Handbook of Cerebrovascular Disease and Neurointerventional Technique (Contemporary Medical Imaging), 4e (Jan 5, 2024)_(3031455975)_(Springer) 9783031455971, 9783031455988

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Handbook of Cerebrovascular Disease and Neurointerventional Technique Mark R. Harrigan John P. Deveikis Fourth Edition

Contemporary Medical Imaging Series Editor U. Joseph Schoepf, Department of Radiology and Radiological Medical University of South Carolin, Charleston, SC, USA

The Contemporary Medical Imaging series focuses on the most recent developments in imaging technology and their applications in areas such as cardiology, pulmonology, endocrinology, and neurology. Individual volumes present the core principles in diagnosing and treating disorders via modalities such as radiofrequency ablation, angiography, computed tomography, magnetic resonance imaging, positron emission tomography, and hybrid techniques such as PET/CT.  Each title is developed by authoritative radiologists who cover the most important topics in this rapidly advancing field.

Mark R. Harrigan • John P. Deveikis

Handbook of Cerebrovascular Disease and Neurointerventional Technique Fourth Edition

Mark R. Harrigan Departments of Neurosurgery, Neurology and Radiology University of Alabama at Birmingham Birmingham, AL, USA

John P. Deveikis Interventional Neuroradiology Bayfront.Health Medical Group Saint Petersburg, FL, USA

ISSN 2626-6431     ISSN 2626-6423 (electronic) ISBN 978-3-031-45597-1    ISBN 978-3-031-45598-8 (eBook) https://doi.org/10.1007/978-3-031-45598-8 Originally published by Humana Press, USA 2009 With a chapter on Ischemic stroke by: Agnieszka A. Ardelt, MD, PhD, MBA, FAHA Professor and Chair, Department of Neurology Medical Director, Stroke Programs MetroHealth/Case Western Reserve University SOM, Cleveland, Ohio, USA © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2009, 2013, 2018, 2023 This work is subject to copyright. All rights are solely and exclusively licensed 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 Humana imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland Paper in this product is recyclable

Introduction

To our enduring disbelief, the publisher agreed to yet another edition of this handbook. The global cerebrovascular community enjoys an advantage that few fields within medicine can match: An ongoing deluge of very high-­ quality scientific data, derived by numerous well designed randomized clinical trials and multicenter registries. These data inform daily management of patients and have contributed to the steady evolution of the field. Proof of this is seen in the steadily declining mortality from stroke over the last several decades. This purpose of this handbook is to serve as a practical guide to endovascular methods, as a reference work for neurovascular anatomy, and as an introduction to the cerebrovascular literature. We have striven to cover the essential aspects of the entire fields of neurointervention and cerebrovascular disease. It is particularly challenging to sift through the cerebrovascular literature because of the uneven quality; badly done and poorly written studies appear side-by-side with high quality publications in even the most prestigious journals. Indeed, so-called “meta-analysis” and “guidelines” publications are notorious for variability and poor quality. Therefore, this handbook should not be a substitute for reading the primary literature. We encourage readers to read the primary research papers, scrutinize them carefully, and form their own opinions. We attempted to enhance the accessibility and ease use of this handbook by arranging it in a semi-outline format. Dense narrative passages have been avoided wherever possible (who has time to read long, thick chapters, anyway?). In that spirit, the rest of this Introduction will be presented in the style of this book… 1. This book is divided into three parts. (a) Fundamentals (i) Essential neurovascular anatomy and basic angiographic techniques provide the foundation of the first section. • The focus of Chap. 1 (Essential Neurovascular Anatomy), remains on vascular anatomy that is pertinent to day-to-day clinical practice. Embryology and discussions of angiographic shift, which is less pertinent these days because of widely available noninvasive intracranial imaging, are left out.

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­ iscussions of anatomic variants include both normal variants D and anomalies. –– New for the second edition are some Angio-Anatomic Correlates that illustrate anatomic structures with angiographic pictures. • Chapters 2 and 3 cover diagnostic angiographic techniques. • Chapter 4 is an introduction to basic interventional access techniques with an appendix on the Neurointerventional Suite, primarily intended for newcomers to the angio suite and for experienced interventionalists planning a new suite. (b) Techniques (i) Endovascular methods, device information, and tips and tricks are detailed. • The second edition is packed with new information on evolving technology. (c) Specific disease states (i) Essential, useful information about each commonly-encountered condition is presented. • Significant clinical studies are summarized and placed into context. • Interesting and novel facts (and “factlets”) are included here and there. (ii) The term “systematic review” is used to refer to useful publications that have analyzed published clinical data in an organized way. The term “meta-analysis” is avoided because it refers to a specific statistical technique that is not always present in review articles purporting to be a meta-analysis. (iii) For readers with extra time on their hands, A Brief History of… sections describe the background and evolution of various techniques. 2. Core philosophy. Within the practical information contained within this book, we hope to impart our underlying patient-­oriented clinical philosophy. In our view, each patient’s welfare is paramount. The clinical outcome of each case takes priority over “pushing the envelope” by trying out new devices or techniques, generating material for the next clinical series or case report, or satisfying the device company representatives standing in the control room. In practical terms, clinical decision-making should be based on sound judgment and the best available clinical data. Moreover, new medical technology and drugs should be used within reason, and whenever possible, based on established principles of sound practice. Thus, while we have the technology and the ability to coil aneurysms in very old patients with Hunt Hess V subarachnoid hemorrhage, embolize asymptomatic and low-risk dural AV fistulas, and perform carotid angioplasty and stenting in patients with asymptomatic stenosis, we should recognize the value of conservative management when it is called for. We hope that this cautious and common sensical outlook is reflected throughout this book. 3. Cookbook presentation. We have made every attempt to present procedures in a plainly written, how-to-do-it format. Although some readers may take issue with the reduction of a field as complex as neurointerven-

Introduction

Introduction

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tion to a relatively simplistic how-to manual, we feel that structure and standardization of technique can only serve to benefit the field in the long run. For comparison, consider commercial air travel in the present era. Air travel fatalities are extremely rare, due to pilot training, standardization of flying techniques and meticulous aircraft maintenance. Even the most skilled and careful neurointerventionalists cannot hold a candle to the stellar safety record obtained by the airline industry. 4. Conventions used in this book (a) Terminology can be confusing. The authors have adopted the most current and commonly-used terms; synonymous terms are listed in parentheses after “aka,” for also known as. (b) We have limited the use of abbreviations to those commonly used in everyday conversation, such as “ICA” and “MCA.” Excessive use of abbreviations, particularly for uncommon terms, can clutter the text and make it difficult to read. (c) The terms, see below and see above, are used to indicate other material within the same chapter. 5. Medico legal disclaimer. This book is meant to serve as a guide to the use of a wide variety of medical devices and drugs. However, the authors and the publisher cannot be held responsible for the use of these devices and drugs by readers, or for failure by the readers of this book to follow specific manufacturer specifications and FDA guidelines. 6. Lastly, we would like to mention six simple truths that have emerged in our field since the last edition: (a) Endovascular treatment of acute ischemic stroke is strongly indicated for selected patients. (b) CTA has replaced catheter angiography for the initial evaluation of spontaneous subarachnoid hemorrhage. (c) Routine catheter angiography for follow-up surveillance imaging of coiled aneurysms is not indicated, as MRA is adequate and often superior than angiography for most cases. (d) Joint Commission-certified Primary and Comprehensive Stroke Centers in the United States, and regionalization of stroke care around the world, have revolutionized the care of patients with cerebrovascular disease and underscore the importance of organized and specialized stroke care. (e) Although live case demonstrations have become popular, they have little actual educational value and exist mainly for self-promotion by certain physicians and as a form of entertainment for the audience. Operators are distracted during live case demonstrations and complications are more likely. We hope that live case demonstrations turn out to become a passing fad. (f) The field is continuing to rapidly evolve making it vital for practitioners (including the authors) to keep abreast of the literature.

Birmingham, AL, USA St. Petersburg, FL, USA

Mark R. Harrigan John P. Deveikis

Acknowledgments

Ethan Tabibian, Kristen Sandefer, David Fisher, Mark Ogilvie, Bart Thaçi, Gustavo Chagoya, Lauren Rotman, Elizabeth Liptrap

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Contents

Part I Fundamentals 1 Essential Neurovascular Anatomy������������������������������������������������    3 1.1 Aortic Arch and Great Vessels������������������������������������������������    3 1.2 Common Carotid Arteries ������������������������������������������������������    7 1.3 External Carotid Artery����������������������������������������������������������    7 1.4 Superior Thyroid Artery����������������������������������������������������������   10 1.5 Ascending Pharyngeal Artery ������������������������������������������������   11 1.6 Lingual Artery������������������������������������������������������������������������   15 1.7 Facial Artery����������������������������������������������������������������������������   16 1.8 Occipital Artery����������������������������������������������������������������������   19 1.9 Posterior Auricular Artery������������������������������������������������������   21 1.10 Superficial Temporal Artery����������������������������������������������������   21 1.11 Maxillary Artery����������������������������������������������������������������������   23 1.12 Other ECA Branches��������������������������������������������������������������   33 1.13 Internal Carotid Artery������������������������������������������������������������   33 1.14 Carotid–Vertebrobasilar Anastomoses������������������������������������   35 1.15 The Infundibulum: A Normal Variant ������������������������������������   48 1.16 Circle of Willis������������������������������������������������������������������������   49 1.17 Anterior Cerebral Artery ��������������������������������������������������������   50 1.18 A1 Segment and Anterior Communicating Artery Complex����������������������������������������������������������������������   50 1.19 A2 Segment����������������������������������������������������������������������������   52 1.20 A3 Branches����������������������������������������������������������������������������   53 1.21 Middle Cerebral Artery ����������������������������������������������������������   55 1.22 Leptomeningeal Collaterals����������������������������������������������������   58 1.23 Posterior Cerebral Artery��������������������������������������������������������   59 1.24 PCA Branches������������������������������������������������������������������������   60 1.25 Vertebral Artery����������������������������������������������������������������������   65 1.26 Basilar Artery��������������������������������������������������������������������������   70 1.27 Venous System������������������������������������������������������������������������   73 1.28 Extracranial Veins ������������������������������������������������������������������   73 1.29 Venous Structures of the Skull������������������������������������������������   76 1.30 Meningeal Veins����������������������������������������������������������������������   76 1.31 Intracranial Venous Sinuses����������������������������������������������������   76 1.32 Superior Group������������������������������������������������������������������������   77 1.33 Inferior Group ������������������������������������������������������������������������   79 xi

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1.34 Supratentorial Cortical Veins��������������������������������������������������   83 1.35 Deep Venous System��������������������������������������������������������������   84 1.36 Infratentorial Venous System��������������������������������������������������   87 1.37 Intracranial Venous System Variants��������������������������������������   88 1.38 Spinal Neurovascular Anatomy����������������������������������������������   89 1.39 Spinal Cord Blood Supply: General Principles����������������������   89 1.40 General Principles of Spinal Arterial Anatomy����������������������   90 1.41 Segmental Contributions to Neural Territories ����������������������   92 1.42 Extrinsic Spinal Cord Arteries������������������������������������������������   93 1.43 Intrinsic Cord Arteries������������������������������������������������������������   94 1.44 Spinal Venous System ������������������������������������������������������������   94 References����������������������������������������������������������������������������������������   96 2 Diagnostic Cerebral Angiography������������������������������������������������  113 2.1 Cerebral Angiography������������������������������������������������������������  113 2.2 Indications������������������������������������������������������������������������������  113 2.3 A Brief History of Cerebral Angiography������������������������������  114 2.4 Complications of Cerebral Angiography��������������������������������  115 2.5 Cerebral Angiography: Basic Concepts����������������������������������  116 2.6 Femoral Artery Sheath (vs. No Sheath)����������������������������������  116 2.7 Sedation and Analgesia ����������������������������������������������������������  117 2.8 Wires and Catheters for Cerebral Angiography����������������������  117 2.9 Prevention of Air Emboli��������������������������������������������������������  120 2.10 Management of Air Emboli����������������������������������������������������  120 2.11 Mechanical Injection��������������������������������������������������������������  121 2.12 Vessel Selection����������������������������������������������������������������������  122 2.13 Angiographic Images and Standard Views ����������������������������  122 2.14 Frame Rates for Digital Subtraction Angiography ����������������  125 2.15 Calibration and Measurement ������������������������������������������������  126 2.16 3D Image Acquisition ������������������������������������������������������������  126 2.17 Cone-Beam CT Acquisition����������������������������������������������������  126 2.18 Femoral Artery Access������������������������������������������������������������  126 2.19 Procedures������������������������������������������������������������������������������  127 2.20 Ultrasound-Guided Access������������������������������������������������������  128 2.21 Aortic Arch Imaging ��������������������������������������������������������������  129 2.22 Carotid Artery Catheterization������������������������������������������������  129 2.23 Vertebral Artery Catheterization ��������������������������������������������  129 2.24 Reconstituting a Simmons 2 Catheter������������������������������������  130 2.25 Femoral Artery Puncture Site Management����������������������������  133 2.26 Closure Devices����������������������������������������������������������������������  133 2.27 Selected Femoral Artery Closure Devices������������������������������  134 2.28 Post-Angiogram Orders����������������������������������������������������������  134 2.29 Radial Artery Access��������������������������������������������������������������  134 2.30 Procedure��������������������������������������������������������������������������������  137 2.31 Avoiding Catheter Kinks and Knots ��������������������������������������  139 2.32 Sheath Removal/Hemostasis��������������������������������������������������  139 2.33 Radial Artery Puncture Site Management������������������������������  140 2.34 Selected Patient-Specific Considerations��������������������������������  140 2.35 Contrast-Induced Nephropathy����������������������������������������������  141

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2.36 Risk Factors for Contrast-­Induced Nephropathy��������������������  141 2.37 Methods to Reduce Risk of Contrast-Induced Nephropathy����������������������������������������������������������������������������  142 2.38 Metformin ������������������������������������������������������������������������������  142 2.39 Metformin-Containing Medications ��������������������������������������  142 2.40 Anaphylactic Contrast Reactions: Prevention and Management��������������������������������������������������������������������  142 2.41 Risk Factors for Contrast Reactions ��������������������������������������  142 2.42 Premedication Regimen����������������������������������������������������������  143 2.43 Acute Contrast Reactions: Signs and Symptoms��������������������  143 2.44 Acute Contrast Reactions: Treatment ������������������������������������  143 2.45 Intraoperative Angiography����������������������������������������������������  144 2.46 Tips for Imaging Specific Vascular Structures and Lesions����  147 References����������������������������������������������������������������������������������������  149 3 Spinal Angiography ����������������������������������������������������������������������  157 3.1 Indications for Spinal Angiography����������������������������������������  157 3.2 Complications of Diagnostic Spinal Angiography ����������������  157 3.3 Selective Spinal Angiography: Basic Concepts����������������������  158 3.4 Special Techniques and Situations������������������������������������������  169 References����������������������������������������������������������������������������������������  171 4 General  Considerations for Neurointerventional Procedures��������������������������������������������������������������������������������������  173 4.1 Pre-procedure Preparation������������������������������������������������������  173 4.2 Vascular Access����������������������������������������������������������������������  175 4.3 Antithrombotic Therapy for Neurointerventional Procedures������������������������������������������������������������������������������  190 4.4 Intervention Phase������������������������������������������������������������������  195 4.5 Provocative Testing ����������������������������������������������������������������  206 4.6 Intra-arterial Chemotherapy����������������������������������������������������  225 4.7 Access Site Closure����������������������������������������������������������������  229 4.8 Post-procedure Care����������������������������������������������������������������  235 4.9 Complication Avoidance and Management����������������������������  235 4.10 Appendix: The Neuroendovascular Suite ������������������������������  240 References����������������������������������������������������������������������������������������  249 Part II Interventional Techniques 5 Intracranial Aneurysm Treatment ����������������������������������������������  265 5.1 Intracranial Aneurysm Embolization��������������������������������������  265 5.2 Endovascular Technique ��������������������������������������������������������  266 5.3 Adjunctive Techniques for the Treatment of Wide-­Necked Aneurysms�������������������������������������������������������  280 5.4 Flow Diverters������������������������������������������������������������������������  294 5.5 Aneurysm Neck Bridging Devices ����������������������������������������  312 5.6 Complications: Avoidance and Management��������������������������  322 5.7 Parent Vessel Sacrifice������������������������������������������������������������  329 5.8 Appendix: Primer on Imaging of Intracranial Aneurysms������  332 References����������������������������������������������������������������������������������������  337

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6 Intracranial Embolization Procedures����������������������������������������  349 6.1 Intracranial Arteriovenous Malformation (AVM) Embolization��������������������������������������������������������������  349 6.2 Carotid Cavernous Fistula (CCF) ������������������������������������������  382 6.3 Dural Arteriovenous Fistulas��������������������������������������������������  389 6.4 Tumor Embolization ��������������������������������������������������������������  393 6.5 Embolization for Treatment of Acute Bleeding����������������������  397 References����������������������������������������������������������������������������������������  401 7 Extracranial  and Spinal Embolization����������������������������������������  409 7.1 Head and Neck Transarterial Embolization��������������������������  409 7.2 Percutaneous Procedures������������������������������������������������������  430 7.3 Spinal Embolization��������������������������������������������������������������  435 References����������������������������������������������������������������������������������������  440 8 Treatment  of Acute Ischemic Stroke��������������������������������������������  447 8.1 Mechanical Thrombectomy����������������������������������������������������  447 8.2 Treatment for Acute Ischemic Stroke: General Considerations����������������������������������������������������������  453 8.3 Intravenous Thrombolysis for Acute Ischemic Stroke������������  456 8.4 Intra-Arterial Therapy for Stroke��������������������������������������������  459 8.5 Special Populations and Special Situations����������������������������  488 8.6 Central Retinal Artery Occlusion��������������������������������������������  498 8.7 Appendix 1: Primer on Imaging in Stroke Joel K. Curé��������  500 8.8 Appendix 2: NIH Stroke Scale ����������������������������������������������  515 References����������������������������������������������������������������������������������������  516 9 Extracranial Angioplasty and Stenting����������������������������������������  535 9.1 Carotid Bifurcation Lesions����������������������������������������������������  535 9.2 Carotid Stenting for Dissection or Pseudoaneurysm��������������  549 9.3 Vertebral Artery Stenosis��������������������������������������������������������  550 9.4 Carotid Artery Origin Lesions������������������������������������������������  552 9.5 Endovascular Revascularization of Chronic ICA Occlusion������������������������������������������������������������������������  554 9.6 Subclavian Artery Origin Stenosis������������������������������������������  556 References����������������������������������������������������������������������������������������  559 10 Endovascular  Treatment of Intracranial Stenosis and Vasospasm�������������������������������������������������������������������������������  565 10.1 Intracranial Atherosclerotic Stenosis������������������������������������  565 10.2 Indications for Intracranial Angioplasty and Stenting����������  567 10.3 Pre-procedure Preparation����������������������������������������������������  568 10.4 Endovascular Technique ������������������������������������������������������  568 10.5 Post-procedure Management������������������������������������������������  573 10.6 Intracranial Angioplasty Tips������������������������������������������������  573 10.7 Management of Intracranial Complications During or After Intracranial Angioplasty������������������������������  574 10.8 Ophthalmic Artery Angioplasty for Age-Related Macular Degeneration����������������������������������������������������������  575 10.9 Endovascular Treatment of Cerebral Vasospasm������������������  575 References����������������������������������������������������������������������������������������  580

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11 Venous Procedures ������������������������������������������������������������������������  583 11.1 Venous Access: Basic Concepts��������������������������������������������  583 11.2 Venography ��������������������������������������������������������������������������  587 11.3 Venous Test Occlusion����������������������������������������������������������  590 11.4 Venous Sampling Procedures������������������������������������������������  593 11.5 Transvenous Embolization����������������������������������������������������  601 11.6 Venous Thrombolysis and Thrombectomy ��������������������������  616 11.7 Transvenous Stenting������������������������������������������������������������  622 11.8 Appendix: Miscellaneous Transvenous Procedures��������������  626 References����������������������������������������������������������������������������������������  629 Part III Specific Disease States 12 Intracranial  Aneurysms and Subarachnoid Hemorrhage ��������  641 12.1 Intracranial Aneurysms: Pathophysiology����������������������������  641 12.2 The Peculiar Infundibulum ��������������������������������������������������  643 12.3 Unruptured Intracranial Aneurysms��������������������������������������  643 12.4 Conditions Associated with Aneurysms�������������������������������  644 12.5 Risk Factors for Aneurysm Formation, Aneurysm Growth, and Subarachnoid Hemorrhage ������������  648 12.6 Natural History����������������������������������������������������������������������  651 12.7 Management of Unruptured Intracranial Aneurysms ����������  654 12.8 Intracranial Aneurysms by Type and Location ��������������������  664 12.9 A Brief History of Endovascular Treatment of Intracranial Aneurysms����������������������������������������������������  677 12.10 Subarachnoid Hemorrhage����������������������������������������������������  679 12.11 Vasospasm����������������������������������������������������������������������������  690 12.12 Subarachnoid Hemorrhage Management Protocol ��������������  699 12.13 Intracranial Aneurysms: Special Situations��������������������������  703 References����������������������������������������������������������������������������������������  721 13 Arteriovenous Malformations������������������������������������������������������  761 13.1 Pathophysiology��������������������������������������������������������������������  761 13.2 Clinical Features ������������������������������������������������������������������  762 13.3 Conditions Associated with AVMs ��������������������������������������  763 13.4 Natural History����������������������������������������������������������������������  765 13.5 Risk Factors for Hemorrhage������������������������������������������������  766 13.6 Outcome after Hemorrhage��������������������������������������������������  766 13.7 Special Section: Cerebral Proliferative Angiopathy ������������  767 13.8 Special Section: AVM Mimics����������������������������������������������  769 13.9 Management��������������������������������������������������������������������������  771 13.10 Specific Considerations��������������������������������������������������������  778 References����������������������������������������������������������������������������������������  790 14 Dural Arteriovenous Fistulas��������������������������������������������������������  805 14.1 Pathophysiology��������������������������������������������������������������������  805 14.2 Pulsatile Tinnitus: What Does it Mean?��������������������������������  808 14.3 Imaging ��������������������������������������������������������������������������������  809 14.4 Natural History����������������������������������������������������������������������  810

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14.5 Management��������������������������������������������������������������������������  811 14.6 Dural AVFs by Location ������������������������������������������������������  812 14.7 Appendix: Direct Carotid-Cavernous Fistulas����������������������  822 References����������������������������������������������������������������������������������������  825 15 Venous  Disorders and Cavernous Malformations����������������������  837 15.1 Developmental Venous Anomalies����������������������������������������  837 15.2 Cavernous Malformations����������������������������������������������������  840 15.3 Venous Anomalies in Vein of Galen Malformations������������  848 15.4 Sinus pericranii ��������������������������������������������������������������������  848 15.5 Extracerebral Venous Malformations������������������������������������  850 15.6 Venous Stenosis��������������������������������������������������������������������  852 15.7 Cerebral Venous Thrombosis������������������������������������������������  857 References����������������������������������������������������������������������������������������  864 16 Ischemic Stroke������������������������������������������������������������������������������  879 16.1 Acute Ischemic Stroke: Initial Management and Evaluation����������������������������������������������������������������������  879 16.2 Acute Ischemic Stroke: Treatment����������������������������������������  883 16.3 Secondary Stroke Prevention������������������������������������������������  894 16.4 Rehabilitation and Neurorepair��������������������������������������������  897 16.5 Epidemiology and Risk Factors��������������������������������������������  898 16.6 Ischemic Stroke Outcomes ��������������������������������������������������  909 16.7 Pathophysiology and Clinical Aspects����������������������������������  909 16.8 Classification of Stroke Etiologies����������������������������������������  927 16.9 Appendix: Kids Korner! Pediatric Ischemic Stroke�������������  951 References����������������������������������������������������������������������������������������  953 17 Intracerebral Hemorrhage������������������������������������������������������������  965 17.1 Epidemiology������������������������������������������������������������������������  965 17.2 Outcomes������������������������������������������������������������������������������  965 17.3 Pathophysiology and Clinical Factors����������������������������������  966 17.4 Imaging ��������������������������������������������������������������������������������  971 17.5 Medical Management of Intracerebral Hemorrhage������������  976 17.6 Surgery for Intracerebral Hemorrhage����������������������������������  982 17.7 Specific ICH Situations��������������������������������������������������������  984 17.8 Appendix Essential Reversal Techniques ����������������������������  989 References����������������������������������������������������������������������������������������  991 18 Extracranial Atherosclerotic Arterial Disease���������������������������� 1001 18.1 Atherosclerosis���������������������������������������������������������������������� 1001 18.2 Management of Carotid Stenosis������������������������������������������ 1003 18.3 Radiographic Evaluation������������������������������������������������������ 1012 18.4 Medical Management������������������������������������������������������������ 1014 18.5 Carotid Angioplasty and Stenting ���������������������������������������� 1017 18.6 Atherosclerotic Carotid Occlusion���������������������������������������� 1024 18.7 Extracranial Vertebral Artery Atherosclerotic Disease �������� 1030 18.8 Rotational Vertebral Artery Occlusion Syndrome���������������� 1032 18.9 Extracranial Cerebrovascular Dissection������������������������������ 1034

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18.10 Fibromuscular Dysplasia������������������������������������������������������ 1041 18.11 Carotid Webs������������������������������������������������������������������������ 1043 References���������������������������������������������������������������������������������������� 1045 19 Intracranial  Cerebrovascular Occlusive Disease������������������������ 1063 19.1 Intracranial Atherosclerotic Disease (ICAD)������������������������ 1063 19.2 Etiology of Symptoms���������������������������������������������������������� 1064 19.3 Imaging �������������������������������������������������������������������������������� 1064 19.4 Natural History���������������������������������������������������������������������� 1065 19.5 Medical Treatment of Symptomatic ICAD�������������������������� 1068 19.6 Intracranial Angioplasty and Stenting���������������������������������� 1068 19.7 Intracranial Arterial Dissections and Cerebral Ischemia������ 1072 19.8 Other Intracranial Artery Stenosis Syndromes �������������������� 1072 19.9 Moyamoya Disease and Moyamoya Syndrome�������������������� 1073 19.10 Kids Korner: ACTA2 Mutation and Cerebrovascular Disease: “Moyamoya-like Syndrome?”�������������������������������� 1086 References���������������������������������������������������������������������������������������� 1088 20 Spinal Vascular Lesions ���������������������������������������������������������������� 1101 20.1 Type I: Dural Arteriovenous Fistula�������������������������������������� 1101 20.2 Type II: Intramedullary Arteriovenous Malformation���������� 1105 20.3 Type III: Juvenile Arteriovenous Malformation ������������������ 1108 20.4 Type IV: Intradural Perimedullary Arteriovenous Fistula������������������������������������������������������������������������������������ 1108 20.5 Epidural Arteriovenous Fistula �������������������������������������������� 1111 20.6 Sacral Arteriovenous Fistula ������������������������������������������������ 1111 20.7 Spinal Cord Aneurysms�������������������������������������������������������� 1112 20.8 Intramedullary Cavernous Malformation������������������������������ 1112 20.9 Vascular Spinal Tumors�������������������������������������������������������� 1112 20.10 Spinal Cord Infarction���������������������������������������������������������� 1112 20.11 Cerebrospinal Fluid-Venous Fistulas������������������������������������ 1117 References���������������������������������������������������������������������������������������� 1117 Index�������������������������������������������������������������������������������������������������������� 1125

Abbreviations

A Amperes AC Alternating current ACAS Anterior cerebral artery ACAS Asymptomatic Carotid Atherosclerosis Study ACCP American College of Chest Physicians ACE Angiotensin converting enzyme A-comm Anterior communicating artery ACST Asymptomatic Carotid Surgery Trial ACT Activated clotting time ACTH Adrenocorticotropic hormone ADAPT A direct aspiration first pass technique ADC Apparent diffusion coefficient ADH Antidiuretic hormone ADPKD Autosomal dominant polycystic kidney disease AED Antiepileptic drug AF Atrial fibrillation AHA American Heart Association AICA Anterior inferior cerebellar artery aka Also known as ALT Alanine aminotransferase AMA Accessory meningeal artery ANA Antinuclear antibody ANGEL-ASPECT Endovascular therapy in acute anterior circulation large vessel occlusive Patients with Large Infarct Core ANP Atrial natriuretic peptide ARCHeR Acculink for revascularization of carotids in high-­ risk patients ARR Absolute risk reduction ARUBA A randomized trial of unruptured brain arteriovenous malformations ASA Aspirin (acetylsalicylic acid), American Stroke Association ASAN Atrial septal aneurysm ASITN American Society of Interventional and Therapeutic Neuroradiology ASNR American Society of Neuroradiology xix

xx

ASPECTS ATACH-2

Alberta Stroke Program Early CT Score Antihypertensive Treatment of Acute Cerebral Hemorrhage 2 Trial atm Atmosphere AV Arterio-venous AVF Arteriovenous fistula AVM Arteriovenous malformation BA Basilar artery BADDASS Balloon guide with large bore distal access catheter with dual aspiration with stent-retriever as standard approach BAER Brainstem auditory evoked potential BAOCHE Basilar artery occlusion Chinese endovascular trial BASICS Basilar Artery International Cooperative Study BCNU 1,3 Bis (2-chloroethyl) 1-nitrosourea. AKA: carmustine BE Bacterial endocarditis BEACH Boston Scientific EPI-A carotid stenting trial for high-risk surgical patients BEAST Biorepository to establish the etiology of sinovenous thrombosis bFGF Basic fibroblast growth factor BNP Brain natriuretic peptide BRANT British Aneurysm Nimodipine Trial BRAT Barrow Ruptured Aneurysm Trial CAA Cerebral amyloid angiopathy CABERNET Carotid Artery Revascularization Using the Boston Scientific FilterWire EX/EZ and the EndoTex NexStent CADASIL Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy CADISS Cervical Artery Dissection in Stroke Study cANCA Circulating antineutrophil cytoplasmic antibody CAPRIE Clopidogrel vs. Aspirin in Patients at Risk of Ischemic Events CAPTIVE Continuous aspiration prior to intracranial vascular embolectomy CAPTURE Carotid Acculink/Accunet Post-Approval Trial to Uncover Rare Events CARASIL Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy CaRESS Clopidogrel and Aspirin for Reduction of Emboli in Symptomatic Carotid Stenosis CAS Carotid angioplasty and stenting CASANOVA Carotid Artery Stenosis with Asymptomatic Narrowing: Operation versus Aspirin

Abbreviations

Abbreviations

xxi

CASES-PMS

Carotid Artery Stenting with Emboli Protection Surveillance- Post-Marketing Study CBC Complete blood count CBF Cerebral blood flow CBV Cerebral blood volume CCA Common carotid artery CCF Carotid cavernous fistula CCM Cerebral cavernous malformation CCNU 1-(2-chloroethyl)-3-cyclohexyl-1-nitosourea. Aka: Lomustine CCSVI Chronic cerebrospinal venous insufficiency CEA Carotid endarterectomy CHADS-VASC Congestive heart failure, hypertension, age, diabetes, stroke, vascular disease, age, sex CHANCE Clopidogrel in high-risk patients with acute nondisabling cerebrovascular events trial CHF Congestive heart failure CHOICE Chemical optimization of cerebral embolectomy CI Confidence interval CISS 3D-constructive interference in steady-state MRI CK Creatine kinase CK-MB Creatine kinase - MB isoenzyme (cardiac-specific CK) CLEAR-IVH Clot lysis evaluating accelerated resolution of intraventricular hemorrhage CM Cardiomyopathy; centimeter CMS Centers for Medicare and Medicaid Services CN Cranial nerve CNS Central nervous system COSS Carotid occlusion surgery study COVID 19 Coronavirus Disease of 2019 CPA Cerebral proliferative angiopathy CPAP Continuous positive airway pressure CPK Creatine phosphokinase CPP Cerebral perfusion pressure Cr Creatinine CREATE Carotid Revascularization with ev3 Arterial Technology Evolution CREST Calcinosis, Raynauds phenomenon, esophageal dysmotility, sclerodactyly and telangiectasia; Carotid Revascularization, Endarterectomy versus Stenting Trial CRH Corticotropin releasing hormone CRP C-reactive protein CRT Cathode ray tube CSC Comprehensive stroke center CSF Cerebrospinal fluid CSW Cerebral salt wasting

xxii

CT CTA CVP CVT DAC DAPT dAVF DAWN

Computed tomography CT angiography Central venous pressure Cerebral venous thrombosis Distal access catheter Dual antiplatelet Dural arteriovenous fistula DWI or CTP assessment with clinical mismatch in the triage of wake-up and late presenting strokes undergoing neurointervention with Trevo Trial DDAVP Desmopressin DEFUSE-3 Endovascular therapy following imaging evaluation for ischemic stroke DEVT Direct endovascular treatment DM Diabetes mellitus DMSO Dimethyl sulfoxide DOAC Direct oral anticoagulant DPD Distal protection device DSA Digital subtraction angiography DSPA Desmodus rotundus salivary plasminogen activator DVA Developmental venous anomaly DVT Deep venous thrombosis DWI Diffusion weighted imaging EAGLE European Assessment Group for Lysis in the Eye EBV Epstein–Barr Virus ECA External carotid artery ECASS European Cooperative Acute Stoke Study ECG Electrocardiogram EC-IC Extracranial to intracranial ECST European Carotid Surgery Trial EDAMS Encephalo-duro-arterio-myo-synangiosis EDAS Encephalo-duro-arterio-synangiosis EDS Ehlers-Danlos syndrome EEG Electroencephalogram EEL External elastic lamina EJ External jugular vein EKG Electrocardiogram EMG Electromyography EMS Encephalo-myo-synagiosis ENRICH Early Minimally Invasive Removal of Intracerebral Hemorrhage Trial EPD Embolic protection device ESCAPE Endovascular treatment for Small Core and Anterior circulation Proximal occlusion with Emphasis on minimizing CT to recanalization times. ESPS European Stroke Prevention Study

Abbreviations

Abbreviations

xxiii

ESR EVA-3S

Erythrocyte sedimentation rate Endarterectomy vs. Angioplasty in Patients with Symptomatic Severe Carotid Stenosis EVOH Ethylene vinyl copolymer. AKA :EVAL EXACT Emboshield and Xact Post Approval Carotid Stent Trial EXTEND-IA Extending the Time for Thrombolysis in Emergency Neurological Deficits-IntraArterial F French FDA Food and Drug Administration FEIBA Factor eight inhibitor bypassing activity FFP Fresh frozen plasma FLAIR Fluid attenuated inversion recovery FMD Fibromuscular dysplasia fMRI Functional magnetic resonance imaging fps Frames per second GCS Glasgow coma scale GDC Guglielmi detachable coil GESICA Groupe d’Etude des Sténoses Intra-Crâniennes Athéromateuses symptomatiques GI Gastrointestinal GIST-UK United Kingdom Glucose Insulin in Stroke Trial GP Glycoprotein GRASP Glucose regulation in acute stroke trial Gy Gray HbF Fetal hemoglobin HbS Hemoglobin S HbSS Hemoglobin S homozygosity HDL High density lipoprotein HeadPoST Head Position in Stroke Trial HEMA 2-hydroxyethyl methacrylate HERMES Highly effective reperfusion evaluated in multiple endovascular stroke trials HERS Heart and Estrogen/progestin study HHT Hereditary hemorrhagic telangiectasia HIPAA Health Insurance Portability and Accountability Act HIT Heparin-induced thrombocytopenia HMG CoA 3-Hydroxy-3-methylglutaryl coenzyme A HRT Hormone replacement therapy IA Intra-arterial ICA Internal carotid artery ICAD Intracranial atherosclerotic disease ICE Intentional cerebral embolism ICG Indocyanine green ICH Intracerebral hemorrhage ICP Intracranial pressure ICP Intracranial pressure

xxiv

ICSS ICU ID IEL IEP II IIH IJ IMA IMS III IMT INR INTERACT2

International Carotid Stenting Study Intensive care unit Internal diameter Internal elastic lamina Intracranial embolization procedure Image intensifier Idiopathic intracranial hypertension Internal jugular vein Internal maxillary artery Interventional Management of Stroke III Intima media thickness International normalized ratio Intensive blood pressure reduction in acute cerebral hemorrhage 2 trial IPS Inferior petrosal sinus IPSS Inferior petrosal sinus sampling IRB Institutional review board ISAT International Subarachnoid Aneurysm Trial ISUIA International Study of Unruptured Intracranial Aneurysms IV Intravenous IVH Intraventricular hemorrhage JAM Japan Adult Moyamoya Trial JUPITER Justification for the use of statins in prevention: an intervention trial evaluating rosuvastatin KHE Kaposiform hemangioendotheliomas KSS Kearns-Sayre syndrome KTS Klippel Trenaunay syndrome kV Kilovolt kW Kilowatt LDL Low density lipoprotein LDS Loeys-Dietz syndrome LINAC Linear accelerator (radiosurgery) LMWH Low molecular weight heparin LOC Level of consciousness; loss of consciousness LV Left ventricle LVAD Left ventricular assist device LVEF Left ventricular ejection fraction LVO Large vessel occlusion MA Maxillary artery MAC Mitral annular calcification MACE Major adverse cerebrovascular events MATCH Management of AtheroThrombosis with Clopidogrel in High-risk patients MAUDE Manufacturer and User facility Device Experience MAVEriC Medtronic AVE Self-Expanding Carotid Stent system with Distal Protection in the Treatment of Carotid Stenosis

Abbreviations

Abbreviations

xxv

MCA MELAS

Middle cerebral artery Mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes MEP Motor evoked potential MERFF Myoclonic epilepsy and ragged red fibers MI Myocardial infarction MISTIE Minimally Invasive Surgery Plus Alteplase for Intracerebral Hemorrhage Evacuation mm Millimeter MMA Middle meningeal artery MR CLEAN Multicenter Randomized Clinical Trial of Endovascular Treatment for Acute Ischemic Stroke in the Netherlands MRA Magnetic resonance angiography MRI Magnetic resonance imaging mRS Modified Rankin Scale MRV Magnetic resonance venography MTT Mean transit time MVP Mitral valve prolapse; most valuable player MyRIAD Mechanisms of Early Recurrence in Intracranial Atherosclerotic Disease Study NA Not available NASCET North American Symptomatic Carotid Endarterectomy Trial NBCA N-butyl-2-cyanoacrylate. Aka: Glue NBTE Nonbacterial thrombotic endocarditis NCRP National Council on Radiation Protection and Measurements NCRP National Council on Radiation Protection and Measurements NCS Nerve conduction study NEMC-PCR New England medical Center Posterior Circulation Registry Newt Newton NG Nasogastric NICU Neurological intensive care unit NIH-SS National Institutes of Health Stroke Scale NNH Number needed to harm NNT Number needed to treat NOACs Novel oral anticoagulants, non-vitamin K antagonist oral anticoagulants NPH Neutral protamine Hagedorn insulin NPO Nil per os (no feeding) NS Not significant NSAID Nonsteroidal anti-inflammatory drug OA-MCA Occipital artery to middle cerebral artery OCP Oral contraceptive oCRH ovine corticotrophin releasing hormone

xxvi

OD Outer diameter OEF Oxygen extraction fraction OKM O'Kelly-Marotta scale OSA Obstructive sleep apnea OTW Over-the-wire PA Posteroanterior PAC Partial anterior circulation stroke PACS Picture archiving and communication system PAN Polyarteritis nodosa PASCAL Performance and Safety of the Medtronic AVE Self-Expandable Stent in the treatment of Carotid Artery Lesions PATCH Platelet Transfusion in Cerebral Hemorrhage Trial pAVF Pial arteriovenous fistula PCA Posterior cerebral artery PCC Prothrombin complex concentrate P-comm Posterior communicating artery PCR Polymerase chain reaction PCWP Pulmonary capillary wedge pressure PCXR Portable chest X-ray PEEP Positive end-expiratory pressure PET Positron emission tomography PFO Patent foramen ovale PHASES Population hypertension age size earlier site PICA Posterior inferior cerebellar artery PKD Polycystic kidney disease PNS Peripheral nervous system POC Posterior circulation stroke POINT Platelet-Oriented Inhibition in New TIA and Minor Ischemic Stroke Trial PPI Proton pump inhibitor PPRF Paramedian pontine reticular formation PROACT Prolyse in acute cerebral thromboembolism Pro-UK Prourokinase PSA Posterolateral spinal arteries PSV Peak systolic velocity PT Prothrombin time PTA Percutaneous transluminal angioplasty PTE Pulmonary thromboembolism PTT Partial thromboplastin time PVA Polyvinyl alcohol PVP Polyvinylpyrollidone RA Rheumatoid arthritis RCVS Reversible cerebrovascular constriction syndrome RECANALISE Recanalization using combined intravenous Alteplase and neurointerventional algorithm for acute ischemic stroke

Abbreviations

Abbreviations

xxvii

REGARDS

Reasons for Geographic and Racial Differences in Stroke Study rem Roentgen-equivalent-man, rapid eye movement sleep stage RESCUE Japan LIMIT Recovery by Endovascular Salvage for Cerebral Ultra-acute Embolism-Japan Large Ischemic Core Trial REVASCAT Endovascular REVAscularlization with a Solitaire Device versus best medical management in Anterior Circulation Stroke Within 8 Hours. REVERSE-AD Reversal Effects of Idarucizumab on Active Dabigatran study RHV Rotating hemostatic valve (aka Y-adapter, aka Touey-Borst Valve) RIND Reversible ischemic neurological deficit RPR Rapid plasma reagin RR Risk reduction RRR Relative risk reduction RVAS Rotational vertebral artery syndrome RX Rapid exchange SAH Subarachnoid hemorrhage SAMMPRIS Stenting vs. Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis SAPPHIRE Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy SAVE Stent-retriever assisted vacuum-locked extraction SBP Systolic blood pressure SCA Superior cerebellar artery SCD Sickle cell disease SCIWORA Spinal cord injury without radiographic abnormality SDH Subdural hematoma SECURITY Study to Evaluate the Neuroshield Bare Wire Cerebral Protection System and XAct Stent in Patients at High Risk for Endarterectomy SELECT2 Randomized Controlled Trial to Optimize Patients selection for Endovascular Treatment in Acute Ischemic Stroke SIADH Syndrome of inappropriate antidiuretic hormone secretion SIM Simmons catheter SIR Society of Interventional Radiology SKIP Direct Mechanical Thrombectomy in Acute LVO Stroke study SLE Systemic lupus erythematosus SOV Superior ophthalmic vein

xxviii

SPACE

Stent-Protected Percutaneous Angioplasty of the Carotid versus Endarterectomy SPACEMAN Stent-pass-aspiration-rescue-microwire-­­angioplasty SPARCL Stroke Prevention by Aggressive Reduction in Cholesterol Levels SPECT Single photon emission computed tomography SSEP Somatosensory evoked potential SSS Superior sagittal sinus SSYLVIA Stenting of Symptomatic Atherosclerotic Lesions in the Vertebral or Intracranial Arteries STA Superficial temporal artery STA-MCA Superficial temporal artery to middle cerebral artery bypass STICH Surgical Trial in Lobar Intracerebral Hemorrhage SWIFT PRIME Solitaire with the intention for thrombectomy as primary endovascular treatment TAC Total anterior circulation stroke TASS Ticlopidine Aspirin Stroke Study TCAR Transcarotid arterial revascularization TCD Transcranial doppler ultrasonography TEE Transesophageal echocardiography TGA Transient global amnesia TIA Transient ischemic attack TOAST Trial of ORG 10172 in Acute Stroke Treatment tPA Tissue plasminogen activator TRA Transradial access TSAT Two-stage aspiration technique TTE Transthoracic echocardiography TTP Time to peak; thrombotic thrombocytopenic purpura U Unit UAC Umbilical artery catheter UOP Urinary output USA United States of America V Volts VACS Veterans Affairs Cooperative Study on Symptomatic Stenosis VAST Vertebral Artery Stenting Trial VBI Vertebrobasilar insufficiency VDRL Venereal Disease Research Laboratory VEGF Vascular Endothelial Growth Factor VERiTAS Vertebrobasilar Flow Evaluation and Risk of Transient Ischemic Attack and Stroke. VERT Vertebral VISSIT Vitesse Intracranial Stent Study VIVA ViVEXX Carotid Revascularization Trial VOGM Vein of Galen malformation VZV Varicella zoster virus

Abbreviations

Abbreviations

xxix

WASID WEAVE WEB WEST WHI WOVEN WSS

Warfarin versus Aspirin for Symptomatic Intracranial Disease Wingspan Stent System Post Market Surveillance Woven endobridge Women Estrogen Stroke Trial Women’s Health Initiative Wingspan One Year Vascular Events and Neurological Outcomes Wall Shear Stress

Part I Fundamentals

1

Essential Neurovascular Anatomy

1.1 Aortic Arch and Great Vessels Aortic arch anatomy is pertinent to neuroangiography because variations of arch anatomy can affect access to the cervicocranial circulation. 1. 2.

Branches (a) Innominate (aka brachiocephalic) artery (b) Left common carotid artery (CCA) (c) Left subclavian artery Variants (Fig. 1.1) (a) Bovine arch (Figs.  1.1b and 1.2). The innominate artery and left common carotid artery (CCA) share a common origin (up to 27% of cases), or the left CCA arises from the innominate artery (7% of cases) [1]. The bovine variant is more common in blacks (10–25%) than whites (5–8%) [2]. (b) Aberrant right subclavian artery. The right subclavian artery arises from the left aortic arch, distal to the origin of the left subclavian artery. It usually passes posterior to the esophagus on its way to the right upper extremity. This is the most common congenital arch anomaly; incidence: 0.4–2.0% [3] associated with Down syndrome. (c) Origin of the left vertebral artery from the arch is seen in 0.5% of cases [1].



(d) Less common variants (Fig. 1.3). Some of these rare anomalies can lead to formation of a vascular ring in which the trachea and esophagus are encircled by connecting segments of the aortic arch and its branches. 3. Effects of aging and atherosclerosis on the aortic arch and great vessels. The aortic arch and great vessels become elongated and tortuous with age (Fig. 1.4); this can have practical implications for neurointervention in the elderly, as a tortuous vessel can be difficult to negotiate with wires and catheters. Although atherosclerosis has been implicated in the etiology of this phenomenon, more recent data suggest that the cervical internal carotid artery (ICA) may undergo metaplastic transformation, in which elastic and muscular tissue in the artery wall is replaced by loose connective tissue [4]. The most common subclavian artery configuration is shown in Fig. 1.5. Major branches are: 1. Vertebral artery (1) 2. Thyrocervical trunk (a) Inferior thyroid artery (2) (b) Ascending cervical artery (most commonly a branch of transverse cervical) (3) (c) Transverse cervical artery (4) (d) Suprascapular artery (5)

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 M. R. Harrigan, J. P. Deveikis, Handbook of Cerebrovascular Disease and Neurointerventional Technique, Contemporary Medical Imaging, https://doi.org/10.1007/978-3-031-45598-8_1

3

1  Essential Neurovascular Anatomy

4

a

b

c

d

Fig. 1.1  Common aortic arch configurations. Clockwise from upper left: (a) Normal arch; (b) bovine arch; (c) aberrant right subclavian artery; and (d) origin of the left vertebral artery from the arch

1.1  Aortic Arch and Great Vessels Fig. 1.2  What exactly is a “bovine arch?” Drawing of an arch from a cow. In cattle, a single great vessel originates from the aortic arch [322]. Presumably, the long brachiocephalic artery is due to the relatively long distance from the aorta to the thoracic inlet in cattle. Because humans do not have a true “bovine arch,” Layton and colleagues proposed that the more precise terms “Common-Origin-of-­ the-Innominate-Artery-and-LeftCommon-Carotid-Artery” and “Origin-of-the-Left-CommonCarotid-Artery-from-the-­ Innominate-Artery” supplant the term bovine arch [323]. This is akin to proposing that the universally understood term “p-comm aneurysm” be replaced by the more accurate “aneurysm-arising-fromthe-internal-carotid-artery-­adjacent-­ to-the-origin-of-the-posteriorcommunicating-­artery.” The authors of this Handbook will continue to use the well understood but anatomically imprecise terms, bovine arch and p-comm aneurysm

5

1  Essential Neurovascular Anatomy

6

a

c

b

d

Fig. 1.3  Selected aortic arch anomalies. (a) Double aortic arch. The arches encircle the trachea and esophagus to form the descending aorta, which is usually on the left. The right arch is larger than the left in up to 75% of cases [1]. (b) Double aortic arch with left arch atresia. (c) Right aortic arch with a mirror configuration. The descending aorta is on the right side of the heart. This anomaly does

e

not form a vascular ring, but is associated with other anomalies such as tetralogy of Fallot [1]. (d) Right aortic arch with a nonmirror configuration and an aberrant left subclavian artery. The descending aorta is on the right side of the heart, and the left subclavian artery arises from the proximal aorta. A common cause of a symptomatic vascular ring [324]. (e) Bi-innominate artery

1.3  External Carotid Artery

7

Fig. 1.4  Aortic arch elongation classification scheme

1.2 Common Carotid Arteries The CCAs travel within the carotid sheath, which also contains the internal jugular (IJ) vein and the vagus nerve. The right CCA is usually shorter than the left. The CCAs typically bifurcate at the C3 or C4 level (upper border of the thyroid cartilage), although the bifurcation may be located anywhere between T2 and C2 [6]. The CCAs do not usually have branches, although anomalous branches can include the superior thyroid, ascending pharyngeal, or occipital arteries [1].

Fig. 1.5  Subclavian artery: (1) vertebral artery; (2) inferior thyroid artery; (3) ascending cervical artery; (4) transverse cervical artery; (5) suprascapular artery; (6) deep cervical artery; (7) supreme intercostal artery; (8) dorsal scapular artery; and (9) internal mammary artery

3. Costocervical trunk (a) Deep cervical artery (6) (b) Supreme or highest intercostal artery (7) 4. Dorsal scapular artery (may also arise from transverse cervical) [5] (8) 5. Internal thoracic (mammary) artery (9)

1.3 External Carotid Artery The external carotid artery (ECA) originates at the common carotid bifurcation. From its origin, the ECA usually curves forward medial to the internal carotid, then immediately begins a c­ ephalad ascent, curving laterally and slightly posteriorly until it ends behind the mandible in its terminal bifurcation into the maxillary and superficial temporal arteries [7]. Thus, on a frontal radiographic view, the external carotid begins medially and swings cephalad and laterally, and on a lateral view it begins anteriorly and then ascends, angling slightly posteriorly.

1  Essential Neurovascular Anatomy

8

Mnemonic for the External Carotid

Branches After reading this book … Some Adoring Linguists Find Our Paragraphs Somewhat Mesmerizing   Superior thyroid   Ascending pharyngeal   Lingual   Facial   Occipital   Posterior auricular   Superficial temporal   Maxillary More amusing and off-color mnemonics are available to assist the novice in remembering these branches. If the readers’ imaginations fail them, the authors would be more than happy to supply additional memory aids for this purpose

1. Branches There are eight major branches of the ECA (Fig. 1.6). Commonly, the branches are listed in order by their point of origin from proximal to distal. (a) Superior thyroid artery (b) Ascending pharyngeal artery (c) Lingual artery (d) Facial artery (e) Occipital artery (f ) Posterior auricular artery (g) Superficial temporal artery (h) Maxillary artery (MA) Occasionally, these branches arise from the ECA trunk. The ventral group arises anteriorly from the ECA and the dorsal group of branches arises posteriorly from the ECA.  Therefore, grouping the ECA branches based on their ventral or dorsal axis is more useful and more consistent. Ventral external carotid branches: (a) Superior thyroid artery (b) Lingual artery

Fig. 1.6  External carotid artery: (1) superior thyroid artery; (2) ascending pharyngeal artery; (3) lingual artery; (4) facial artery; (5) posterior auricular artery; (6) maxillary artery; (7) occipital artery; and (8) superficial temporal artery

(c) Facial artery (d) Maxillary artery Dorsal external carotid branches: (a) Ascending pharyngeal artery (b) Occipital artery (c) Posterior auricular artery (d) Superficial temporal artery 2. Territories The ECA supplies much of the soft tissue and bony structures of the head and face, the deep structures of the upper aero-digestive tract, and much of the dura of the intracranial compartment. Numerous anastomoses are present between ECA branches and the branches of the internal carotid and vertebral arteries. These anastomoses provide collateral flow to the vascular territories distal to a ­proximal occlusion. Anastomoses to carotid or vertebral arteries can also be considered “dangerous anastomoses” when attempting to embolize vascular lesions in the head and neck via external carotid branches. See below

1.3  External Carotid Artery

9

for discussion of individual ECA branch anastomoses and Tables 1.1, 1.2, 1.3, and 1.4. 3. Variants (a) The most frequent branching pattern seen at the common carotid bifurcation (in 48.5%) is the external carotid arises anteromedially while the internal carotid arises posterolaterally. The most frequent branching pattern seen at the common



carotid bifurcation finds the external carotid arising anteromedially. Occasionally, the ECA arises posterolaterally or directly laterally [8, 9]. (b) The ECA and ICA may rarely arise as separate branches of the aortic arch [7, 10]. (i) Some ECA branches, especially the superior thyroid artery, may arise from the CCA.

Table 1.1  Anastomosis to anterior circulation Anastomosis from Ascending pharyngeal, neuromeningeal trunk Ascending pharyngeal, inferior tympanic branch Ascending pharyngeal, superior pharyngeal Ascending pharyngeal, superior pharyngeal Accessory meningeal (cavernous branch) Middle meningeal (cavernous branch) Middle meningeal (cavernous branch) Distal maxillary (artery of foramen rotundum)

Anastomosis to Cavernous carotid via meningohypophyseal trunk

Comments/ Reference [14]

Petrous carotid via caroticotympanic

[14]

Cavernous carotid via inferolateral trunk

[14]

Petrous carotid via mandibular branch

[14]

Cavernous carotid via inferolateral trunk, posterior branch Cavernous carotid via inferolateral trunk, posterior branch Cavernous carotid via meningohypophyseal trunk Cavernous carotid via inferolateral trunk, anterolateral branch

[14] [14] [14] [14]

Table 1.2  Common anastomosis to ophthalmic artery Anastomosis from Middle meningeal, sphenoidal branch Middle meningeal, frontal branch Inferolateral trunk, anteromedial branch Distal maxillary, anterior deep temporal Distal maxillary, infraorbital Distal maxillary, sphenopalatine Distal facial Transverse facial Superficial temporal, frontal branch Cavernous carotid, inferolateral trunk

Anastomosis to Ophthalmic Ophthalmic via anterior falx artery Ophthalmic Ophthalmic Ophthalmic Ophthalmic via ethmoidal branches Ophthalmic Ophthalmic Ophthalmic Ophthalmic via recurrent meningeal branch

Comments/Reference [14] [14] [14] [14] [14] [14] [14] [14] [14] [14]

Table 1.3  Common anastomoses to posterior circulation Anastomosis from Ascending cervical Deep cervical Occipital, muscular branches Ascending pharyngeal, muscular branches Ascending pharyngeal, neuromeningeal trunk

Anastomosis to Vertebral segmental branches Vertebral segmental branches Vertebral segmental branches Vertebral segmental branches

Comments/Reference [14] [14] [14] [14]

C3 segmental vertebral via odontoid Odontoid arch connects side-to-side arch [14]

1  Essential Neurovascular Anatomy

10 Table 1.4  More trouble: cranial nerve blood supply Cranial nerve I: Olfactory II: Optic III: Oculomotor IV: Trochlear V: Trigeminal VI: Abducens VII: Facial VIII: Auditory IX: Glossopharyngeal X: Vagus XI: Spinal accessory XII: Hypoglossal







Arterial supply Anterior cerebral Supraclinoid carotid, ophthalmic Basilar, superior cerebellar, posterior cerebral, inferolateral trunk, ophthalmic Inferolateral trunk, meningohypophyseal trunk Inferolateral trunk, meningohypophyseal trunk, middle meningeal, accessory meningeal, artery of foramen rotundum, infraorbital Inferolateral trunk, meningohypophyseal trunk, middle meningeal, accessory meningeal, ascending pharyngeal (jugular branch) Stylomastoid (from post auricular or occipital), middle meningeal (petrous branch), ascending pharyngeal (inferior tympanic and odontoid arcade) Basilar, AICA, ascending pharyngeal jugular branch Ascending pharyngeal jugular branch

References [14] [14] [14, 70] [14, 70] [14, 70]

Ascending pharyngeal jugular branch, superior and inferior thyroid, laryngeal branches Ascending pharyngeal (jugular, inferior tympanic, and musculospinal branches)

[14, 19]

[14, 19, 70] [14, 71] [14, 72] [14, 19]

[14, 19]

Ascending pharyngeal, hypoglossal branch and proximal trunk, occipital, directly [14, 73] from external carotid, lingual

(ii) Some branches (especially the ascending pharyngeal or occipital arteries) may originate from the ICA. (iii) A common origin of superior thyroid, occipital, and ascending pharyngeal arteries from the ICA has been reported [11]. (iv) Rarely, all external carotid branches may arise from the ICA [12]. (v) External carotid branches may arise as common trunks with other branches including: linguofacial trunk (20% of cases), thyrolingual trunk (2.5% of cases), thyrolinguofacial trunk (2.5% of cases), and occipitoauricular trunk (12.5% of cases) [13].

1.4 Superior Thyroid Artery Whether it arises above or below the common carotid bifurcation, the superior thyroid artery originates from the anterior surface of the parent artery and immediately turns caudally to supply the anterior soft tissue structures of the neck.

1. Branches (a) Infrahyoid (hyoid) artery travels medially from its origin, and then follows along the lower hyoid bone. It can anastomose with the submental artery, providing a collateral pathway to the facial artery [14]. (b) Superior laryngeal artery travels alongside the internal laryngeal nerve inferomedially from its origin and pierces the thyrohyoid membrane to supply the mucosa of the larynx superior to the vocal cords and taste buds of the epiglottis [15]. (i) Branches • The superior thyroid artery has two major branches and a small epiglottic branch. Its ventral branch anastomoses with both the cricothyroid artery and superior laryngeal arcade. The dorsal branch anastamoses with the longitudinal laryngeal arcade [14]. (ii) Territory • The superior laryngeal artery supplies the pharyngeal and laryngeal structures as well as the internal laryngeal nerve. It anastamoses with its contralateral

1.5  Ascending Pharyngeal Artery









2.

partner and with the inferior laryngeal artery from the inferior thyroid artery. (iii) Variants • May arise as a separate branch from the ECA or ascending pharyngeal artery [14]. • In 6 of 22 anatomic specimens, the superior laryngeal artery does not pierce the thyrohyoid membrane but instead passes through a foramen in the thyroid cartilage to supply the soft tissues of the larynx [16]. (c) Sternocleidomastoid artery (i) The sternocleidomastoid artery feeds the middle part of the sternocleidomastoid muscle. It anastomoses superiorly with the muscular branches of the occipital and posterior auricular and inferiorly with the thyrocervical trunk and suprascapular. It can also connect with the glandular branches of the superior thyroid artery. (d) Cricothyroid artery (i) Anastomoses with the superior laryngeal artery and feeds the upper trachea. (e) Glandular branches. (i) These are a continuation of the superior thyroid trunk with superior, medial, and lateral arcades to supply the thyroid gland. They freely anastomose with their contralateral counterparts. Territories (a) The superior thyroid artery supplies the majority of the blood to the larynx, its associated musculature, and the upper pole of the thyroid gland [7]. In a minority of cases the superior thyroid provides blood flow to the parathyroid glands [17]. The superior laryngeal branch accompanies and can supply the internal laryngeal nerve. The superior thyroid branches freely anastomose with their contralateral

11

counterparts and the inferior thyroid artery (from the thyrocervical trunk). 3. Variants (a) The superior thyroid artery arises from the ECA in 46% of cases and more commonly, from the CCA in 52% of cases [18]. (b) The superior thyroid artery may arise in a common trunk with the lingual as a thyrolingual trunk. (c) Rarely, the superior thyroid artery may arise from the ICA [11].

