run at the end of the procedure (j) confirmed that blood circulation in the aneurysm had sufficiently reduced. The lobulated focal dilatation of the aneurysm wall adjacent to the inferior trunk of the MCA (M2) was still present in the final DSA run

procedure; VerifyNow (ARU 384; P2Y12 PRU: 4, 98% inhibition) and Multiplate (AUC: ADP 14 U, ASPI 19 U) 4 days prior the procedure confirmed sufficient dual platelet function inhibition

Access; right common femoral artery, 8F sheath (Terumo); guide catheter: 8F Guider Softip (Boston Scientific); intermediate catheter: Syphontrak (InNeuroCo/Cerenovus); microcatheters, 1


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Fig. 3 Follow-up MRI examination after the first endovascular session. No procedure-related FLAIR abnormalities were present (a). DSA examination 2 months after the pCONUS2 implantation (b, c). No in-stent stenosis, coil

migration, or overpacking was noted. The lobule adjacent to the inferior branch was patent and unchanged in size and shape

Prowler Select Plus 90 (Cerenovus); 1
Prowler Select Plus 45 (Cerenovus); 1
Marathon (Medtronic), 1
Echelon-10 90 (Medtronic), 1
pORTAL 14 (phenox); microguidewires: 2
Mirage (Medtronic), 1
Synchro2 0.01000 300 cm, 1
Synchro2 0.01400 300 cm (Stryker) Implants: 2 flow diverters: 1
p48MW 3/18 and 1
p48MW 3/12 (phenox) Course of treatment: access to the aneurysm was achieved via the right ICA. The catheterization of the right M2 inferior trunk was not straightforward. However, this was facilitated by the presence of the pCONUS2 device and the obliterated neck of the aneurysm. The right distal M2/M3 branches were catheterized with a Marathon/Mirage microcatheter/ microguidewire combination, crossing the petals of the pCONUS2 device. After the Mirage had been withdrawn, a Synchro2 0.010 “(300 cm) microguidewire was inserted, and the Marathon microcatheter was replaced by an Echelon-10 90 microcatheter. This was followed by the Synchro2 0.010” microguidewire being replaced by a Synchro2 0.01400 (300 cm) microguidewire, which allowed us to replace the Echelon-10 with a Prowler Select Plus 90 microcatheter. This catheter was then used to deploy the first p48MW 3/18 across the aneurysmal neck and inside the crown of the previously implanted pCONUS2. The flow

modulation device was then completely unsheathed. However, the proximal portion of the p48MW had a slight “fish mouth” presentation with incomplete wall apposition to the vessel wall. Navigating a Prowler Select Plus 45 microcatheter across the whole p48MW resolved the proximal kinking of said implant. In order to avoid any potential collapse of the device and possible occlusion of the parent artery, a second p48MW 3/12 was carefully implanted proximal to the terminal carotid artery. This allowed approximately 30% of the mesh of the two devices to overlap. The final DSA run confirmed that the dependent target vessels were still fully patent (Fig. 4). Duration: 1st–21st DSA run: 230 min; fluoroscopy time: 93 min Complications: none Postmedication: 1
100 mg ASA PO daily for life and 1
10 mg prasugrel PO daily for 12 months; 2
3000 IU certoparin (MonoEmbolex, Aspen) SC daily for 1 week

Follow-Up Examinations MRI after the second treatment did not reveal any procedure-related silent emboli. The diagnostic angiography performed 12 months after

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Fig. 4 (continued)

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Fig. 4 The second and final phase of staged endovascular treatment of a complex MCA bifurcation aneurysm. The microcatheter used for the p48MW was navigated distally (a), and the procedure was straightforward (b). The first low-profile flow modulation device p48MW 3/18 was carefully loaded and positioned inside the microcatheter (c). Once the p48MW stent had been completely deployed (d), this stent was fully expanded inside the crown of the

the second procedure showed complete patency of the intraluminal stents, normal perfusion of the superior trunk of the MCA, and complete obliteration of the target aneurysm lobule (Fig. 5).

Clinical Outcome Both endovascular procedures were well tolerated, and the patient’s neurological condition remained unchanged from baseline in the following months. Postprocedural MRI did not show any relevant abnormalities. The patient was discharged home on day 4 after treatment in both cases.

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pCONUS2 implant (e). Note the partial resolution of the “fish mouth” narrowing of the stent (e, arrow) through gentle nudging with the microcatheter. Implanting the second p48MW 3/12 resolved the proximal narrowing of the first flow diverter (f), while adequate vessel apposition was achieved. A final DSA run at the end of the procedure confirmed the patency of both flow diverters and the parent arteries (g)

Discussion Dangerous aneurysmal flow changes and the related hemodynamic patterns may result in aneurysm sac changing shape. Should certain geometric features such as irregularities, focal bulging, or lobulation be present, there is considered to be a higher likelihood of a significant future aneurysmal rupture (de Rooij et al. 2009; Schneiders et al. 2014). Aneurysms that have an unfavorable dome-to-neck ratio (De Leacy et al. 2019) or incorporated arterial branches could be particularly challenging for any intervention. Although nowadays we have recourse to

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Fig. 5 Follow-up DSA 12 months after the staggered endovascular treatment of a right-hand MCA aneurysm. DSA with contrast medium injected into the right ICA (a)

Fig. 6 Glass model of an MCA bifurcation aneurysm showing a pCONUS2 bifurcation stent implanted with its petals at the neck level of the “aneurysm.” A p48MW 2/15 mm has been deployed through the pCONUS2 from the “inferior MCA trunk” to the “M1 segment.” There is only a small amount of metal connecting the six petals with the shaft of the p48MW. This allows the flow diverter to expand without hindrance fully

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showed that the target aneurysm had been entirely and definitively occluded. Note the patency of the implanted pCONUS2 device and both p48 MWs (b, c)

various new and advanced techniques, such complex aneurysms are still particularly tricky to treat. Most of the devices on the market are designed to reconstruct either the aneurysm neck or the parent artery of the aneurysm itself, whether temporarily or permanently (Henkes and Weber 2015; Khattak et al. 2018). In certain scenarios, it is crucial to either use alternative techniques or to combine techniques to secure the patency of the incorporated branches or the awkward aneurysm anatomy. This case portrays a situation in which a pCONUS2 device was used to successfully cover the aneurysmal neck while the incorporated efferent arterial branches were protected (Lylyk et al. 2018). Secondly, applying the p48MW low-profile flow modulation device across the aneurysmal neck and inside the pCONUS2 implant resulted in a significant hemodynamic alternation. As the p48MW was introduced at the level of the arterial bifurcation, it could successfully provoke the reconstruction of the parent artery and the aneurysm neck by

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redirecting the blood flow away from the aneurysm as intended. Due to its structure, the pCONUS2 implant contains less metal than the pCONUS1. It was purposely designed to enable it to be combined with the p48MW flow diverter (Fig. 6). We did not observe any technical difficulties in navigating the microcatheter across the crown and the intraluminal portion of the implant. The radial force of the p48MW shaft allowed adequate wall apposition of the stent while it was being deployed. The coil retention afforded by the six petals appeared to be at least as robust as known from the pCONUS1 (Bhogal et al. 2019). We believe that the combined use of this “waffle cone technique” for assisted coil occlusion together with an extrasaccular flow diversion device enables better treatment results for selected, complex bifurcation aneurysms. A true “bifurcation flow diverter,” however, might have the potential even further to facilitate the endovascular treatment of complex bifurcation aneurysms.

Therapeutic Alternatives Microsurgical Clipping Stent Assisted Coil Occlusion WEB Y-Stent Assisted Coil Occlusion

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References Bhogal P, Bleise C, Chudyk J, Lylyk I, Viso R, Perez N, Henkes H, Lylyk P. The p48mw flow diverter – initial human experience. Clin Neuroradiol. 2019; https://doi. org/10.1007/s00062-019-00827-8. De Leacy RA, Fargen KM, Mascitelli JR, Fifi J, Turkheimer L, Zhang X, Patel AB, Koch MJ, Pandey AS, Wilkinson DA, Griauzde J, James RF, Fortuny EM, Cruz A, Boulos A, Nourollah-Zadeh E, Paul A, Sauvageau E, Hanel R, Aguilar-Salinas P, Novakovic RL, Welch BG, Almardawi R, Jindal G, Shownkeen H, Levy EI, Siddiqui AH, Mocco J. Wide-neck bifurcation aneurysms of the middle cerebral artery and basilar apex treated by endovascular techniques: a multicentre, core lab adjudicated study evaluating safety and durability of occlusion (BRANCH). J Neurointerv Surg. 2019;11(1):31–6. https://doi.org/10.1136/neurintsurg-2018-013771. De Rooij NK, Velthuis BK, Algra A, Rinkel GJ. Configuration of the circle of Willis, direction of flow, and shape of the aneurysm as risk factors for rupture of intracranial aneurysms. J Neurol. 2009;256(1):45–50. https://doi.org/10.1007/s00415-009-0028-x. Henkes H, Weber W. The past, present and future of endovascular aneurysm treatment. Clin Neuroradiol. 2015;25 (Suppl 2):317–24. https://doi.org/10.1007/s00062-0150403-1. Khattak YJ, Sibaie AA, Anwar M, Sayani R. Stents and stent mimickers in endovascular management of wideneck intracranial aneurysms. Cureus. 2018;10(10): e3420. https://doi.org/10.7759/cureus.3420. Lylyk P, Chudyk J, Bleise C, Sahl H, Pérez MA, Henkes H, Bhogal P. The pCONus2 neck-bridging device: early clinical experience and immediate angiographic results. World Neurosurg. 2018;110:e766–75. https://doi.org/ 10.1016/j.wneu.2017.11.097. Schneiders JJ, Marquering HA, van den Berg R, VanBavel E, Velthuis B, Rinkel GJ, Majoie CB. Rupture-associated changes of cerebral aneurysm geometry: high-resolution 3D imaging before and after rupture. AJNR Am J Neuroradiol. 2014;35(7):1358–62. https://doi.org/10.3174/ajnr.A386.

Part XVIII Distal Segments (M2 and Beyond) of the Middle Cerebral Artery

Middle Cerebral Artery (M3) Aneurysm: Ruptured Mycotic Distal Aneurysm: Treatment by Deconstructive Technique Using a Liquid Embolic Agent

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Jorge Chudyk, Esteban Scrivano, Nicolas Perez, Carlos Bleise, and Pedro Lylyk

Abstract

Keywords

A 30-year-old female patient presented with headache and fever. She had aortic valve replacement in her medical history and was anticoagulated. The CT scan showed a subarachnoid hemorrhage (SAH). DSA revealed a small distal aneurysm of the left middle cerebral artery. The SAH was considered to have arisen due to the rupture of this very small distal mycotic aneurysm. The size and location of the aneurysm justified parent vessel occlusion as the treatment concept of choice. Both the aneurysm and its parent artery were therefore occluded by injecting nBCA diluted with Lipiodol. The patient was asymptomatic when she was discharged home after 15 days. The management of mycotic aneurysms is the main topic of this chapter.

Middle cerebral artery · Mycotic aneurysm · Distal aneurysm · Parent artery occlusion · Deconstructive technique

Patient A 30-year-old female patient presented with a severe headache and fever. She had a medical history including mechanical aortic valve replacement due to a bicuspid aortic valve and was therefore under oral anticoagulation. Medical work-up confirmed bacterial endocarditis.

Diagnostic Imaging In September 2013, the patient presented at the emergency room with a severe headache and neck stiffness. CT and CTA were performed showing a cortical SAH in the left parietal lobe and a very small distal aneurysm in the left M3 segment. The location of the aneurysm and the concomitant cardiological disorder suggested this aneurysm

J. Chudyk · E. Scrivano · N. Perez · C. Bleise · P. Lylyk (*) Interventional Neuroradiology, Clinica La Sagrada Familia, ENERI, Buenos Aires, Argentina e-mail: [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_53

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Fig. 1 NCCT (a) showing cortical hyperdensity in the left parietal lobe and effacement of the surrounding sulci, corresponding to a superficial SAH with light surrounding hypodensity. CTA (b) showing a small distal dilation of a

cortical branch of the left MCA compatible with a mycotic aneurysm in an area adjacent to the SAH (white circle). DSA run in a lateral projection (c) and 3D DSA reconstruction (d) showing the small mycotic aneurysm

was of mycotic origin. Diagnostic 2D and rotational angiography with 3D reconstruction confirmed the presence of the mycotic aneurysm in a very distal M3 segment of the left middle cerebral artery (MCA), less suitable for coiling due to its small size (under 2 mm) (Fig. 1).

endocarditis and prevent new emboli. Parent artery occlusion with liquid embolic agent was the technique chosen to treat the aneurysm. At the same time, treatment with antibiotic drugs was initiated to prevent further septic emboli.

Treatment Treatment Strategy The primary goal of the treatment was to prevent further growth and re-rupture of the mycotic aneurysm. The secondary goal was to treat the

Procedure, 05.09.2013: treatment of a ruptured distal mycotic MCA aneurysm by parent vessel occlusion, using embolization with nBCA glue

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Fig. 2 Microcatheter injection of a cortical branch of the left MCA (a), showing a small mycotic aneurysm. A more distal position of the tip of the microcatheter was achieved for an even better controlled injection of the liquid embolic agent. Once in position, the microcatheter was flushed with 10 cc of dextrose solution. A 0.5 cc mixture of nBCA and Lipiodol was slowly injected. The target segment of the

MCA together with the mycotic aneurysm was completely occluded with the solidified polymer (b, c). There was no glue migration outside of the target arterial segment. A post-embolization DSA immediately after the procedure shows occlusion of the parent vessel and the mycotic aneurysm (d)

Anesthesia: general anesthesia, 10,000 IU unfractionated heparin (Reviparin, Ribero) IV Premedication: The patient was under oral anticoagulation with an international normalized ratio (INR) of 4.3. Vitamin K and 1.000 IU of Prothromplex were used to reverse the effect of anticoagulation prior to the procedure. Access: right femoral artery, 8 F sheath (Terumo). Guiding catheter: triaxial system with a shuttle long sheath 6F (Cook) and 6F Fargo Max (Balt Extrusion) intermediate catheter; microcatheter: Magic 1.2 F (Balt Extrusion); microguidewire: Hybrid 0.00700 (Balt Extrusion)

Liquid embolic agent: n-butyl-cyanoacrylate (Histoacryl, B. Braun), Lipiodol (Guerbet), 1:3, 0.5 cc injected Course of the treatment: Although the patient was young, a triaxial system was chosen to ensure sufficient support, considering the far distal location of the aneurysm. The left ICA was catheterized with a 5 F vertebral diagnostic catheter that was exchanged for a Shuttle and Fargo Max guiding catheter, using a 300 cm 0.03500 exchange guidewire. A Magic 1.2 F microcatheter and a Hybrid 0.00700 microwire were used to navigate the

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microcatheter as close to the aneurysm as possible (Fig. 2). Duration: 1st–25th DSA run: 140 min; fluoroscopy time: 50 min Complications: none Post medication: none Antibiotic therapy IV and PO for the treatment of bacterial endocarditis was initiated.

Clinical Outcome The general anesthesia was worn off in the angiography suite, and the patient woke up without neurological deficit. The patient was discharged 15 days after the endovascular treatment in order to complete antibiotic treatment. mRS at discharge was 0.

Follow-Up Examinations NCCT scans were performed at 48 h and 15 days after the treatment (Fig. 3), showing no residual SAH and a small area of hypodensity around the glue. Additional follow-up MRI/MRA examinations were performed at 12 and 24 months, showing no recanalization of the aneurysm and a very small gliosis around the glue.

Fig. 3 Follow-up NCCT (a) and T2WI MRI (b, c) showing reabsorption of the SAH, the hyperdense glue cast (a), and an adjacent gliotic scar (c). Neither a new hemorrhage

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Discussion Mycotic aneurysms represent one of the most serious neurological complications of endocarditis and account for 0.7–6.5% of all intracranial aneurysms. Although the risk of rupture is about 2%, the mortality rate after rupture is as high as 60–90% (Kannoth and Thomas 2009). The most accepted theory concerning the formation, growth, and rupture of these aneurysms assumes septic emboli from the heart that cause both an occlusion of cerebral arteries and a severe inflammation of the vessel wall (i.e., an endarteritis), leading to weakening of the arterial wall and finally resulting in arterial enlargement and aneurysm formation. Usually they are located in the anterior circulation at far distal locations (Kuo et al. 2010). The most common clinical presentation is headache, fever, and vomiting in more than 50% of the patients. When a rupture occurs, the hemorrhage can be subarachnoid, intraparenchymal, or intraventricular (Ducruet et al. 2010). CT and MRI images are used to diagnose parenchymal brain abnormalities, and angiographic studies such as CTA or MRA can reveal the presence of mycotic aneurysms. Digital subtraction angiography is necessary to confirm the lesion and plan the treatment.

nor a major infarct in the area of the occluded artery can be found

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Treatment options include medical, surgical, and endovascular approaches (Zanaty et al. 2013). Medical treatment involves empiric or culture-guided antimicrobial agents for 4–6 weeks. Surgical treatment is an effective approach when intraparenchymal hematoma is associated with the aneurysm in order to evacuate the blood and also surgically exclude the aneurysm. Endovascular treatment has the advantage of decreased risk of anesthesia in patients with previous coronary and valve dysfunction, rapid reinstitution of anticoagulation therapy, and shorter procedure overall. Endovascular treatment of these aneurysms can be achieved using different techniques including coil occlusion, stent-assisted coiling, and deconstructive technique with liquid embolic agents (Zanaty et al. 2013). Because of the fragility of the wall and also the anatomy, coil occlusion was not considered appropriate. Using a stent in an “infected aneurysm” was also not considered. Due to the very small size of the aneurysm and the distal location, embolization with liquid agents and occlusion of the parent artery were preferred. ONYX and nBCA are the most frequently used agents. ONYX has the advantages of slow precipitation and multiple injections from a single catheter but requires DMSO compatible microcatheters and some experience in using it. nBCA allows rapid obliteration, minimal inflammatory effect, but with higher risk of collateral embolization or gluing the microcatheter. With the experience from previous cases, a low profile microcatheter and microguidewire combination and nBCA were chosen for the embolization. The Magic 1.2 F microcatheter allows for very distal, flow-guided, and therefore atraumatic navigation in very tortuous anatomy and small arteries. The mixture of nBCA and Lipiodol of 33% allowed progressive propagation of the polymerizing glue and a precise obliteration of the aneurysm, decreasing the risk of an

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unintended collateral vessel occlusion. The embolization is observed under fluoroscopy or high-frame-rate DSA. Once reflux of the polymerizing liquid is observed, the microcatheter is immediately withdrawn. Angiographic control usually shows complete obliteration of the aneurysm together with the target vessel (Ducruet et al. 2010). The good clinical and angiographic outcome and the absence of further septic or embolic complications in this case confirm the efficacy of the endovascular treatment using a deconstructive technique in the management of distal mycotic aneurysms.

Therapeutic Alternatives Conservative Management Onyx Embolization Surgical Clipping

References Ducruet AF, Hickman ZL, Zacharia BE, Narula R, Grobelny BT, Gorski J, Connolly ES Jr. Intracranial infectious aneurysms: a comprehensive review. Neurosurg Rev. 2010 Jan;33(1):37–46. https://doi.org/ 10.1007/s10143-009-0233-1. Kannoth S, Thomas SV. Intracranial microbial aneurysm (infectious aneurysm): current options for diagnosis and management. Neurocrit Care. 2009;11(1):120–9. https://doi.org/10.1007/s12028-009-9208-x. Kuo I, Long T, Nguyen N, Chaudry B, Karp M, Sanossian N. Ruptured intracranial mycotic aneurysm in infective endocarditis: a natural history. Case Rep Med. 2010;2010:168408. https://doi.org/10.1155/ 2010/168408. Zanaty M, Chalouhi N, Starke RM, Tjoumakaris S, Gonzalez LF, Hasan D, Rosenwasser R, Jabbour P. Endovascular treatment of cerebral mycotic aneurysm: a review of the literature and single center experience. Biomed Res Int. 2013;2013:151643. https://doi.org/ 10.1155/2013/151643.

Middle Cerebral Artery (M3) Aneurysm: Atypical Primary Morphology and Early Recurrence After Stent-Assisted Coil Occlusion During the Long-Term Left Ventricular Assist Device Treatment, Accompanied by Temporary Septicemia; Parent Vessel Occlusion as the Final Treatment with Good Clinical Outcome

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Vera Reuschel, Matthias Groll, Ulf Quäschling, Karl-Titus Hoffmann, and Stefan Schob Abstract

A 58-year-old male patient presented with a subarachnoid hemorrhage (SAH) due to the rupture of a distal aneurysm of a left middle cerebral artery (MCA, M3) branch. Stentassisted coil occlusion was performed successfully, preserving the parent artery lumen. The patient was undergoing long-term treatment with a left ventricular assist device (LVAD) for his progressive congestive cardiac failure and had encountered long episodes of impaired wound healing and LVAD-associated infections. During an assessment for a heart transplant, a non-enhanced cranial CT scan was performed, which raised the suspicion of

V. Reuschel · U. Quäschling · K.-T. Hoffmann · S. Schob (*) Abteilung für Neuroradiologie, Universitätsklinikum Leipzig AöR, Leipzig, Germany e-mail: [email protected]; [email protected]; [email protected]; [email protected]; [email protected]

aneurysmal parenchymal hemorrhage. DSA showed further growth and recurrent perfusion in the aneurysm, which had been occluded 21 months earlier. There was no recurrent hemorrhage. Since the parent artery no longer supplied a large volume of brain parenchyma, it was decided to treat it with proximal parent vessel occlusion (PVO) using coils. This was performed successfully and followed by a course of antimicrobial chemotherapy. The patient recovered without neurological deficit. In the presence of sepsis or other systemic infections, an early and morphologically atypical recurrence of a previously treated intracranial aneurysm suggests an underlying bacterial infection. This scenario requires immediate antibiotic therapy and rigorous treatment of the aneurysm. Long-term treatment with cardiac assist devices can create ideal conditions for chronic infection, as a biofilm may form along the intra-corporal parts of the device, which then serve as a focus for septicemia.

M. Groll Klinik und Poliklinik für Neurochirurgie, Universitätsklinik Leipzig AöR, Leipzig, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_76

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This carries significant risk of primary aneurysm formation as well as of superinfection of previously occluded aneurysms where the infection infiltrates, inflames, and thus weakens the vessel wall. This latter scenario could cause an initially sufficiently treated aneurysm to rapidly relapse and grow further. For distally located infectious aneurysms, PVO is a viable treatment option. The management of “mycotic” aneurysms is the main topic of this chapter.

Treatment Strategy

Keywords

Treatment

Middle cerebral artery · Mycotic aneurysm · Parent vessel occlusion · Left ventricular assist device

Patient A 58-year-old male patient suffering from dilated cardiomyopathy which was progressively leading to congestive heart failure was in urgent need of a left ventricular assist device (LVAD). After receiving the implant, his sternal wound healing was hampered by prolonged infection from Staphylococcus aureus and Proteus vulgaris. During one of the multiple revision operations, he suffered an epileptic seizure. After extubation, the patient was found to be suffering from global aphasia and a right hemiparesis.

Diagnostic Imaging The patient was immediately transferred to the Department of Neuroradiology, where a non-enhanced cranial computed tomography (NCCT) was performed which showed a subarachnoid hemorrhage (SAH) Fisher grade 4. A digital subtraction angiography (DSA) was initiated without further delay and revealed an atypical distal MCA aneurysm arising from an M3 branch, which was responsible for the supply of a significant portion of the left sided MCA territory posterior to the sensory and motor cortex (Fig. 1).

Since the aneurysm not only arose from but also included part of a potentially important left M3 branch, simple coil occlusion would not have been possible without risking significant cerebral ischemia. Consequently, it was decided to treat the aneurysm using stent-assisted coiling, aiming to preserve the perfusion of the dependent brain parenchyma.