1.5 Ascending Pharyngeal Artery The ascending pharyngeal artery is a thin, slender branch that arises from the very proximal posterior aspect of the ECA or in the crotch of the CCA (Fig. 1.7). It travels cephalad parallel to the ICA. Its termination in the superior pharynx creates a forward and medial right-angle turn. 1. Branches (a) Inferior pharyngeal artery (i) A relatively small vessel arising from the proximal ascending pharyngeal, the inferior pharyngeal travels anteriorly in a zigzag fashion. It supplies the pharyngeal muscles and mucosa. It anastomoses with its contralateral counterpart. (b) Musculospinal artery (i) The vessel may arise from the ascending pharyngeal itself or from the neuromeningeal trunk. It extends posteriorly and superiorly for a short distance before curving inferiorly. It primarily supplies muscles, but also may supply the ipsilateral upper spinal nerve roots, the eleventh cranial nerve, and superior sympathetic ganglion. In addition, it may anastomose with the ascending and deep cervical and vertebral arteries [14, 19].

1  Essential Neurovascular Anatomy

12



Fig. 1.7 Ascending pharyngeal artery. A common branching pattern of the ascending pharyngeal artery is shown. Note internal carotid (ICA), external carotid (ECA), superior thyroid (STh), ascending pharyngeal (AscPh), inferior pharyngeal (IP), middle pharyngeal (MP), superior pharyngeal (SP), inferior tympanic (IT), musculospinal branches (MS), neuromeningeal trunk (NMT), jugular branch (JB) entering the jugular foramen, hypoglossal branch (HG) entering the hypoglossal foramen, and prevertebral (not shown)



(c) Neuromeningeal trunk (i) This is a major branch of the ascending pharyngeal artery that continues cephalad but angles gently to the posterior. It has several important branches that pass through foramina in the skull base.

(ii) Branches • Musculospinal artery –– This branch may variably arise from the neuromeningeal trunk instead of originating from the ascending pharyngeal artery. • Jugular artery –– Often the largest branch of the neuromeningeal trunk, this vessel heads straight cephalad to the jugular foramen. It supplies the ninth through the eleventh cranial nerves and their ganglia. A medial branch ascends on the clivus to supply the eleventh cranial nerve. Its lateral branch travels along the dura around the sigmoid sinus. It can be a major contributor to the dura of the posterior fossa. Anastomoses with the lateral clival branch of the meningohypophyseal trunk and dural branches of the vertebral artery are possible [14]. • Hypoglossal artery –– This branch enters the hypoglossal canal and supplies the twelfth cranial nerve. It also supplies the dura in the posterior cranial fossa and anastomoses with the jugular branch, medial clival branches of the meningohypophyseal trunk, the contralateral hypoglossal artery, and the odontoid arcade [14, 20]. • Prevertebral artery –– It often arises from the neuromeningeal trunk and contributes to the odontoid arcade. It anastomoses with its contralateral counterpart, the anterior meningeal branch of the vertebral and hypoglossal artery branches [20].

1.5  Ascending Pharyngeal Artery



(iii) Territories • The very important neuromeningeal trunk of the ascending pharyngeal artery supplies cranial nerves VI, IX, X, XI, and XII, and potentially collateralizes to the upper three spinal nerves and the superior sympathetic ganglion. Its meningeal territory includes a large portion of the posterior fossa meninges. Anastomotic channels exist to its contralateral counterpart and meningeal branches of the vertebral artery and the meningohypophyseal trunk [19]. (iv) Variants • All branches of the neuromeningeal trunk are in vascular equilibrium with each other and with their anastomotic connecting vessels. Hypoplasia or absence of one or more vessels is accompanied by hypertrophy of the existing branches. (d) Prevertebral artery (i) Occasionally, this artery arises directly from the ascending pharyngeal artery and contributes to the odontoid arcade [20]. (e) Inferior tympanic artery (i) Branches [14] • Ascending branch connects to petrosal branch of middle meningeal artery. • Anterior branch connects to the caroticotympanic branch. • Posterior branch connects to the stylomastoid artery, a branch of the posterior auricular artery. (ii) Territories • Supplies the middle ear cavity and associated nerves, including the twelfth nerve and tympanic branch of the ninth cranial nerve (aka Jacobson’s nerve).

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(iii) Variants • May arise from the neuromeningeal branch, the ascending pharyngeal artery, or it may appear as a trifurcation with the inferior tympanic artery arising in between neuromeningeal and pharyngeal divisions [14]. (f ) Middle pharyngeal artery (i) Branches • No named branches. (ii) Territories • Supplies mucosa and muscles of the naso- and oropharynx as well as the soft palate [21]. Anastomoses with contralateral middle pharyngeal artery, ipsilateral ascending palatine artery, greater palatine artery, and branches of the accessory meningeal artery. (iii) Variants • May arise from ascending pharyngeal artery proximal or occasionally distal to the origin of neuromeningeal trunk. (g) Superior pharyngeal artery (i) As the most cephalad anterior branch of the ascending pharyngeal artery, this tends to be a small vessel. The pharyngeal branches take an abrupt anterior and medial angulation from the vertical ascending pharyngeal artery. (ii) Branches • There are several common branches of the superior pharyngeal artery, but only one is named. • The carotid branch actually traverses the cartilage filling the foramen lacerum and connects to the cavernous ICA via the inferolateral trunk. • Anterior unnamed branches to the upper nasopharynx and adjacent tissues.

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(iii) Territories • Supplies upper nasopharynx including the orifice of the Eustachian tube as well as associated muscles, including superior constrictor. Has many potential anastomoses, including accessory meningeal, pterygovaginal, and contralateral superior pharyngeal. If a Vidian branch is present, this is a potentially dangerous anastomosis during embolization procedures and it may also contribute to cavernous carotid fistulas via the petrous ICA. (iv) Variants • Pharyngeal territories of the superior pharyngeal artery may be primarily supplied by the accessory meningeal artery, Vidian artery, and other nasopharyngeal feeders. 2. Territories (a) Ascending pharyngeal artery supplies the mucosa and adjacent muscles of the pharynx, soft palate, odontoid process, bones, and muscles and nerve roots at C1 and C2. It also supplies the lower cranial nerves (IX–XII and potentially

3.



VI and VII); lower clivus and medial skull base; meninges of the posterior fossa; portions of the middle cranial fossa; and the middle ear. The ascending pharyngeal artery has extensive anastomoses with its contralateral counterpart, the occipital, middle, and accessory meningeal and distal maxillary arteries. Moreover, it has particularly dangerous anastomosis with the internal carotid and vertebral arteries [19]. This is a very busy little artery. Variants (a) The ascending pharyngeal artery may arise from the ICA. (b) Often arises as a common trunk with the occipital artery. (c) Ascending cervical artery may supply the territory of the ascending pharyngeal artery [14]. (d) Can contribute to the persistent hypoglossal artery variant. (e) Can reconstitute an occluded or aplastic vertebral artery. (f) The so-called “aberrant ICA” in the middle ear cavity is probably more appropriately termed the ascending pharyngeal artery, providing a collateral pathway for the territory of a segmentally occluded ICA [22, 23].

1.6  Lingual Artery

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Angio-Anatomic Correlate! Ascending Pharyngeal Artery Collaterals (Fig. 1.8) a

Fig. 1.8  Lateral view selective injections of the ascending pharyngeal artery in a patient with a dural arteriovenous fistula. Early arterial phase (a) starts to show faint anastomotic filling of the vertebral

1.6 Lingual Artery Arises from the ventral aspect of the external carotid and takes a gentle anterior-inferior path creating a characteristic “U” shaped curve on both frontal and lateral angiographic projections. It then curves upward, as the dorsal lingual branch forms an arc through the tongue with an arcade of radiating branches. 1. Branches (a) Suprahyoid artery (i) This small branch runs along the superior aspect of the hyoid bone and anastomoses with the contralateral suprahyoid artery [7]. (b) Dorsal lingual artery (i) May consist of two or three upwardly arching branches that curve up over the tongue, forming radiating branches that follow the pattern of the radiating intrinsic lingual muscle. The dorsal lingual artery anastomoses with its contralateral counterpart [7].

b

artery at the C1 level (arrow). Later arterial phase (b) shows considerable filling of the vertebral and basilar arteries (arrows)



(c) Sublingual artery (i) This branch angles anteriorly to supply the sublingual gland and floor of the mouth. It anastomoses with the submental branch of the facial artery and with its contralateral counterpart. A small branch pierces the lingual foramen of the mandible and supplies the adjacent bone [7]. (d) Deep lingual artery (i) This is a small terminal branch to the frenulum of the tongue [7]. 2. Territories (a) The lingual artery provides generous arterial supply to the tongue and floor of the mouth. There are anastomoses with the contralateral lingual and ipsilateral facial arteries via the submental branch. However, remember that branches extending to the tip of the tongue are effectively end arteries. Distal embolization with small particles or liquid agents can produce ischemic necrosis of the tip of the tongue, especially if the emboli are forced

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3.





across the midline via the side-to-side anastomosis, or if bilateral embolization is intentionally done. Variants (a) The lingual artery often arises with the facial artery from a common facial-­ lingual trunk (20% of cases) [13]. (b) Occasionally, it can arise with the superior thyroid artery as a common thyrolingual trunk (2.5% of cases), or thyrolinguofacial trunk (2.5% of cases) [13]. (c) It rarely arises from the CCA. (d) The lingual artery can supply variable amounts of the submental artery’s supply to the floor of the mouth.

1.7 Facial Artery The facial artery is usually one of the larger ECA branches and arises from the anterior aspect of the ECA. It then curves in a slightly redundant fashion through the submandibular gland, under and around the angle of the mandible, and then angles forward and cephalad, as well as medially to extend up along the angle of the nose as the angular artery. The facial artery has a number of named and unnamed branches that anastomose freely from one to the other and with other vessels in the face (Fig. 1.9). 1. Branches (a) Ascending palatine artery (i) This artery ascends for a few centimeters from its origin, and then takes a right angle forward to the soft palate by making a small loop-de-loop as it curves around the tonsils. Consequently, the ascending palatine artery can be a casualty of tonsillectomy or palatal surgery [21] and, along with the smaller tonsillar arteries, a source of postoperative bleeding.

Fig. 1.9  Facial artery: (1) ascending palatine artery; (2) tonsillar artery; (3) submental artery; (4) inferior masseteric artery; (5) jugal trunk; (6) middle mental artery; (7) inferior labial artery; (8) anterior jugal artery (not shown); (9) superior labial artery; (10) lateral nasal artery; and (11) angular artery

• Branches –– A cadaver study of palatine blood supply found three fairly constant and several less constant branches [24]. Glossal branch. Arises at the level of the upper border of the tongue and supplies the palatoglossus muscle. Tonsillar branch. Arises at the level of the oropharyngeal tonsil and supplies the tonsil and palatopharyngeus muscle and sometimes the palatoglossal muscles. Hamular branch. Arises adjacent to the hamulus of the medial pterygoid plate and mucosa and palatoglossus muscle.

1.7  Facial Artery







Variable branches to uvula, levator palatini, palatoglossus, and palatopharyngeus muscles. (ii) Territories • Supplies mucosa and muscles of the lateral oropharynx and soft palate. Anastomoses with contralateral ascending palatine artery, ipsilateral middle pharyngeal artery, the greater palatine artery, and the branches of accessory meningeal artery. (ii) Variants • Usually arises from the proximal facial artery. May arise directly from the ECA, from a common trunk with the submandibular branch, and occasionally from the middle pharyngeal artery (from the ascending pharyngeal artery) or even from the accessory meningeal artery [14]. (b) Tonsillar artery (i) This artery is comprised of one or more small proximal facial branches to the tonsils. The tonsillar artery, along with the ascending palatine artery, pharyngeal branches of the ascending pharyngeal, dorsal lingual branch of the lingual, and greater palatine branch of the maxillary, provides the dominant supply to the palatine (oropharyngeal) tonsil [7]. The tonsillar artery must, therefore, be considered a culprit, along with the ascending palatine artery, in postoperative bleeding after tonsillectomy. The tonsillar branches of the facial artery can also contribute to the nasopharyngeal tonsils, but most of the blood supply to that tonsil comes from the superior pharyngeal artery, ascending palatine artery, pterygovaginal artery, and occasionally the inferior hypophyseal branch of the meningohypophyseal trunk [7].

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(c) Submandibular branches (i) A small branch or branches to the submandibular gland region may arise from the submental artery and anastomose to the lingual and superior thyroid branches [25]. (d) Submental artery (i) This fairly large artery travels along the inferior margin of the mandible. It supplies the floor of the mouth in conjunction with the lingual artery. The submental artery anastomoses with the lingual artery via its submandibular branch and with the superior thyroid artery via its infrahyoid branch. It also has side-to-side anastomoses with its contralateral partner [25]. Its terminal branches curve up to the chin to anastomose with the middle mental and inferior labial arteries [7]. (e) Inferior masseteric artery (i) This anterior-superior angling branch follows and supplies the lower masseter muscle. It may have a small amount of collateral flow to the superior masseteric branch of the maxillary artery [25]. (f) Jugal trunk (i) The name is derived from the Latin jugālis, and refers to the zygoma or cheek. The jugal trunk is one of the three main superior-to-inferior anastomoses in the soft tissues of the cheek. • Branches • Two angiographically visible branches arise from the jugal trunk: –– Bucco-masseteric (aka buccal). Arises from the jugal trunk at the level of the ramus of the mandible, then heads in a cephalad direction and deeply into the cheek. It gives rise to a buccal branch that supplies the mucosa and deep parts of the cheek and a masseteric branch

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that feeds its namesake—the masseter. The buccal artery anastomoses with the distal maxillary artery via its buccal branch and the superior masseteric. The masseteric branch anastomoses with the trans- verse facial and infraorbital arteries. It characteristically crosses the transverse facial artery at a right angle on lateral angiographic views [25]. –– Posterior jugal. This branch travels obliquely anterior-­ superiorly and anastomoses with the infraorbital branch of the maxillary, superior alveolar, and the transverse facial arteries [25]. (g) Middle mental artery (i) A small horizontal branch along the body of the mandible that supplies skin and adjacent subcutaneous tissues. It anastomoses to adjacent facial artery branches and the inferior alve- olar branch of the maxillary artery [7]. (h) Inferior labial artery (i) This anterior and medially directed branch is the major supplier to the lower lip. It anastomoses with the contralateral inferior labial artery and the ipsilateral superior labial and submental arteries [25]. In 10% of angio- 2. grams this artery shares a common origin with the superior labial artery [26]. (i) Middle jugal artery (i) An inconstant branch that parallels and potentially anastomoses with the anterior and posterior jugal trunks [25]. ( j) Superior labial artery (i) Anterior and medially directed branch to the upper lip. It runs parallel to the inferior labial artery and is usually larger than that artery. It has septal and alar branches to the nose. It

1  Essential Neurovascular Anatomy

freely anastomoses with the contralateral superior labial artery and has potentially dangerous anastomoses with nasal branches of the ophthalmic artery [7, 25]. (k) Anterior jugal artery (i) The anterior-most of the upward angulated branches in the cheek, it supplies the anterior cheek and lateral aspect of the upper lip and nose. It freely anastomoses with the infraorbital, the posterior and middle jugal arteries, the transverse facial artery, and superior alveolar artery [25]. (l) Lateral nasal (aka alar) artery (i) This small branch extends anteriorly to supply the nostril and anastomoses with the contralateral alar artery [7]. (m) Nasal arcade (i) These arteries are a network of anastomotic channels curving over and across the nose. They collect and connect inputs bilaterally from the facial and ophthalmic arteries [25]. (n) Angular artery (i) Travels up along the angle lateral to the nose, hence its name. It supplies the cheek beside the nose and the lateral aspect of the nose, contributing to the nasal arcade. It has dangerous anastomoses with inferior palpebral and nasal branches of the ophthalmic artery [25]. Territories (a) The facial artery is the major supplier to the superficial soft tissues of the face and contributes to the masseter muscle, parotid gland, palate and tonsils, floor of the mouth, and portions of the buccal mucosa. It provides vasa nervosa to distal facial artery branches in the face. There are numerous anastomoses between facial branches and to virtually every other artery in the facial region, including major connections to the maxillary artery, transverse facial artery, and important collaterals to distal ophthalmic artery branches.

1.8  Occipital Artery

3. Variants Lasjaunias proposed a theory of hemodynamic balance in the face to explain the variety of arterial configurations [14, 25]. At six regions in the face (termed jugal, infraorbital, and ophthalmic superiorly, and mandibular, labial, and nasal inferiorly), dominance of blood flow to the region by one or the other potential inputs determines the course and size of the facial artery. For instance, there is balance between the buccal and masseteric arteries in the posterolateral aspect of the face and balance between the infraorbital and transverse facial arteries in the midportion. Numerous variations are possible. (a) The facial artery frequently arises as a common trunk with the lingual (20% of cases) [13]. (b) The proximal facial artery may have a posterolateral “jugal” course through the jugal region [14]. (c) The facial artery may also travel anteromedially through the labial point for a “labial course.” [14]. (d) The left and right facial arteries are symmetrical in 68% of autopsy cases [27]. (e) The facial artery terminates in: [27]. (i) Angular artery (68%) (ii) Lateral nasal branch (26%) (iii) Superior labial artery (4%)

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Fig. 1.10 Occipital artery: (A) sternocleidomastoid branches; (B) stylomastoid artery; (C) mastoid branch; (D) descending branch; (E) lateral meningeal branch; and (F) occipital branches

1.8 Occipital Artery The occipital artery is a large branch of the posterior aspect of the ECA and travels posteriorly and superiorly. The initial segment is straight as it goes up through the upper neck, and the artery becomes more tortuous and redundant as it travels up the posterior scalp (Fig. 1.10). 1. Branches (a) Sternocleidomastoid branches (aka muscular branches) There may be multiple muscular branches. The hypoglossal nerve hooks around the lowest branch of this artery as the nerve first heads inferiorly and then



anteriorly toward the tongue [7]. Each muscular branch characteristically tends to curve cephalad for a short distance before taking an abrupt turn posteroinferiorly. Each muscular branch corresponds to a vertebral level and provides segmental supply to the muscles, nerves, and bone at the corresponding levels. The occipital artery shares segmental vertebral blood supply with the vertebral artery, ascending pharyngeal artery, and deep cervical artery, which all anastomose extensively with the occipital artery muscular branches. The muscular branches that usually come from the occipital artery may also arise from the posterior auricular artery or directly from the ECA [14]. (b) Stylomastoid artery The stylomastoid artery arises from the occipital artery in 20–50% of cases [14, 28]. It is a common source of blood flow to the facial nerve and middle ear and it has anastomoses with the inferior tympanic, anterior tympanic, and superior tympanic arteries.

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(c) Mastoid artery This vessel angles cephalad and medially from the occipital artery, giving some supply to the soft tissue in the adjacent scalp before entering the skull via the occipital foramen. (i) Branches After it enters the skull, the mastoid commonly divides into three groups of branches: [14] • Descending branches. These approach the jugular foramen and anastomose with the jugular branch of the ascending pharyngeal. • Ascending branches. These approach the internal auditory canal and can anastomose with the sub arcuate branch of the anterior-inferior cerebellar artery (AICA). • Posteromedial branches. These spread out into the lateral dura of the posterior fossa and anastomose with branches of the hypoglossal branch of the ascending pharyngeal artery or the posterior meningeal branch arising from the vertebral (or posterior-­ inferior cerebellar) artery [14]. (ii) Territories The mastoid artery supplies the superficial soft tissue, bone, and dura in the mastoid and temporal bone region. It may supply large areas of the dura in the posterior fossa. (iii) Variants The mastoid artery may be absent or hypoplastic. Its territory may be supplied by middle meningeal artery, hypoglossal artery, jugular branches, or the meningeal branches of the vertebral artery. (d) Descending branch The most cephalad muscular branch at the occipital-C1 junction tends to be quite prominent, usually with large anastomotic connections to the vertebral artery





2.

3.





and a descending branch connecting to the deep cervical artery. (e) Lateral meningeal branches Distal to the origin of the mastoid branch, there may be one or more branches entering the skull via a small parietal foramen to supply the supratentorial dura. There are usually anastomoses with middle meningeal branches. (f ) Occipital branches Multiple scalp vessels, with a redundant zigzag configuration, arise from the occipital to supply the scalp, muscles, and pericranium. These anastomose with the contralateral occipital branches, the scalp branches of the posterior auricular, and the superficial temporal arteries [7]. Territories The occipital artery travels 3 cm lateral to the inion. It generally supplies the posterior third of the scalp; the occipital-frontalis, trapezius, and sternocleidomastoid muscles; portions of the occipital, mastoid, and temporal bones; dura; the seventh and ninth cranial nerves; and the first few spinal nerves. There are numerous anastomoses to the contralateral occipital artery, the ipsilateral ascending pharyngeal artery, vertebral artery, middle meningeal artery, superficial temporal artery, posterior auricular artery, deep cervical artery, and even the anterior-inferior cerebellar artery. Variants (a) The ascending pharyngeal may arise from the occipital artery. (b) There can be a common origin of the occipital with the posterior auricular artery as an occipitoauricular trunk (12.5% of cases) [13]. (c) The occipital artery may arise from the ICA. (d) The occipital artery can be a part of persistent carotid-vertebral anastomoses, such as a persistent proatlantal artery. (e) The occipital artery may originate from C1 or C2 segmental branches of the vertebral artery or from the ascending cervical artery [14, 29].

1.10  Superficial Temporal Artery

1.9 Posterior Auricular Artery This posterior branch of the distal external carotid is fairly small and can be identified angiographically by the tortuous scalp branch curving cephalad behind the ear. 1. Branches (a) Sternocleidomastoid (aka muscular) branch Proximal branch of the posterior auricular can assist the occipital in providing blood flow to the sternocleidomastoid, digastric, and stylohyoid muscles [7]. (b) Parotid branches Small branches from the proximal posterior auricular to the parotid that can supply portions of the facial nerve. (c) Stylomastoid branch The stylomastoid artery arises from the posterior auricular in 50–70% of cases [28, 30]. In order of frequency, it may also arise from the occipital or directly from the external carotid. It feeds the facial nerve and middle ear, mastoid air cells, and portions of the inner ear [7]. It can anastomose with anterior tympanic artery (from middle meningeal) and inferior tympanic (from ascending pharyngeal) artery. (d) Auricular branch A fairly constant branch seen in 65% of cases, this vessel supplies much of the posterior aspect of the pinna [31]. It branches from a dense arterial network in the ear. (e) Occipital (aka retroauricular) branch Also a fairly constant branch and is seen in 65% of cases. It supplies the scalp behind the ear. (f ) Parietal branch A fairly inconstant branch seen only when the superficial temporal does not have a dominant parietal branch. It has the typical ascending, tortuous appearance of a scalp vessel. 2. Territories The posterior auricular artery supplies the auricle and enters the middle part of the ear posteriorly [32]. It is the major supplier of blood

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flow to the ear [33]. It can supply portions of the parotid gland, facial nerve, sternocleidomastoid, digastric and stylohyoid muscles [7]. It has variable supply to the scalp posterior and superior to the ear, depending on the dominance of the superficial temporal and occipital arteries. It anastomoses with the superficial temporal and occipital arteries via the scalp and auricular branches. It also anastomoses with the middle meningeal artery (anterior tympanic branch) and ascending pharyngeal artery (inferior tympanic branch) via the stylomastoid artery. 3. Variants (a) Shares a common origin with the occipital artery (occipitoauricular trunk) in 12.5% of cases [13]. (b) The scalp territories of the posterior auricular artery are in a hemodynamic balance with the superficial temporal and occipital arteries. If one is hypoplastic, the adjacent vessels are hypertrophic, and vice versa.

1.10 Superficial Temporal Artery One of the two terminal branches of the external carotid (the other is the maxillary artery), this vessel continues the general vertical course of the ECA.  The superficial temporal artery arises behind the neck of the mandible within the parotid gland. It is easily palpable anterior to the ear at the tragus [7]. The superficial temporal artery typically provides two major branches that then angle cephalad in a wavy, redundant fashion typical of scalp vessels. 1. Branches (a) Transverse facial artery Originating anteriorly from the superficial temporal artery (within the parotid gland) the transverse facial artery travels anteriorly and slightly inferiorly between the parotid duct and zygomatic arch, supplying facial structures [7]. On a lateral angiogram it crosses the buccal artery at a right angle [14]. With agenesis or diminution of the facial artery, this branch may be the dominant artery of the face.

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(i) Branches The transverse facial artery commonly has a number of branches, but only one (superior masseteric) has a well-described formal name. • Parotid branches. These supply the parotid gland and duct and may contribute to facial nerve branches. • Superior masseteric. Prominent branch to the masseter muscle that anastomoses with the buccal artery (from the facial artery) [14]. • Jugal branches. One or more descending branches to the cheek that may anastomose with the jugal branches of the facial artery. • Zygomatic branches. These spread out into the face and anastomose with branches of the zygomatico-orbital branch of the superficial temporal artery [14]. Distally, these terminal branches may anastomose with the infraorbital and lacrimal arteries [7]. (ii) Territories The transverse facial artery supplies the superficial soft tissues of the upper face. It anastomoses with other superficial temporal and facial branches, as well as collaterals to the infraorbital and ophthalmic arteries. (iii) Variants The transverse facial artery may arise directly from the ECA. (b) Anterior auricular artery It is a proximal branch of the superficial temporal, supplying blood primarily to the anterior aspect of the ear. It has three branches, the most superior of which curves up over the helix to anastomose with posterior auricular artery. The lower two branches only provide limited supply to the anterior ear [32]. (c) Zygomatico-orbital artery (aka zygo­ maticotemporal)







This variably prominent, anteriorly directed branch of the superficial temporal artery runs just superior to the zygomatic arch toward the lateral aspect of the orbit. It supplies the scalp and the orbicularis occuli muscles [7]. It has numerous anastomoses with the frontal branch of the superficial temporal artery, transverse facial artery, and the supraorbital, frontal, palpebral, and lacrimal branches of the ophthalmic ­ artery [14]. (d) Middle temporal artery Also called the posterior deep temporal by some authors, this is a relatively small branch supplying the temporalis muscle, specifically its posterior aspect [34]. It potentially anastomoses with the deep temporal branches of the maxillary [7]. (e) Frontal branch One of the two large terminal branches of the superficial temporal takes a tortuous course over the frontal scalp and supplies tissue from skin down to pericranium. It anastomoses with its contralateral counterpart across the midline, the ipsilateral zygomatico-orbital branch of the superficial temporal, and the supraorbital and supratrochlear branches of the ophthalmic artery [7]. The distal frontal branch over the vertex can also provide branches that pass through foramina for emissary veins to anastomose with middle meningeal branches [14]. This is why superficial temporal arteries sometimes supply intracranial lesions such as meningiomas. (f ) Parietal branch The other, usually larger terminal branch of the superficial temporal, angles more posteriorly to supply the parietal scalp. It anastomoses with the contralateral parietal branch, ipsilateral frontal branch, posterior auricular, and occipital branches. It can also provide some transcranial anastomoses with the middle meningeal branches.

1.11  Maxillary Artery

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2. Territories The superficial temporal is a major contributor of blood flow to the scalp and is in a hemodynamic equilibrium with the occipital and posterior auricular arteries. There are extensive anastomoses between the superficial temporal branches and branches of the occipital, posterior auricular, middle meningeal, ophthalmic, and facial arteries. 3. Variants The major superficial branches vary considerably in size and territory. Hemodynamic balance exists between individual superficial temporal artery branches and competing scalp arteries. Therefore, when one artery is large and covers a wide territory, adjacent arteries may be small or absent.

was referred to as the external maxillary artery. The term IMA is still in popular use despite the anachronism. The MA arises at a right angle from the external carotid behind the neck of the ­mandible and travels anteriorly [7]. Anatomically, it can be divided into three segments: (1) the proximal mandibular part that travels horizontally, first posterior and then medial to the mandible; (2) the middle pterygoid part that travels anteriorly and cephalad (in a slightly oblique fashion) adjacent to the lateral pterygoid muscle (medial or lateral to it depending on whether it is the superficial or deep variant as described below); and (3) the distal pterygopalatine part that passes between the upper and lower heads of the lateral pterygoid, curves medially, and travels through the pterygomaxillary fissure into the pterygopalatine fossa [7]. The MA is found in two configurations:

1.11 Maxillary Artery The maxillary artery (MA) is the larger of the two terminal branches of the ECA. The MA was formally known as the internal maxillary artery (IMA), from an earlier time when the facial artery

1. The superficial-type MA travels lateral to the lateral pterygoid. In this variant, the accessory meningeal artery arises from the middle meningeal artery. The inferior alveolar and the middle deep temporal arteries arise separately from the MA (Fig. 1.11) [35, 36].

Fig. 1.11  Maxillary artery, superficial-type variant. The maxillary artery (MA) travels lateral to the lateral pterygoid muscle, and is characterized by separate origins of the middle deep temporal (MDT) and inferior alveolar artery (IAA). The accessory meningeal (AMA) arises from the proximal middle meningeal (MMA). Other IMA branches include deep auric-

ular (DA), anterior tympanic (AT), posterior deep temporal (PDT), pterygoid branches (not shown), masseteric branches (MaB), buccal artery (BuA), anterior deep temporal (ADT), posterior superior alveolar (PSA), infraorbital (IOA), greater palatine (GPA), pterygovaginal (PVA), artery of foramen rotundum (AFR), and sphenopalatine (Sph)

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Fig. 1.12  Maxillary artery, deep-type variant. The deep-­ type maxillary (MA) is medial to the lateral pterygoid muscle. This variant has a common trunk (arrow) that gives rise to the middle deep temporal (MDT) and inferior alveolar artery (IAA). Also note separate origins of the accessory meningeal (AMA) and middle meningeal artery (MMA). Superficial temporal origin (STA) and distal external carotid (ECA) are also shown

2. The deep-type MA travels medial to the lateral pterygoid. It gives rise to a common origin of the inferior alveolar and middle deep temporal arteries. The accessory meningeal artery, in this variant, arises directly from MA [35, 36]. Hint: Remember that the Deep-type MA has a common origin of the inferior alveolar and middle deep temporal arteries (Fig. 1.12). (a) Branches The mandibular part of the MA gives rise to the deep auricular, anterior tympanic, middle meningeal, accessory meningeal, and inferior alveolar arteries (i.e., branches that traverse foramina or fissures). The pterygoid part usually has deep temporal, pterygoid, masseteric, and buccal branches (i.e., muscular branches). The pterygopalatine part provides the posterior superior alveolar, infraorbital, artery of foramen rotundum, pterygovaginal, descending palatine, Vidian, and sphenopalatine arteries [7].

(i) Deep auricular artery • Tiny branch of very proximal maxillary artery • Branches –– No named branches. • Territories –– Supplies external auditory meatus, tympanic membrane, and temporomandibular joint [7]. • Variants –– May arise in a common trunk with the anterior tympanic artery (ii) Anterior tympanic artery • Very small branch of very proximal maxillary artery • Branches –– No named branches. • Territories –– Supplies tympanic cavity and anastomoses with the stylomastoid artery, pterygovaginal branch of the MA, and caroticotympanic artery from petrous ICA [7]. • Variants –– Analysis of 104 cadaveric specimens revealed extremely variable anterior tympanic artery origins [37]. –– May arise as a common trunk with deep auricular artery, middle meningeal artery, accessory meningeal artery, or posterior deep temporal artery. –– The anterior tympanic artery is a branch of the right MA in 78% of cases and a branch of the left MA in 45% of cases. –– Next most common site of origin: superficial temporal artery.

1.11  Maxillary Artery

25

–– 1–4% arise directly from the ECA. –– Rarely, the anterior tympanic artery may be duplicated, triplicated, or absent [37]. (iii) Middle meningeal artery (Fig. 1.13) • The first substantial ascending branch of the maxillary enters the cranial cavity through foramen spinosum. It then takes a characteristic right-angle turn.

In the sagittal plane, it turns anteriorly and in the coronal plane it turns laterally. • Branches –– Accessory meningeal branch This may be a major extracranial branch of the middle meningeal or may arise separately from the maxillary artery. The accessory meningeal artery is discussed in detail below.

Fig. 1.13  Middle meningeal artery: branches and anastomoses. The middle meningeal artery (MMA) often has a large extracranial branch, the accessory meningeal artery (AMA), which, in turn, has anastomoses with the greater palatine (Gr. Palatine) and ascending palatine (Asc. Palatine) arteries before entering the skull via the foramen ovale and anastomosing with cavernous branches of the internal carotid (ICA). The middle meningeal artery continues into the skull via the foramen spinosum. The petrous branch (Petrous Br.)

is the first intracranial branch and anastomoses with ascending pharyngeal branches in the temporal bone and with ICA branches via its cavernous branch (CB). Petrosquamosal (PSB), temporal, parietal, and frontal branches supply the dura over the middle and anterior fossa. Transcranial anastomoses with the superficial temporal (STA) and midline anastomoses with the anterior falx (AFA) branch of the ophthalmic (Ophth.) are depicted. The sphenoidal branch (Sph. Br.) is a major collateral to the ophthalmic



1  Essential Neurovascular Anatomy

26

–– Petrous branch The small but important petrous branch first gives a medial cavernous branch to the cavernous sinus that can anastomose with the posterior branch of the inferolateral trunk. It then gives a posterior basal tentorial branch, which anastomoses with basal tentorial branches of the petrosquamosal branch of the middle meningeal artery and cavernous branches of the ICA [14]. The artery then follows along the greater petrosal nerve and sends the superior tympanic branch to the facial nerve and geniculate ganglion. This portion of the artery anastomoses with the stylomastoid artery [7]. –– Petrosquamosal branch A posteriorly directed branch of the proximal intracranial middle meningeal artery, the petrosquamosal branch supplies the middle cranial fossa dura. It can have a basal tentorial branch to the dura of the posterior fossa, and it anastomoses with the jugular branch of the ascending pharyngeal [14]. –– Sphenoidal branch This branch supplies dura along the planum sphenoidale and then enters the orbit via the superior orbital fissure to communicate with the ophthalmic artery [38]. Sphenoidal collaterals to

the ophthalmic artery are present in 16% of cadaveric specimens [39]. –– Meningolacrimal branch The orbital branch is derived from the superior branch of the primitive stapedial artery and enters the orbit through the cranioorbital foramen (of Hyrtl) and directly fills the lacrimal artery [38]. This branch is present in 43% of cadaveric specimens [39]. –– Temporo-occipital (aka temporal) branch This branch arises distal to the sphenoidal branch and curves posteriorly. It supplies skull and dura of the middle cranial fossa. It may extend completely around the calvaria to the midline and contribute to the posterior falx and tentorium, but this is generally seen only in pathological states. It anastomoses with the petrosquamosal and parietal branches of the middle meningeal artery and with scalp arteries via transcranial collaterals. –– Parietal branch One of the two terminal branches of the middle meningeal artery, this vessel supplies the anterior cranial fossa dura. It can vary in size and distribution, since it anastomoses with and is in a hemodynamic balance with the frontal and t e m p o r o -­o c c i p i t a l branches. The parietal branch reaches the vertex

1.11  Maxillary Artery

and contributes to the walls of the superior sagittal sinus (SSS) and falx. At the midline, it anastomoses with the contralateral middle meningeal artery. Transcranial anastomoses with scalp arteries (superficial temporal and occipital) are present in nearly all cadaveric specimens [40]. –– Frontal branch Usually the last branch of the middle meningeal artery, this branch is in hemodynamic balance with the parietal branch; therefore, it can vary in size and distribution. It is a major contributor to the anterior cranial fossa dura. It can reach the midline and frequently anastomoses with the anterior falx branch of the ophthalmic artery. Other anastomoses include the ipsilateral parietal branch, the contralateral frontal branch, and transcranial collaterals of the scalp arteries, especially the frontal branch of the superficial temporal artery. • Territories –– The middle meningeal artery provides extensive flow to the calvaria and meninges of the anterior and middle fossae (Table 1.5). It has important collaterals to the ICA circulation [41]. The middle meningeal artery also contributes to the cranial nerves in the cavernous sinus via the cavernous branch and also to the facial nerve via the superior tympanic branch.

27

• Variants –– The middle meningeal artery develops from the fetal ­stapedial artery. The stapedial artery arises from the fetal hyoid artery, a branch that becomes the petrous ICA, and passes through the mesenchyme that later becomes the stapes (hence the name). The stapedial artery gives off supraorbital, maxillary, and mandibular branches, which are later incorporated into the ECA.  The supraorbital artery anastomoses with the developing ophthalmic artery [7]. Persistence of portions of fetal arteries that usually regress and/or regression of segments that usually persist, results in a number of congenital variants [42]. –– The distal middle meningeal artery frequently arises from the ophthalmic artery [43]. –– The middle meningeal artery may arise from the ICA [44, 45]. –– The ophthalmic artery may arise from the middle meningeal artery [46–49]. –– A number of extracranial branches may arise from the middle meningeal artery, including a palatine branch [50], as well as the posterior superior alveolar artery [51]. –– Tentorial branches (usually arising from cavernous ICA) may arise from the middle meningeal artery [52]. –– Occasionally, the middle meningeal artery may arise from the basilar artery [53–55].

1  Essential Neurovascular Anatomy

28 Table 1.5  Intracranial dural vascular supply Dural structure/ Region Posterior fossa

Tentorium

Falx cerebri

Anterior cranial fossa

Middle cranial fossa

Feeding arteries Petrosquamosal Petrous Mastoid Jugular Hypoglossal Posterior meningeal Anterior meningeal Artery of Bernasconi and Cassinari (marginal tentorial) Basal tentorial Petrosquamosal Mastoid Artery of Davidoff and Schechter Anterior falx artery Frontal and parietal branches Artery of Davidoff and Schechter Ethmoidals Recurrent meningeal Anterior falx Sphenoidal Frontal and parietal branches Inferolateral trunk Accessory meningeal Temporo-occipital Recurrent meningeal Carotid branch

Which usually arise from Middle meningeal Middle meningeal Occipital Ascending pharyngeal Ascending pharyngeal Vertebral Vertebral Cavernous carotid Cavernous carotid Middle meningeal Occipital Posterior cerebral Ophthalmic Middle meningeal Posterior cerebral Ophthalmic Ophthalmic Ophthalmic Middle meningeal Middle meningeal Cavernous carotid Middle meningeal Middle meningeal Ophthalmic Ascending pharyngeal

Reference

[6] [6] [6] [6] [14] [14] [14] [14] [209]

[209] [6]

[6] [6] [6] [6] [6]

These arteries should be considered with evaluating vascular lesions in and around the dura

–– The size and direction of the distal middle meningeal branches is extremely variable. –– Dural-to-pial collateral flow from middle meningeal artery branches to anterior or middle cerebral branches can occur. However, these variants are usually seen in the presence of occlusive disease (such as carotid occlusion with impaired collateral flow) [56] or with high-flow lesions (such as brain arteriovenous malformations). These are likely acquired connections due to high flow demand and release of angiogenic factors, rather than true congenital variants.



(iv) Accessory meningeal artery • This small branch arising either from the proximal middle meningeal or, less commonly, from the IMA just distal to the middle meningeal artery takes a characteristic gently curving antero-superior course. Ironically, in spite of its name, only about 10% (range 0–40%) of its blood supply is intracranial [57]. • Branches –– Terminal branches of the accessory meningeal vary in size and configuration and are variably named in the literature [58]. The major branches, ascending, descending, and recurrent rami, are named for the direction they take after

1.11  Maxillary Artery

a­rising from the accessory meningeal artery [57]. –– Lateral territory ascending ramus (aka posterior branch). –– Medial territory ascending ramus (aka inferomedial branch). –– Intracranial ascending ramus (aka intracranial branch). –– Small branch usually enters the skull via foramen ovale. –– Descending companion ramus to the medial pterygoid nerve (aka arteria pterygoida medialis). –– Anterior descending ramus (aka inferopalatine branch). This is the continuation of the main accessory meningeal artery and supplies the soft palate and the nasal cavity. –– Variable recurrent rami to mandibular nerve and otic ganglion. • Territories –– There are lateral, medial, and intracranial territories. Most of the blood supply is extracranial supplying lateral and medial pterygoid, the levator veli palatine muscles, the pterygoid plates, the greater wing of the sphenoid bone, the mandibular nerve, and otic ganglion. The artery also supplies the posterior nasal cavity and can be a source of nasal bleeding [59]. The intracranial contribution is usually small and enters the skull through foramen ovale (most commonly) or the sphenoidal emissary foramen of Vesalius (in 22% of cases) [57]. The intracranial rami supply the meninges of vari-

29



able portions of the middle cranial fossa, portions of the cavernous sinus and the trigeminal nerve and its ganglion. It can anastomose with the posterior limb of the inferolateral trunk of the cavernous ICA [60]. • Variants –– The origin of the accessory meningeal artery is from the middle meningeal artery when the internal MA is lateral to the lateral pterygoid muscle (superficial-type MA). –– The origin is from the maxillary artery when the MA is medial to the lateral pterygoid (deep-type MA). –– There can be multiple accessory meningeal arteries (25% of cases), but the artery is rarely absent (4% of cases) [57]. –– The rare persistent trigeminal variant consists of an anastomosis from the accessory meningeal artery to the superior cerebellar artery (SCA) [61]. (v) Inferior alveolar artery (aka dental artery) • This branch takes an anterior-­ inferior angulation from its origin from the proximal maxillary artery. It then enters the mandibular foramen, following along the mandibular canal. • Branches –– Mylohyoid branch. This is a small branch to the mylohyoid muscle arising from the inferior alveolar artery before entering the ­mandibular canal. It anastomoses with the submental branch of the facial artery [7].

1  Essential Neurovascular Anatomy

30



–– Incisive branch. One of two terminal branches of the inferior alveolar. Under the incisor teeth, the incisive branch reaches the midline, anastomosing with the contralateral incisive branch [7]. –– Mental branch. This branch travels out through the mental foramen of the mandible to anastomose with the submental and inferior labial branches of the facial artery [7]. • Territories –– The inferior alveolar supplies the mylohyoid muscle, the mandible, mandibular teeth, inferior alveolar nerve, and the soft tissues of the chin. • Variants –– The inferior alveolar artery arises as a common trunk with the middle deep temporal artery in the deep-type maxillary artery variant. –– The inferior alveolar artery may arise directly from the ECA [62]. (vi) Middle deep temporal artery • Complicating things further, some authors refer to this branch as the posterior deep temporal artery, but most authorities refer to it as the middle deep temporal artery. The deep temporal arteries ascend in a relatively straight course unlike the redundant superficial temporal branches. The middle deep temporal artery provides approximately one-half of the blood flow to the temporalis muscle [34]. It anastomoses with the superficial temporal artery and occasionally the transcranial collaterals from













this vessel can anastomose with the middle meningeal artery branches. A component of the deep-type maxillary artery variant is a common origin of the inferior and middle deep temporal arteries [35, 36]. (vii) Pterygoid branches • Small inferiorly directed branches of the distal pterygoid part to the pterygoid muscles that are not often visualized angiographically. (viii) Masseteric artery • Small, inferiorly directed branch to the masseter that anastomoses with masseteric branches of the facial and the transverse facial arteries. (ix) Buccal artery • Inferiorly directed branch that connects to the jugal trunk of the facial artery and supplies the soft tissues of the cheek from mucosa to skin. It provides collateral flow between the distal maxillary and facial arteries and has a connection to the transverse facial artery. (x) Anterior deep temporal artery • This artery angles cephalad in a fairly straight course to provide approximately 30% of the blood supply to the temporalis muscle [34]. This artery has important anastomoses to the lacrimal branch of the ophthalmic artery. (xi) Posterior superior alveolar artery • This artery descends behind the maxilla before sending branches to bone, teeth, and gingiva in the posterior aspect of the maxilla. (xii) Infraorbital artery • Anterior-most branch of the IMA that passes through the inferior orbital fissure, then

1.11  Maxillary Artery

enters the infraorbital canal to outline the roof of the maxillary sinus [7]. • Branches –– Middle superior alveolar branch. Contributes to the alveolar process of the mandible. –– Anterior superior alveolar branch. Also contributes to the supply of the maxillary teeth. –– Orbital branch. This artery primarily supplies the adipose tissue in the inferior aspect of the orbit and can anastomose with the ophthalmic artery [63]. –– Palpebral branch. Distal branch to the lower eyelid. It anastomoses with the dorsal nasal branch of the ophthalmic artery. –– Naso-orbital branch. Small branches to the anterior-­ inferior orbit and side of the nose that anastomose with the ophthalmic artery. –– Zygomatic branches. Lateral branch (or branches) supplying the cheek and connecting to the transverse facial artery and jugal trunk of the facial artery. • Territories –– The infraorbital artery supplies the adjacent infraorbital (maxillary) nerve, mucosa, and bony margin of the maxillary sinus [64]. Distal branches contribute to the lower eyelid and pre-­ maxillary cheek soft tissue [7]. Both the orbital branch and the distal infraorbital branch (palpebral branch) anastomose with the ophthalmic artery, putting vision

31









at risk when anything toxic is injected in the infraorbital artery [65]. The infraorbital artery connects to the posterior superior alveolar, sphenopalatine, and facial arteries. • Variants –– May be hypoplastic or hypertrophic, depending on the size of the facial artery. –– Can arise in a common trunk with the posterior superior alveolar artery. (xiii) Pterygovaginal artery • This is a small branch running posteriorly from the IMA into the pterygoid canal. It anastomoses with the accessory meningeal artery and ascending pharyngeal artery branches to the Eustachian tube region, and may connect with the petrous ICA. (xiv) Vidian artery (aka artery of the pterygoid canal) [66, 67]. • This artery may arise from the pterygovaginal artery, or separately from the IMA.  It enters the Vidian canal and may anastomose with a Vidian branch of the petrous ICA. (xv) Artery of foramen rotundum • Small, posteriorly directed branch with a characteristic wavy appearance as it passes through the foramen rotundum. Supplies the maxillary nerve and adjacent skull base. It is an important collateral to the anterolateral branch of the inferolateral trunk of the cavernous ICA. (xvi) Descending palatine artery • This large artery descends obliquely from its origin, travels in the pterygopalatine (aka greater palatine) canal, turns

1  Essential Neurovascular Anatomy

32

abruptly forward horizontally, and travels medial to the maxillary teeth to supply the palate. When it emerges from the greater palatine foramen, it then becomes the Greater palatine artery. • Branches –– Lesser palatine artery. Smaller branch or branches running parallel to the greater palatine artery in a separate bony canal, usually without a distal horizontal segment. May arise independently from the IMA [24]. –– Palatine branch. It is a small branch turning posteriorly to supply the soft palate and anastomoses with the middle pharyngeal and/or the ascending palatine. –– Septal branch. It is the terminal branch of the greater palatine at the incisive canal. It supplies the nasal septum and anastomoses with sphenopalatine and ethmoidal arteries. • Territories –– A major contributor to the blood supply of the hard palate, it also contributes to the mucosa, gingiva, soft palate, and tonsils [7]. Anastomotic connections exist with the contralateral greater palatine artery, ipsilateral middle pharyngeal artery, ascending palatine artery, sphenopalatine artery, and ethmoidal branches of the ophthalmic [14]. • Variants –– The greater palatine artery may be hypoplastic or absent on one or both sides.



–– Bilateral hypoplasia of the greater palatine artery is seen in cleft palate syndrome [68]. (xvii) Sphenopalatine artery • This is a major branch of the terminal IMA that enters the sphenopalatine foramen to supply the nasal cavity. This artery can be a major source of bleeding in epistaxis cases. The sphenopalatine artery can also supply vascular lesions in the nasal cavity such as juvenile nasopharyngeal angiofibromas. • Branches –– Septal branch This is a small branch that first goes straight medially, takes a right angle cephalad and another right angle medially before spreading out into the nasal septum. It also supplies the superior turbinate in 72% of cases [69]. –– Lateral nasal branch (aka posterior lateral nasal branch). This branch travels inferiorly before ramifying along the nasal turbinates to supply the nasal cavity mucosa. • Territories –– Sphenopalatine arteries supply the mucosa of nasal cavity and are a very common source of bleeding in idiopathic epistaxis. They anastomose with ethmoidal branches of the ophthalmic artery, the greater palatine artery, and the septal branch of the superior labial artery [7]. • Variants –– None described.

1.13  Internal Carotid Artery

(b) Territories (IMA) (i) The IMA supplies bones in the mid and lower face, muscles of mastication mucosa in the nasal cavity, the palate, numerous cranial nerves (III– VII), and large areas of dura [7]. There are multiple potential anastomoses with the internal carotid directly, and with the ophthalmic and numerous other vessels in the face and head. (c) Variants (IMA) (i) Superficial-type versus deep-type IMA (see beginning of IMA section, above). (ii) Rarely, the IMA shares a common origin with the facial artery [70].

1.12 Other ECA Branches Variable unnamed branches of the ECA are present. They are usually small and not well seen on angiography unless they are involved with a vascular malformation or neoplasm. The named branches that occasionally arise from the ECA usually arise from one of its major branches: 1. Tiny carotid body branches arise from the proximal ECA itself or from the proximal branches of the ECA. 2. The sternocleidomastoid branch (or branches) can arise from the ECA, but usually arises from the superior thyroid, occipital, or posterior auricular artery. 3. The superior laryngeal artery usually originates from the superior thyroid artery but can arise separately from the ECA. 4. A recurrent pharyngeal branch to the upper oropharynx and palate can arise directly from the ECA [24].

33

5. A small branch to the stylomastoid muscle arises from the distal ECA. 6. A small masseteric branch originates from the distal ECA. 7. The ascending palatine artery usually arises from the facial artery, but may originate directly from the proximal ECA. 8. The transverse facial artery frequently arises separately from the distal ECA, although it is more often a branch of the superficial temporal artery.

1.13 Internal Carotid Artery Several classification schemes exist for the segments of the ICA, including various numbering systems (Fig. 1.14). The numbering systems can be confusing and needlessly arcane for the purposes of everyday clinical work. The authors of this Handbook favor the following simple system (corresponding to the description by Gibo and colleagues): [71]. 1. 2. 3. 4.

Cervical Petrous Cavernous Supraclinoid

The segmental nomenclature used by Bouthillier and coworkers will be used in this chapter for the purpose of anatomic description [72]. The system established by Fischer in 1938 was intended to describe angiographic patterns of arterial displacement by intracranial tumors, numbered the ICA segments against the flow of blood, and excluded the extracranial ICA [73]. Subsequent systems have included the cervical segment and have numbered the segments with the flow of blood.

1  Essential Neurovascular Anatomy

34

Fig. 1.14  Selected segmental classification schemes of the internal carotid artery [71–73]

Angio-Anatomic Correlate! Carotid Bifurcation (Fig. 1.15) a

Fig. 1.15  The ICA usually arises lateral to the ECA, and is thought to be fixed at birth. Exceptions can occur, however. In this patient with lupus, the

b

ICA changed from a lateral position (a) to a medial position (b) after 4 months on high-dose steroids

1.14  Carotid–Vertebrobasilar Anastomoses

Cervical Segment (C1) This segment begins at the carotid bifurcation and ends at the skull base and usually has no branches. The carotid bifurcation is usually at the level of C3. The ICA receives approximately 80% of the flow from the CCA. The ICA is encircled by sympathetic fibers, and travels in the carotid sheath, which also contains the internal jugular vein and the vagus nerve. The uppermost portion of the carotid sheath (superior to the nasopharynx) also contains cranial nerves IX, XI, and XII. 1. Divisions (a) Carotid bulb. Focal dilation of the ICA at the origin, measuring 7.4 mm in diameter on average, compared to 7.0 mm for the CCA and 4.7 mm for the ICA distal to the carotid bulb [74]. (b) Ascending cervical segment. The diameter remains relatively constant throughout its course. Coiling or complete looping of the vessel is seen in up to 15% of angiograms [1]. 2. Branches: None 3. Variants (a) Position of origin. The carotid bifurcation can be found as low as T2 or as high as C1 [1]. Rarely, the ICA may arise directly from the aortic arch; in these cases the non-bifurcating carotid artery gives rise to all of the branches normally supplied by the ECA and then continues as the ICA [75]. (b) Agenesis and hypoplasia (i) Congenital absence or hypoplasia of the ICA may occur sporadically in association with other congenital anomalies, such as anencephaly or basal telangectasia [76]. Intracranial aneurysms are associated in 67% of cases [77]. (ii) Agenesis of the ICA has a prevalence of 0.01% [78] and can be distinguished from ICA occlusion by imaging of the skull base; in patients with agenesis, the carotid canal is

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absent [79]. Agenesis is more frequent on the left [80]. (iii) Bilateral ICA agenesis is seen in 3.0.CO;2-­V. 287. Zhang W, Ye Y, Chen J, et al. Study on inferior petrosal sinus and its confluence pattern with relevant veins by MSCT. Surg Radiol Anat. 2010;32(6):563– 72. https://doi.org/10.1007/s00276-­009-­0602-­z. 288. Tubbs RS, Watanabe K, Loukas M, Cohen-Gadol AA.  Anatomy of the inferior petro-occipital vein and its relation to the base of the skull: application to surgical and endovascular procedures of the skull base. Clin Anat. 2014;27(5):698–701. https://doi. org/10.1002/ca.22268. 289. Kurata A, Suzuki S, Iwamoto K, et al. A new transvenous approach to the carotid-cavernous sinus via the inferior petrooccipital vein. J Neurosurg. 2012;116(3):581–7. https://doi.org/10.3171/2011.4. JNS102155. 290. San Millan Ruiz D, Gailloud P, Rufenacht DA, Delavelle J, Henry F, Fasel JH.  The craniocervical venous system in relation to cerebral venous drainage. AJNR Am J Neuroradiol. 2002;23(9):1500–8. https://www.ncbi.nlm.nih.gov/pubmed/12372739 291. Braun JP, Tournade A. Venous drainage in the craniocervical region. Neuroradiology. 1977;13(3):155–8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve&db=PubMed&dopt=Citation&l ist_uids=865680 292. Arnautovic KI, Al-Mefty O, Pait TG, Krisht AF, Husain MM.  The suboccipital cavernous sinus. J Neurosurg. 1997;86(2):252–62. https://doi. org/10.3171/jns.1997.86.2.0252. 293. Galligioni F, Bernardi R, Pellone M, Iraci G.  The superficial sylvian vein in normal and pathologic cerebral angiography. Am J Roentgenol Radium Therapy, Nucl Med. 1969;107(3):565–78. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?

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1  Essential Neurovascular Anatomy 305. Raybaud CA, Strother CM, Hald JK.  Aneurysms of the vein of Galen: embryonic considerations and anatomical features relating to the pathogenesis of the malformation. Neuroradiology. 1989;31(2):109– 28. http://www.ncbi.nlm.nih.gov/entrez/query.fcg i?cmd=Retrieve&db=PubMed&dopt=Citation&l ist_uids=2664553 306. Gailloud P, O’Riordan DP, Burger I, Lehmann CU. Confirmation of communication between deep venous drainage and the vein of galen after treatment of a vein of Galen aneurysmal malformation in an infant presenting with severe pulmonary hypertension. AJNR Am J Neuroradiol. 2006;27(2):317–20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve&db=PubMed&dopt=Citation&l ist_uids=16484400 307. Lewis SB, Chang DJ, Peace DA, Lafrentz PJ, Day AL.  Distal posterior inferior cerebellar artery aneurysms: clinical features and management. J Neurosurg. 2002;97(4):756–66. http://www.ncbi. nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=P ubMed&dopt=Citation&list_uids=12405360 308. Siclari F, Burger IM, Fasel JH, Gailloud P.  Developmental anatomy of the distal vertebral artery in relationship to variants of the posterior and lateral spinal arterial systems. AJNR Am J Neuroradiol. 2007;28(6):1185–90. http://www.ncbi. nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=P ubMed&dopt=Citation&list_uids=17569985 309. Chakravorty BG. Arterial supply of the cervical spinal cord (with special reference to the radicular arteries). Anat Rec. 1971;170(3):311–29. http://www. ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve& db=PubMed&dopt=Citation&list_uids=5088404 310. Schalow G.  Feeder arteries, longitudinal arterial trunks and arterial anastomoses of the lower human spinal cord. Zentralbl Neurochir. 1990;51(4):181–4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve&db=PubMed&dopt=Citation&l ist_uids=2099053 311. Rodriguez-Baeza A, Muset-Lara A, Rodriguez-­ Pazos M, Domenech-Mateu JM.  The arterial supply of the human spinal cord: a new approach to the arteria radicularis magna of Adamkiewicz. Acta Neurochir. 1991;109(1–2):57–62. http://www.ncbi. nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=P ubMed&dopt=Citation&list_uids=2068969 312. Biglioli P, Roberto M, Cannata A, et  al. Upper and lower spinal cord blood supply: the continuity of the anterior spinal artery and the relevance of the lumbar arteries. J Thorac Cardiovasc Surg. 2004;127(4):1188–92. http://www.ncbi.nlm.nih. gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed &dopt=Citation&list_uids=15052221 313. Lo D, Vallee JN, Spelle L, et al. Unusual origin of the artery of Adamkiewicz from the fourth lumbar artery. Neuroradiology. 2002;44(2):153–7. http://www. ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve& db=PubMed&dopt=Citation&list_uids=11942368

References 314. Tveten L.  Spinal cord vascularity. III.  The spinal cord arteries in man. Acta Radiol Diagn (Stockh). 1976;17(3):257–73. http://www.ncbi.nlm.nih.gov/ entrez/query.fcgi?cmd=Retrieve&db=PubMed&dop t=Citation&list_uids=937044 315. Adamkiewicz A.  Die Blutgefasse des menschlichen Ruckenmarkes. I.  Theil. Die Gefasse der Ruckenmarkssubstanz. Sitzungsberichte der Kaiserlichen Akademie der Wissenschaften, mathematisch-naturwissenschaftliche Classe. 1881;84:469–502. (In German) 316. Adamkiewicz A.  Die Blutgefasse des menschlichen Ruckenmarkes. II.  Theil. Die Gefasse der Ruckenmarks-Oberflache. Sitzungsberichte der Kaiserlichen Akademie der Wissenschaften, mathematisch-naturwissenschaftliche Classe. 1882;85:101–30. (In German) 317. Desproges-Gotteron R. Contribution á l’étude de la sciatque paralysante (thése). Paris; 1955. 318. Gregg L, Gailloud P.  Transmedullary venous anastomoses: anatomy and angiographic visualization using flat panel catheter angiotomography. AJNR Am J Neuroradiol. 2015;36(7):1381–8. https://doi. org/10.3174/ajnr.A4302. 319. Koutsouflianiotis K, Daniil G, Paraskevas G, Piagkou M, Chrysanthou C, Natsis K.  Computed tomography angiography study of the azygos vein course and termination into superior vena cava: gender and age impact. Surg Radiol Anat. 2021;43(3):353–61. https://doi.org/10.1007/s00276-­020-­02583-­8. 320. Tatar I, Denk CC, Celik HH, et al. Anatomy of the azygos vein examined by computerized tomography imaging. Saudi Med J. 2008;29(11):1585–8. https:// www.ncbi.nlm.nih.gov/pubmed/18998005 321. Yeh BM, Coakley FV, Sanchez HC, Wilson MW, Reddy GP, Gotway MB.  Azygos arch valves: prevalence and appearance at contrast-enhanced CT.  Radiology. 2004;230(1):111–5. https://doi. org/10.1148/radiol.2301021216. 322. Habel RE, Budras KD.  Bovine anatomy: an illustrated text. Hanover: Schlütersche GmbH & Co.; 2003. 323. Layton KF, Kallmes DF, Cloft HJ, Lindell EP, Cox VS.  Bovine aortic arch variant in humans: clarification of a common misnomer. AJNR Am J Neuroradiol. 2006;27(7):1541–2. http://www.ncbi. nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=P ubMed&dopt=Citation&list_uids=16908576

111 324. Pickhardt PJ, Siegel MJ, Gutierrez FR.  Vascular rings in symptomatic children: frequency of chest radiographic findings. Radiology. 1997;203(2):423– 6. http://www.ncbi.nlm.nih.gov/entrez/query.fcg i?cmd=Retrieve&db=PubMed&dopt=Citation&l ist_uids=9114098 325. Gottfried ON, Soleau SW, Couldwell WT.  Suprasellar displacement of intracavernous internal carotid artery: case report. Neurosurgery. 2003;53(6):1433–4; discussion 1434–5. http://www. ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve& db=PubMed&dopt=Citation&list_uids=14633312 326. Hayreh SS, Dass R. The ophthalmic artery. II. Origin and intracranial and intra-canalicular course. Br J Ophthalmol. 1962;46:165–85. 327. Marinkovic S, Kovacevic M, Gibo H, Milisavljevic M, Bumbasirevic L.  The anatomical basis for the cerebellar infarcts. Surg Neurol. 1995;44(5):450– 60; discussion 460–1. http://www.ncbi.nlm.nih.gov/ pubmed/8629230 328. Acar F, Naderi S, Guvencer M, Ture U, Arda MN. Herophilus of Chalcedon: a pioneer in neuroscience. Neurosurgery. 2005;56(4):861–7; discussion 861–7. http://www.ncbi.nlm.nih.gov/entrez/ query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citat ion&list_uids=15792526 329. Zouaoui A, Hidden G. Cerebral venous sinuses: anatomical variants or thrombosis? Acta Anat (Basel). 1988;133(4):318–24. http://www.ncbi.nlm.nih.gov/ entrez/query.fcgi?cmd=Retrieve&db=PubMed&dop t=Citation&list_uids=3227793 330. van Rooij SB, van Rooij WJ, Sluzewski M, Sprengers ME.  Fenestrations of intracranial arteries detected with 3D rotational angiography. AJNR Am J Neuroradiol. 2009;30(7):1347–50. https://doi. org/10.3174/ajnr.A1563. 331. Uchino A, Nomiyama K, Takase Y, Kudo S. Anterior cerebral artery variations detected by MR angiography. Neuroradiology. 2006;48(9):647–52. https:// doi.org/10.1007/s00234-­006-­0110-­3. 332. Kobayashi S, Yuge T, Sugita Y, et al. Azygos anterior cerebral artery aneurysm associated with fenestration of the anterior cerebral artery. Kurume Med J. 1986;33(3):149–53. http://www.ncbi.nlm.nih.gov/ pubmed/3599873

2

Diagnostic Cerebral Angiography

2.1 Cerebral Angiography Noninvasive vascular imaging including computed tomography (CT) and magnetic resonance angiography (MRA) can give high-resolution depiction of cerebral vascular anatomy and pathology. However, cerebral arteriography, which predated these noninvasive tests, still provides greater detail in the depiction of small vessels and subtle changes in the lumen. It is less prone to artifacts and also provides information on the speed and direction of flow in vessels, which may only be indirectly evident on computed tomography angiography (CTA) or MRA. No question, a cerebral arteriogram is a much more involved procedure for the patient than a simple “X-ray of the brain arteries,” which is how it is often described. The procedure has benefitted from technological advancement with smaller catheters, lower-dose fluoroscopic equipment, and less-toxic contrast agents. Most importantly, the operators performing the procedure can benefit from the errors and follies of their predecessors and perform the procedure safely and effectively. Angiography remains an invaluable tool for workup of patients with suspected neurovascular abnormalities. Diagnostic angiography is also frequently an important part of any neurointerventional proce-

dure. Mastery of diagnostic angiography is a prerequisite for neurointerventional training. Training standards formulated by the American Society of Interventional and Therapeutic Neuroradiology (ASITN), the Joint Section of Cerebrovascular Neurosurgery, and the American Society of Neuroradiology (ASNR) recommend the performance of at least 100 diagnostic angiograms before entering neuroendovascular training [1]. This Handbook authors’ preference, however, is for a neurointerventionalist-in-­ training to perform at least 250 diagnostic cerebral angiograms prior to becoming the lead operator in neurointerventional cases.