Procedure #1, 27.01.2016: endovascular stentassisted coil occlusion of a ruptured left M3 aneurysm Anesthesia: general anesthesia; 5000 IU unfractionated heparin (Heparin-Natrium, B. Braun) IV after securing the femoral access Premedication: 1
500 mg ASA (aspirin IV, Bayer Vital) IV and 1
14 mg eptifibatide (Integrilin, GlaxoSmithKline) IV during the procedure prior to stent deployment; 1
300 mg clopidogrel (Clopidogrel, Zentiva) PO following the procedure Access: right common femoral artery, 1
6F sheath (Terumo); guide catheter: 1
6F Envoy (Codman); microcatheter: 2
Excelsior SL10 (Stryker); microguidewire: 1
Traxcess 14 EX 0.01400 200 cm (MicroVention) Implants: 1
stent: Leo+ Baby 2/25 mm (Balt Extrusion); 5
coils: Target 360 ultra 3/8, Target 360 soft 4/8, Target 360 soft 4/6, Target helical ultra 2/8, Target helical ultra 2/4 (Stryker) Course of treatment: cerebral angiography of all intracranial vessels was performed. Left ICA angiography revealed a distal aneurysm of the left MCA located on a branch of the superior division. The aneurysm measured 8
5
4.7 mm. The aneurysm was more fusiform than saccular in shape and included a significant portion of the circumference of its parent artery. No further aneurysms or other vascular pathologies were detected. The guide catheter was placed into the proximal left ICA. Then, the affected MCA branch was probed with two microcatheters. The first one was placed distally to the aneurysm,

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Fig. 1 Emergency NCCT and DSA of a patient with aneurysmal SAH. The NCCT (a) shows the left-sided sulcal blood, suggesting a ruptured MCA aneurysm. The

injection of the left ICA confirms an oval-shaped aneurysm on the left-sided M3 segment, the most likely cause of the SAH (posterior-anterior view (b), lateral view (c))

ready for the Leo + Baby stent to be deployed as part of a jailed catheter coiling technique. The second microcatheter was placed within the aneurysm sac. The Leo + Baby stent was deployed to protect the parent vessel and provide scaffolding for the coils. Eventually, a loose coil occlusion of the aneurysm was performed. The aneurysm was considered sufficiently occluded to prevent

recurrent rupture, and the parent artery remained patent (Fig. 2). Duration: 1st–12th DSA run: 160 min; fluoroscopy time: 32 min Complications: none Postmedication: 1
100 mg ASA PO daily lifelong, 1
75 mg clopidogrel PO daily for 6 months

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Fig. 2 DSA with injection of the left MCA (a) showing the dependent brain parenchyma and the left M3 aneurysm as the likely cause of the SAH. Preparation of stent-assisted coiling (b): the stent delivery catheter is placed distally to the aneurysm; the coiling microcatheter is placed within the aneurysm sac. After deploying the stent, the coiling

catheter is jailed in situ, and coils can be safely inserted (c). The final injection (d) confirms the satisfactory occlusion of the aneurysm and the patency of the stent and that all dependent branches still have unimpaired left hemispheric perfusion

Outcome

Follow-Up Imaging

The patient recovered from the SAH and the endovascular treatment with no residual neurologic symptoms apart from some subjective dysarthria.

The NCCTs performed after the procedure showed the continuing resorption of subarachnoid blood. No complications such as recurrent hemorrhage or cerebral infarction were observed.

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Over a period of several months, the patient continued to suffer from massively impaired sternal and abdominal wound healing as well as an infection of the LVAD driveline. A swab of the wound confirmed a number of pathogens, including Staphylococcus aureus, Streptococcus agalactiae, and Proteus hauseri. A complex, resistogram-based therapy with antibiotics was initiated and continued for approximately 2 months. This included gentamicin (Gentamicin Ratio, Ratiopharm; 0-1-0, blood level tailored), rifampicin (Eremfat, Riemser Pharma; 600 mg 1–0–0), meropenem (Merrem, Pfizer Pharma; 1000 mg, 1-1-1), and clindamycin (Clindamycin, Aristo; 600 mg, 1-1-1). While the patient was unwell, no follow-up DSA examination was performed. After a brief recovery, his overall condition deteriorated significantly, and he was listed for an urgent heart transplant. While being evaluated prior to receiving a transplant, an NCCT was performed which showed a parenchymal hyperdensity in the left hemisphere adjacent to the coil bundle. An intracerebral aneurysmal hemorrhage was suspected, and a DSA was performed immediately. This showed a major dislodging of the coil bundle and a significant, morphologically atypical growth of the previously occluded aneurysm. The risk of re-rupture was considered to be extraordinarily high, and the decision was made to attempt endovascular re-treatment (Fig. 3).

Treatment Strategy Since the microcatheter injection revealed high velocity flow into the aneurysm originating from the proximal third of the stent-bearing vessel, reconstructive flow diversion and parent vessel occlusion were both contemplated as treatment options. Given the failure of the first treatment so soon after the intervention, the small caliber of the feeding vessel, the distal localization of the aneurysm, and relatively small volume of dependent brain parenchyma, parent vessel occlusion (PVO) was considered to yield the better riskbenefit ratio. It was felt that retrograde supply and further growth of the aneurysm as a

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consequence of retrograde perfusion via the leptomeningeal collaterals following proximal occlusion was unlikely.

Treatment Procedure #2: 18.10.2017: endovascular treatment of a recurrent left M3 aneurysm by parent artery occlusion with coils Anesthesia: general anesthesia; 5000 IU unfractionated heparin IV after securing the femoral access Premedication: none Access: right common femoral artery; 1
8F sheath (Terumo); guide catheter: 1
6F Neuron MAX (Penumbra); distal access catheter, 1
6F Sofia (MicroVention); microcatheters: 1
Excelsior SL-10 (Stryker), 1
Excelsior XT27 (Stryker); microguidewires: 1
Traxcess 0.01400 , 1
Transend Floppy 0,01400 300 cm (Boston Scientific) Implants: 3 coils: 1
Codman Deltapaq 10 stretch-resistant coil 2/6, 1
Codman Deltapaq 10 stretch-resistant coil 2/8, 1
Codman Deltapaq 10 stretch-resistant coil 1.5/4 Course of treatment: an angiography showing the left ICA and its branches was performed. The microcatheter injection of the stent-carrying vessel revealed that the stent-bearing segment was patent and that there was delayed yet prolonged contrast filling of the aneurysm sac, mainly via the proximal stent-bearing third of the treated branch. Once the guide catheter had been placed in the left ICA, the intermediate catheter was advanced into the M1 segment of the left MCA. The stent-carrying vessel was successfully catheterized using the microcatheter. Subsequently, the proximal portion of the stentcarrying branch was occluded using three detachable coils. This successfully excluded the aneurysm from the intracranial circulation. The final injection demonstrated good opacification of the left hemisphere without significant ischemia. The patient was extubated the same day and did not exhibit any focal neurological deficit (Fig. 4).

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Fig. 3 An NCCT was performed 21 months after successful stent-assisted coil occlusion while the patient was being evaluated for a heart transplant. The images showed a hyperdense mass, medial and caudal adjacent to the coil

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bundle, which was interpreted as a parenchymal hematoma (a, b). Subsequent DSA revealed a significant aneurysm growth (diameters now reaching about 10
10 mm with the coil bundle loosening and becoming dislodged (c, d, e)

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Fig. 4 (continued)

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Clinical Outcome The patient developed an infection of the peripheral driveline of the LVAD system adjacent to the transverse colon. Antibiotic treatment was continued successfully and complemented by VAC therapy. The patient was transferred to a dedicated cardiovascular rehabilitation center with no focal neurological deficit.

Discussion The occurrence of an infective intracranial aneurysm (IA) as a result of focal bacterial cerebral vasculitis secondary to septic emboli from bacterial endocarditis (BE) was first reported by Church (1869) in a 13-year-old boy. A few years later, Osler (1885) coined the slightly misleading term “mycotic aneurysm” for this specific entity, as its microscopic appearance was reminiscent of “fresh fungal vegetations.” In patients with BE, the development of an IA is a not uncommon scenario and occurs in 10–30% of all cases (Peters et al. 2006). Nowadays, an IA may also emerge as an epiphenomenon in the increasingly common use of invasive bridging technologies such as an LVAD in advanced cardiac failure. This is because these devices often predispose to chronic infection, even sepsis as a bacterial biofilm forms along their intra-corporal parts (Koval and Rakita 2013). The formation of intracranial aneurysms has furthermore been observed in virally caused immunodeficiency (Mahadevan et al. 2008). In this case, both the primary formation of the aneurysm and its atypical relapse may be interpreted as a consequence of a focal cerebral vasculitis secondary to LVAD-associated septicemia. Both the

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distal location and the distinct, unusual morphology of the ruptured primary aneurysm in a patient with a known, LVAD-related infection suggest a causal relationship between bacterial focus and aneurysm formation. So far, only sporadic reports of IA formation associated with LVAD therapy exist (Hill et al. 2014; Remirez et al. 2017). To the best of our knowledge, no case of IA recurrence after initial successful therapy has so far been reported. However, the morphologically atypical, early relapse of the initially occluded aneurysm during septicemic episodes of LVAD treatment strongly indicates infectious colonization of the vessel wall as an adjunctive factor. Certainly, a locally persisting infection as a consequence of insufficient antimicrobial therapy – or less likely a procedure-related dissection – may have been responsible for the relapse. In any case, the illustrated course demonstrates the importance of a successful combination of anti-microbial chemotherapy and sufficient endovascular treatment (Kannoth and Thomas 2009) as well as the necessity for stringent follow-up imaging of patients with IAs. Moreover, this case exemplifies the plasticity of cerebral perfusion in the long term. At the time of the initial treatment, sacrificing the parent artery would have caused a significant infarct in the left MCA territory. After stent-assisted coiling, supply to the brain parenchyma reorganized. During this process, the large recurrent aneurysm may have behaved as an elastic reservoir, causing a Windkessel effect in which pooling of the blood in the lumen of the aneurysm with reduced perfusion into the efferent artery could have triggered the recruitment of leptomeningeal collaterals to supply the dependent parenchyma, eventually allowing

ä Fig. 4 PVO as a treatment of a recurrent left MCA/M3 “mycotic” aneurysm. A proximal microcatheter injection of the parent branch shows both jet-like inflow into the aneurysmal sac originating from the proximal third of the stented segment and opacification of distal parenchyma (a). The injection further distal and close to the source of aneurysmal inflow reveals predominant opacification of

the aneurysm with no contrast filling relevant downstream cortical MCA territory (b). Dense coil occlusion of the proximal third of the stented segment, which was responsible for continued aneurysmal inflow (c), was performed. The final ICA injection shows good opacification of the ICA territory with no signs of ischemia arising from the performed branch occlusion (d, e)

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the coil occlusion of the said parent artery without clinically relevant ischemia or infarct.

Therapeutic Alternatives Induced Asystole For Embolization Microsurgical Clipping nBCA Embolization Onyx Embolization Parent Vessel Occlusion

References Church WS. Aneurysm of right cerebral artery in a boy of thirteen. Trans Pathol Soc Lond. 1869;20:109. Hill JA, Mokadam NA, Rakita RM. Intracranial mycotic aneurysm associated with left ventricular assist device infection. Ann Thorac Surg. 2014;98:1088–9. https:// doi.org/10.1016/j.athoracsur.2013.10.094.

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Kannoth S, Thomas SV. Intracranial microbial aneurysm (infectious aneurysm): current options for diagnosis and management. Neurocrit Care. 2009;11:120–9. https://doi.org/10.1007/s12028-009-9208-x. Koval CE, Rakita R. Ventricular assist device related infections and solid organ transplantation. Am J Transplant. 2013;13:348–54. https://doi.org/ 10.1111/ajt.12126. Mahadevan A, Tagore R, Siddappa NB. Giant serpentine aneurysm of vertebrobasilar artery mimicking dolichoectasia-an unusual complication of pediatric AIDS. Report of a case with review of the literature. Clin Neuropathol. 2008;27:37–52. Osler W. The Gulstonian lectures. On malignant endocarditis. Lancet. 1885;1:415–8. Peters PJ, Harrison T, Lennox JL. A dangerous dilemma: management of infectious intracranial aneurysms complicating endocarditis. Lancet Infect Dis. 2006;11:742–8. https://doi.org/10.1016/S1473-3099 (06)70631-4. Remirez JM, Sabet Y, Baca M, Maud A, Cruz-Flores S, Rodriguez GJ, Mukherjee D, Abbas A. Mycotic intracranial aneurysm secondary to left ventricular assist device infection. J Vasc Interv Neurol. 2017;3:23–5.

Middle Cerebral Artery (M2) Aneurysm: Endovascular Treatment of a Ruptured Left MCA (M2) Aneurysm in an Elderly Patient with Good Clinical Outcome

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Muhammad AlMatter and Hans Henkes

Abstract

An 80-year-old female patient presented with a spontaneous Hunt and Hess II, Fisher 4 aneurysmal subarachnoid hemorrhage (SAH) associated with a parenchymal hematoma secondary to the rupture of a small left middle cerebral artery (MCA) M2 segment aneurysm. This was treated with endovascular coilocclusion and the patient made a good recovery. The affected superior trunk of the left MCA was found to be almost occluded on follow-up DSA without clinical sequelae. The management of ruptured intracranial aneurysms in elderly patients is the main topic of this chapter. Keywords

Middle cerebral artery · Subarachnoid hemorrhage · Intracranial aneurysm · Advanced age · Coil occlusion

Patient An 80-year-old female patient presented to the local emergency department with a sudden onset of severe headache associated with profound

fatigue and loss of appetite. Her husband reported several intermittent episodes of speech difficulties. The past medical history included hypertension, type II diabetes mellitus, and obesity. The neurological examination confirmed sensorimotor aphasia.

Diagnostic Imaging With the working diagnosis of an acute stroke, the patient underwent an emergent cranial magnetic resonance imaging (MRI) examination. This showed a left hand-sided parenchymal hematoma in the inferior frontal gyrus, measuring about 3 cm in diameter, an associated sulcal subarachnoid hemorrhage (SAH), and a thin film of subdural hematoma (SDH) along the convexity and infratentorial region with mild compression of the left lateral ventricle. The MR angiography revealed a small aneurysm close to the left middle cerebral artery (MCA) bifurcation, which was considered to be the most likely cause of the hemorrhage. The patient was transferred to our service, where diagnostic catheter angiography was performed and confirmed a 3.5 mm aneurysm located at the origin of the superior trunk (M2) of the left MCA (Fig. 1).

M. AlMatter (*) · H. Henkes Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_101

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Middle Cerebral Artery (M2) Aneurysm: Endovascular Treatment of a Ruptured Left MCA (M2). . .

Fig. 1 Diagnostic imaging in an elderly woman with suspected ischemic stroke. Cranial MRI (FLAIR) demonstrating diffuse sulcal SAH over the left hemisphere (a) with parenchymal hematoma (b) in the left frontal lobe and a thin SDH extending into the posterior fossa (c, d). TOF

Treatment Strategy Due to the good clinical condition of the patient, treatment of the ruptured aneurysm was considered appropriate despite her advanced age. As the hematoma was located in an eloquent area and didn’t cause significant compression, we refrained from craniotomy and hematoma evacuation. Since the configuration of the aneurysm was favorable for endovascular coil occlusion, this was considered to be the best treatment strategy.

Treatment Procedure, 28.10.2013: endovascular treatment of a ruptured left MCA (M2) aneurysm with endovascular coil-occlusion Anesthesia: general anesthesia; medications: 500 mg sodium thiopental (Trapanal, Nycomed) IV Premedication: none Access: right common femoral artery, 1
6F sheath (Terumo); guide catheter: 1
6F Heartrail II (Terumo); microcatheter: 1
Echelon-10 (Medtronic); microguidewire: 1
Synchro2 0.01400 200 cm (Stryker)

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MRA (e) and 2D DSA (f) and volume-rendered rotational angiography (g and h), demonstrating a 3 mm aneurysm with an irregular contour (arrows), arising from the proximal segment of the left superior MCA trunk (M2)

Coils: 1
Morpheus 3D 3/8 (Medtronic), 2
MicroPlex-10 2/6 (MicroVention) Course of treatment: the guiding catheter was placed in the midcervical segment of the left internal carotid artery (ICA). Based on the 3D DSA, a suitable working projection showing the aneurysm in profile was chosen. Atraumatic navigation of an Echelon-10 microcatheter into the fundus of the MCA(M2) aneurysm followed, using the road map function. A 3/8 3D Morpheus coil was then inserted to form a cage inside the aneurysm sac, which was then followed by dense filling of the aneurysm sac using two helical coils each measuring 2 mm/6 cm. The aneurysm sac was eventually sufficiently occluded with a significant neck remnant (Fig. 2). Duration: 1st – 21st DSA run: 102 min; fluoroscopy time: 58 min Complications: none Postmedication: none

Clinical Outcome The patient tolerated the procedure very well and was extubated immediately afterwards. The remainder of the hospital course was unremarkable except for a minor urinary tract

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Fig. 2 Endovascular treatment of a ruptured left MCA (M2) aneurysm. The working projection shows an ectasia of the superior MCA trunk at the origin of the aneurysm (a). A steam-shaped Echelon-10 microcatheter was navigated inside the aneurysm sac (b) followed by forming a

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cage with a 3D coil (c). The aneurysm was then obliterated with two helical coils (d). The final DSA run confirmed the complete occlusion of the aneurysm sac, a significant neck remnant, and the patency of the superior MCA trunk (e)

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infection. There was no evidence of cerebral vasospasm on the daily transcranial Doppler ultrasound examinations. The clinical condition of the patient remained unchanged with sensorimotor aphasia but no paresis. She was discharged to a rehabilitation facility 12 days after the initial presentation, where she experienced a moderate recovery from the aphasia (mRS 2).

Follow-Up Examinations An MRI performed 8 months after the treatment showed a complete resorption of the frontal hematoma with marked gliosis in the inferior frontal gyrus causing ex vacuo dilatation of the left lateral ventricle. The MRA was remarkable for loss of vessel signal in the vicinity of the hematoma. A follow-up DSA was performed, which showed a marked atrophy of the superior trunk of the left MCA with some leptomeningeal collaterals to its vascular territory (Fig. 3). The patient reported no history of acute deterioration of her residual, incomplete aphasia. Thus, the vessel occlusion was considered asymptomatic and maybe related to a reduced demand of the dependent supply territory or a result of a dissection underlying the previous aneurysm formation.

Discussion Treatment of intracranial aneurysms in elderly patients is a controversial topic. On the one hand, advanced age is associated with many physiological and anatomical changes that render the management in this population challenging. The global increase in the life expectancy, on the other hand, means that the treating physicians will be increasingly dealing with elderly patients diagnosed with ruptured and unruptured cerebral aneurysms, which means that devising an optimal treatment strategy for these patients is a pressing concern. The superiority of endovascular treatment over conservative management in patients with acute ischemic stroke due to a large vessel occlusion has been demonstrated in multiple randomized controlled trials. The meta-analysis of

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these trials showed a similar favorable treatment effect in patients aged 80 years or older (HERMES Collaborators 2016). It is, however, unlikely that a similar RCT will be performed to compare the treatment effect in elderly patients with aneurysmal SAH. Treatment strategies in these patients will therefore depend on personal and institutional experience, the results of limited series and individual patient preference. Due to its minimally invasive nature, endovascular management is a favorable option in the elderly patient compared with neurosurgery (Jang et al. 2011; Stovell and Jenkinson 2014). Advanced age is, however, associated with increased tortuosity and atherosclerosis of the cranio-cervical vessels, which may increase the difficulty of the endovascular treatment and the risk of embolic complications, respectively (Gonzalez et al. 2010; Khosla et al. 2012). Elderly patients also usually suffer from multiple comorbidities that increase the risk of general anesthesia and prolong the subsequent recovery (Papaioannou et al. 2005). Elderly patients are more likely to succumb to severe and lifethreatening complications on the ICU during the acute phase after aSAH (Van Den Noortgate et al. 1999). Multiple retrospective series reported that the treatment of high grade aneurysmal SAH in the elderly might be futile, since the majority of the treated patients eventually succumbed to the sequelae of the severe primary hemorrhage despite the successful treatment of the ruptured aneurysms (Park et al. 2014). In the series described by Cai et al. (2005), 13 out of 63 consecutive patients age 70 and older were treated by endovascular coiling for intracranial aneurysms after a SAH grade Hunt and Hess >III. In this series, 10 out of 13 patients (77%) with SAH Hunt and Hess > III died or had a poor outcome. In our case series of ruptured intracranial aneurysms, we treated a total of 40 patients aged 75 years or older using endovascular techniques over a 10-year period. Over 67% of the treated elderly patients had a poor outcome and those with severe SAH (Hunt and Hess > III) had the worst outcomes, with a modified Rankin scale >3 (AlMatter et al. 2018). Endovascular treatment of unruptured intracranial aneurysms, or in patients

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Fig. 3 Follow-up examinations 8 months after a spontaneous SAH and the subsequent coil occlusion of a left MCA (M2) superior trunk aneurysm. T2WI MRI (a) at the level of the frontal horns of the lateral ventricles shows marked volume loss at the level of the absorbed intraparenchymal hematoma with compensatory dilatation of the adjacent ventricle. There is a paucity of vessel signal in the corresponding TOF MRA (b) and DSA (d). DSA

performed at the same time showing a significant reduction in caliber of the superior trunk of the left MCA (c). This might have been due to a reduced demand, following the gliosis of the dependent vascular supply territory after resoption of the previous hematoma. Another explanation would be an initial dissection of the parent artery, which was possibly the reason for the aneurysm formation

with less severe SAH, seems to be associated with a favorable clinical outcome in older patients, suggesting that age is not a major limiting factor for the procedure (Stiefel et al. 2010; Hwang et al. 2011; Oishi et al. 2015). Considering both the

poor prognosis of ruptured intracranial aneurysms in the elderly population and the seemingly acceptable safety profile of endovascular aneurysm treatment in this population, it seems plausible to afford preventive endovascular treatment

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of unruptured aneurysms to these patients, after weighing up the likely risks and benefits with the individual patient in light of their current medical and physical condition.

Therapeutic Alternatives Conservative Management Flow Diversion Microsurgical Clipping

References 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;167:106–11. https://doi.org/10.1016/ j.clineuro.2018.02.022. Cai Y, Spelle L, Wang H, Piotin M, Mounayer C, Vanzin JR, Moret J. Endovascular treatment of intracranial aneurysms in the elderly: single-center experience in 63 consecutive patients. Neurosurgery. 2005;57(6):1096–102. https://doi.org/10.1227/01. NEU.0000185583.25420.DF. Gonzalez NR, Dusick JR, Duckwiler G, Tateshima S, Jahan R, Martin NA, Viñuela F. Endovascular coiling of intracranial aneurysms in elderly patients: report of 205 treated aneurysms. Neurosurgery. 2010;66(4):714–20. https://doi.org/10.1227/01.NEU.0 000367451.59090.D7. HERMES Collaborators. Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials. Lancet. 2016;387(10029):1723–31. https://doi.org/ 10.1016/S0140-6736(16)00163-X. Hwang SK, Hwang G, Oh CW, Jin SC, Park H, Bang JS, Kwon OK. Endovascular treatment for unruptured

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intracranial aneurysms in elderly patients: single-center report. AJNR Am J Neuroradiol. 2011;32(6):1087–90. https://doi.org/10.3174/ajnr.A2458. Jang EW, Jung JY, Hong CK, Joo JY. Benefits of surgical treatment for unruptured intracranial aneurysms in elderly patients. J Korean Neurosurg Soc. 2011;49(1):20–5. https://doi.org/10.3340/jkns.2011.49 .1.20. Khosla A, Brinjikji W, Cloft H, Lanzino G, Kallmes DF. Age-related complications following endovascular treatment of unruptured intracranial aneurysms. AJNR Am J Neuroradiol. 2012;33(5):953–7. https://doi.org/ 10.3174/ajnr.A2881. Oishi H, Yamamoto M, Nonaka S, Shimizu T, Yoshida K, Mitsuhashi T, Arai H. Treatment results of endosaccular coil embolization of asymptomatic unruptured intracranial aneurysms in elderly patients. J Neurointerv Surg. 2015;7(9):660–5. https://doi.org/ 10.1136/neurintsurg-2014-011305. Papaioannou A, Fraidakis O, Michaloudis D, Balalis C, Askitopoulou H. The impact of the type of anaesthesia on cognitive status and delirium during the first postoperative days in elderly patients. Eur J Anaesthesiol. 2005;22(7):492–9. https://doi.org/ 10.1017/S0265021505000840. Park JH, Kim YI, Lim YC. Clinical outcomes of treatment for intracranial aneurysm in elderly patients. J Cerebrovasc Endovasc Neurosurg. 2014;16(3):193–9. https://doi.org/10.7461/jcen.2014. 16.3.193. Stiefel MF, Park MS, McDougall CG, Albuquerque FC. Endovascular treatment of unruptured intracranial aneurysms in the elderly: analysis of procedure related complications. J Neurointerv Surg. 2010;2(1):11–5. https://doi.org/10.1136/jnis.2009.001685. Stovell MG, Jenkinson MD. Neurosurgery in octogenarians. Br J Neurosurg. 2014;28(5):611–5. https://doi. org/10.3109/02688697.2014.889809. Van Den Noortgate N, Vogelaers D, Afschrift M, Colardyn F. Intensive care for very elderly patients: outcome and risk factors for in-hospital mortality. Age Ageing. 1999;28(3):253–6. https://doi.org/10.1093/ ageing/28.3.253.

Middle Cerebral Artery (M3) Aneurysm: Treatment of a Mycotic Aneurysm of the Distal Middle Cerebral Artery with Coil Occlusion of Both the Aneurysm and the Parent Vessel

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Dominik F. Vollherbst and Markus A. Möhlenbruch

Abstract

A 44-year-old male patient presented with a mycotic aneurysm located in the M3-segment of the left middle cerebral artery (MCA). The aneurysm was detected by a follow-up cranial MRI examination, which was being performed for pre-existing septic-embolic encephalitis caused by infective endocarditis. Endovascular coil occlusion treatment was carried out for the aneurysm and the parent vessel. The patient did not develop any infarction around the occluded artery during follow-up. Cerebral angiography 3 months after the treatment showed that the aneurysm and the parent vessel had been completely and stably occluded. The treatment of mycotic intracranial aneurysms is the main topic of this chapter. Keywords

Middle cerebral artery · Mycotic intracranial aneurysm · Infectious intracranial aneurysm · Endocarditis · Parent vessel occlusion

Patient A 44-year-old male patient was referred to the neurovascular department with a mycotic intracranial aneurysm (MIA) located in the M3-segment of the left middle cerebral artery (MCA). The patient was suffering from infectious endocarditis, caused by Staphylococcus aureus, with septic-embolic encephalitis and multiple known cerebral septic lesions and infarctions. He was on an antibiotic regime of flucloxacillin and rifampicin. The patient was suffering from motor and coordination issues; however, no cognitive disabilities were present.

Diagnostic Imaging Diagnostic, pre-interventional magnetic resonance imaging (MRI) showed a partially thrombosed aneurysm in the M3 segment of the left MCA with a size of 25  21  19 mm. The aneurysm involved more than half of the circumference of the parent vessel over a distance of 16 mm (Fig. 1).

Treatment Strategy D. F. Vollherbst · M. A. Möhlenbruch (*) Department of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany e-mail: [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_155

The decision to treat the patient was taken because of how the aneurysm had increased in size. Because of the extensive cerebral inflammatory changes and the patient’s general condition, the patient was recommended endovascular 1019

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Fig. 1 MRI showing a MIA of the left MCA (contrastenhanced T1-weighted sequence). The partially thrombosed aneurysm distinctly increased in size between the examination 3 months before treatment (a) and the immediate pre-interventional MRI (b), while other

inflammatory changes, such as abscess formation (double arrow), decreased in size under antibiotics. The aneurysm showed a perfused part (arrow) and peripheral thrombus (arrowhead) and broad-based contact to the MCA

treatment. Due to the broad-based contact of the aneurysm to the MCA, which involved most of the vessel’s circumference and meant there was no circumscribed aneurysmal neck, coiling both the aneurysm and the parent vessel was considered to be the best treatment strategy for this aneurysm.

VFC 3–6/15, 1 MicroPlex18 16/39, 1 MicroPlex10 Hypersoft 2/4, 1 MicroPlex 3D Hypersoft 1.5/4, 1 Hydrosoft 1/3, 1 VFC 10–15/40, 4 VFC 6–10/30, 1 VFC 10–15  30, 1 MicroPlex 10 2/4, 1 MicroPlex Complex 8/20, 1 MicroPlex Complex 9/24, 1 MicroPlex Complex 7/18, 1 MicroPlex Compass Complex 6/18, 2 MicroPlex Compass Complex 5/16, 1 MicroPlex Compass Complex 5/10 (MicroVention) Course of treatment: the guiding catheter was placed in the left internal carotid artery. Suitable working projections were chosen based on the 3D DSA. Subsequently, the first microcatheter was navigated into the aneurysm and the second microcatheter into the parent artery. First, a framing coil was placed within the aneurysm using the first microcatheter, followed by coil occlusion of the parent artery. This was performed in order to minimize the degree of bleeding in the event of an aneurysmal rupture. Afterward, the MIA was occluded with coils. Before, during, and after coiling, control DSA runs were performed and showed complete perfusion of the brain distal to the occluded M3 branch. DSA after coil occlusion

Treatment Procedure, 02.08.2019: endovascular treatment for an MIA located in the M3 segment of the left MCA encompassing coil occlusion of both the aneurysm and the parent vessel Anesthesia: general anesthesia; anticoagulation was initiated with a bolus of unfractionated heparin (80 IU/kg), followed by intravenous administration to maintain an activated clotting time of 250 s Premedication: none Access: right common femoral artery, 1 7F sheath (Terumo); guide catheter: 1 7F Envoy (Codman); microcatheter: 2 Headway Duo (MicroVention); microguidewire: 1 Traxcess 14, Implants: 22 coils: 1 VFC 3–6/10, 3

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Middle Cerebral Artery (M3) Aneurysm: Treatment of a Mycotic Aneurysm of the Distal. . .

showed complete obliteration of both the parent vessel and the aneurysm (Fig. 2). Duration: 1st–6th DSA run: 71 min; fluoroscopy time: 33 min Complications: none Postmedication: none

Fig. 2 (continued)

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Follow-Up Examinations MRI and DSA were performed 3 months after the treatment, showing complete and stable occlusion of the aneurysm with no ischemic damage to the dependent brain parenchyma (Fig. 3).

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Fig. 2 Endovascular treatment of an MIA of the left MCA. After DSA in the working projection (a, b) and 3D DSA (c), two microcatheters were placed within the aneurysm and the parent artery, respectively. Subsequently, a framing coil was placed within the aneurysm, followed

by coil occlusion of the parent artery (black arrow (d)) and coiling of the aneurysm (e, f). The final DSA run showed complete occlusion of the aneurysm, while the brain was still perfused distal to the occluded M3 branch (g, h)

Clinical Outcome

hospital course was unremarkable apart from his pre-existing illness. Six days after the procedure, the patient was discharged to a rehabilitation clinic, still with motor and coordination issues, although these had

The patient tolerated the procedure with no adverse events. He was extubated immediately after the procedure. The remainder of the

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Middle Cerebral Artery (M3) Aneurysm: Treatment of a Mycotic Aneurysm of the Distal. . .

Fig. 3 Follow-up imaging after the endovascular coil occlusion of a MIA together with the parent artery. On contrast-enhanced T1WI (a) 3 months after the treatment, susceptibility artifacts, caused by the occluded parent artery (arrowhead) and the coil-occluded aneurysm (arrow), were

stabilized. Under an antibiotic regime of flucloxacillin and rifampicin, administered over a 4-week period following his surgery, the patient’s clinical condition had improved significantly during the 3-month follow-up period.

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visible, with no signs of aneurysmal reperfusion. T2WI (b) did not show any infarction in the supply area of the occluded M3 branch. Furthermore, DSA at 3 months (posterior-anterior projection (c), lateral projection (d)) confirmed stable occlusion of the aneurysm and its parent artery

Discussion “Mycotic” aneurysms (also known as “infectious aneurysms”) were first described by Osler in the nineteenth century and nowadays refer not only to

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aneurysms resulting from fungal infections but to aneurysms caused by any infectious etiology (Osler 1885). They can occur in any artery throughout the body and account for 1–5% of all intracranial aneurysms (Ducruet et al. 2010; Gross and Puri 2013). These aneurysms can be caused by a myriad of pathogens; most commonly they are identified after or concomitantly with systemic bacterial infections. In more than 80% of cases, the primary source of infection is bacterial endocarditis (Peters et al. 2006). Up to 30% of patients with bacterial endocarditis develop neurological manifestations, such as septic embolic stroke or abscess formation, while MIAs are observed in only 2–4% of these patients (Peters et al. 2006). Aneurysms form following the inflammatory degradation of the arterial wall secondary to microbial infiltration of the tunica media and adventitia of the vessel wall (Kannoth and Thomas 2009). MIAs are typically thin-walled, friable, and often broad-based with no circumscribed aneurysmal neck, leading to a high risk of progression, hemorrhage, and recurrence after treatment (Gross and Puri 2013). They are most frequently located in the distal vasculature of the middle cerebral artery, followed by the posterior cerebral artery and the anterior cerebral artery (Ducruet et al. 2010; Ringer 2018). Bacterial infection or another causative infection is found in less than 50% of MIAs (RangelCastilla et al. 2018). In these cases, 4 weeks of intravenous antibiotic/antifungal therapy is recommended. There are no clear criteria for the interventional treatment of MIAs. However, the high mortality rates of both unruptured and ruptured MIAs suggest that the aneurysm should be treated if risk factors such as large aneurysm size or previous hemorrhage are present and if treatment can be performed without a substantial risk of further neurological impairment (RangelCastilla et al. 2018; Ringer 2018). For small MIAs where risk factors are not present, conservative therapy and close observation can be a reasonable strategy since antibiotic treatment can cause small MIAs of up to 10 mm to completely regress (Peters et al. 2006).

D. F. Vollherbst and M. A. Möhlenbruch

Most MIAs can be treated via endovascular means (Zanaty et al. 2013). Due to an MIA’s friable walls, clipping the aneurysm in open surgery is often not feasible (Gross and Puri 2013). In particular situations, for example, in cases of symptomatic intracranial hemorrhage, craniotomy and clot evacuation with microsurgical treatment of the aneurysm by either clip reconstruction or proximal occlusion can be helpful options (Ringer 2018). Multiple endovascular technical approaches have been described for the treatment of MIAs, including coiling with and without stent or balloon assistance, liquid embolization using n-butyl-2-cyanoacrylate (NBCA) or ethylene vinyl alcohol (EVOH) copolymers, and detachable balloon inflation (Dhomne et al. 2008; Ding et al. 2014; Esenkaya et al. 2016; Gross and Puri 2013; Rangel-Castilla et al. 2018). A distal location, vessel tortuosity, and a small parent vessel caliber all make treating these aneurysms difficult (Rangel-Castilla et al. 2018). Implanting a stent or inflating a balloon is often not possible because of the small caliber and the friable wall of the parent vessel. A combined occlusion of the aneurysm and the parent artery, as in the case above, can be a treatment option for distally located aneurysms if the occluded vessel does not supply an eloquent brain area. Data on the treatment success of the different treatment options for MIAs is rare. A review published by Ducruet et al. (2010) reported a pooled technical success rate of 96% for the endovascular management of MIAs. With regard to the high risk of progression and recurrence, close follow-up is recommended both when following conservative management and after interventional treatment.

Therapeutic Alternatives Conservative Management Flow Diversion Microsurgical Clipping nBCA Occlusion

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Middle Cerebral Artery (M3) Aneurysm: Treatment of a Mycotic Aneurysm of the Distal. . .

References Dhomne S, Rao C, Shrivastava M, Sidhartha W, Limaye U. Endovascular management of ruptured cerebral mycotic aneurysms. Br J Neurosurg. 2008;22(1):46–52. https://doi.org/10.1080/02688690701593561. Ding D, Raper DM, Carswell AJ, Liu KC. Endovascular stenting for treatment of mycotic intracranial aneurysms. J Clin Neurosci. 2014;21(7):1163–8. https:// doi.org/10.1016/j.jocn.2013.11.013. Ducruet AF, Hickman ZL, Zacharia BE, Narula R, Grobelny BT, Gorski J, Connolly ES Jr. Intracranial infectious aneurysms: a comprehensive review. Neurosurg Rev. 2010;33(1):37–46. https://doi.org/ 10.1007/s10143-009-0233-1. Esenkaya A, Duzgun F, Cinar C, Bozkaya H, Eraslan C, Ozgiray E, Oran I. Endovascular treatment of intracranial infectious aneurysms. Neuroradiology. 2016;58(3): 277–84. https://doi.org/10.1007/s00234-015-1633-2. Gross BA, Puri AS. Endovascular treatment of infectious intracranial aneurysms. Neurosurg Rev. 2013;36 (1):11–9; discussion 19. https://doi.org/10.1007/ s10143-012-0414-1.

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Kannoth S, Thomas SV. Intracranial microbial aneurysm (infectious aneurysm): current options for diagnosis and management. Neurocrit Care. 2009;11(1):120–9. https://doi.org/10.1007/s12028-009-9208-x. Osler W. The Gulstonian lectures, on malignant endocarditis. Br Med J. 1885;1(1264):577–9. https://doi.org/ 10.1136/bmj.1.1264.577. Peters PJ, Harrison T, Lennox JL. A dangerous dilemma: management of infectious intracranial aneurysms complicating endocarditis. Lancet Infect Dis. 2006;6 (11):742–8. https://doi.org/10.1016/S1473-3099(06) 70631-4. Rangel-Castilla L, Nakaji P, Siddiqui A, Spetzler R, Levy E, editors. Decision making in neurovascular disease. New York: Thieme Publishers; 2018. Ringer A, editor. Intracranial aneurysms. 1st ed. Amsterdam: Elsevier; 2018. Zanaty M, Chalouhi N, Starke RM, Tjoumakaris S, Gonzalez LF, Hasan D, Rosenwasser R, Jabbour P. Endovascular treatment of cerebral mycotic aneurysm: a review of the literature and single center experience. Biomed Res Int. 2013;2013:151643. https://doi. org/10.1155/2013/151643.

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Middle Cerebral Artery (M3) Aneurysm: Two “Mycotic” Aneurysms of the Middle Cerebral Artery Due to Bacterial Endocarditis; Endovascular Treatment of One Aneurysm with Glue (nBCA) Injection During Adenosine-Induced Asystole; Spontaneous Resolution of the Second Aneurysm

Alexander Sirakov, Hosni Abu Elhasan, Marta Aguilar Pérez, Carmen Serna Candel, Hansjörg Bäzner, and Hans Henkes Abstract

A 58-year-old male patient presented with phonemic paraphasia, pyrexia of 39.5
C, chronic fatigue, and exhaustion. The patient reported experiencing mild but persistent left flank

A. Sirakov Neuroradiology, University Hospital St. Ivan Rilski, Sofia, Bulgaria Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] H. A. Elhasan Department of Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel e-mail: [email protected] M. Aguilar Pérez · H. Henkes (*) Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; [email protected] C. Serna Candel Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] H. Bäzner Neurologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_165

pain, weight loss of 14 kg, and excessive sweating during sleep for the past 6 months. Echocardiography revealed mobile vegetation on the mitral valve, and his blood culture was positive for Enterococcus faecalis. He was diagnosed as having infective endocarditis (IE), and intravenous antibiotic medication was started. He was also given oral anticoagulation agents due to an elevated serum D-dimer level. Initial abdominal and cranial MRI examinations revealed the presence of a previous splenic infarct and a left frontoparietal hemorrhagic infarction accompanied by time-of-flight (TOF) magnetic resonance angiography (MRA) signal abnormality among the changes. The cerebral infarction was suspected of being associated with a “mycotic” (inflammatory) aneurysm of the left middle cerebral artery (MCA) secondary to the IE. A digital subtraction angiography (DSA) examination was performed and confirmed the presence of two left-hand distally located MCA infectious intracranial aneurysms (IIA). The larger of the two aneurysms was successfully occluded by selective intrasaccular injection of nBCA/Lipiodol under adenosine-induced asystole to prevent hazardous migration of the embolic material during the embolization. The smaller and distally 1027

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located aneurysm (2 mm fundus diameter) resolved spontaneously. The aneurysm treatment was well tolerated. Under continuous IV antibiotic infusion and with the complete resolution of the somatic symptoms, echocardiography revealed no mitral valve vegetation, suggesting the IE was under control. Long-term follow-up confirmed persistent aneurysm occlusion and the permanent clinical improvement of the patient. The management of IIA by parent vessel occlusion using glue injection under adenosineinduced asystole is the main topic of this chapter. Keywords

Middle cerebral artery · Mycotic aneurysm · Infectious intracranial aneurysm · Parent vessel occlusion · Adenosine · Induced asystole · nBCA · Lipiodol

Patient A 58-year-old male patient was admitted to hospital due to pyrexia of 39.5
C, chronic fatigue, and exhaustion. The neurological examination revealed phonemic paraphasia without any other chronic progressive or acute neurological deficits. The patient reported experiencing mild but persistent left flank pain, weight loss of 14 kg, and excessive sweating during sleep for the last 6 months. Echocardiography revealed mobile vegetation on the mitral valve, and a blood culture sample was positive for Enterococcus faecalis. He was diagnosed as having infective endocarditis (IE), and intravenous antibiotic medication was started. He was also given a course of oral anticoagulation agents due to elevated serum D-dimer level. The patient’s clinical history had included a transurethral resection of the prostate gland.

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of cortical and white matter hyperintensities on the T2WI and DWI, which also showed nodular and peripheral rim enhancement. All of the changes were restricted to the territory of the left MCA. The hyperintensities shown contained foci of susceptibility artifact on the gradient echo T2 sequence. Distal septic emboli due to clinically confirmed infective endocarditis were the most probable cause of the changes. A subsequent DSA run confirmed the presence of two lefthand distal and irregular MCA “mycotic” (i.e., infectious) intracranial aneurysms (IIA) (Fig. 1).

Treatment Strategy With IV administration of antibiotic drugs for over 2 weeks, the patient’s clinical condition remained stable. Due to the distal location and the relatively small diameter of the parent artery, the patient was ineligible for a conventional endovascular stent procedure as it carried a high risk of intraprocedural complications. Since “mycotic” aneurysms are notorious for being fragile, the usage of a liquid embolic agent was preferred over standard coil occlusion. The anticipated impact on the aneurysm wall was thought to be less traumatic with glue than with coils. Superselective endovascular application of nBCA/Lipiodol during adenosine-induced asystole was the technique we decided on to achieve our goals. The aim was to occlude the aneurysm sac without passing the glue into the distal vasculature. Preserving the cortical branch of the MCA distal to the aneurysm would potentially allow the following recruitment of leptomeningeal collaterals, thus preventing focal parenchymal ischemic damage. On the other hand, microsurgical clipping was considered possible, but the chances of occluding the inflammatory aneurysm and preserving the patency of the parent vessel were expected to be poor.

Diagnostic Imaging Treatment Initial brain magnetic resonance imaging (MRI) examination at admission and following MRI scans carried out 8 and 16 days after the onset of the neurological deficit carefully documented the status of the patient. MRI (1.5T) revealed a couple

Procedure, 05.12.2014: endovascular treatment of an inflammatory left MCA/M3 aneurysm via selective injection of nBCA/Lipiodol under adenosine-induced asystole

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Middle Cerebral Artery (M3) Aneurysm: Two “Mycotic” Aneurysms of the Middle. . .

Fig. 1 (continued)

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Fig. 1 (continued)

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Middle Cerebral Artery (M3) Aneurysm: Two “Mycotic” Aneurysms of the Middle. . .

Fig. 1 (continued)

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Fig. 1 Diagnostic imaging in a patient with infective endocarditis (IE). Cranial MRI performed right after the onset of the neurological deficit revealed left-hand cortical and white matter hyperintensities on the T2WI (a) and DWI (b, c). The hyperintensities shown contained foci of susceptibility artifact on the gradient echo T2 sequence (d). Nodular T1WI contrast enhancement (arrows (e, f)) was seen over the changes that were restricted to the territory of the left MCA. Time-of-flight (TOF, (g)) MRA signal abnormality at the distal branches of the left middle cerebral artery suggesting the underlying presence of an inflammatory aneurysm

secondary to the IE. Following MRI examinations carried out 8 days (h, i, j, k) and 16 days (l, m, n) after the admission confirmed a slight reduction in the size of the FLAIR and T2WI changes with almost absent DWI hyperintensities. However, gradually increasing nodular and intense peripheral rim enhancement was noted on the following contrast-enhanced T1WI (o, p) series. Initial DSA (posterior-anterior view (q), lateral view (r, s)) confirmed the presence of two left-hand distal and irregular middle cerebral artery “mycotic” aneurysms. The larger and more proximal aneurysm measured approximately 5 mm in diameter (t, u)

Anesthesia: general anesthesia; bolus injection of 1 36 mg adenosine (Adrekar, Sanofi-Aventis) IV via a 4F Tempo4 vertebral (Cordis) catheter, which was introduced via femoral venous access with the tip positioned in front of the right atrium Premedication: none Access: right common femoral artery, 1 6F sheath (Terumo), right femoral vein, 1 4F sheath (Cordis); guide catheter: 1 6F Heartrail II (Terumo); catheter for adenosine injection: Tempo4 vertebral (Cordis); microcatheter: 2

Marathon (Medtronic); microguidewire: 1 Mirage 0.00800 (Medtronic) Liquid embolic agent: nBCA (Glubran2, GEM), ethiodized oil (Lipiodol ultrafluid, Guerbet), mixed in a relation of 1:1 Course of treatment: via femoral venous access, a 4F diagnostic catheter was carefully navigated and placed into the right atrium. A 6F guide catheter was introduced into the left internal carotid artery. DSA revealed that the smaller and more distally located aneurysm had

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Middle Cerebral Artery (M3) Aneurysm: Two “Mycotic” Aneurysms of the Middle. . .

spontaneously thrombosed. However, the 5 mm fusiform aneurysm on the precentral M2/M3 MCA branch was unchanged. The parent artery and the aneurysmal sac itself were catheterized with a Marathon catheter. The bolus injection of 36 mg adenosine via the venous 4F catheter induced over 20 s of asystole. During the initial 5 s of the cardiac arrest, the dead space of the Marathon was slowly filled with Glubran2/ Lipiodol 1:1. Under cerebral circulation arrest, the liquid embolic agent was slowly and carefully injected into the aneurysm under DSA with a frame rate of 4/s. The highly viscous nature of the embolic material and the complete absence of cerebral circulation, allowed a single polymerized drop of glue to be formed at the tip of the microcatheter. Under careful application, the embolic mass was able to take the shape of a sphere, filling most of the aneurysmal sac. Once the aneurysm appeared to have been filled with glue, the microcatheter was abruptly withdrawn. No glue got into the efferent vessel of the aneurysm during the embolization procedure. On the spontaneous return of the sinus rhythm over approximately 20 s after the adenosine had been applied, the solidified glue cast inside the aneurysm neither moved nor migrated. However, following contrast injections revealed that the aneurysm had not been completely occluded. There was a notable gap between the glue cast and the aneurysm wall. The presence of residual aneurysmal filling was considered to be a risk factor for dangerous aneurysm regrowth and potential rupture. The parent artery was, therefore, catheterized once again. Since distal passage was no longer a concern, there was no need to induce any asystole. The second selective glue injection (again Glubran2/Lipiodol) resulted in the complete obliteration of the aneurysm. When the contrast medium was injected into the left ICA, this confirmed the complete occlusion of the IIA and the retrograde perfusion of the efferent artery via leptomeningeal collaterals (Fig. 2). Duration: 1st–12th DSA run: 160 min; fluoroscopy time: 32 min Complications: none Postmedication: none

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Clinical Outcome Immediately after the endovascular treatment, a right-hand side hemiparesis and right central facial nerve palsy were noted. Conservative management and elevation of the arterial blood pressure by administering noradrenaline was issued. Over the following days, the neurological deficit fully resolved. During the follow-up, no recurrence of bacterial endocarditis had occurred.