2.2 Indications 1. Diagnosis of primary neurovascular disease (e.g., intracranial aneurysms, arteriovenous malformations [AVMs], dural arteriovenous fistulas, atherosclerotic stenosis, vasculopathy, cerebral vasospasm, acute ischemic stroke). 2. Planning for neurointerventional procedures. 3. Intraoperative assistance with aneurysm surgery. 4. Follow-up imaging after treatment (e.g., after aneurysm coiling or clipping, treatment of arteriovenous fistulas).

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 M. R. Harrigan, J. P. Deveikis, Handbook of Cerebrovascular Disease and Neurointerventional Technique, Contemporary Medical Imaging, https://doi.org/10.1007/978-3-031-45598-8_2

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2.3 A Brief History of Cerebral Angiography The first report of X-ray angiography of blood vessels was in 1896. In Vienna, E. Haschek and O.T. Lindenthal obtained X-rays of blood vessels by injecting a mixture of petroleum, quicklime, and mercuric sulfide into the hand of a cadaver [2]. António de Egas Moniz, a Portuguese neurologist, is credited with the introduction of cerebral angiography. Moniz was interested in developing “arterial encephalography” as a means to localize brain tumors. He obtained cerebral angiograms in cadavers using a solution of strontium bromide and sodium iodide. These early studies demonstrated universal branching patterns among the intracranial arteries, which were contrary to popular theories based on cadaver dissection. After studies in dogs and monkeys, Moniz and his pupil Almeida Lima performed the first angiogram on living human patients in 1927 [3]. The initial attempts were done using percutaneous injections of strontium bromide, which failed to show any opacified vessels [4]. In later attempts, the cervical internal carotid artery (ICA) was surgically exposed and temporarily occluded with a ligature while a total of 5 mL of a solution of 25% sodium iodide was injected into the vessel. Flow was restored in the artery while simultaneously obtaining an X-ray. After the ninth attempt, successful visualization of the vessels was obtained. Monitz declared: “Nous avons realise notre desideratum” (“Now that’s what I needed”). [4] Although no complications were noted during the procedure, one patient died two days later in status epilepticus [5]. Moniz went on to obtain successful angiograms in other patients with epilepsy, brain tumors, and postencephalitic Parkinsonism [6, 7]. The first cerebral venogram was accomplished in 1931 when an inadvertent delay in photographing an angiographic plate led to an image of the venous angiographic phase, which Moniz termed a “cerebral phlebogram.” The technique became fully developed in the 1930s. By then, cerebral angiography involved direct percutaneous puncture of the carotid artery

2  Diagnostic Cerebral Angiography

and injection of iodinated organic contrast media [8]. Despite a flurry of publications about cerebral angiography over the ensuing decade, many by Moniz himself, ventriculography and encephalography remained more popular as methods to image intracranial pathology [9]. Moniz was awarded the Nobel Prize in Physiology and Medicine in 1949 for his work on frontal leukotomy for psychiatric disorders, which, unlike cerebral angiography, gained early and widespread acceptance by the medical community [10]. The popularity of cerebral angiography did rise significantly by the 1950s, becoming the premier method to image the intracranial space. The neurosurgeon Gazi Yasargil performed some 10,000 angiograms between 1953 and 1964 [9]. Direct percutaneous puncture of the cervical carotid artery remained the primary technique for cerebral angiography in the 1950s and 1960s. Direct puncture of the vertebral artery was reported in 1956 [11]; the posterior circulation was also imaged by puncture of the right brachial artery and retrograde injection of the contrast into the vertebral artery [12, 13]. The movie The Exorcist (1973) featured a graphic (and realistic) depiction of a direct carotid stick. The transition from direct puncture of the cervical vessels to transfemoral artery arteriography began in the late 1960s [14] and became widespread in the 1970s. The introduction of computed tomography (CT) in the early 1970s sharply reduced the demand for diagnostic angiography, although the field continued to develop because of the advent of interventional cardiology and other interventional fields. Metrizamide, introduced in the 1970s, was the first nonionic iso-osmolar iodinated contrast medium. Nonionic contrast media improved the safety and comfort of angiographic procedures considerably. Digital subtraction angiography (DSA) was introduced in the 1980s as a method for intravenous (IV) injection of contrast for imaging the arterial system, as the contrast in the arterial system following intravenous injection was too dilute to be imaged with standard X-rays. Over the ensuing decade, the spatial resolution of DSA imaging

2.4 Complications of Cerebral Angiography

improved to the extent that it began to rival the resolution of unsubtracted X-ray images. Further technical refinements in recent years include rotational angiography, three-­dimensional (3D) angiography, and flat panel detectors for imaging. In the last decade, the rapid evolution of CTA and MRA has made DSA obsolete for the routine evaluation of subarachnoid hemorrhage and follow-up after endovascular treatment of intracranial aneurysms. Indeed, it is disappointing that catheter angiography is still widely used for routine followup of aneurysms in many centers. Global Gem! European Origins of Cerebral Angiography

Europe was the cradle of cerebral angiography. After Moniz introduced cerebral angiography in Portugal, numerous other Old World pioneers contributed to the early development of the technique, including Herbert Olivecrona, Erik Lysholm, Georg Schönander, and Sven-Ivar Seldinger (Sweden); Norman Dott (Scotland); Arne Torkildsen (Norway); Sigurd Wende (Germany); Fedor Serbinenko (Russia); Georg Salamon and René Djindjian (France); and George Ziedses des Plantes (the Netherlands).

2.4 Complications of Cerebral Angiography Informed consent prior to an angiogram should include quantitative estimates of the risk of complications. 1. 24-h risk of stroke and death:  50; 5F CK-1 (aka HN-5): Left common carotid or right vertebral artery; 5F H1 (aka Headhunter): Right subclavian artery, right vertebral artery; and 4 or 5F Newton: Tortuous anatomy, patients >65

dle. This incomprehensible gauge system was developed by the British Catheters: French (F), defined as the outer diameter of a catheter measured as a multiple of thirds of a millimeter (French number/3 = outer diameter in mm) Wires: Measured in thousandths of an inch. (a 0.035 wire is 0.035 in. thick)

Catheter Navigation Diagnostic catheters should usually be advanced over a hydrophilic wire. The wire keeps the catheter tip from rubbing against the wall of the vessel and causing intimal injury. When advancing the wire and catheter toward the aortic arch from the femoral artery, the tip of the wire should be followed by direct fluoroscopic visualization. Avoid advancing the catheter/wire assembly with 50 years), and those with a bovine arch configuration, the Simmons II

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catheter is helpful for accessing the left common carotid. 5. If selective internal carotid artery catheterization is planned, first do angiography of the cervical carotid system to check for internal carotid artery stenosis in any patient at risk of atherosclerosis. Catheterization of the internal carotid artery should be done under roadmap guidance. 6. Turning the patient’s head away from the carotid being catheterized may allow the wire and/or catheter to enter the vessel more easily. 7. Once the common carotid is catheterized, turning the head away from the side being catheterized facilitates internal carotid catheterization, and turning toward the ipsilateral side facilitates external carotid catheterization. 8. When the wire or catheter does not advance easily into the vessel of interest, ask the patient to cough. It often bounces the catheter into position.

2.23 Vertebral Artery Catheterization 1. Place an angled diagnostic catheter over a hydrophilic wire and into the subclavian artery. Intermittent “puffing” of contrast will allow identification of the vertebral artery origin. 2. Make a roadmap and pass the wire into the vertebral artery until the tip of the wire is in the upper third of the cervical portion of the vessel. Placing the wire relatively high in the vertebral artery provides adequate purchase for advancement of the catheter, will help straighten out any kinks in the artery that may be present near the origin, and will also facilitate smooth passage of the catheter past the entrance of the artery into the foramen transversarium at C6. The C6 foramen transversarium is where the vertebral artery makes a transition from free-floating to fixed, and is a region at risk for iatrogenic dissection if the catheter is allowed to scrape against the wall of the vessel.

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3. Remember that the vertebral artery makes a right-angle turn laterally at C2, so be careful not to injure the vessel at that point with the wire. 4. After removal of the wire, and double flushing, do an angiogram with the tip of the catheter in view, to check for dissection of the vessel during catheterization. 5. For patients at risk of atherosclerosis, do an angiogram of the vertebral artery origin prior to accessing the vessel to check for stenosis. 6. In approximately 5.8% of patients [59], the left vertebral artery arises directly from the aorta, which should be kept in mind when the origin of the vessel cannot be found on the left subclavian artery. 7. When kinks or loops in the vessel prevent catheterization, ask the patient to tilt their head away from the vertebral artery being catheterized.

2  Diagnostic Cerebral Angiography

great vessels or atherosclerotic stenosis, inflate a blood pressure cuff on the ipsilateral upper extremity and inject 100% contrast into the subclavian artery with a power injector. The inflated cuff will direct flow away from the arm and toward the vertebral artery. Be careful not to place the catheter with its tip in the thyrocervical or costocervical trunks. A large volume contrast injection in these small vessels can be painful, and can cause spinal cord injury in cases where large spinal cord feeders arise from these branches, or even directly from the subclavian artery. If the catheter tip cannot be placed in a stable position in the subclavian artery proximal to the origin of the vertebral artery, place the tip distal to the origin of the vertebral artery. 5. Set the power injector to allow a good injection without kicking the catheter out: 6 mL/s, total of 25 mL; linear rate-rise: 0.5 s.

Several options exist for patients in whom vessel tortuosity (usually of the innominate artery) makes catheterization of the vertebral artery difficult.

2.24 Reconstituting a Simmons 2 Catheter

1. Do a roadmap with an ipsilateral oblique Towne view; this will show the vertebral artery origin and separate the vertebral artery from the common carotid artery. 2. Try a Headhunter catheter. It is well suited for navigation through a tortuous innominate artery. 3. Other catheters that can be helpful in negotiating a difficult right vertebral artery are the Vertebral catheter and the Dural arteriovenous fistula (DAV) catheter. 4. When catheterization of the vertebral artery is not possible because of tortuosity of the

The Simmons 2 catheter is useful in the catheterization of the left common carotid artery, particularly when there is a bovine configuration, when the aortic arch is tortuous, and in patients aged >50. The catheter can be reconstituted in the left subclavian artery, the aortic arch, or the aortic bifurcation (Figs.  2.7 and 2.8). Reconstitution in the left subclavian or aortic bifurcation is preferred to the aortic arch, to minimize risk of dislodging atherosclerotic plaque material and subsequent embolization into the intracranial circulation. Remember that the tip of the Simmons catheter advances into the vessel when the catheter is

2.24 Reconstituting a Simmons 2 Catheter

a

b

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c

Fig. 2.7  Reconstituting a Simmons 2 catheter in the left subclavian artery. The catheter is advanced over a hydrophilic wire into the left subclavian artery so that the tip is in the subclavian artery (a), and the primary bend in the catheter (the “elbow”) is in the aortic arch. The wire is

then withdrawn until the tip is proximal to the elbow (b), and the catheter is then pushed forward, until the elbow moves into the proximal part of the aortic arch (c), and the tip of the catheter is out of the subclavian artery, directed backward toward the shaft of the catheter

pulled back at the groin and pulls out of the vessel when the catheter is pushed forward at the groin. This effect is the reverse of the behavior of more simple-curved or angled catheters. The

Simmons catheter can also be advanced antegrade over a wire, allowing for selective catheterization of the internal or external carotid arteries.

2  Diagnostic Cerebral Angiography

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a

b

c

d

Fig. 2.8  Alternative method for reconstituting a Simmons 2 catheter. The catheter is advanced over a hydrophilic wire so the tip of the catheter is in the ascending aorta (a). The wire is then withdrawn until the wire tip is proximal

to the elbow, and the catheter is rotated clockwise as it is simultaneously withdrawn so that the loop is in the descending aorta (b, c). The wire is then advanced swiftly (d), to reconstitute the catheter

2.26 Closure Devices

2.25 Femoral Artery Puncture Site Management The “gold standard” for management of the arteriotomy after an angiogram is manual compression. 1. Remove the sheath and apply pressure to the groin 1–2 cm superior to the skin incision. 2. Apply pressure for 15 min: usually 5 min of occlusive pressure, followed by 10  min of lesser pressure. (a) For patients on aspirin and/or clopidogrel, a longer time is required, usually 40 min. 3. At the end of the time period, release pressure on the groin slowly and apply a pressure dressing. 4. The Chito-seal™ pad (Abbott Laboratories, Abbott Park, IL) and the Syvek® NT Patch (Marine Polymer Technologies, Inc., Danvers, MA) are topical hemostatic agents that can be applied to the incision after sheath removal to accelerate hemostasis. (a) In an animal model, the Syvek® Patch was found to control bleeding better than Chito-seal™ [60]. (b) These topical agents cannot be expected to produce the same security of hemostasis as the closure devices described below, especially if the sheath size is greater than 5F. 5. A balloon compression dressing (FemoStop®plus Femoral Compression System, Radi Medical Systems, Wilmington, MA) compresses the site with a balloon, but the balloon must be deflated after 1 h to prevent pressure injury to the skin. The dressing is then left in place and the balloon can be reinflated if oozing from the site occurs. 6. After compression, the patient should remain supine for 5  h, then be allowed to ambulate but remain under nursing observation for one more hour prior to discharge. 7. Of note: A study of coronary angiographic procedures showed no difference in vascular complications between 2, 4, and 6  h bedrest after hemostasis, even when using abciximab [61].

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8. Early mobilization even as early as 1.5 h after hemostasis does not significantly increase the incidence of hematomas but definitely reduces complaints of back pain [62]. 9. Using topical hemostatics, the patient should generally remain flat in bed for 2 h, and can ambulate in 3 h.

2.26 Closure Devices Percutaneous femoral artery closure devices can allow the patient to ambulate sooner than with compression techniques, and can be helpful when the patient is on antiplatelet or anticoagulant medications. Most closure device instructions recommend puncture site arteriograms (Fig. 2.9) since use of these devices may be contraindicated if a bifurcation or excessive plaque is at the puncture site. When a closure

Fig. 2.9  Femoral artery angiogram done prior to the use of a closure device. Injection of contrast through the sheath shows that the sheath enters the femoral artery proximal to the bifurcation. Optimal visualization of the femoral bifurcation is usually obtained with an ipsilateral or contralateral oblique angiogram

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device is used, the patient should remain supine for 1 h. However, there is a greater risk of complications with the use of closure devices. In a meta-analysis to assess the safety of closure devices in patients undergoing percutaneous coronary procedures, an overall analysis favored mechanical compression over closure devices [63].

2  Diagnostic Cerebral Angiography

ing Mynx to Angio-Seal found a higher rate of device failure with Mynx [67].

2.28 Post-Angiogram Orders

1. Bed rest with the accessed leg extended, head of bed ≤30°, for 5 h, then out of bed for 1 h (if a closure device is used, bed rest, with head of bed ≤30°, for 1 h, then out of bed for 1 h). 2.27 Selected Femoral Artery 2. Vital signs: Check on arrival in recovery room, Closure Devices then Q 1 h until discharge. Call physician for Systolic blood pressure (SBP) 120. Abbott Park, IL). 3. Check the puncture site and distal pulses upon (a) Closure method: A proline stitch is placed arrival in recovery room, then Q 15 min × 4, Q in the arteriotomy. 30 min × 2, then Q 1 h until discharge. Call (b) Requires a femoral artery angiogram; the physician if: puncture site must be at least 1 cm away (a) Bleeding or hematoma develops at puncfrom major branches of the vessel, such ture site. as the femoral artery bifurcation (b) Distal pulse is not palpable beyond the (Fig. 2.8). puncture site. (c) Advantage: The same artery can be re-­ (c) Extremity is blue or cold. punctured immediately if necessary. 4. Check puncture site after ambulation. 2. Angio-Seal™ (Terumo Medical, Somerset, 5. Intravenous fluids (IVF): 0.9 N.S. at a mainteNJ). nance rate until patient is ambulatory. (a) Closure method: The device creates a 6. Resume pre-angiogram diet. mechanical seal by sandwiching the arte- 7. Resume routine medications. riotomy between a bioabsorbable anchor 8. Per oral (PO) fluids 400 mL. and a collagen sponge, which dissolves 9. D/C IV prior to discharge. within 60–90 days. (b) May be used at femoral artery branch points. 2.29 Radial Artery Access (c) If re-puncture of the same femoral artery is necessary within 90  days, then the Why Radial Artery Access? reentry site should be 1  cm proximal to the previous site [64, 65]. The radial artery is an easily palpable vessel and is a 3. Mynx™ Cadence (AccessClosure, Mountain common access point for arterial pressure monitorView, CA). ing. The arteries of the upper extremity were used as (a) Closure method: The device places an an alternative to the femoral artery for both diagnosexpanding glycolic sealant over the tic cerebral angiography and some neurointervenarteriotomy. tional procedures. Access via the brachial artery [68] (b) In a series of 146 devices deployed in 135 or radial artery [69] is advantageous when vessel patients, 18% were found to have intravas- tortuosity makes access to the vertebral artery difficular Mynx sealant on follow-up vascular cult from a femoral approach, or iliac or femoral imaging, and 11% were found to have pseu- occlusive disease prevents access from the femoral doaneurysms [66]. Another study compar- artery. Previously, arm access was a bailout only for

2.29 Radial Artery Access

selected cases since using sheaths and catheter systems designed for femoral catheterization via radial access was awkward at best. Radial access has the advantage of being far more convenient for patients since they can sit up and even ambulate immediately after the procedure. Although neurointerventionalists have been using transradial artery access (TRA) selectively for decades [69], the interventional cardiology world has fully embraced the technique. An array of studies comparing TRA to transfemoral artery access in cardiology patients have shown tangible benefits with TRA [70–73]. The 2015 European Society of Cardiology recommended TRA as the preferred method of access for acute coronary syndrome intervention [74], and a 2018 American Heart Association guidelines document also supported a “radial-first” approach in this setting [75]. In the last several years, TRA has also become widely popular in the neurointerventional community, with book appearing on the topic in 2021 [76]. Device manufactures have slowly come up with more options for lower profile sheaths and catheters better suited for a radial approach. Advantages of TRA 1. Easier hemostasis. 2. Quicker recovery for the patient. 3. Some vessels difficult to access via femoral approach such as right vertebral are much easier to access. 4. Tortuous iliacs or distal aortic disease can be avoided. 5. Happy customers: Patients prefer radial access [77]. 6. There are fewer complications (2% radial vs. 7% femoral) [78] largely because the superficial location of the radial artery allows for easy and secure hemostasis. Disadvantages of TRA 1. Small access vessels and tendency to spasm limit the sizes of sheaths and catheters. 2. Radial artery loop can impair access to the aortic arch. Radial anomalies are seen in 13.8% of patients [79].

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3. Some vessels difficult to access via radial approach such as left vertebral from right radial access. 4. Tortuous subclavian arteries can be problematic. 5. An aberrant right subclavian artery can make it impossible to access cranial vessels via a right radial approach.

Is an Allen Test Necessary Prior to Radial Access?

No. The Allen test, for variations of the Allen test, named for Edgar Van Nuys Allen [80], is a method to assess collateral circulation to the hand by compressing the radial artery. Use of the Allen test prior to puncture of the radial artery was dogma for decades but has been discredited by the interventional cardiology community. In a study of 206 patients undergoing transradial cardiac procedures, 60 had Allen test results indicating poor collateral circulation during radial artery compression, but lactate levels and other indicators of ulnar collateral flow were not found to be significantly different among the patients, and no hand ischemic complications occurred [81]. A 2018 American Heart Association guidelines document about transradial access declared that “…performing an Allen test…to confirm patency of dual arterial circulation to the hand…is only of historical interest” [75].

Site Selection Right versus left radial access: Routine use of right-sided access is common, since it is easier for right-handed operators. Left radial access may be better if left vertebral catheterization is the primary goal. A known radial artery occlusion would direct one to the opposite radial artery. If there is a concern based on a history of

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trauma, prior arm surgery, or multiple radial catheters, pre-procedure screening of the radial arteries with an ultrasound can confirm vessel patency. Proximal versus distal radial access: Distal access from the anatomic snuff box has the advantage that the procedure is done without extreme supination of the wrist, making it much more comfortable for the patient. Distal access with the left arm positioned on rather than lateral to the patient’s body makes left radial access ­easier for right-handed operators. There is theoretically lower risk of hand ischemia because the entry site is distal to the origin of the superficial palmar branch that gives extensive supply to the deep palmar arch [82]. Distal access also allows for use of the standard distal site for catheterization when distal catheterization fails [83]. The advantage of the standard proximal access at the ventral wrist is that the vessel there is larger and straighter and is able to accept larger-sized sheaths. A prospective comparison of the two access sites showed 30% failure with distal radial attempts versus 2% with standard site attempts [84]. Even though most operators prefer the wrist flat in supination for proximal radial access, if using ultrasound guidance, it is not necessary to use extreme wrist supination for standard radial access, making each site equally comfortable for the patient with either site.

Sheath Selection Sheaths for radial access are lower profile, have a smooth, hydrophilic coating, and have a long, tapered introducing dilator to allow smooth, atraumatic introduction to the small radial artery. Radial sheath kits come with a low-profile puncture needle, a small caliber platinum tip wire, and the sheath/dilator assembly. This allows one-step introduction into the vessel without a separate step for dilating the tract. The slick hydrophilic coating also allows atraumatic withdrawal. It should be as long as possible (usually 23 cm) to bypass much of the radial artery and have the inner catheter exit in the larger brachial artery, reducing the risk of spasm [85]. Selected radial sheath specifications:

2  Diagnostic Cerebral Angiography

1. Prelude EASE™ (Merit Medical, South Jordan, UT) (a) Available 4–7 Fr sizes and 7, 11, 16, and 23 cm lengths (i) 4 Fr nominal measures 1.78  mm outer diameter (OD), 1.57 mm inner diameter (ID) (ii) 5 Fr nominal measures 2.13 mm OD, 1.9 mm ID (iii) 6 Fr nominal measures 2.44 mm OD, 2.24 mm ID (iv) 7 Fr nominal measures 2.77 mm OD, 2.57 mm ID 2. Glidesheath Slender® (Terumo Medical, Somerset, NJ) (a) Available 5–7 Fr nominal sizes and 10 or 16 cm lengths (i) 5 Fr nominal measures 2.13 mm OD (ii) 6 Fr nominal measures 2.46 mm OD (iii) 7 Fr nominal measures 2.79 mm OD 3. Rain Sheath® (Cordis, Miami Lakes, FL) (a) Available 4–7 Fr nominal sizes and 10 or 16 cm lengths (i) 4 Fr nominal measures 1.79 mm OD, 1.54 mm ID (ii) 5 Fr nominal measures 2.14 mm OD, 1.89 mm ID (iii) 6 Fr nominal measures 2.47 mm OD, 2.22 mm ID (iv) 7 Fr nominal measures 2.80 mm OD, 2.55 mm ID

Catheter Selection Catheterization of the vertebral ipsilateral to the radial artery sheath can be easily catheterized with a simple curve such as a vertebral or Berenstein curve. However, the remaining branches of the aortic arch require a reverse curve Simmons or Sidewinder curve. The short Simmons 1 curve is easier to reform and torque. Using a Glidewire® (Terumo Medical, Somerset, NJ) advanced well distally into the vessel, the internal carotid, external carotid, or contralateral vertebral arteries can be selectively catheterized. A Simmons 2 curve may be more stable for proximal common carotid or subclavian injections.

2.30 Procedure

Catheters should be 4 or 5 French for diagnostic studies and hydrophilic coating is very important. A braided catheter shaft is also useful to improve catheter torque and limit the risk of catheter kinking. Standard 100 cm length may be sufficient for smaller patients, especially for common carotid catheterization, but tall patients with long arms and those with tortuous vessels frequently require longer catheter lengths such as 130 cm for selective catheterization.

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5. Make a 3  mm incision parallel to the skin with an 11-blade scalpel. The artery is very superficial so it is imperative to avoid incising it. 6. Most sheath sets come with an appropriate 21-gauge needle. Insert the needle with the bevel facing upward under ultrasound guidance. Gently wiggle the tip if unsure where it is. Adjust the ultrasound probe to keep the artery in view and watch for deflection of the anterior wall of the vessel. 7. Continue advancing the needle and look for Guidewire Selection blood return. Advance the needle 1–2  mm after the first blood return and ensure brisk Navigation through the arm vessels can be difficult blood return continues from the needle. Then with many side branches or loops that can hang up gently advance the soft-tip wire appropriate a guidewire and risk spasm or dissection. An effecfor the sheath system. tive solution is the 1.5  mm  J-tip (Baby-J) 0.035 8. Alternatively, make a two-wall puncture by Glidewire® (Terumo Medical, Somerset, NJ). This advancing the needle through-and-through gently glides around curves and loops and stays in both vessel walls, then slowly withdraw the the main vessel, avoiding side branches. needle until pulsatile blood return is Selective catheterization is facilitated by using obtained. an angled hydrophilic Glidewire® (Terumo 9. When bright red, pulsatile arterial blood is Medical, Somerset, NJ) that usually must be encountered, gently advance introducing advanced for some distance to provide sufficient wire through the needle for at least the support to advance the catheter. Standard 150 cm length of the sheath (usually 23  cm). The lengths will work for 100 cm catheters but longer-­ wire must go smoothly and effortlessly. It is length catheters will require a 260 cm Glidewire®. a good habit to check on fluoroscopy that the wire is well up the arm in the brachial artery. 2.30 Procedure 10. Exchange the needle for the radial sheath (usually 4 or 5 Fr for diagnostic studies). It Radial Artery Puncture should effortlessly advance over the wire. 11. Secure the sheath at the wrist with a stitch or 1. Consider pretreating with topical lidocaine with a small Tegaderm™ (3  M, St. Paul, applied to the wrist, or nitropaste patch, MN) adhesive dressing. which can produce a 10% increase in the 12. Consider a gentle angiogram immediately diameter of the radial artery [86]. after placement of the sheath to rule out a 2. Prepare and drape the wrist and forearm. dissection and to confirm that antegrade flow Consider also prepping the groin area if in the artery is preserved after placement of radial access fails. the sheath. 3. Always use ultrasound guidance. Scan the 13. Cocktail time: Slowly inject a radial artery wrist and locate the pulsatile radial artery. cocktail via the sheath: 10 mL of saline conEnsure it is large enough to accept the chosen taining heparin (5000  international units sheath size. (IU)), verapamil (2.5 mg), cardiac lidocaine 4. Give local anesthesia (2% lidocaine without (2%, 1.0  mL), and nitroglycerin (0.2  mg). epinephrine), by raising a wheal approxi(Enjoy responsibly.) mately 1 cm distal to the expected entry point 14. Consider repeat dose with catheter exchange into the artery. and prior to sheath removal.

2  Diagnostic Cerebral Angiography

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Navigating Through Loops and Angles in the Radial Artery Abrupt turns and 360° loops in the radial artery are possible. A number of options helps navigate these pesky loops. 1. Advance a hydrophilic Simmons diagnostic catheter over a 1.5  mm  J-Tip hydrophilic Baby-J Glidewire® (Terumo Medical, Somerset, NJ) around the loop and into the ascending aorta. 2. A triaxial system with a hydrophilic catheter over a microcatheter over a microwire can be navigated around the loop with roadmap guidance. 3. Balloon-assisted tracking of the catheter involves a low-profile balloon sized to match the catheter diameter with 50% of the balloon protruding from the end of the catheter. This is advanced over a 0.014 wire through the loops. The balloon reduces the offset with the guiding catheter [87, 88]. 4. Similar to the reasoning behind the balloon, microcatheters such as the Wedge™ (MicroVention/Terumo, Aliso Viejo, CA) can be advanced to the catheter tip and offset the ledge between the microwire and the guide

a

b

Fig. 2.10  Access to the great vessels from the right arm. A 0.035-in. hydrophilic wire is advanced into the ascending aorta and reflected off of the aortic valve (a). A

catheter. This system can be advanced as a unit around the loops in the vessel.

Carotid Artery Catheterization 1. Advance a hydrophilic Simmons diagnostic catheter over a J-Tip hydrophilic wire into the ascending aorta. 2. The Baby-J Glidewire® (Terumo Medical, Somerset, NJ) can be gently reflected off the aortic valve and superiorly in the right common carotid artery, followed by the catheter. This reforms the Simmons curve (Fig. 2.10). 3. To engage the left common carotid artery, ensure that the primary angle of the Simmons catheter is in the innominate, insert an angled Glidewire® (Terumo Medical, Somerset, NJ) up to the primary curve, then gently and slowly push and turn the catheter so that it backs out of the innominate artery. Then with the wire inside the catheter and the tip facing to the patient’s left, rotate and pull until the catheter “clicks” into the left common carotid. Then advance the wire superiorly, followed by the catheter. 4. From a right radial approach, the left carotid in a bovine arch configuration can be easily

c

Simmons 2 catheter is then advanced over the wire and into the right or left common carotid artery (b), or the left subclavian artery (c)

2.32 Sheath Removal/Hemostasis



catheterized, often directly from the right subclavian with a Glidewire® (Terumo Medical, Somerset, NJ). One can skip the step of forming the Simmons curve prior to this step. (a) When finished studying the left carotid, the Simmons curve can be constituted by pulling the catheter just far enough the elbow of the primary curve at the origin of the left carotid. Then the catheter is rotated and gently pushed, which should back the catheter into the aorta and reform the curve.

Vertebral Artery Catheterization 1. Vertebral artery ipsilateral to radial puncture is often easily accessed by carefully advancing an angled Glidewire® (Terumo Medical, Somerset, NJ) up and into the vertebral and following with the hydrophilic catheter. 2. Contralateral vertebral catheterization requires a hydrophilic Simmons 2 or 3 diagnostic catheter reconstituted as above over a J-Tip hydrophilic wire. 3. To engage the left subclavian artery from a right radial approach, ensure that the primary angle of the Simmons catheter is in the innominate, insert an angled Glidewire® (Terumo Medical, Somerset, NJ) up to the primary curve, then gently and slowly push and turn the catheter so that it backs out of the innominate artery. Then with the wire inside the catheter and the tip facing to the patient’s left, rotate and pull until the catheter “clicks” into the left common carotid. Then advance the catheter gently to click into the left subclavian. 4. Gently pull back on the catheter and it should advance into the subclavian. Rotation of the catheter may be required. (a) Pulling back too abruptly can cause the Simmons curve to unform. 5. A long enough primary curve may allow the catheter to engage the vertebral artery origin. 6. A left subclavian injection can be done to obtain a roadmap. 7. An angled Glidewire® (Terumo Medical, Somerset, NJ) may then be advanced up into

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the vertebral but extensive wire support is required to be able to advance the Simmons over the wire without backing out the whole assembly into the aorta. 8. Subclavian injections may suffice for routing diagnostic studies but difficulties may be encountered getting a good selective vertebral catheterization from a contralateral radial access. Consider doing an ipsilateral radial puncture if a good selective vertebral arteriogram is desired.

2.31 Avoiding Catheter Kinks and Knots Using Simmons catheters requires catheter rotation to form it and to catheterize the great vessels. This can risk kinking or knotting the catheter. Any manipulations should be done with care and under fluoroscopic observation. Any motion at the hub of the catheter that does not immediately translate to the catheter tip should raise the suspicion that something bad is happening. The cause of the catheter problem could be arterial spasm, catheter looping, kinking, or other failure and the cause should be investigated and corrected rather than continuing to rotate the catheter in the same way. Braided, hydrophilic catheters rotate more easily and are somewhat more resistant to kinks. It is tempting to rotate the catheter while repeatedly puffing contrast to try to engage the target vessel but keeping a guidewire in the catheter will support it, transmit the torque, and help prevent kinks and knots.

2.32 Sheath Removal/Hemostasis 1. Slowly withdraw the catheter. If resistance, there may be spasm. This can usually be overcome by gentle, continuous traction. Remove the catheter. 2. Slowly withdraw the sheath for several centimeters to ensure that spasm is not entrapping the sheath. 3. Apply the hemostatic TR band® (Terumo Medical, Somerset, NJ). The Terumo logo

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should be on the ulnar side (little finger side) of the band. The green box on the clear balloon should be 1–2 mm proximal to the puncture site. (a) Attach a pulse-oximeter probe to the ipsilateral index finger to monitor blood flow to the hand. 4. Inflate the balloon of the TR band to 16 mL with the attached purple syringe. (The maximum capacity is 18 mL.) Fully withdraw and remove the sheath. 5. Check that the pulse oximeter still shows pulsatile flow. If not, slowly deflate the balloon until pulsatile flow returns. 6. Manually compress the ulnar artery. If the pulsatile pattern stops, slowly deflate the balloon until it returns. When the waveform remains pulsatile, the radial is patent. This is patent hemostasis and has been shown to significantly reduce the risk of radial artery occlusion [89]. 7. If a distal radial access site was used, a hemostatic band designed for distal puncture such as Prelude SYNCH Distal™ must be used. This has a maximum volume in the balloon of 10 mL. The device is applied with the target 1–2  mm proximal to the skin entry site. Management of this device is otherwise similar to the standard balloon bands. 8. Always ensure that the plastic syringe supplied with the hemostatic band stay with the patient. This will allow inflation or deflation as needed. The usual luer lock syringes will not work with the system.

2.33 Radial Artery Puncture Site Management 1. After leaving the balloon band inflated for 45 min, begin the deflation process. 2. Remove 3  mL air from the balloon every 15 min. 3. Watch for bleeding at the puncture site; reinflate enough to stop bleeding. 4. When balloon is completely deflated, observe for another 15 min. 5. Remove the band and cover the puncture site with sterile gauze and Tegaderm.

2  Diagnostic Cerebral Angiography

2.34 Selected Patient-Specific Considerations 1. Patients receiving heparin: The heparin infusion should be stopped 6  h prior to the angiogram when feasible. (a) If the need is urgent, an angiogram can still be done in patients on heparin or who are coagulopathic with minimal risk. Radial access angiography should be considered due to easier and more secure hemostasis. 2. Patients receiving warfarin: Hold warfarin (the patient should be placed on a heparin infusion or low-molecular-weight heparin if necessary) until the international normalized ratio (INR) ≤ 1.4. 3. Patients receiving metformin. See below. 4. Thrombocytopenia: Minimum platelet count for angiography is 75,000/μL. 5. Diabetic patients: (a) Patients taking insulin: Reduce the insulin dose to half of the usual dose on the morning of the procedure, when the patient is nothing by mouth (NPO).  Do the procedure as early in the day as possible, and the patient’s usual diet and insulin should then be resumed. (b) Patients taking metformin-containing oral anti-hyperglycemic medications: See below. (c) Protamine should not be used to reverse heparin if the patient has received neutral protamine Hagedorn (NPH) insulin [90, 91]. 6. Pregnant patients: Every effort should be made to study pregnant patients noninvasively. Occasionally, a catheter angiogram is necessary (e.g., head and neck trauma with possible vascular injury, spontaneous epistaxis, intracranial AVM). Cerebral angiography can be performed safely during pregnancy. (a) Informed consent of the patient or guardian should include a theoretical risk of injury to the fetus. (b) Current recommendations for radiation exposure of the fetus include a maximum dose of 0.5  rem (roentgen-equivalent-­ man) [92].

2.36 Risk Factors for Contrast-­Induced Nephropathy



(i) By shielding the uterus with a lead apron, the maximum dose to the fetus is less than 0.1  rem during cerebral angiography [93]. (ii) In general, fetal malformations only occur above a threshold dose of 100– 200 mGy (~10–20 rem) [94]. (c) Iodinated contrast agents are physiologically inert and pose little risk to the fetus [95]. (i) Provide adequate hydration to avoid fetal dehydration [96]. (ii) Fluoroscopy: Minimize time and pulse/s during the procedure. (iii) Decrease fps during diagnostic runs to a minimum. 7. Pediatric patients. See Kid’s Korner below.

2.35 Contrast-Induced Nephropathy Iodinated contrast-induced nephropathy usually appears as an acute wo++rsening in renal function within three to four days of the procedure [97]. Contrast-induced nephropathy is usually defined as an increase in serum creatinine of 25–50% over baseline, or an absolute rise in serum creatinine of 0.5–1  mg/dL [98, 99]. Patients with renal insufficiency are up to ten times more likely to develop contrast-induced renal failure with administration of iodinated contrast than patients in the general population [100]. Patients with renal insufficiency (creatinine ≥1.5 mg/dL) [101] require measures to minimize the risk of contrast-­ induced injury nephropathy during angiography. Nonionic, lowosmolality contrast agents, such as iodixanol (Visipaque™, GE Healthcare, Princeton, NJ) and iopromide (Ultravist®, Schering, Berlin), have been shown to be less renal-toxic when compared to iohexol (Omnipaque®) [102]. The smallest possible amount of contrast should be used during the procedure. One of this Handbook authors was able to do a carotid angioplasty and stent procedure using a total of 27 mL of Visique™ by diluting the contrast with saline and using it sparingly. Forty-eight hours should be allowed to elapse between procedures utilizing iodinated contrast when possible [103]. The antioxidant, N-acetylcysteine (Mucomyst®, Bristol-

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Myers Squibb, New York), is thought to function as a free-radical scavenger and to stimulate intrarenal vasodilation. Acetylcysteine was shown in a randomized trial to reduce serum creatinine elevation in patients undergoing radiological procedures using nonionic, low-osmolality contrast material [104]. Prophylactic administration of acetylcysteine (600 mg PO twice a day (BID)) and 0.45% saline IV, before and after administration of the contrast agent, leads to a significant decrease in serum creatinine compared to patients receiving saline only. Subsequently, isotonic IV fluid was found to be superior to half-isotonic IV fluid in reducing the incidence of contrast-induced nephropathy in patients undergoing coronary angioplasty [105]. Gadolinium contrast has also been used as a noniodinated contrast agent in cerebral angiography in patients with contrast allergy [106, 107], but extensive testing has not been done to ensure the safety of gadolinium compounds in the cerebral arteries, and, moreover, there is evidence of an association of the use of gadolinium contrast agents in patients with renal insufficiency with later development of nephrogenic systemic sclerosis, a debilitating and potentially fatal condition, precluding its use in patients with renal failure [108]. Hemofiltration has been shown to reduce creatinine elevations after angiography [109]. For patients with dialysis-­dependent renal failure, arrangements should be made with the patient’s nephrologist to schedule dialysis after the angiogram.

2.36 Risk Factors for Contrast-­ Induced Nephropathy 1. Serum creatinine level ≥1.5 mg/dL. 2. Diabetes mellitus. 3. Dehydration. 4. Cardiovascular disease and the use of diuretics. 5. Age ≥ 60 years. 6. Para-proteinemia (e.g., multiple myeloma). 7. Hypertension. 8. Hyperuricemia. The patients at greatest risk for contrast nephrotoxicity are those with both diabetes and renal insufficiency [110, 111].

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2.37 Methods to Reduce Risk of Contrast-Induced Nephropathy 1. Minimize the use of contrast. 2. Use Visipaque™ (270  mL I/mL) instead of Omnipaque™ [102]. 3. PO hydration (water, 500 mL prior to the procedure and 2000 mL after the procedure). 4. IV hydration with 0.9% sodium chloride [105]. 5. IV hydration with sodium bicarbonate [112]. 6. Acetylcysteine 600 mg (3 mL) PO BID on the day before and the day of the procedure [104].

2.38 Metformin Metformin is an oral anti-hyperglycemic and is used in several preparations (listed below). Metformin-associated lactic acidosis is rare but has been reported to have a mortality rate as high as 50% [113]. Metformin use should be held for 48 h after the procedure, and restarted only after serum creatinine has been checked and found to be unchanged. The procedure may be done even if the patient has taken metformin earlier on the same day of the procedure [114]. Although metformin use seems to be associated with lactic acidosis, a systematic review article has questioned whether there is a causal relationship [115].

2.39 Metformin-Containing Medications 1. 2. 3. 4. 5.

Metformin (generic) Glucophage® Avandamet® Glucovance® Metaglip®

2.40 Anaphylactic Contrast Reactions: Prevention and Management Although the overall rate of anaphylactic iodinated contrast reactions with IV administration is 0.7–2% [116, 117], the rate of anaphylactic

reactions with cerebral angiography is much lower. This is thought to be because a passage of a bolus of contrast through the pulmonary vasculature, which occurs with IV administration, is more likely to incite an anaphylactic reaction than the relatively diluted dose given during an arteriogram. Large series of cerebral angiograms have reported the following incidences of allergic reactions: 0 out of 1358 cases (0/1358) [118], 0/2154 [119], 1/2924 [120], and 0/3636 [121].

2.41 Risk Factors for Contrast Reactions 1. History of a reaction to iodinated contrast agents (except flushing, a sensation of heat, or a single episode of nausea). 2. History of serious allergic reactions to other materials. 3. Asthma. 4. Renal insufficiency. 5. Significant cardiac disease (e.g., patients with angina, congestive heart failure, severe aortic stenosis, primary pulmonary hypertension, severe cardiomyopathy). 6. Anxiety. Previous reaction to contrast medium is the most important risk factor in the prediction of an adverse event [122]. Patients who have had a previous reaction to ionic contrast may not have a reaction to nonionic agents [123]. A history of seafood allergies, without a specific history of an iodine reaction, usually indicates a hypersensitivity to tasty allergens in seafood, and does not indicate that the patient is unable to tolerate contrast media [124]. Premedication with steroids can reduce the risk of a serious contrast reaction [125]. Repeat contrast reactions in patients with a history of previous reactions to iodinated contrast occur in 10–18% of cases despite premedication [117, 126]. Gadolinium has been used for cerebral angiography in patients with a sensitivity to iodinated contrast material [107, 127]. However, IA gadolinium produces images that are reduced in qual-

2.44 Acute Contrast Reactions: Treatment

ity compared to iodinated contrast, and patients undergoing coronary angiography with gadolinium have a relatively high rate (21%) of complications, such as cardiac arrhythmias and hemodynamic instability [128].

2.42 Premedication Regimen 1. Prednisone 50  mg PO (or hydrocortisone 200  mg IV) 13, 7, and 1  h prior to contrast injection. 2. Diphenhydramine (Benadryl®) 50  mg IV, intramuscular (IM) or PO 1 h prior to contrast injection. Steroids should be given at least 6 h prior to the procedure; administration less than 3 h prior to the procedure does not reduce the risk of an adverse reaction [114].

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2.43 Acute Contrast Reactions: Signs and Symptoms 1. Cutaneous signs (flushing, urticaria, pruritis). 2. Mucosal edema. 3. Generalized edema. 4. Sudden loss of consciousness. 5. Hypotension + tachycardia (anaphylactic reaction). 6. Hypotension + bradycardia (vasovagal reaction). 7. Respiratory distress.

2.44 Acute Contrast Reactions: Treatment Effective treatment depends on prompt recognition of the problem and rapid management (Table 2.4) [129].

Table 2.4  Management of acute contrast reactions in adults Urticaria  1. Discontinue procedure if not completed  2. No treatment needed in most cases  3. Give H1-receptor blocker: Diphenhydramine (Benadryl®) PO/IM/IV 25–50 mg. If severe or widely disseminated: Alpha agonist (arteriolar and venous constriction) epinephrine SC (1:1000) 0.1–0.3 mL (= 0.1–0.3 mg) (if no cardiac contraindications) Facial or laryngeal edema  1. Give alpha agonist (arteriolar and venous constriction): Epinephrine SC or IM (1:1000) 0.1–0.3 mL (= 0.1–0.3 mg) or, if hypotension evident, epinephrine (1:10,000) slowly IV 1 mL (=0.1 mg). Repeat as needed up to a maximum of 1 mg  2. Give O2 6–10 L/min (via mask)  3. If not responsive to therapy or if there is obvious acute laryngeal edema, seek appropriate assistance (e.g., cardiopulmonary arrest response team) Bronchospasm  1. Give O2 6–10 L/min (via mask)  2. Monitor: Electrocardiogram, O2 saturation (pulse oximeter), and blood pressure  3. Give inhaled beta-agonist (bronchiolar dilator, such as albuterol [Proventil® or Ventolin®]), 2 to 3 puffs from metered dose inhaler. Repeat as needed (PRN). If unresponsive to inhalers, use SC, IM, or IV epinephrine  4. Give epinephrine SC or IM (1:1000) 0.1–0.3 mL (= 0.1–0.3 mg) or, if hypotension evident, epinephrine (1:10,000) slowly IV 1 mL (= 0.1 mg)  5. Repeat as needed up to a maximum of 1 mg. Alternatively: Give aminophylline: 6 mg/kg IV in D5W over 10–20 min (loading dose), then 0.4–1 mg/kg/h, as needed (caution: Hypotension) Call for assistance (e.g., cardiopulmonary arrest response team) for severe bronchospasm or if O2 saturation 5 fps) can help clarify anatomy of AVMs, as they are typically high-­ flow lesions. High-speed runs may also permit more precise measurements of arteriovenous transit times. 3. Intranidal aneurysms can be identified and distinguished from enlarged veins by their location on the arterial side of the nidus [140]. In contrast, nidal “pseudoaneurysms” have been described in the arterial or venous side of the nidus; they can be recognized

2  Diagnostic Cerebral Angiography

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when they appear as a new finding on subsequent angiography [141]. 4. Small, obscure AVMs may sometimes be made to be more apparent on angiography by having the patient deliberately hyperventilate for several minutes. Normal vessels will constrict and AVM vessels will be unchanged. [142]

 erebral Proliferative Angiopathy C (See Chap. 13) 1. A complete six-vessel angiogram should be done (bilateral internal and external carotid and vertebral arteries), to identify meningeal feeders, which are frequently present [143]. 2. Feeding vessels (such as the ICAs and M1 segments) should be imaged well to look for the presence of arterial stenosis.

Dural Arteriovenous Fistulas 1. All feeding vessels should be identified; selective catheterization of branches of the external carotid artery is usually necessary. 2. After each injection, the angiogram should be allowed to continue until the draining vein (or venous sinus) is imaged. 3. On internal carotid and vertebral injections, the venous drainage pathways of the normal brain must be determined to see how it relates to the drainage pathways of the fistula. 4. DynaCT angiography is useful to accurately determine the site at which artery connects to vein [52].

 irect (High-Flow) Carotid-Cavernous D Fistulas 1. High-speed runs (>5 fps) are usually helpful. 2. Huber maneuver: Injection of contrast into the ipsilateral vertebral artery with manual compression of the carotid artery; reflux of contrast into the carotid artery can demonstrate the defect in the cavernous carotid artery [144].

3. Slow injection into the internal carotid artery with a compression of the carotid artery below the catheter tip in the neck can also demonstrate the defect in the vessel [145]. 4. Special attention should be given to venous drainage and determining whether there is a retrograde cortical venous flow.

Aortic Arch 1. Angiography of the aortic arch is best done with a power injector and a pigtail catheter positioned in the ascending aorta. The optimal projection is left anterior oblique, 30°, with the patient’s head rotated to the left to face the image intensifier. Power injector settings are 20 mL/s, total of 25 mL. 2. For these high-volume injections, care should be taken that the injection pressure does not exceed the nominal rating for the catheter and any stopcock.

Assessment of the Circle of Willis 1. Patency and caliber of the posterior communicating artery can be assessed with the Huber (or Allcock) maneuver: Injection of contrast into the ipsilateral vertebral artery with manual compression of the carotid artery. Reflux of contrast into the carotid artery can demonstrate posterior communicating artery. 2. The anterior communicating artery can be demonstrated by “cross compression” of the carotid artery. Manual compression of the contralateral common carotid artery, while wearing a lead glove during injection of contrast into the ipsilateral internal carotid artery, will help visualize the anterior communicating artery.

Carotid Siphon and MCA Candelabra 1. The “Haughton view” can be used to open up the carotid siphon (useful for imaging the origins of the P-comm and anterior choroidal arteries) and to unfurl the branches of the

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2  Diagnostic Cerebral Angiography 117. Davenport MS, Cohan RH, Caoili EM, Ellis JH.  Repeat contrast medium reactions in premedicated patients: Frequency and severity. Radiology. 2009;253(2):372–9. (In eng). https://doi. org/10.1148/radiol.2532090465. 118. Horowitz MB, Dutton K, Purdy PD.  Assessment of complication types and rates related to diagnostic angiography and interventional neuroradiologic procedures. A four year review (1993-1996). Interv Neuroradiol. 1998;4(1):27–37. (In eng). http://www. ncbi.nlm.nih.gov/pubmed/20673388 119. Leonardi M, Cenni P, Simonetti L, Raffi L, Battaglia S. Retrospective study of complications arising during cerebral and spinal diagnostic angiography from 1998 to 2003. Interv Neuroradiol. 2005;11(3):213– 21. (In eng). http://www.ncbi.nlm.nih.gov/ pubmed/20584477 120. Dawkins AA, Evans AL, Wattam J, et  al. Complications of cerebral angiography: A prospective analysis of 2,924 consecutive procedures. Neuroradiology. 2007;49(9):753–9. (In eng). https:// doi.org/10.1007/s00234-­007-­0252-­y. 121. Fifi JT, Meyers PM, Lavine SD, et  al. Complications of modern diagnostic cerebral angiography in an academic medical center. J Vasc Interv Radiol. 2009;20(4):442–7. (In eng). S1051-­ 0443(09)00014-1 [pii]. https://doi. org/10.1016/j.jvir.2009.01.012. 122. Bettmann MA, Heeren T, Greenfield A, Goudey C.  Adverse events with radiographic contrast agents: Results of the SCVIR contrast agent registry. Radiology. 1997;203(3):611–20. http://www.ncbi. nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=P ubMed&dopt=Citation&list_uids=9169677 123. Osborn AG.  Diagnostic cerebral angiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1999. 124. Dewachter P, Trechot P, Mouton-Faivre C. “Iodine allergy”: Point of view. Ann Fr Anesth Reanim. 2005;24(1):40–52. http://www.ncbi.nlm.nih.gov/ entrez/query.fcgi?cmd=Retrieve&db=PubMed&dop t=Citation&list_uids=15661464 125. Lasser EC, Berry CC, Mishkin MM, Williamson B, Zheutlin N, Silverman JM.  Pretreatment with corticosteroids to prevent adverse reactions to nonionic contrast media. AJR Am J Roentgenol. 1994;162(3):523–6. http://www.ncbi.nlm.nih.gov/ entrez/query.fcgi?cmd=Retrieve&db=PubMed&dop t=Citation&list_uids=8109489 126. Freed KS, Leder RA, Alexander C, DeLong DM, Kliewer MA.  Breakthrough adverse reactions to low-osmolar contrast media after steroid premedication. AJR Am J Roentgenol. 2001;176(6):1389– 92. (In eng) http://www.ncbi.nlm.nih.gov/ pubmed/11373198 127. Sakamoto S, Eguchi K, Shibukawa M, et al. Cerebral angiography using gadolinium as an alternative contrast medium in a patient with severe allergy to iodinated contrast medium. Hiroshima J Med Sci.

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3

Spinal Angiography

3.1 Indications for Spinal Angiography 1. Evaluation of patients with myelopathy and suspected to have spinal dural arteriovenous fistulas (most common indication). 2. Evaluation of patients with known or suspected spinal arteriovenous malformations or vascular neoplasms (e.g., with spinal intramedullary or subarachnoid hemorrhages). 3. Rarely for the evaluation of suspected spinal cord ischemia (since cord blood supply is so variable, and treatment options for cord ischemia are so limited, angiography is mainly done to rule out a fistula as the cause of symptoms). 4. Planning for neurointerventional procedures on spine or spinal cord. 5. Preoperative mapping of cord vasculature prior to spinal or aortic procedures that risk occlusion of the spinal vessels. 6. Intraoperative assistance with surgery on spinal vascular lesions. 7. Follow-up imaging after treatment (e.g., after treatment of arteriovenous fistulas or malformations).

Spinal Imaging Strategy

Adjunctive cross-sectional imaging techniques can replace or complement catheter spinal angiography. Also, a spine MRA or CTA can direct attention to the pertinent segmental artery prior to the catheter angiogram and save considerable time during the angiogram. 1. Spinal MR angiography 2. Spinal CT angiography (a) CTA combined with DSA [1]. This approach combines the anatomic precision of DSA with high-resolution bony imaging from fine-cut CT.  Technique: A pigtail catheter is positioned in the aorta proximal to the area of interest. Scanning is done twice during the injection to obtain arterial- and venous-phase images to differentiate between arterial and venous structures. Selective catheterization is then done based on the DSA/CT findings.

3.2 Complications of Diagnostic Spinal Angiography Informed consent prior to an angiogram should include a quantitative estimate of the risk of complications.

Spinal angiography is invasive and can be technically challenging, particularly in older patients. © The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 M. R. Harrigan, J. P. Deveikis, Handbook of Cerebrovascular Disease and Neurointerventional Technique, Contemporary Medical Imaging, https://doi.org/10.1007/978-3-031-45598-8_3

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158

Neurological Complications

Pre-angiogram Orders

Neurological complications in spinal angiography may include the same risk of cerebral ischemic events that may occur during cerebral angiography when the cervical region is being studied (see Chap. 2). In addition, there is the risk of vessel dissection, embolic occlusion with thrombus, atherosclerotic plaque, or air emboli occluding the spinal cord vessels and producing myelopathy. In a study of 134 spinal angiograms, there were three (2.2%) neurological complications, all transient [2]. Two more recent series, with over 300 cases, found zero neurological complications from diagnostic spinal angiography [3, 4]. High-volume contrast injection in vessels feeding the spinal cord (although not necessarily performed as part of spinal ­angiography) has also been shown to produce temporary or permanent injury to the spinal cord [5–7].

1. NPO except medications for 6 h prior to the procedure. 2. Place peripheral IV (two if an intervention is anticipated). 3. Place Foley catheter (almost always, unlike cerebral angiography).

Non-neurological Complications Non-neurological complications of spinal angiography via the femoral artery include the same local and systemic complications seen in cerebral angiography. A recent study found 1% rate of puncture site complications and 0.7% rate of systemic complications [4].

3.3 Selective Spinal Angiography: Basic Concepts Pre-procedure Evaluation 1. Brief neurological exam should be done to establish a baseline, should a neurologic change occur during or after the procedure. 2. The patient should be asked for a history of iodinated contrast reactions. 3. The femoral pulse as well as the dorsalis pedis and posterior tibialis pulses should be examined. 4. Blood work, including a serum creatinine level and coagulation parameters, should be reviewed.

Sedation/Analgesia/Anesthesia The choice between general anesthesia and conscious sedation for spinal angiography depends upon the circumstances. General anesthesia allows for patient immobility including prolonged interruption of respiration, while imaging tiny spinal vessels that are present in the thoracic and lumbar region. General anesthesia also spares the patient the potential discomfort of a long, involved angiographic procedure. Using nonionic, iso-osmolar contrast, procedures can be done under local anesthesia with minimal sedation, and adequate image quality is possible in cooperative patients. The advantage of local anesthesia is the avoidance of any of the potential complications of general anesthesia and the ability to monitor the neurological status of the patient during the procedure. The limited ability to monitor the neurological status of the patient during general anesthesia may be partially mitigated by the use of neurophysiological monitoring, such as somatosensory and/or motor evoked potentials [3]. However, neurophysiological monitoring adds to the cost and complexity of the procedure, and may not be readily available or reliable, depending on the institution.