Follow-Up Examinations Postprocedural MRI examination confirmed the presence of perianeurysmal FLAIR and DWI hyperintensities. Follow-up examinations were scheduled for July 2015 and November 2017. Both clinical and radiological follow-up examinations confirmed the complete resolution of the neurological deficit as well as the complete obliteration of the target aneurysm (Fig. 3).

Discussion The term “mycotic” cerebral aneurysm is a misnomer because the pathophysiological mechanism behind the aneurysmal formation is often associated with the presence of emboli containing bacteria. “Infectious intracranial aneurysm” (IIA) appears a more appropriate term. Septic emboli lead to subsequent necrosis and further inflammation of the vessel wall. Rapid neutrophil infiltration and disintegration of the vessel wall, fragmentation of the internal elastic lamina, and proliferation of the intima can be seen on microscopic histological samples. The water-hammer effect of the disturbing local blood flow over the already weakened vessel wall leads to rapid aneurysmal formation. Molinari et al. (1973) confirmed that an acute inflammatory response due to local bacterial invasion of the lamina muscularis with underlying aneurysmal formation could be seen within 24 h after a septic embolism has occurred. When endocarditis is associated with a distal aneurysm, the diagnosis of a “mycotic” (i.e., IIA)

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aneurysm is most likely (Henkes et al. 1993). Other less common etiologies include contiguous and excessive infection due to meningitis, adjacent osteomyelitis, and sinusitis. The type of microorganism may be isolated, but the most common causative organism is the Gram-positive

Fig. 2 (continued)

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bacteria streptococcus, followed by staphylococci, enterococci, pneumococcus, and haemophilus species (Venkatesh et al. 2000). Intravenous drug abuse and “immunocompromised” conditions are becoming more commonly associated with IIA.

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Fig. 2 Endovascular treatment of a left mycotic middle cerebral artery aneurysm via selective glue obliteration and induced asystole. Note the fragile nature and the angiographic (a) appearance of the aneurysm. Distal navigation of a Marathon microcatheter and the successful catheterization of the aneurysmal sac under roadmap guidance (b). Under adenosine-induced asystole, n-butyl

2-cyanoacrylate (nBCA)/Lipiodol (c) was injected into the sac. Following the retraction of the microcatheter, control angiography revealed incomplete obliteration (arrow (d)). The second successful (e) application of nBCA/Lipiodol resulted in the complete occlusion (f) of the aneurysm. Retrograde perfusion of the distal efferent artery was seen on the control (g, h) angiograms

Many authors suggest that these IIA carry a significant risk of rupture with subsequent intracerebral and or subarachnoid hemorrhage (Ducruet et al. 2010; Tunkel and Kaye 1993). However, to date, the true incidence of rupture in IIA remains unknown. Nowadays, there are no established guidelines and clinical standards for the management of IIA. Treatment modalities include conservative management, microvascular surgery, endovascular treatment, or a combination of therapies. In a comprehensive literature review, Ragulojan et al. (2019) found that in 56% of IIA for which conservative management had been intended, in the end, either active treatment was required or the patient died. The development of IIA can be often unpredictable as they may suddenly disappear, involute, or even rapidly enlarge and rupture. In contrast to a “regular” saccular intracranial aneurysm, IIAs are usually thin-walled and extremely fragile, often with a broad or absent neck, making them difficult to deal with by microsurgical means. For IIA affecting distal arteries, endovascular parent vessel occlusion using coils,

embolization particles, or liquid embolic agents is an accepted treatment (Chapot et al. 2002). The embolization material commonly used in endovascular treatment of IIAs are detachable coils (Champeaux et al. 2017) or liquid embolic agents (Grandhi et al. 2014). Introducing foreign body materials into an already damaged and infected vessel wall may, however, cause further inflammation or malicious abscess formation. Liquid embolic agents are, from a theoretical perspective, the ideal material for the complete endovascular occlusion of IIA (Misser et al. 2005). The key to the success of this procedure is the controlled depositing of the liquid into the aneurysm without losing any either proximal or distal. However, the embolic cast needs to attach to the aneurysm wall firmly. Any gap between the embolic material and the vessel wall carries the risk of residual aneurysm perfusion leading to subsequent growth and rupture. Despite promising reports (Cekirge et al. 2006) and its nonadhesive nature, ethylene vinyl alcohol copolymer (Onyx, Medtronic) has been widely abandoned in the treatment of intracranial aneurysms.

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Fig. 3 (continued)

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Middle Cerebral Artery (M3) Aneurysm: Two “Mycotic” Aneurysms of the Middle. . .

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Fig. 3 Follow-up examinations after the treatment of a left-hand MCA infectious aneurysm with nBCA embolization under induced asystole. Perianeurysmal FLAIR (a) and DWI (b) hyperintensities were noted on the postprocedural MRI examination. DSA follow-up confirmed the successful obliteration of the aneurysm (c, d) as well as the patency of the distal MCA branches. A complete

reversal of the cerebral changes was noted on the first follow-up MRI (e) examination conducted 7 months after the embolization. There was no distal migration of the embolic cast, as seen on the corresponding native images (f). Final DSA and MRI examinations performed 12 months after the treatment confirmed the success of the endovascular procedure

This statement, however, is not valid for IIA (Gross and Puri 2013). On the other hand, cyanoacrylate derivatives such as NBCA have led to a higher number of stand-alone curative endovascular embolization procedures for infective cerebral aneurysms. Our case report suggests that selective glue embolization of an infective cerebral aneurysm secondary to bacterial endocarditis can be accomplished. The adenosine-induced asystole provided an alternative method to achieve the temporary cerebral circulatory arrest that was needed for precise fluoroscopic embolization control (Lylyk et al. 2017). The inherent adhesive nature of the NBCA guaranteed that the cast would hold long term, protecting the aneurysmal wall. The lack of luminal blood flow into the parent vessel during the embolic cast delivery showed that NBCA could successfully go into a spherical form that conforms to the wall and thus filling the peripheral portion of the aneurysmal lumen. The glue was injected at an angled view of the aneurysmal neck under high-resolution, subtracted, and real-time fluoroscopic roadmap imaging, which facilitated the procedure. The concentration of the embolic

mixture meant that it would have been possible to retrieve the microcatheter safely. Finally, our treatment strategy resulted in successful immediate and long-term angiographic obliteration of the target aneurysm and recovery from the neurologic deficit with no periprocedural technical or clinical complications.

Therapeutic Alternatives Coil Occlusion Conservative Management Microsurgical Clipping

References Cekirge HS, Saatci I, Ozturk MH, Cil B, Arat A, Mawad M, Ergungor F, Belen D, Er U, Turk S, Bavbek M, Sekerci Z, Beskonakli E, Ozcan OE, Ozgen T. Late angiographic and clinical follow-up results of 100 consecutive aneurysms treated with Onyx reconstruction: largest single-center experience. Neuroradiology. 2006;48(2):113–26. https://doi.org/ 10.1007/s00234-005-0007-6.

1038 Champeaux C, Walker N, Derwin J, Grivas A. Successful delayed coiling of ruptured growing distal posterior cerebral artery mycotic aneurysm. Neurochirurgie. 2017;63(1):17–20. https://doi.org/ 10.1016/j.neuchi.2016.10.005. Chapot R, Houdart E, Saint-Maurice JP, Aymard A, Mounayer C, Lot G, Merland JJ. Endovascular treatment of cerebral mycotic aneurysms. Radiology. 2002;222(2):389–96. https://doi.org/ 10.1148/radiol.2222010432 Ducruet AF, Hickman ZL, Zacharia BE, Narula R, Grobelny BT, Gorski J, Connolly ES Jr. Intracranial infectious aneurysms: a comprehensive review. Neurosurg Rev. 2010;33(1):37–46. https://doi.org/ 10.1007/s10143-009-0233-1. Grandhi R, Zwagerman NT, Linares G, Monaco EA 3rd, Jovin T, Horowitz M, Jankowitz BT. Onyx embolization of infectious intracranial aneurysms. J Neurointerv Surg. 2014;6(5):353–6. https://doi.org/10.1136/ neurintsurg-2013-010755. Gross BA, Puri AS. Endovascular treatment of infectious intracranial aneurysms. Neurosurg Rev. 2013;36(1):11–9; discussion 19. https://doi.org/ 10.1007/s10143-012-0414-1. Henkes H, Terstegge K, Felber S, Jänisch W, Nahser HC, Kühne D. “Mykotisches”, infektionsbedingtes intrakranielles Aneurysma. In: Henkes H, Kölmel HW, editors. Die entzündlichen Erkrankungen des Zentralnervensystems, Handbuch und Atlas, II-1. Landsberg/Lech: Ecomed; 1993. p. S1–71.

A. Sirakov et al. Lylyk P, Chudyk J, Bleise C, Serna Candel C, Aguilar Pérez M, Henkes H. Endovascular occlusion of pial arteriovenous macrofistulae, using pCANvas1 and adenosine-induced asystole to control nBCA injection. Interv Neuroradiol. 2017;23(6):644–9. https://doi.org/ 10.1177/1591019917720921. Misser SK, Lalloo S, Ponnusamy S. Intracranial mycotic aneurysm due to infective endocarditis – successful NBCA glue embolisation. S Afr Med J. 2005;95(6):397–9.. 403-4 Molinari GF, Smith L, Goldstein MN, Satran R. Pathogenesis of cerebral mycotic aneurysms. Neurology. 1973;23:325–32. https://doi.org/10.1212/ wnl.23.4.325. Ragulojan R, Grupke S, Fraser JF. Systematic review of endovascular, surgical, and conservative options for infectious intracranial aneurysms and cardiac considerations. J Stroke Cerebrovasc Dis. 2019;28(3):838–44. https://doi.org/10.1016/j.jstrok ecerebrovasdis.2018.11.035. Tunkel AR, Kaye D. Neurologic complications of infective endocarditis. Neurol Clin. 1993;11(2):419–40. Venkatesh SK, Phadke RV, Kalode RR, Kumar S, Jain VK. Intracranial infective aneurysms presenting with haemorrhage: an analysis of angiographic findings, management and outcome. Clin Radiol. 2000;55(12):946–53. https://doi.org/10.1053/crad. 2000.0596.

Part XIX Vertebral Artery (V4)

Vertebral Artery Aneurysm: Incidental Large Vertebral Aneurysm with Medullary Compression, Incorporation of the PICA, Treatment with a Single p64 Flow Diverter, and Complete Aneurysm Occlusion

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André Kemmling, Thomas Eckey, Dirk Rasche, and Peter Schramm

Abstract

A large incidental saccular sidewall aneurysm of the right vertebral artery (VA) incorporating the posterior inferior cerebellar artery (PICA) was treated by endovascular coverage with a p64 flow diverter. The patient initially presented with neck pain because of a substantial sized aneurysm (21/20/18 mm). The aneurysm caused significant dorsal deflection of the medulla at the level of the foramen magnum with myelopathic edema on MRI. This mass effect required a careful treatment strategy. Prior to endovascular treatment, occipital decompressive surgery was performed to avoid any further harmful compression of the medulla in the event of a PICA infarct after endovascular treatment. Furthermore, to reduce the uncertainty with regard to flow diverter size and behavior during and after deployment, a precise 3D vascular model of the large aneurysm was manufactured from 3D

A. Kemmling (*) · T. Eckey · P. Schramm Institut für Neuroradiologie, Universitätsklinikum Schleswig-Holstein, Lübeck, Germany e-mail: [email protected]; [email protected]; [email protected] D. Rasche Klinik für Neurochirurgie, Universitätsklinikum Schleswig-Holstein, Lübeck, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_14

rotational DSA image data. Deployment of the flow diverter within the 3D model was straightforward, with sufficient coverage at the landing zones of the afferent and efferent aneurysm parent vessel. During controlled release, there was no flow diverter foreshortening across the large uncovered portion within the aneurysm. The patient was treated accordingly without technical difficulty. DSA after one week showed partial obliteration of the aneurysm with minimal expansion of the flow diverter into the aneurysm at the expense of minimal proximal narrowing without movement of the proximal or distal landing zones. The patient was discharged after 2 weeks without a neurological deficit. Within 1 month after discharge, there was cerebral spinal fluid (CSF) effusion from surgery at the neck causing soft tissue compression at the foramen magnum with intermittent hydrocephalus, which was treated by ventriculoperitoneal shunt. On follow-up after 3 months, the DSA showed near-complete aneurysm obliteration. There were spontaneous right VA occlusion and retrograde filling of the patent PICA. A possible reason for the VA occlusion was attributed to an incompliant intake of dual antiplatelet medication by the patient. The patient completed his rehabilitation without any sequelae. This case

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illustrates the feasibility of treatment simulation to anticipate flow diverter sizing and deployment behavior in complex giant aneurysms using patient-specific 3D vascular models. The deployment of a single flow diverter can result in a complete obliteration of a large VA aneurysm without compromise of the adjacent side branch (PICA). The occlusion of the parent artery during follow-up underlines the importance of patient compliance for medication intake of dual platelet inhibition in vertebrobasilar flow diverters. Keywords

Vertebral artery · PICA · Flow diversion · p64 · 3D model

Patient 59-year-old, male, neck pain

Diagnostic Imaging Diagnostic imaging was requested as a work-up for neck pain. MRI (Fig. 1a–c) and DSA (Fig. 2) showed a large, wide-necked sidewall aneurysm (21/20/18 mm) of the right VA proximal to the

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origin of the right PICA with significant dorsal deflection of the medulla at the level of the foramen magnum. There was significant compression of the myelon with early myelopathic edema on MRI (Fig. 1c).

Treatment Strategy Prevention of further growth and rupture were the goals of this treatment, aiming at the obliteration with shrinkage of the aneurysm and the preservation of the adjacent PICA. Prior to endovascular treatment, occipital decompressive surgery was performed to prevent compression of the medulla in the event of infratentorial swelling due to a PICA infarct (Fig. 3). Also, this was to avoid potential bleeding complications of post hoc decompressive surgery under dual platelet inhibition after flow diverter treatment. The goal was to treat the aneurysm with minimal mass effect, i.e., no coils and without sacrificing the PICA. After endovascular simulation of sizing and device deployment in a 1:1 3D printed vascular model of the aneurysm (Fig. 4), treatment using a single flow diverter to cover the aneurysm was chosen.

Fig. 1 Diagnostic imaging. MRI showed a large wide-necked sidewall VA aneurysm (21/20/18 mm) with compression of the medulla oblongata. (a) Coronal, (b) sagittal contrast enhanced T1WI, (c) T2WI

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Fig. 2 Diagnostic imaging. DSA of a large right VA aneurysm (21/20/18 mm) (a) posterior-anterior projection, (b) lateral projection, and (c) 3D DSA rendering of the

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aneurysm with the PICA at the distal efferent parent artery at the neck

Fig. 3 Site of occipital decompressive surgery with giant VA aneurysm lurking behind the medulla (a). CT after surgery shows the extend of the decompressive craniectomy (b)

Treatment Procedure #1, 19.07.2017: flow diversion of a large aneurysm of the right VA, according to the results of a previous 3D model Anesthesia: general anesthesia; 3000 IU heparin IV, weight-adapted tirofiban (Aggrastat, Correvio) IV infusion during device deployment Premedication: 1
100 mg ASA (Aspirin, Bayer Vital) PO and 1
75 mg clopidogrel (Plavix, Sanofi-Aventis) PO, both started 5 days

prior to treatment. Effective ASA and clopidogrel platelet function inhibition was tested by Multiplate analyzer (Roche Diagnostics) with ASPI test and ADP test, respectively. Access: right femoral artery; sheath: soft tip 6F Neuron Max (Penumbra) long sheath; 5F intermediate guide catheter: 5MAX ACE (Penumbra); microcatheter: Excelsior XT-27 (Stryker) for the flow diverter; microguidewire: Synchro2 0.01400 200 cm (Stryker) Implant: flow diverter: 1
p64 4.5/27 (phenox)

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Fig. 4 DSA of the 3D vascular model (a). Road map during device deployment into the 3D model (b). Photograph of a 1:1 3D printed vascular model of the aneurysm with a deployed p64 flow diverter (c)

Fig. 5 Pre-procedural (a) and immediate post-procedural DSA (b, c) showing significant flow diversion with contrast stasis within the large aneurysm

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Fig. 6 3D DSA confirmed the proper deployment of the flow diverter with patent lumen and without kinking or stenosis. Thick slab MIP (a), thin slab MIP (b), and

proximal (c) and distal (d) thin cross-sectional imaging of the deployed flow diverter

Course of treatment: the dominant right VA was proximally catheterized with a 6F soft tip long sheath with distal placement of a 5F intermediate guide catheter. DSA showed the large sidewall VA aneurysm and the origin of the right PICA, which was incorporated in the distal part of the aneurysm neck. The vessel diameter of the anticipated proximal landing zone was 4.5 mm, of the distal landing zone 2.5 mm. An Excelsior

XT-27 was brought to the basilar artery, and the p64 was released across the aneurysm (Fig. 5). The final DSA run confirmed a delayed washout of the contrast medium from the aneurysm sac and opacification of the patent right PICA within normal limits. 3D DSA confirmed the proper deployment of the flow diverter (Fig. 6). Duration: 1st – 12th DSA run: 51 minutes; fluoroscopy time: 27 minutes

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Fig. 7 Compared to MRI at discharge (a), MRI revealed an intermittent hydrocephalus after one month (b). CSF effusion had developed at the neck after decompressive surgery (c). The CSF effusion into the cervical soft tissue had caused local compression and hindered CSF flow

through the foramen magnum. Surgery with dural ligation and ventriculoperitoneal shunt (d) was performed to prevent further CSF leakage and hydrocephalus. The flow diverter is seen at the foramen magnum

Complication: none Post medication: 1
100 mg ASA PO daily for life, 1
75 mg clopidogrel (Plavix, SanofiAventis) PO daily for 6 months

presented with gait disturbance. MRI revealed that CSF effusion had developed at the neck after decompressive surgery. The CSF effusion into the soft tissue caused local compression and hindered CSF flow through the foramen magnum with intermittent hydrocephalus. The aneurysm itself showed no signs of growth in MRI (Fig. 7a–c). After drainage of the effusion, the patient improved immediately. A second surgery with dural ligation and ventriculoperitoneal shunt was performed to prevent further CSF leakage and

Clinical Outcome The patient remained without neurological deficit (mRS 0, GOS V) at immediate follow-up and until discharge at 2 weeks. After 1 month, the patient

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Fig. 8 Pre-procedural (a), post-procedural (b), and follow-up DSA after 1 week (c) and 3 months (d) (the upper row shows posteroanterior and the lower row lateral projections). DSA follow-up examinations after 1 week showed partial obliteration of the aneurysm with a minor expansion of the flow diverter into the aneurysm at the

expense of proximal narrowing. The proximal and distal landing zones remained unchanged and in place. DSA at 3 months showed near-complete aneurysm obliteration with occlusion of the right VA while the right PICA remained patent

hydrocephalus (Fig. 7d). Upon follow-up after 3 months, DSA showed near-complete aneurysm obliteration with a patent PICA by retrograde filling via the V4 segment. Spontaneous right VA occlusion had occurred. The patient completed rehabilitation without sequelae (mRS 0, GOS V).

showed near-complete aneurysm obliteration with spontaneous occlusion of the right VA. The PICA remained patent with retrograde filling.

Follow-Up Examinations Pre-procedural, post-procedural, and follow-up DSA after 1 week and 3 months, respectively, are shown in Fig. 8. At 1 week, there was partial obliteration of the aneurysm with a minor expansion of the flow diverter into the aneurysm with minimal proximal narrowing. DSA at 3 months

Discussion The main reasons to treat this aneurysm were the anticipated risks of hemorrhage and further growth at already subcritical compression of the medulla oblongata. Dense coil occlusion of the aneurysm sac was therefore not an option. Coil placement would also require challenging technical solutions, e.g., retrograde catheterization of the right PICA via the left vertebral artery across the vertebral artery junction with deployment of a

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stent from the right PICA toward the distal right V4 segment, followed by coil occlusion of the aneurysm sac (Heye et al. 2015). Occlusion of the dominant right VA with reversal of flow direction was considered to be suboptimal for spontaneous aneurysm occlusion with a large PICA arising from the neck of the aneurysm. For flow diverter placement, the technical feasibility was a concern with regard to proper flow diverter deployment across a long uncovered portion within the aneurysm (approximately 20 mm). Ballooning or kinking within the aneurysm with proximal foreshortening was a potential risk. Furthermore, the PICA at the neck was a concern since this feature may lead to a reduced obliteration rate (Moshayedi et al. 2017). Loose coil embolization prior to flow diverter placement could have accelerated obliteration after the treatment (Park et al. 2016). However, the goal was to minimize the risk of any thromboembolism into the PICA to prevent cerebellar infarct with swelling causing a potentially devastating mass effect on the medulla. Covering both aneurysm and PICA with a flow diverter was expected to result in aneurysm occlusion and induce shrinkage without compromise of the PICA. In order to better anticipate the optimal size and behavior of the flow diverter during placement into this large sidewall aneurysm, a precise 3D vascular model was manufactured by stereo-lithographic 3D printing (at 0.025-mm resolution) from 3D rotational DSA image data. Multiple device deployment tests within the 3D model were performed showing maximum control during release and resheathing. Release occurred with a homogenous lumen width across the aneurysm. A p64 flow diverter with 27 mm length at 4.5 mm diameter was chosen for optimal coverage at the landing zones of the afferent and efferent aneurysm parent vessel. The procedure in the patient after practicing in the model was straightforward and rapidly performed with identical device behavior as predicted from the 3D model. Dual antiplatelet function

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inhibition was intended to be maintained for six months with clopidogrel and ASA, followed by ASA for life. There was no PICA occlusion or any cerebellar infarct; thus, prior decompressive surgery at the neck as a preventive measure for critical medullary compression was in retrospect not necessary in this particular case. Unexpectedly, CSF leakage with effusion at the neck induced a soft tissue mass effect at the foramen magnum leading to intermittent hydrocephalus, which was treated successfully. At three months follow-up, there was nearcomplete obliteration of the aneurysm with spontaneous right VA occlusion and retrograde filling of the patent PICA. A possible cause was attributed to patient’s incompliance with regard to dual antiplatelet medication. The patient completed his rehabilitation without any sequelae.

Therapeutic Alternatives Coil-Assisted Flow Diversion Parent Vessel Occlusion Stent-Assisted Coil Occlusion

References Heye S, Stracke CP, Nordmeyer H, Heddier M, Stauder M, Chapot R. Retrograde access to the posterior inferior cerebellar artery in balloon-assisted coiling of posterior inferior cerebellar artery aneurysms. J Neurointerv Surg. 2015;7:824–8. https://doi.org/10.1136/neurintsurg-2014011417. Moshayedi H, Omofoye OA, Yap E, Oyekunle TO, SasakiAdams DM, Solander SY. Factors affecting the obliteration rate of Intracranial Aneurysms treated with a single Pipeline Embolization Device. World Neurosurg. 2017;104:205. pii: S1878–8750(17) 30619–8. https://doi.org/10.1016/j.wneu.2017.04.111. Park MS, Nanaszko M, Sanborn MR, Moon K, Albuquerque FC, McDougall CG. Re-treatment rates after treatment with the pipeline embolization device alone versus pipeline and coil embolization of cerebral aneurysms: a singlecenter experience. J Neurosurg. 2016;125:137–44. https://doi.org/10.3171/2015.7.JNS15582.