Contrast Agents Nonionic contrast agents are almost always used due to their lower osmolality and better tolerance when injected into the small vessels feeding the spine. Iodixanol (Visipaque™, GE Healthcare, Princeton, NJ), an iso-osmolar and a nonionic contrast agent, is more expensive and more viscous than other contrast agents commonly used but is the best tolerated agent for spinal angiography.

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3.3 Selective Spinal Angiography: Basic Concepts

1. Diagnostic angiogram: Omnipaque®, 300 mg I/mL, or Visipaque™, 320 mg I/mL. 2. Neurointerventional procedure: Omnipaque®, 240 mg I/mL or Visipaque™, 270 mg I/mL. Patients with normal renal function can tolerate up to 400–800 mL of Omnipaque®, 300 mg I/ mL without adverse effects [8]. Contrast volumes in spinal angiography can routinely approach these limits, given the large number of injections required.

 emoral Artery Sheath Versus No F Sheath Spinal angiography is almost always done with a femoral artery sheath. 1. Sheath (a) Advantages: allows the rapid exchange of catheters and less potential for blood loss from the arteriotomy site. Spinal angiography frequently requires several different catheters per case. (b) Unlike cerebral angiography, catheter position is often tenuous in the vessels being selected, and the sheath allows for more precise manipulation and positioning of the catheter. (c) Short sheath (10–13-cm arterial sheath) is used most commonly. (d) Longer sheath (25  cm) is useful when iliac or femoral artery tortuosity or atherosclerosis can impair catheter navigation. Longer sheaths may need to be pulled back, partially out of the iliac artery, when selective catheterization of the ipsilateral internal iliac artery is needed. (e) Technique: Standard arterial puncture techniques are used. Most commonly, a 5 or 6F sheath (Pinnacle® Sheath; Terumo Medical, Somerset, NJ) is used. The lumen of the sheath (and the angiographic catheter) is continuously perfused with heparinized saline (10,000 U heparin/L of saline) under arterial pressure.

2. No sheath (a) Spinal angiography without a sheath offers the advantage of a slightly smaller arteriotomy, but is rarely done. (b) Situations in which a sheath may not be needed include pediatric cases in which a smaller arteriotomy is desired and very limited follow-up angiograms in which only one catheter may be used for a quick procedure.

Suggested Wires and Catheters for Diagnostic Spinal Angiography 1. Guidewires (a) Use a 0.035′ or 0.038′ J-tip wire for sheath insertion. (b) The 0.035′ angled Glidewire® (Terumo Medical, Somerset, NJ) is soft, flexible, and steerable. (c) The 0.038′ angled Glidewire® (Terumo Medical, Somerset, NJ) is slightly stiffer than the 0.035  in. may be helpful when added wire support is needed. 2. Catheters (a) In general, catheters for spinal angiography (Table 3.1 and Fig. 3.1) are the same shapes typically used for visceral angiography, although cerebral-type catheters may be used for catheterization of brachiocephalic vessels. Occasionally, straight catheters may be steam-shaped to an appropriate curve for a particular application. Straight catheters may also be used as-is for retrograde flush aortic injections (see below). Table 3.1  Catheters for spinal angiography Catheter 5F Angled Taper 5F Mikaelsson 5F Simmons 1 4 or 5F Cobra 5.5F RDC 5F Straight

Use Good all-purpose diagnostic catheter for supra-aortic vessels Good all-purpose catheter for intercostal and lumbar arteries Alternative to Mikaelsson Intercostal and lumbar arteries in younger patients Very stable and torqueable, but stiff For retrograde flush aortic runs

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Fig. 3.1  Recommended diagnostic catheters used for spinal arteriography

Vessel Catheterization Selective spinal angiography may be either complete spinal angiography, or a partial, focused study for a specific lesion. Complete spinal angiography is a major undertaking, in which all vessels that may relate to the spinal canal are selectively catheterized and studied. This is most often used in the evaluation of a patient with a suspected dural arteriovenous fistula causing myelopathy. The vascular lesion can be anywhere from the head to the sacrum, and evaluation of all vessels supplying these structures may be required (Table  3.2). When the lesion is obviously confined to a specific region of the spine, a more focused study may be more appropriate. This should include all the vessels that supply the area of interest, and the levels above and below the lesion, given the possibility of collateral flow from adjacent spinal vessels. Another useful rule of thumb is to visualize normal spinal cord vessels above and below any lesion affecting the cord. Assessing spinal cord blood supply may require selective angiography of the vertebral arteries (Fig. 3.2), thyrocervical and costocervical trunks, subclavian arteries, intercostal arteries (Fig. 3.3), lumbar arteries (Fig. 3.4), and lateral and medial sacral arteries.

Table 3.2  Blood supply to various spinal regions Level Upper cervical Lower cervical Upper thoracic Mid-lower thoracic Upper-to-mid lumbar Lower lumbar Sacrum

Feeding arteries Vertebral, ascending pharyngeal, occipital, deep cervical Vertebral, deep cervical, ascending cervical Supreme intercostal, superior intercostal Intercostal Lumbar Iliolumbar Anterior and lateral sacral

Roadmapping Roadmapping aids catheterization of the supra-­ aortic vessels, such as vertebral arteries, and the thyrocervical and costocervical trunks. Roadmapping is less helpful in catheterizing the intercostal and lumbar arteries, since respiratory motion degrades the image.

Double Flushing Catheter flushing technique is discussed in Chap. 2. Although some operators use double flushing of catheters only in the supra-aortic arteries, it

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Fig. 3.2 Lateral vertebral artery angiogram showing anterior spinal artery (arrows)

makes more sense to use a meticulous flushing technique anywhere in the vascular system. This ensures that one will not forget to use good technique when it is most needed. Moreover, ­thrombus or air emboli in spinal cord vessels can be just as disabling as cerebral ischemia.

Continuous Saline Infusion Three-way stopcock or manifolds can be used to provide a heparinized saline drip through the catheter. This is particularly useful for long spinal angiographic procedures. In-line air filters (B. Braun, Bethlehem, PA) on the saline drip tubing provide added protection from bubbles (as discussed in Chap. 4). A rotating adapter on the stopcock is needed to prevent the stopcock from being a drag on free manipulation of the catheter. Using both a rotating three-way stopcock and a rotating hemostatic valve on the catheter allows for two pivot points to allow free rotation of the catheter. This is important, as the catheter may not be in a stable position in the small lumbar and intercostal arteries.

Fig. 3.3  Typical intercostal artery

Hand Injection Frequent small injections (“puffing”) of contrast can be used to help manipulate the catheter into the desired lumbar and intercostal arteries. A 20  mL syringe containing contrast can be left attached to the catheter for these injections, and then used immediately for hand injections of contrast for angiographic runs. As is done in the cerebral vasculature, the syringe is held vertically and care is taken not to allow bubbles to enter the

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graphic run, but the phase of respiration at which the breath-holding should occur depends on the spinal level being imaged (see below).

Mechanical Injection A power contrast injector is necessary for thoracic or lumbar aortic angiograms, and for large vessels such as subclavian or iliac arteries. As stated in Chap. 2, the pressure and flow rate settings should not exceed the ratings of the stopcock or catheter. Common power injector settings for vessels studied in spinal angiograms using a 5F catheter are listed in Table 3.3. Note that one may need to increase or decrease these rates and volumes, depending on the size of the vessels, the stability of the catheter, and the quickness of the runoff of the contrast on a test injection. Use extreme caution if the catheter is wedged in the vessel and be especially careful if there is a possibility that a spinal cord vessel is arising from the branch one is injecting, since high-pressure power injections can damage the cord [7]. When in doubt, use careful hand-injections of contrast.

Vessel Selection

Fig. 3.4  Typical lumbar artery

catheter. Most spinal vessels are best imaged with hand injections of contrast, to allow for modulation of the injection rate and volume, depending on the size of the vessel and stability of the catheter. An adequate angiographic run can be usually done with a single 2–3 s injection of 4–6 mL (100% contrast) of contrast. The goal is to adequately opacify the vessel of interest without displacing the catheter or refluxing too much into the aorta or into the ever-present collaterals to other spinal vessels. Patients should be warned that they will experience warmth and/or cramping in the territory of the injected vessel, and breathing should be suspended during the angio-

If the exact level of the lesion is known from noninvasive imaging, the spinal angiogram should begin with those vessels supplying that area. Following catheterization of the vessel of interest, it is then customary to work systematically above and below the lesion to include normal terTable 3.3  Standard power injector settingsa Vessel Aortic arch Retrograde aortic flush Iliac artery Subclavian artery Vertebral artery Lumbar or intercostal artery For 3D imaging

Power injector settings 20 mL/s; total of 25 mL 10 mL/s; total of 30 mL 10 mL/s; total of 20 mL 6 mL/s; total of 15 mL 6 mL/s; total of 8 mL 2 mL/s; total of 6 mL 0.5–2 mL/s; total 7–30 mL (higher doses for high flow AVF)

 For digital subtraction angiography using a 5F catheter

a

3.3 Selective Spinal Angiography: Basic Concepts

ritory adjacent to the lesion. Lesions of the cord itself usually require mapping of the spinal cord supply above and below the lesion. For complete spinal angiography, it is particularly important to image the intercostal and lumbar arteries in a ­systematic fashion so that one does not inadvertently miss or repeat a level. It is helpful to maintain a worksheet during the procedure, and list the sides and vessels injected during each angiographic run. Radio-opaque marker rulers can be placed under the patient on the table or marker tapes can be affixed to the patient’s back, slightly off midline to have a reference available on each film to help confirm the levels studied. Additionally, bony landmarks, such as the 12th rib, can also help with keeping track of the vessels being studied.

 ngiographic Images and Standard A Views Spinal angiography has a number of features that make it less desirable to use biplane imaging routinely. The vascular anatomy is usually quite simple compared to cerebral vessels. Moreover, lateral views require higher doses of X-rays to adequately penetrate the thoracic or lumbar region to give good visualization of the structures. To limit the radiation dose to the patient and operator, and to prevent over-heating the X-ray tube, obtain single plane frontal images of the thoracic, lumbar, and sacral spine. Later, obtain lateral views when the vessels supplying the lesion are found. Additionally, when a complex vascular lesion is found, 3D rotational imaging can add useful information. 3D imaging is better than conventional angiography for determining the relationship of AVMs to the spinal cord and detecting intranidal aneurysms [9]. 3D spine angiography requires general anesthesia to ensure immobility during the 15 s imaging acquisition and contrast must be slowly injected in the vessel of interest for approximately 15–17  s beginning 1 s prior to starting the acquisition to ensure that the vessels are opacified throughout the full rotation of the gantry.

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1. When viewing the spinal angiographic images, the normal anatomic features should be recognized. Segmental spinal vessels have osseous branches that supply the vertebra at that level, radicular branches, variable radiculomedullary branches that connect to the anterior spinal artery, variable radiculopial branches that feed the posterolateral spinal arteries, muscular branches, and anastomoses to the contralateral and cephalad and caudal adjacent segmental branches. 2. Other imaging features worthy of attention during the performance of a spinal angiogram: (a)  Vessel contour and size (angioarchitecture). (b) Presence or absence of evident contribution to spinal cord. Look for the hair-pin turn of the artery of Adamkiewicz (Fig.  3.5) and fairly straight ascending and/or descending vessels in the spinal canal. (c)  Presence of abnormal or unexpected vascular channels (neovascularity). (d) Presence or absence of an abnormal vascular blush. Note that normal muscle and bone normally display a vascular blush. (e)  Early venous filling indicates an AV shunt. (f) When there is a shunt, you must ask yourself: where do the veins drain to? (g) Injection of intercostal or lumbar arteries that fill the anterior spinal artery should be examined for the appearance of the coronal venous plexus of the spinal cord within about 15 s after contrast injection. Lack of visualization or delayed visualization of the veins along the cord and the radicular veins that anastomose with the epidural veins can be evidence of severe spinal venous hypertension. Pearl

Remember that the anterior spinal artery is in the midline. The posterolateral spinal arteries are slightly off midline.

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arterial, capillary, and venous phases. However, when screening for causes of spinal venous hypertension, such as a spinal dural AVF, injection of the segmental vessel supplying the artery of Adamkiewicz may require imaging for 20 s to visualize the venous phase of the spinal cord vasculature.

Calibration and Measurement Size measurements and calibration can be done as described in Chap. 2. In spinal angiography, radioopaque rulers may be placed under the patient for reference and can also be utilized for calibration.

Spinal Angiographic Procedures  emoral Artery Puncture F 1. Standard arterial access is obtained (see Chap. 2). 2. A femoral arterial sheath is placed (5 or 6F).

Fig. 3.5  L1 lumbar artery injection showing the artery of Adamkiewicz (black arrows), with the characteristic hairpin turn, followed by the anterior spinal artery (white arrow)

 rame Rates for Digital Subtraction F Angiography Most spinal angiography can be done with relatively slow frame rates of 1 or 2 frames per second (fps). Most arteriovenous fistulas in the spine are relatively slow filling. Only very high flow arteriovenous shunts would require 3 fps or faster imaging. Routine use of fast frame rate while imaging the spine below the cervical region will soon overheat the X-ray tube and may not even be possible with lower quality imaging equipment. For most spinal arteriography, a 10–12  s imaging sequence allows for visualization of

 adial Artery Access R 1. Very rarely, spinal angiography may require access from the arm if there are femoral, iliac, or aortic occlusions. 2. For the most part, radial access is only used when a focused study is needed. 3. If lower lumbar arteries must be imaged using an upper extremity artery for access, use an axillary approach, since even 100  cm catheters may not reach from a radial or even brachial approach. Aortic Imaging 1. Screening aortic injections by pigtail catheter are a way to get a rough idea of vascular anatomy in the thoracic and lumbar region. 2. It is most helpful in elderly patients with aortic atherosclerosis or aortic aneurysms to see which segmental vessels may be occluded. 3. As a rule, aortic injections provide poor visualization of small spinal vessels, so they do not eliminate the need for selective spinal angiography. 4. In the lumbar region, pigtail catheter injections fill all the visceral vessels as well as the

3.3 Selective Spinal Angiography: Basic Concepts

lumbar arteries. This can obscure even fairly extensive vascular abnormalities in the spine. 5. For most cases, it is not worth wasting the time or contrast on aortic injections.

 etrograde Aortic Flush R 1. Better visualization of the segmental spinal arteries can be obtained with a retrograde aortic flush, as opposed to standard pigtail injections [10, 11]. 2. Bilateral femoral arterial sheaths are required (5 or 6F). 3. A straight catheter (5 or 6F) is positioned in each common iliac artery. 4. Simultaneous power injection of contrast in each catheter is needed. A sterile Y-connector that is rated for high pressure can connect the tubing from the injector to both catheters. Alternatively, two separate injector machines may be used. 5. 20  mL/s for a total of 50  mL distributed equally between the two catheters is injected. 6. Contrast usually streams up the posterior wall or the aorta, providing visualization of the lumbar, and lower intercostal arteries, with less obscuration of the anterior visceral arteries. 7. More viscous contrast, such as Omnipaque 350 or Visipaque 320 works best with this technique. 8. Usually no more than five vertebral levels are well imaged by this technique. The catheters may need to be positioned in the upper lumbar aorta to visualize the higher thoracic levels. 9. This technique is still not a replacement for selective spinal angiography. 10. Retrograde aortic flush is contraindicated in very tortuous aorta or iliac vessels, in the presence of extensive atherosclerosis, or aortic or iliac aneurysmal disease, due to a risk of dissection or plaque disruption. I ntercostal and Lumbar Artery Catheterization 1. For complete spinal angiography, spinal segmental vessels constitute the majority of the vessels to be studied.

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2. Unless the exact site of a lesion is known from other imaging studies, the segmental spinal vessels should be studied in a systematic fashion to ensure that all are being visualized. 3. Using a Mikaelson or Simmons catheter, it is often most efficient to go from caudal to cranial, to avoid un-forming the curve of the catheter. 4. Using most other catheters, such as Cobra catheters, it works best to go from cranial to caudal. 5. From one level to the next, the segmental vessels come off at similar positions along the wall of the aorta, so it is best to go from one level to the next and do all on one side before going back and doing all on the other side. This is much quicker than rotating the catheter from one side to the other at each level. 6. The catheter is slowly rotated and moved forward or backward, while puffing small amounts of contrast until the desired vessel is engaged. 7. The catheter is gently pulled back to ensure it is seated in the vessel. 8. The catheter should be held in position with one hand to prevent it from rotating out of the vessel, and contrast injected for an angiographic run, during transient arrest of respiration. 9. Keeping the catheter at the same angle of rotation, it is then gently pushed forward (for Mikaelsson or Simmons) or withdrawn (for Cobra) to disengage from the vessel. 10. Again keeping the same angle of rotation, the catheter is moved to the next vertebral level and it should just pop into the lumbar or intercostal branch. 11. Alternatively, the catheter can be left in the branch, then slowly rotated toward the right or left until it enters the contralateral segmental branch at the same vertebral level. 12. Continue the process in a systematic fashion until all the desired vessels are studied.

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 ptimizing Images by Reducing O Respiratory and Other Motion

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3. The right and left lower lumbar arteries may have a common origin from the aorta. 4. In lumbar and lower thoracic regions, segmental branches usually arise just below the level of the pedicle. 5. In the more cephalad levels in the thoracic region, the intercostal arteries are closer together, and slope cephalad to supply vertebral levels above the level of the aorta from which they arise. 6. The highest intercostal arteries are close together, and their angulation often makes it difficult to keep the catheter in a stable position in the vessel. 7. Just below the aortic arch, the superior intercostals ascend and variably supply two or three thoracic vertebral levels above the origins of the vessels (Fig. 3.7). 8. Do not forget that the supreme intercostals are at the costocervical trunks (hence, the name “costo-” cervical) and supply the most cranial two or three thoracic levels.

General anesthesia can be used to prevent patient motion. With or without general anesthesia, imaging the intercostal and lumbar arteries should be done during breath-holding. For lower lumbar imaging, the patients can hold their breath in either inspiration or expiration, whichever moves aerated bowel away from the area of interest. Upper lumbar and lower thoracic imaging is best if the patients hold in expiration, to keep the interface of lung and diaphragm out of the imaging field. In the mid-thoracic region above the diaphragm, the patients should hold their breath in inspiration, to keep the diaphragm below the area of interest. In the upper thoracic region, catheter positioning is frequently very tenuous, and deep respirations in anticipation of breath holding can displace the catheter. In this region, it is best to have the patient suspend respiration without deep inspiration or expiration. In the lumbar region, bowel peristalsis can sometimes degrade subtraction images. Bowel movement can be temporarily slowed by injecting 1 mg of glucagon or 40 mg of hyoscine-N-­ butylbromide (Buscopan®; Boehringer Ingelheim GmbH, Germany) IV just prior to acquiring the Sacral and Iliolumbar Artery images [12].

Pearls

To facilitate catheterization of the intercostal and lumbar arteries, remember the following facts: 1. The more caudal the spinal level, the more posterior the origins of the segmental vessels [13] and the more symmetrical the origin of the right and left segmental vessels. 2. Upper thoracic right-sided intercostal arteries arise from the lateral wall of the aorta; the left is more posterior. Right and left lower lumbar arteries both arise from the posterior wall of the aorta (Fig. 3.6).

Catheterization 1. The anterior sacral artery arises from the aortic bifurcation and can be catheterized with any reverse-curve catheter (like Mikaelsson or Simmons). 2. Iliolumbar and lateral sacral arteries come off the internal iliac arteries. 3. Common iliac injections can be done to locate the spinal vessels to be selected. 4. Iliac arteries and their branches contralateral to the femoral puncture site are catheterized by engaging the iliac with the catheter, then advancing a hydrophilic wire well down into the contralateral femoral artery. The catheter is then advanced antegrade over the wire into the external iliac. While injecting small amounts of contrast, it is slowly pulled back and rotated until the desired vessel is catheterized.

3.3 Selective Spinal Angiography: Basic Concepts

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Fig. 3.6  Orientation of segmental arteries. Upper thoracic: Right intercostal arises from lateral aspect of aorta, the right from posterior surface. Thoracolumbar: both intercostal/lumbar arteries arise from lateral aspect of aorta. Lower lumbar: Both lumbar arteries arise from posterior wall of aorta. A anterior, P posterior

Fig. 3.7  Superior intercostal artery. This is the most cephalad intercostal artery arising from the aorta, ascending to supply several vertebral levels. Not to be confused with supreme intercostal arising from the costocervical trunk

5. Iliac arteries ipsilateral to the femoral puncture require a fully formed Mikaelsson or Simmons in the aorta, which is slowly withdrawn and rotated so that it points back into the ipsilateral iliac. As small amounts of contrast are injected, it is withdrawn and rotated into the vessel of interest. 6. The ipsilateral iliac vessels can often be well imaged from a retrograde injection of a catheter or sheath with its tip in the distal external iliac artery. 7. If a femoral artery sheath is being used, it may have to be pulled back into the external iliac to allow catheterization of the iliac branches. 8. Truly selective injections of the iliolumbar and lateral sacral arteries may require the use of a microcatheter/micro-guidewire assembly placed coaxially through the 5F catheter positioned with its tip at the origin of the internal iliac artery. 9. Iliolumbar arteries are at the very proximal internal iliac and the lateral sacral a little more distally off the posterior division of the internal iliac. 10. Warn patients that they will feel the heat of the contrast in very private places when injected in the iliac arteries and their branches.

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 ertebral Artery Catheterization V 1. For complete spinal angiography, the vertebral arteries must be studied. 2. Vertebral artery catheterization is discussed in detail in Chap. 2. 3. The vertebral arteries fill the anterior spinal arteries at the vertebrobasilar junction and the posterolateral spinal arteries proximal to, or directly from, PICA. 4. Remember that segmental branches of the vertebral may contribute also to the spinal cord. If the catheter tip is positioned too high up in the vertebral artery, lower segmental feeders to the cord may be overlooked. Thyrocervical/Costocervical Trunk Catheterization 1. For complete spinal angiography, these subclavian artery branches must be studied. 2. For most cases, a simple curve on the catheter (Angled Taper, Vertebral, or Berenstein curve) works best. 3. Advance the catheter over a wire into the subclavian artery well beyond the origin of the vertebral artery. 4. Double flush the catheter, then slowly withdraw the catheter, keeping the tip pointed cephalad, while gently injecting small quantities of contrast until the catheter engages the desired vessel. 5. The costocervical trunk is just distal to the thyrocervical trunk, which is just distal to the vertebral artery. 6. There may be an anomalous artery of the cervical enlargement, supplying the cord directly from the subclavian. 7. With tortuous vessels or confusing anatomy, a subclavian injection, using a slight ipsilateral oblique view can help.  arotid Artery Catheterization C 1. For complete spinal angiography, branches of the carotid arteries must be studied. 2. Carotid artery catheterization is discussed in detail in Chap. 2. 3. External and internal carotid injections, and preferably, selective injections of ascending pharyngeal and occipital arteries are needed.

The middle meningeal artery may also contribute to AV fistulas that drain to the spinal cord veins.

Reconstituting a Mikaelsson Catheter The Mikaelsson catheter has a reverse curve that must be reconstituted after the catheter is introduced into the aorta, similar to the Simmons catheter. The Simmons 2 catheter is discussed in detail in Chap. 2. The Mikaelsson can be reconstituted if a wire is advanced into the contralateral iliac artery or a renal artery. The catheter is then advanced over the wire until the primary curve is just into the iliac or renal artery. Then the wire is pulled back and the catheter gently advanced, reforming the shape of the reverse curve. As the catheter continues to advance, it will pull out of the engaged renal or iliac artery and be fully formed in the aorta. Sometimes the catheter will spontaneously reform its shape if it is advanced up to the aortic arch distal to the left subclavian artery, and then rotated. Reconstitution in the left subclavian or the aortic valve is usually not an option due to the short length of the catheter. Remember that pulling back on the Mikaelsson can engage intercostal arteries, lumbar arteries, and those pesky visceral vessels, which can un-­ form the catheter curve if it is pulled back further. The catheter should always be pulled back slowly under fluoroscopic visualization as the catheter is constantly rotated to avoid snagging vessels along the way.

 emoral Artery Puncture Site F Management Arterial puncture site management and closure techniques and devices are discussed in Chap. 2.

Postangiogram Orders 1. Bed rest with accessed leg extended, head of bed ≤30°, for 6 h, then out of bed for 1 h. (If

3.4 Special Techniques and Situations

a closure device is used, bed rest, with head of bed ≤30°, for 1 h, then out of bed for 1 h). 2. Vital signs: Check on arrival in recovery room, then Q 1  h until discharge. Call ­physician for SBP ≤90  mmHg or decrease 25 mmHg; pulse ≥120. 3. Check puncture site and distal pulses upon arrival in recovery room, then Q 15 min × 4, Q 30 min × 2, then Q 1 h until discharge. Call physician if: (a) Bleeding or hematoma develops at puncture site. (b) Distal pulse is not palpable beyond the puncture site. (c) Extremity is blue or cold. 4. Check puncture site after ambulation. 5. IVF: 0.9  N.S. at 100  mL/h until patient is ambulatory. 6. Resume pre-angiogram diet. 7. Resume routine medications. 8. PO fluids at least 500 mL. 9. D/C Foley catheter and IV prior to discharge. 10. Check BUN and creatinine 24–48 h post-­ procedure if very large volumes of contrast were used.

3.4 Special Techniques and Situations Intraoperative Spinal Angiography Intraoperative spinal angiography can be done during surgery for spinal AV fistulas and arteriovenous malformations [14]. It can localize small lesions and to confirm complete removal of lesions. It correlates well with postoperative angiography in the angiography suite, and can show an unexpected residual AV shunt in up to 33% of cases [15]. Intraoperative spinal angiography poses technical challenges compared to intraoperative cerebral angiography: 1. Patient is usually prone during the operation. (a) This requires that a long (at least 25 cm) sheath be placed in the femoral artery prior

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to the patient being positioned prone. The sheath is only inserted a short distance and is positioned so that its hub is along the lateral aspect of the hip, so it can be accessed after the patient is turned prone. (b) An alternative for arterial access is a transradial approach [16]. This will allow catheterization of cervical or upper thoracic feeders, but lumbar feeders may require extra, extra-long catheters. (c) Popliteal artery access may be a better option for lumbar and low thoracic feeders. Ultrasound guided puncture of the popliteal artery with placement of a 4F sheath can be easily done in the prone position [17]. 2. Another challenge is the fact that most operating room tables are not radiolucent, which can make it a challenge getting the right C-arm angle to visualize the catheter and the desired vessels. (a) A Jackson frame should be used instead of an operating table if possible. 3. Prone positioning can also confuse the angiographer and make catheterization of the desired vessels difficult [18]. (a) An easy aid to catheterization is to reverse the fluoroscopic image side-to-side when working the catheter on a prone patient. 4. These challenges may be overcome, but are one reason why intraoperative spinal angiography is not more commonly practiced.

Tips for Imaging Specific Lesions  ype I Spinal Dural Arteriovenous T Fistulas 1. By far the most common indication for spinal angiography. 2. Noninvasive imaging such as MRI may suggest the diagnosis, but the sensitivity of MR in detecting fistulae is only 51% [4]. 3. Even if the area of myelopathy is known from clinical symptoms and noninvasive imaging, the site of the arteriovenous fistula may be remote from the area affected, so be prepared to do complete spinal angiography.

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4. Look for an enlarged vein filling from a radicular of a lumbar or intercostal artery in most cases. 5. Occasionally, the fistula may be found at the craniocervical junction [19], intracranially [20], or in the paraspinal region [16]. 6. Seek out and carefully study the artery supplying the artery of Adamkiewicz (Fig. 3.5). 7. In cases of thoracic myelopathy from a dural AV fistula, lack of visualization of the coronal venous plexus and radicular veins after injection of the artery of Adamkiewicz provides convincing evidence for venous hypertension and suggests the diagnosis of an AV fistula [21]. 8. Conversely, good visualization of normal spinal cord veins within 15  s after seeing the artery of Adamkiewicz makes the diagnosis of AV a fistula much less likely. Caveat: there may still be visualization of the venous phase in 25% of dural AV fistulas [22]. 9. An exception to this rule is the cranial dAVF draining into cord veins. Injection of the artery of Adamkiewicz may look normal [23].

 pinal Intramedullary or Perimedullary S Arteriovenous Malformations 1. All feeding arteries and draining veins should be identified; this requires visualization of the spinal cord vessels at the level of the lesion, and several segmental levels above and below the lesion. 2. Normal spinal arteries should be seen above and below the lesion to ensure all feeders have been seen. 3. Biplane, magnified runs are useful to evaluate the architecture and relationship to the cord. 4. Rapid imaging rates of 3–5 fps can sometimes provide a better visualization of the angioarchitecture of the lesion. 5. Images should be carefully evaluated to determine how the lesion relates to the anterior and posterolateral spinal arteries. 6. Look for intranidal aneurysms and pseudo-aneurysms. 7. 3D imaging can be useful.

3  Spinal Angiography

 ype IV Spinal Perimedullary T Arteriovenous Fistulas 1. These are uncommon congenital fistulas that are usually obvious on noninvasive imaging. 2. Like other vascular malformations, normal spinal arteries should be seen above and below the lesion to ensure all feeders have been seen. 3. Biplane, magnified runs are useful to evaluate the architecture and relationship to the cord. 4. These are high flow lesions, requiring rapid imaging rates of 3–15 fps. 5. 3D imaging may be useful. Spinal Intramedullary Vascular Tumors 1. The most common indication is spinal hemangioblastoma, usually preoperative and/or pre-embolization. 2. All feeding arteries and draining veins should be identified; this requires visualization of the spinal cord vessels at the level of the lesion, and several segmental levels above and below the lesion. 3. Biplane, magnified runs are useful to evaluate the architecture and relationship to the cord. Spinal Extradural Vascular Tumors 1. Common indications are in cases of preoperative evaluation of patients with aneurysmal bone cyst or vascular metastases such as renal or thyroid cancer. 2. All feeding arteries should be identified; this requires visualization of the segmental spinal vessels bilaterally at the level of the lesion, and several segmental levels above and below the lesion. 3. Normal spinal arteries at the level of the lesion or at nearby levels should be identified so that they can be carefully spared during any anticipated embolization procedure or at the time of surgery.  reoperative Angiography for Surgery P That May Risk Occlusion of the Spinal Cord Blood Supply 1. Major spinal surgery, aortic aneurysm repair, or stent-grafts may carry a risk of myelopathy if radiculomedullary contributors to the ante-

References

rior spinal artery and adjacent segmental collateral vessels are all occluded. 2. Preoperative spinal angiography can locate the variable spinal cord vessels. If a dominant spinal cord feeder is at risk in the surgical field, it could be spared, or the feeding intercostal or lumbar artery could be reimplanted into the aorta. 3. On the other hand, one study of over 100 cases in which preoperative spinal angiography was done showed no impact on neurological outcome when vessels were preserved or reimplanted based on angiographic findings [24].

References 1. Yamamoto S, Kanaya H, Kim P.  Spinal intraarterial computed tomography angiography as an effective adjunct for spinal angiography. J Neurosurg Spine. 2015;23(3):360–7. https://doi.org/10.3171/2014.12. SPINE14584. 2. Forbes G, Nichols DA, Jack CR Jr, et al. Complications of spinal cord arteriography: prospective assessment of risk for diagnostic procedures. Radiology. 1988;169(2):479–84. http://www.ncbi.nlm.nih.gov/ entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt =Citation&list_uids=3174997. 3. Niimi Y, Sala F, Deletis V, Setton A, de Camargo AB, Berenstein A. Neurophysiologic monitoring and pharmacologic provocative testing for embolization of spinal cord arteriovenous malformations. AJNR Am J Neuroradiol. 2004;25(7):1131–8. http://www.ncbi. nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=Pu bMed&dopt=Citation&list_uids=15313696. 4. Chen J, Gailloud P.  Safety of spinal angiography: complication rate analysis in 302 diagnostic angiograms. Neurology. 2011;77(13):1235–40 (in Eng). https://doi.org/10.1212/WNL.0b013e3182302068. 5. Moseley IF, Tress BM.  Extravasation of contrast medium during spinal angiography: a case of paraplegia. Neuroradiology. 1977;13(1):55–7. Case Reports (in Eng). http://www.ncbi.nlm.nih.gov/ pubmed/557752. 6. Ramirez-Lassepas M, McClelland RR, Snyder BD, Marsh DG.  Cervical myelopathy complicating cerebral angiography. Report of a case and review of the literature. Neurology. 1977;27(9):834–7. Case Reports (in Eng). http://www.ncbi.nlm.nih.gov/ pubmed/561339. 7. Miller DL.  Direct origin of the artery of the cervical enlargement from the left subclavian artery. AJNR Am J Neuroradiol. 1993;14(1):242–4. Case

171 Reports (in Eng). http://www.ncbi.nlm.nih.gov/ pubmed/8427098. 8. Rosovsky MA, Rusinek H, Berenstein A, Basak S, Setton A, Nelson PK.  High-dose administration of nonionic contrast media: a retrospective review. Radiology. 1996;200(1):119–22. http://www.ncbi. nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=Pu bMed&dopt=Citation&list_uids=8657898. 9. Prestigiacomo CJ, Niimi Y, Setton A, Berenstein A.  Three-dimensional rotational spinal angiography in the evaluation and treatment of vascular malformations. AJNR Am J Neuroradiol. 2003;24(7):1429– 35. http://www.ncbi.nlm.nih.gov/entrez/query.fcg i?cmd=Retrieve&db=PubMed&dopt=Citation&l ist_uids=12917141. 10. Rauste J, Somer K.  Semiselective renal angiography, a useful method for evaluating the vascular supply in both kidneys. Radiol Clin (Basel). 1977;46(4):281–8 (in Eng). http://www.ncbi.nlm.nih. gov/pubmed/877260. 11. Ogawa R. [Semiselective renal and lumbar angiography: experimental and clinical evaluation of this new angiographic method]. Nippon Igaku Hoshasen Gakkai Zasshi. 1995;55(1):20–33 (in Jpn). http:// www.ncbi.nlm.nih.gov/pubmed/7899062. 12. Kozak RI, Bennett JD, Brown TC, Lee TY. Reduction of bowel motion artifact during digital subtraction angiography: a comparison of hyoscine butylbromide and glucagon. Can Assoc Radiol J. 1994;45(3):209– 11. http://www.ncbi.nlm.nih.gov/entrez/query.fcg i?cmd=Retrieve&db=PubMed&dopt=Citation&l ist_uids=8193968. 13. Shimizu S, Tanaka R, Kan S, Suzuki S, Kurata A, Fujii K.  Origins of the segmental arteries in the aorta: an anatomic study for selective catheterization with spinal arteriography. AJNR Am J Neuroradiol. 2005;26(4):922–8. http://www.ncbi.nlm.nih.gov/ entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt =Citation&list_uids=15814947. 14. Barrow DL, Colohan AR, Dawson R.  Intradural perimedullary arteriovenous fistulas (type IV spinal cord arteriovenous malformations). J Neurosurg. 1994;81(2):221–9. http://www.ncbi.nlm.nih.gov/ entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt =Citation&list_uids=8027805. 15. Schievink WI, Vishteh AG, McDougall CG, Spetzler RF.  Intraoperative spinal angiography. J Neurosurg. 1999;90(1 Suppl):48–51. http://www.ncbi.nlm.nih. gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed& dopt=Citation&list_uids=10413125. 16. Lang SS, Eskioglu E, R AM.  Intraoperative angiography for neurovascular disease in the prone or three-quarter prone position. Surg Neurol. 2006;65(3):283–9; discussion 289. http://www.ncbi. nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=Pu bMed&dopt=Citation&list_uids=16488250. 17. Barbetta I, van den Berg JC.  Access and hemostasis: femoral and popliteal approaches and closure devices-why, what, when, and how? Semin

172 Intervent Radiol. 2014;31(4):353–60. https://doi. org/10.1055/s-­0034-­1393972. 18. Benes L, Wakat JP, Sure U, Bien S, Bertalanffy H.  Intraoperative spinal digital subtraction angiography: technique and results. Neurosurgery. 2003;52(3):603–9; discussion 608–9. http://www. ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&d b=PubMed&dopt=Citation&list_uids=12590685. 19. Pulido Rivas P, Villoria Medina F, Fortea Gil F, Sola RG. [Dural fistula in the craniocervical junction. A case report and review of the literature]. Rev Neurol. 2004;38(5):438–442. http://www.ncbi.nlm.nih.gov/ entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt =Citation&list_uids=15029522. 20. Li J, Ezura M, Takahashi A, Yoshimoto T. Intracranial dural arteriovenous fistula with venous reflux to the brainstem and spinal cord mimicking brainstem infarction—case report. Neurol Med Chir (Tokyo). 2004;44(1):24–8. http://www.ncbi.nlm.nih.gov/ entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt =Citation&list_uids=14959933. 21. Willinsky R, Lasjaunias P, Terbrugge K, Hurth M.  Angiography in the investigation of spinal

3  Spinal Angiography dural arteriovenous fistula. A protocol with application of the venous phase. Neuroradiology. 1990;32(2):114–6 (in Eng). http://www.ncbi.nlm.nih. gov/pubmed/2398936. 22. Eckart Sorte D, Obrzut M, Wyse E, Gailloud P.  Normal venous phase documented during angiography in patients with spinal vascular malformations: incidence and clinical implications. AJNR Am J Neuroradiol. 2016;37(3):565–71. https://doi. org/10.3174/ajnr.A4601. 23. Trop I, Roy D, Raymond J, Roux A, Bourgouin P, Lesage J. Craniocervical dural fistula associated with cervical myelopathy: angiographic demonstration of normal venous drainage of the thoracolumbar cord does not rule out diagnosis. AJNR Am J Neuroradiol. 1998;19(3):583–6. Case Reports (in Eng). http:// www.ncbi.nlm.nih.gov/pubmed/9541323. 24. Minatoya K, Karck M, Hagl C, et al. The impact of spinal angiography on the neurological outcome after surgery on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg. 2002;74(5):S1870– 2; discussion S1892–8 (in Eng). http://www.ncbi.nlm. nih.gov/pubmed/12440683.

4

General Considerations for Neurointerventional Procedures

4.1 Pre-procedure Preparation General preparations for most neurointerventional procedures: 1. Routine pre-procedure workup: (a) History and physical (b) Neurological examination (c) Imaging (d) Blood work (CBC, Cr, PT, PTT) (e) EKG (f ) Anesthesia evaluation, if needed 2. Informed consent. 3. One or two peripheral IV lines. 4. Foley catheter (a) Insert in the patient’s private room or preoperative area for awake patients (b) Insert in the angiography suite, after induction of anesthesia, for asleep patients 5. NPO after midnight or 6 h prior to the procedure except for medications. 6. Place thigh-high sequential compression device (SCD) sleeves on both legs for deep venous thrombosis prophylaxis. 7. Make sure that all devices that may be needed are available in the angiography suite prior to the procedure. 8. Premedication: (a) Dual antiplatelet therapy. Necessary for any stenting case, and an option for other interventions such as intracranial aneurysm coiling and liquid embolic proce-

dures. See below (Antiplatelet Therapy) for dosing. (b) Protection against nephrotoxicity for patients with renal insufficiency (creatinine ≥1.5 mg/dL): (i) PO hyTdration (water, 500 mL prior to the procedure and 2000 mL after the procedure) (ii)  IV hydration with 0.9% sodium chloride [1] (iii) Acetylcysteine 600  mg (3  mL) PO BID on the day before and the day of the procedure [2] (c) Protection against anaphylaxis for patients with a history of contrast allergy: (i) Prednisone 50 mg PO (or hydrocortisone 200  mg IV) 13, 7, and 1  h prior to contrast injection. (ii) Diphenhydramine (Benadryl®) 50 mg IV, IM or PO 1 h prior to contrast injection. (iii)  Steroids should be given at least 6  h  prior to the procedure; ­administration less than 3 h prior to the procedure does not reduce the risk of an adverse reaction [3]. 9. Routine steroid premedication: (a) Dexamethasone may reduce swelling associated with tumors [4]. (b) Whereas some studies suggest some benefit to steroids protecting against effects

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 M. R. Harrigan, J. P. Deveikis, Handbook of Cerebrovascular Disease and Neurointerventional Technique, Contemporary Medical Imaging, https://doi.org/10.1007/978-3-031-45598-8_4

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of ischemia [5], other studies show no benefit [6] or even a detrimental effect of steroids [7]. (c) Chronic steroids worsen effects of ischemia, but short-term steroids prior to the procedure may be less detrimental [8]. (d) The authors of this handbook do not routinely premedicate with steroids, except in tumor cases. 10. Make sure that all devices that may be needed are available in the angiography suite prior to the procedure.

Awake or Asleep? Some operators prefer general anesthesia for most neurointerventional cases whereas others prefer to do them with the patient awake. Each approach has advantages and disadvantages. General anesthesia eliminates procedural discomfort, which can be substantial during some procedures, such as liquid embolic embolization and intracranial angioplasty. It also helps patients endure lengthy procedures, keeps them still for precise intracranial maneuvering, and simplifies the procedure for the operators somewhat, eliminating the need for constant coaching and neurological assessment of an awake patient. General anesthesia makes it possible to pause respirations intermittently in order to obtain highly precise angiograms and road maps. However, general anesthesia makes it difficult to detect neurological changes in the patient, although electroencephalography and monitoring of somatosensory and/or motor evoked potentials can help remedy this. On the other hand, physiological monitoring during general anesthesia can cause crowding of the angiography suite during procedures, and the reliability of monitoring is less than certain. Doing neurointerventional procedures awake eliminates the risks associated with general anesthesia, permits constant monitoring of the patient’s neurological status, and reduces procedure time and room turnover time. Occasional patients simply cannot tolerate general anesthesia, most often because of cardiac or pulmonary disease. Shepherding an awake patient through a

complex intracranial intervention, however, takes patience and skill on the part of the operator, and the judicious use of sedation and analgesia. Whatever the institutional practice is at any given center, it behooves the operator—and particularly those in training—to do cases awake occasionally to maintain the skills and comfort level necessary to do awake cases.

Awake Technique 1. Obtain IV access and a Foley catheter placement before the patient is brought to the angiography suite. 2. An abbreviated neurological examination is rehearsed with the patient prior to draping (e.g., the patient is asked to say “Methodist Episcopal,” show their teeth and gums, wiggle their toes, and squeeze a rubber duckie (Fig.  4.1) with the hand contralateral to the side being treated). 3. Throughout the case, the patient is reminded to stay completely still. The patient’s head can be lightly taped to the head holder with a piece of plastic tape across the forehead, to remind him or her to stay still. Place a piece of nonadherent Telfa™ dressing (Kendall/

Fig. 4.1  Rubber duckie. Other squeaky toys may be substituted if a duck is not available

4.2 Vascular Access

Covidien, Mansfield, MA) between the tape and the forehead to ensure that the skin is not injured. 4. Warn the patient prior to contrast injections or potentially uncomfortable catheter movements, so there are no surprises. 5. Check on the patient with gentle questions and reminders constantly throughout the procedure. 6. Keep sedation and analgesia to a minimum to facilitate the patient’s full cooperation. Options for sedation: (a) Midazolam (Versed®) 1–2  mg IV for sedation; lasts approximately 2 h. (b) Fentanyl (Sublimaze®) 25–50  μg IV for analgesia; lasts 20–30 min.

Asleep Technique 1. The patient is placed under general anesthesia on the angiography table. (a) Endotracheal anesthesia is better than laryngeal mask anesthesia, which will not allow the patient to be chemically paralyzed during the procedure. (b) If arterial blood pressure monitoring is needed during induction (e.g., when intubating patients with a ruptured aneurysm), then several options exist: (i) Radial arterial line (SAH patients usually arrive in the angiography suite with an arterial line). (ii) Femoral artery sheath. The sheath may be placed prior to induction and used to transduce blood pressure. A femoral artery sheath is less uncomfortable than a radial arterial line. 2. Pay strict attention to blood pressure during induction. 3. If neurophysiological monitoring is planned, obtain baseline evoked potentials immediately prior to the case. Depending on the anatomic location of the lesion, electroen­ cephalography or monitoring of somatosensory, motor, visual, or auditory evoked potentials may be useful. The authors of this handbook routinely use monitoring for procedures involving the spinal cord.

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4. Ask the anesthesiologist to report any abrupt changes in blood pressure or heart rate during the case, which can indicate intracranial hemorrhage. 5. Assess the patient’s neurological status following anesthesia.

Contrast Agents 1. For most cases use iohexol (Omnipaque®, GE Healthcare, Princeton, NJ) 240  mg I/ mL.  Patients with normal renal function can tolerate as much as 400–800  mL of Omnipaque®, 300  mg I/mL without adverse effects [9]. 2. For patients with renal insufficiency use iodixanol (Visipaque™, GE Healthcare, Princeton, NJ) 270 mg I/mL. 3. See Chap. 2 for more detail about contrast agents, renal insufficiency, and iodinated contrast agent anaphylaxis.

4.2 Vascular Access All neurointerventional procedures consist of (1) an access phase and (2) an intervention phase. The access phase usually consists of placement of a guide catheter in the carotid or vertebral artery via the femoral artery. 1. Femoral access. The traditional access site is still used frequently for neurointerventional procedures. (a) Place the patient on the angiography table. (b) Find and mark the dorsalis pedis and posterior tibialis pulses. (c) Clip, prep, and drape both groins. (i) Clipping is better than shaving since it creates less skin irritation [10]. (ii) Be sure to prep both groins in case femoral artery access cannot be obtained on one side or if a second sheath needs to be inserted.

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(iii) For younger patients and those with a low pain threshold, apply EMLA® (AstraZeneca, Wilmington, DE), a topical anesthetic cream to the puncture site under an occlusive dressing 30 min prior to the procedure. (d) Bring the PA C-arm into position to enable fluoroscopy of the femoral artery, if needed for puncture of the vessel. (e) Insert a sheath in the femoral artery. (f ) The size of the sheath depends on the intervention. For most intracranial cases, a 6F is suitable. A 7F sheath has the advantage of being large enough to accommodate a 6F guide catheter and still permit arterial line transduction through the sheath. (g) Sheaths are available in various lengths, most commonly 10 or 25 cm. The 25-cm version has the advantage that it bypasses any tortuosity in the iliac arteries. Having the distal end of the sheath in the aorta prevents any danger of injuring the iliac artery during catheter introduction through the sheath. (h) Use a 0.038-in.  J-tip wire (“safety wires”) for sheath placement. (i) If a femoral artery closure device is planned, do a femoral artery angiogram at the beginning of the case right after insertion of the sheath, because the C-arm is positioned over the groin. 2. Radial access. Now it is used frequently as a first-choice option in many centers. (a) Prepare and drape the wrist and forearm. Consider also prepping the groin area if radial access fails. (b) Always use ultrasound guidance. Scan the wrist and locate the pulsatile radial artery. Ensure it is large enough to accept the chosen sheath size. (c) Give local anesthesia (2% lidocaine without epinephrine), by raising a wheal approximately 1 cm distal to the expected entry point into the artery. (d) Make a 3-mm incision parallel to the skin with an 11-blade scalpel. The artery is very superficial, so it is imperative to avoid incising it.

















(e) Radial sheath sets come with an appropriate 21-gauge puncture needle. Insert the needle with the bevel facing upward under ultrasound guidance. Gently wiggle the tip if unsure where it is. Adjust the ultrasound probe to keep the artery in view and watch for deflection of the anterior wall of the vessel. (f ) Continue advancing the needle and look for blood return. Advance the needle 1–2  mm after the first blood return and ensure brisk blood return continues from the needle. Then gently advance the softtip wire appropriate for the sheath system. (g) Alternatively, make a two-wall puncture by advancing the needle throughand-through both vessel walls, then slowly withdraw the needle. When bright red, pulsatile arterial blood is encountered, gently advance the introducing wire through the needle for at least the length of the sheath (usually 23 cm). The wire must go smoothly and effortlessly. (h) It is a good habit to check on fluoroscopy that the wire is well up the arm in the brachial artery. (i) Exchange the needle for the radial sheath (e.g., 6F Prelude EASE™ (Merit Medical, South Jordan, UT)). It is low profile with the 2.44-mm OD and inner dilator with a long, smooth taper. It should easily advance over the wire. ( j) Secure the sheath at the wrist with a stitch or with a small Tegaderm™ (3M, St. Paul, MN) adhesive dressing. (k) Consider a gentle angiogram immediately after placement of the sheath to rule out a dissection and to confirm that antegrade flow in the artery is preserved after placement of the sheath. (l) Cocktail time: Slowly inject a radial artery cocktail via the sheath: 10  mL of saline containing heparin (5000  IU), verapamil (2.5  mg), cardiac lidocaine (2%, 1.0 mL), and nitroglycerin (0.2 mg). (Enjoy responsibly.)

4.2 Vascular Access



(i) Consider repeat dose with catheter exchange and prior to sheath removal. (m) Remove the inner dilator and insert a Simmons curve hydrophilic catheter over a hydrophilic 1.5-mm  J-tip (Baby-J) 0.035 Glidewire® (Terumo Medical, Somerset, NJ) to the aorta. (i) The tight J-tip wire works well to circumnavigate loops and bypass branches. 3. If needed, do a diagnostic angiogram prior to the intervention. Prior to the intervention, do intracranial PA and lateral angiograms, to serve as a baseline for later comparison, to check for the possibility of thromboembolism or hemorrhage in the intracranial circulation during or after the procedure. 4. Obtain angiographic images of the access vessel (carotid or vertebral artery). Biplane imaging is preferred. 5. Guide catheter selection. There are five major groups of guide catheters suitable for neurointerventional procedures. Traditional guide catheters are large-bore supportive catheters (5–7F) that are 90 or 100 cm long, which are placed in the proximal internal carotid or vertebral arteries. Guiding sheaths are 4–8F inner diameter 80–110 cm in length, and these are much more stable than traditional guide catheters. Hybrid guide/intermediate catheters have a supportive large-bore 6F proximal segment like a traditional guide catheter but a progressively soft, flexible distal segment that can be placed safely positioned in the intracranial vessels. These can be used primarily through a short groin sheath or with a longer guiding sheath for added support. Intermediate catheters have soft, flexible distal segments that can be safely placed in the intracranial vessels for greater stability; however, the more proximal segments of these catheters are also very soft and flexible. These are therefore only used in conjunction with a traditional guide catheter or a guiding sheath to provide added stability. Finally, several dedicated radial guide catheters are available. They are designed to have strategically positioned flex-

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ible and supportive segments that offer stability when positioned from a radial approach. (a) Traditional guide catheters (best for femoral access) (i) 6F Guider Softip™ XF guide catheter (Stryker Neurovascular, Fremont, CA) • Advantages: Soft atraumatic tip. Minimizes risk of vasospasm and dissection in small, tortuous vessels. Available angled tip allows it to be navigated into position primarily. • Disadvantages: Relatively flimsy and prone to prolapse back in the arch when the vasculature is tortuous. (ii) 6F Envoy® (Cerenovus, Irvine, CA): • Advantages: Relatively rigid, provides a good platform in tortuous vessels, large internal lumen. Nice for working in the external carotid artery. Angled tip allows it to be navigated primarily. • Disadvantages: Stiff and sharpedged tip. (iii) 6F Northstar® Lumax® Flex Catheter (Cook, Inc., Bloomington, IN) • Advantages: The device comes packaged with an inner dilator, which provides a smooth transition to the guidewire, minimizing trauma to the vessel wall. The dilator also allows the catheter to be introduced without a groin sheath. Relatively rigid, providing stability. • Disadvantages: Relatively stiff distal tip. Extremely lubricious catheter can slip out of tortuous vessels. (b) Guiding sheaths (also best for femoral access) (i) 6F 90-cm Flexor® Shuttle® (Cook, Inc., Bloomington, IN):

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• Very large, stable platform. • Available from 4- to 8F size. Most neurovascular cases use 6F with a 0.087-in. lumen. (ii) Benchmark™ BMX 96 Large Lumen Catheter (Penumbra, Inc., Alameda, CA) • Large lumen, for use as a guide catheter. The 4-cm distal tip is soft, flexible, and stable. • Available 6F Neuron Select™ catheters can also be used within it, to facilitate quick primary access to the vessel of choice without needing a catheter exchange. • Available in 80-, 90-, and 100cm lengths. (iii) AXS Infinity LS Plus® 91 (Stryker Neurovascular, Fremont, CA) • 8F outer diameter but the large 0.091-in. lumen. • Easily access vessel of choice and provides a stable platform. • Available lengths 70, 80, and 90 cm. (iv) Fubuki® Long Sheath (Asahi, Irvine, CA) • Designed as a long sheath to act as a guide catheter. Available in 4–6F nominal sizes, which are 2F larger in the outer diameter. The inner dilator provides a smooth transition to the guidewire as it is advanced. • Available in 80-, 90-, 100-, and 110-cm length. (v) Ballast® Long Sheath (Balt, Boston, MA) • Designed as a long sheath to act as a guide catheter. Available in 6F nominal size, 8F outer diameter, 0.088-in. lumen. The inner dilator provides a smooth transition to the guidewire as it is advanced. • Available in 80-, 90-, and 100cm length.

(vi) Cerebase™ DA Guide Sheath (Cerenovus, Irvine, CA) • Designed as a long sheath to act as a guide catheter. Available in 6F nominal size, 8F outer diameter, 0.090-in. lumen. The inner dilator provides a smooth transition to the guidewire as it is advanced. • The distal segment very flexible to allow more distal atraumatic positioning of the tip. • Available in 90-cm length. (vii) Guide sheath technique: • For 6F size, it requires either an 8F sheath or sheathless by exchange for a smaller sheath (e.g., for carotid stent cases). If a smaller sheath (e.g., 5 or 6F) is inserted first, position a diagnostic catheter in the neck artery and then exchange it over an exchange-length (260–300  cm) hydrophilic wire for the guide sheath with the obturator still in place. Note that when inserting the sheath over a wire directly into the vessel, the tip may be easily damaged and become wrinkled. This can impair insertion in the vessel and increase trauma to the vessel. • When the guide sheath is ∼2 cm proximal to the desired final position, remove the obturator and aspirate several milliliters of blood backwards out of the sheath, to remove any bubbles or clot. In anterior circulation cases, position the exchange wire in the external carotid territory and do the first flush in the external carotid before repositioning the guide sheath into its final position. This strategy minimizes the risk of clinically significant dissection and emboli during this process. Note: The obturator is not radio-opaque.

4.2 Vascular Access

• The guide sheath may be primarily positioned in the vessel of interest without doing a catheter exchange if an inner catheter is used with an appropriate curve. –– If the guide sheath is advanced in the aorta, then remove the dilator and insert the desired 125-cm Neuron Select™ (Penumbra, San Leandro, CA) or other catheter over a 0.038-in. Glidewire® (Terumo Medical, Somerset, NJ) to the target vessel (carotid or vertebral artery). Available curves include Berenstein for fairly straight vessels or Simmons for more tortuous vessels. –– Note that the Neuron Select catheters may require an exchange length (260  cm) wire for navigation since these catheters are longer than routine diagnostic catheters. –– Tip: If the guide sheath becomes displaced back in the aortic arch, reaccess to the great vessels can be obtained by advancing a hydrophilic wire and a 125cm 5F Simmons or Vitek catheter within it. The Vitek has a shape similar to a Simmons 2 catheter, and can be used to navigate the sheath back into the carotid or subclavian arteries. (c) Hybrid guide/intermediate catheters: (i) 6F 0.71-in. Benchmark™ Intracranial Access System (Penumbra, Inc., Alameda, CA). • 6F OD, 0.071-in. (∼5.4F) ID.  Comes packaged with a curved Neuron Select™ catheter

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for smooth access over a hydrophilic wire. • Advantages: Large lumen, able to accommodate two microcatheters (e.g., ideal for balloon-remodeling). Permits good angiograms with even larger microcatheters in position. Can be used for radial access cases. With the large lumen and reasonable stability, it is a good option for most interventional procedures. • Disadvantage: Somewhat more stiff, navigable less distally than the smaller Neuron. • Technique and tips: –– Can be exchanged into position, but often using the inner Neuron Select™ it may be positioned primarily in the vessel of interest. –– Two lengths are available: 95 and 105  cm, and the corresponding Neuron Select™ is available in 120- or 130-cm lengths. –– Also available in straight or multipurpose curve. –– A standard hydrophilic wire is used for initial positioning of the Neuron™. –– Coaxial microcatheter technique for final positioning of the Benchmark™ 0.071-in. catheter: Advance a microcatheter over a microwire through the Benchmark™ into the target vessel distal to the desired final position of the guide catheter. Then advance the Benchmark™ over the microcatheter to its final position. A more substantial microcatheter such as a Velocity® (Penumbra, Inc., Alameda, CA), XT-27® (Stryker

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4  General Considerations for Neurointerventional Procedures

Neurovascular, Fremont, CA), or Prowler® Plus (Cerenovus, Irvine, CA) with a substantial 0.016-­in. or larger guidewire can provide good support to facilitate distal placement of the Neuron™. The more distal the tip, the more stable the catheter will be; e.g., position the tip in the horizontal segment of the petrous ICA or the V4 segment of the vertebral artery for maximum stability. Optimal positioning is distal to at least two 90° turns in the vessel to provide sufficient support for the coaxial placement of a microcatheter. Guide catheter angiograms may be of marginal quality when multiple microcatheters are inside the guide catheter, because of the relatively narrow lumen. Injection of 100% contrast in a 3-mL syringe, rather than a 10-mL syringe, will produce better angiograms. Warning: When the Benchmark™ is in its final intracranial position, use caution when flushing or injecting contrast. Use smaller volumes and lower pressures since the pressure is transmitted directly to the intracranial vessels. This can be particularly dangerous if there is an aneurysm near the catheter tip. Avoid using a power injector.

(ii) Envoy® DA Guiding Catheters (Cerenovus, Irvine, CA) • OD 6F, ID 0.071 in. Available in 95 and 105-cm lengths. Available in straight and multipurpose tips. • Also available in Envoy DA XB with a stiffer distal segment when added support is needed. • Advantages: Large lumen, can accommodate multiple microcatheters. Somewhat more supportive than other hybrid guiding/distal access catheter systems. • Disadvantages: The stiffer distal segment may not allow safe access as distally as other catheter systems. Limited size and length options. The radio-opaque distal marker is located proximal to the actual tip. • Technique: Similar to Neuron™ catheters. (d) Intermediate catheters: (i) AXS Catalyst™ catheter (Stryker Neurovascular, Fremont, CA) • CAT® 5 OD 5.3F distal, 5.6F proximal, ID 0.058  in. Length 115 cm. • CAT® 6 OD 5.4F distal, 6.0F proximal, ID 0.060  in. Length 132 cm. • Advantages: Very soft and flexible, and can be advanced safely in tortuous vessels to a distal location to support the working microcatheter. Available in a variety of sizes and lengths. When used in procedures requiring use of multiple microcatheters such as AVM embolization [11], the distally placed intermediate catheter greatly facilitates and speeds repeated access of the distal vessels.