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Vertebral Artery Aneurysm: Acute Subarachnoid Hemorrhage Due to a Dissecting V4 Aneurysm, Treatment with a Flow Diverter Stent, and Complete Reconstruction of the Vessel Lumen

Muhammad AlMatter, Marta Aguilar Pérez, and Hans Henkes

Abstract

We describe the clinical course, radiological findings, and endovascular treatment of a 58year-old male patient who presented with headache due to a minor subarachnoid hemorrhage (SAH) resulting from a dissecting aneurysm of the intradural segment (V4) of the right vertebral artery. The aneurysm was treated on day 7 after the onset of the headache by means of flow diversion with complete obliteration on the angiographic follow-up studies. The affected segment of the vertebral artery was reconstructed, and the posterior inferior cerebellar artery (PICA), which was covered by the flow diverter, remained patent. There was no recurrent hemorrhage, and the patient was asymptomatic apart from headache and neck stiffness during the follow-up period. The use of flow diversion in the setting of acute SAH due to intracranial arterial dissection is the main topic of this case report. Keywords

Vertebral artery · Dissecting aneurysm · SAH · Flow diverter · Vertebrobasilar aneurysm

M. AlMatter (*) · M. Aguilar Pérez · H. Henkes Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; [email protected]; [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_30

Patient 58-year-old, male, spontaneous SAH, Hunt and Hess grade I, Fisher grade 1

Diagnostic Imaging This previously healthy patient presented to the emergency department of the referring hospital due to a sudden and severe nocturnal headache. The initial computer tomography (CT) of the head was within normal limits. The diagnostic lumbar puncture revealed xanthochromic cerebrospinal fluid (CSF) with an elevated cell count. Under the assumption of viral meningitis, he was then admitted and treated with intravenous acyclovir. A follow-up magnetic resonance imaging (MRI) revealed a fusiform, dissecting aneurysm of the right vertebral artery (VA) (Fig. 1). In keeping the possibility of a minor subarachnoid hemorrhage as the cause of the initial symptoms, a transcranial Doppler (TCD) ultrasound was performed, demonstrating accelerated flow in the vertebrobasilar circulation. The patient was then referred to our center for further evaluation and management. A diagnostic catheter angiography was performed. The selective injection of the right vertebral artery confirmed the MR findings of a fusiform, dissecting aneurysm of the right vertebral artery just distal to the origin of the right posterior 1049

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Fig. 1 Axial source images of the “time-of-flight” angiography (a) and sagittal T2 TSE (b) demonstrating a fusiform dilatation in the terminal V4 segment of the right vertebral artery

inferior cerebellar artery (PICA) with a maximal diameter of 7 mm over an 8 mm segment of the vessel (Fig. 2).

Treatment Strategy The treatment goals were the prevention of a recurrent SAH, the reconstruction of the parent artery, and the preservation of the right PICA. Endovascular placement of a flow diverter (FD) along the affected segment was chosen as the most appropriate strategy for achieving the abovementioned goals. The patient was started on dual antiplatelet medication with ASA and ticagrelor (Brilique, AstraZeneca), and the adequate response was confirmed with a Multiplate test (Roche Diagnostics). The endovascular treatment was performed on the following day (hence, 7 days after the onset of headache) with successful placement of one FD. The patient was extubated immediately after the procedure and was discharged 10 days thereafter.

Treatment Procedure, 22.03.2017: endovascular reconstruction of the dissected V4 segment of the right vertebral artery via flow diversion

Anesthesia: general anesthesia; 3000 IU unfractionated heparin (Heparin-Natrium, B. Braun) IV, 500 mg ASA (Aspirin i.v.500mg, Bayer Vital) IV, 1 g thiopental (Trapanal, Nycomed) IV, 2 mg glyceryl trinitrate (Nitrolingual infus., G. Pohl-Boskamp) IA Premedication: 1
500 mg ASA and 180 mg ticagrelor PO, 12 h prior to the intervention and 7 days after the SAH 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 0.01400 200 cm (Stryker) Implant: flow diverter, 1
p64 3.5 / 18 mm (phenox) Course of treatment: the treatment started with an angiographic examination of all intracranial vessels. The selective injection of the right vertebral artery revealed a fusiform aneurysm just distal to the origin of the right PICA with moderate narrowing of the parent vessel at the origin of the PICA. The guide catheter was navigated into the mid-cervical segment of the right vertebral artery, which was followed by atraumatic advancement of the Excelsior XT-27 microcatheter up to the mid-third of the basilar artery over the 0.01400 microguidewire. DSA of the right vertebral artery in multiple projections were used for the appropriate sizing of the FD; this was then advanced

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Fig. 2 Posteroanterior (pa) (a), lateral (b), and right and left 45 oblique (c, d) projections of the selective digital subtraction angiography after injection of the right vertebral artery confirming the MRA findings of a fusiform aneurysm of the right vertebral artery just distal to the origin of the right PICA. Note the moderate stenosis just proximal to the aneurysm, which might represent an intracranial dissection resulting in the formation of the aneurysm

through the microcatheter to the level of the fusiform aneurysm. After partial deployment, the appropriate vessel wall apposition was confirmed (Fig. 3), and the FD was then completely unsheathed and mechanically detached. The final DSA run showed a delayed washout of the contrast from the aneurysm and normal perfusion of both the basilar artery and the right PICA, with no evidence of peripheral emboli (Fig. 4). Duration: 1st-6th DSA run: 38 m; fluoroscopy time: 19 m Complications: none Post medication: In addition to the oral dual antiplatelet medication of 1
100 mg ASA daily and 2
90 mg ticagrelor daily, the patient also received 2
3000 IU of certoparin

(Mono-Embolex, Aspen) SC daily for 2 weeks and 4
4 mg of dexamethasone (Fortecortin, Merck Pharma) PO daily for 3 days, which was then tapered off over the 2 following weeks.

Clinical Outcome The postoperative course was uneventful, and the patient was discharged home on the 10th day post procedure. The most recent clinical follow-up examination eight months after the treatment showed no residual neurological or functional deficits (modified Rankin Scale 0, Glasgow Outcome Score 5).

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Fig. 3 Deployment of the p64 flow diverter (FD) into the V4 segment of the right VA. a and b demonstrate the fully unsheathed length of the FD while still in the microcatheter. c and d show the partial deployment of the FD with a good wall apposition of the distal half

Follow-Up Examinations The postoperative cranial MRI showed no evidence of an ischemic or hemorrhagic complication. An early follow-up DSA performed 8 days after the endovascular treatment (EVT) confirmed

the patency of the right PICA. The second angiographic follow-up was performed 2 months after the treatment and revealed the shrinkage of the aneurysm with normal perfusion of the right VA and right PICA (Fig. 5). The latest angiographic follow-up 8 months after the EVT showed complete obliteration of the fusiform aneurysm with

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Fig. 4 Selective injection of the right VA after full deployment of the FD (a), the struts completely cover the aneurysm. The late arterial phase (b) shows some flow stagnation inside the aneurysm

Fig. 5 PA (a) and lateral (b) projections of the first angiographic follow-up showing almost complete occlusion of the fusiform aneurysm with smoothening of the vessel contour. The right PICA is still patent despite being covered with the FD

preserved patency of the previously narrowed segment of the right vertebral artery. The covered origin of the right PICA was still patent with uncompromised anterograde perfusion (Fig. 6).

Discussion Intracranial dissecting aneurysms represent a rare but an important cause of spontaneous SAH (Friedman and Drake 1984; Rinkel et al. 1993). The underlying pathology is often a dissection between the media and adventitia or a disruption of the entire vessel wall (Endo et al. 1993). If left untreated, ruptured dissecting vertebrobasilar

aneurysms have a high tendency for re-rupture with high mortality rates. Surgical treatment options include parent vessel occlusion, wrapping, trapping, or partial clipping of the susceptible portion (Mizutani et al. 1995; Yamada et al. 2004). Endovascular treatment options include parent vessel occlusion and exclusion of the aneurysm by using coils with or without a stent (Rabinov et al. 2003; Ramgren et al. 2005). The management strategy for dissecting aneurysms of the intracranial segment of the VA is mainly influenced by their individual location. Lesions that do not involve the PICA can be managed by trapping the dissected segment. For lesions that involve or are in the vicinity of the

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Fig. 6 Selective DSA of the right VA from the latest angiographic follow-up (a: pa, b: lateral, c and d: 45 oblique projections) showing the complete obliteration of the aneurysm and preserved anterograde flow of the right PICA 8 months after the FD implantation

PICA, proximal occlusion of the parent vessel can in some cases be the only viable option (Iihara et al. 2002). Safe proximal occlusion of the vertebral artery, however, depends on the patency and diameter of the contralateral vessel. The emergence of FD has widely expanded the spectrum of endovascular treatment of intracranial aneurysms and has been used for the treatment of intracranial dissections and fusiform aneurysms with promising results (Fischer et al. 2012; Bhogal et al. 2017a). Reconstructing the dissected segment of the vessel using a FD, as in this presented example, is an elegant technique for preserving the flow

in the parent artery and the important branches arising from the affected segment. Although the coverage of the orifice of side branches is often associated with modulation of the flow dynamics and can lead to progressive narrowing or complete occlusion, these tend to be clinically well tolerated (Bhogal et al. 2017b). A major limitation for the use of the today available FD in the acute setting of a spontaneous SAH is the need for dual platelet function inhibition medication and the associated increased risk of hemorrhagic complications, especially those associated with the insertion of a ventricular drain (Kung et al. 2011).

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Therapeutic Alternatives Conservative Management Parent Vessel Occlusion Telescoping Stents

References Bhogal P, Pérez MA, Ganslandt O, Bäzner H, Henkes H, Fischer S. Treatment of posterior circulation non-saccular aneurysms with flow diverters: a single-center experience and review of 56 patients. J Neurointerv Surg. 2017a;9 (5):471–81. https://doi.org/10.1136/neurintsurg-2016012781. Bhogal P, Ganslandt O, Bäzner H, Henkes H, Pérez MA. The fate of side branches covered by flow diverters – results from 140 patients. World Neurosurg. 2017b;103:789–98. https://doi.org/10.1016/j.wneu.2017.04.092. Endo S, Nishijima M, Nomura H, Takaku A, Okada EA. Pathological study of intracranial posterior circulation dissecting aneurysms with subarachnoid hemorrhage: report of three autopsied cases and review of the literature. Neurosurgery. 1993;33(4):732–8. Fischer S, Vajda Z, Aguilar Perez M, Schmid E, Hopf N, Bäzner H, Henkes H. Pipeline embolization device (PED) for neurovascular reconstruction: initial experience in the treatment of 101 intracranial aneurysms and dissections. Neuroradiology. 2012;54(4):369–82. https://doi.org/10.1007/s00234-011-0948-x.

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Friedman AH, Drake CG. Subarachnoid hemorrhage from intracranial dissecting aneurysm. J Neurosurg. 1984;60 (2):325–34. Iihara K, Sakai N, Murao K, Sakai H, Higashi T, Kogure S, Takahashi JC, Nagata I. Dissecting aneurysms of the vertebral artery: a management strategy. J Neurosurg. 2002;97(2):259–67. Kung DK, Policeni BA, Capuano AW, Rossen JD, Jabbour PM, Torner JC, Howard MA, Hasan D. Risk of ventriculostomy-related hemorrhage in patients with acutely ruptured aneurysms treated using stent-assisted coiling. J Neurosurg. 2011;114(4):1021–7. https://doi. org/10.3171/2010.9.JNS10445. Mizutani T, Aruga T, Kirino T, Miki Y, Saito I, Tsuchida T. Recurrent subarachnoid hemorrhage from untreated ruptured vertebrobasilar dissecting aneurysms. Neurosurgery. 1995;36(5):905–11; discussion 912–3. Rabinov JD, Hellinger FR, Morris PP, Ogilvy CS, Putman CM. Endovascular management of vertebrobasilar dissecting aneurysms. AJNR Am J Neuroradiol. 2003;24(7):1421–8. Ramgren B, Cronqvist M, Romner B, Brandt L, Holtås S, Larsson EM. Vertebrobasilar dissection with subarachnoid hemorrhage: a retrospective study of 29 patients. Neuroradiology. 2005;47(2):97–104. Rinkel GJ, van Gijn J, Wijdicks EF. Subarachnoid hemorrhage without detectable aneurysm. A review of the causes. Stroke. 1993;24(9):1403–9. Yamada M, Kitahara T, Kurata A, Fujii K, Miyasaka Y. Intracranial vertebral artery dissection with subarachnoid hemorrhage: clinical characteristics and outcomes in conservatively treated patients. J Neurosurg. 2004;101(1):25–30.

Vertebral Artery Aneurysm: Severe Subarachnoid Hemorrhage, Dissecting Pseudoaneurysm of the Vertebral Artery, and Reconstructive Treatment Using Telescoping Pipeline Flow Diverters

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Franziska Dorn Abstract

A dissection of the V4 segment of the left vertebral artery (VA) was treated with telescoping flow diverters. The patient presented with severe subarachnoid hemorrhage (SAH), Fisher grade 4, 3 days after he had undergone tumor nephrectomy at an external hospital. After the surgery, he complained about neck pain before he progressively developed a rightsided hemiparesis and finally lost consciousness. An external ventricle drainage was applied after intubation, and the patient was transferred to our center. DSA confirmed a dissection of the left intradural vertebral artery (V4), including the origin of the posterior inferior cerebellar artery (PICA), and reconstructive treatment with a total of three telescoping Pipeline Embolization Devices (PED, Medtronic) was performed under antiplatelet medication with tirofiban. Follow-up DSA examinations 7 and 11 days after the treatment revealed progressive yet incomplete occlusion of the false vessel lumen. Finally, the follow-up DSA after 5 months demonstrated the complete reconstruction of the previously dissected artery with patency of the PICA. No procedure-related ischemic events occurred.

F. Dorn (*) Department of Neuroradiology, University Hospital of Munich, Campus Grosshadern, Munich, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_34

Ruptured vertebrobasilar dissecting aneurysms are associated with a poor natural history with high rates of re-rupture, stroke, and death when left untreated. For decades, parent vessel occlusion has been the treatment of choice. It is technically straightforward and has the advantage of an immediate occlusion of the pseudoaneurysm, and there is usually no need for antiplatelet medication; however, more sophisticated treatment options, such as bypass surgery or reconstructive endovascular treatment with flow diverters, must be discussed if the origin of the PICA and/or the anterior spinal artery is involved or in patients with a dissection of a dominant vertebral artery or in an isolated vertebrobasilar circulation. Keywords

Vertebral artery · Dissecting aneurysm · Pseudoaneurysm · SAH · Flow diverter · Telescoping

Patient A 52-year-old male patient with a history of renal cell carcinoma. Spontaneous SAH, Hunt and Hess IV, Fisher 4, 3 days after he underwent tumor nephrectomy and complained about neck pain afterward. He developed right-sided hemiparesis (3/5) and lost consciousness. At the time of arrival at our hospital, he was intubated. 1057

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Diagnostic Imaging

Treatment

Emergency CT in the referring hospital showed massive SAH in the posterior fossa (Fisher 4, Fig. 1) with subsequent hydrocephalus. A diagnostic angiography was performed one day later and revealed a circumscribed dilatation of the V4 segment of the left vertebral artery (VA) including the origin of the PICA consistent with an underlying dissection (Fig. 2).

Procedure, 11.04.2016: reconstructive treatment using three telescoping Pipeline flow diverters Anesthesia: general anesthesia Premedication: tirofiban (Aggrastat, Correvio) over 30 min in weight-adjusted loading dose (40 ml/h) and afterward in maintenance dose (10 ml/h) Access: right femoral artery, 8F sheath (Terumo); guide catheter: 7F Envoy (Codman Neurovascular); microcatheter: Marksman (Medtronic); microguidewire: Synchro2 0.01400 200 cm (Stryker) Implants: 3 Pipeline Embolization Device with Shield Technology (PED, Medtronic) 3/ 20 mm, 3.25/20 mm, 3.5/20 mm

Treatment Strategy The aim of the treatment was to prevent rebleeding from the dissecting pseudoaneurysm and to avoid occlusion of the PICA.

Fig. 1 Emergency CT at the referring hospital was performed after severe clinical deterioration and revealed a massive SAH with hydrocephalus

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Fig. 2 The initial angiogram (a, posterior-anterior (PA); b, lateral projection; c, 3D reconstruction of the rotational angiography) confirmed the dissection of the V4 segment of the left VA involving the origin of the dominant PICA

Course of treatment: The left VA was catheterized with a 7F guide catheter. The pseudoaneurysm was then crossed with a microguidewire/microcatheter combination (Fig. 3a, b), and a PED 3/20 mm was deployed using the push-and-pull technique, starting distally from the pseudoaneurysm (Fig. 3c–e). After complete deployment of the first PED, the microcatheter was advanced distally over the pusher wire, and the second PED (3.25/20 mm) was deployed in a telescoping fashion as described (Fig. 3f–h). The maneuver was repeated with the third PED (3.5/ 20 mm), and full coverage of the dissected vessel segment was achieved (Fig. 3i–k). The final DSA showed no thromboembolic events and proved patency of the PICA (Fig. 4a, b). Duration: 1st-40th DSA run: 91 min; fluoroscopy time: 45 min Complications: none Postmedication: tirofiban (Aggrastat, Correvio) in weight-adapted maintenance dose (10 ml/h) for 48 h, followed by 1 100 mg ASA PO daily lifelong, and 1 75 mg clopidogrel (Plavix, Sanofi-Aventis) daily for 6 months

difficulties with time and place orientation yet no sensomotoric or speech deficits.

Clinical Outcome

Discussion

The patient recovered gradually and received a ventriculoperitoneal shunt system. Eighteen months after the SAH, he had moderate

Dissecting-type VA pseudoaneurysms are rare causes of SAH with a particularly poor prognosis (Cerejo et al. 2017; Santos-Franco et al. 2008).

Follow-Up Examinations The first follow-up DSA was performed 7 days after the treatment and showed incomplete occlusion of the pseudoaneurysm. The flow diverters had created a second lumen bypassing the stentcovered arterial segment with considerable slower flow compared to the stent-covered segment and the PICA (Fig. 5). The second follow-up DSA was performed 11 days after the treatment and confirmed progressing contrast medium stasis in the pseudoaneurysm (Fig. 6). A midterm follow-up angiography was performed 5 months after the treatment. Finally, it demonstrated complete reconstruction of the dissecting segment with patency of the PICA. Apart from a minor dilatation at the origin of the PICA, the second lumen was now completely occluded while patency of the PICA was maintained (Fig. 7).

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Fig. 3 (continued)

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Vertebral Artery Aneurysm: Severe Subarachnoid Hemorrhage, Dissecting Pseudoaneurysm of. . .

Fig. 3 A microguidewire/microcatheter combination was navigated into the basilar artery crossing the pseudoaneurysm (a, pa; b, lateral road map). A PED 3/20 mm was deployed using the push-and-pull technique starting distally from the pseudoaneurysm (c–e), then the

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microcatheter was advanced over the pusher wire, and the second PED (3.25/20 mm) and third PED (3.5/20 mm) were deployed in an overlapping/telescoping fashion until full coverage of the dissected vessel segment was achieved (d–f and g–i)

Fig. 4 Post-interventional angiography showed no thrombotic events and full patency of the PICA (a, pa; b, lateral view)

With up to 70%, the risk of rebleeding in unsecured lesions is particularly high, with more than half of them occurring in the first 24 h after the initial SAH (Mizutani et al. 1995; Rabinov et al. 2003).

The best therapeutic choice for the treatment of VA dissecting-type aneurysms is yet to be defined. Due to an underlying fragility of the vessel wall and requirement to treat the entire diseased vessel segment (and not just the aneurysmal pouch),

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Fig. 5 Early follow-up DSA after 7 days showed patency of the stent-covered V4 segment as well as of the PICA with creation of a “bypass” lumen (arrows) with

Fig. 6 A second DSA after 11 days with progressing but still incomplete occlusion of the false lumen (arrows)

F. Dorn

considerably slower flow compared to the V4 segment, as well as the PICA (*) (a–c, pa projection; d, reconstruction of the 3D rotational DSA)

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Vertebral Artery Aneurysm: Severe Subarachnoid Hemorrhage, Dissecting Pseudoaneurysm of. . .

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Fig. 7 Follow-up DSA 5 months after the treatment demonstrated complete reconstruction of the dissecting vessel segment with preservation of the PICA (a, PA; b, oblique

projection; c, 3D reconstruction from the rotational DSA). A minor dilatation at the origin of the PICA is all what is left from the pseudoaneurysm (b and c, arrow)

direct surgical approaches have been largely abandoned in favor of endovascular techniques. Several endovascular approaches to the treatment of VA dissecting-type aneurysms exist comprising deconstructive and reconstructive techniques. While deconstruction (i.e., occlusion) of the dissected artery segment (either by permanent parent vessel occlusion or by trapping of the pseudoaneurysm) has been the treatment of choice for many years, reconstructive techniques have emerged with the advent of stents and flow diverters (Sönmez et al. 2015). Permanent occlusion of the parent artery offers the advantage of an immediate occlusion of the pseudoaneurysm and usually does not require antiplatelet medication, which potentially can avoid secondary complications (Rabinov et al. 2003; Matouk et al. 2012). However, sacrifice of the parent artery is associated with significant mortality and morbidity as a result of occlusion and ischemia of perforating arteries and the anterior spinal artery (Madaelil et al. 2016). This applies in particular for more complex cases (e.g., with involvement of the predominant vertebral artery and/ or major branches such as the PICA arising from the diseased segment) (Kashiwazaki et al. 2013).

Reconstructive treatment techniques have the potential to create a complete reconstruction of the affected vessel segment – even if this effect is not entirely predictable and may take several weeks or even months. The successful use of flow diverters has been described in several cases of dissecting vertebral artery aneurysms (Ducruet et al. 2013, Mazur et al. 2016; Fang et al. 2017). A metaanalysis comparing reconstructive with deconstructive techniques for the treatment of vertebral dissecting aneurysms found higher angiographic occlusion rates after permanent artery occlusion but no difference in recurrence, retreatment, and rebleeding rates (Sönmez et al. 2015). Potentially, angiographic results will further improve with an increasing use of new generation flow diverters and with the use of multiple overlapping stents. Several series demonstrated higher rates of longterm angiographic occlusion with multiple overlapping stents compared with single-stent treatment (Kabbasch et al. 2016; Kim et al. 2011; Zhao et al. 2013). Our case illustrates the feasibility of reconstructive flow diverter treatment in intracranial dissecting-type pseudoaneurysms of the VA. It resulted in a complete angiographic remodeling of the dissecting segment of the artery under

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preservation of the PICA and a good clinical outcome of the patient.

Therapeutic Alternatives Bypass Surgery Parent Vessel Occlusion Telescoping Stents

References Cerejo R, Bain M, Moore N, Hardman J, Bauer A, Hussain MS, Masaryk T, Rasmussen P, Flow TG. Diverter treatment of intracranial vertebral artery dissecting pseudoaneurysms. J Neurointerv Surg. 2017;9(11):1064–8. https://doi.org/10.1136/neurintsurg-2017-013020. Ducruet AF, Crowley RW, Albuquerque FC, McDougall CG. Reconstructive endovascular treatment of a ruptured vertebral artery dissecting aneurysm using the pipeline embolization device. J Neurointerv Surg. 2013;5(4):e20. https://doi.org/10.1136/neurintsurg2012-010358. Fang YB, Wen WL, Yang PF, Zhou Y, Wu YN, Hong B, Xu Y, Zhao WY, Liu JM, Huang QH. Long-term outcome of Tubridge flow diverter(s) in treating large vertebral artery dissecting aneurysms-a pilot study. Clin Neuroradiol. 2017;27(3):345–50. https://doi.org/ 10.1007/s00062-015-0494-8. Kabbasch C, Mpotsaris A, Behme D, Dorn F, Stavrinou P, Liebig T. Pipeline Embolization LT. Device for treatment of intracranial aneurysms – the more, the better? A single-center retrospective observational study. J Vasc Interv Neurol. 2016;9(2):14–20. Kashiwazaki D, Ushikoshi S, Asano T, Kuroda S, Longterm HK. Clinical and radiological results of endovascular internal trapping in vertebral artery dissection. Neuroradiology. 2013;55(2):201–6. https://doi.org/ 10.1007/s00234-012-1114-9. Kim BM, Shin YS, Kim SH, Suh SH, Ihn YK, Kim DI, Kim DJ, Park SI. Incidence and risk factors of recurrence after

F. Dorn endovascular treatment of intracranial vertebrobasilar dissecting aneurysms. Stroke. 2011;42(9):2425–30. https://doi.org/10.1161/STROKEAHA.111.617381. Madaelil TP, Wallace AN, Chatterjee AN, Zipfel GJ, Dacey RG Jr, Cross DT 3rd, Moran CJ, Derdeyn CP. Endovascular parent vessel sacrifice in ruptured dissecting vertebral and posterior inferior cerebellar artery aneurysms: clinical outcomes and review of the literature. J Neurointerv Surg. 2016;8(8):796–801. https://doi.org/10.1136/neurintsurg-2015-011732. Matouk CC, Kaderali Z, terBrugge KG, Willinsky RA. Long-term clinical and imaging follow-up of complex intracranial aneurysms treated by endovascular parent vessel occlusion. AJNR Am J Neuroradiol. 2012;33 (10):1991–7. https://doi.org/10.3174/ajnr.A3079. Mazur MD, Kilburg C, Wang V, Pipeline TP. Embolization device for the treatment of vertebral artery aneurysms: the fate of covered branch vessels. J Neurointerv Surg. 2016;8(10):1041–7. https://doi.org/10.1136/neurintsurg2015-012040. Mizutani T, Aruga T, Kirino T, Miki Y, Saito I, Recurrent TT. Subarachnoid hemorrhage from untreated ruptured vertebrobasilar dissecting aneurysms. Neurosurgery. 1995;36:905–11. Rabinov JD, Hellinger FR, Morris PP, Ogilvy CS, Putman CM. Endovascular management of vertebrobasilar dissecting aneurysms. AJNR Am J Neuroradiol. 2003;24(7):1421–8. Santos-Franco JA, Zenteno M, Lee A. Dissecting aneurysms of the vertebrobasilar system. A comprehensive review on natural history and treatment options. Neurosurg Rev. 2008;31(2):131–40.; ; discussion 140. https://doi.org/10.1007/s10143-008-0124-x. Sönmez Ö, Brinjikji W, Murad MH, Lanzino G. Deconstructive and reconstructive techniques in treatment of vertebrobasilar dissecting aneurysms: a systematic review and meta-analysis. AJNR Am J Neuroradiol. 2015;36(7):1293–8. https://doi.org/10.3174/ajnr. A4360. Zhao KJ, Fang YB, Huang QH, Xu Y, Hong B, Li Q, Liu JM, Zhao WY, Deng BQ. Reconstructive treatment of ruptured intracranial spontaneous vertebral artery dissection aneurysms: long-term results and predictors of unfavorable outcomes. PLoS One. 2013;8(6):e67169. https://doi.org/10.1371/journal.pone.0067169.

Vertebral Artery Aneurysm: Partially Thrombosed Dissecting Aneurysm, Symptomatic Through Brainstem Compression, Treatment with Telescoping Surpass Streamline Flow Diverters

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Marin Irizoiu, Andrik Aschoff, Christoph Schul, and Christian Taschner Abstract

A 57-year-old patient presented with progressive gait ataxia and paresthesia of the upper extremities. CT and MRI revealed a large fusiform aneurysm of the intradural segment of the left vertebral artery (VA), with the right VA only supplying the posterior inferior cerebellar artery (PICA). The aneurysm was partially thrombosed and the aneurysm wall was calcified. A previous dissection was assumed to be the underlying cause of this aneurysm. The aneurysm was treated by the endovascular insertion of two Surpass Streamline (Stryker) flow diverters using a telescoping technique. A DSA carried out 3 months later confirmed the complete angiographic obliteration of the fusiform vessel dilatation. Significant shrinkage of

M. Irizoiu (*) · A. Aschoff Klinik für diagnostische und interventionelle Radiologie und Neuroradiologie, Klinikum Kempten, Kempten, Germany e-mail: [email protected]; andrik. [email protected] C. Schul Klinik für Neurochirurgie, Klinikum Kempten, Kempten, Germany e-mail: [email protected] C. Taschner Klinik für Neuroradiologie, Universitätsklinikum Freiburg, Freiburg, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_43

the thrombosed saccular component did not, however, occur. The calcification of the aneurysm wall and an incomplete hemodynamic isolation of the aneurysm from the parent artery are potential reasons for the aneurysmal mass effect not having reduced. Treating a dissecting aneurysm with flow diversion is often technically easier than stent-assisted coil occlusion. A potential issue after stenting and coil occlusion is a recurrent perfusion of the aneurysm due to the coil compaction, leading to secondary aneurysm growth and coil migration into an intrasaccular thrombus. The use of flow diverters for treating chronic dissecting aneurysms located in the posterior circulation remains controversial. The large number of perforating and branching arteries in the posterior circulation potentially increases the risk involved in flow diversion, exposing patients to thromboembolic complications and a potential brainstem stroke. The main topic of this report is a case in which two flow diverting implants were combined in a large fusiform aneurysm with the expectation of reducing brainstem compression, which has not yet occurred. Keywords

Vertebral artery · Fusiform aneurysm · Dissection · Flow diversion · Surpass Streamline 1065

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Patient

Treatment Strategy

A 57-year-old, male patient, presenting with progressive gait abnormality which he had for 1 month and tingling paresthesia of both hands and the right shoulder, which had been present for 1 week.

The aims of this treatment were to prevent further growth and further brainstem compression and rupture and ultimately to obliterate the aneurysm. It was decided to go for flow diverter coverage of the aneurysm since neither microsurgical clipping nor parent vessel occlusion were viable options.

Diagnostic Imaging Treatment CT, MRI, and DSA examinations showed a large fusiform aneurysm of the left VA at the V4 segment. The aneurysm wall was calcified. A saccular component of the aneurysm was partially thrombosed and had caused significant brainstem compression. The right vertebral artery was only supplying the right PICA (Fig. 1).

Procedure, 17.02.2017: endovascular treatment of a dissecting left V4 aneurysm comprising telescopic implantation of two Surpass Streamline flow diverters Anesthesia: general anesthesia; 1 5000 IU unfractionated heparin (Heparin-Natrium,

Fig. 1 Diagnostic imaging from the work-up of suspected brainstem compression. CT (a) and MRI (b, c) showing a large, partially thrombosed VA aneurysm, compressing the adjacent pons. A DSA with contrast medium injected into

the right-hand VA showed exclusive supply of the right PICA (d). The contrast medium injected into the left-hand VA (e) confirmed a dissecting aneurysm of the V4 segment with a length of 23 mm and a width of 14 mm

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Vertebral Artery Aneurysm: Partially Thrombosed Dissecting Aneurysm, Symptomatic Through. . .

B. Braun) IV, 1 500 mg ASA (Aspirin i.v., Bayer Vital) IV Premedication: 1 300 mg ASA (Aspirin, Bayer Vital) PO, 1 180 mg ticagrelor (Brilique, AstraZeneca) PO, both given 5 days before the treatment as “loading dose.” After that 1 100 mg ASA (Aspirin, Bayer Vital) PO daily, 2 90 mg ticagrelor (Brilique, AstraZeneca) PO daily. A VerifyNow test (Accriva) confirmed platelet function inhibition from the ASA and ticagrelor (ARU 350, P2Y12 inhibition 45%, PRU 112, base 204). Access: right femoral artery, 6F long sheath (Stryker); Catalyst as a distal access catheter (Stryker); microguidewire, Transend 14 300 cm (Stryker). Implants: flow diverter: 1 Surpass Streamline 4/50, 1 Surpass Streamline 4/20 (both Stryker). Course of treatment: the left VA was catheterized with a 6F long sheath. A microguidewire was placed through the aneurysm in the left posterior cerebral artery. The first flow diverter was positioned from the basilar artery to the left vertebral artery. The size of the aneurysm and the foreshortening of the device upon deployment made complete coverage including the proximal stenosis impossible. A second flow diverter was telescopically deployed which allowed both the aneurysm and the stenosis to be completely covered. The final DSA run confirmed a delayed washout of the contrast medium from the aneurysm sac (Fig. 2). Duration: 1st–8th DSA run: 85 min; fluoroscopy time: 27 min Complications: none Postmedication: 1 100 mg ASA (Aspirin) PO daily lifelong, 2 90 mg ticagrelor (Brilique) PO daily for one year, 3 4 mg dexamethasone (Fortecortin, Merck Serono) PO daily for 4 days, followed by dexamethasone 3  2 mg for 8 days and after that 1  2 mg for 16 days.

Clinical Outcome The clinical condition of the patient remained unchanged after the treatment and during followup, with continuing gait disturbance and paresthesia of the upper extremities.

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Follow-up Examinations DSA and MRI follow-up examinations after 3 months and 12 months showed complete obliteration of the perfused component of the partially thrombosed aneurysm. Despite this, the thrombosed component of the aneurysm had not shrunk (Fig. 3).

Discussion Spontaneous dissection of the intradural segment of the vertebral artery is not rare. Further development is unpredictable, and the artery normalizing, a subarachnoid hemorrhage, stenosis, or the formation of an aneurysm are possible outcomes (Akiyama et al. 1996; Jung et al. 2016). Fusiform, partially thrombosed aneurysms of the V4 are mostly the aftermath of a previous dissection. A rupture with a subarachnoid hemorrhage (SAH) would usually be encountered in the acute dissection phase with a fusiform dilatation of the V4 segment (Kocaeli et al. 2009; Sasaki et al. 1991). In the chronic phase, while the possibility of an SAH remains a concern, issues from mass effect are far more frequent (Yoon et al. 2007). The most straightforward way to treat acute and chronic dissecting V4 aneurysms is through endovascular parent vessel occlusion (PVO) (Leibowitz et al. 2003; Naito et al. 2002). However, this treatment strategy requires a suitable contralateral vertebral artery or at least a posterior communication artery – P1 collateral, which can take on the task of supplying the entire posterior circulation. If this is not the case, PVO is unlikely to be tolerated. Prior to the availability of flow diverters, both stent-assisted coil occlusion of dissecting pseudoaneurysms and telescoping stenting had been advocated in reconstructive treatment (Sönmez et al. 2015). Flow diverters in general have been found to be useful in reconstructing dissected intracranial arteries (Fischer et al. 2012). The use of flow diverters to treat aneurysms located in the posterior circulation remains controversial. The large number of perforating and branching arteries of the posterior circulation potentially increases the risk in flow diversion, exposing patients to thromboembolic

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Fig. 2 DSA with contrast medium injected into the left VA during the endovascular treatment with the Surpass catheter in position (a), after deployment of the first (b) and second (c) Surpass Streamline flow diverter. The final DSA

run confirms that the aneurysm has been completely covered by the two flow diverters (d, e) with delayed washout of the contrast medium

complications and a potential brainstem stroke. Flow diverter treatment of giant, fusiform aneurysms of the vertebrobasilar junction or basilar trunk has been associated with high morbidity and mortality of up to 71% (Kiyofuji et al. 2017; Taschner et al. 2017). Despite some sobering experiences, flow diverter reconstruction of large and giant V4 aneurysms might be a viable option for carefully selected patients for whom PVO is not feasible. The complete separation of a large aneurysm from the blood circulation in its parent artery should induce shrinkage of said aneurysm (Mohammad et al. 2017). If this is not the case, a variety of reasons might be responsible. These

include incomplete interruption of blood circulation inside the aneurysm (e.g., due to an endoleak), calcification of the aneurysm wall, or the effect of vasa vasorum on the aneurysm wall. In such aneurysms, endothelialization can be delayed or not occur at all (Szikora et al. 2015). For the patient described above, the aneurysm wall calcifying was potentially the reason why the mass effect deriving from the aneurysm did not decrease. A follow-up MRI, however, showed that the saccular component of the dissecting aneurysm was not hemodynamically separated from the parent artery. This case confirms our previous experience that in large and giant

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Fig. 3 DSA and MRI follow-up examinations after flow diverter treatment of a dissecting left VA aneurysm. DSA 3 months after the endovascular treatment (a) confirmed the angiographic obliteration of the aneurysm and the patency of the left PICA. One year after the treatment, a DSA examination (b) showed a stable angiographic

obliteration of the aneurysm, but an MRI (c) revealed only a minor decrease in aneurysm diameter of about 2 mm. A comparison of unenhanced (d) and Gd-enhanced T1WI (e) showed persistent contrast enhancement of the aneurysm wall and inside the thrombus adjacent to the lumen of the left V4 segment

aneurysms, follow-up after flow diversion needs to include both DSA and an MRI. A plain and a contrast-enhanced T1WI is particularly helpful. Contrast enhancement of chronic dolichoectatic dissecting aneurysms on T1WI after angiographically confirmed aneurysm occlusion can be observed regularly during follow-up. This most likely is related to the inflammatory processes of the vessel wall or the organizing thrombus.

Stent Graft Telescoping Stents

Therapeutic Alternatives Parent Vessel Occlusion Stent Assisted Coiling

References Akiyama Y, Itoh T, Kumai J, Iwamuro Y, Miyake H, Nishikawa M. Vertebral artery dissection without subarachnoid hemorrhage studied by serial angiography. No Shinkei Geka. 1996;24(5):443–9. Fischer S, Vajda Z, Aguilar Perez M, Schmid E, Hopf N, Bäzner H, Henkes H. Pipeline embolization device (PED) for neurovascular reconstruction: initial experience in the treatment of 101 intracranial aneurysms and dissections. Neuroradiology. 2012;54(4):369–82. https://doi.org/10.1007/s00234-011-0948-x. Jung SC, Kim HS, Choi CG, Kim SJ, Kwon SU, Kang DW, Kim JS. Spontaneous and unruptured chronic

1070 intracranial artery dissection: high-resolution magnetic resonance imaging findings. Clin Neuroradiol. 2016. Kiyofuji S, Graffeo CS, Perry A, Murad MH, Flemming KD, Lanzino G, Rangel-Castilla L, Brinjikji W. Metaanalysis of treatment outcomes of posterior circulation non-saccular aneurysms by flow diverters. J Neurointerv Surg. 2017. pii: neurintsurg-2017013312. https://doi.org/10.1136/neurintsurg-2017013312. Kocaeli H, Chaalala C, Andaluz N, Zuccarello M. Spontaneous intradural vertebral artery dissection: a singlecenter experience and review of the literature. Skull Base. 2009;19(3):209–18. https://doi.org/10.1055/s0028-1114296. Leibowitz R, Do HM, Marcellus ML, Chang SD, Steinberg GK, Marks MP. Parent vessel occlusion for vertebrobasilar fusiform and dissecting aneurysms. AJNR Am J Neuroradiol. 2003;24(5):902–7. Mohammad LM, Coon AL, Carlson AP. Resolution of giant basilar artery aneurysm compression and reversal of sensorineural hearing loss with use of a flow diverter: case report. J Neurosurg Pediatr. 2017;20(1):81–5. https://doi.org/10.3171/2016.9.PEDS16428. Naito I, Iwai T, Sasaki T. Management of intracranial vertebral artery dissections initially presenting without subarachnoid hemorrhage. Neurosurgery. 2002;51 (4):930–7. discussion 937–8

M. Irizoiu et al. Sasaki O, Ogawa H, Koike T, Koizumi T, Tanaka R. A clinicopathological study of dissecting aneurysms of the intracranial vertebral artery. J Neurosurg. 1991;75 (6):874–82. Sönmez Ö, Brinjikji W, Murad MH, Lanzino G. Deconstructive and reconstructive techniques in treatment of vertebrobasilar dissecting aneurysms: a systematic review and meta-analysis. AJNR Am J Neuroradiol. 2015;36(7):1293–8. https://doi.org/10.3174/ajnr. A4360. Szikora I, Turányi E, Marosfoi M. Evolution of flowdiverter endothelialization and thrombus organization in giant fusiform aneurysms after flow diversion: a histopathologic study. AJNR Am J Neuroradiol. 2015;36(9):1716–20. https://doi.org/10.3174/ajnr. A4336. Taschner CA, Vedantham S, de Vries J, Biondi A, Boogaarts J, Sakai N, Lylyk P, Szikora I, Meckel S, Urbach H, Kan P, Siekmann R, Bernardy J, Gounis MJ, Wakhloo AK. Surpass flow diverter for treatment of posterior circulation aneurysms. AJNR Am J Neuroradiol. 2017;38(3):582–9. https://doi.org/ 10.3174/ajnr.A5029. Yoon W, Seo JJ, Kim TS, Do HM, Jayaraman MV, Marks MP. Dissection of the V4 segment of the vertebral artery: clinicoradiologic manifestations and endovascular treatment. Eur Radiol. 2007;17(4):983–93.

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Vertebral Artery Aneurysm: Stent-Assisted Coil Occlusion, Early Reperfusion, ASA/Metamizol Interaction with Poorly Controlled Platelet Function Inhibition, p64 Implantation, Aneurysm Reperfusion and Thrombus-Related Inflammation, Telescoping PED Implantation and Anti-Inflammatory Medication, Angiographic Exclusion of the Aneurysm, Regression of the Inflammation and Good Clinical Outcome Cindy Richter, Karl-Titus Hoffmann, Katharina Köhlert, Ulf Quäschling, and Stefan Schob Abstract

A 58-year-old female patient was diagnosed with an incidental aneurysm of the left vertebral artery (VA) adjacent to the origin of the posterior inferior cerebellar artery (PICA). The

C. Richter Cindy Richter Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany Abteilung für Neuroradiologie, Universitätsklinikum Leipzig, Leipzig, Germany e-mail: [email protected] K.-T. Hoffmann · U. Quäschling · S. Schob (*) Abteilung für Neuroradiologie, Universitätsklinikum Leipzig, Leipzig, Germany e-mail: [email protected]; [email protected]; schob. [email protected] K. Köhlert Klinik für Neurochirurgie, Universitätsklinikum Leipzig, Leipzig, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_52

wide-necked saccular aneurysm was partially thrombosed and exerted a minor space occupying effect on the brain stem. Stent-assisted coil occlusion was followed by a major recurrent perfusion of the aneurysm 6 months later. After a further 19 months, the reperfusion of the aneurysm had further increased. When the intended p64 flow diverter (FD) was implanted, the aneurysm was found to be almost entirely thrombosed. This was most likely related to the intake of metamizole, which undermines the ability of acetylsalicylic acid (ASA) to inhibit platelet function. Just 3 months after implanting the p64 flow diverter (FD), another significant reperfusion of the aneurysm was observed. In the meantime, the patient had continued occasional taking of metamizole, but now mostly separate from ASA. In addition, a significant perianeurysmal inflammatory reaction and contrast enhancement of the aneurysm wall was observed. 1071

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Almost 5 months after implanting the p64, a PED Flex FD was telescopically deployed into the left V4 segment. This second FD, alongside anti-inflammatory medication, led to the aneurysm being excluded from blood circulation. The thrombus-induced inflammation of the aneurysm wall and the adjacent brain stem ceased. The interaction of ASA and metamizole in the context of treating aneurysms by flow diversion is the main topic of this chapter.

C. Richter et al.

Diagnostic Imaging This 58-year-old female patient presented with a persistent headache, poorly responsive to conventional analgesic medication. As part of the diagnostic work-up, a cranial MRI examination was performed which showed an incidental aneurysm of the left vertebral artery. Said aneurysm was partially thrombosed with minor displacement of the pons and the medulla oblongata (Fig. 1).

Keywords

Vertebral artery · Metamizole · Acetylsalicylic acid · Platelet inhibition · p64 · PED Flex · Inflammation

Treatment Strategy

A 58-year-old woman, otherwise healthy, with an incidental aneurysm of the left vertebral artery arising from the PICA orifice.

The goal of the treatment was to prevent the aneurysm growing further and rupturing. Its size had already impacted upon and displaced the ponto-medullary junction. The morphology of this incidental saccular aneurysm appeared suitable for stent-assisted coil occlusion; since the neck of the aneurysm was wide, it was anticipated

Fig. 1 MRI examination of a patient with a mid-size VA aneurysm. The transversal constructive interference in steady state (CISS) image (a) shows a minor displacement of the brainstem due to the partially thrombosed aneurysm,

confirmed by sagittal T2 weighted imaging (b). TOF MRA (c) demonstrates the wide-necked, cranially oriented saccular aneurysm of the left V4 segment adjacent to the PICA origin

Patient

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Vertebral Artery Aneurysm: Stent-Assisted Coil Occlusion, Early Reperfusion, ASA/Metamizol. . .

that the coil could be protruded into the parent vessel without a stent.

Treatment Procedure #1, 19.08.2015: endovascular stentassisted coil occlusion of an incidental left VA (V4) aneurysm arising from the origin of the PICA Anesthesia: general anesthesia; 5000 IU unfractionated heparin (Heparin-Natrium, B. Braun) IV after securing the femoral sheath, rinsing solution with 1000 IU heparin IA per liter Premedication: 1
300 mg clopidogrel PO and 1
500 mg ASA (Aspirin, Bayer Vital) PO as a loading dose 24 h prior to the intervention; 1
75 mg clopidogrel (Clopidogrel Zentiva 75 mg, Zentiva Pharma) PO and 1
100 mg ASA PO 4 h prior to the intervention Access: right common femoral artery, 1
6F sheath (Terumo); guide catheter: 1
6F Envoy (Codman); 1
5F vertebral catheter 125 cm (Cordis); microcatheters: stenting: 1
Prowler select plus (Codman); coiling: 1
Excelsior SL10 (Stryker); microguidewire: 1
Traxcess 1400 200 cm (MicroVention) Implants: 20 coils: 1
Target 360 Standard 5/15; 18
Target 360 Ultra: 2
5/15, 2
5/10, 1
4/10, 3
4/8, 4
4/6, 3
3/8, 3
3/6 (Stryker); 1
Deltapaq 4/6 (then Codman, now Cerenovus); 1 stent: Enterprise2 4/23 mm (then Codman, now Cerenovus) Course of treatment: A DSA examination covering all intracranial vessels was performed. The injection of the left vertebral artery revealed the wide-necked saccular aneurysm (neck 4 mm, fundus width 6 mm, fundus depth 11 mm) arising from the PICA orifice. The guide catheter was placed in the distal V2 segment. A working projection showing the entire aneurysm sac including the neck plane was selected. A Prowler select plus microcatheter was placed distally to the aneurysm in the basilar artery for stent deployment. The aneurysm was catheterized with an Excelsior SL-10 microcatheter. The coil occlusion procedure was started, preserving the PICA origin,

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and continued, until a coil loop prolapsed into the vertebral artery. As a consequence, an Enterprise2 stent had to be put in place to protect the parent vessel and provide scaffolding for the coils. Coiling was then continued until the final DSA run showed complete occlusion of the aneurysm and uncompromised opacification of the left PICA (Fig. 2). Duration: 1st–25th DSA run: 300 min; fluoroscopy time: 71 min Complications: none Postmedication: 1
75 mg clopidogrel PO daily for 6 months, 1
100 mg ASA PO daily for life

Follow-up and Subsequent Treatments The follow-up DSA at 6 months revealed a significant recurrent perfusion of the previously coil occluded vertebral artery aneurysm (8
5 mm), accompanied by loosening and displacement of the coils (Fig. 3). Further treatment using extra-aneurysmal flow diversion was considered a viable therapeutic option. However, due to the patient’s hesitation, 19 months passed before the patient presented again. A DSA was performed to re-assess the state of the aneurysm, showing further growth accompanied by enhanced loosening and dislocation of the coil package (Fig. 4). It was imperative that the aneurysm be retreated.