4.2 Vascular Access

• Disadvantages: A very floppy catheter is not supportive unless advanced quite distally around several turns and also requires proximal support from a guiding catheter or guiding sheath. The catheter may advance so distally in smaller vessels it may be occlusive. If the chosen catheter is too long, the microcatheter advanced through it may not be long enough to reach the desired location. Requires an addition pressurized saline infusion line. • Tip: When the guide catheter is in position, advance a microcatheter over a microwire through the intermediate catheter and into the target vessel distal to the desired final position of the access catheter. Then advance the intermediate over the microcatheter to its final position. A more substantial microcatheter such as a Velocity® (Penumbra, Inc., Alameda, CA), Renegade® (Stryker Neurovascular, Fremont, CA), or Prowler® Plus (Cerenovus, Irvine, CA) with a beefier 0.016in. guidewire can provide good support to facilitate distal placement of the DAC™. (ii) Navien™ Intracranial Support Catheter (Medtronic PLC, Minneapolis, MN) • Navien™ 058 OD 5.2F; ID 0.058 in. Available in 105-, 115-, 125-, and 130-cm lengths. • Navien™ 072 OD 6.3F; ID 0.072 in. Available in 95-, 105-, 115-, 125-, and 130-cm lengths. Also available with a 25° angled tip. • Advantages: Very soft and flexible. Can be advanced quite distally. Somewhat more supportive

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than DAC™ catheters. Multiple sizes are available. • Disadvantages: Floppy proximal segment requires support with a guiding sheath. More size options compared to the AXS Catalyst™ catheter. • Technique: When the guide catheter is in position, advance a microcatheter over a microwire through the Navien™ and into the target vessel distal to the desired final position of the access catheter. Then advance the Navien™ over the microcatheter to its final position. A more substantial microcatheter such as a Marksman (Medtronic PLC, Minneapolis, MN) with a beefier 0.016-in. guidewire can provide good support to facilitate distal placement of the Navien™. (iii) SOFIA® and SOFIA® Plus Distal Access Catheters (Microvention/ Terumo, Aliso Viejo, CA) • OD 6F, ID 0.070-in. SOFIA® available in 110-cm length and SOFIA® Plus 125 and 131 cm. • Advantages: Very soft distal segment that can be advanced quite distally. Very large lumen. • Disadvantages: Proximal segment not supportive enough to use without a guiding sheath. Limited variety of sizes and lengths. • Technique: Similar to DAC™ catheters. (iv) Revive™ IC (Cerenovus, Irvine, CA) • REVIVE 044: 4.1F OD, ID 0.044 in. (3.3F) • Available in 115- and 130-cm (usable) lengths • Will fit in a Neuron™ 6F 070 guide catheter

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4  General Considerations for Neurointerventional Procedures

• REVIVE 056 (4.3F ID, 5.0F OD) • Available in 115- and 125-cm (usable) lengths –– May barely fit in an 070 Neuron™ (v) Fargo and FargoMAX (Balt Extrusion, Montmorency, France). These are CE mark approved, but not yet available in the United States. • Fargo 6F OD 6.0F, ID 4.2F • Available in 105, 115, 125, and 135 cm lengths • Available in straight or preshaped multipurpose curve • Fargo MAX OD 6.0F, ID 5.3F • Available in 105-, 115-, and 125-cm lengths • Available in straight or preshaped multipurpose curve (e)   Dedicated radial access guide catheters: (i) Rist™ Guide Catheter (Medtronic, Minneapolis, MN) • Rist™ 079: 7F OD, ID 0.079 in. (6F) • Available in 95-, 100-, and 105cm lengths • Available 5.5F Berenstein or Simmons curve Rist inner catheters 120 or 130  cm to facilitate positioning • Rist 071: 6F OD, ID 0.071  in. (5.5F) • Available in 95-, 100-, and 105cm lengths • Available 5.5F Berenstein or Simmons catheters will also fit (ii) Armadillo™ Radial Access System (Q’Apel Medical, Fremont, CA) • Armadillo 7F (0.095 in.) OD, ID 0.072 in. (6F) • Uses SelectFlex™ technology in which an outer chamber of the catheter makes it very flexible when filled with fluid, allowing navigation through curves. When in position, the fluid in the cath-

eter wall is withdrawn, making the catheter body rigid for support 6. Guide catheter sizing: (a) The guide catheter should be 90 cm long (and no longer) for use with the Wingspan stent system. (b) Use 6F for most cases. (c) Use 5F if the vessel caliber is small and collateral circulation is limited: (i) e.g., for use in a small vertebral artery when the contralateral vessel is hypoplastic. (ii) Disadvantage: Angiograms with a microcatheter or balloon in place are more difficult to obtain because of limited space within the guide catheter. 7. Straight or angled? (a) The straight guide catheter is useful in relatively straight vessels, or in situations where the guide catheter is gently navigated through a convoluted vessel: (i) Usually requires exchanging (see below). (ii) Preferred for the vertebral artery. (b) The angled guide catheter is useful when the final position of the catheter tip is in a vessel curve. (c) Angled catheters are easier to navigate through the aortic arch than straight catheters. 8. Traditional guide catheter placement technique: (a) Position the guide catheter in the ICA or vertebral artery only after the heparinization is therapeutic (usually 5  min or more after the IV loading dose is given). (b) Exchange method: (i) Exchanging is usually necessary for Neuron™ guide catheters and other straight guide catheters because the absence of an angle at the tip makes it difficult to navigate the catheter primarily. Exchanging minimizes risk of dissection and is useful in patients with tortuous anatomy, atherosclerosis, and fibromuscular dysplasia.

4.2 Vascular Access















(ii) Guide a 4- or 5F diagnostic catheter into the CCA or vertebral artery over an exchange length (260  cm) 0.035- or 0.038-in. hydrophilic wire. The 0.035-in. Glidewire® Advantage® (Terumo Medical, Somerset, NJ) works well. (iii) Advance the tip of the hydrophilic wire into a distal branch of the ECA or the distal extracranial vertebral artery (usually the first 90° turn of the vessel at C2) using a road map. (iv) Gently remove the diagnostic catheter while the tip of the hydrophilic wire is continuously visualized on fluoroscopy. (v) Wipe down the hydrophilic wire with a dripping-wet Telfa™ (Kendall/Covidien, Mansfield, MA) sponge. • Avoid wiping hydrophilic wires with dry cotton sponges, which can leave numerous thrombogenic cotton fibers on the wire. (vi) Advance the guide catheter over the wire while continuously visualizing the tip of the wire. (c) Direct navigation method: (i) Possible in patients with nontortuous, nonatherosclerotic vessels. (ii) Navigate an angled guide catheter gently into the carotid or vertebral artery over a 0.035- or 0.038-in. hydrophilic wire. (d) Guide catheter position: (i) Carotid artery • Using a road map, advance the guide catheter over a hydrophilic wire into the ICA as distally as possible. A “high position” of the guide catheter will maximize the stability of the guide and improve control over the microcatheter and microwire. • In a nontortuous, healthy carotid system, the authors of this handbook prefer to position the tip of the guide catheter in the vertical

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segment of the petrous ICA. In a cervical ICA with a significant curve in the vessel, the guide can be adequately positioned immediately proximal to the curve. • A curvaceous carotid or proximal vertebral artery can sometimes be straightened out by tilting the patient’s head toward the opposite shoulder (Fig. 4.2). • Moderate curves in the vessel can be straightened out by guiding a relatively stiff hydrophilic wire (e.g., a 0.038-in. wire) through the affected segment, followed by the catheter, but this may compromise flow in the vessel due to kinking or spasm. Consider a catheter with the softer distal segment such as Neuron™ 053 (Penumbra, Alameda, CA) or a soft intermediate catheter to navigate around the curves without compromising the lumen. (ii) Vertebral artery • Using a road map, position the guide catheter in the distal extracranial vertebral artery, usually at the first curve (at C2). (e) Once the guide catheter is in position, do a gentle injection of contrast through the guide catheter under fluoroscopy, to examine the configuration of the vessel around the tip and to check for the presence of vasospasm or vessel dissection around the tip. If catheter tip-induced vasospasm is present and flow-limiting, withdrawal of the catheter tip by several millimeters is often sufficient to restore flow. (f ) Keep the tip of the guide catheter in view on one or both biplane fluoroscopic views for the duration of the case. For correct placement of the guide catheter tip, and, if the catheter appears to be unstable, consider replacement with a more stable guide catheter system.

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4  General Considerations for Neurointerventional Procedures

Fig. 4.2  Head tilt technique. Lateral angiogram of the left carotid system in a neutral position (left) and with the head tilted toward the opposite shoulder (right)

9. Guide catheter care and maintenance (a) Continuous irrigation of the guide with heparinized saline (10,000 units of heparin per liter of saline) is important. (b) Meticulous attention to the RHV and the guide catheter is necessary throughout the procedure in order to identify thrombus or bubbles. 10. Tips to minimize or treat guide catheter induced vasospasm (a) Withdraw the catheter into a lower segment of the vessel when significant catheter-induced vasospasm appears.



(b) Keep the catheter tip away from kinks and bends in the vessel if possible. (c) Selective injection of IA nitroglycerin (30 μg per injection). (d) IA nitroglycerin can also help distinguish vasospasm from vessel dissection, if a dissection is suspected. (e) Use Visipaque™ (GE Healthcare, Princeton, NJ) contrast instead of Omnipaque; according to the manufacturer, this contrast material is less spasmogenic than Omnipaque®.

4.2 Vascular Access

(f) Use a soft-tipped guide catheter or a hybrid guide/intermediate catheter (e.g., Neuron™, Penumbra, Alameda, CA). (g) Use a guide catheter with an inner obturator (e.g., Northstar® Lumax® Flex Catheter, Cook, Inc., Bloomington, IN). 11. Tips for guide catheter navigation via a radial approach (a) See Chap. 2 for detailed radial access tips. (b) Via a 6F radial sheath catheterize the vessel of interest with a 6F 0.71-in. Benchmark™ (Penumbra, Inc., Alameda, CA) over a 5F Neuron Select Simmons curve all over a 0.038260-cm Glidewire. (i) Alternatively, a Simmons 2 curve catheter is placed in the vessel of interest and exchanged over a 260cm Glidewire® Advantage® (Terumo Medical, Somerset, NJ) for a 6F 0.71-in. Benchmark™ Intracranial Access System (Penumbra, Inc., Alameda, CA). (c) Via a 7F radial sheath, the 5.5F Rist™ (Medtronic, Minneapolis, MN) Simmons catheter can be used coaxially within the 079 Rist™ (Medtronic, Minneapolis, MN) Guide catheter for primary catheterization. (i) If using the smaller 071 Rist™, one can use a 6F radial sheath but the 5.5F Simmons can still fit. (ii) Simmons catheters can also initially be placed separately in the vessel of interest with exchange over an exchange length hydrophilic guidewire for the guide catheter. (d) Try to access the target vessel with as few catheter exchanges as possible to avoid causing spasm. (i) Consider a repeat dose of the radial cocktail with each exchange.

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Kids Korner! Pediatric Vascular Access

1. Femoral arterial access (a) Use a 4F micropuncture kit, which contains a 22-gauge needle. (b) Ultrasound guidance is recommended to reliably access the vessel. (c) Be very careful when puncturing the vessel to minimize the chance of spasm, which can cause artery occlusion in kids. (d) After puncturing the vessel, carefully advance the 0.018-­micropuncture wire into the aorta. (e) Exchange the needle for the 3–4F coaxial dilator. (f   ) Remove the inner 3F dilator and advance a 0.038-in.  J-tip wire and position its tip in the descending aorta. (g) Remove the dilator and advance a 4F nonbraided 40-cm Berenstein catheter (Angiodynamics, Latham, NY) over the wire. Longer catheters may be required in older, larger children. (h) Always be gentle while inserting and manipulating the catheter. (i) Consider heparinizing the patient with a 50-unit/kg bolus. ( j) Attach an RHV to the catheter and a slow, continuous flush of heparinized saline. 2. Femoral venous access (a) See Chap. 11. 3. Umbilical artery access (Fig. 4.3) [12]. The paired umbilical arteries connect to the iliac arteries and are available for catheter access for about 3–5 days after birth. Tip: Neonatal ICU physicians are typically experienced at obtaining umbilical artery access, and can assess or perform this procedure if needed.

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(a) Prepare and drape the umbilicus and adjacent abdomen in a sterile fashion. (b) If placing the catheter de novo, an Argyle™ single-lumen umbilical vessel catheter (UAC) and insertion tray (Covidien, Mansfield, MA) should be available. (c) Flush the catheter and dilator with heparinized saline (1 unit/mL). (d) Estimate the length of catheter required to reach the aorta. UAC catheters have centimeter gradations. (e) Gently place a sterile tourniquet around the base of the umbilical cord. (f ) Cleanly cut the distal end of the cord with a scalpel. (g) The single, bigger, thin-walled lumen is the vein and the paired thicker walled vessels are arteries. (h) Have an assistant grasp the outer edge (Wharton’s jelly) of the cord with two hemostats and stabilize it. (i) Gently probe the artery with a dilator to dilate the vessel. ( j) Further dilate the end of the artery by gently spreading it open with curved iris forceps. (k) While holding the vessel open with the forceps, grasp the UAC with a straight forceps and gently insert it millimeter by millimeter until it is solidly in the vessel for 2 cm. (l) Slowly and gently insert the catheter by hand. If resistance is encountered, apply continuous gentle forward pressure for 30 s to try to overcome spasm. (i) A sudden popping sensation means trouble and may indicate puncture of the umbilical artery, which requires switching to the other umbilical artery for access.

(m) Usually the catheter easily passes up to the aorta, although sometimes it will go down into the femoral artery. (n) The catheter can usually be seen fluoroscopically without using contrast. (o) When the catheter is in the aorta, insert a 300-cm, exchange length 0.010- or 0.014-in. wire into the aorta and exchange the UAC for either a 3F sheath with a microcatheter by itself in smaller newborns, or a coaxial assembly of a microcatheter with a 4F 65-cm angled Glidecath® (Terumo, Somerset, NJ) in larger babies. The softer microcatheter can more easily negotiate the sharp turns around the internal iliac artery; the hydrophilic 4F can then be advanced over the microcatheter and wire and into the desired carotid or vertebral artery. (p) Avoid using a standard 4F sheath in the umbilical artery, as this will not make the sharp turn into the aorta and may not be stable. (q) Whenever doing a catheter exchange in the umbilical artery, have an assistant stabilize the umbilical cord to avoid excessive blood loss and loss of access. (r) Any blood leakage around the catheter during the procedure can be managed by gently tightening the tourniquet at the base of the cord. (s) When the procedure is complete, either remove the catheter, and tie the cord with a silk suture for hemostasis, or exchange for a standard UAC catheter to maintain vascular access for the neonatologists. (t) For patients with an in-dwelling UAC, all the work of finding and

4.2 Vascular Access

catheterizing the umbilical artery is already done, but the trick is to carefully remove all the tape and sutures that are usually fixing the catheter firmly in place. Exchange the UAC over a 0.014-in. exchange wire for the coaxial microcatheter/ guide catheter assembly described above. Be careful not to traumatize the cord and not kink or damage the catheter in the process. 4. Radial artery access (a) Larger, older children may have large enough radial arteries for access. (b) Thirty-five diagnostic cerebral arteriograms and 24 interventional procedures were reported in children (mean age 14  years, mean body weight 57  kg, and radial artery diameter 2 mm) [13]. (i) Significant vasospasm encountered in 13% of radial access cases, and conversion to femoral access in 8.3%. (c) For larger children use a hydrophilic 4F Prelude Ideal™ (Merit Medical, South Jordan, UT) sheath preferably 23 cm long, and 4F catheters can then be used for angiography or microcatheter delivery. (d) Small children with smaller radial arteries are best treated by accessing the radial artery with a 4F micropuncture kit and attaching a rotating hemostatic valve to the outer 4F introducer and use the introducer as a sheath. Larger microcatheters can be advanced through the introducer and used for angiography and intervention such as intra-arterial chemotherapy [13]. 5. Direct carotid puncture [14, 15] (a) Infants with high-flow fistulas requiring treatment may have poor umbilical or femoral access, making direct carotid puncture a bailout option.

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(b) Some cases may also require carotid access as the primary option if tortuous carotids are expected to impede intracranial access [15]. (c) Technique: (i) Ultrasound-guided anterior wall puncture of the mid-­ common carotid with 21-g Angiocath of a micropuncture kit. (ii) Remove the inner needle and inject contrast to confirm good intravascular position and obtain a road map. (iii) Insert a steerable hydrophilic wire such as 0.018-in. Aristotle (Scientia, West Valley, UT) well up into the internal or external carotid, depending on the vascular target. Be careful that the Angiocath does not back out of the vessel as the wire is steered through the distal vessel. (iv) Insert a 4F micropuncture dilator up into a stable position in the carotid. • Alternatively, a low-profile 4F Prelude Ideal™ (Merit Medical, South Jordan, UT) sheath directly over the wire. This allows placement of a 4F guide catheter such as Fargo Mini (Balt, Montmorency, France) for additional support. (v) Remove the inner 3F dilator and attach an RHV to the hub of the dilator, which now functions as a sheath. (vi) Secure the sheath to the skin with a suture or sterile transparent film dressing (Tegaderm™, 3M, Maplewood, MN). (vii) Microcatheters can then be introduced through the sheath to perform the intervention. • Tip: If using a 4F Prelude Ideal™ (Merit Medical, South Jordan, UT) or other

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6.

4  General Considerations for Neurointerventional Procedures

standard sheath, it may be difficult to introduce a floppy microcatheter into the standard diaphragm valve. Options include a short peelaway sheath (if available) or a short 4F dilator to get it through the diaphragm. Some operators use a microwire inserted in the microcatheter backwards with the stiff end just enough to get the tip of the microcatheter through the diaphragm, but never, ever allow the stiff end of the wire to enter the vessel. (viii) Use low-dose heparin in the heparinized saline infusions and be careful to limit the volume of fluids and contrast. Infants can easily get overheparinized and fluid overloaded. (ix) On completion of the procedure, pull the sheath and apply gentle manual compression, checking with ultrasound to confirm distal patency. Usually 20  min of compression is sufficient. (x) Watch the child carefully in the ICU.  Periodic ultrasound and neck circumference measurements can check for occlusive or hemorrhagic complications. (xi) A small series using carotid access had no access site complications [15]. Transcardiac access (a) This is venous access via the femoral or umbilical vein and then passing a balloon catheter through the

foramen ovale to the left heart and into the aorta. The balloon catheter is exchanged for a 4F guide catheter. (b) A series of 15 neonatal fistulas treated by a senior neurointerventionalist used transcardiac access in three cases [14]. (c) Catheter manipulations in the heart can cause scary arrhythmias, which are best done with the assistance of an experienced pediatric cardiologist.

Fig. 4.3  Umbilical artery access. Drawing showing basic anatomy of the umbilical arteries (left) and an abdominal X-ray in a newborn (right) showing an umbilical catheter taking a sharp turn as it enters the iliac artery (arrow) before it ascends up the aorta

4.2 Vascular Access

Kids Korner! Guide Catheters for Pediatric Interventions

Guide catheters are designed by catheter manufacturers for adults, since that is where sales volumes are the greatest. These catheters are too large for small children and consequently, pediatric neurointerventionalists are often forced to improvise. An acceptable guide catheter for microcatheter placement in infants and small children is a 4F 65-cm straight or simple Berenstein or Kumpe curve (e.g., Soft-Vu®, AngioDynamics, Latham, NY, or Glidecath®, Somerset, NJ). These catheters can be inserted via femoral or umbilical access without a sheath, since using a sheath adds 2F (0.6 mm) to the size of the hole in these small, fragile vessels. For larger children, 5F catheters or the even low-­profile 80-cm guide sheath with a 6F outer diameter such as 4F Fubuki® (Asahi Intec, Santa Ana, CA) may be used, to allow for more support with larger devices, such as reperfusion catheters and stents.

Kids Korner! Growth of Cerebral Vessels in Children

Children are small people, but how small are their vessels? A recent study found diameters of the common carotid artery in young infants to be 5.6 mm, high cervical internal carotid artery 3.9 mm, carotid terminus 3.1 mm, and M1 2.6 mm [16]. These diameters increased an average of 0.069 mm per year up to age 5, then slowed to 0.005 mm per year after that. Compared to the arteries in 15–18-year olds, a 5-year old’s cerebral arteries are 94% of the diameter and a neonate’s is 59%. These findings indicate that devices should be smaller in children, especially in those younger than 5  years. These tender young arteries are also more sensitive with a high risk of vasospasm compared to adults.

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Tips for Difficult Access Cases 1. Femoral artery is not accessible. (a) Use an alternative route (see below). 2. Aortic arch or great vessels are tortuous. (a) Use the ECA to anchor the wire. (i) During the initial placement of the diagnostic catheter in the CCA, use a 0.035-in. hydrophilic wire to advance the diagnostic catheter into a branch of the ECA. (ii) Then remove the wire and replace it with a stiffer exchange-­length wire, such as a 0.038-in. hydrophilic wire or an Amplatz stiff wire. (iii) Then exchange the diagnostic catheter for the 90-cm sheath. (iv) This technique works well in the left CCA using a Simmons 2 catheter as the diagnostic catheter. 3. “Tower of power” technique to add stability to the 90-cm sheath: (a) Advance a 6F guide catheter, e.g., 6F Envoy (Cerenovus, Irvine, CA), inside a 6F 90-cm sheath. (b) Larger diameter 90-cm sheath (e.g., 7 or 8F) will add stability. (c) Use an intermediate catheter (e.g., DAC®, Stryker Neurovascular, Fremont, CA) inside a guide catheter inside a 90-cm sheath to create the ultimate “tower of power.” 4. Grappling hook technique: (a) A very distal guide catheter position may be achieved even in tortuous vessels with this technique [17]. (b) Use a 6F 90-cm guiding sheath (e.g., Neuron™ Max, Penumbra, Alameda, CA). (c) Coaxially advance a flexible guide catheter (e.g., Navien™, Medtronic, Minneapolis, MN, or Neuron™, Penumbra, Alameda, CA) over a very soft, compliant balloon catheter (e.g., Scepter® XC, Microvention, Aliso Viejo, CA, or TransForm™, Stryker, Fremont, CA), all over a 0.014-in. wire. (d) Inflate the balloon in a straight segment of the carotid and provide gentle traction on

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4  General Considerations for Neurointerventional Procedures

the balloon as the guide catheter is advanced. 5. Buddy wire technique: (a) Use a larger diameter 90-cm 7- or 8F sheath and a 0.014- or 0.018-in. wire anchored into the subclavian artery or a branch of the ECA.

High Body Mass Index

Tips and tricks for neurointerventional procedures in the obese patient. In many regions, particularly the southern United States, obesity is a problem of epidemic proportions. These patients pose a number of challenges for health care providers in general and specifically for neurointerventionalists. A large body habitus may make it difficult to access vessels percutaneously and the following tips may be useful to keep in mind; 1. The femoral artery may be unexpectedly medial in location. 2. The abdominal pannus can be taped up to allow access to the groin. 3. Ultrasound guidance for puncturing the femoral artery is very helpful. 4. Be aware of hematoma formation at the femoral puncture site may not be noticeable until the patient becomes hypotensive. (Large hematomas can hide in large thighs). 5. Strongly consider radial arterial access in morbidly obese patients. 6. Be sure that the angiographic table will hold the weight of the patient.

Alternative Access Routes If the femoral artery cannot be accessed (e.g., because of high-grade iliac or femoral artery stenosis or occlusion, innominate or subclavian artery tortuosity, patients unable to tolerate lying flat, morbid obesity, or aortic disease), several other options exist. The radial approach is nicely suited for access to the ipsilateral vertebral artery. For access to the great vessels from the arm, use

a 5F Simmons 2 catheter to access the target artery (Fig. 2.7) and then exchange a guide catheter into position over an exchange-­length 0.035or 0.038-in. hydrophilic wire. See Chap. 2 for further details about radial artery access. 1. Radial artery [18] (see Chap. 2) (a) Advantages: (i) Easier to get hemostasis after the sheath is removed, compared to the femoral artery approach. (ii) Less potential for nerve injury than brachial or axillary approaches. (b) Disadvantages: (i) Smaller vessel. Usually limited to a 6F sheath [19]. (ii) Requires different techniques than femoral access (see Chap. 2). (iii) Has the potential for hand ischemia. (iv) Radial artery cocktail is usually necessary. 2. Carotid artery (a) Cut-down and direct puncture of the common carotid artery [20]. (b) Direct percutaneous puncture can be done for embolization procedures with few complications [21]. (c) Stent-assisted coiling by direct carotid puncture and closure with the AngioSeal™ closure device (St. Jude Medical, Minnetonka, MN) has been reported (Blanc 2002, 16).

4.3 Antithrombotic Therapy for Neurointerventional Procedures The overall risk of thromboembolic complications during neurointerventional procedures is significant. Aneurysm coiling carries a 2–8% risk of symptomatic thromboembolic complications [22, 23]. Strategies for antithrombotic medication management vary widely. Anticoagulation with heparin is standard for most procedures. Dual antiplatelet therapy is standard for all stenting procedures. Some operators also advocate routine antiplatelet therapy (e.g., aspirin) for many neurointerventional procedures.

4.3 Antithrombotic Therapy for Neurointerventional Procedures

Anticoagulation 1. Heparin for flushes and irrigation. (a) Use heparinized saline—10,000  units of heparin per liter of saline (except in pediatric patients 33 different alleles of the CYP2C19 gene have been identified. Each allele is defined by variations in the DNA sequence, which may result in functional differences in the CYP2C19 enzyme [57]. The CYP2C19*1 allele is common in people of European origin and the CYP2C19*2 allele is present in 30%, 15%, and 17% of Asian, Caucasian, and black patients, respectively [58]. Carriers of CYP2C19*2 have reduced effectiveness of clopidogrel [59, 60] and have an elevated risk of cardiovascular events and coronary stent thrombosis [61]. Because of these findings the FDA issued a safety warning in May 2009 that clopidogrel has reduced effectiveness in patients who are poor metabolizers of the drug [58, 62]. Aside from genetic tendencies, other causes of poor responsiveness to clopidogrel include noncompliance, drug interactions [63], inadequate absorption [64], body mass

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index [65, 66], and increased platelet activity related to an acute thrombotic event [67]. Platelet activation is a significant threat in neurointervention, contributing to overall rates of acute thromboembolic events up to 8% [23]. Several techniques are available for the socalled point-of-care detection of poor responsiveness to antiplatelet therapy [68]. Among the most commonly used are the VerifyNow™ Rapid Platelet Function Assay (Accumetrics, San Diego, CA), Innovance® Platelet Function Analyzer (Siemens Healthcare Diagnostics, Inc., Deerfield, IL), and the Multiplate® Multiple electrode aggregometry device (Dynabyte Medical, Munich) [68]. Point-of-care testing is meant to identify patients who are at higher risk of thromboembolic complications during percutaneous interventional procedures. Point-of-care testing has become de rigueur in some cardiac catheterization laboratories and neuroangio suites, but the vast majority of published experience with point-of-care testing has been from cardiology [69]. Several studies of point-of-care platelet function testing in neurointerventional procedures have been published. In a study of 414 Pipeline procedures, clopidogrel nonresponders had a significantly higher rate of thromboembolic complications compared to clopidogrel responders [70]. In a series of 50 patients undergoing cerebrovascular stenting procedures, 28% were classified as clopidogrel nonresponders, and there was a significant correlation between clopidogrel nonresponse (as assessed by the Multiplate® device) and procedural adverse events [71]. In another study of 76 patients undergoing cerebrovascular stenting procedures, clopidogrel resistance (as assessed by the VerifyNow™ assay) was reported in 51.9% [72]. A study of 186 aneurysm coiling patients found that diminished clopidogrel responsiveness (by VerifyNow™) correlated with thromboembolic events [73]. Another study of 216 neurointerventional patients found that inadequate platelet inhibition (by VerifyNow™) was found in 13% of patients on aspirin and 66% of patients on clopidogrel [74]. Yet another study of 106 neurointerventional patients found that 42.9% were poor responders to clopidogrel (by

VerifyNow™), and that all cases of intraprocedural thrombosis occurred in the poor-response group [65]. VerifyNow™ interpretation: A systematic review including data on 1464 Pipeline cases found that PRU values greater than 200–240 had absolute 15% greater risk of thrombotic events and PRU values less than 60–70 had absolute 12% greater risk of hemorrhagic events [75].

 hould Routine Platelet Function S Testing Be Done Prior to Neurointerventional Procedures? Point-of-care platelet function testing is controversial. In the medical management of ischemic stroke, recent editorials have argued for and against platelet function testing [76–78]. A number of publications have concluded that routine platelet function testing is not justified [57, 68]. No standards, guidelines, or randomized trial data exist for the use of platelet function testing for neurointerventional procedures, yet some operators use it routinely while others do not. This practice remains an option until more definitive data on the question are available. 1. Arguments in favor of routine point-of-care platelet function testing: (a) A significant percentage of patients (28– 66%) are poor responders to clopidogrel [71, 74]. (b) Acute thrombosis due to platelet activation is a significant source of morbidity. (c) Point-of-care testing is relatively easy and feasible. (d) Identification of poor responders serves to heighten awareness of the possibility of acute thrombosis during neurointerventional procedures. (e) A contingency plan may be activated for these patients; e.g., an additional antiplatelet drug, such as abciximab, can be made available for quick use should a thromboembolic complication occur. (f) Alternative treatment strategies can be formulated for poor responders (e.g., if

4.4 Intervention Phase





2.











stent-assisted coiling was planned, then a balloon remodeling procedure might be done instead, or a patient might have a carotid endarterectomy instead of a stent). (g) Poor responders may be pre-treated with dual antiplatelet therapy for a prolonged period, if feasible. (h) Poor responders can be treated with alternative drugs such as ticagrelor. (i) Longer periods of treatment with antiplatelet agents (e.g., >7 days) are associated with heightened antiplatelet activity [74, 79]. Arguments against routine point-of-care platelet function testing: (a) Point-of-care testing is not universally available. (b) There is no consensus on the definition of “poor responsiveness” to antiplatelet medication [68]. (c) Optimal management based on point-ofcare testing has not been defined. Does one increase the clopidogrel dose, switch to ticagrelor or prasugrel, or consult a witch doctor? (d) There is no evidence that management based on point-of-care testing improves outcome. (e) Point-of-care testing techniques vary widely. (f ) The results of studies using the VerifyNow device, for instance, cannot be extrapolated to centers where other platelet function tests are used. (g) Other medications with better effectiveness than clopidogrel (such as ticagrelor) may gain better evidence of safety and efficacy in neurointervention. (h) A multistudy review showed no significant effect on outcomes after Pipeline™ embolization based on platelet function testing [80].

 lopidogrel and Proton Pump C Inhibitors Current American Heart Association guidelines recommend that in order to minimize gastrointes-

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tinal complications, all patients on dual antiplatelet therapy be prescribed a proton pump inhibitor (PPI) [81]. PPIs suppress CYP2C19 activity, and omeprazole (Prilosec®, AstraZeneca, Wilmington, DE) has shown more of this effect than newer PPIs such as pantoprazole (Protonix®, Pfizer, New York, NY) [82]. For patients taking omeprazole and clopidogrel, there is a significant increase in residual platelet activity compared to patients taking clopidogrel alone [83]. In 2009, the FDA issued an announcement recommending against the concomitant use of clopidogrel and omeprazole. However, studies of interactions between other PPIs and clopidogrel have been inconsistent. Although a number of retrospective studies have linked concomitant use of PPIs and clopidogrel with an increased risk of cardiovascular adverse events and death [84, 85], other studies have found no evidence of increased risk [85, 86]. A recent case–control study of clopidogrel in 2765 stroke patients found no association between proton pump inhibitors and an increased risk of recurrent stroke [87]. Furthermore, alternatives to PPIs, such as H2 blockers, have not been found to be as beneficial as PPIs in reducing GI bleeding risk when used in combination with aspirin or clopidogrel [88]. Therefore, considering the conflicting evidence, it seems reasonable to use PPIs in patients who are on a dual antiplatelet regimen [57].

4.4 Intervention Phase The intervention usually consists of microcatheter access to the lesion followed by treatment that is specific to the lesion. This section covers general microcatheter selection and techniques.

Devices 1. Microcatheter selection (a) Microcatheters vary in size and design. (b) All modern microcatheters have a hydrophilic coating to reduce thrombogenicity [89]. (c) Microcatheters are either fiber-braided or metal coil-braided, which serves to pre-

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serve the inner lumen when the catheter is curved and enhances pushability. (d) Smaller microcatheters permit better guide catheter angiograms, particularly when smaller guide catheters (e.g., 5F) are employed. (e) Some situations call for larger and/or stiffer microcatheters to deliver larger devices. (i) When the catheter access to the lesion is tenuous because of vascular anatomy, increased microcatheter stiffness will add stability. (f  ) Single-tip versus two-tipped microcatheters. Two-tipped microcatheters, rather than single-tipped catheters, are required for aneurysm coiling. The two tips in microcatheters used in aneurysm coiling are always 3  cm apart—this feature can be used for calibration and measurements. (g) Common microcatheters for most cases: (i) Excelsior® SL-10 (Stryker, Fremont, CA) • OD 2.4F proximal, 1.7F distal, ID 0.0165 in. • Can be used for 10-system and 14-system coils. • Retains its shape better after steam-shaping than other microcatheters of the same size [90]. • Polished tip less likely to hang up on side branches or if advancing through a stent compared with other microcatheters. (ii) Excelsior® XT-17™ (Stryker Neurovascular, Fremont, CA) • OD 2.4F proximal, 1.7F distal, ID 0.017 in. • Comparable to SL-10 but more support for greater stability. (iii) Echelon™ 10 (Medtronic Neurovascular, Minneapolis, MN) • OD 2.1F proximal, 1.7F distal, ID 0.017 in. • The small proximal outer diameter of 2.1F (versus 2.4F for the Excelsior® SL-10), permits bet-

ter guide catheter angiograms when a 5F guide catheter is used. • Compatible with Onyx®. • Nitinol wire braiding produces a stable platform in spite of its small diameter. (iv) Marathon™ (Medtronic Neurovascular, Minneapolis, MN) • OD 3.0F proximal, 1.5F distal, ID 0.013 in. • “Flow directed,” small-caliber, flexible microcatheter. • Designed for Onyx® embolization. (v) Magic® microcatheter (Balt, Montmorency, France) • Magic® 1.8: OD 2.7F proximal, 1.8F distal, ID 0.012 in. • Magic® 1.5: OD 2.7F proximal, 1.5F distal, ID 0.010 in. • Magic® 1.2: OD 2.7F proximal, 1.2F distal, ID 0.008 in. • By far, the most flow-directed microcatheter of them all. • The catheter is only compatible with n-butyl cyanoacrylate (nBCA). • Both Magic® 1.8, and also 1.5, available in 155- and 165-­ cm lengths. Magic® 1.2 available in 165-cm length only, but choice of 3- or 12-cm length of distal floppy segment. (vi) Marksman™ (Medtronic Neurovascular, Minneapolis, MN) • OD 3.2F proximal, 2.8F distal, ID 0.027 in. • Robust microcatheter, resistant to ovalization. • Useful for Neuroform® EZ (Stryker Neurovascular, Fremont, CA) stent and Pipeline™ flow diverter (Medtronic, Minneapolis, MN) deployment. • Comes in 105-, 135-, 150-, and 160-cm lengths.

4.4 Intervention Phase

(vii) Phenom™ 027 (Medtronic Neurovascular, Minneapolis, MN) • OD 3F proximal, 2.7F distal, ID 0.027 in. • Microcatheter with beveled and polished distal opening for more optimized delivery of Pipeline™ Flex. • Comes in a 15-cm or more flexible 30-cm distal segment. (viii) Plato® 17 (Scientia Vascular, West Valley, UT) • OD 2.0F proximal, 1.7F distal, ID 0.017 in. • Versatile microcatheter, can accommodate coils or liquid embolics. • Vert maneuverable yet kink resistant. Maintains a stable inner diameter, minimizes friction for advancing coils or wires. (ix) Prowler® Select™ Plus (Cerenovus, Irvine, CA) • OD 2.8F proximal, 2.3F distal, ID 0.021 in. • Large microcatheter, intended for use with the Enterprise™ Vascular Reconstruction System (Codman, Raynham, MA). • Available in 150- or 170-cm lengths. (h) Steerable microcatheters (i) The Plato™ microcatheter (Scientia Vascular, West Valley, UT) is steerable and FDA and CE mark approved for intracranial access. (ii) Bendit21® and Bendit27® catheters (Bendit, Petah Tikva, Israel) have a deflectable tip for steering and FDA approved. (iii) SwiftNINJA® (Sumitomo Bakelite, Tokyo, Japan) has a deflectable tip and is available in Japan. (iv) Stiffer steerable microcatheters such as Direxion™ and Direxion™ Hi-Flo (Boston Scientific, Marlborough, MA)

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are not FDA approved for neurovascular procedures. (i) Microcatheter shape: Pre-shaped versus straight versus steam-shaped (i) A shaped microcatheter can be advantageous in accessing aneurysms that arise from the parent vessel at an acute angle, and in stabilizing the microcatheter during coiling. (ii) Pre-shaped microcatheters retain their shape better than steam-shaped microcatheters [91]. Steam-shaping can obtain catheter shapes that are not available in pre-shaped devices. (iii) Steam-shaping technique: • Shape the wire mandrel into the desired shape, with an exaggerated degree of curvature (as the microcatheter will recoil to some degree after steam-shaping). • Hold over steam for 10 s. • Cool in sterile water and remove mandrel. (iv) Fiber-braided (e.g., Excelsior®) microcatheters are more likely to retain their shape after steam-­ shaping, than metal coil-braided (e.g., Prowler and Echelon™) microcatheters [91]. ( j) Detachable-tip microcatheters (i) Designed to prevent catheter entrapment when injecting liquid embolic agents. (ii) Apollo™ Onyx™ delivery catheter (Medtronic, Minneapolis, MN) has a 0.013-in. inner lumen and 165cm length, with the available 1.5- or 3-cm detachable tip. (iii) Sonic microcatheter (Balt, Montmorency, France) has 1.2F catheters with 15- or 25-cm detachable segments and 1.5F catheters with 25-cm detachable segments. This Sonic catheter is CE mark approved but not available in the United States.

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4  General Considerations for Neurointerventional Procedures

2. Microwires (a) A variety of microwires are available, with differing properties such as size, softness, visibility on fluoroscopy, shapeability, and steerability, trackability, and torque control. (b) Preferred microwires for most cases: (i) Aristotle®-14 0.014  in. (Scientia Vascular, West Valley City, UT) • Very soft, flexible distal tip, good for navigation into small aneurysms or through difficult anatomy. • Available Standard and Soft distal segments. • Precise torque control. • Available in 0.018- and 0.024-in. sizes for larger microcatheters. (ii) Synchro®-14 0.014  in. (Stryker Neurovascular, Fremont, CA) • Very soft, flexible distal tip, good for navigation into small aneurysms or through difficult anatomy. • Good torque control. (iii) Transend™ EX 0.014  in. (Stryker Neurovascular, Fremont, CA) • Smooth, nonabrasive tip, similar to the Synchro®. • Available in Standard, Soft-tip, Floppy, or more Platinum versions. • Superior torque control compared to many other microwires. (iv) Glidewire® GT and Glidewire® Gold 0.018  in. (Terumo Medical Corporation, Somerset, NJ) • Provides support for larger microcatheters. • GT version tapers distally to minimize vessel trauma. • GT available in 90° or double angle tips, which can be helpful to negotiate difficult anatomy. • Very lubricious. 3. Exchange length microwires (a) A variety of microwires are available in 300-cm lengths. This allows for place-

ment of a small microcatheter to a desired location and exchange for a larger or stiffer working catheter or balloon catheter. (b) Preferred microwires for most cases: (i) Aristotle®-14 0.014  in. (Scientia Vascular, West Valley City, UT) • Very soft, flexible distal tip, good for navigation into small aneurysms or through difficult anatomy. • Available Standard and Soft distal segments. • Precise torque control. • Also available in 0.018- and 0.024-in. sizes. (ii) Synchro®-14 0.014  in. 300  cm (Stryker Neurovascular, Fremont, CA) • Very soft, flexible distal tip, good for navigation through difficult anatomy. • “Supreme torque control.” • Comes in Soft, Standard, or Extra Support versions for delivery of stiffer catheters or devices. (iii) Synchro®-10 0.010  in. 300  cm (Stryker Neurovascular, Fremont, CA) • More torque control than other 0.010-in. wires. (iv) Transend™ EX 0.014-in. Floppy tip 300 cm (Stryker Neurovascular, Fremont, CA) • Soft tip is atraumatic. • Heightened radio-opacity makes the tip easy to see on fluoroscopy. • Smooth coating on wire facilitates smooth catheter exchanges. • Comes in Floppy or Extra Support versions for delivery of stiffer catheters or devices. (v) Neuroscout™ 14 XL 300-cm Guidewire (Cerenovus, Irvine, CA) • Comes in Soft or Standard versions.

4.4 Intervention Phase

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Guidewire Extension

Ever wish that guidewire was just a little bit longer? This may happen when using 0.014-in. wires or other devices (e.g., filter wires and stentrievers) and a catheter exchange needs to be done with any catheter or balloon not designed to be rapid exchange. Wires on devices such as the Trevo®-ProVue (Stryker Neurovascular, Fremont, CA) or GuardWire® Temporary Occlusion and Aspiration System (Medtronic, Minneapolis, MN) have a thinner, slightly undulating proximal end, which fits nicely with the DOC® Guidewire Extension (Abbott, Abbott Park, IL) to extend the wire to 300  cm. The Asahi Guidewire extension (Asahi Medical, Northbrook, IL) and Runthrough® NS Extension Wire (Terumo Medical, Sommerset, NJ) are also guidewire extenders compatible with 0.014-in. wires. Always ensure the extender is properly attached to the wire according to manufacturer’s package insert, to avoid disconnection of the extender during catheter exchange.

Microcatheter Technique

Fig. 4.4  Proper microwire technique. Grasp the microwire with your palm facing up (top). This permits fine finger control of the microwire; with the palm facing down (below), operating the microwire becomes more of a wrist action than a fine motion

1. Do angiograms when the guide catheter is in optimal position and working views are selected. 2. The guide catheter must be visible on at least one view for the duration of the case. 3. Find optimal working views for both PA and lateral detectors. Sometimes the orthogonal views can provide critical complementary information. Even if an ideal working view is present on the PA view, do not let the lateral view “go to waste.” 4. Using a road map, advance the microcatheter over the microwire into position. Grasp the microwire with the palm facing up (Fig. 4.4). Fix the wire when it is at the vessel of interest while advancing the microcatheter. If the

microcatheter does not advance effortlessly, gently rotate the wire to reduce the friction. 5. Always keep the tip of the guide catheter in view since the microcatheter can push the guide catheter back if there is friction around multiple curves. 6. Any redundancy (i.e., slack) in the microcatheter should be removed by gently pulling back on the microcatheter to straighten it out. 7. Once the microcatheter tip is positioned at the target, the microwire should be withdrawn and advanced several times for most of the distance between the guide catheter and tip of the microcatheter. This maneuver helps to straighten out any remaining redundancy in the microcatheter, eliminating potential

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4  General Considerations for Neurointerventional Procedures

energy in the microcatheter that may cause it to leap forward unexpectedly. 8. When guide catheter angiograms are done, the RHV should be tightened around the microcatheter, securing it to prevent the microcatheter from being carried forward by the contrast as it is injected. 9. A 3-mL syringe should be used for guide catheter angiograms when a microcatheter is within the 6F 0.053-in. Neuron™. A 3-mL syringe will provide a higher injection pressure than a 10-mL syringe.

Tips for Handling Difficult Curves 1. Large catheters (such as the Penumbra reperfusion catheters or DACs) often get hung up in the carotid siphon, particularly at the origin of the ophthalmic artery. Options: (a) Use microcatheters with a wider segment designed to reduce offset between the microcatheter and reperfusion catheter/ DAC.  These include the Wedge™ (Microvention-Terumo, Tustin, CA) and AXS Offset™ (Stryker, Fremont, CA). (b) Use a larger wire such as Aristotle®-24 0.024 in. (Scientia Vascular, West Valley City, UT) in the large catheter. (c) Navigate a compliant balloon catheter (such as a Hyperglide™ [Medtronic, Minneapolis, MN] or Scepter XC® [Microvention, Aliso Viejo, CA]) into the siphon and inflate with the balloon positioned halfway out of the large catheter; the inflated balloon will take the edge off the large catheter and allow it to glide through the siphon [92]. 2. Try shaping the microcatheter to match curve of the artery. 3. Anterior cerebral catheterization: (a) Wire access can be difficult because of the sharp reverse curve origin of the A1 segment. (b) Using the “advancing loop technique” [93] a microwire with a C-shaped curve is manipulated through the carotid siphon to obtain a U-shaped loop. Advance the loop

into the MCA until the wire tip has passed distal to the A1 origin. Then slowly withdraw the wire, turning the loops that the wire tip is pointing cephalad. The wire loop is pulled back just like a Simmons 2 catheter and if the tip is positioned in the right direction, it will advance into the A1 segment. (c) It may take several tries, but usually this technique works. (d) When sufficient wire has advanced into the A1 to undo the loop, a combination of microcatheter advancement and wire manipulation more distally in the A2 segment of the ACA will get the microcatheter into the ACA. 4. Middle cerebral branch catheterization: (a) Stent-assisted coiling of middle cerebral aneurysms may require a branch arising from the aneurysm neck be catheterized and stented to prevent inadvertent occlusion of the branch during coiling. (b) Especially when a middle cerebral branch comes off at a sharp angle, it may be difficult to catheterize with standard techniques. (c) “Microcatheter looping technique” [94] is a variation on the advancing loop technique, in which a microcatheter (e.g., J-tip Excelsior® SL-10, Stryker, Fremont, CA) is looped in the carotid and advanced just distal to the branch that one wishes to catheterize. (d) With the tip of the looped catheter pointing toward the acutely angled branch, carefully advance a 0.014-in. Aristotle® wire (Scientia, West Valley, UT) as far as possible in the branch. (e) Pull back on the microcatheter to straighten the loop and then advance the microcatheter over the wire into the branch. A stent (LVIS™ Jr., Microvention, Aliso Viejo, CA) may then be deployed. (f ) If necessary, the microcatheter may be exchanged over a 300-­ cm exchange microwire for a larger microcatheter or balloon.

4.4 Intervention Phase

Flow-Directed Microcatheter Technique 1. Flow-directed microcatheters are often used for liquid embolic delivery. The high flow state in AVMs and dAVFs greatly makes for rapid and accurate placement of the microcatheter to the desired position. A DMSOcompatible microcatheter must be used with Onyx® (ev3, Irvine, CA). 2. Most flow-directed microcatheters are packaged with a long mandrel that can be used to stiffen the catheter and allow insertion through the RHV into the guide catheter. Never advance the mandrel beyond the tip of the microcatheter or use it like a guidewire in the vascular system. The mandrel is not soft enough for intravascular use. 3. Flush the plastic hoop in which the microcatheter is packaged to hydrate the hydrophilic coating. 4. Remove the catheter from the hoop and immerse the catheter in a large bowl of sterile, heparinized saline. 5. If packaged with a mandrel, remove the mandrel from the microcatheter. Having the microcatheter immersed in saline prevents aspirating air into the catheter as the mandrel is withdrawn. 6. Attach an RHV and flush the system to purge all air. 7. Insert a microwire (0.012 in. or smaller) through the RHV and into the microcatheter to the distal tip. The authors use the 0.007-in. Hybrid™ (Balt, Montmorency, France) or 0.010-in. Synchro®-10 (Stryker Neurovascular, Fremont, CA). 8. Insert the microcatheter into the RHV of the guide catheter and advance it to the distal tip of the guide catheter. Both the Marathon™ and Apollo™ (Medtronic, Irvine, CA) have a marker on the shaft of the catheter that indicates that the tip is approaching the end of a 90-cm guide catheter, to limit fluoroscopy time. 9. Under road map guidance, advance the flowdirected microcatheter into the vascular sys-

201

tem. Note that the tips of most flow-directed microcatheters are quite small and tend to move very quickly, so good fluoroscopic imaging equipment and a watchful eye are needed to keep the tip in view. 10. Let the blood flow carry the tip forward, and advance the catheter forward at a rate fast enough to keep the catheter moving, but not so fast that redundant loops form in the proximal vessel. It is helpful to have one plane of a biplane road map system include the tip of the guide catheter to ensure that the microcatheter does not loop in the neck or displace the guide catheter. 11. Keep the microwire within the microcatheter most of the time and do not advance it beyond the tip. Arteries can be damaged or perforated with a microwire more easily than with a soft catheter. 12. A curved microwire can be rotated within the microcatheter to direct the tip of the catheter. 13. If the tip of the microcatheter does not advance as the microcatheter shaft is advanced at the groin, often pulling the microwire back gently will cause the tip to advance. 14. Only in rare situations when a very sharp angle must be negotiated, the microwire may need to be cautiously advanced beyond the tip of a flow-directed microcatheter and torqued into a sharp curve or sharply angulated side branch. 15. Note: There can be considerable friction between the soft microcatheter and the microwire, especially with Magic® microcatheters (Balt, Montmorency, France). This can cause the microwire to jump forward if advanced too vigorously or cause the catheter to “accordion” and crumple on itself as the wire is pulled back. These problems can be minimized by gently rotating the wire or moving it in and out slightly to break the friction. (a) Microwires cannot be usually advanced beyond the tip of the Magic® 1.2 microcatheter (Balt, Montmorency, France): the distal lumen is only 0.008 in.

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4  General Considerations for Neurointerventional Procedures

16. Another technique that can be used to facilitate catheter advancement is to remove the microwire and gently puff saline or contrast through the microcatheter. This will cause the tip of the microcatheter to move proximally a millimeter or two and allow flow to carry the tip in a different direction. 17. Steam-shaping a 45° curve on the microcatheter can also help keep the tip of the microcatheter in the center of the vessel when making a turn. 18. Another solution to the problem of insufficient flow-direction is to switch to a different microcatheter. The Ultraflow™ (Medtronic, Minneapolis, MN) is more flow directed than the Marathon™ (Medtronic, Minneapolis, MN). The Magic® Standard microcatheter (Balt, Montmorency, France) is far more flow directed than other catheters. The very floppy Magic® 1.2 microcatheter is extremely flow directed. 19. If one cannot negotiate a sharp turn into a branch from a larger vessel, position a balloon catheter such as the Hyperglide™ (Medtronic, Minneapolis, MN) in the main vessel beyond the branch. Use the balloon to temporarily occlude flow distal to the side branch. This will allow flow to carry the microcatheter into the branch. This technique adds to the complexity of the case and the presence of another intravascular catheter can add friction and impair the flow-­ directional capabilities of the microcatheter. Therefore, this method is not recommended except in very unusual circumstances where no other options are available. 20. Gently pull back on the microcatheter periodically to remove redundancy. 21. Inject a small amount of contrast through the microcatheter to confirm catheter positioning, and also to confirm patency of the microcatheter. When all slack is removed, perform a high-resolution superselective arteriogram. 22. Do a microcatheter angiogram to determine: (a) The desired position has been reached. (b) No normal brain vessels filling.



(c) The flow rate, in order to choose an embolic agent and the injection rate needed. (d) No sign of contrast exiting the microcatheter proximal to the distal tip. Danger! Leaking contrast indicates that the microcatheter has been irreparably damaged or even ruptured and must not be used for embolization! 23. Once the microcatheter is in position, provocative testing may be performed if necessary or the embolization phase may begin.

Steerable Microcatheter Technique 1. The Plato™ 14 microcatheter (Scientia Vascular, West Valley City, UT) is currently available. Steerable microcatheters require gentle rotations along with forward or backward movement. The following is a general technique for steerable microcatheters: 2. Use a preshaped catheter or steam-shape a curve on the microcatheter. 3. Preload and shape an appropriate microwire into the microcatheter, such as Aristotle®-14 0.014  in. (Scientia Vascular, West Valley City, UT). 4. Use a guide catheter that is placed as high as safely possible in the cervical carotid or vertebral artery. 5. Use the peel-away introducer to insert the microcatheter into the guide catheter. 6. Carefully advance the microcatheter under road map guidance over the guidewire. When encountering a sharp turn in the vessel, rotate the catheter during advancement, to make the turn. 7. Keep the tip of the guide catheter on the road map working view, and remember that the steerable microcatheter will try to push the guiding catheter back, as it is advanced. 8. When rotating the microcatheter, hold the flange at the microcatheter hub. Ensure that any slack in the microcatheter or guiding catheter is removed and that the RHV on the guide catheter is not too tight.

4.4 Intervention Phase

9. If the microcatheter tip is not moving forward as it is advanced at the groin, rotate it slightly, and it may move forward again. 10. Beware that the microcatheter can jump forward abruptly as it is being rotated, especially if pushing it forward results in little response at the tip. All that pushing has stored energy into the system and it releases quickly when the catheter is rotated. 11. If the microcatheter does not advance and the guide catheter pushes back, pull back to release tension, and try again, using various combinations of forward pushing and rotating of the microcatheter, as well as gentle rotation of the guidewire. 12. The stiffness of the microcatheter can straighten small, sharply curved vessels, so it may be advisable to use a smaller catheter system for very distal catheterization of small vessels. 13. Similar technique is used for tip deflectable catheters such as Bendit® (Bendit, Petah Tikva, Israel) except that these catheters allow adjustment of the tip angle in addition to the ability to torque the microcatheter. This can help negotiate complex curves quickly and efficiently [95].

Specific Interventional Techniques 1. Aneurysm treatment: Chap. 5. (a) Includes coiling, stent-assisted coiling, balloon-remodeling, and flow diversion. 2. Intracranial embolization: Chap. 6. (a) Includes liquid embolic and coil embolization of tumors and vascular malformations. 3. Extracranial embolization: Chap. 7. (a) Includes transarterial embolization of head and neck lesions and spinal lesions, and percutaneous injection procedures. 4. Thrombectomy and thrombolysis for acute ischemic stroke: Chap. 8. 5. Extracranial angioplasty and stenting: Chap. 9. 6. Intracranial angioplasty and stenting: Chap. 10.

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(a) Includes treatment of atherosclerotic stenosis and cerebral vasospasm. 7. Venous procedures including transvenous embolization: Chap. 11.

Intermediate Catheter Technique The introduction of the distal access catheter (DAC) (CAT® 5 or CAT® 6, Stryker Neurovascular, Fremont, CA), which is intermediate in size between a guide catheter and a microcatheter, inspired the development of the so-called “intermediate” (or triaxial) catheter technique. The DAC was originally developed for buttressing access for thrombectomy with the old MERCI devices (Stryker Neurovascular, Fremont, CA), but it quickly became clear that the DAC can provide stable access to the intracranial target by functioning as a bridge and support between the guide catheter and the microcatheter (Fig. 4.5). By softening the curves of the microcatheter within it, the DAC reduces the ovalization forces in the microcatheter that add friction and resistance to the microcatheter and microwire. The DAC is also advantageous because it has a ­relatively large lumen, but it is as navigable as many microcatheters. The intermediate catheter technique is very helpful in a number of settings, including aneurysm and AVM embolization and treatment of acute ischemic stroke and intracranial stenosis. Catheters that can be used as the intermediate catheter besides CAT® 5 and CAT® 6 include the Penumbra Distal Delivery Catheters (Penumbra, Alameda, CA), the Navien™ (Medtronic, Minneapolis, MN), and the Sophia® (Medtronic, Aliso Viejo, CA). Technique: 1. Case selection (a) Intermediate catheter technique is helpful in certain situations: (i) Tortuous and redundant proximal anatomy. (ii) Tortuous intracranial anatomy. (iii) Need for remote intracranial access (e.g., a distal MCA AVM pedicle).

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4  General Considerations for Neurointerventional Procedures

a

b

Fig. 4.5  Intermediate catheter technique. Microcatheter positioning in an ophthalmic segment ICA aneurysm without (a) and with (b) a distal access catheter (DAC). Without a DAC, some redundancy is present in the microcatheter throughout the carotid siphon, which diminishes microcatheter stability, ovalizes the microcatheter in the

sharp turns, and lengthens the amount of microcatheter subject to movement during the coiling. With the microcatheter positioned within the DAC, the curviness of the microcatheter is reduced and the unconstrained length of microcatheter is minimized, improving stability and control





(iv) Need for a large microcatheter (e.g., when a larger microcatheter cannot be guided through the carotid siphon, placing it within a DAC might help). (v) Acute ischemic stroke cases in which the operating microcatheter must be advanced and withdrawn repeatedly, such as in stentriever cases. (vi) Intracranial venous sinus thrombosis aspiration. 2. DAC selection (a) Be careful to choose a DAC™ that will be small enough to fit inside the guide catheter and large enough to accommodate the microcatheter. Generally, a larger guide catheter is necessary. DACs come in four different sizes and two to three lengths for each size. The Excelsior® SL-10 is small enough to fit inside all of the DACs.

(b) DAC compatibilities: (i) AXS Vecta® 71 (5.4F ID, 6.45F OD) • 115-, 125-, and 132-cm lengths available • This DAC has a large lumen for multiple microcatheters (ii) CAT® 5058 (4.3F ID, 5.6F OD) • 115-cm length (iii) CAT® 6060 (4.5.F ID, 6.0F OD) • 132-cm length (c) Choose the length of the DAC very carefully and use the shortest length necessary. It must be long enough to extend out of the guide catheter and reach distal enough to provide support for the catheter. However, it must not be so long that there is not enough length of the microcatheter to extend the desired length beyond the tip of the DAC.

4.4 Intervention Phase

3. Triaxial technique (a) Prepare three heparinized flushes with RHVs. (b) Position the guide catheter. (i) Advance the microwire, microcatheter, and DAC within the guide catheter as a single unit. Maintain the microcatheter and DAC on continuous heparin saline flush throughout the procedure. 4. Intermediate catheter tips (a) Be sure the microcatheter is long enough and/or the DAC short enough to extend out of the DAC by a meaningful distance. (b) Use a 3- or 5-mL syringe for guide catheter angiograms. (c) Attempt to make a road map with the guide catheter before the DAC is introduced that will be useable throughout the procedure. Alternatively, remove the microcatheter and do the road map injecting through the DAC. Because of crowding within the guide catheter, later guide catheter angiograms are of limited quality. 5. At-a-glance triaxial combinations: The most challenging part of using the intermediate catheter technique can be simply figuring out which catheters will fit within which other catheters. Here are some triaxial combinations that work: (a) 6F Cook Shuttle/Penumbra 054/ Penumbra 032 (b) Neuron 088 MAXX/Penumbra 054/ Penumbra 032 (c) Neuron 088 MAXX/Penumbra 041/ SL-10 (d) Neuron 070/DAC 044/any microcatheter (i) May barely fit in a 070 Neuron™

Imaging Techniques for Neurointervention Flat panel angiography technology allows for rapid three-dimensional (3-D) rotational angiog-

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raphy and road mapping, and rotational flat panel computed tomography. 1. 3-D angiography (a) Rotational flat panel three-dimensional angiography creates a 3-D image on a workstation that can be rotated, edited, and measured. Particularly helpful for finding the optimal working view for treatment of intracranial lesions. (b) Technique (i) Park the lateral C-arm out of the way. (ii) Adjust to the narrowest possible field of view, centered on the target. (iii) Position the patient at isocenter. (iv) Connect the power injector. • For carotid, settings: 3 mL/s for 21 mL total. (v) All personnel should step out of the angiography suite and into the control room during acquisition of the images, if possible, because of the large amount of radiation scatter. (vi) Post-processing is automatic. Adjust windowing, magnification, and view of the image on the workstation as needed. (vii) Some angiographic suites allow a 3-D angiography to be a mask for road mapping, as in the syngo iPilot (Siemens) and Dynamic 3D Roadmap (Philips). 2. Cone beam CT (a) Rotational flat panel CT (also known as “cone beam” CT) generates a fine-cut head CT with less contrast resolution compared to conventional multidetector CT [96–98]. Useful in neurointervention for identifying new intracranial hemorrhage, hydrocephalus, ventriculostomy catheter position, and other anatomic information [99, 100]. (b) Siemens’ version: DynaCT [101]. (c) Philips’ version: XperCT [102]. (d) GE version: Innova CT HD. (e) Toshiba version: Low Contrast Imaging. (f ) Shimadzu version: SCORE CT.

4  General Considerations for Neurointerventional Procedures

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(i) Technique. (ii) Park the lateral C-arm. (iii) Adjust to a wide field of view. (iv) Position the patient at the isocenter. (v) Routinely program the system to acquire “low definition” images. The low definition setting provides faster image acquisition with a lower radiation dose compared to “high definition.” (vi) All personnel should step out of the angiography suite and into the control room during acquisition of the images, if possible, because of the large amount of radiation scatter. Image acquisition takes only several seconds. (vii) Post-processing of the CT images is automatic and usually takes several minutes.

4.5 Provocative Testing Provocative testing is used to determine if any clinical deficit would result from the occlusion of an artery or vessel or resection of the territory supplied by that vessel. Provocative testing may be mechanical, in which a vessel is temporarily occluded, usually using a balloon, or pharmacological, in which an agent is injected to temporarily anesthetize and inactivate a neuroanatomical territory in the brain, spinal cord, or a nerve. When the provocative test is being done, examine the patient to check for new neurological deficits that may result from either the lack of blood flow to a vascular territory in the case of balloon test occlusion, or an anesthetic infusion into the neural tissue supplied by the vessel being tested pharmacologically. Provocative testing can also be done under general anesthesia with motor or somatosensory evoked potentials. These procedures may be done preoperatively or as part of a therapeutic endovascular procedure to ensure the safety of occluding a vessel by open surgical or endovascular methods. This section focuses on arterial procedures. See Chap. 11 for venous provocative testing.

Balloon Test Occlusion Background Temporary occlusion of a vessel is a safe and predictable way to estimate the effect of permanent vascular occlusion. Test occlusion is done to predict whether occlusion of the vessel will have negative hemodynamic consequences, which can result in ischemic injury to neural tissue and result in a permanent functional deficit. Temporarily occluding a vessel to predict the functional effects was first reported by Rudolph Matas, a New Orleans surgeon, in the early twentieth century, and therefore, the test occlusion procedure is sometimes referred to as the Matas test [103]. The use of an endovascular balloon allows for reversible occlusion of the vessel in a predictable fashion. Balloon test occlusion is generally performed prior to endovascular or surgical occlusion of a major cerebral artery in the management of aneurysms, tumors, and other neurosurgical problems. There are two conditions that must be met to ensure the reliability of the test occlusion results: 1. The vessel being occluded must be at the proper site and level to simulate the anticipated permanent occlusion. (a) It is important to test-occlude beyond any potential collateral vessels that may still provide flow to the brain during the test, yet may be lost after more distal permanent occlusion. (b) In the carotid circulation, more than half the population have angiographically apparent branches of the proximal intracranial carotid that can be pathways for collateral flow to the brain, during a test occlusion in the cervical carotid [104]. (c) The ophthalmic artery is a significant collateral pathway in many patients and some patients pass a test occlusion with a balloon proximal to the ophthalmic, but fail when the balloon is placed at the level of the ophthalmic, which occludes the collateral flow via that vessel [105]. A simple rule of thumb is to perform a test occlusion of a vessel with balloon infla-

4.5 Provocative Testing

tion at the same level as the anticipated permanent occlusion. 2. The test should reliably predict neurological consequences of the vascular occlusion. (a) Temporary occlusion of a vessel could sufficiently lower the blood flow to an eloquent neuroanatomical region, so that a demonstrable neurological deficit occurs. (b) The situation is simple if the test result is abnormal, and the patient exhibits a neurological deficit during the test: It is very likely that the patient would suffer some hemodynamic ischemic injury due to permanent occlusion of that vessel. (c) When a neurological change occurs during a test occlusion, it may not always be true that a permanent deficit would occur with permanent occlusion of the artery, thanks to the potential for collateral enlargement (arteriogenesis) after occlusion. However, it is never wise to ignore a test occlusion that produces a deficit. (d) Somewhat more problematic is the situation in which no deficit occurs during the test occlusion. Does this imply that the patient will never have an ischemic problem from permanent occlusion of the vessel, or is there a potential for false-negative test occlusions? (e) Combine the neurological examination during arterial test occlusion with additional maneuvers, when possible, to corroborate the clinical findings. These include cerebral blood flow imaging, acetazolamide administration, and pharmacological lowering of blood pressure. Carotid artery test occlusion is done frequently, and experience with the procedure has shown the predictive power of the test. A systematic review of 254 patients in five studies in which an internal carotid was therapeutically sacrificed without a test occlusion found an average stroke rate of 26%, and mortality of 12% [106]. These results are in contrast to a study of 262 patients in eight studies in which the internal carotid was occluded after perform-

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ing a test occlusion with an average stroke rate of 13% and mortality of 3%. This difference in stroke and death rate reached statistical significance. The significant morbidity associated with permanent carotid artery occlusion, even with prior test occlusion, indicates that test occlusion is an imperfect predictor with a significant falsenegative rate. Adjunctive evaluation techniques (the additional maneuvers mentioned above) were added to the neurological assessment to reduce the chances of a false-negative test occlusion. The rationale for the use of these additional tests is that occlusion of the carotid or other vessels may produce a drop in blood flow that puts the patient at risk for stroke, yet not enough of a drop to produce detectable neurological dysfunction during a trial occlusion for a reasonable period. These adjunctive tests look for subtle signs of neurological dysfunction or look for the effects of the vessel occlusion on blood flow to the target territory.

Adjunctive Tests of Neurological Function 1. Hypotensive challenge [107, 108]. Lowering the blood pressure magnifies the hemodynamic effect of vascular occlusion. When the carotid artery is occluded and no deficit occurs in a normotensive patient, the blood pressure is pharmacologically lowered to a target pressure (e.g., 66% of mean baseline pressure [109]), or until the patient develops a focal neurological deficit (or becomes too nauseated and uncomfortable to allow adequate clinical assessment). Agents that can be used for lowering blood pressure should be fast-acting and quickly reversible, such as nitroprusside or esmolol. (a) Advantages: Cheap and easy to perform. Does not require moving the patient from the angiography suite. (b) Disadvantages: Headaches and nausea are common for the patient (and the physician). A small series [110] had a 15% false-negative rate, which is no better than just a clinical test occlusion. 2. Neuropsychological testing [111]. In addition to simple neurological testing during temporary vessel occlusion, a battery of standard-

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3.





4.



4  General Considerations for Neurointerventional Procedures

ized neuropsychological tests are given to test higher cortical functions. (a) Advantages: Cheap and easy to perform. Can be performed in the angiography suite. Standardized tests of higher cortical function can detect subtle signs of neurological dysfunction, even if the patient does not have an apparent motor or sensory deficit [111]. (b) Disadvantages: Requires skilled personnel to administer testing in an accurate and consistent manner. Most centers have limited experience with this test. Accuracy is unproven. Electroencephalography (EEG) [112]. Continuous EEG monitoring is done throughout the procedure. Slowing or other deviations from baseline conditions can be secondary signs of developing ischemia. (a) Advantages: Does not require moving the patient with the balloon in place. Can still be done with patients under light general anesthesia. Monitored results can be ­ recorded and examined carefully at a later time, to look for changes corresponding to events during the procedure. (b) Disadvantages: Adds cost and complexity to the procedure. Requires pre-placement of EEG leads prior to starting the procedure. Requires skilled personnel to monitor the readings. Careful neurological testing will almost always reveal a deficit when EEG changes are present, making the use of this modality redundant when the patient is awake and can be tested neurologically. Somatosensory evoked potentials (SSEP) [113]: EEG electrodes are attached and electrical stimulation of a peripheral nerve (usually the median nerve), contralateral to the hemisphere being tested, is performed. Cortical responses are recorded and the timing and amplitude of the response indicates cortical function. Testing is done prior to and following balloon inflation. (a) Advantages: Does not require moving the patient with the balloon in place. Can still be done with patients under light general

anesthesia. Monitoring results can be recorded and examined carefully at a later time to look for changes corresponding to events during the procedure. (b) Disadvantages: Adds cost and complexity to the procedure. Requires pre-placement of EEG leads and nerve stimulation leads prior to starting the procedure. Stimulation of the nerve can be uncomfortable and distracting to the patient. Results may be difficult to interpret in the setting of underlying spinal or peripheral nerve disease. Requires skilled personnel to monitor the readings. The value of this test is unclear, compared to standard neurological testing. 5. Cerebral oximetry [114]. A commercially available cerebral oximeter, such as INVOS® (Somanetics, Troy, MI) can be applied to the forehead and allows measurement of frontal lobe oxygenation. (a) Advantages: Does not require movement of the patient with the balloon in place. Results seem to correlate with neurological deficits and single-photon emission computed tomography (SPECT) imaging [114]. (b) Disadvantages: Gives only a limited evaluation of frontal lobe oxygenation. Results can be affected by underlying brain pathology. Sensitivity and specificity are unproven.

 djunctive Tests of Blood Flow A 1. Angiography [115, 116]. Cerebral angiography before and during balloon test occlusion allows qualitative, semiquantitative assessment of brain blood flow and potential collateral circulation to the occluded vascular territory. A posterior communicating artery diameter 0.3 mL/min risk vascular injury due to DMSO toxicity. (ii) Continue injecting Onyx® as long as it is flowing forward into desired areas of the abnormal vessels. If it refluxes along the catheter, passes into the proximal part of the vein, or refluxes into other arterial feeders, pause the injection for 15  s, then resume injecting. If the Onyx® continues to flow in the wrong direction, pause again for 15–30  s, then try again. If the Onyx® finds another, more desirable pathway, continue the slow injection. (iii) Make a new roadmap mask periodically. New roadmaps subtract out the already deposited embolic agent and make the newly injected material easier to see. Guide catheter angiograms can be done during the Onyx injection to determine if there are still portions of the feeding artery or nidus that could be occluded from this microcatheter position. (iv) The Onyx® injection requires patience and usually takes at least several minutes.

• Some reflux back along the catheter tip is not a problem, due to the nonadhesive nature of the product. Avoid more than 1 cm of reflux, however, since even Onyx® may glue a microcatheter into the vessel. • Do not pause the injection for >2  min at a time because the Onyx® may solidify and clog the microcatheter. • Never try to inject against resistance. A clogged microcatheter may burst if the injection is forced. (v) When adequate filling of the desired vascular spaces is achieved, or if the Onyx® repeatedly flows in the wrong direction, stop injecting, aspirate back on the syringe, and steadily pull back on the microcatheter, disengage it from the deposited Onyx® and remove it. (vi) After the microcatheter is withdrawn from the guide catheter, examine the RHV of the guide catheter for any retained droplets of Onyx®, then aspirate and double flush the stopcock, RHV, and guide catheter. (vii) Once the guide catheter is thoroughly inspected and flushed, do a guide catheter angiogram to see what has been accomplished. 4. Ethanol embolization technique. (a) Ethanol embolization is seldom done for extracranial embolization. It may be useful in occasional situations in which the microcatheter tip is very close to the lesion, and for direct puncture of superficial tumors or vascular malformations (see below). (b) Some operators use Swan-Ganz catheter monitoring for AVM embolization with ethanol, to watch for signs of pulmonary hypertension due to the pulmonary effects of ethanol. (c) When added to particles, the technique is essentially the same as standard par-

7.1 Head and Neck Transarterial Embolization

ticulate embolization (see below). When used without particles, the technique is more like that for glue. (d) Be sure to use syringes, stopcocks and microcatheter hubs that will not degrade when exposed to ethanol. Often, those that can be used with glue or DMSO will withstand ethanol, but it is wise to test it first. Since ethanol is not an FDA-­ approved embolic material, manufacturers state that their products are not approved for use with ethanol. (e) Position the microcatheter and do provocative testing as needed. (f) Prior to embolizing, do test injections of contrast through the microcatheter to estimate the rate and volume required to fill the vessels that will be treated. If the flow is very rapid, consider placing a coil or two to slow the flow. (g) Flush the microcatheter with saline because ethanol can cause contrast to precipitate. (h) Inject the absolute ethanol at a rate similar to the rate that was used for the microcatheter angiogram but use only approximately 50% of the volume of contrast that was used for the microcatheter angiogram. (i) Wait a few minutes, then repeat the contrast injection. If the target vessels remain patent, inject another small bolus of ethanol, and wait again. (j) If spasm is seen on repeat test injections, wait until it resolves and decrease the volume of the ethanol bolus. (k) After a few boluses of ethanol have been given, wait at least 5–10  min between ethanol injections before checking for patency of the vessel. (l) If there is no change after 20 mL of ethanol, consider placement of additional coils to slow the flow and help the ethanol work, or try a better embolic agent. (m) Remember that ethanol can affect the endothelium for some time and can also spread through the vessel wall into the

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adjacent tissues, so keep the total ethanol volume to a minimum. 5. Particle embolization technique. (a) Most particles are used in a similar fashion for extracranial embolization. (b) To avoid major problems with particles clogging the microcatheter, use a larger lumen microcatheter, such as a RapidTransit® (Codman Neurovascular, Raynham, MA). (c) The microcatheter tip must be close to the lesion being embolized and in a stable position distal to normal branches. (d) Choose a particle size depending on the size of the vessels in the target lesion. In general, use particles 300  μm for AVMs. (e) If there are potential connections to cranial nerves use particles >300 μm. (f) Mix the particles with 50:50 contrast in saline and draw up the emboli in a labeled 10-mL syringe. This acts as a reservoir for emboli. (g) The particles should be fairly dilute to limit the risk of clogging the microcatheter. (h) Attach the syringe to one female connection on a 3-way stopcock and attach a labeled 3-mL Luer-lock syringe to the other female connection. This syringe is used to inject the embolic mixture through the microcatheter. (i) The stopcock is then attached to the hub of the microcatheter. (j) The stopcock is turned to connect the 10- and 3-mL syringes, and the ­contrast/ emboli mixture is flushed into the 3-mL syringe and then back into the 10-mL syringe, back and forth several times, to ensure uniform suspension of particles. (k) The 3-mL syringe is then filled with 1–2 mL of the emboli suspension. (l) Using a blank roadmap, slowly inject the emboli in small (0.2 mL) increments and ensure that the contrast freely flows from the microcatheter tip.

7  Extracranial and Spinal Embolization

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(m) Increase or decrease the rate of injection, depending on the speed of runoff away from the microcatheter. (n) Every 3–5  mL of embolic suspension, or sooner if emboli are seen to collect in the hub of the microcatheter, disconnect the 3-mL syringe and reconnect another labeled 3-mL syringe filled with dilute 50:50 contrast. (o) Gently flush the microcatheter with the contrast under fluoroscopy, remembering that the microcatheter is still full of emboli. (p) As long as a good runoff of contrast is seen, reconnect the 3-mL embolic syringe, refill it with embolic mixture, and continue to inject emboli. (q) When the 10-mL syringe is empty, consider obtaining a control superselective angiogram via the microcatheter to see whether the flow pattern is changing. (r) Especially with AVMs it may require some time and a considerable number of emboli to occlude a feeder. (s) If an entire vial of emboli is injected with no change in the flow pattern, consider modifying the flow with a coil or two, or switching to a different embolic agent. (t) Avoid creating reflux of the embolic mixture back along the microcatheter when injecting. Slow or stop the injections if reflux is seen. (u) If resistance is encountered during the injections, stop, disconnect the 3-mL embolic syringe and check the hub of the microcatheter. If emboli are bunched up in the hub, it may be possible to rinse them out with a needle or guidewire introducer, then attempt to gently flush with contrast. (v) If resistance continues, do not attempt to force the emboli through by a forceful injection, and do not use a 1-mL syringe to achieve higher pressures. Forcibly injecting through a microcatheter clogged with particles can cause the

microcatheter to rupture and even break into pieces. (w) When the flow in the feeder is significantly slowed, injections of emboli are stopped. (x) If more definitive closure of the vessel is needed after particle embolization, a coil or a tiny pledget of Gelfoam may be deposited to finish the job. (y) Be certain to flush out the microcatheter with contrast or saline before inserting a coil. Particles in the microcatheter can cause the coil to bind in the microcatheter. (z) Even if the microcatheter seems free of particles, it is best to withdraw and discard the used microcatheter and use a new microcatheter prior to attempting catheterization of another feeder. 6. Silk suture embolization technique. (a) See Chap. 6. 7. Detachable balloon technique. (a) See Chap. 6. 8. Pushable coil technique. (a) See Chap. 6. 9. Detachable coil technique. (a) Use of detachable coils is discussed in detail in Chap. 5. Use of detachable coils for fistulas is covered in Chap. 6. 10. Stent placement for AVF technique. (a) The use of stents for aneurysm coiling is discussed in Chap. 5 and for AV fistulas in Chap. 6. 11. Stent-graft placement for active bleeding. (a) Begin by obtaining large guide catheter access (a 6F Cook Shuttle is best). Consider placing a second sheath in the opposite femoral artery; this will allow a temporary balloon catheter to be placed in the target vessel to buy time to prepare for stenting. During the access phase, external packing may control the bleeding while the endovascular procedure is underway. In a dire situation, someone may need to manually compress the bleeding site until it is controlled, but their hands will be exposed in the X-ray

7.1 Head and Neck Transarterial Embolization



















field and potentially make fluoroscopic imaging difficult. (b) In the setting of massive bleeding from trauma or a carotid blow-out, pretreatment with antiplatelet agents is not advisable. Loading the patient with clopidogrel (usually 300–600 mg) only after the stent placement and only after the bleeding has stopped seems to be the most prudent way to handle antiplatelet therapy in this setting. (c) Size the stent-graft appropriately for the parent artery (usually a little wider than the parent artery) and for the lesion being stented (usually at least 4 mm coverage on either side of the lesion). (d) Obtain a good roadmap that shows the bleeding site to be treated and, as much as possible, the vessel proximally and distally. Even if the patient moves, consider placing an external radio-opaque marker over the bleeding site to ensure coverage by the stent-graft. (e) Advance a microcatheter with a 0.014 in. 300 cm exchange as distal as possible to the lesion being stented. Then remove the microcatheter and leave the exchange-length microwire in place. Take care not to traumatize the bleeding vessel during this process. Always keep the wire tip in view and ensure that it stays in a larger vessel and does not injure the vessel wall. (f) Advance the stent delivery catheter over the wire, gently pulling back on the wire to make sure the tip remains in a stable position. (g) Once the stent is in position, remove any slack in the wire and stent delivery catheter. This is critical for obtaining easy and accurate deployment. (h) Do a guide-catheter angiogram. If the stent is not in proper position, change the position and repeat the angiogram. (i) When a good position is achieved across the neck of the lesion, the stent is ready for deployment. (j) Self-expanding stent technique.

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(i) The use of self expanding stent-­ grafts for bleeding vessels is similar to the placement of self-expanding carotid stents. (ii) The Wallgraft™ and Viabahn® stents require a very large sheath. A 6F or 7F Cook Shuttle™ is suitable. (iii) Once the guide catheter or sheath is in place, advance a 300-cm microwire distal to the lesion. (iv) Advance the stent delivery catheter over the microwire while gently pulling back on the wire to make sure the tip remains in a stable position. (v) As with other self-expanding stents, the stent-graft is deployed by stabilizing the inner part of the delivery system as the outer part of the delivery catheter is pulled back, exposing the stent, and allowing it to expand. (vi) Remove the stent delivery catheter and do a guide catheter angiogram to determine whether the stent-­ graft has sealed the bleeding site. (vii) If the stent is not fully apposed to the vessel wall, do a post-stent angioplasty. Use the minimum pressure required to slightly dilate the stent. Do not allow the balloon to inflate outside of the stent. (viii) If a continued leak is present, consider using a second self-­ expanding stent or stent-graft. (k) Balloon-expandable stent technique. (i) For a balloon mounted stent such as Jostent®, the stent is deployed by inflating the balloon under roadmap guidance to match the size of the parent artery. Do not exceed the maximum recommended pressure, and be careful not to disrupt the site of bleeding. (ii) When it appears that the stent is opened up to the proper size, deflate the balloon and carefully disengage

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7  Extracranial and Spinal Embolization

it from the open stent. It may be 5. Pay close attention to blood pressure after stuck to the stent and may require embolization of a high-flow AVF or an another inflation/deflation cycle to actively bleeding artery. free it up. Be careful not to move 6. Patients who do not have planned surgery the stent when trying to pull back after extracranial embolization procedures on the balloon. can be discharged to home on post-procedure (iii) Once the balloon is deflated and day 1. disengaged, do a guide catheter 7. Patients undergoing embolization of tumors angiogram. should be observed for a few days to watch (iv) If the stent is not fully apposed to for signs of swelling and/or venous the vessel wall, re-insert the balcongestion. loon into the stent and attempt to 8. Depending on the lesion treated, there may or dilate further. Do not exceed maximay not be a need for routine radiographic mum pressure for the balloon. If follow-up. Most patients are followed clininecessary, the balloon could be cally and with cross-sectional imaging. exchanged for a new low-­ compliance coronary angioplasty balloon sized to the vessel diameter Tips on Specific Diseases and no longer than the stent. (v) Remember that the outer diameter Head and Neck Embolization of the stent is more than that of the 1. Extracranial arteriovenous malformation inner lumen, so the vessel will be (AVM) dilated around the stent to a greater (a) Indications: preoperative flow reduction degree than expected for the size of or palliation for bleeding, cosmetic deforthe balloon used. mity, pain or tinnitus. (vi) Assuming that the stent was prop- (b) Since these are infiltrative lesions that erly sized and positioned in the first intimately involve normal structures, place, it should nicely fit the vessel complete cure is rare, even with radical and occlude the lesion when fully embolization plus surgery. deployed. If not, consider a second (c) Particle embolization is effective for prestent-graft. operative embolization, but is not useful for palliative treatment since the occlusion will be temporary and the clinical benefits transient. Post-procedure Management (d) Embolization with n-BCA glue will be permanent when the glue is placed 1. Complete the neurological exam. within the nidus. The microcatheter tip 2. Admit to the ICU with vital signs, neuro must be placed as close to the nidus as exams and groin checks Q 1 h. possible. (a) It is not uncommon for patients undergo (e) An alternative to transarterial embolizaing embolization procedures to have some tion is direct puncture and embolization pain in the area treated the evening after with glue [7] or sclerotherapy with ethathe procedure. nol [8] (see below). In patients whose 3. IV fluids (normal saline) at 100 mL/h until the external carotid arteries have been previpatient is taking oral fluids well. ously ligated in a desperate attempt to 4. Stented patients require dual antiplatelet thertreat the lesion, embolization may still be apy (clopidogrel 75  mg and aspirin 325  mg possible by a direct needle puncture of daily). Other post-embolization patients are the feeding vessels and embolization with not routinely treated with antithrombotic glue distal to the ligation [9]. agents.

7.1 Head and Neck Transarterial Embolization

(f) Flow control with either transarterial embolization or percutaneous needle injection can be achieved by direct external compression of external draining veins during the glue or ethanol injection. (g) A more complicated solution is to surgically reconstruct the ligated vessel, which can be a reasonable option if ischemic symptoms are present in the territory distal to the ligation [10]. (h) Take extreme care not to allow the occlusive agent to enter dangerous anastomoses to the brain, spinal cord, or eye (see Chap. 1 for a listing of anastomoses). (i) Keep the glue, ethanol, or even small (less than 300 μm) particles out of the vessels supplying cranial nerves, by doing provocative testing, if possible, or at least by keeping the embolic agent strictly within the nidus. (j) Also, keep liquid embolics or small particles out of cutaneous branches of the superficial temporal or facial arteries. Embolization of these arteries will cause pain, blistering, and necrosis of the skin. (k) The bottom line: Less is more. Do not be too aggressive and the risk of complications will be reduced. 2. Extracranial arteriovenous fistula (AVF) (a) Congenital head and neck AVFs are rare, but often present with a pulsatile mass, tinnitus, or high-output cardiac failure. They have a predilection for arising from the internal maxillary artery [11, 12]. (b) These congenital AVFs were previously treated with detachable balloons, but more recently, transarterial embolization using GDC coils and glue has been successful [13]. (c) The goal is to occlude the fistula directly because proximal occlusion is destined to fail, thanks to the presence of generous facial collaterals. (d) In high-flow AVFs, care must be taken to size the coils (or balloon) large enough to

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prevent passage through the fistula into the veins and eventually into the lungs. (e) Post-traumatic and post-surgical AVFs in the head and neck can occur in a wide variety of locations and the treatment depends on the symptoms and vascular anatomy. (f) In an expendable vessel, such as an external carotid branch, coil and/or glue occlusion of both the fistula and parent artery may be an option. When possible the fistula and proximal vein should be occluded to prevent collateral vessels from maintaining patency of the fistula. (g) If there is adequate collateral flow to the brain, occlusion of the carotid or vertebral artery can be done to treat some fistulas. Prior test occlusion is mandatory (Chap. 6). (h) Case reports of stent-grafts to treat carotid or vertebral AVFs have shown the devices are effective in occluding the fistula and maintaining the flow in the parent artery, at least in the acute phase [14–16]. However, the long-term patency of these devices is unknown. (i) Vertebro venous AVFs are usually post-­ traumatic, but may be spontaneous [17, 18], especially in children, or those with an underlying collagen vascular such as Ehlers Danlos or neurofibromatosis. These fistulas can often be treated with balloons or coils on the venous side of the fistula, preserving arterial flow [19, 20]. 3. Idiopathic epistaxis (a) Endovascular treatment for nosebleeds consists of selective catheterization and particle embolization of the nasal vessels, usually the sphenopalatine arteries. (b) Coil embolization is not recommended for idiopathic epistaxis: Coils only block access for later re-embolization, should bleeding recur. (c) A study of 70 patients treated with embolization for epistaxis found that 86% had effective relief of bleeding, and only one

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(1.4%) had a serious neurological complication. (d) Two other reports of over 100 patients each found acute complication rates of up to 17% and a 1–2% rate of long-term neurological deficits [21, 22]. (e) Complications can be minimized by careful attention to angiographic anatomy and awareness of dangerous anastomoses. Provocative testing with amobarbital and lidocaine prior to embolization is an added safety factor [1]. (f) Always check the contralateral sphenopalatine artery angiographically, even if the bleeding is obviously unilateral, because there can be side-to-side collaterals [23]. The authors of this handbook nearly always embolize the sphenopalatine arteries bilaterally. (g) Smaller particles may be used on the side of active bleeding, but always use large particles (≥500  μm) on the contralateral side to minimize the risk of nasal mucosal necrosis. Remember: large particles call for large microcatheters. (h) Ethmoidal branches from the ophthalmic artery may be the cause of treatment failure after embolization of the internal maxillary artery. There has been a case report of embolization of the ophthalmic artery for epistaxis [24] but this is not recommended due to the risk of vision loss and the availability of a fairly easy and safe surgical procedure to ligate these vessels. (i) Accessory meningeal arteries may also rarely be a source of bleeding in epistaxis and can be embolized [25]. (j) A review of embolization compared to internal maxillary ligation suggested that ligation was more effective and, although the complications were more frequent than for embolization, the major complications of embolization (stroke) were more serious [26]. (k) In some centers, endoscopic ligation of the sphenopalatine artery is becoming a minimally invasive, safe, and effective

first choice for the treatment of epistaxis [27]. (l) Embolization may become a second line choice after a failed endoscopic ligation, or where the expertise for endoscopic ligation is unavailable. 4. Post-traumatic and post-surgical bleeding (a) Treatment of post-traumatic or post-­ surgical bleeding is very similar to treatment of post-traumatic and post-surgical AVF (above). The main difference is the urgency of the situation. (b) A general rule: Damaged, bleeding vessels must be occluded definitively, except in cases when an obvious major neurological deficit will result. (c) For quick and definitive closure of the bleeding vessels, the main endovascular tools are detachable coils (for larger vessels), n-BCA (for smaller vessels) and detachable balloons (if available). (d) Consider the use of a proximal balloon catheter in the parent artery to control bleeding during catheterization and embolization of the damaged vessel. (e) Coiling of bleeding pseudoaneurysms extending into sinuses should always be avoided. The walls of pseudoaneurysms are too fragile to contain a coil mass beyond the acute phase, and the coils will inevitably erode through the walls of the pseudoaneurysm. The authors of this handbook have managed a patient with a previously coiled ICA pseudoaneurysm that extended into the sphenoid sinus; 1 year after treatment, the patient presented with coil strands coming out of his nose and down his throat [28]. (f) If occlusion of the carotid does not appear to be an option, based on limited collateral flow to the brain or a positive test occlusion, stent-graft placement may be the only endovascular option. (g) Prior to any major vascular occlusion, consider surgical options such as vascular repair or bypass, if the anatomic location is favorable.

7.1 Head and Neck Transarterial Embolization

5. Bleeding tumors (a) Embolization of tumors is usually done with particles, since they tend to lodge in the small vessels of the tumor bed and produce sufficient devascularization for surgical excision. (b) Particles may also be used for actively bleeding tumors, but, n-BCA is quicker and a more definitive to stop the bleeding, as long the microcatheter is positioned close to the lesion and no dangerous anastamoses are present. (c) If endovascular microcatheter access to the bleeding vessel is not possible, direct needle puncture and glue injection may be feasible. 6. Carotid blow-out syndrome. (a) Carotid blow-out syndrome is catastrophic, sudden bleeding from the carotid in patients after surgical treatment for head and neck malignancy [29]. In popular jargon, the term often refers to any sudden, spontaneous bleeding from the carotid. (b) Carotid blow-outs occur in ≤5% cases of advanced cancer patients after surgery and does not seem to be necessarily related to preoperative radiation therapy [30] although anecdotally, it may be seen soon after radiation therapy [31]. In any case, carotid blow-outs tend to occur in patients whose carotid may be minimally covered by healthy connective tissue. (c) Carotid blow-out is one of the most urgent situations imaginable, since patients can bleed to death, often drowning in their own blood, in minutes. (d) The airway should be secured by intubation, if not already done. (e) The bleeding site is packed to control bleeding and emergent angiography is helpful if there is time, since often the exact site of bleeding may be uncertain. (f) A large caliber sheath should be placed to maximize options for devices. (g) In patients who are not actively bleeding at the time of the arteriogram, a pseudoa-

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neurysm is the usual angiographic sign of the bleeding site [32]. (h) Parent artery occlusion was the usual treatment historically, unless the collateral flow is limited by angiographic criteria. Test occlusion could be performed if the patient is clinically stable. (i) Delayed ischemic complications occur in 15–20% of cases with carotid occlusion, so stent-graft placement seems to be an attractive option, when feasible [6]. (i) Reported results with self-expanding stent-grafts have been promising, but long-term patency rates are unknown. In a series of three patients treated for carotid with stent-grafts, two went on to be thrombosed and/or exposed [33]. (ii) A more recent study showed that placement of Viabahn® Endoprosthesis(Gore, Flagstaff, AZ) may be a reasonable treatment for actual or threatened carotid blow-out due to head and neck cancer [34]. • Rebleed from the treated vessel after stent-graft placement is unusual unless there is incomplete wall apposition of the stent [34]. • Ischemic events are also rare using the heparin-impregnated Viabahn® [34]. (j) Carotid blow-out syndrome can be a long-term problem in some patients; multiple episodes of massive bleeding were reported in 26% of patients with carotid blow-out syndrome [35]. 7. Tips for large vessel occlusion (see also Chap. 5) (a) Indications. (i) Post-traumatic bleeding. (ii) Carotid blow-out syndrome. (iii) Pre-operative occlusion of large vessel involved with a tumor. (iv) Treatment of certain difficult aneurysms, pseudoaneurysms, AVFs, AVMs.

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(b) Whenever possible, perform a test occlusion first. (i) In emergency situations, tolerance of a large vessel occlusion may be estimated by angiographic evaluation of collaterals. (c) Whenever possible, use proximal flow control with a balloon guide catheter. 8. Extracranial vascular tumors (a) Juvenile nasopharyngeal angiofibroma. (i) Hypervascular tumor in young boys usually presents with nasal bleeding and nasal obstruction. In females, hemangiopericytoma can have a similar clinical presentation. (ii) Angiographically, these lesions show an intense tumor blush supplied mainly by the distal internal maxillary artery branches with variable contributions from the accessory meningeal and ascending pharyngeal arteries. Larger tumors may be supplied from the petrous and cavernous carotid branches, the middle meningeal artery, and even the transverse facial artery. (iii) Preoperative particle embolization of the feeding arteries is effective in reducing blood loss, especially in larger tumors [36]. (iv) Vision loss from central retinal artery embolization [37] and facial nerve palsy [38] are complications of angiofibroma embolization. These complications underscore the need for careful attention to technique, vigilance for dangerous anastomoses, and the use of provocative testing. (v) Direct tumor needle puncture and embolization with glue is an option for these tumors [39]. Tumors may have feeders from the carotid, potentially allowing retrograde flow of glue to the carotid, so constant vigilance for visualization of dangerous collaterals during the glue injection is mandatory.













(b) Paraganglioma (aka chemodectoma, glomus tumor). (i) These tumors include glomus jugulare, glomus tympanicum, carotid body tumors, glomus vagale, or rare paragangliomas of the larynx, orbit, paranasal sinuses, or elsewhere in the head and neck. (ii) The jugulare, tympanicum, carotid body, and vagale tumors all tend to have dominant vascular supply from one or more branches of the ascending pharyngeal artery. On angiography, these lesions have an intense tumor blush, often with some arteriovenous shunting. (iii) When these tumors become very large, it is sometimes difficult to determine from which location they have arisen. Larger tumors may have intracranial, even intradural extension, usually in the posterior fossa, with blood supply from the anterior inferior cerebellar artery or other intracranial branches in the posterior fossa. (iv) The primary indication for endovascular treatment is preoperative embolization. Rarely, palliative embolization may be done for inoperable lesions to slow progression of the tumor. (v) Embolization is usually done with particles from a transarterial route [40]. Provocative testing should be done because of the tendency of feeding vessels to also supply cranial nerves (Chap. 4). If a neurological deficit occurs with provocative lidocaine injection, embolization with larger particles (>300  μm) can still be done, because these particles are too large to get into branches going to cranial nerves. (vi) Onyx® embolization of both the arteries and veins may provide good hemostasis for the surgeon

7.1 Head and Neck Transarterial Embolization

removing large paragangliomas [41]. (vii) Onyx® embolization using the Scepter® balloon catheter (Microvention, Aliso Viejo, CA) has been advocated as a way to achieve deep penetration of the tumor vessels in paragangliomas [42]. (viii) Vascular tumors may also be directly punctured with a needle and injected with n-BCA [43–46]. Direct puncture with glue embolization still carries a risk of stroke through reflux of glue into carotid branches [47]. (c) Other vascular tumors. (i) Preoperative or palliative embolization can be helpful for vascular metastases and other rare tumors in the head and neck. (ii) Transarterial particle embolization is most commonly done for any lesion with a capillary bed to trap small particles. (iii) Rarely, direct puncture with glue injection may be done when arterial access is difficult [43, 45]. (d) Special situation: Kasabach Merritt syndrome. (i) Kasabach Merritt syndrome is a consumptive coagulopathy with platelet and fibrinogen consumption associated with large vascular lesions, often in the head and neck. • Classically, the tumors were called involuting infantile hemangiomas, but more recently they have been referred to as Kaposiform hemangioendotheliomas (KHE) [48]. • Medical therapy with aspirin, steroids, vincristine and alpha interferon has been helpful controlling the coagulopathy [49–51]. • Transarterial embolization of the primary feeding vessels with particles, if needed, appears safe and

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effective and does not prevent re-­ embolization [49, 50, 52]. • A single case report trumpets Onyx as a good agent for KHE [53]. However, the dark tantalum in the agent can stain very superficial lesions and the occlusion of feeding arteries can prevent access for later embolization.

 omplications of Head and Neck C Embolization Informed consent prior to any interventional procedure must include a discussion of the risk of complications. Published reports of series of embolization procedures should not be relied on to indicate the true risk of complications. It is human nature to publicize good results and gloss over bad results. Especially in the case of extracranial embolization, the procedures are widely varied in the techniques and agents used and territories involved, so results and complications of, for example, epistaxis embolization with particles, cannot be used to predict results from facial AVMs with n-BCA.  The operator’s personal experience and complication rates should also be disclosed if known.

Neurological Complications 1. Head and neck embolization carries a 1–2% risk of stroke due to thromboembolism. Stroke, blindness, or spinal cord infarction may occur from reflux of embolic material or passage through dangerous anastomoses. 2. Cranial nerve defect can occur with embolic material entering the blood supply to the nerve. 3. In spinal AVMs and AVFs passage of emboli into the veins, or even thrombosis induced by the embolization, may worsen venous congestion of the cord and cause worsening symptoms [54, 55].

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4. AVFs with large draining veins may swell and compress neural structures after embolization. 5. Access complications can occur with dissection of access vessels, specifically the common carotid or subclavian. 6. Microcatheters or wires may fracture and embolize. 7. Use of liquid embolics can cause the microcatheter to be glued in place.

Nonneurological Complications 1. Embolization of superficial vessels in the head and neck can result in ischemia and necrosis of skin, mucosa, and other tissue. 2. In AV fistulas, embolic material may travel to the pulmonary circulation [56, 57]. 3. Anaphylactic reactions to iodinated contrast or any of the medications used can occur as with any endovascular procedure. 4. Similarly, groin hematomas or other groin arterial injury can occur, as in any endovascular procedure. 5. Deep venous thrombosis and pulmonary embolism can occur. 6. Anesthesia-related complications can occur if using general anesthesia. 7. Use of Onyx in the external carotid circulation can cause bradycardia and asystole, presumably by induction of the trigeminocardiac reflex by toxic effects of the DMSO [58]. (a) Reflexive bradyarrhythmia occurred in 7.5% of dural AVFs treated with Onyx [59].

7  Extracranial and Spinal Embolization

3. Familiarize yourself with the devices that will be used during the case, particularly if it is a device not commonly used (like a stent-­ graft or detachable balloons). 4. Focus on basic techniques such as flushing and microcatheter navigation. 5. In awake patients do provocative testing with amobarbital and lidocaine. 6. Use neurophysiological monitoring and provocative testing even when using general anesthesia in spinal embolization cases. 7. When embolizing with any agent, inject no faster than was done for the contrast injection during the microcatheter angiogram. 8. Immediately stop injecting when reflux occurs or if different vessels (potentially dangerous anastomoses) appear. 9. Do periodic guide catheter and microcatheter angiograms to monitor progress and to decide when to stop. 10. Pay constant attention to the patient: vital signs, neurological status, neurophysiological monitoring, and comfort level. It is all too easy to expend all of one’s attention on the procedural aspects and forget the person underneath the sterile drape.

7.2 Percutaneous Procedures Indications

1. Superficial venous and lymphatic malformation (a) These lesions are usually cosmetic problems that were present at birth and can usually be accurately diagnosed on MRI imaging. (b) These lesions can be differentiated from How to Avoid Extracranial AVMs by the absence of a bruit and thrill. Embolization Complications in Ten (c) Unlike AVMs, there is no role for transarEasy Steps terial embolization of any kind. Sadly, the authors of this handbook have seen too 1. Carefully study the angiograms and cross-­ many patients who have been misdiagsectional imaging of the lesion and surroundnosed and even previously treated by ing structures to have a clear understanding transarterial embolization with absolutely of the anatomy and pathology in the case. no benefit. 2. Do microcatheter angiograms prior to embo (d) Percutaneous sclerotherapy and/or laser lization to look for reflux into normal territotreatments and/or surgical excision are ries or filling of dangerous anastomoses. the effective treatments [8].

7.2 Percutaneous Procedures

2. Superficial arteriovenous malformations (a) These lesions are percutaneously accessible vascular tumors. Embolization is done pre-operatively (common) or for palliation (rare). (i) Juvenile nasopharyngeal angiofibroma. (ii) Paraganglioma (aka chemodectoma, glomus tumor). (iii) A wide variety of other primary and metastatic vascular tumors.

Percutaneous Sclerotherapy: Technique This technique is used for the treatment of superficial arteriovenous malformations as well as venous and lymphatic malformations [8]. It is also useful for preoperative or definitive treatment of hemangiomas [60]. When using the sclerotherapy technique for arteriovenous malformations, an arterial catheter is used to angiographically localize the target lesion and monitor progress. Angiographic catheters are not used when treating venous or lymphatic malformations. A recent systematic review including 37 papers and 2067 patients summarizes what has been reported on sclerotherapy for venous malformations [61]. It results in overall cure rate of 64.7%. The highest cure rate is using pingyangmycin (82.9%) and lowest is using Sotradecol (55.5%). On the other hand, overall quality of life improvement was seen in 78.9% and patient satisfaction in 91%. Interestingly, patient satisfaction was lowest (72.8%) using Sotradecol and highest (96%) using alcohol. Permanent morbidity was low at 0.8% and there was no mortality. 1.

Sclerosing agents (a) Bleomycin (most commonly used) (b) Pingyangmycin (c) Sotradecol (d) Ethanol (e) Doxycycline (f) Ethanolamine (g) Polidocanol (h) OK-432

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2. Anesthesia (a) Percutaneous ethanol sclerotherapy is almost always performed under general anesthesia because the ethanol injection is very painful, and doxycycline and Sotradecol are moderately painful. (b) Bleomycin is less painful, although many practitioners still use anesthesia. 3. Access (a) The area of the lesion is localized by palpation or ultrasonic localization, or in the case of AVM, by contrast injection in the feeding artery for roadmap guidance. (b) For an AVM, the lesion can be accessed by puncturing the artery close to the nidus, the nidus itself, or the proximal vein close to the nidus. For venous and lymphatic malformations, the ideal puncture site is the larger cavernous spaces within the lesion. Prep and drape the skin overlying the lesion and inject local anesthetic. (c) Insert a 22-gauge spinal needle for deep lesions or butterfly for superficial lesions. Place the tip at the expected depth of the lesion. Check for return of blood or lymphatic fluid. Reposition the needle if good return is not obtained. Bright red pulsatile blood indicates that AVM has been punctured; dark blue blood indicates puncture of venous malformation, and straw-­colored or slightly bloody fluid is seen with puncture of lymphatic malformations. Once good return from the needle is seen, do an angiogram with injection of contrast through the needle. (d) For venous and lymphatic malformations, use a second needle to puncture another part of the now contrast-filled malformation. The second needle allows drainage of fluid from the lesion as the ethanol is injected to remove the diluting blood or fluid and reduce the risk of over-­ pressurizing the lesion with ethanol and creating leakage back along the needle [62]. 4. Injection

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(a) Study the angiogram images to ensure that the needle is in a vascular space and that it fills the lesion. Estimate the rate and volume required to opacify the territory that is to be occluded. (b) If the flow is extremely rapid, place a coil or two through the needle to slow the flow. Ten-system fibered coils will pass through a 22-gauge needle; 18-system coils will pass through thin-wall 19-gauge or any 18-gauge needle. Most cases will not require coils, especially if the flow can be manually slowed by manual compression of the draining veins, or by placement over the area of a compressive O-ring affixed to the skin over the lesion. Do a repeat percutaneous angiogram when the venous outlets are compressed to assess the change in flow and to check the rate and volume required to opacify the lesion. (c) Flush the needle with saline because ethanol can cause contrast to precipitate. It is usually easiest to attach a short extension tubing to the needle with a one-way stopcock at the end of the tubing to control back-bleeding through the needle. (d) Inject absolute ethanol at a rate similar to that which opacified the vessel, but use only approximately 50% of the volume of contrast used. If a second needle is positioned in the lesion, remove the stylet and let it back-bleed during the ethanol injection to relieve the pressure within it. (e) After the first injection, allow 5  min to elapse and then release the pressure on the veins and check for back-bleeding from the injected needle. If rapid return is obtained, inject another dose of ethanol equal to 50% of the volume of contrast needed to opacify the lesion. After waiting another 5  min, again check for return from the needle. If the return is still brisk, repeat the contrast injection. If the vessel remains patent, inject another small bolus (1 or 2 mL) of ethanol, and wait again.























(f) If vasospasm is seen on repeat test injections, wait until it resolves and decrease the volume of ethanol boluses. (g) Stop the ethanol injections when there is no longer blood return or if blanching or discoloration of the skin is seen to prevent damage to the soft tissues and skin. (h) If there is no change after 20 mL of ethanol, consider placement of additional coils to slow the flow and help the ethanol work, or use n-BCA as the embolic agent. (i) Remember that ethanol can work on the endothelium for some time and can also spread through the vessel wall into the adjacent tissues, so it is best to keep the ethanol volumes to a minimum. (j) To minimize local tissue damage, it is best to stage the procedure rather than attempting to cure the lesion with a single session. The maximum recommended ethanol dose per session is 1 mL/kg body weight [62, 63]. (k) When the puncture cavity appears to be thrombosed, wait another 5 min and then remove the needle and hold manual pressure for approximately 5–10 min or when hemostasis is obtained. (l) If only a few mL of ethanol have been injected, a second needle puncture (use a new needle) and additional ethanol injections may be done. (m) It is time to stop when swelling or discoloration at the puncture site is seen or if the ethanol dose gets over 20–30 mL, and absolutely if the total dose of 1 mL/kg is reached [63]. (n) When using bleomycin, inject a volume approximately 1 mL at a time and plan on injecting approximately the total volume of contrast required to fill the space. (o) Wait 5  min between injections and be certain to check that blood or fluid can be aspirated between injections. Note that thrombosis of the space is not as common with bleomycin. (p) Keep the total dose of bleomycin each day to less than 0.5 units/kg body weight.

7.2 Percutaneous Procedures



(q) If using Sotradecol or polidocanol as the agent, these agents can be converted into foam by using 2 syringes connected to a 3 way stopcock. One has a few milliliters of sclerosant and the other with air. Injecting the sclerosant back and forth quickly between the syringes will result in a uniform foam. This can then be injected in the vein and the foam will result in the agent filling the vein for a longer time than liquid alone [64].

 ercutaneous n-BCA Injection: P Technique This technique involves direct puncture and glue embolization of feeding vessels that may have been ligated [9], or direct puncture and embolization of AVMs [65] or vascular tumors in the head, neck [43–45] or spine [66]. 1. Access (a) Park an arterial catheter in the feeding artery to the vascular lesion to allow for roadmap imaging and control angiography. (b) Prep and drape the skin overlying the target and inject local anesthetic (2% lidocaine). (c) Using a roadmap, plan a trajectory to allow direct needle access to the target without hitting any vital structures. Biplane or 3D roadmapping is particularly useful. (d) For very superficial lesions plan an oblique trajectory to allow the skin and tissues to stabilize the needle once it is positioned in the lesion. (e) Insert a 22-gauge spinal needle with a metal hub under roadmap guidance to the desired position. Remove the stylet when the needle seems deep enough to look for blood return. If no return is obtained the needle should be advanced or withdrawn until good blood flow is obtained. (f) In the scalp and face the tumor or vessels may be mobile and it may take some

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2.









3.

manipulation to puncture the lesion and not glance off it. (g) Once good blood return is obtained, do an angiogram with injection of contrast through the needle to: (i) Confirm proper positioning. (ii) Look for any filling of normal vessels or dangerous anastomoses. (iii) Time the volume required to fill the lesion. (iv) Determine the arteriovenous transit time. n-BCA preparation (a) Prepare the n-BCA on a second sterile back table that is saline-free. As always when using glue, all persons near the sterile field should wear glasses or other eye protection. If a connection comes loose during injection, the glue can spray and stick to whatever it touches. (b) Rule of thumb: For high-flow fistulas use a concentrated mixture such as a 75% glue (three parts n-BCA to one part Ethiodol®). Most tumors require a dilute mixture such as 20% (one part n-BCA to four parts Ethiodol). (c) Tantalum powder greatly increases the radio-opacity of glue, but is not absolutely necessary unless the glue mixture is greater than 70% n-BCA. Tantalum is messy and can clump, and also the pigment may be visible through the skin in superficial vessels, so most operators usually avoid it in the extracranial circulation. (d) Draw up the Trufill® n-BCA (Codman Neurovascular, Raynham, MA) using a labeled, glue-compatible 3-mL syringe (avoid polycarbonate plastic... it softens). (e) Draw up the Ethiodol® in a labeled syringe, and add the proper volume to the glue syringe. (f) Have several labeled 3-mL syringes filled with 5% dextrose solution ready. Injection (a) Re-confirm proper needle positioning with a small contrast injection.

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(b) Select a projection that shows the needle tip and its relationship to any curves in the arterial feeder distal to the needle, any visible normal branches, and the lesion. (c) Attach a glue-compatible stopcock directly to the needle. One-way stopcocks are sufficient, but three-way are preferred since it allows a flush syringe of dextrose to remain attached even when the glue syringe is attached. Be careful not to move the needle when attaching stopcocks or syringes. (d) Thoroughly flush the needle with 5% dextrose solution. About 2–3 mL is sufficient to clear all saline and/or blood from the needle lumen. As the last mL of dextrose is being injected, close the stopcock to prevent blood backflow into the needle. (e) Make a blank roadmap to make the glue easy to visualize. (f) Attach a 3-mL syringe loaded with the glue mixture and slowly and steadily inject the glue using the blank roadmap. Watch to make sure that the glue column is continuously moving forward during the injection. Fill the arterial feeder and as much of the nidus or tumor bed as possible. (g) Be on the alert for reflux of glue back along arterial feeders, passage of glue into the vein, or reflux of glue through the nidus or tumor bed into other potentially dangerous arterial branches feeding the lesion. If any of these conditions is occurring, with dilute glue it is possible to aspirate to stop forward motion, then after a brief pause, resume cautiously. Sometimes the glue will find another pathway through the nidus. (h) In high-flow AVMs, flow can be controlled during the glue injection by manual compression of draining veins or by placement of a compressive dressing or O-ring [7] over the skin overlying superficial lesions.





(i) Close the stopcock when the glue injection is complete and wait. Polymerization will be complete within a few minutes. Rotate the needle to break the bond with the injected glue and then remove it. (j) Once the needle is removed and hemostasis obtained at the puncture site, do a follow-­ up arteriogram to ensure that the desired result is obtained. If other segments of the lesion remain patent, additional needle punctures and glue injections may be done.

Complications of Percutaneous Injection Procedures Neurological Complications 1. Nerve damage is possible, particularly to the facial nerve, if the sclerosing agent is injected near the nerve. 2. Cranial nerve injury can occur with embolic material entering the blood supply to the nerve. 3. Stroke, blindness, and spinal cord infarction can occur from embolic material reflux or passage through dangerous anastomoses. 4. Large lesions may swell and compress neural structures after treatment. Nonneurological Complications 1. Sclerotherapy in the head and neck can result in ischemia and necrosis of skin, mucosa, or other tissues. 2. Pulmonary embolization is possible during treatment of AV fistulas and venous malformations. 3. Anaphylactic reactions to iodinated contrast or any of the medications used can occur as with any endovascular procedure. 4. Similarly, groin hematomas and other groin arterial injury can occur, as in any endovascular procedure. 5. Anesthesia-related complications can occur.

7.3 Spinal Embolization

7.3 Spinal Embolization Indications: Spinal Embolization 1. Type I spinal dural arteriovenous fistula (dAVF) (not common, but not rare) (a) Preoperative embolization (b) Definitive embolization 2. Type II spinal intramedullary AVM (rare) (a) Preoperative embolization (b) Palliative embolization for symptom reduction (c) Focused embolization of features at risk for bleeding (e.g., intranidal aneurysms) 3. Type III juvenile AVM (very rare) (a) Palliative embolization for symptom reduction 4. Type IV perimedullary AVF (very rare) (a) Definitive embolization (b) Pre-operative embolization 5. Spinal vascular tumors: Pre-operative embolization (a) Hemangioblastoma (rare) (b) Primary bone lesions (e.g., aneurysmal bone cyst) (uncommon) (c) Vascular metastatic tumors (e.g., renal cell cancer, thyroid cancer) (very common)

Awake or Asleep? Use of glue or ethanol can cause considerable pain due to the toxic nature of these agents, and the pain makes it difficult for even sedated patients to remain motionless. General anesthesia eliminates this discomfort and allows the operator to focus on the procedure rather than on coaching and assessing the patient. It can make the procedure much more palatable for anxious patients. Another advantage of general anesthesia is that it allows for patient immobility including prolonged interruption of respiration while imaging tiny spinal vessels. The limited ability to monitor the neurological status of the patient during general anesthesia may be partially mitigated by the use of neurophysiological monitoring, such as somatosensory and/or

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motor evoked potentials. Neurophysiological monitoring adds to the cost and complexity of the procedure, and may not be readily available or reliable, depending on the institution. However, the authors of this handbook find monitoring very useful for spinal embolization, and use it for virtually all embolization of intramedullary lesions, even in awake patients. Less complicated bone or paraspinal soft tissue tumor embolization can be easily done under local anesthesia with minimal sedation, and adequate image quality is possible in cooperative patients. Embolization with the patient awake permits continuous neurological monitoring, eliminates the risks of general anesthesia, can shorten the length of the case, and is done in many centers. The authors of this handbook prefer to do most cases of embolization other than intramedullary spinal embolization awake with conscious sedation, to allow for provocative testing. Vascular navigation in the extracranial circulation is also much less challenging than in intracranial embolization procedures, so it is less critical that the patient remains motionless.

 uide Catheters for Spinal G Embolization Guide catheters for spinal intervention have two special characteristics 1. They have complex curves that allow the catheter to have relatively stable positioning in the transversely oriented spinal branches. 2. They are relatively short (60–80  cm), since that is all that is needed to access these vessels. (a) Standard spinal angiography catheters, like the 5F Mikaelsson and the 5F Simmons I (Merit Medical, South Jordan, UT), are complex-curved catheters that can readily engage side-branches of the aorta. (i) Advantages: Reverse curve provides stability in transverse branches of the aorta. Nonhydrophilic coating makes the catheter more stable in the vessel.

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(ii) Disadvantages: These catheters are soft and may back out and disengage from the vessel as the microcatheter is advanced through it. Microcatheters fit tightly in these catheters, so guide catheter angiograms cannot usually be done while the microcatheter is in place. (b) The 4F angled Glidecath® (Terumo Medical, Somerset, NJ) [5] and 4F Berenstein II (Cordis Endovascular, Miami Lakes, FL) [67] can be advanced distally into the intercostal or lumbar arteries. The usual technique for these catheters is use a standard spinal angiography catheter to first engage the spinal artery and then exchange it for the 4F catheter over an exchange-length wire [67]. (i) Advantages: Soft, atraumatic tip. Minimizes risk of vasospasm and dissection in narrow and tortuous vessels. When placed distally in a segmental vessel, these catheters are a fairly stable platform for 10-system microcatheters. (ii) Disadvantages: Relatively flimsy and prone to becoming displaced, especially when the vasculature is tortuous. Requires the use of an exchange wire to access the lumbar or intercostal artery. Larger caliber microcatheters may not easily pass through these catheters. Even small microcatheters are a tight fit and it is not possible to inject contrast around the microcatheter. (c) 6 and 7F coronary guide catheters like the Runway™ (Boston Scientific, Marlborough, MA) can be obtained with various curves such as the Amplatz left or allRight™ curve that can engage segmental spinal vessels. (i) Advantages: Very stable platforms with gigantic internal lumen. Will accept various devices and microcatheters with room to spare for contrast injections.

7  Extracranial and Spinal Embolization

(ii) Disadvantages: These big, stiff catheters can be traumatic to the vessel and are not easily used in tortuous vessels. May not engage vessels that arise at a sharp angle from the aorta. Often require the use of an exchange wire to access the vessel of interest. (d) Standard 5 and 6F guide catheters such as the Envoy® (Codman Neurovascular, Raynham, MA) or Guider Softip™ XF (Stryker Neurovascular, Fremont, CA) work well if spinal vessels in the cervical or upper thoracic region are accessed through subclavian artery branches.

 uide Catheter Technique: Segmental G Spinal Arteries 1. Direct navigation method: Useful in young patients with non-tortuous, non-­ atherosclerotic vessels, and when using a catheter with a complex, reverse curve shape. (a) Flush the catheter with heparinized saline and attach it to an RHV with continuous flush. (b) Advance the hydrophilic wire to the tip of the guide catheter to stiffen it and allow passage through the valve in the hub of the sheath. Use the peel-away introducer to insert the tip of the catheter into the sheath, but do not peel it off. Just slide it back to the hub of the catheter to keep it out of the way and available to use again if needed. (c) Advance the catheter over the hydrophilic wire into the abdominal aorta. Reconstitute the shaped catheter by one of two methods: (i) If the hydrophilic wire can easily be advanced into the contralateral iliac artery or a renal artery, the curve of the complex curve catheter (e.g., Mikaelsson or Simmons) may be formed by advancing the catheter just enough to engage the renal or iliac artery. Then, withdraw the hydrophilic wire into the catheter and gently push and rotate the catheter to form the curve.

7.3 Spinal Embolization









2.



3.

(ii) Alternatively, advance the catheter into the aortic arch. When the hydrophilic wire is pulled back, the catheter usually reconstitutes as the catheter is rotated. (d) Withdraw the wire completely and double flush the catheter with heparinized saline. (e) Position the tip of the catheter at the target spinal level. With small puffs of contrast, gently rotate and manipulate the catheter tip into the origin of the segmental artery. Gently pull the catheter back to advance it into the segmental artery for 1–2 cm to obtain a stable position. (i) If the catheter does not advance into the vessel when it is pulled back, park it at the origin of the artery and place a microcatheter into the artery over a microwire. The guide catheter can then be pulled back, advanced forward, or rotated very gently into a more stable position. Movement that is too vigorous will push the guide catheter back into the aorta. (f) Occasionally, in younger patients with large segmental spinal arteries, a simple curved guide catheter can be manipulated into a segmental artery using a steerable hydrophilic wire such as a 0.035  in. or 0.038  in. Glidewire® (Terumo Medical, Somerset, NJ). Exchange method: Useful when using a 4F guide catheter and also often when using larger coronary-type guide catheters. (a) Place a 5F diagnostic spinal catheter in the segmental spinal artery over an exchange length (270–300 cm) wire, usually a hydrophilic wire like Glidewire® (Terumo Medical, Somerset, NJ). (b) Advance the tip of the wire into a distal branch of the artery using a roadmap. (c) Exchange the diagnostic catheter for the guide catheter under fluoroscopy. Optimizing guide catheter position in spinal cases (a) Guide catheter stability can be a huge problem in spinal embolization cases given the continual movement of the vessels with respiration and the fairly proxi-

437



4.

5.

6.

mal guide catheter position that is necessary in many cases. In a lumbar or intercostal artery with a significant proximal curve, the guide catheter may easily advance beyond the origin of the vessel. Moderate curves in the vessel usually cannot be straightened out by guiding a relatively stiff catheter around them, and may cause spasm or even dissection. If added guide catheter stability is needed, a relatively stiff 0.014 inch wire can be advanced through the guide catheter as a buddy wire, and if the catheter has a large enough lumen, a microcatheter can be advanced along side it. The buddy wire will help keep the guide catheter in place. Buddy wires cannot be used when 5F or smaller catheters are used as guide catheters. (b) Many times only very tenuous catheter positioning is possible, and one must keep an eye on the guide catheter position constantly during the case and gently adjust its position as necessary. Guide catheter irrigation (a) Continuous irrigation of the guide with heparinized saline (5000  U heparin per 500-mL saline) is important. Contrast injections (a) Frequent puffing of contrast can be used to help manipulate the guide catheter into spinal segmental arteries. A 20-mL syringe containing contrast can be left attached to the catheter for these injections, and then used immediately for hand injections of contrast for angiographic runs. As is done in the cerebral arteries, the syringe is held vertically with care not to allow bubbles to enter the catheter. Spinal arteries are best imaged with hand injections of contrast, to allow for modulation of the injection rate and volume, depending on the size of the vessel and stability of the catheter. Maintaining guide catheter position (a) Monitor the position of the guide catheter constantly during the microcatheter access and embolization phases of the procedure.