Treatment Procedure #2, 06.11.2017: implantation of a p64 FD into the stent-bearing segment of the left vertebral artery Anesthesia: general anesthesia; 5000 IU unfractionated heparin IV after securing the femoral sheath, rinsing solution with 1000 IU unfractionated heparin IA per liter Premedication: 1
180 mg ticagrelor and 1
100 mg ASA the night before the procedure, from the day of the procedure 2
90 mg ticagrelor (1-01) and 1
100 mg ASA PO daily

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Fig. 2 Initial DSA and stent-assisted coil occlusion of a left-hand side V4 aneurysm. Posterior-anterior view of the pretreatment injection (a) of the left vertebral artery shows the aneurysm involving the PICA orifice (magnified view (b)). The working projection (b) for stent-assisted coiling

showing the Enterprise2 stent, which was used to prevent coil dislocation into the parent artery (c). The postprocedural injection (d) demonstrates sufficient occlusion of the aneurysm with uncompromised patency of the vertebral artery and the PICA

Access: right common femoral artery, 1
8F sheath (Terumo); guide catheter: 1
6F Neuron MAX (Penumbra); intermediate catheter: 1
6F SOFIA 115 cm (MicroVention); 1
5F vertebral catheter 125 cm (Cordis); microcatheters: 1
Excelsior SL-10 (Stryker) and 1
Excelsior XT27 (Stryker); microguidewire: 1
Transend 14 ex platinum 205 cm (Stryker) Implants: flow diverter: p64 4/21 mm (phenox) Course of treatment: The injection of the left VA, 1 month after the previous DSA, showed a

significant reduction of the previously observed recurrent perfusion of the V4 aneurysm, indicating sudden (and unexpected) subtotal intraaneurysmal thrombus formation. Upon inquiry it became obvious that the patient had been taking analgesic medication (1–2 g metamizole PO daily) for on-going severe neck pain over the last few weeks, which most likely undermined the ASA’s ability to inhibit platelets clotting, causing intra-aneurysmal thrombosis. Since this thrombosis was not considered a stable aneurysm

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Fig. 3 Follow-up DSA 6 months after the initial treatment shows significant recurrent perfusion of the aneurysm (a), loosening and migration of the coil mesh (b). A proposed

continuation of the treatment with extra-aneurysmal flow diversion was not immediately accepted by the patient

Fig. 4 Due to the patient’s hesitation, re-treatment was not performed for an additional period of 19 months. Subsequent follow-up DSA revealed further progress of the

recurrent aneurysm perfusion (a). Magnified views (b, c) show the loosening and displacement of the coil mesh

occlusion, the intervention was continued. The guide catheter was placed in the left distal V2 segment and the intermediate catheter was used to probe the Enterprise2 stent. A microcathetermicroguidewire combination was then advanced to the distal basilar artery and a p64 FD was deployed telescopically within the Enterprise2 stent (Fig. 5). Duration: 1st – 20th DSA run: 60 min; fluoroscopy time: 13 min Complications: none

Postmedication: 2
90 mg ticagrelor PO daily for 12 months, 1
100 mg ASA PO daily for life

Follow-up and Subsequent Treatment An MRI examination of the head was performed and showed a thrombotic occlusion of the aneurysm sac and a significant contrast enhancement of the aneurysm wall as a correlate of mural, thrombus-induced inflammation. The space

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Fig. 5 DSA with injection of the left VA in posterioranterior view (a) shows remarkable reduction of the aneurysm reperfusion 4 weeks after the follow-up DSA shown in Fig. 4. In the meantime metamizole had been prescribed to be taken on demand by the primary care physician for persistent neck pain. Metamizole taken at the same time as

ASA is known to interfere with ASA-induced platelet function inhibition. This was the most likely cause for the subtotal thrombosis of the recurrent aneurysm. A p64 FD was deployed into the stent-bearing segment of the left vertebral artery. Note the suspension of the aneurysmal perfusion after the FD implantation (b)

Fig. 6 MRI performed 7 days after the FD implantation. The patient continued the intake of metamizole against advice. An MRI shows growth of the predominantly

thrombosed aneurysm (a) accompanied by significant thrombus-related contrast enhancement on T1WI (b)

occupying effect of the aneurysm had meanwhile increased in comparison to the initial MRI examination (Fig. 6). Hence, a combination of platelet inhibition and anti-inflammatory medication was prescribed: 1
100 mg ASA PO daily for life, 2
90 mg ticagrelor (1-0-1) PO daily for 12 months, 2
3000 IU certoparin (Mono-Embolex, Aspen) SC daily during in-patient care, 3
4 mg dexamethasone (Fortecortin, Merck Serono) PO daily for 10 days and afterwards reduced gradually, 2


150 mg ranitidine (Ranitidin 150, 1A Pharma) PO daily, gradually reduced according to the dexamethasone intake, 1
200 mg celecoxib (Celecoxib, Heumann Pharma) for 6 weeks. The follow-up DSA 3 months after the p64 implantation again revealed a massive recanalization and growth of the formerly thrombosed part of the aneurysm (Fig. 7). The patient admitted occasionally taking metamizole (1–2 g for some days) PO, mostly together with her other medication, while taking ASA and

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Fig. 7 DSA 3 months after the implantation of a p64 FD. Posterior-anterior projection (a), an oblique view (b) and a 3D rotational DSA (c) at 3 months follow-up after the p64 implantation show massive recanalization and further growth of the formerly thrombosed vertebral artery

aneurysm under continuation of the metamizole medication and dual platelet inhibition. As a consequence, another endovascular treatment with an additional flow diverter was proposed to the patient

Fig. 8 The patient had been continuing to occasionally take metamizole against advice for analgesic reasons. However, she had changed her habits and was now generally taking ASA and metamizole separately from each other. About 18 weeks after the p64 implantation, she complained of sudden dizziness, sensory disturbance, and

gait impairment. Immediate MRI including transversal T2w imaging (a) revealed further brain stem displacement and brain stem edema. A T1WI postcontrast (b) showed progressive peripheral thrombus-related transmural contrast enhancement, indicating an inflammatory reaction together with significant reperfusion of the aneurysm

ticagrelor for dual platelet function inhibition until the day before the DSA examination. Due to sudden dizziness, sensory impairment of the lower limbs, and weakness of the legs, an MRI examination was performed. A progressive brain stem edema with increased displacement of the brainstem was encountered. T1 weighted postcontrast imaging indicated an inflammatory condition (Fig. 8). After achieving informed consent

and explicit explanation of the high-risk situation, a further FD implantation was scheduled.

Treatment Procedure #3, 26.03.2018: telescopic implantation of a PED into the p64 in the left vertebral artery

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Fig. 9 DSA prior to the implantation of the second FD – a PED Flex – once again shows a slightly decreased perfusion of the aneurysm sac (a). This might have been the consequence of an uncontrolled ASA/metamizole interaction with temporarily improved platelet function

inhibition. A PED Flex was implanted into the previously placed p64 (b) to increase the hemodynamic effect. The subsequent contrast injection of the left VA (c) confirmed a reduced aneurysm perfusion as a consequence of the synergistic effect of the two non-matching FDs

Anesthesia: general anesthesia; 5000 IU unfractionated heparin IV after securing the femoral sheath, rinsing solution with 1000 IU heparin IA per liter Premedication: 2
90 mg ticagrelor (1-0-1) PO and 1
100 mg ASA PO daily Access: right common femoral artery, 1
8F sheath (Terumo); guide catheter: 1
6F Neuron MAX (Penumbra); 1
5F vertebral catheter 125 cm (Cordis); intermediate catheter: 1
6F SOFIA 115 cm (MicroVention); microcatheter: 1
Phenom 0.02700 150 cm (Medtronic); microguidewire: 1
Traxcess 14 200 cm (MicroVention) Implant: flow diverter: Pipeline Embolization Device (PED) Flex (Medtronic) 4/25 mm Course of treatment: the third treatment started with a selective injection of the left vertebral artery, again demonstrating slightly decreased aneurysmal perfusion (6
8 mm) as a consequence of temporarily improved platelet function inhibition. The telescoping Enterprise2 and p64 construct appeared as expected. After positioning the guide catheter in the distal V2 segment, the p64 was carefully catheterized via the intermediate catheter in order to place the tip of the inserted microcatheter-microguidewire combination in the proximal segment of the left posterior cerebral artery. Subsequently, a telescoping deployment of the PED Flex FD within the previously implanted p64 FD was performed. The final

DSA run already showed a reduction of the aneurysm perfusion as a sign of increased extraaneurysmal flow diversion and endovascular flow-redirection (Fig. 9). Duration: 1st – 18th DSA run: 40 min; fluoroscopy time: 18 min Complications: none Postmedication: The combination of platelet function inhibition and anti-inflammatory medication was continued as follows: 1
100 mg ASA PO daily for life, 2
90 mg ticagrelor (1-0-1) PO daily for 12 months, 2
3000 IU certoparin SC daily during in-patient care, 3
4 mg dexamethasone PO daily for 10 days and afterwards reduced gradually, concomitant 2
150 mg ranitidine PO daily reduced according to the tapering dexamethasone intake, 1
200 mg celecoxib for 6 weeks. The patient was repeatedly informed of the risks of continuing to take either metamizole or ibuprofen.

Follow-Up Examination An MRI/MRA examination including transversal T2WI (a), and sagittal T1WI (b) 6 weeks after the implantation of the PED as a second FD confirmed the regression of the inflammatory reaction and the exclusion of the aneurysm from blood circulation (Fig. 10).

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Fig. 10 MRI 6 weeks after the telescoping implantation of a PED Flex as a second FD. The patient had stopped taking metamizole. A follow-up MRI including transversal T2WI imaging (a) revealed decreasing brain stem

Clinical Outcome Dizziness, motor symptoms, and sensory symptoms improved shortly after the – so far – final intervention. The most recent routine clinical follow-up examination showed no neurological deficit (mRS 0).

Discussion The case impressively demonstrates potentially life-threatening interactions of metamizole with ASA given for platelet function inhibition during the course of complex endovascular treatment of an intracranial aneurysm. As reported previously, platelet inhibition is weakened in more than 90% of co-medication scenarios with metamizole (Polzin et al. 2013, 2015; Schmitz et al. 2017). As a consequence, metamizole administered for pain treatment at the same time as platelet function inhibiting drugs considerably increases the likelihood of thrombus-related complications. In our case, sudden and fluctuating thrombosis of the residual aneurysm sac occurred secondary to metamizole medication and caused wall inflammation, aneurysm growth, and compression of the

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displacement and lower brain stem edema. T1WI postcontrast imaging (b) showed significant reduction of the aneurysm perfusion and a partial resolution of the thrombus associated transmural inflammation

adjacent ponto-medullary junction, eventually resulting in startling neurological deficits. Also, it took considerably longer for the endovascular treatment to be a success. In a worst case scenario, a combination of predominantly thrombotic mural inflammation and secondary inflow with significant growth of the aneurysm may eventually lead to rupture and subarachnoid hemorrhage – despite adequate initial endovascular therapy. Another probable outcome associated with undermined platelet inhibition is thrombotic occlusion of the vessel segment which carries the flow diverter-in stent construct, resulting in ischemia of the dependent arterial territory and – ultimately – disabling or even lethal cerebral ischemia. Therefore, medication with nonsteroidal antiinflammatory drugs (NSADs) like metamizole or ibuprofen must be strictly avoided in the context of platelet function inhibition necessitated by recent implantation of stents or FD in the cerebral vasculature. Another relevant aspect of this report is the possible escalation strategy of endovascular treatment in case of early aneurysm recurrence after stent assisted coiling with braided FD. In many patients, stent assisted coil occlusion performed with braided stents results in permanent occlusion

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of the aneurysm and does not require repeated interventions (Sedat et al. 2018; Voigt et al. 2017). However, especially complicating circumstances, as present in our case, may cause reperfusion despite successful initial treatment and necessitate rather early re-treatment in combination with complex pharmacotherapy to control uncommonly dynamic courses of recurrent aneurysms. As braided FDs are composed of a densely braided mesh, re-coiling through a previously implanted FD is technically impossible. Therefore, only extra-saccular options remain open. We decided to continue the endovascular therapy by implanting a p64, an effective FD consisting of 64 tightly braided nitinol wires (Fischer et al. 2015). As demonstrated above, the initial success was excellent, but continued intermittent intake of metamizole alongside a dual platelet inhibition regime caused a hyperdynamic process with iterated early relapse – even after subsidiary FD implantation. Therefore, an additional escalation step became necessary. To further increase the flow diverting effect, we decided to deploy a Pipeline Embolization Device (PED Flex) into the previously implanted p64. The PED Flex is a second generation flow diverter composed of 48 strands consisting of 75% cobalt chromium and 25% platinum alloy (Fischer et al. 2012). This has a different geometry to a p64, thus creating an overlapping, synergistic mesh that covers the aneurysm neck and enhances extra-saccular flow redirection. Conclusively, overlapping nonmatching flow diverters may offer a successful add-on strategy for difficult cases of previously treated, directly inaccessible aneurysms (Xu et al. 2015).

Therapeutic Alternatives Derivo FRED Parent Vessel Occlusion Stent Graft

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Surpass Telescoping Flow Diverters Telescoping Stents

References Fischer S, Vajda Z, Aguilar Perez M, Schmid E, Hopf N, Bäzner H, Henkes H. Pipeline embolization device (PED) for neurovascular reconstruction: initial experience in the treatment of 101 intracranial aneurysms and dissections. Neuroradiology. 2012;54(4):369–82. https://doi.org/10.1007/s00234-011-0948-x. Fischer S, Aguilar-Pérez M, Henkes E, Kurre W, Ganslandt O, Bäzner H, Henkes H. Initial experience with p64: a novel mechanically detachable flow diverter for the treatment of intracranial saccular sidewall aneurysms. AJNR Am J Neuroradiol. 2015;36 (11):2082–9. https://doi.org/10.3174/ajnr.A4420. Polzin A, Zeus T, Schrör K, Kelm M, Hohlfeld T. Dipyrone (metamizole) can nullify the antiplatelet effect of aspirin in patients with coronary artery disease. J Am Coll Cardiol. 2013;62(18):1725–6. https://doi.org/10.1016/ j.jacc.2013.07.039. Polzin A, Richter S, Schrör K, Rassaf T, Merx MW, Kelm M, Hohlfeld T, Zeus T. Prevention of dipyrone (metamizole) induced inhibition of aspirin antiplatelet effects. Thromb Haemost. 2015;114(1):87–95. https:// doi.org/10.1160/TH14-11-0922. Schmitz A, Romann L, Kienbaum P, Pavlaković G, Werdehausen R, Hohlfeld T. Dipyrone (metamizole) markedly interferes with platelet inhibition by aspirin in patients with acute and chronic pain: a case-control study. Eur J Anaesthesiol. 2017;34(5):288–96. https:// doi.org/10.1097/EJA.0000000000000581. Sedat J, Chau Y, Gaudart J, Sachet M, Beuil S, Lonjon M. Stent-assisted coiling of intracranial aneurysms using LEO stents: long-term follow-up in 153 patients. Neuroradiology. 2018;60(2):211–9. https://doi.org/ 10.1007/s00234-017-1965-1. Voigt P, Schob S, Jantschke R, Nestler U, Krause M, Weise D, Lobsien D, Hoffmann KT, Quäschling U. Stent-assisted coiling of ruptured and incidental aneurysms of the intracranial circulation using moderately flow-redirecting, braided Leo stents – initial experience in 39 patients. Front Neurol. 2017;8:602. https:// doi.org/10.3389/fneur.2017.00602. Xu J, Wu Z, Yu Y, Lv N, Wang S, Karmonik C, Liu JM, Huang Q. Combined effects of flow diverting strategies and parent artery curvature on aneurysmal hemodynamics: a CFD study. PLoS One. 2015;10(9):e0138648. https://doi.org/10.1371/journal. pone.0138648.

Vertebral Artery Aneurysm: Ruptured Dissecting Aneurysm, Implantation of Telescoping p48MW HPC Flow Diverter Stents Under Antiaggregation with ASA Only

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Frances Colgan, Marta Aguilar Pérez, Victoria Hellstern, Matthias Reinhard, Stefan Krämer, Hansjörg Bäzner, Oliver Ganslandt, and Hans Henkes Abstract

A 66-year-old male patient sustained blunt trauma to the head and neck during a seizure

F. Colgan Department of Radiology, University of Otago, Christchurch Hospital, Christchurch, New Zealand e-mail: [email protected] M. Aguilar Pérez · H. Henkes (*) Neuroradiologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; [email protected] V. Hellstern Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected]; victoria. [email protected] M. Reinhard Klinik für Neurologie und klinische Neurophysiologie, Klinikum Esslingen, Esslingen, Germany e-mail: [email protected] S. Krämer Klinik für Radiologie und Nuklearmedizin, Klinikum Esslingen, Esslingen, Germany e-mail: [email protected] H. Bäzner Neurologische Klinik, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] O. Ganslandt Neurochirurgische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_80

following alcohol withdrawal. Two days later, he developed massive subarachnoid hemorrhage (SAH) and was found to have a ruptured left vertebral artery dissecting aneurysm (V4 segment). He was successfully treated with the insertion of telescoping p48MW HPC flow diverter stents under monoantiplatelet therapy and made a full recovery. Flow diverter stents offer a possibility for effective treatment in intracranial hemorrhage in the absence of other clinically viable options or as an alternative to parent vessel occlusion. The usage of flow diverter stents with reduced thrombogenicity due to hydrophilic surface coating is the main topic of this chapter. Keywords

Vertebral artery · Dissecting aneurysm · Subarachnoid hemorrhage, SAH · p48MW HPC Flow diversion · Hydrophilic coating · ASA only

Patient A 66-year-old male patient with hypercholesterolaemia but no other significant medical history was admitted to a community hospital after a seizure with blunt trauma to the head and neck. Three previous seizures were reported, 15 years, 1 year, and 6 weeks previously, and 1081

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two of these were related to train journeys and sleep deprivation. Neurological examination and routine blood testing were within normal limits. The patient reported significant alcohol intake and was treated with a B12 infusion. Further investigations for seizures performed over the next 48 h were also unremarkable. The patient reported some neck pain, but plain radiographs demonstrated no fracture. He was treated for seizures without defined underlying cause, with sleep deprivation and regular alcohol consumption as possible trigger factors. He was commenced on lamotrigine and an MRI was planned. On the afternoon of the second day after the head trauma, the patient complained about severe sudden headache. He presented neck stiffness before he lost consciousness. A CT examination of his head revealed a massive subarachnoid hemorrhage (SAH). Instantaneous intubation and ventilation and an emergent ventricular drain were required.

Diagnostic Imaging A non-contrast CT (NCCT) performed on admission was unremarkable. Before the MRI could be performed, the patient developed increasingly severe headache, arm tremors and signs of meningism, and lost consciousness thereafter. CT was immediately performed and demonstrated acute large volume SAH with early hydrocephalus (Fisher 4). The patient was intubated and ventilated and was transferred to our center (Fig. 1).

Treatment Strategy Upon arrival, bilateral external ventricular drains (EVD) were inserted. The goal of the treatment was to prevent a recurrent hemorrhage from the dissected left V4 segment. Several options were contemplated, including conservative management, coil occlusion of the dissected vessel segment, stabilizing this artery with a single or telescoping self-expanding stent(s) or the deployment of a one or more flow diverter stent(s). Concerning the flow diversion option, the usage

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of implants with a surface with reduced thrombogenicity was also considered. The issue of conservative management was the high risk of a recurrent hemorrhage. The anticipated drawback of a parent vessel occlusion was the possible development of post-hemorrhagic vasospasm, which could also affect the remaining right V4 segment, resulting in a severe compromise of the blood supply to brain stem and cerebellum after the left V4 segment had been occluded. The main argument in the balance of self-expanding stent (s) versus flow diverter(s) was the fact that the expected vessel wall protection was more effective with a flow diverter due to the reduced porosity. Both implants would have required dual platelet function inhibition to prevent thrombus formation on the device surface with the risk of device occlusion and distal emboli. The use of a flow diverter with low thrombogenicity, which would have allowed a reduced antiaggregation medication, appeared as the most promising treatment strategy to us. After extensive multidisciplinary discussions and consent of the patient’s wife, a decision was made to proceed with compassionate use of the hydrophilic coated flow diverter stents.

Treatment Procedure, 26.01.2018: endovascular treatment of a ruptured left V4 dissecting aneurysm with overlapping flow diverter stents with hydrophilic surface coating under ASA only Anesthesia: general anesthesia Premedication: on the day prior to the procedure, Multiplate (Roche Diagnostics) and VerifyNow (Accrive) tests showed no platelet function inhibition; 1 500 mg ASA (Aspirin i.v. 500 mg, Bayer Vital) IV were given 20 h prior to the start of the procedure; Multiplate and VerifyNow 15 h after the ASA administration and 5 h prior to the procedure confirmed the ASA effect on the platelet function. Access: bilateral common femoral artery; sheaths: right 6F, left 4F (Terumo); diagnostic and guide catheters: Tempo4 vertebral catheter (Cordis), 6F Heartrail II (Terumo); microcatheter:

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Vertebral Artery Aneurysm: Ruptured Dissecting Aneurysm, Implantation of Telescoping. . .

Trevo Pro 18 Microcatheter (Stryker); microguidewire: pORTAL 14 (phenox) Flow diverters: 2 p48MW HPC 3/18 (phenox) Course of treatment: the left vertebral artery was catheterized and angiography performed, confirming the left V4 dissection. A microguidewire was advanced with the aid of a microcatheter and two overlapping p48MW HPC stents were inserted. The final DSA run demonstrated adequate stent placement with some residual

Fig. 1 (continued)

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contrast stagnation within the dissection. During the observation, no thrombus formation was observed (Fig. 2). Due to the hydrophilic coating of the flow diverter surface, their thrombogenicity is significantly reduced, allowing their implantation under single antiplatelet medication with ASA only. Duration: 1st–7th DSA run: 139 min; fluoroscopy time: 33 min Complications: none

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Fig. 1 (continued)

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Fig. 1 (continued)

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Fig. 1 (continued)

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Post medication: After the procedure, the patient returned to the ICU intubated and ventilated and was commenced on a daily dose of 500 mg + 250 mg ASA IV daily. On the second day, the dosage was reduced to 500 mg ASA IV daily, which turned out to be insufficient based on the above-mentioned response tests. Since Aspirin i.v. 500 mg (Bayer Vital) was on backorder, 1000 mg Flectadol (Vademecum) IV and 500 mg Aspirin i.v. 500 mg were given on day 3 to 7, with adequate response confirmed in the above-mentioned tests. From there on 2 500 mg ASA IV daily was given. Monitored with frequent response tests, the ASA dosage was gradually reduced to 2 100 mg ASA PO daily over the following 6 weeks.

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Follow-Up Examinations An early follow-up DSA and a CTA examination were carried out 6 days and 10 days after the treatment, respectively. They showed that the dissection had meanwhile not increased, the perfusion around the outer surface of the flow diverters had almost entirely stopped, and there was no visible thrombus formation inside of the flow diverters nor emboli distal to them (Fig. 3). Angiography and MRI performed 7 months after the initial flow diverter procedure demonstrated patent bilateral vertebral arteries and the flow diverter stents without evidence of in-stent stenosis. MRI showed no further ischemic insult of brain stem, cerebellum, or posterior cerebral artery supply territory (Fig. 4).

Clinical Outcome Discussion The postoperative course was complicated by tracheobronchitis, hyponatremia, and an episode of tachyarrhythmia treated with beta-blockade but was otherwise unremarkable. EVDs were removed 15 days after the stenting procedure under ASA. The patient subsequently developed recurrent hydrocephalus necessitating the insertion of a ventriculo-peritoneal shunt. This operation was performed under ASA 1 month after the SAH without issues. The patient was discharged to a rehabilitation facility 43 days after initial presentation. At this time, he was not fully oriented, mentally slow, and physical examination showed a resolving paresis of his left arm. He presented for a follow-up examination 8 months after the treatment without a neurological deficit.

Traumatic vertebral artery dissection is an infrequent but well-recognized complication of blunt and penetrating trauma to the head and cervical spine (Fusco and Harrigan 2011; Mohan 2014) and is associated with significant morbidity (Majidi et al. 2014). Dissections occurring in the extracranial segments, particularly V1 and V3, carry a risk of embolic stroke and those occurring in the intra-dural segment of V4 carry an additional risk of subarachnoid hemorrhage in the event of rupture (Ali et al. 2012). First-line management options for uncomplicated traumatic vertebral artery dissection include antithrombotic therapy, with platelet aggregation inhibitors or anticoagulation (Harrigan et al. 2013). Endovascular and surgical interventions are

ä Fig. 1 NCCT after a seizure with blunt trauma to the head and neck. The first CT examination hours after the trauma was essentially within normal limits, especially concerning the distal vertebral arteries (a–c). A second NCCT examination was carried out 2 days later, after the clinical condition of the patient had deteriorated and revealed a massive SAH (d–f). A CTA (g–l) showed a fusiform dilatation of the left V4 segment due to a dissection. This dissecting aneurysm was considered the most likely cause of the SAH. The

following NCCT another 2 days later demonstrated blood around the brain stem and in both lateral ventricles but no apparent parenchymal damage (m, n). Diagnostic DSA was performed on the second day after the SAH and showed a normal right VA (o). The dissecting fusiform aneurysm of the left V4 segment was confirmed (maximum diameter 5.5 mm, a length of 8 mm) (p, q). This dissecting fusiform aneurysm was the most likely source of the SAH and became the target for the subsequent treatment

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Fig. 2 (continued)

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Fig. 2 (continued)

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Fig. 2 Endovascular treatment of a ruptured dissecting left V4 aneurysm by telescoping deployment of two p48MW HPC flow diverters. Catheterization of the left VA with a Trevo Pro 18 microcatheter and deployment of the first p48MW HPC 3/18 flow diverter (a). The right VA was injected to make sure that the vertebral artery junction was not covered (b). The injection of the left VA showed that the first p48MW HPC was in the right position distally. Due to the proximal foreshortening, the dissection was

only partially covered (c). A second p48MW HPC 3/18 was therefore implanted in a telescoping way (d). A magnified image shows that the dissecting aneurysm is now completely covered (e). A first DSA run after the implantation of both flow diverters (f) was followed by DSA runs after 16 min (g), 34 min (h), 56 min (i), 77 min (j), 94 min (k), and 113 min (l, m). Neither thrombus formation within the flow diverters nor distal emboli were observed

usually reserved for cases in which there is subarachnoid hemorrhage, compromised cerebral circulation, and recurrent thrombotic events despite optimal pharmacological management and/or aneurysmal expansion (Mohan 2014; Medel et al. 2014). Endovascular options have been well-described and encompass both deconstructive techniques and preservation of the parent vessel lumen when possible (Hernández-Durán and Ogilvy 2014; Medel et al. 2014). In the context of complicated vertebral artery dissection, these techniques have been demonstrated to be effective and relatively safe (Hernández-Durán and Ogilvy 2014). In the setting of acute SAH associated with V4 segment dissection, deconstructive techniques are usually employed as long as there is adequate collateralization of the posterior cerebral circulation (Hernández-Durán and Ogilvy 2014; Huang et al. 2009; Medel et al. 2014).

Recently, technological advances have led to the development of flow diverter stents, which are effective in the treatment of intracranial aneurysms including those of the posterior circulation (Becske et al. 2017; Kallmes et al. 2015, 2017; Yeung et al. 2012). However such flow diverter stents are associated with an increased risk of thromboembolic events and necessitate inhibition of platelet function (Saber et al. 2018). Aneurysm occlusion is not immediate after flow-diverter stent insertion and thus platelet inhibition carries a risk of bleeding in the event of aneurysm rupture (Briganti et al. 2015). However, in patients undergoing coiling of ruptured aneurysms, antiplatelet therapy has been demonstrated to be safe and effective in the reduction of thromboembolic events in patients considered highrisk patients for these events, without significantly increasing serious hemorrhagic complication (Edwards et al. 2017).

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Fig. 3 DSA 6 days (a, b) and CTA 10 days (c) after the flow diverter implantation into the dissected left V4 segment under ASA only. The fusiform aneurysm of the left V4 segment due to the dissection is still visible. Perfusion

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outside the implanted flow diverters has almost completely ceased and there is no visible thrombus formation in the vessel lumen

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Fig. 4 (continued)

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Fig. 4 Mid-term follow-up 7 months after the endovascular treatment of a dissecting aneurysm of the left V4 segment using two flow diverters with hydrophilic coating under ASA only. On DSA (a–c), the dissection is angiographically healed, the previous fusiform aneurysm is no longer visible. A digital radiograph shows that the

telescoping p48MW HPC flow diverters are intact (d). Contrast enhanced MRA (e) matches better than ToF MRA (f) with the angiographic finding. FLAIR MRI images show no ischemia-related changes of the brainstem and the cerebellum (g–i)

Recent advances in polymer coating technology and stent design have led to increased biocompatibility of flow-diverter stents (e.g., PED Shield; Medtronic). They reduce platelet aggregation in experimental situations (Girdhar et al. 2015; Marosfoi et al. 2018) and demonstrate short-term clinical safety, with further results awaited (Martínez-Galdámez et al. 2017). In animal models treated with antiplatelet monotherapy, the PED Shield displays faster endothelialization with comparable neointimal volume and less thrombus formation than with the PED Flex (Matsuda et al. 2018). Two reports of PED Shield insertion without effective dual antiplatelet therapy have been published. In the first, the PED Shield was used in the treatment of an AcomA aneurysm, with an intraprocedural aneurysm perforation. Postoperative platelet aggregometry was impaired, presumed due to

malabsorption. The patient was treated with single agent antiplatelet (ASA) owing to the large interhemispheric hematoma and indwelling EVD, with no reported thromboembolic or occlusive event at 30 days (Orlov et al. 2018). Another report describes a PED Shield stent inserted for ruptured dissection aneurysm after bolus dose of abciximab and subsequent treatment with single antiplatelet agent (Aspirin) with no stent occlusion or further embolic infarct at 6 weeks (Chiu et al. 2017). Successful use of flow modulating stents has been reported in the treatment of traumatic vertebral artery dissection in the extracranial vertebral artery; it is proposed that the small mesh size and the distal-to-proximal deployment result in thrombus trapping and reduces the risk of intraprocedural embolization (Cohen et al. 2013, 2016). Their use has also been described in the

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treatment of ruptured intracranial vertebral artery aneurysm (Ducruet et al. 2013; McAuliffe and Wenderoth 2012; Narata et al. 2012). In this situation, a flow-diverter stent was inserted to optimize the arterial supply to the posterior circulation. It was felt that it would not be in the patient’s interest to permanently occlude the left vertebral artery and off-licence treatment was agreed within the multidisciplinary team and by the family. To our knowledge, this is the first report of such a technique being described in the treatment of a ruptured intracranial vertebral artery dissection secondary to trauma. When considering stent insertion, the subsequent inhibition of platelet aggregation in our patient was considered in detail. In the event that the vertebral artery remained incompletely treated by the flowmodulating stent, this bleeding risk would persist. Furthermore, platelet aggregation in patients with acute subarachnoid hemorrhage is known to be impaired (Perez et al. 2018), which could lead to suboptimal platelet inhibition, risking stent thrombosis and distal embolization. The patient required high doses of aspirin to achieve inhibition of platelet aggregation, as is expected in the context of acute subarachnoid hemorrhage. The case demonstrates successful use of a flow-diverter stent in acute SAH secondary to traumatic vertebral artery dissection. In the context of acute intracranial hemorrhage, platelet anti-aggregation should be precisely controlled to minimize the risks of further bleeding and stent-associated embolic events.

Therapeutic Alternatives Parent Vessel Occlusion Pipeline Embolization Device, PED Stent Graft Telescoping Stents

References Ali MS, Amenta PS, Starke RM, Jabbour PM, Gonzalez LF, Tjoumakaris SI, Flanders AE, Rosenwasser RH, Dumont AS. Intracranial vertebral artery dissections:

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trauma. Neurosurgery. 2013;72(Suppl 2):234–43. https://doi.org/10.1227/NEU.0b013e31827765f5. Hernández-Durán S, Ogilvy CS. Clinical outcomes of patients with vertebral artery dissection treated endovascularly: a meta-analysis. Neurosurg Rev. 2014;37(4):569–77. https://doi.org/10.1007/s10143014-0541-y. Huang YC, Chen YF, Wang YH, Tu YK, Jeng JS, Liu HM. Cervicocranial arterial dissection: experience of 73 patients in a single center. Surg Neurol. 2009;72(Suppl 2):S20–7; discussion S27. https://doi. org/10.1016/j.surneu.2008.10.002. Kallmes DF, Hanel R, Lopes D, Boccardi E, Bonafé A, Cekirge S, Fiorella D, Jabbour P, Levy E, McDougall C, Siddiqui A, Szikora I, Woo H, Albuquerque F, Bozorgchami H, Dashti SR, Delgado Almandoz JE, Kelly ME, Turner R 4th, Woodward BK, Brinjikji W, Lanzino G, Lylyk P. International retrospective study of the pipeline embolization device: a multicenter aneurysm treatment study. AJNR Am J Neuroradiol. 2015;36(1):108–15. https://doi.org/ 10.3174/ajnr.A4111. Kallmes DF, Brinjikji W, Cekirge S, Fiorella D, Hanel RA, Jabbour P, Lopes D, Lylyk P, McDougall CG, Siddiqui A. Safety and efficacy of the pipeline embolization device for treatment of intracranial aneurysms: a pooled analysis of 3 large studies. J Neurosurg. 2017;127(4):775–80. https://doi.org/10.3171/2016.8. JNS16467. Majidi S, Hassan AE, Adil MM, Jadhav V, Qureshi AI. Incidence and outcome of vertebral artery dissection in trauma setting: analysis of national trauma data base. Neurocrit Care. 2014;21(2):253–8. https:// doi.org/10.1007/s12028-013-9937-8. Marosfoi M, Clarencon F, Langan ET, King RM, Brooks OW, Tamura T, Wainwright JM, Gounis MJ, Vedantham S, Puri AS. Acute thrombus formation on phosphorilcholine surface modified flow diverters. J Neurointerv Surg. 2018;10(4):406–11. https://doi. org/10.1136/neurintsurg-2017-013175. Martínez-Galdámez M, Lamin SM, Lagios KG, Liebig T, Ciceri EF, Chapot R, Stockx L, Chavda S, Kabbasch C, Farago G, Nordmeyer H, Boulanger T, Piano M, Boccardi EP. Periprocedural outcomes and early safety with the use of the pipeline flex embolization device with shield technology for unruptured intracranial aneurysms: preliminary results from a prospective clinical study. J Neurointerv Surg. 2017;9(8):772–6. https://doi.org/10.1136/neurintsurg-2016-012896. Matsuda Y, Jang DK, Chung J, Wainwright JM, Lopes D. Preliminary outcomes of single antiplatelet therapy

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for surface-modified flow diverters in an animal model: analysis of neointimal development and thrombus formation using OCT. J Neurointerv Surg. 2018. https://doi.org/10.1136/neurintsurg-2018-013935. pii: neurintsurg-2018-013935. McAuliffe W, Wenderoth JD. Immediate and midterm results following treatment of recently ruptured intracranial aneurysms with the pipeline embolization device. AJNR Am J Neuroradiol. 2012;33(3):487–93. https://doi.org/10.3174/ajnr.A2797. Medel R, Starke RM, Valle-Giler EP, Martin-Schild S, El Khoury R, Dumont AS. Diagnosis and treatment of arterial dissections. Curr Neurol Neurosci Rep. 2014;14(1):419. https://doi.org/10.1007/s11910-0130419-3. Mohan IV. Current optimal assessment and management of carotid and vertebral spontaneous and traumatic dissection. Angiology. 2014;65(4):274–83. https://doi. org/10.1177/0003319712475154. Narata AP, Yilmaz H, Schaller K, Lovblad KO, Pereira VM. Flow-diverting stent for ruptured intracranial dissecting aneurysm of vertebral artery. Neurosurgery. 2012;70(4):982–8; discussion 988–9. https://doi.org/ 10.1227/NEU.0b013e318236715e. Orlov K, Kislitsin D, Strelnikov N, Berestov V, Gorbatykh A, Shayakhmetov T, Seleznev P, Tasenko A. Experience using pipeline embolization device with shield technology in a patient lacking a full postoperative dual antiplatelet therapy regimen. Interv Neuroradiol. 2018;24(3):270–3. https://doi.org/ 10.1177/1591019917753824. Perez P, Lukaszewicz AC, Lenck S, Nizard R, Drouet L, Payen D. Platelet activation and aggregation after aneurysmal subarachnoid hemorrhage. BMC Neurol. 2018;18(1):57. https://doi.org/10.1186/s12883-0181062-z. Saber H, Kherallah RY, Hadied MO, Kazemlou S, Chamiraju P, Narayanan S. Antiplatelet therapy and the risk of ischemic and hemorrhagic complications associated with pipeline embolization of cerebral aneurysms: a systematic review and pooled analysis. J Neurointerv Surg. 2018. https://doi.org/10.1136/ neurintsurg-2018-014082. pii: neurintsurg-2018014082. Yeung TW, Lai V, Lau HY, Poon WL, Tan CB, Wong YC. Long-term outcome of endovascular reconstruction with the pipeline embolization device in the management of unruptured dissecting aneurysms of the intracranial vertebral artery. J Neurosurg. 2012;116(4):882–7. https://doi.org/10.3171/2011.12. JNS111514.

Vertebral Artery Aneurysm: Unruptured Dissecting Intradural Right Vertebral Artery Aneurysm with Brainstem Compression; Coil Occlusion of the Aneurysm and the Parent Artery with Resolution of the Mass Effect; Good Clinical Outcome with Long-Term Follow-up

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Hegoda Levansri Dilrukshan Makalanda, Sundip D. Udani, Grainne McKenna, Ken Wong, and Pervinder Bhogal Abstract

A 31-year-old female patient was suffering headaches, mainly occipital, for a year following childbirth. She presented with a 4-week history of spastic paresis on the right side (MRC 4/5) and paraesthesia down her left leg. An MRI scan demonstrated brainstem compression at the craniocervical junction secondary to an unruptured aneurysm of the V4 segment of the right vertebral artery (VA). A CTA confirmed a dilated intradural (V4) segment of the right VA with a multilobulated, fusiform, dissecting

H. L. D. Makalanda (*) · S. D. Udani · K. Wong Department of Interventional Neuroradiology, The Royal London Hospital, London, UK e-mail: [email protected]; [email protected]; [email protected] G. McKenna Department of Neurosurgery, The Royal London Hospital, London, UK e-mail: [email protected] P. Bhogal Department of Interventional Neuroradiology, The Royal London Hospital, London, UK

aneurysm, and a dominant right AICA-PICA. DSA further delineated the anatomy and demonstrated the right PICA to be originating from the caudal part of the aneurysm. Given the mass effect, a deconstructive treatment strategy was employed using a combination of coils and a detachable balloon. A follow-up MRI at 7 days confirmed successful right vertebral artery occlusion, with reduction in the mass effect on the brainstem. There was retrograde filling of the PICA territory via the right AICA with no sequelae of ischemia or infarction. Six-month MRI follow-up confirmed continued vessel occlusion and a further reduction in the size of the aneurysm. The current treatment options for a dissecting aneurysm along the vertebral artery is the main focus of this chapter. Keywords

Vertebral artery · Dissecting aneurysm · Endovascular treatment · Reconstructive techniques · Deconstructive techniques · Parent vessel occlusion · Flow diverter stents · Detachable Goldbal balloon

Neuroradiologische Klinik, Neurozentrum, Klinikum Stuttgart, Stuttgart, Germany e-mail: [email protected] © Springer Nature Switzerland AG 2020 H. Henkes et al. (eds.), The Aneurysm Casebook, https://doi.org/10.1007/978-3-319-77827-3_87

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Patient A 31-year-old, female patient presenting with a one-year history of headache following childbirth, 4/5 right-sided spastic paresis and left leg paraesthesia due to a multilobulated dissecting right V4 segment vertebral artery aneurysm.

Diagnostic Imaging MRI demonstrated brainstem compression at the craniocervical junction secondary to an unruptured aneurysm of the V4 segment of the right vertebral artery. CTA confirmed a multilobulated, fusiform, dissecting aneurysm arising from the right V4 segment of the vertebral artery with a dominant right AICA-PICA. DSA demonstrated the right PICA originating from the caudal extent of the aneurysm (Fig. 1). The anterior spinal artery was not visualized.

Treatment Strategy The goal of treatment was to exclude the aneurysm from the circulation and reduce the mass effect and pulsatility on the brainstem. Although flow diversion was considered, the potential for acute enlargement of the aneurysm due to thrombus formation following stent placement, resulting in potentially life-threatening brainstem compression, was felt to outweigh the potential benefits of vessel reconstruction.

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(Micrus); diagnostic catheter: 1 5F vertebral catheter (Cordis); 1 Hyperform balloon (ev3); microcatheter: 1 Excelsior SL-10 (Stryker); microguidewire: 1 Traxcess14 (MicroVention); balloon/microcatheter: 1 Goldbal balloon/ Baltacci (Balt Extrusion) Implants: 11 coils: Axium FX coils (ev3) Course of treatment: a 5F diagnostic vertebral catheter was positioned in the left vertebral artery to allow angiography during the procedure and to enable balloon test occlusion. Angiography of the right vertebral artery demonstrated a fusiform dissecting aneurysm of the V4 segment. The right PICA was originating from the caudal aneurysm. The SL-10/Traxcess combination was used to navigate through the aneurysm into the right V4 segment proximal to the vertebrobasilar junction, which appeared normal. Several Axium FX coils were deployed to occlude the vessel outflow. The catheter was then retracted into the V3 segment of the right vertebral artery and the vessel occluded with Axium FX coils and a detachable Goldbal balloon. The final DSA run confirmed satisfactory isolation of the right V4 with neither anterograde nor retrograde flow (Fig. 2). Bilateral 6F Angioseals were used to achieve hemostasis at the groin puncture sites. Duration: 1st–14th run: 118 min; fluoroscopy time: 41 min Complications: none Post medication: 24 h heparin IV, reducing steroid course 8 mg TDS PO daily for 4 days followed by 4 mg TDS PO daily for 1 week (to reduce perianeurysmal inflammation from thrombus formation).

Treatment Procedure, 31.12.2012: endovascular treatment of an unruptured dissecting right vertebral artery aneurysm using a deconstructive technique Anesthesia: general anesthesia; 7,000 IU unfractionated heparin IV Premedication: none Access: infiltration of 1% lidocaine followed by ultrasound guided puncture of bilateral common femoral arteries; 2 6F short sheath (Cordis); guide catheter: 1 6F Neuropath

Clinical Outcome The patient’s left sided paraesthesia improved, but the right arm and leg weakness persisted. She was provided further community input to help improve strength and functional use of her right hand, arm, and leg. She presented 5 years later with headache. The CT/CTA confirmed that the aneurysm remained excluded from circulation with no evidence of SAH.

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Fig. 1 Diagnostic imaging in a dissecting aneurysm of the right VA. MRI demonstrates significant mass effect on the brainstem (sagittal T1WI(a), magnified detail (b)). 3D CTA shows the multilobulated right V4 segment dissecting

aneurysm (c). DSA shows the right PICA originating from the caudal extent of the aneurysm (posterior anterior view (d), lateral view (e))

Follow-Up Examinations

Discussion

A repeat MRI at 7 days postprocedure confirmed successful right vertebral artery occlusion, with slight increase in the previously observed mass effect on the brainstem. The right PICA supply had been taken over by the right AICA with no ischemia or infarct. MRI at 6 months confirmed persistent vessel occlusion and significant reduction in size of the aneurysm (Fig. 3).

Dissecting aneurysms of the VA represent approximately 3.3% of all intracranial aneurysms (Lylyk et al. 2001). These lesions should not be underestimated as they are associated with a high morbidity and mortality. Whereas carotid dissections tend to occur in the second or third decades, vertebral artery dissections occur later, usually in the fourth decade (Schievink 2001).

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Fig. 2 DSA after endovascular coil occlusion of a dissecting aneurysm of the right VA (V4), demonstrating successful deconstruction and trapping of the right V4

segment and exclusion of the dissecting aneurysm from the circulation (a, b)

The most commonly involved segments are V1 and V3, presumably due to their relative mobility. Our patient had disease involving the intradural V4 segment, which is much less common. A histological analysis of the VA showed that the intima thins after the origin of the PICA and that defects in the internal elastic lamina are more frequently related to the vertebral artery before penetration of the dura mater and near the branching of the PICA (Sato et al. 2004). This would be consistent with the clinical observation of the location of VA dissections and also in our patient who had involvement of the PICA origin. Dissecting VA aneurysms can lead to significant morbidity and mortality by three main mechanisms – ischemia, hemorrhage, and compression. Like other aneurysms, they are at risk of rupture. The intradural vertebral artery aneurysm is more susceptible to rupture than the extradural segments. This is because the intradural segment has a thinner adventitia, fewer elastic fibers in the media, it lacks an external elastic lamina and

has a thicker internal elastic lamina (SantosFranco et al. 2008; Halbach et al. 1993; Ramgren et al. 2005). Rupture of an intradural vertebral artery aneurysm can result in massive SAH and serious neurological deficit. Due to the critical location of the dissecting V4 aneurysms, hemorrhage can result in occlusion of the foramen of Magendie and Luschkae or the cerebral aqueduct leading to acute obstructive hydrocephalus (Pan et al. 2016). The rate of further rebleeding has been shown to be 30% (Ramgren et al. 2005) and as high as 58% (Yamada et al. 2004). A rebleeding rate of 57% has been reported within the first week after an initial bleed (Mizutani et al. 1995). It should be remembered that the walls of these particular subtypes of aneurysms are extremely thin and provide one explanation of the observed high re-rupture frequency and hence significant morbidity and mortality. The second cause of their significant morbidity and mortality is again related to their location near the brainstem. It has been shown that the risk of

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Fig. 3 Follow-up MRA at 7 days confirmed exclusion of the right VA from the circulation (TOF (a)) with a slightly increased mass effect (b). At 6 months, MRI demonstrated

a significant reduction in mass effect on the brainstem compared with the initial images (c)

ischemic stroke (28%) was higher than the risk of hemorrhage (3%) (Flemming et al. 2005). Potential mechanisms described include the occlusion of small perforating arteries due to distortion of the parent vessel, parent vessel emboli, and in situ thrombus formation in the perforating arteries and/or parent artery (Bhogal et al. 2016).

Dissecting V4 aneurysms can result in significant mass effect upon the brainstem. Compressive symptoms were seen in almost a quarter (22%) of patients in one cohort (Flemming et al. 2005). Cranial nerve palsies commonly affect CN V-VIII, although IX-XI can also be compressed. Therefore, by their dynamic expanding nature,

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these aneurysms can lead to worsening compressive symptoms and posterior fossa ischemia resulting in poor patient outcome. It is therefore the author’s opinion that aggressive treatment options should be considered in view of the natural history of symptomatic dissecting VA aneurysms.

Treatment Strategies Conservative A retrospective review of 100 patients presenting with an unruptured vertebral artery dissecting aneurysm demonstrated that the aneurysm remained unchanged in 70 patients over a 2-year follow-up period (Kai et al. 2011). A proposed pathological classification (Mizutani et al. 1999) differentiated a classic dissecting aneurysm (acute disruption of the IEL without compensatory intimal thickening) from dolichoectatic dissecting aneurysm (with thickened intima) and saccular aneurysms (minimal IEL disruption without thickened intima). Therefore, patients initially presenting with rupture might be considered as a different entity to those that hemorrhage after presenting with other symptoms (Flemming et al. 2005). This heterogeneity in disease pathology must be appreciated if successful conservative treatment options are to be safely employed. However, as previously discussed since these lesions frequently rupture (Santos-Franco et al. 2007; Yamada et al. 2004), a low threshold for intervention should be employed and close longterm follow-up should be the standard. However, it is important to remember that the risk factors for bleeding cannot be anticipated on angiographic data alone.

Surgical The aim of surgery is to achieve flow reduction to the dissecting aneurysm, if there is inadequate collateral supply or flow reversal if there is adequate collateral supply. In cases of poor collaterals or involvement of the PICA, bypass surgery can

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be performed prior to flow reversal/reduction. This is usually via a superficial temporal artery to superior cerebellar/posterior cerebral artery bypass. If there is significant mass effect, then hematoma decompression with segmental trapping is performed. Good supply from the posterior communicating arteries (PcomA) significantly reduces the chance of ischemic complications. There was a 7% chance of ischemia in patients with at least one large PcomA (>1 mm diameter) compared with 43% in patients with two small PcomAs (