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(b) The guide catheter may become displaced during microcatheter navigation, which can result in kinking of the microcatheter and can cause sudden, undesired displacement of the microcatheter. (c) Any displacement of the guide catheter tip should be corrected. If the guide catheter becomes too unstable, consider replacing it with a more stable guide catheter. (d) Consider use of a 0.014 inch, 300  cm buddy wire advanced in the distal segmental artery to stabilize the guide catheter [68].

 echniques and Tips on Spinal T Embolization for Specific Lesions See Chap. 20 for details about spinal vascular lesions.

7  Extracranial and Spinal Embolization

6. Onyx® (Medtronic, Minneapolis, MN) embolization via a Scepter® dual lumen balloon (Microvention, Alisa Viejo, CA) allows for flow control and helps prevent reflux [68, 76, 77]. The Scepter® Mini balloon has also been reported for spinal AVF embolization [78]. 7. A post-embolization CT, confirming intradural venous location of the glue column, is a good way to predict who will have a long-­ term cure [54]. 8. Both surgery and endovascular treatment can lead to improvement in gait but not bladder dysfunction if the symptom duration prior to treatment is >1 year [79]. 9. Several groups advocate an attempt at endovascular treatment first, reserving surgical treatment for unsuccessful embolization [80, 81]. 10. Close clinical and imaging follow-up is needed in all spinal fistula patients. Recurrence of symptoms after successful treatment should prompt a full angiographic workup, since collaterals may enlarge to supply the fistula and even remote new fistulas may develop [74].

Type I spinal dural arteriovenous fistulas (dAVF) 1. Caution! In 14% of dAVF patients the feeder and the normal origin of the anterior or posterior spinal artery (such as Adamkiewicz) arise from the same segmental artery [69]. 2. Particle embolization of dAVFs has been shown to be a temporary solution, and recur- Type II spinal intramedullary AVMs rence is the rule and not the exception [70, 1. Carefully study the spinal angiogram to determine all arterial feeders, draining veins, and 71]. Embolization with n-BCA is more effecthe relationship of the AVM with normal spitive, with 55% improvement in gait and a nal cord vessels. Look for associated feeding 15% recurrence rate [72]. Embolization with artery and intranidal aneurysms. Do not treat Onyx has also been reported [73]. the lesion until the anatomy is thoroughly 3. A contraindication to embolization is a spiunderstood and a plan of action has been nal cord feeder arising from the same radicuformulated. lar artery supplying the fistula, which is 2 . Slow PVA particle embolization has been present in approximately 6% of cases [74]. advocated for intramedullary AVMs [82, 4. Endovascular treatment consists of full-­ 83]. The endpoint of particle embolization column n-BCA injection in the radicular can be objectively determined by serial artery feeding the fistula with glue dilute provocative testing (stop when the provocenough to be pushed through the fistula into ative testing shows neurological changes) the intradural vein. and/or serial pressure measurements from 5. The authors of this handbook frequently the microcatheter (stop when the microplace a microcoil in the lumbar or intercostal catheter pressure rises to 90% of systemic feeder beyond the radicular branch, to prepressure) [5]. However, AVMs treated with vent the glue from entering muscular particle embolization frequently recanalize branches. Embolization of muscular [70, 84]. branches can cause severe pain [75].

7.3 Spinal Embolization

3. Embolization with n-BCA may be more effective and safer than particle embolization in experienced hands [2, 85]. 4. Monitoring with SSEPs and MEPs, as well as provocative testing prior to embolization, may reduce the risk of complications [2–4, 86]. 5. Catheterization of the nidus with a flow-­ directed microcatheter is the goal, with a careful full column glue injection after a negative provocative testing. 6. Aneurysms associated with the AVM should be specifically targeted for embolization to reduce the risk of AVM bleeding [87]. 7. A study 17 patients with intramedullary AVMs treated with Onyx® embolization reported a 37% acute cure rate; 82% had a good clinical result with no permanent neurological procedural complications [88, 89]. 8. A study of functional and emotional quality of life in spinal cord AVM patients after embolization showed significantly worse scores compared to patients with post-traumatic spinal cord problems [90]. This suggests that further improvements in treatment of these patients are necessary. Type III juvenile AVMs 1. These diffuse AVMs with cord and segmental spinal and paraspinal nidus are difficult to treat, or at least to cure, but are extremely rare. 2. Palliative embolization with glue or Onyx® for symptom reduction has been reported [91, 92]. 3. Successful surgical resection following embolization has been reported [93–96]. Combined arterial and venous embolization followed by surgical resection of a large AVM associated with Cobb syndrome has also been reported [97]. Type IV perimedullary AVFs 1. These lesions are rare perimedullary fistulas without an intervening nidus. They can present with hemorrhage or progressive myelopathy. They can have multiple arterial feeders and prominent congestion of the perimedullary veins that can make the angiogram challenging to figure out.

439

2. As with all spinal vascular malformations, a high-quality spinal angiogram and a thorough visualization and understanding of the vascular anatomy and pathology are mandatory before considering treatment. 3. Preoperative embolization via a transarterial route has been successful and reported in several small series [98–101]. 4. Surgical treatment is reserved for accessible fistulas and for those in which embolization failed to occlude the fistula [102, 103]. 5. Conus and filum terminale AVFs are usually best treated surgically [85, 103]. 6. Some large fistulas (so-called Type IV-c lesions) can be treated with transvenous coiling either via a standard transfemoral venous approach [102] or through surgical access to the dilated veins [104]. 7. Primary endovascular treatment for giant fistulas with detachable balloons in 10 patients reported six good clinical results and one complication caused by migration of the balloon into the draining vein [55]. 8. A French study of transarterial n-BCA embolization reported a 67% rate of angiographic cure; 22% had transient neurological deficits, but all had improvement at follow-up [105]. Clinical improvement was stable in cases in which complete angiographic cure was not obtained [106]. 9. Use highly concentrated n-BCA preparations (≥70%) for high-flow fistulas. 10. Careful and complete angiographic follow­up is needed in these patients, since they can develop co-existing separate Type I dural fistulas, which likely develop because of venous hypertension [107]. Epidural and paraspinal AVFs 1. These are rare congenital or acquired fistulas often presenting with radiculopathy, but occasionally with myelopathy if venous drainage backs up into the spinal cord veins [108, 109]. 2. Treatment may be transarterial embolization, or surgical interruption of the radicular veins that provide the conduit for arterialized blood to the intradural veins.

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Spinal vascular tumors: Pre-operative embolization 1. Preoperative embolization of spinal cord hemangioblastomas has been reported [110, 111]. One of four patients undergoing preoperative embolization for thoracolumbar hemangioblastomas had transient worsening myelopathy [112]. 2. Vascular tumors in the spinal region, most commonly metastatic renal cell cancer or less commonly thyroid cancer, seem to benefit greatly from preoperative particle embolization [113–115]. 3. Primary bone lesions (e.g., aneurysmal bone cyst) can benefit from preoperative particle embolization. 4. Do a vigilant angiographic search for collateral connections to normal spinal cord arteries. Serial provocative testing with clinical and/or SSEP and MEP monitoring can reduce the risk of inadvertent passage of emboli to the spinal cord circulation [114]. 5. Symptomatic spinal osseous hemangiomas may benefit from transarterial preoperative embolization [116] or percutaneous vertebroplasty [117]. These lesions may also be treated with direct needle puncture and ethanol injection, but the total ethanol volume should be kept 50% intracranial stenosis who have failed medical therapy, balloon angioplasty with or without stenting should be considered. 2. Patients who have an asymptomatic intracranial arterial stenosis should first be counseled regarding optimizing medical therapy. There is insufficient evidence to make definite recommendations regarding endovascular therapy in asymptomatic patients with severe intracranial atherosclerosis. They should be counseled regarding the nature and extent of their disease, monitored for new neurological symptoms, and have periodic noninvasive imaging (MRA or CTA) at regular intervals of 6–12 months initially, and later with cerebral angiography if warranted. Optimal prophylactic medical therapy should be instituted, which might include antiplatelet and/or statin therapy. 3. Continued evaluation and improvements in both pharmacological and catheter-based therapies are needed to reduce the possibility of stroke from intracranial atherosclerosis. *ASITN, American Society of Interventional and Therapeutic Neuroradiology; SIR, Society of Interventional Radiology; and ASNR, American Society of Neuroradiology.

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10  Endovascular Treatment of Intracranial Stenosis and Vasospasm

 urrent FDA Indications for Use C of Wingspan Stent Following the release of the SAMMPRIS results, the FDA changed the indications for its use under the HDE designation [15]. 1. Wingspan is approved for patients between 22 and 80 years of age, and who meet all the following criteria: 2. Have had two or more strokes in spite of aggressive medical management. 3. Most recent stroke occurred greater than 7 days prior to treatment with Wingspan. 4. Stenosis of the vessel in the territory of the two stokes is 70–99%. 5. Recovery since the last stroke must be sufficient to allow for modified Rankin scale of 3 or better. 6. Wingspan should not to be used: (a) For treatment of vessel causing symptoms with onset within 7 days. (b) For treatment of vessel causing only TIAs without stroke.

Other Contraindications 1. Patient inability to have antiplatelet therapy and/or anticoagulation. 2. Highly calcified lesions or anatomy, which prevents endovascular access.

10.3 Pre-procedure Preparation 1. Informed consent 2. Dual antiplatelet therapy. (a) Do platelet function testing if desired (see Chap. 4). 3. Two peripheral IVs. 4. Foley catheter. 5. NPO after midnight or 6 h prior to the procedure except for medications. 6. Ensure all devices required are available in the angio suite prior to the procedure.

10.4 Endovascular Technique The access phase involves placing a guide catheter in the internal carotid or vertebral artery. The intervention phase includes advancing a microwire across the stenotic lesion, followed by angioplasty with or without stent deployment.

Awake or Asleep? Intracranial angioplasty can be uncomfortable, as stretching and pulling on intracranial vessels are painful. Although the authors of this Handbook use general anesthesia in most cases and the SAMMPRIS protocol required the used of general anesthesia, good results have been obtained without anesthesia. Avoiding anesthesia permits continuous neurological surveillance and eliminates anesthesia-associated risks: 1. Patients who are awake should rehearse the neurological exam on the angio suite table prior to draping. A squeeze toy should be placed in the patient’s hand contralateral to the side being treated. 2. In a report of 37 intracranial angioplasty and stenting cases without general anesthesia, technical success was achieved in all patients [16]. About 61% experienced intra-procedural symptoms that led to some alteration of the interventional technique. Headache was the most common symptom, and, when persistent, signaled the occurrence of intracranial hemorrhage.

Access Phase Patients with intracranial atherosclerosis are also prone to extracranial disease. The reader is referred to Chap. 9, Extracranial Angioplasty and Stenting, for a detailed discussion of access techniques and tips for difficult situations. Compared to other intracranial procedures, angioplasty procedures require extra-rigid guide catheter support.

10.4 Endovascular Technique

1. Obtain guide catheter access in the usual manner (see Chap. 4). 2. Systemic anticoagulation. Thromboembolic complications can occur during angioplasty, when there is slowing of flow in the parent vessel caused by the guide catheter, or in the target vessel by the microwire or angioplasty balloon. 3. A loading dose of IV heparin is given (5000 units or 70 units/kg). Additional doses of heparin are necessary only for cases lasting several hours. 4. Protamine on standby—Critical: (a) A syringe containing enough protamine to reverse the total amount of heparin the patient has received should be kept on the back table for easy access to the operator, should hemorrhage occur: (i) Dose of protamine required to reverse heparin: 10  mg protamine/1000  U heparin. 5. Guide catheter selection and positioning: (a) The guide catheter should be 90 cm long (and not longer) for use with the Wingspan stent system. (b) Guide catheter support is more important for intracranial angioplasty procedures than most other intracranial interventions. Angioplasty balloons and stents are relatively rigid and difficult to navigate; forward motion of these devices can cause unexpected high amounts of downward-­ directed force on the guide catheter. Therefore, due caution should be used in guide catheter selection and positioning. (c) Stiffer guide catheters and positioning of the guide catheter as high as possible helps to maximize support for the intervention. (d) The catheter tip may slide up and down and rub against the vessel wall with each heart beat; this is to be taken into account when positioning the catheter.

Intervention Phase Once the guide catheter is in position, a good working view must be obtained. The working

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view should be under high magnification and demonstrate the target lesion and distal vessels, and guide the catheter clearly. In most situations, a microcatheter is advanced through the stenotic intracranial vessel over an exchange-length microwire. The purpose of the microcatheter is to facilitate atraumatic and smooth passage of the microwire into a distal vessel; the microcatheter is then removed and the balloon is guided over the microwire into position within the region of stenosis. If stenting is planned, the “pre-dil” balloon is removed and a self-expanding stent (e.g., Wingspan™, Stryker, Fremont, CA) is deployed. Alternatively, a balloon-mounted stent (e.g., PHAROS™ Vitesse™, Codman Neurovascular, San Jose, CA) is navigated into position and the stent is deployed.

Device Selection Essential devices for intracranial angioplasty include an exchange-length microwire, a microcatheter, and a balloon. The Wingspan™ Stent System with Gateway™ PTA Balloon Catheter (Stryker, Fremont, CA) was specifically designed for intracranial angioplasty and stenting. It is available on a Humanitarian Device Exemption basis; the use of the Wingspan system currently requires Institutional Review Board (IRB) approval. The Wingspan devices and technique are discussed in detail in a separate section below. The PHAROS™ Vitesse™ (Codman Neurovascular, San Jose, CA) balloon-­ expandable stent is an alternative to the Wingspan stent and is also covered in a separate section below. 1. Microwires: (a) “Beefiness,” trackability, and torque control are microwire properties that are most important for intracranial angioplasty. A relatively soft distal tip is helpful as well, to minimize the chances of distal vessel vasospasm and perforation. (b) The authors prefer the following microwires for most cases: (i) Transend™ 0.014 in. 300 cm Floppy Tip (Stryker, Fremont, CA):

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10  Endovascular Treatment of Intracranial Stenosis and Vasospasm

• Superior torque control, compared to other microwires. • Heightened radio-opacity makes the tip easy to see on fluoroscopy. (ii) Aristotle™ 0.014  in. 300  cm Soft (Scientia, West Valley, UT): • Supreme torque control. • Better tip-shape retention. (iii) X-Celerator™ 0.014  in. 300  cm (Medtronic, Minneapolis, MN): • Soft tip, relatively supportive body, very lubricious. 2. Microcatheters: (a) A low-profile, straight microcatheter, usually of any kind, is sufficient. (b) The 1.7F Echelon-10 microcatheter (Medtronic, Minneapolis, MN) can navigate through tortuous and stenotic vessels easier than other microcatheters. 3. Angioplasty balloons: (a) Noncompliant coronary angioplasty balloons are designed to create sufficient radial force to dilate vessels thickened by atherosclerotic plaque. NC: noncompliant: (i) Selected balloons: • Gateway™ PTA Balloon Catheter (Stryker, Fremont, CA) is used with the Wingspan stent (see below). • Maverick2™ Monorail™ balloon Catheter (Boston Scientific, Natick, MA). • NC Raptor™ balloon catheter (Cordis, Miami, FL). • Size: –– The diameter of the balloon should correspond to or be smaller than the normal diameter of the vessel; 2.0–2.5  mm diameter balloons are usually appropriate. –– The length of the balloon should be kept to a minimum to optimize trackability. 4. Stents: (a) Wingspan (see below). (b) Balloon-mounted coronary stents are not FDA approved in the intracranial circula-







tion. The intracranial arteries, which float freely in cerebrospinal fluid (CSF), are not surrounded by fibrous connective tissue like coronary arteries and they are more vulnerable to dissection and perforation during deployment of balloon-­ mounted stents. Relatively high complication rates have been reported with balloon-mounted coronary stents [16–18]. (i) If a balloon-mounted coronary stent must be used, cobalt–chromium coronary stents are the easiest to deliver compared to other balloon-mounted stents [16]. (ii) The PHAROS™ Vitesse™ (Codman Neurovascular, San Jose, CA) is a balloon-mounted stent specifically designed for the intracranial circulation, although the prospective VISSIT trial showed outcomes worse than medial therapy using this device [12]. (iii) There is increasing interest in use of coronary drug-eluting stents for intracranial atherosclerotic stenosis [19]. • A single-center report of a database including 58 patients treated using Resolute Onyx™ (Medtronic, Minneapolis, MN) and 126 patients treated with Wingspan. –– Reported better outcomes with the coronary stent compared with Wingspan including lower incidence of restenosis. –– Certainly, using a rapid-­exchange balloon-­mounted stent is a simpler procedure compared with the multiple exchanges required for Wingspan. –– Study included patients within 7  days of last stroke, which is off-label for Wingspan. The implication is that this would be expected to result in worse outcomes compared to on-­ label usage of Wingspan.

10.4 Endovascular Technique

Angioplasty Without Stent Deployment Angioplasty alone is less morbid than angioplasty and stenting with balloon-expandable stent. A systematic review of submaximal angioplasty for intracranial stenosis showed a pooled peri-procedural 30-day stroke rate of 4.9% and 3.7% after 30 days [20]. By itself, angioplasty is a reasonable option for patients with symptomatic intracranial stenosis, particularly because intracranial stenting has not yet been shown to reduce the risk of stroke, and the use of a stent (even the Wingspan system) adds complexity and expense to the procedure. The balloon should be sized to cover the length of the lesion, and the diameter should be ≤ the normal diameter of the vessel.

Wingspan Procedure The manufacturer of the Wingspan™ Stent System with Gateway™ PTA Balloon Catheter has obtained a Humanitarian Device Exemption from the U.S. FDA. The system is authorized for use in improving cerebral artery lumen diameter in patients with intracranial atherosclerotic disease, refractory to medical therapy, in intracranial vessels with 70–99% stenosis that are accessible to the system. An IRB approval is currently necessary to use the system. 1. Devices (a) Guide catheter should be ≥6F and ≤90 cm long. (b) Microwire. Synchro2™ or Transend™ 0.014  in. Floppy Tip (Boston Scientific, Inc., Natick, MA) is the recommended microwire. Use an exchange-length microwire (300 cm) to maintain microwire access after stent placement in case additional stent placement or post-stent angioplasty is needed. (c) Gateway™ PTA Balloon Catheter: (i) The Gateway™ is a modified version of the Maverick2™ balloon catheter, with silicone coating on the balloon

571

and hydrophilic coating on the catheter to facilitate access. Radio-opaque markers on the balloon permit visualization of the proximal and distal ends of the balloon on fluoroscopy. (ii) Available sizes: • Balloon diameters (mm): 1.5, 2.0, 2.25, 2.75, 3.0, 3.25, 3.5, 3.75, 4.0. • Balloon lengths (mm): 9, 15, 20. • Nominal inflation pressure: 6 atm. Rated burst pressure: 12  atm. (14 atm. For 2.25–3.25 mm diameters only). (iii) Size selection: • Plan angioplasty to achieve approximately 80% of normal vessel diameter. For example, for a vessel with a 3.0 mm normal diameter, angioplasty to produce a diameter of about 2.4  mm would be appropriate. • If the target vessel has different diameters proximal and distal to the lesion, size the balloon to the smaller of the two. (iv) Preparation: • Use 50/50 mixture of contrast in heparinized saline. • Prepare the inflator and attach it with a three-way stopcock and an empty 20-mL syringe to the balloon catheter. • Apply suction to the balloon but do not pre-inflate it. • Continuously flush through the lumen of the balloon catheter with heparinized saline via a stopcock and a rotating hemostatic valve. (d) Wingspan™ Stent: (i) The Wingspan is a 3.5F nitinol over-­ the-­wire (OTW) self-expanding stent. The design is very similar to the Neuroform2™ stent (Boston Scientific, Natick, MA); it has four platinum markers at each end for visualization, and is deployed from the delivery microcatheter (called the outer body) with the inner body. The

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10  Endovascular Treatment of Intracranial Stenosis and Vasospasm

inner body is analogous to the stabimicrowire can be advanced into a dislizer device that is used to deploy tal intracranial vessel within a microNeuroform stents. catheter, which can be exchanged for (ii) Available sizes: the Gateway balloon. • Stent diameters (mm): 2.5, 3.0, 3.5, (ii) After flushing, advance the balloon 4.0, 4.5. catheter over the microwire into the • Stent lengths (mm): 9, 15, 20. guide catheter. When positioned at the (iii) Size selection: RHV, a marker on the balloon catheter • Select a stent length that extends a shaft indicates the guide catheter tip. minimum of 3 mm on both sides of This feature saves fluoroscopy time. the lesion. (iii) With roadmap guidance, advance the • If the target vessel has different balloon until the balloon markers are diameters proximal and distal to across the lesion. Perform a guide the lesion, size the stent to the catheter angiogram with the balloon in larger of the two. position, to confirm proper • After deployment, the stent may positioning. shorten up to 2.4% in 2.5  mm (iv) Inflate the balloon slowly to nominal stents and up to 7.1% in 4.5  mm pressure, at a rate of ~1  atm./10  s, stents [21]. under fluoroscopy. When the balloon (iv) Preparation: is fully inflated, leave it up for another • Flush the Wingspan system with 10–20 s and then deflate. Do a guide heparinized saline, as indicated in catheter angiogram prior to removing the diagram on the package. the balloon. • The more flushes, the better. (v) In most cases a single inflation will be Continuous flushes with heparinsufficient. Occasionally, a second ized saline should be connected via inflation at a slightly higher pressure stopcocks and RHVs to both the (e.g., 8 atm.) is helpful. Wingspan deployment catheter (b) Stent deployment: (the outer body) and the inner (i) Tighten the RHV on the inner body to body. prevent migration and advance the • Loosen the tapered tip of the inner outer body of the Wingspan system body slightly, with about 1 mm of over the exchange-length microwire: space between the spearhead-­ • The delivery system should be shaped tip of the inner body and advanced only by grasping the the distal end of the outer body, to outer body, to avoid inadvertently allow adequate flushing and preadvancing the inner body and prevent corking, or binding, of the maturely deploying the stent. inner body tip to the outer body (ii) Advance the outer body slightly past catheter. Heparinized saline should the region of stenosis. be seen dripping from the inner (iii) Using the marker bands to identify the lumen and from between the inner position of the stent, advance the inner and outer bodies. body just proximal to the stent. 2. Technique: (iv) Pull back on the outer body, to bring (a) Angioplasty: the outer body tip into position just (i) The Gateway balloon may be taken up past the region of stenosis; this should primarily, over a nonexchange-­length be the final maneuver prior to stent microwire, if the anatomy is favorable. deployment. Alternatively, an exchange-­ length

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10.6  Intracranial Angioplasty Tips



(v) Deploy the stent by holding the inner body in a stable position with the right hand, while, with the left hand, slowly withdraw the outer body. • Do not attempt to change the position of the stent during deployment. (vi) Once the stent is deployed, bring the deployment system into the proximal part of the vessel, or into the guide catheter, while leaving the microwire in position. Do a guide catheter angiogram. 3. Gateway and Wingspan tips [21] (a) Do not overtighten the RHV around the balloon catheter shaft. (b) If the balloon is difficult to inflate, remove it and use another device. (c) If the balloon “watermelon-seeds” (i.e., slips forward or backward during inflation): (i) Apply gentle traction to the balloon catheter during inflation, to stabilize the balloon and prevent it from migrating distally during inflation, or. (ii) Select a longer balloon. (d) If the stent system binds with the microwire during navigation through tortuous vessels: (i) Affirm that adequate flush is being applied to both the inner and outer body catheters. (ii) Try a softer microwire (e.g., Synchro2®-14, Stryker, Fremont, CA). (e) Keep in mind that the tapered tip of the inner body extends for 10–12 mm past the distal tip of the outer body, and is radiolucent (in contrast to the Neuroform system, which does not have anything that extends out of the deployment catheter). Care should be taken to avoid jamming the distal end of the system into a curving vessel. (f) Once the stent catheter is advancing over the microwire, advantage may be taken of the forward momentum and tracking continued to a site distal to the lesion. It is

easier to move the system from distal to proximal than vice versa. (g) If the stent is malpositioned during deployment, consider placing a second stent.

10.5 Post-procedure Management 1. Complete neurological exam. 2. Admit to the neuro intensive care unit (NICU) or step-down unit with neuro exams and groin checks Q 1 h. 3. Antiplatelet therapy: (a) Antiplatelet therapy: Aspirin 325 mg per oral (PO) QD indefinitely, and. (b) Clopidogrel (Plavix®) 75 mg PO QD for ≥30 days after the procedure. (i) Note: Some operators maintain patients on dual antiplatelet therapy for 3–6 months, longer than is usually done for cervical carotid or Neuroform stent cases. Cardiologists are recently moving toward longer periods of dual antiplatelet treatment (3, 6, or 12 months) after coronary angioplasty and stenting [22]. It can be argued that atherosclerotic intracranial arteries are similar in size and pathology to similarly diseased coronary arteries. Or (c) Antiplatelet therapy: Aspirin 325 mg PO QD indefinitely, and (d) Ticlopidine (Ticlid®) for 30  days after the procedure. (i) Note: Monitor for neutropenia. 4. Most patients can be discharged from the hospital post-procedure day 1 or 2.

10.6 Intracranial Angioplasty Tips 1. Operator experience and careful patient selection were shown to be critically important to improve outcomes, as was shown in the WEAVE study [23]. No Class I data exist yet to show that intracranial angioplasty and

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10  Endovascular Treatment of Intracranial Stenosis and Vasospasm

stenting is beneficial to patients; therefore, the odds must be stacked in the patient’s favor. Patients undergoing intracranial angioplasty should be managed by experienced operators or not treated by endovascular methods at all. 2. All devices needed for the procedure are to be prepared before the case, immediately prior to the groin stick, and placed in a stack on the back table or at the foot of the patient’s table, with each device separated by a sterile towel in the order that they will be used. This will permit rapid and efficient access to each device as required. 3. A hand-injection angiogram has to be done after each step, to check for contrast extravasation, dissection, intraluminal thrombi, positioning of devices, and documentation. If a complication should arise during or after the case, a complete set of angiograms can help sort out and manage the problem. 4. If the patient is awake, a brief neurological exam after each step of the procedure has to be completed. 5. Overdilation during angioplasty must be avoided. It is better to undersize the angioplasty balloons than to oversize them. 6. In-stent restenosis: (a) Consider endovascular treatment only if the in-stent stenosis is symptomatic. (b) If treatment is necessary, consider doing a redo angioplasty with or without another stent. (c) Consider use of a drug-eluting coronary stent.

10.7 Management of Intracranial Complications During or After Intracranial Angioplasty 1. Prompt recognition of a change is critical. 2. If an abrupt change in blood pressure or heart rate occurs, or if a neurological change occurs in an awake case: (a) Obtain antero-posterior (AP) and lateral intracranial angiograms. (b) Look for contrast extravasation and other signs of vessel perforation (such as a

wire tip in the wrong location), intraluminal thrombus, intracranial vessel dropout, or slowing of contrast passage through distal intracranial vessels (indicates a shower of emboli into multiple small branches). (c) Look for signs of dissection caused by devices. 3. Options for thrombolysis if needed: (a) IV GP IIb/IIIa inhibitor (e.g., eptifibatide or abciximab): (i) Advantages: Powerful antiplatelet agent, particularly useful for platelet-­rich thrombosis, which can occur with stent deployment. (ii) Disadvantages: Carries a risk of ICH [24], relatively long half-life. (iii) The authors prefer abciximab, which, unlike eptifibatide, can be reversed with platelet transfusion if necessary: • Abciximab: • Loading dose of 0.25 mg/kg, followed by a 12-h intravenous infusion at a rate of 10 μg/min. • Eptifibatide: • Loading dose of 135  μg/kg followed by a 20–24  h infusion of 0.5 μg/kg/min. (b) Intra-arterial (IA) thrombolytic (e.g., tPA or urokinase): (i) Advantage: Short half-life. (ii) Disadvantages: May not be as effective as a GP IIb/IIIa inhibitor if the thrombus is platelet-rich. Also carries a risk of ICH. 4. Intracranial hemorrhage (a) Suspect a hemorrhage if sudden hypertension or bradycardia occurs, or if the patient complains of a headache. (b) Do an angiogram to look for contrast extravasation. (c) If ICH is identified: (i) Reverse heparin with protamine (10 mg IV per 1000 units of heparin given). (ii) Maintain tight blood pressure control.

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(iii) Platelet transfusion (to reverse antiplatelet medications). (d) Obtain a head computed tomography (CT); leave the sheath in place for the trip to the scanner. 5. Post-procedure neurological change (a) Obtain head CT. (b) Consider return to the angio suite for a diagnostic angiogram and possible intra-­ arterial thrombolysis. 6. When angiography or CT imaging does not explain a neurological change, consider magnetic resonance imaging (MRI) with diffusion-­ weighted imaging, which can identify subtle ischemic changes.

10.8 Ophthalmic Artery Angioplasty for Age-Related Macular Degeneration Age-related macular degeneration is a cause of progressive blindness in the elderly. Although the blood supply to the choroid is not the primary cause of the disease, decreased perfusion may contribute to the progression of the disease [25]. Lylyk et al. describe a retrospective series of ophthalmic artery angioplasty in five patients with advanced stages of macular degeneration [26]. The patients’ visual acuity improved after the procedure. No objective measurement of perfusion such as using optical coherence tomography is reported. Could this study be a good example of the power of the placebo effect? The study’s authors admit that ophthalmic artery angioplasty is technically very challenging, and that more thorough investigation is required before this procedure can be widely recommended.

10.9 Endovascular Treatment of Cerebral Vasospasm Indications for Endovascular Treatment of Cerebral Vasospasm 1. New onset of a neurologic change not due to other causes.

2. Radiographic evidence of ischemia due to vasospasm in a brain territory that corresponds to the neurologic deficit, with or without prior treatment with hyperdynamic therapy: (a) A trial of hyperdynamic therapy is first-­ line for vasospasm prior to resorting to angioplasty [27, 28]. (b) In contrast to treatment of acute ischemic stroke, evidence of infarction on CT is not necessarily a contraindication to treatment: (i) In a series of 17 cases in which angioplasty was done despite a CT scan showing a new hypodensity, there was no hemorrhages or worsening of symptoms [29]. There was resolution of the CT hypodensities in 5 of the 17 patients and a majority of the patients improved clinically. 3. Balloon angioplasty is an option for symptomatic vasospasm affecting intracranial arteries >1.5 mm in diameter [30], such as the intracranial ICA, the M1, A1, and the vertebral and basilar arteries and P1 segments. 4. Intra-arterial injection of pharmacologic agents is an option for vessels that are not accessible or safely treatable with a balloon, such as distal ACA or MCA branches, or the A1 segment (which can be difficult to reach with a balloon).

Awake or Asleep? Symptomatic vasospasm typically manifests as confusion and a decline in the level of consciousness, making it difficult for patients to cooperate with an endovascular procedure. General anesthesia makes the procedure easier and safer. A practical alternative to general anesthesia is to intubate the patient prior to the procedure (usually in the NICU) and place him or her on a mechanical ventilator with chemical paralysis and continuous analgesia and sedation.

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Techniques Access Phase The procedure for carotid or vertebral artery access for vasospasm is nearly identical to that used for angioplasty for atherosclerotic intracranial stenosis as seen above. Several issues pertinent to treatment of vasospasm are: 1. Guide catheter positioning depends on whether balloon angioplasty is planned, or if IA drug infusion only is anticipated. Balloon angioplasty requires the guide catheter be placed as high as possible, for maximal support, whereas drug infusion through a microcatheter can be accomplished with the guide catheter in a relatively low position. 2. Use of systemic heparin: (a) Systemic heparinization can be used in selected patients, but is associated with theoretical increased risk of hemorrhage in postcraniotomy patients: (i) Procedural anticoagulation with systemic heparinization can be done safely in SAH patients with a ventriculostomy [31, 32].



(ii) Systemic heparinization in patients with a recent craniotomy carries a 1.8% risk of major hemorrhage [33]. (b) Systemic heparin should be reserved for cases in which there is guide catheter-­ induced interruption of antegrade flow in the access vessel, or a relatively long period of interruption of flow in an intracranial vessel due to the microcatheter or angioplasty balloon: (i) A loading dose of IV heparin is given (70  U/kg) and 5  min later, a 5-mL specimen of blood for an activated clotting time (ACT) is drawn from the sheath. The ACT should be kept between 250 and 300  s for the duration of the procedure.

Balloon Angioplasty 1. Device selection: (a) There are two views about the kind of balloon to use to treat vasospasm, i.e., compliant or noncompliant balloons. The arguments for and against each kind of device are summarized in Table  10.1.

Table 10.1  Balloon selection for angioplasty for vasospasm Advantages Compliant balloons • More easily placed in small, tortuous vessels

• Balloon and catheter are softer and less traumatic to vessels • Smaller, softer microwires are less likely to traumatize or perforate the vessel • Balloon can be inflated and deflated repeatedly, since it deflates completely (noncompliant balloons get “krinkly” after one inflation) • With slow, careful, low-pressure inflation, the balloon gently teases open the vessel • Single-lumen balloons, such as the HyperGlide and HyperForm, can be deflated quickly and easily by withdrawing the wire (note: the balloon cannot be reinflated after it is deflated by pulling back on the wire) Noncompliant balloons

Disadvantages • The diameter of the balloon varies greatly with the amount of inflation; overdilation and rupture of the vessel is a greater threat than with noncompliant balloons

• Lower inflation pressure may require multiple inflations to adequately dilate the target vessel; occasionally, the low-pressure balloon will not adequately open the affected vessel

10.9 Endovascular Treatment of Cerebral Vasospasm

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Table 10.1 (continued) Advantages • If appropriately sized for the target vessel, there will be less likelihood of overdilation and/or rupture of the vessel, since they reach the nominal size and then stop inflating • They are used with a 0.014 in. microwire, which provides more torquability and support than smaller wires • Because they are difficult to navigate into small distal vessels, angioplasty is usually limited to larger proximal vessels, where one is less likely to face problems







Good results have been obtained with either device [34]. The authors of this Handbook are evenly divided in their preferences. (i) Compliant balloons: • HyperGlide™ (Medtronic, Minneapolis, MN): • Available sizes: 4  ×  10  mm; 4  ×  15  mm; 4  ×  20  mm; 4 × 30 mm. • HyperForm™ (Medtronic, Minneapolis, MN): • Available sizes: 4  ×  7  mm; 7 × 7 mm. • For most cases the HyperGlide™ 4  ×  10  mm balloon is most suitable. (ii) Microwires: • X-pedion™ 0.010  in. microwire (ev3, Irvine, CA). This wire comes with the HyperGlide balloon and is useful in most cases. • Synchro2®-10 (Stryker, Fremont, CA). This wire is more steerable than the X-pedion and has an added advantage of being slightly smaller, so that slow contrast leakage will occur from the balloon when it is inflated, which helps prevent overinflation of the balloon. (iii) Noncompliant balloons: • Maverick2™ Monorail™ Balloon Catheter (Boston Scientific, Natick, MA).

Disadvantages • Heavier, bulkier, and more rigid than compliant balloons

• They require a heavier microwire for support, which may carry a greater risk of vessel injury or perforation • Noncompliant balloons get “krinkly” after one inflation, increasing possibility of vessel injury when maneuvering a balloon that has already been inflated and deflated

–– A wide range of sizes are available; the 1.5 × 9 mm and the 2.0 × 9 mm sizes are most suitable. • NC Ranger™ Balloon Catheter (Boston Scientific, Natick, MA). • NC Raptor™ (Cordis, Miami, FL). 2. Compliant balloon technique with the HyperGlide system: (a) Preparation: (i) Attach the HyperGlide balloon catheter to an RHV and flush using a 10-mL syringe containing 50/50 contrast in heparinized saline. (b) Compliant balloon catheter assembly: (i) Fill a 3-mL syringe with 50/50 contrast in heparinized saline and attach it to the side port of the RHV (Fig. 10.1). (ii) Insert the X-pedion microwire through the RHV until the distal tip emerges from the distal tip of the balloon catheter, and shape the tip. (iii) Note: The microwire should not be allowed to extend more than 10  cm beyond the tip of the balloon catheter; if it extends any further than 10  cm, the balloon will not function correctly. To prevent this, advance the microwire until the tip of the microwire is 4–5  cm and then tighten the torque device onto the microwire at the mouth of the RHV. (iv) Test inflation. Place the distal end of the balloon catheter in a bowl of sterile saline and use the 3-mL syringe to

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10  Endovascular Treatment of Intracranial Stenosis and Vasospasm Table 10.2  HyperGlide balloon inflation volumes Infusion volume (mL) 0.02 0.04 0.06 0.08 0.10 0.12 0.14 0.16

Balloon size (mm) 2.0 2.6 3.0 3.3 3.5 3.7 3.9 4.1

Infusion volume required for the 4 × 10 mm HyperGlide balloon [35]

Fig. 10.1 Setup for using the HyperGlide™ and HyperForm™ systems: 3-mL syringe (C), 10-mL syringe containing 50/50 contrast in heparinized saline (S), X-pedion microwire (X), and balloon catheter (B)

fully inflate the balloon under direct visualization (the maximum rated volume for the 4 × 10 mm HyperGlide balloon in 0.16 mL). During the first inflation, the balloon typically inflates in an eccentric manner, which is why a test inflation is required. Subsequent balloon inflations should be symmetric. (c) Angioplasty technique: (i) Advance the microwire and balloon into the target vessel under roadmap fluoroscopy. (ii) Carefully and gently inflate the balloon under fluoroscopic visualization: • For the 4 × 10 mm HyperGlide balloon, see Table  10.2 for infusion volumes required to obtain each balloon diameter. (iii) Deflate the balloon with the syringe: • Note: Do not withdraw the microwire into the tip of the balloon catheter unless rapid deflation of the

balloon is needed, as this will introduce blood into the balloon catheter; the manufacturer recommends the balloon not be inflated once this happens. (iv) Reposition the balloon for additional angioplasties as needed. 3. Noncompliant balloon technique with the Maverick angioplasty balloon: (a) Preparation: (i) Use 50/50 mixture of contrast in heparinized saline. (ii) Prepare the inflator and attach it with a three-way stopcock and an empty 20-mL syringe to the balloon catheter. (iii) Apply suction to the balloon but do not pre-inflate it. (iv) Continuously flush through the lumen of the balloon catheter with heparinized saline via a stopcock and a rotating hemostatic valve. (b) Angioplasty technique: (i) The balloon can be taken up primarily, without exchanging over an exchangelength microwire, when the target vessel is fairly proximal, like the ICA or the vertebral artery, and sometimes the basilar artery. For treatment of the M1 and A1 segments, and frequently the basilar artery, exchange-length microwire should be advanced within a microcatheter first. With the microwire tip positioned in a distal vessel, the microcatheter is then exchanged for the balloon catheter.

10.9 Endovascular Treatment of Cerebral Vasospasm



4.





(ii) The balloon is advanced into position under roadmap guidance and inflated to the appropriate pressure briefly, for 1–2 s. It has to be ensured that the balloon is completely deflated before it is repositioned. • Eskridge and Song [36] recommend a four-step angioplasty technique, in which the balloon is sequentially inflated and deflated at progressively larger diameters and advanced a slight distance after each inflation (25% inflation, deflation; 50% inflation, deflation; 75% inflation, deflation; and then 100% inflation). (iii) Reposition the balloon for additional angioplasties as needed. Angioplasty tips: (a) In general, the smaller and shorter the balloon, the better. (b) Work in a proximal-to-distal direction. Improvement in the caliber of proximal vessels will sometimes lead to the same in distal vessel calibers. (c) In cases of severe vasospasm, when the target vessel is too constricted to accept the balloon, pretreatment by intra-arterial injection of nitroglycerin, 20  μg, can help. A microcatheter is positioned in the proximal part of the vessel and the drug is slowly infused. A very limited amount of papaverine may be safe and effective for this maneuver; better drug options include nitroglycerine, nicardipine, and verapamil. Nitroglycerin works faster than other agents used for vasospasm, such as nicardipine and verapamil: (i) Some operators recommend that pharmacologic dilation prior to angioplasty should be avoided, on the basis that predilation makes angioplasty less likely to work. Theoretically, angioplasty is effective because it stretches the vessel wall, and dilation of the vessel before angioplasty may make this less likely to occur.

579

(d) When both the A1 and M1 segments require treatment, treat the A1 segment first [37]. If a vasodilating drug is injected into the A1 segment after successful treatment of the M1 segment, the drug may be diverted away from the A1 segment and into the M1 segment. (i) Alternatively, temporary balloon occlusion of the M1 segment can help divert the drug into the ACA [36].

Retrievable, Adjustable Stent The Comaneci™ (Rapid Medical, Yokneam, Israel) is a retrievable stent-like mesh device that can be inflated like a balloon to fit the size of a parent vessel and keep coils from protruding while coiling wide-neck aneurysms. Unlike a balloon, it allows continued flow through the parent artery during expansion and unlike most stents, it is removed after the procedure. The device has been used to successfully dilate vasospasm [38]. Comaneci™ expands up to 4.5 mm, Comaneci™ Petit up to 3.5  mm, and both are deployed using 0.021  in. lumen microcatheters. Comaneci™ 17 expands up to 2.5 mm and can be deployed through a 0.0165  in. microcatheter. These devices are similar to the Tigertriever™ from Rapid Medical used in acute ischemic stroke. Other self-expanding stentrievers have been used for vasospasm treatment, although in a small series the authors note that the radial force of the stentriever was insufficient to expand the vessel to normal size [39]. The controlled inflation of the Comaneci™ may make it more effective but larger series are needed to better assess the effectiveness of this device for vasospasm angioplasty. Another stent-retriever-based device, the NeVa™ VS (Vesalio Nashville, TN), can be used to dilate intracranial vasospasm, and this was able to achieve restoration of flow to at least 50% of pre-vasospasm diameter in 64 out of 74 vessels (86.5%) treated [40]. Vasodilator medications were frequently used. Thrombotic complications were seen in 3.2%. There was no vessel rupture

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related to the device but one patient experienced middle cerebral artery rupture when balloon angioplasty was utilized.

Infusion of Pharmacologic Agents Intra-arterial administration of the calcium channel blockers nicardipine, nimodipine, and verapamil has been reported. No single agent has been shown to be more efficacious than the others. Parenteral nimodipine is not currently available in the United States. Reports of intravenous [41] or intrathecal [42] milrinone infusions have shown positive benefits in small series. Intra-­ arterial milrinone plus or minus balloon angioplasty can be used as a rescue strategy for those patients unresponsive to the intravenous infusion [43], although at least one study showed no added benefit from intra-arterial therapy compared to intravenous milrinone [2]. IA infusion of these agents can be used to treat vessels that cannot be dealt with, or are difficult to treat with, balloon angioplasty, such as distal branches and the A1 segment. IA papaverine administration is no ­longer recommended. See Chap. 12, Intracranial Aneurysms and Subarachnoid Hemorrhage, for a discussion of the published data. 1. Nicardipine. (a) Nicardipine (Cardene IV; ESP Pharma, Inc., Edison, NJ) is diluted in 0.9% NaCl (without heparin) to a concentration of 0.1 mg/mL. Inject 1 mL aliquots through the microcatheter to a maximal dose of 5  mg per vessel [35]. Note: Nicardipine precipitates in heparinized saline, so ensure the system is flushed with unheparinzed saline before and after injecting nicardipine. 2. Verapamil. (a) Verapamil HCl Injection. Dilute a 5  mg vial with 0.9% NaCl to a concentration of 1 mg/mL. Inject 10–20 mg per vessel for a maximum of 20 mg per carotid. Watch for transient hypotension. 3. Combined verapamil + nitroglycerin continuous infusion. Multiple-agent infusion may be



more effective than infusion of a single agent [44]. (a) Add nitroglycerin (500 μg) and verapamil (50 mg) to a 1-L bag of 0.9% NaCl. Place a microcatheter in the target vessel and infuse the solution at approximately 25  mL/min for 20  min per vessel; plan about three vessels per bag. Two bags of saline are typically necessary for treatment of all vascular territories.

Treatment-Related Complications A review of published reports indicates major complications with endovascular treatment were seen at 5%, for vasospasm with an incidence of 1.1% vessel rupture [45]: 1. Reported complications include thromboembolism, arterial dissection, reperfusion hemorrhage, branch occlusion, bleeding from untreated aneurysms, retroperitoneal hemorrhage, groin hematoma, and vessel rupture [46].

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27. Macdonald RL. Management of cerebral vasospasm. Neurosurg Rev. 2006;29(3):179–93. 28. Harrigan MR. Hypertension may be the most important component of hyperdynamic therapy in cerebral vasospasm. Crit Care. 2010;14(3):151. (Comment) (In eng). https://doi.org/10.1186/cc8983. 29. Jabbour P, Veznedaroglu E, Liebman K, Rosenwasser RH.  Is radiographic ischemia a contraindication for angioplasty in subarachnoid hemorrhage? AANS annual meeting. San Francisco: American Association of Neurological Surgeons; 2006. 30. American Society of Interventional and Therapeutic Neuroradiology. Mechanical and pharmocologic treatment of vasospasm. AJNR Am J Neuroradiol. 2001;22(90080):26S–27. http://www.ajnr.org 31. Bernardini GL, Mayer SA, Kossoff SB, Hacein-Bey L, Solomon RA, Pile-Spellman J.  Anticoagulation and induced hypertension after endovascular treatment for ruptured intracranial aneurysms. Crit Care Med. 2001;29(3):641–4. http://www.ncbi.nlm.nih. gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed& dopt=Citation&list_uids=11373436 32. Hoh BL, Nogueira RG, Ledezma CJ, Pryor JC, Ogilvy CS.  Safety of heparinization for cerebral aneurysm coiling soon after external ventriculostomy drain placement. Neurosurgery. 2005;57(5):845–9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve&db=PubMed&dopt=Citation&l ist_uids=16284554 33. Raabe A, Gerlach R, Zimmermann M, Seifert V.  The risk of haemorrhage associated with early postoperative heparin administration after intracranial surgery. Acta Neurochir. 2001;143(1):1–7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve&db=PubMed&dopt=Citation&l ist_uids=11345711 34. Terry A, Zipfel G, Milner E, et  al. Safety and technical efficacy of over-the-wire balloons for the treatment of subarachnoid hemorrhage-induced cerebral vasospasm. Neurosurg Focus. 2006;21(3):E14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve&db=PubMed&dopt=Citation&l ist_uids=17029338 35. ev3.Package insert, Occlusion Balloon System 2007. 36. Eskridge JM, Song JK.  A practical approach to the treatment of vasospasm. AJNR Am J Neuroradiol. 1997;18(9):1653–60. http://www.ajnr.org 37. Murayama Y, Song JK, Uda K, et al. Combined endovascular treatment for both intracranial aneurysm and symptomatic vasospasm. AJNR Am J Neuroradiol. 2003;24(1):133–9. http://www.ajnr.org/cgi/content/ abstract/24/1/133

38. Badger CA, Jankowitz BT, Shaikh HA.  Treatment of cerebral vasospasm secondary to subarachnoid hemorrhage utilizing the Comaneci device. Interv Neuroradiol. 2020;26(5):582–5. https://doi. org/10.1177/1591019920945554. 39. Bhogal P, Loh Y, Brouwer P, Andersson T, Soderman M.  Treatment of cerebral vasospasm with self-­ expandable retrievable stents: proof of concept. J Neurointerv Surg. 2017;9(1):52–9. https://doi. org/10.1136/neurintsurg-­2016-­012546. 40. Gupta R, Woodward K, Fiorella D, et  al. Primary results of the Vesalio NeVa VS for the treatment of symptomatic cerebral vasospasm following aneurysm subarachnoid hemorrhage (VITAL) study. J Neurointerv Surg. 2022;14(8):815–9. https://doi. org/10.1136/neurintsurg-­2021-­017859. 41. Steiger HJ, Ensner R, Andereggen L, Remonda L, Berberat J, Marbacher S.  Hemodynamic response and clinical outcome following intravenous milrinone plus norepinephrine-based hyperdynamic hypertensive therapy in patients suffering secondary cerebral ischemia after aneurysmal subarachnoid hemorrhage. Acta Neurochir. 2022;164(3):811–21. https://doi. org/10.1007/s00701-­022-­05145-­6. 42. Koyanagi M, Fukuda H, Lo B, et al. Effect of intrathecal milrinone injection via lumbar catheter on delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. J Neurosurg. 2018;128(3):717–22. https://doi.org/10.3171/2016.10.JNS162227. 43. Abulhasan YB, Ortiz Jimenez J, Teitelbaum J, Simoneau G, Angle MR.  Milrinone for refractory cerebral vasospasm with delayed cerebral ischemia. J Neurosurg. 2020;134(3):971–82. https://doi.org/10 .3171/2020.1.JNS193107. 44. Chen PR, Bulsara K, Lopez-Rivera V, et  al. Use of single versus multiple vasodilator agents in the treatment of cerebral vasospasm: is more better than less? Acta Neurochir. 2021;163(1):161–8. https://doi. org/10.1007/s00701-­020-­04415-­5. 45. Hoh BL, Ogilvy CS. Endovascular treatment of cerebral vasospasm: transluminal balloon angioplasty, intra-arterial papaverine, and intra-arterial nicardipine. Neurosurg Clin N Am. 2005;16(3):501–16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve&db=PubMed&dopt=Citation&l ist_uids=15990041 46. Sayama CM, Liu JK, Couldwell WT. Update on endovascular therapies for cerebral vasospasm induced by aneurysmal subarachnoid hemorrhage. Neurosurg Focus. 2006;21(3):E12. http://www.ncbi.nlm.nih. gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed& dopt=Citation&list_uids=17029336

Venous Procedures

11.1 Venous Access: Basic Concepts Pre-Procedure Evaluation 1. Do a brief neurological exam to establish a baseline, should a neurologic change occur during or after the procedure. 2. Ask the patient if they have a history of iodinated contrast reactions. 3. Examine both groins. The femoral arterial pulse provides a landmark for femoral venous access. 4. Ask the patient about any history of deep venous thrombosis that may require using special sites for venous access. 5. Review blood work, including a serum creatinine level, serum glucose if diabetic, and coagulation parameters.

Pre-Procedure Orders 1. NPO except medications for 6 h prior to the procedure. 2. Patients on insulin for hyperglycemia should get half their normal dose prior to the procedure. 3. Place a peripheral IV. 4. Place Foley catheter if a long procedure is anticipated.

11

Contrast Agents Nonionic contrast agents are well tolerated and are usually used for these procedures. Iohexol (Omnipaque®, GE Healthcare, Princeton, NJ), a low osmolality, nonionic contrast agent, is relatively inexpensive and is the most commonly used agent in venographic procedures. In patients with a history of severe anaphylactic reactions to iodinated contrast, small quantities of gadolinium-­ based MR contrast agents may be used instead.

Sedation/Anesthesia Diagnostic venography and intracranial venous pressure measurements generally cause minimal discomfort. Intracranial venous interventions, such as venous sinus stenting, can be uncomfortable and may require general anesthesia.

Venous Access 1. Femoral vein access (a) Most commonly used venous access site. (b) Technique: (i) Inject local anesthetic. (ii) Use ultrasound guidance to locate the femoral vein. It will be medial to the artery and more easily compressible.

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 M. R. Harrigan, J. P. Deveikis, Handbook of Cerebrovascular Disease and Neurointerventional Technique, Contemporary Medical Imaging, https://doi.org/10.1007/978-3-031-45598-8_11

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(iii) Advance a 22-gauge needle with a syringe half-full of heparinized saline just medial to a palpable femoral arterial pulse. (iv) Apply continuous suction as the needle is advanced by pulling back on the plunger. (v) If ultrasound not available and if the arterial pulse is not palpable, the fluoroscopic landmark is that the vein lies over the most medial aspect of the femoral head. In many cases, it is medial to the femoral head. (vi) When the vein is punctured, there may not be good spontaneous blood return from the needle. If blood can be freely aspirated, the needle is in the vein. (vii) Using a micropuncture access kit, insert the 0.018  in. wire into the needle, remove the needle, place a coaxial dilator in the vein, and then remove the inner dilator. (viii) Carefully advance a J-tip 0.038 in. wire under fluoroscopic visualization and confirm intravenous positioning visualization of the wire to the right of the spine. (ix) Advance the sheath into the vein. • A 6F, 25  cm long Pinnacle® (Terumo Medical, Somerset, NJ) sheath is useful for most cases. • Larger sheaths are usually well tolerated. Alternative routes (a) Internal jugular vein. The jugular vein can be used for access to the ipsilateral dural venous sinuses. (i) Retrograde jugular punctures are done using ultrasound guidance with a small vessel access system. (ii) The larger, more compressible jugular vein is lateral to the carotid. (iii) Palpate the carotid pulse and insert a 22-gauge needle just lateral to the pulse, angling cephalad. Attach a

syringe to the needle and gently aspirate as the needle is advanced until dark venous blood freely flows back. (If the blood is bright red and pulsatile, that is the carotid artery. Pull out and hold pressure for 5–10  min, then reattempt more laterally). (iv) When the needle is in the vein, advance the 0.018  in. platinum-tip wire of the access kit carefully up the jugular vein, remove the needle and insert the coaxial dilator. (v) Microcatheters may be advanced directly through the outer 4F coaxial dilator. Always attach a rotating hemostatic valve with a continuous saline flush to the hub of the dilator. (vi) If larger catheter systems are used, the dilator may be exchanged over a 0.035–0.038  in.  J-tip wire for a 10  cm long sheath of appropriate size. Since there is less soft tissue support and only a short length of the guidewire can usually be advanced up the jugular, it can be challenging to get the sheath into the vessel without buckling the wire and potentially losing access. Use progressively larger dilators to dilate the tract. Rotating the dilators and sheath as they are advanced over the wire helps. (b) Arm or subclavian veins can also be used to access the venous system. However, angulation at the entry of the jugular veins to the brachiocephalic veins and valves in these locations can make it difficult to access the jugular or more cephalad veins from the arm.

Catheter Navigation 1. Advance all catheters over a steerable hydrophilic wire. 2. When the tip of the wire enters the junction of the inferior vena cava and right atrium, keep

11.1  Venous Access: Basic Concepts

the curved tip of the wire pointing laterally to facilitate passage into the superior vena cava. 3. Keep an eye on the electrocardiographic (ECG) monitor, since arrhythmias can be induced if the wire irritates the wall of the atrium or if it enters the right ventricle. 4. Once the catheter is in the superior vena cava, it can either be advanced straight up the right internal jugular, or angled sharply to the left to enter the left brachiocephalic vein. It must then be advanced in a cephalad direction if catheterization of the left internal jugular is desired. 5. Valves in the proximal internal jugular veins sometimes can impede advancement of the guidewire up the internal jugular veins. The valves can be gently probed with an angled Glidewire® (Terumo Medical, Somerset, NJ) as the patient breathes deeply. Other useful wires for navigating through venous valves are the 0.016 in. Gold-tip Glidewire® (Terumo Medical, Somerset, NJ) or 0.024 in. Aristotle® (Scientia Vascular, West Valley City, UT). Once the wire is past the valve, the catheter can then be advanced into the more cephalad jugular vein. 6. Catheterization of more cephalad venous structures requires use of a coaxial microcatheter/microwire assembly, usually placed through a 5 or 6F guide catheter. 7. When advancing a microcatheter through any guide catheter, always remember that movement of the microcatheter forward creates retrograde force on the guide catheter. 8. Attempts at advancing the microcatheter very distally can make the guide catheter buckle in the right atrium, causing arrhythmias. (a) Arrhythmias will resolve when the slack is taken out of the guide catheter. (b) Buckling of the guiding catheter may be minimized by always using a relatively stiff guide sheath, such as a 90  cm Benchmark™ BMX™ 96 (Penumbra, Inc., Alameda, CA), with a Tower of Power arrangement with the 90 cm sheath combined with a 100 cm guide catheter to create a stiffer platform.

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 ips for Catheter Navigation T in Difficult Situations 1. Veins are more mobile than arteries and are therefore less supportive to catheters. Stiff guide catheters are necessary for support. 2. Veins are generally tortuous and require a steerable soft-tip wire to get to the target vessel. 3. Veins are more variable in their anatomy than arteries. Moreover, many pathological venous conditions involve venous occlusions. 4. When in doubt about where the catheter tip is, periodically inject contrast through the catheter under fluoroscopy or make roadmaps. 5. Veins carry blood toward the heart. It can be difficult to navigate against the flow of blood. Stiff, steerable wires, and steerable catheters are helpful in the venous system. 6. Direct access to a target in the venous system may be difficult. Sometimes it is helpful to use a more circuitous route to obtain access in the intracranial venous system. A multiple catheter, snare assisted technique may help in accessing the target in this situation (Fig. 11.1).

Roadmapping Roadmapping is less effective for venous procedures compared to arterial procedures. It is difficult to opacify the venous structures for more than a few centimeters beyond the tip of the catheter, since the contrast is injected against the flow of blood. Excellent roadmap images of the target venous structures can be obtained by injecting contrast in the arterial feeding vessels via a separate angiographic catheter in the arterial side when performing venous catheterization for transvenous embolization of arteriovenous fistulas. A diagnostic catheter can be parked in the internal carotid artery during intracranial venous procedures specifically for making venous-phase roadmaps.

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11  Venous Procedures

Fig. 11.1  Snare-assisted catheterization 1. The dilemma In an attempt to obtain transvenous access to the site of an arteriovenous fistula (*), difficult angles make it impossible to advance a microcatheter (A) directly. Neither the microcatheter nor the microwire can be navigated directly via the small venous channel (X). A wire may be advanced into an indirect pathway (Y), but the microcatheter cannot make the sharp turn and displaces the wire and pushes beyond the turn 2. Place the microwire Carefully navigate a soft microwire into the small venous channel (X), and into the larger vessel below. This microwire does not provide sufficient support to allow the microcatheter to follow around the turn 3. Snare the microwire Position a second microcatheter (B) with its tip near the end of the microwire. Advance a snare through this microcath-

eter and maneuver it around the end of the microwire. Then pull the snare back into the microcatheter to grasp the wire 4. Pull the microcatheter up Gently pull the microwire (now snared) back into the first microcatheter (A) and push the second microcatheter (B) to slowly advance it up the small arterial pedicle (X) 5. Disengage the microwire from the snare The snare is then pushed out slightly from the second microcatheter (B) tip to disengage the wire. The wire and first microcatheter (A) can then be withdrawn. The second microcatheter is then advanced to the desired target over either the snare itself, or, preferably, the snare can be removed and a microwire is used to guide the microcatheter into position

Double Flushing

cally evident problems on the venous side, use good angiographic techniques, including double flushing at all times, to limit the risk of complications.

Double flushing is covered in Chap. 2 and is more appropriately termed “double aspiration.” One heparinized saline-filled syringe is used to aspirate blood, bubbles, and/or clot from the catheter, and is discarded. The second syringe is connected and a slight aspiration of blood used to confirm the absence of bubbles after which saline is flushed into the catheter. Although small bubbles or clot emboli are less likely to create clini-

Continuous Saline Infusion Three-way stopcocks or manifolds are necessary to provide a heparinized saline drip through the catheter. Always use a rotating hemostatic valve

11.2 Venography

on the catheter so that the catheter hub is never left open to the air. When the catheter is in the venous system, low venous pressure may pull air into the catheter. Careful double flushing is also required if a wire is inserted and removed or if any blood is present in the lumen. The use of multiple hemostatic valves and continuous infusions is mandatory for any coaxial catheterization.

Anticoagulation Heparinization limits thrombus formation in the catheter system, which can impair normal functioning of these systems. Moreover, thrombus in or around the catheter can cause venous thrombosis, potentially resulting in deep venous thrombosis, pulmonary emboli, and/or local thrombotic occlusion of the cerebral venous structures being catheterized. However, published data on whether systemic heparin is effective in preventing complications of venous procedures is lacking.

Hand Injection A 10  mL syringe containing contrast should be attached to the stopcock on the catheter, and the syringe should be snapped with the middle finger several times to release bubbles stuck to the inside surface of the syringe. The syringe should be held in a vertical position, with the plunger directed upward, to allow bubbles to rise away from the catheter. Contrast injections through a microcatheter are usually done with 3 or 1 mL syringes.

Mechanical Injection There is generally no role for power injections during venous procedures.

Puncture Site Care Manual compression should be applied to the femoral vein puncture site for 5–10  min after

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removal of the sheath. The patient should be kept on strict bed rest with the legs extended for at least 2 h, depending on the sheath size. A Syvek Excel® hemostatic patch (Marine Polymer Technologies, Danvers, MA) can be helpful. Bleeding from venous punctures is less of a concern compared to arterial punctures, but closure devices such as Mynx Control® (Cordis, Miami Lakes, FL), Perclose Proglide® (Abbott, North Chicago, IL), and Vascade® (Cardiva, Santa Clara, CA) are approved for venous access site closure and could be used. See Chap. 4 for more details on closure devices.

11.2 Venography Background Catheter venography is rarely done in the head and neck due to the availability of excellent noninvasive imaging techniques, such as magnetic resonance venography (MRV) to study the venous system [1]. Most commonly, direct catheter angiography of the venous system is only performed as part of another venous procedure.

Indications for Venography 1. To confirm catheter placement and to assess venous drainage patterns in venous sampling procedures. 2. To evaluate for stenosis or occlusion in patients with suspected venous hypertension. 3. To evaluate for stenosis or occlusion in patients with unexplained tinnitus. 4. To assess collateral pathways in anticipation of surgical or endovascular occlusion of dural venous sinuses. 5. To evaluate for potential routes of access for transvenous embolization procedures. 6. In cases of transarterial embolization of arteriovenous shunts, venous catheterization may be done to monitor pressure, and determine the degree of reduction of venous hypertension.

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Complications of Venography Neurological Complications 1. Since venography is usually performed as part of another venous procedure, the patient should be informed of the potential complications of the more involved procedure. 2. Statistics on complications of venography alone are lacking, since it is not a commonly performed procedure. 3. Theoretically, there is always a risk of venous infarction and hemorrhage with intracranial venous structures, but the risk of these complications is unknown and probably very low. Non-neurological Complications 1. Anaphylactic reactions to iodinated contrast or any of the medications used can occur as with any endovascular procedure. 2. Access-site hematomas can occur, but are less common and less severe compared to arterial punctures. 3. Venous thrombosis can occur, producing symptoms of deep venous thrombosis, or pulmonary emboli.

Venography: Procedural Aspects Suggested Wires and Catheters for Venography Hydrophilic Wires 1. The 0.035  in. angled Glidewire® (Terumo Medical, Somerset, NJ) is soft, flexible, and steerable. 2. The 0.038  in. angled Glidewire® (Terumo Medical, Somerset, NJ) is slightly stiffer than the 0.035 and helpful when added wire support is needed, but is too stiff for routine use in smaller veins or intracranial veins. 3. Softer, yet torquable wires such as the Headliner™ (Microvention, Tustin, CA) or Gold-tip Glidewire® (Terumo Medical, Somerset, NJ) can be helpful for navigating the sometimes difficult valves in the lower

11  Venous Procedures

internal jugular and for accessing the intracranial sinuses.

Catheters for Venography There is one principle to keep in mind when doing venography: blood flows back toward the heart. Therefore, contrast injected in head or neck veins through a catheter placed via a femoral approach will flow back toward the heart and opacify the vessel caudal to the tip of the catheter. In the larger dural sinuses, it can be difficult to inject contrast more than a few centimeters beyond the tip of the catheter. 1. Soft-tip, simple angle catheters for catheterizing the caudal IPS or jugular bulb: (a) 4 or 5F Berenstein curve Soft-Vu® (Angiodynamics, Queensbury, NY). (b) 4 or 5F Angled Glide-catheter® (Terumo Medical, Somerset, NJ). 2. Guiding catheters used for coaxial approach: (a) 5 or 6F angle-tip Envoy® (Cerenovus Neurovascular, Irvine, CA). 3. Microcatheters used for the coaxial approach should be braided with a relatively large internal lumen: (a) RapidTransit® (Cerenovus Neurovascular, Irvine, CA). 4. Catheterization of the superior sagittal sinus in adults requires a 170 cm microcatheter: (a) RapidTransit® (Codman Neurovascular, Raynham, MA) is available in a 170 cm length, and works well for this purpose. (b) Remember to use a 200  cm or longer microwire: (i) 0.012  J-Tip Headliner® (Microvention, Tustin, CA). (ii) 0.014 Soft-Tip Transend™ (Stryker Neurovascular, Fremont, CA). 5. Excellent opacification of dural sinuses can be obtained using intermediate catheter systems. (a) DAC® (Stryker Neurovascular, Fremont, CA), whose 038 and 044 systems come in up to 136 cm, which is sufficient for most cases.

11.2 Venography

Techniques Femoral Venous Access. Place a 5 or 6F sheath in the right or left femoral vein. Catheter Manipulation 1. Attach all catheters to rotating hemostatic valves and attach a three-way stopcock and continuous infusion of saline containing 10,000 units heparin per liter. 2. Through the femoral venous sheath, advance the catheter into the desired internal jugular vein. 3. Once in the internal jugular vein, direct the catheter superomedially to point into the inferior petrosal sinuses, or superolaterally to point to the jugular bulb. 4. If the venous structures being studied are more cephalad than the jugular bulb or IPS, advance a large-lumen microcatheter coaxially through the rotating hemostatic valve of the guiding catheter. 5. Warn awake patients that the catheter manipulation may cause discomfort. 6. Carefully and gently advance the microcatheter over a soft-tip guidewire into the venous sinus cephalad to the area to be studied. 7. Do test injections of 1–2  mL of contrast to ensure proper catheter position and to estimate the amount of contrast required for a selective venogram. 8. Intracranial venograms are performed with hand injections of contrast. 9. Large dural venous sinuses may require injection volumes of 3–5  mL or more, and smaller sinuses, like the IPS may only require 1–3 Ml 10. Cortical veins or deep veins like the internal cerebral veins should be cautiously injected with small volumes of contrast. 11. Perform venograms with high-quality DSA imaging systems using 2–4 frames per second.  ips for Evaluating Venogram Images T 1. Inevitably, when using microcatheters for venography of large dural sinuses, a stream-

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ing of contrast and unopacified blood from tributary veins will be seen, creating apparent filling defects in the vein. 2. Apparent filling defects from streaming will change in size and configuration from frame-­ to-­ frame during the angiographic run, and have vague margins, whereas true filling defects or stenoses are static and more clearly demarcated. 3. If it is not clear if a filling defect is real or not, adjusting catheter position and repeating the run may help confirm the presence of a real defect. 4. Remember that potentially large Pacchionian granulations are normally expected within the dural sinuses, usually in lateral aspect of the transverse sinuses, and smaller ones can be seen in the superior sagittal sinus.

 enous Pressure Measurements V Stenosis seen on venography may or may not be hemodynamically significant. Therefore, patients with suspected venous hypertension should have venous pressure measurements obtained proximal and distal to any potential stenosis. The simplest method is to connect saline-filled extension tubing from a three-way stopcock or manifold connected between the catheter and a standard pressure transducer. For full evaluation of the intracranial sinuses, it is necessary to take the measurements using a microcatheter that can be advanced into the superior sagittal sinus, ipsilateral and contralateral transverse and sigmoid sinuses and jugular veins, obtaining pressure measurements at each of these sites. Waveforms of pressure measurements obtained via a microcatheter will inevitably be inaccurate, but studies have shown the mean values are accurate [2]. If the pressure waveform is completely flat, it may be necessary to change the display scale on the monitor. If the waveform is flat and the pressure measurements do not seem correct, the microcatheter may be wedged against the wall of the vessel, or it may be kinked, so gentle withdrawal of the catheter may improve the reading. More accurate pressure measurements may be obtained by inserting a 0.014  in. PressureWire ™ Certus (St. Jude Medical Systems, St. Paul, MI) in the microcatheter.

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Venous pressure measurements can also be useful during transarterial embolization of arteriovenous malformations or fistulas. Particularly in the palliative embolization of extensive lesions, intracranial venous pressure measurements can provide objective data about the effect of embolization on flow through the lesion. Reduction of pressure to more normal levels suggests the patient will gain a clinical benefit from the procedure. In similar fashion, a Doppler guidewire can document alterations in blood flow by measuring changes in velocity in the veins draining arteriovenous shunts as the arterial feeders are embolized [3].

11.3 Venous Test Occlusion Background Venous test occlusion can predict whether occlusion of the vein will have negative hemodynamic consequences. There are significant differences between arterial and venous test occlusion. On the arterial side, occlusion of the vessel can quickly cause a sufficient drop in blood flow to a vascular territory to cause a demonstrable neurological deficit. However, there is less of a linear relationship of blood flow to patency of a venous structure; hence, neurological deficits may not occur quick enough to be detected during the test. Moreover, many of the potentially disabling signs and symptoms of venous occlusive disease, such as intractable headaches and visual loss, may develop weeks or months after venous occlusion. There are reports of balloon test occlusions failing to predict disastrous venous hypertension and brain swelling after permanent occlusion of the tested venous sinus [4]. Venous sinuses have reportedly been safely occluded when collateral venous flow appears adequate on angiographic studies and if the pressure proximal to the site of occlusion increased 2 for all IPS samples before CRH administration and >3 post-CRH. Therefore, the source of the ACG must be in the pituitary. The right IPS is greater than 1.4 times the left IPS, so the lesion should be on the right. All samples dramatically exceed the threshold ratios. DIAGNOSIS: A right-sided pituitary adenoma was successfully located and removed at surgery.

SAMPLE PATIENT B R IPS L IPS Peripheral

T: −10 min 59 321 28

T: −5 min 184 236 27

T: 0 min 127 405 26

T: 1 min 26 266 322

T: 3 min 5154 4912 26

T: 5 min 1086 1757 50

T: 10 min 1159 1422 74

All values are ACTH levels in ng/L; T Time, min Minutes before and after administration of CRH

DISCUSSION: MRI suggested a right pituitary adenoma. All readings show a 2:1 IPS:peripheral ratio pre-CRH and almost all readings show at least 3:1 IPS:peripheral ratio post-CRH, indicating Cushing’s disease from a pituitary adenoma. Notice at 1 min post-CRH the RIPS value is the same as the previous peripheral value. This likely indicates the samples were mixed up somehow. Note also that at 3 min post-­CRH, there is higher ACTH in the right IPS, even though the remaining

times show higher values in the left IPS, predicting a left pituitary source of ACTH, in contradiction to the right-sided prediction by MRI. DIAGNOSIS: A right-sided adenoma was removed at surgery. The IPSS therefore was incorrect as to the side. The venography during the study showed no venous anomalies or asymmetry. This shows the major limitation to IPSS, since it correctly lateralizes the lesion only about 70% of the time [18].

SAMPLE PATIENT C R IPS L IPS Peripheral

T: −10 min 46 141 12

T: −5 min 35 157 11

T: 0 min 46 201 14

T: 1 min 255 477 14

T: 3 min 542 1185 24

T: 5 min 827 1416 41

All values are ACTH levels in ng/L; T Time, min Minutes before and after administration of CRH

T: 10 min 600 1419 77

600

DISCUSSION: Consistently higher values are seen in either IPS compared to peripheral and left compared to right. DIAGNOSIS: A left-sided pituitary adenoma was removed and the patient’s serum ACTH and cortisol returned to normal.

 avernous Sinus Sampling C The results of cavernous sinus sampling are variable. 1. A study of 93 patients from an experienced endovascular group reported successful catheterization of the cavernous sinuses with zero complications, and sampling successfully diagnosed a pituitary source of ACTH in 93% of cases pre-CRH and 100% post-CRH correctly predicting the side of the lesion in 83% of all cases, and 89% of those with symmetrical venous anatomy and good catheter position [22]. (a) This is similar to the larger IPS sampling studies in terms of safety and accuracy, although cavernous sinus sampling seems better for lateralizing the lesion. 2. Another study of 90 patients from another experienced endovascular group also had no complications but showed accuracy of diagnosing Cushing’s disease of 86% for cavernous sinus sampling compared to 97% for IPS sampling and 100% using both sites, but successful lateralization in only 62–68% [31]. 3. Cavernous sinus sampling accuracy suffers when CRH is not used, [32, 33] or if samples from each sinus are not obtained simultaneously [34]. 4. Transient sixth cranial nerve palsies have been reported in two cases [35]. 5. Most centers prefer IPS sampling since it is simpler, less invasive, and there is more experience with that technique. 6. The authors of this handbook use cavernous sinus sampling in selected cases when venous anatomic variants make IPS sampling more difficult or in cases in which IPS sampling results are equivocal.

11  Venous Procedures

Jugular Venous Sampling In centers where there is limited experience with petrosal sinus catheterization, jugular venous catheterization is a much simpler and somewhat safer alternative. 1. A study comparing jugular sampling to IPS sampling found jugular venous sampling to have 83% sensitivity and100% specificity, compared to sensitivity of 94% and specificity of 100% for IPS sampling [36]. 2. Consequently, if jugular venous sampling is positive for Cushing’s disease, then the patient should respond to trans-sphenoidal surgery, and if the sampling results are negative or equivocal, the patient could be referred to a center with more experience in IPS or cavernous sinus sampling.

 enous Sampling in Suspected Ectopic V ACTH Production If the IPS:peripheral ACTH gradients is 2) for 403 subjects available for follow-up: [619] (a) 23.2% in the endovascular group (b) 33.7% in the surgical group (p = 0.02) 3. Six-year rate of poor outcome for 336 subjects available for follow-up: [620] (a) 35.2% in the endovascular group (b) 41.4% in the surgical group (p = 0.24) 4. Notable aspects of BRAT: (a) A large percentage (38%) of patients assigned to coiling crossed over to clipping, while 1.9% of patients assigned to clipping crossed over to coiling, which likely reflects both the skill and stature of the surgeons but also the culture at the center involved in the study. (b) Whereas complete aneurysm obliteration was achieved in 96% of clipping patients and only 48% of coiling patients, rebleeding after initial treatment was observed in only two patients, both in the clipping group [619]. No known rebleeds occurred in either group at the 6-year follow-up [620], suggesting that coiling is protective against rehemorrhage even with incomplete obliteration. 5. Controversies. The BRAT has been criticized along several lines, including design of the trial, analysis of the results, gaps in the data, the randomization scheme, and the high number of crossovers in the group assigned to coiling [621, 622]. Indeed, the original design of the trial intended it to be a pilot study and not a definitive Phase III trial; therefore, the trial was underpowered to detect a significant difference in the primary outcome measure. Nevertheless, a number people have interpreted the trial as supporting the continued use of clipping for the treatment of ruptured aneurysms [623, 624].

12.13 Intracranial Aneurysms: Special Situations

12.13 Intracranial Aneurysms: Special Situations KIDS KORNER! Pediatric Aneurysms Pediatric intracranial aneurysms are uncommon but have a number of features that are distinct from aneurysms found in adults. Epidemiology and Characteristic Features 1. Pediatric cases account for 90% arise along the nonbranching dorsal (superior) wall of the supraclinoid carotid. [714] (vii) Occasionally reported in atypical locations including anterior communicating artery, middle cerebral, basilar, posterior cerebral, anterior cerebral, and posterior-inferior cerebellar artery. [715] Presentation: (a) In contrast to most fusiform and dolichoectatic aneurysms, the evolution and presentation of dissecting aneurysms is an acute and progressive process [716]. (b) The most common presentation is SAH, occurring in 53% of patients in the Japanese nationwide study [709]. (c) Cerebral ischemia or infarction is also a common mode of presentation. In a series of patients with lateral medullary infarction (Wallenberg syndrome), 18% were attributable to intracranial vertebral artery dissection [717]. In anterior circulation cases, presentation with ischemic symptoms are more common than hemorrhage [709, 710]. Radiographic appearance: (a) Dissecting aneurysms often arise from an arterial trunk, such as the vertebral or basilar arteries or the ICA, in contrast to saccular aneurysms, which usually arise from arterial branch points. (b) Dissecting aneurysms are typically irregular structures, often including a narrow tapered parent vessel lumen associated with proximal or distal focal dilatation (“pearl and string” sign). Arterial occlusion, an intimal flap, a double lumen, extension of the aneurysm into distal branches, and retention of contrast material into the late venous phase are also angiographic features of dissecting aneurysms [329, 718] (c) The single pathognomonic sign of a dissecting aneurysm is a double lumen [719].

(d) On MRI, enhancement of the dissecting aneurysm with gadolinium is seen in 95% of cases [720]. 6. Pathogenesis: (a) Compared to the extradural arteries, normal intradural arteries have a thin media and adventitia with relatively few elastic fibers, making them more vulnerable to dissection, hemorrhage, and pseudoaneurysm formation [721]. Also, intracranial arteries have diminished vasa vasorum, which may limit healing [722]. (b) Spontaneous intradural dissecting vertebral artery aneurysms have been hypothesized by Ro and colleagues to begin with focal weakening of the media through a process termed segmental arterial mediolysis (Fig. 12.13) [723]. Next, the intima and elastic lamina rupture because of a lack of support by the media, causing blood to flow into the false lumen. Under arterial pressure and without the support by the other layers of the artery, the adventitia expands and ultimately ruptures at the point of greatest dilation. This hypothesis was based on an autopsy study of 50 cases of fatal ruptured dissecting intradural vertebral artery aneurysms [723]. Interesting findings from this study: (i) Every ruptured dissecting aneurysm had a single point of adventitial rupture where the adventitia was maximally dilated. The mean size of the adventitial defect was 1.9  mm and was located an average of 14.6  mm proximal to the vertebrobasilar junction. (ii) Defects in the media were common, were larger than the length of the dilated segment, and averaged 15.6 mm in length. (c) Dissecting aneurysms are dynamic lesions, with evolution of the angiographic appearance characteristically occurring over 2–3 months. (d) Most spontaneous dissecting aneurysms are idiopathic, although associated risk factors include atherosclerosis, hyperten-

12.13 Intracranial Aneurysms: Special Situations

a

b

715

c

d

Fig. 12.13  Pathogenesis of ruptured intradural vertebral artery dissecting aneurysms. Ro and coworkers proposed that spontaneous ruptured dissecting intracranial vertebral artery aneurysm originates with a focal weakening of the media (a) [723]. Next, the defects occur in the intima and

elastic lamina due to lack of support by the media (b), causing blood to flow into and expand the false lumen (c). The adventitia then expands and ruptures at the point of greatest dilation (d)

sion, a history of tumor resection, aneurysm clipping, or head injury, mucoid degeneration of the media, syphilis, migraines, fibromuscular dysplasia, homocystinuria, strenuous physical exertion, periarteritis nodosa, moyamoya disease, Guillain–Barré syndrome, and Marfan syndrome.

vascular options include proximal occlusion and parent vessel occlusion [324, 725], stenting [726, 727],flow diversion [728], and parent vessel sacrifice [729]. • A series of 29 patients reported overall morbidity and mortality rates of 13.8 and 17.2%, respectively [725]. Parent vessel sacrifice carries an 8.3% risk of ischemic stroke with very low or zero chance of recurrence [729]. • A series of ten blister like aneurysms treated with Pipeline flow diversion had nine good outcomes with complete occlusion of the blister on follow-up angiography [730]. (ii) Surgical techniques include proximal occlusion of the parent vessel, trapping of the lesion, and wrapping. When sacrifice of a portion of a vessel with critical branches is anticipated, surgical bypass may be necessary. Clipping of the aneurysm at the neck, as is done with saccular aneurysms, is generally not feasible. (iii) A systematic review of the literature revealed 27.8% poor outcome (mRS 4–6) with surgical treatment of blister aneurysms versus 14.7% poor

Management 1. Hemorrhagic dissecting aneurysms: (a) The risk of rebleeding for ruptured dissecting aneurysms is significant and may be higher than that for saccular aneurysms. In a series of 31 patients with ruptured vertebrobasilar dissecting aneurysms managed either with or without surgery, the rate of rebleeding was 71.4%, with an associated mortality rate of 46.7% [724]. A more recent study found a rebleeing rate of 17.1% [708]. (b) Management: Most agree that either surgery or endovascular treatment to prevent rebleeding is critical. In a study of ruptured dissecting aneurysms, the mortality rate in the treated group was 20%, whereas that in the untreated group was 50%: [324] (i) Endovascular treatment is first-line for the management of ruptured dissecting aneurysms. Primary endo-





716

12  Intracranial Aneurysms and Subarachnoid Hemorrhage

outcome with endovascular treatment [714]. 2. Nonhemorrhagic dissecting aneurysms: (a) For symptomatic dissecting aneurysms without hemorrhage, conservative management may be the best option. In the Japanese nationwide study, the majority of nonhemorrhagic dissecting aneurysms were managed without surgery or intervention, and a good recovery (by Glasgow outcome scale) was achieved in 79% of patients [709]. Dolichoectatic, Fusiform, and Serpentine Aneurysms Dolichoectatic and fusiform aneurysms are uncommon, accounting for 7  mm and symptomatic progression (b) Mortality: 0.51% per year 2. Atherosclerotic fusiform aneurysms (a) Aneurysm progression: 12% per year (b) Mortality: 5.2% per year Growth and rupture rates of vertebrobasilar nonsaccular aneurysms: [736] 1. 2. 3.

Fusiform (a) Annual growth rate: 6.4% (b) Annual rupture rate: 1.7% Dolichoectasia (a) Annual growth rate: 2.4% (b) Annual rupture rate: 0.4% Transitional aneurysms (a) Annual growth rate: 15.8% (b) Annual rupture rate: 3.5%

Management Surgery or endovascular treatment is indicated for select patients with symptomatic lesions who are good candidates for a major intracranial procedure. Surgery of fusiform and dolichoectatic aneurysms

718

12  Intracranial Aneurysms and Subarachnoid Hemorrhage

can be complex. In some cases, the parent vessel can be reconstructed with a series of stacked fenestrated clips. Wrapping of fusiform aneurysms with cotton or some other material is of unclear benefit. Surgical trapping or proximal occlusions, with or without a bypass, and with or without debulking of the aneurysm are other options. Trapping is superior to proximal occlusion when possible. Because of the rarity of these lesions, endovascular reports are limited to case reports and small series. Good results have been obtained with endovascular parent vessel occlusion [701, 749]

and intravascular stenting combined with coiling [705]. Flow diversion may be an even better option. A study of 77 basilar trunk and vertebrobasilar junction aneurysm patients showed either stent-assisted coiling or flow diversion could effectively treat small (35%: 4.1% –– EF 29–35%: 7.8% –– EF ≤28%: 8.9% (iii) Reduction of stroke risk in patients with cardiomyopathy. • Anticoagulation has been compared to antiplatelet therapy in several randomized trials with mixed results • The 2014 AHA Guidelines for Primary Prevention of Stroke recommends either anticoagulation or antiplatelet therapy in patients with heart failure and without AF or a previous stroke • For secondary prevention, anticoagulation with warfarin is recommended for at least 3 months [92] (e) Endocarditis (i) Endocarditis accounts for less than 1% of thromboembolic ischemic strokes and is classified as either bacterial [229] (aka infective) or nonbacterial thrombotic endocarditis (aka marantic or verrucous) [230]. Conditions predisposing to bacterial endocarditis (BE) include valvular abnormalities, catheter-­



related blood stream infections, intravenous drug use, and immune suppression. BE can occur on native or prosthetic valves, and in the majority of cases, either streptococci or staphylococci are involved. NBTE is most often associated with malignancy, disseminated intravascular coagulation, systemic lupus erythematosus with antiphospholipid syndrome, and primary hypercoagulability in the setting of previously normal valves. In these conditions, valvular vegetations are sterile and typically consist of fibrin and platelets. The term Libman-­Sacks endocarditis refers to sterile endocardial lesions in patients with systemic lupus erythematosus and the antiphospholipid syndrome (see Coagulopathy section below). (ii) Diagnosis • Bacterial endocarditis (Table 16.5) –– Clinical exam findings of systemic embolization

Table 16.5  Modified Duke criteria for diagnosis of bacterial endocarditis [229] Major criteria • Microorganisms isolated from two separate blood cultures, persistent bacteremia, or a single culture with Coxiella burnetii • Evidence of endocardial lesion (new valvular regurgitation or positive echocardiogram) Minor criteria • Predisposition (IV drug use, previous BE, prosthetic heart valve, mitral valve prolapse, etc.) • Fever • Evidence of embolization • Immunologic phenomena (Osler nodes, Janeway lesions, etc.) • Microbiologic findings not meeting major criteria Definite bacterial endocarditis  Two major criteria OR one major and three minor criteria OR 5 minor criteria Possible bacterial endocarditis  One major and one minor criteria OR three minor criteria

16.8  Classification of Stroke Etiologies

Osler nodes: tender nodules on finger and toe pads, present in 10–25% of patients with BE, but not specific to BE Janeway lesions: nodular hemorrhages on palms and soles, most likely associated with BE when seen on physical exam Petechiae and palpable purpura Splinter hemorrhages: subungual, dark red streaks; may also be seen with trauma Roth spots: oval retinal hemorrhages with pale centers –– New cardiac murmur –– Positive blood cultures –– Evidence of vegetation on echocardiography Transthoracic echo can detect large lesions but transesophageal echo is more sensitive –– Culture-negative endocarditis Blood cultures are sterile in up to 5% of cases of bacterial endocarditis diagnosed using strict criteria outlined earlier Causes of sterile cultures: prior use of antibiotics, right heart endocarditis, slow-growing organisms, fungi, intracellular pathogens, and nonbacterial thrombotic endocarditis [229] • Nonbacterial thrombotic endocarditis –– Diagnosis Echocardiographic evidence of vegetation Sterile blood cultures

931







Evidence of systemic embolization Frequently there is a prothrombotic condition present, such as cancer or antiphospholipid syndrome Cardiac murmurs are infrequent (unlike in bacterial endocarditis) Osler nodes: tender nodules on finger and toe pads, present in 10–25% of (iii) Ischemic stroke risk • Bacterial endocarditis –– Up to 20% of patients have ischemic stroke and up to 65% may have embolization elsewhere –– Vegetations on the anterior leaflet of the mitral valve and >10 mm in size [231] are most likely to embolize –– Cerebral embolization of vegetations containing bacteria can result in cerebral ischemia, abscess, arteritis and infectious aneurysm formation, and hemorrhage • Nonbacterial thrombotic endocarditis –– Systemic (including brain) emboli are present on autopsy in almost half of patients with NBTE [232] (iv) Other complications of bacterial endocarditis [229] • Congestive heart failure in up to 50% of patients • Glomerulonephritis • Annular abscess or cardiac conduction system disruption (v) Management • Bacterial endocarditis –– Obtain blood cultures –– Begin empiric IV antibiotics targeting the most likely organisms

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–– Adjust antibiotics based on culture sensitivities –– If valves are prosthetic, continue systemic anticoagulation, unless there is evidence of hemorrhage or the infarct is large, i.e., at risk for hemorrhagic transformation –– There is no role for systemic anticoagulation in the case of native valves, and initiation may increase the risk of hemorrhagic conversion of cerebral infarcts –– Surgical management is reserved for cases of valvular insufficiency, heart failure, continued embolization, or persistent bacteremia despite appropriate antibiotic therapy, highly resistant virulent organisms, immediate relapse after completion of therapy, or large vegetations on the mitral valve • Nonbacterial thrombotic endocarditis [230] –– Evaluate the patient for malignancy, primary hypercoagulability, and antiphospholipid syndrome and treat the primary condition accordingly –– Unless contraindicated (i.e., in the setting of hemorrhage or moderate-to-large acute cerebral infarcts), systemic anticoagulation should be used In patients with malignancy, heparins may be more effective than warfarin or other vitamin K antagonists In patients with primary hypercoagulability or antiphospholipid syndrome, warfarin should be used

Consider surgery for patients with large vegetation or destructive valvular lesions [233] –– Yada (f) Valvulopathies (i) Abnormalities of cardiac valves may lead to ischemic stroke. Mitral valve prolapse is the most common valvulopathy in adults and is thought to be a cause of cerebral embolism in rare patients with cryptogenic stroke. Mitral valve prolapse may also predispose to bacterial endocarditis. Mitral annular calcification may be linked with cardiac conduction abnormalities and is thought to be a risk factor for cardioembolism. Prosthetic mechanical valves are extremely thrombogenic and require life-long anticoagulation with warfarin sodium. Rheumatic mitral valve disease and other valvulopathies may be associated with atrial fibrillation, dramatically increasing the risk of cardioembolism. (ii) Ischemic stroke risk [116]. • Rheumatic mitral valve disease, recurrent embolism: 30–65%, most within 6 months of the initial event • Mechanical prosthetic heart valves: Four percent per year without anticoagulation; 1% per year with anticoagulation [234] • Bioprosthetic valves: One percent per year, risk highest within 3  months of valve replacement surgery [234] (iii) Management of ischemic stroke risk in patients with valvulopathies. • Rheumatic heart disease –– Primary prevention [235] With atrial fibrillation: Life-long warfarin therapy, goal INR 2–3

16.8  Classification of Stroke Etiologies

With mitral or tricuspid stenosis and sinus rhythm with enlarged atrium or atrium with clot: Long-­ term warfarin therapy, goal INR 2–3 –– Secondary prevention Long-term warfarin therapy, goal INR 2–3 Add aspirin, 81 mg/day, to warfarin in cases of recurrent embolism despite proper warfarin anticoagulation • Prosthetic heart valves –– Modern mechanical valves Life-long anticoagulation with warfarin, goal INR 2.5–3.5 Add aspirin in cases of thromboembolism despite proper warfarin anticoagulation Consider a higher INR goal (3.0–4.5) for patients with caged ball or disk valves [234] –– Bioprosthetic valves Primary prevention: For patients with a mitral bioprosthetic valve, oral anticoagulation to goal INR 2–3 for 3 months after surgery, then aspirin 325  mg per day if in sinus rhythm; the same approach may be considered for aortic bioprosthetic valves [234] Secondary prevention: Long-term warfarin therapy, goal INR 2–3 (g) Atrial myxoma (i) The incidence of primary cardiac tumors is 1 in 5000 [236]. Atrial myxoma is the most common primary cardiac tumor in adults and is usually located in the left atrium. There is a

933

3.

4.

2:1 female predominance; diagnosis is most common between the third and sixth decade; and some cases are familial [237]. Patients with atrial myxoma present with symptoms related to flow obstruction (50–70% of patients), peripheral or central embolization (16–30%), and/or constitutional disturbance (50–58% of patients). Embolization is related to a thrombus located on the surface of the myxoma or embolization of tumor fragments. Tumor emboli may subsequently evolve into mass lesions (myxomatous metastasis) or vascular erosion and aneurysm formation may occur. Myxomatous cerebral aneurysms are similar to infectious aneurysms and feature fusiform shape and distal locations [237] (see Fig.12.2 in Chap. 12). The diagnosis of atrial myxoma can be made on transesophageal echocardiography; treatment centers on surgical resection, which is typically curative. Small artery occlusion (SAO, 23% of stroke cases [204]) (a) Most commonly atherosclerotic perforator and small distal vessel occlusion (see Lacunar syndromes, above) (b) May overlap with presentations of vasculitis or CADASIL (see below) Other determined cause (OC, only 2% of stroke cases [204]) (a) Vasculitis (i) The vasculitis syndromes are inflammatory vasculopathies. CNS vasculitis may be part of a systemic vasculitis; it can be primary, i.e., isolated to the CNS; or it can be related to a connective tissue disease or another systemic disease process [238, 239]. Vasculitis syndromes can be classified according to many schemes, including the size of predominantly involved blood vessels (small, medium, or large) or type of

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pathologic process (necrotizing, immune complex-mediated, granulomatous, etc.). Classification of selected primary systemic vasculitidies [240] Vessel size Pathophysiology Examples Large (aorta, Granulomatous Giant cell arteritis large arteries) vasculitis Takayasu arteritis Medium Necrotizing Polyarteritis (arteries, arteritis nodosa arterioles) Small Vascular immune Lupus vasculitis, (arterioles, complexes rheumatoid capillaries, vasculitis venules, Rare vascular Wegener’s veins) immune granulomatosis, complexes Churg–Strauss syndrome





(ii) CNS involvement with vasculitis generally presents with a prolonged and progressive functional decline, encephalopathy, seizures, and cerebral ischemic and hemorrhagic lesions [238, 239]. Although “vasculitis” is often invoked when interpreting cerebral angiograms showing features characteristic of inflammatory vasculopathy, it is important to keep in mind that the diagnosis of CNS vasculitis cannot be made solely on the basis of angiography. Vasculitis is a pathologic diagnosis; and in the absence of a tissue diagnosis, appropriate clinical history, physical exam findings, CSF, and other laboratory values, along with appropriate imaging [241], are required to make the diagnosis. (iii) Systemic vasculitis syndromes • Giant cell arteritis (aka temporal arteritis, Horton’s disease, Hutchinson-Horton disease) –– Characteristics Most common primary vasculitis in adults >50 years old

Perivascular inflammation leads to intimal hyperplasia, usually without thrombosis Largely extracranial involvement, but 20–50% can present with vision loss or ischemic stroke [238] Headache is the most common symptom; occurs in 65–75% of patients [242] Scalp tenderness and jaw claudication may occur and are highly suggestive of the diagnosis –– An elevated erythrocyte sedimentation rate (ESR, >50 mm/h) is a useful marker for giant cell arteritis [243]; however, ESR is normal in up to 20% of cases [244] –– Diagnostic criteria (3 of 5 are required) [242] Age of onset ≥50 New onset or new type of headache Temporal artery tenderness or attenuated pulsation Westergren ESR >50 mm/h [50] Positive temporal artery biopsy [240] –– Management Immune suppression with corticosteroids Consider antithrombotic therapy for patients with ischemic stroke [245] • Takayasu arteritis (aka pulseless disease) –– Characteristics Involves the aorta and branches, but intracranial involvement may occur Media and adventitia thickening leads to stenosis and occlusion

16.8  Classification of Stroke Etiologies

Neurologic symptoms are usually transient (TIA), although cerebral infarcts can also occur [246] –– Associated finding: Exacerbation of the disease may be associated with an elevated ESR –– Diagnostic criteria (3 of 6 required) [247] Age 10-mmHg blood pressure difference between arms Subclavian artery bruit Abnormal arteriogram –– Management Immune suppression with corticosteroids Cyclophosphamide, azathioprine, or methotrexate may be necessary • Polyarteritis nodosa (PAN) –– Characteristics Most common of the necrotizing vasculitis syndromes Features destruction of the vessel wall and aneurysm formation Organs involved include the brain, nerves, skeletal muscle, heart, and kidney Microangiopathic brain involvement is more common than medium cerebral vessel vasculitis [248] –– Associated findings Hepatitis may be present Peripheral nerve involvement is usually a mononeuropathy multiplex (scattered, asymmetric involvement of nerves at multiple sites).

935

–– Diagnostic criteria (3 of 10 required) [249] Weight loss ≥4kg Livedo reticularis Testicular tenderness Myalgias, weakness, leg tenderness Mono- or polyneuropathy Diastolic blood pressure >90 mmHg Elevation of blood urea nitrogen or creatinine Hepatitis B surface antibody or antigen positive Arteriogram showing visceral artery aneurysms or occlusion Biopsy showing granulocytes, or granulocytes and monocytes in the artery wall –– Management Immune suppression with corticosteroids; cyclophosphamide, azathioprine, or methotrexate may be necessary • Granulomatosis with polyangiitis (aka Wegener’s granulomatosis) [250] –– Characteristics Necrotizing vasculitis Granulomatous infiltration of the respiratory tract and necrotizing glomerulonephritis –– Associated findings Presence of circulating antineutrophil-cytoplasmic antibodies (cANCA) Generalized disease: in addition to lung and kidney involvement, manifests with arthritis, palpable purpura, neuropathy, and rarely cerebral infarction (infarcts may be due to

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nonbacterial thrombotic endocarditis or cerebral vasculitis) [251] –– Diagnostic criteria (2 of 4 required) [252] Oral ulcers or purulent or bloody nasal discharge Chest X-ray showing nodules, infiltrates, or cavities Microhematuria or red cell casts in the urine Biopsy with granulomatous inflammation within or around artery or arteriole –– Management Immune suppression with corticosteroids; cyclophosphamide, azathioprine, or methotrexate may be necessary • Allergic granulomatous angiitis (aka Churg–Strauss vasculitis) [250] –– Characteristics Necrotizing vasculitis Respiratory system involvement Rare cerebral infarction due to diagnostic criteria (4 of 6 required) [253, 254] –– Associated findings Eosinophilia, pulmonary infiltrates, nasal polyps, skin rash, and GI disturbances –– Diagnostic criteria (4 of 6 required) [253, 254] Asthma Peripheral eosinophilia >10% of total white blood count Peripheral neuropathy due to vasculitis Transient pulmonary infiltrates Paranasal sinus abnormalities

Biopsy showing eosinophils around blood vessels –– Management Immune suppression with corticosteroids; cyclophosphamide, azathioprine, or methotrexate may be necessary • Primary CNS vasculitis (aka CNS angiitis, CNS granulomatous angiitis, primary angiitis of the CNS, isolated angiitis of the CNS) [238, 255, 256] –– Characteristics Involvement of cortical and leptomeningeal vessels, usually small arteries Segmental granulomatous angiitis T-cell mediated process –– Clinical features [255] Slight male predominance (4M:3F), onset usually in middle age Presentation typically subacute, evolving over weeks to months with headache, cognitive decline, encephalopathy, seizures, and focal neurologic deficits –– Diagnostic criteria [255] Definite: Brain biopsy showing perivascular granulomatous infiltrates. Possible. Arteriogram with vascular beading Neurologic decline for at least 3 months Increased CSF protein and leukocyte count Other possible causes are excluded Brain biopsy: Although cortical and leptomeningeal biopsy may sometimes be negative (due to missing

16.8  Classification of Stroke Etiologies

inflammatory foci with the biopsy needle), the biopsy is important, especially if the patient is declining and cyclophosphamide therapy is being contemplated, as biopsy may provide an alternate diagnosis such as intravascular lymphoma. –– Management Immune suppression with corticosteroids; in some cases, cyclophosphamide may be necessary • Secondary CNS vasculitis [238, 239] –– Characteristics: Inflammatory exudates around arteries result in fibrosis and constriction or direct vascular infection/invasion results in lumenal stenosis –– Infections associated with CNS vasculitis Meningovascular syphilis (aka Heubner’s arteritis) involving small and medium-sized vessels Basal meningitis with M. tuberculosis or fungi involving the basilar artery and pontine perforators Bacterial meningitis with involvement of pial vessels Human immunodeficiency virus (HIV), although the etiology may be related to a co-existing infectious agent like varicella zoster (see below) Varicella zoster vasculitis

937

Varicella Zoster Vasculitis

Reactivation of latent varicella zoster virus (VZV) usually occurs in patients >60 years old and may or may not cause the characteristic dermatomal distributed rash. In immunocompetent hosts, VZV reactivation in the trigeminal ganglia may sometimes be followed several weeks later by ischemic stroke. Pathologically, cerebral ischemia is due to a granulomatous-necrotizing vasculitis of cerebral arteries: usually the internal carotid artery, middle cerebral artery, or anterior cerebral artery. In immunocompromised hosts, VZV reactivation may result in small-vessel vasculitis, concomitant encephalitis, and/or myelitis [257]. CSF anti-VZV IgG is a sensitive marker of VZV vasculopathy [258].

–– Diagnosis of CNS vasculitis associated with infections HIV testing; evaluation of CSF, including white cell count, red cell count, protein glucose, gram stain and culture, specific viral polymerase chain reaction (PCR) tests, anti-VZV IgG antibody, acid-fast stain, India ink fungal stain, cryptococcal antigen, VDRL as well as bacterial, fungal, and tuberculosis culture. Serum cryptococcal antigen is also a useful test in suspected cryptococcal meningitis. Interferon gamma release assays have

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supplemented the tuberculosis diagnostic armamentarium [259]. Brain MRI. Cerebral angiography (Fig. 16.11). Brain biopsy, if needed. –– Management Treat underlying infection using appropriate antibiotics at CNS doses Concomitant corticosteroids Dexamethasone started prior to the first dose of antibiotic in community-­ acquired bacterial meningitis improves outcome [260] Steroids used together with antiviral therapy have been used in VZV vasculitis and may be helpful in other similar conditions [257] • CNS vasculitis associated with connective tissue diseases

Fig. 16.11  CNS vasculitis. Lateral view of a carotid artery angiogram of a patient with HIV-related CNS vasculitis. Note the widespread characteristic beading of distal arteries that is typical—but nonspecific—for CNS vasculitis. Other conditions (e.g., RSVS) can look quite similar

–– Characteristics: Inflammatory exudates around arteries result in fibrosis and constriction resulting in luminal stenosis –– Selected connective tissue disorders associated with CNS vasculitis Systemic lupus erythematosus (SLE): Autoimmune inflammatory disease that involves multiple organs

Systemic Lupus Erythematosus (SLE)

Although cerebral vasculitis is frequently invoked as a cause of cerebral infarction in SLE, it is relatively rare. A seminal study of pathologic specimens from SLE patients showed that true vasculitis with intramural inflammation was present only in 3 of 24 cases [261]. Other, more common, causes of cerebral ischemia in SLE: noninflammatory cerebral vasculopathy; antiphospholipid antibody syndrome (see Coagulopathy section); cerebral microangiopathy due to hypertension; and cardioembolism due to Libman–Sacks endocarditis (see Endocarditis section) [262, 263].

Rheumatoid arthritis (RA): A multisystem disorder that can affect the brain by causing a lymphocytic pachymeningitis and arteritis Sjogren’s Syndrome: Characterized by keratoconjunctivitis, xerostomia, and a PAN-like vasculitis, which may involve multiple organs including the brain; associated with the presence in the blood of Ro ([SS]-A) and La ([SS]-B)

16.8  Classification of Stroke Etiologies

939

antibodies, the detection of which can aid with diagnosis –– Diagnosis of connective tissue diseases Clinical and historical evidence of a connective tissue disease Laboratory evaluation appropriate for the suspected condition, including serum rheumatoid factor (RA); SS-A, SS-B antibodies (Sjogren’s); antinuclear antibody, and anti-DNA antibodies (SLE) –– Management is disease-­ specific, usually involving immunosuppression • CNS vasculitis associated with drug use [264] –– Characteristics: Necrotizing arteritis, similar to polyarteritis nodosa –– Specific agents: Amphetamines and cocaine

Cocaine and Stroke

Cocaine administration by any route predisposes to ischemic and hemorrhagic strokes. Acute hypertension is thought to be related to hemorrhage especially in the setting of chronic hypertensive vasculopathy or in patients harboring intracranial aneurysms. Chronic hypertensive vasculopathy, microangiopathy, and acute vasospasm are thought to relate to ischemic stroke risk. Intravenous use can also predispose to endocarditis. Unlike in cases of amphetamine-related cerebral vasculitis, true cerebral vasculitis in chronic cocaine use has not been frequently demonstrated [264].

–– Heroin and other opioids: Vasculopathy leading to cerebral ischemia has been observed, although histological proof of an inflammatory etiology is lacking [265]; endocarditis is another common etiology of cerebral ischemia with heroin use –– Diagnosis: History, physical exam (needle tracks), urine drug screen –– Management: Abstinence from drug use • CNS vasculitis associated with other selected systemic diseases [238, 239] –– Behçet’s disease: Characterized by oral and genital ulcers, and iritis; the associated vasculitis may involve the brain; treatment is of the underlying disease [266] –– Paraneoplastic cerebritis: Perivascular inflammation has sometimes been associated with cerebritis; treatment is of the underlying malignancy –– Lymphoma: An associated CNS vasculitis similar to primary CNS vasculitis has been observed; treatment is of the underlying malignancy (b) Vasospasm (i) The term vasospasm indicates functional contraction of vascular smooth muscle cells. Although most cases of vasospasm are reversible or self-­ limited, the length of time during which the vessel is in spasm may be variable, from seconds to days. Post-­ subarachnoid hemorrhage vasospasm occurs 3–14  days after the hemorrhage. Postsubarachnoid hemorrhage vasospasm is characterized by initial functional arterial contraction result-

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ing in luminal narrowing, followed by progression to actual structural changes within the arteries: intimal proliferation with progressive luminal narrowing and, subsequently, necrosis of the tunica media. In a subset of patients, these vascular changes lead to cerebral ischemia: 5–10% of hospitalized patients with aneurysmal subarachnoid hemorrhage die from severe cerebral vasospasm. Subarachnoid hemorrhage and vasospasm are discussed in Chap. 12. (ii) Reversible cerebrovascular constriction (RCVS, aka Call Fleming syndrome, benign cerebral angiopathy, and postpartum cerebral angiopathy) [267]. • Characteristics –– The majority of patients are female; prevalence is low –– Presentation is with a thunderclap headache mimicking subarachnoid hemorrhage; seizures, nausea, and vomiting may accompany the headache –– CT is usually normal in the acute phase and CSF analysis is unremarkable; cerebral angiography and MRA demonstrate

diffuse arterial luminal narrowing, sometimes mimicking angiographic findings of vasculitis (Fig. 16.12) • Associated conditions, possibly precipitating factors –– Sympathomimetic and serotonergic drugs –– Migraine –– Pregnancy/puerperium (aka postpartum cerebral angiopathy) • Diagnostic criteria [269] –– Acute and severe headaches with or without focal deficits or seizures –– Uniphasic course without new symptoms for more than 1 month –– Segmental constriction of cerebral arteries on cerebral or MR angiography –– No evidence of aneurysmal subarachnoid hemorrhage –– Normal or near-normal CSF (protein 80% of patients in the Rotterdam Study had calcification of the intracranial internal carotid artery (ICA) [3]. Distribution of symptomatic ICAD by location [4]: 1. 2. 3. 4. 5.

ICA—20.3% MCA—33.9% Vertebral artery—19.6% Basilar artery—20.3% Multiple arteries—5.9% Risk factors:

1. Black, Asian, or Hispanic ethnicity [5] (a) Black patients with TIA or stroke are more likely than white patients to have ICAD, whereas whites are more likely to have extracranial carotid atherosclerotic stenosis [6].

19



(i) In a comparison of white and black patients with symptomatic posterior circulation disease, black patients had more lesions of the distal basilar artery, more high-grade lesions of intracranial branch vessels, and more symptomatic intracranial branch disease. Race was found to be the only factor increasing the risk of intracranial posterior circulation occlusive disease [7]. (b) Asian patients have a higher proportion of ICAD compared to Caucasians [1]. (i) The Chinese IntraCranial Atherosclerosis Study (CICAS) reported on 2,846 patients with non-cardiogenic ischemic stroke [8]. The prevalence of ICAD (≥50%) was 46.6%. (c) Reasons for the dramatic differences in intracranial atherosclerosis among ethnic groups are likely multifactorial, and due to differences in genetic susceptibility, lifestyles, and risk factors. 2. Hypertension is present in up to 75% of patients [9]. Diabetes, coronary artery disease, cigarette smoking, hypercholesterolemia, and peripheral arterial occlusive disease are also strongly associated. 3. Patients without carotid bifurcation disease are more likely to demonstrate progression of ICAD compared with patients with it [10].

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 M. R. Harrigan, J. P. Deveikis, Handbook of Cerebrovascular Disease and Neurointerventional Technique, Contemporary Medical Imaging, https://doi.org/10.1007/978-3-031-45598-8_19

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4. Metabolic syndrome is present in about 50% volumetric flow rates. Some 25% of of patients with symptomatic intracranial athpatients had reduction of flow >20% erosclerotic disease and is associated with a below normal and had a significantly substantially higher risk of major vascular higher risk of ischemic stroke in the events. affected territory compared to patients (a) Metabolic syndrome is a cluster of interwith normal flow (28% vs. 9%, related risk factors that together increase p  =  0.4, median follow-up period of an individual’s risk of cardiovascular dis24 months). ease [11]. The syndrome consists of four (b) Collateral circulation main categories of metabolic abnormali- (i) Collateral circulation, or the collatties: atherogenic dyslipidemia (elevated erome [14], is defined as the suppletriglycerides and decreased high-density mentary network of vascular channels lipoproteins), increased blood pressure, that stabilize cerebral blood flow elevated plasma glucose, and a pro-­ when the principal conduit fails [15]. thrombotic state. Some 24% of the US Although chronic ischemia can lead adults have metabolic syndrome [12]. to expansion of the collateral circulation [16], the capacity of collaterals to protect against ischemia remains Global Gem! ICAD highly variable among individuals. An Intracranial arterial stenosis is more prevaanalysis of WASID subjects (see lent among Asian and African people combelow) found that patients with ≥70% pared to whites [6]. Based on racial and ICAD an poor, or absent collaterals, ethnic patterns, ICAD may be the most had a six-fold higher chance of having important cause of ischemic stroke in the a stroke compared to patients with world. good collaterals [17]. 2. Occlusion of branches of the artery by the atherosclerotic plaque. (a) An MRI study of 80 patients with stroke 19.2 Etiology of Symptoms due to ICAD found [18]: (i) Branch occlusions were present in Cerebral ischemia due to ICAD occurs as a result 45% of cases, and were milder degrees of one or a combination of mechanisms. The of stenosis compared to non-branch pathophysiology of atherosclerosis is covered in occlusion cases. Chap. 18. 3. Thrombosis at the site of stenosis due to plaque rupture or hemorrhage within the 1. Hypoperfusion. Impaired perfusion results plaque [19]. from a combination of reduction of flow through the region of stenosis and impaired 4. Artery-to-artery thromboembolism distal to the stenosis. collateral circulation. (a) Reduction of flow (i) The Vertebrobasilar flow Evaluation and Risk of Transient Ischemic Attack 19.3 Imaging and Stroke (VERiTAS) study used quantitative MRA to assess arterial All four imaging modalities, listed below, proflow in patients with ischemic symp- vide useful and complementary information toms due to stenosis ≥50% [13]. about patients with ICAD.  The authors of this Quantitative MRA combines time-of-­ handbook favor using both MRI/MRA and CTA flight and phase-contrast MRA tech- for most patients and catheter angiography for niques to derive vessel-specific some patients.

19.4  Natural History

1. MRI/MRA (a) Advantages: (i) Detailed brain imaging; can distinguish remote infarction (on FLAIR) from acute infarction (on DWI and ADC). (ii) MRA is better than CTA for imaging the petrous and cavernous ICA. (iii) High-resolution MRI can provide information about plaque composition and morphology [20]. (iv) Quantitative MRA can assess blood flow to provide information about additional risk of stroke [13]. (v) No ionizing radiation or contrast needed. (b) Disadvantages: (i) A flow gap on MRA suggests >50% stenosis, although it can be hard to distinguish stenosis from artifact or occlusion [21]. (ii) MRA is also limited in distinguishing atherosclerotic stenosis from arterial dissection, vasospasm, or thrombosis. (iii) MR studies may be contraindicated in some patients with implanted devices (e.g., implanted defibrillators or pacemakers) (iv) Claustrophobic patients may not tolerate being in a closed MR scanner. 2. CTA (a) Advantages: (i) Provides more precise anatomic detail compared to MRA. (ii) More readily available than MRA in many institutions. (b) Disadvantages: (i) Limited visualization of the petrous and cavernous ICA. (ii) Image quality may be poor in patients with poor cardiac output. (iii) Requires adequate venous access for rapid contrast bolus. (iv) Requires ionizing radiation and intravenous contrast. 3. Catheter angiography (a) Advantages:

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(i) High anatomic resolution. (ii) Permits assessment of collateral circulation. (iii) Often uses a lower volume of contrast than CTA studies. (b) Disadvantages: (i) Invasive and costly. (ii) Requires ionizing radiation and intravascular contrast. 4. Transcranial Doppler ultrasonography (a) Optimal velocity criteria for diagnosis of ≥70% stenosis [22]. (i) MCA: >120  cm/s, stenotic/prestenotic ratio ≥3, or low velocity. (ii) Vertebral/basilar artery: >110 cm/s or stenotic/prestenotic ratio ≥3. (b) Advantages: (i) Noninvasive and low-risk. (ii) TCD can assess for emboli, arterial steal, and collateral circulation. (iii) Can provide quantitative flow velocity. (iv) No ionizing radiation and no intravenous contrast. (c) Disadvantage: (i) Provides very little anatomic information. (ii) Limited number of vessels are visualized. (iii) Strongly dependent on both operator skill and patient anatomy to be able to visualize desired vascular structures.

19.4 Natural History Intracranial atherosclerotic stenoses are dynamic lesions that may demonstrate both progression and regression on serial imaging. 1. In a study of patients with ICAD undergoing repeat angiography at an average interval of 26.7 months, 40% of lesions were stable, 20% regressed, and 40% progressed [10]. 2. Stenosis progression, as detected by TCD, is an independent predictor of stroke recurrence [23].

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3. Extracranial-intracranial (EC-IC) bypass ­therapy had an annual ipsilateral ischemic stroke surgery promotes progression of the lesion rate of 7.8% per year [24]. The EC/IC Bypass and occlusion of MCA in patients with non-­ Study is discussed in detail in Chap. 18. occluded MCA stenosis [24]. Asymptomatic ICAD is generally believed to be benign. In a series of 50 patients with asymptomatic MCA stenosis followed for a mean of 351 days, no patient had an ischemic stroke in the corresponding territory [9]. The best studies of the natural history of symptomatic stenosis have been from several prospective studies of medical therapy. Estimates of the overall annual ipsilateral stroke risk in patients with ICAD from prospective studies range from 2.3 to nearly 13%. The most definitive studies so far are the EC/IC Bypass trial [24], the prospective WASID trial [4], SAMMPRIS [25], and MyRIAD [26].

EC/IC Bypass Study

 arfarin vs. Aspirin for Symptomatic W Intracranial Disease (WASID) studies The WASID studies compared anticoagulation to antiplatelet agents in the management of patients with symptomatic ICAD.  Two separate studies were done. The first study was retrospective and suggested that warfarin is superior to aspirin [27]. The second study was a prospective, multicenter, double-blinded randomized trial. Warfarin was associated with significantly higher rates of adverse events and did not provide a benefit over aspirin [4].

WASID Prospective Trial

The subset of patients in the EC/IC Bypass Study with MCA stenosis randomized to medical

A total of 569 patients with TIA or stroke attributable to angiographically verified 50–99% stenosis of a major intracranial artery (Fig.  19.1)

Fig. 19.1  WASID technique for measuring ICAD.  The equation used for determining percent stenosis of a major intracranial artery in WASID [28]. Dstenosis the diameter of the artery at the site of the most severe degree of stenosis, Dnormal the diameter of the proximal normal artery. Dnormal is selected according to the following criteria: (1) First choice (left): The diameter of the proximal part of the artery at its widest, nontortuous, normal segment is selected. Stenotic region (arrow); reference area (Dnormal)

(open arrow). (2) Second choice (right): If the lesion is at the origin of the vessel, or if the proximal artery is diseased (e.g., proximal basilar artery stenosis or M1 segment origin stenosis), the diameter of the distal portion of the artery at its widest, parallel, nontortuous normal segment is used. Stenotic region (arrow); reference area (Dnormal) (open arrow). (3) Third choice: If the entire intracranial artery is diseased, the most distal, parallel, nontortuous normal segment of the feeding artery is measured

19.4  Natural History

were randomized to receive warfarin (target INR, 2.0–3.0) or aspirin (1300  mg per day) [4]. Enrollment was stopped prematurely (enrollment of 806 patients was originally planned) because of a significantly higher rate of hemorrhage in the warfarin group. The median time from qualifying event to randomization was 17  days, and the mean follow-up period was 1.8  years. Principal finding: The risk of ischemic stroke was similar for both antiplatelets and anticoagulation, but the rate of bleeding was higher in the anticoagulation group. 1. The primary end point of ischemic stroke, brain hemorrhage, or death from vascular causes other than stroke: (a) 21.8% in the warfarin group (b) 22.1% in the aspirin group (p = 0.83) 2. Rate of death: (a) 9.7% in the warfarin group (b) 4.3% in the aspirin group (p = 0.02) 3. Major hemorrhage (a) 8.3% in the warfarin group (b) 3.2% in the aspirin group (p = 0.01) 4. Myocardial infarction or sudden death: (a) 7.3% in the warfarin group (b) 2.9% in the aspirin group (p = 0.02) 5. Rate of death from vascular causes: (a) 5.9% in the warfarin group (b) 3.2% in the aspirin group (p = 0.16) 6. Rate of death from nonvascular causes (a) 3.8% in the warfarin group (b) 1.1% in the aspirin group (p = 0.05) The risk of ischemic stroke in the territory of the stenotic artery at 1 year in patients treated with aspirin was 12%, and in patients treated with warfarin, the risk was 11% (p = 0.31). Because of the high adverse event rates for patients treated with warfarin, and lack of therapeutic benefit of warfarin over aspirin for prevention of ischemic stroke caused by ICAD, the WASID investigators concluded that aspirin should be used in preference to warfarin for patients with intracranial arterial stenosis.

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 ASID Prospective Trial Subgroup W Analyses  ASID Predictors of Ischemic Stroke W in the Territory of a Symptomatic Intracranial Stenosis The majority of strokes (73%) in WASID patients were in the territory of the stenotic artery [29]. The risk of stroke in the territory of the stenotic artery was greatest in patients with the following characteristics: 1. Severe (≥70%) stenosis (p = 0.0025). 2. Patients enrolled early (≤17 days) (p = 0.028). 3. There was a statistical trend toward an increased risk for women (p = 0.051). 4. Location of stenosis, type of qualifying event, and prior use of antithrombotic medications were not associated with increased risk.

MyRIAD Prospective, in-depth observational study of 102 patients after stroke or TIA due to ICAD 50–99% and treated with aggressive medical therapy [26]. The primary outcome was ischemic stroke in the territory of the affected artery; mean follow-up was 253 days. 1. The primary outcome occurred in 8.8% of patients and a TIA attributable to the symptomatic artery occurred in 5.9%. 2. A new infarct in the territory of the affected artery was found in 24.7%. 3. An assortment of mechanisms for recurrent symptoms were identified, underscoring the complexity and heterogeneity of ICAD. (a) A low-flow state on quantitative MRA: 25.5% of all patients (b) Poor distal perfusion on perfusion-weighted MRI: 43.5% (c) Impaired vasoreactivity: 67.5% (d) Microemboli on ultrasound: 39.0%

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19.5 Medical Treatment of Symptomatic ICAD

19.6

The aggressive medical management-only group in SAMMPRIS (see below) did unexpectedly well in terms of risk of stroke, both compared to the stenting group in SAMMPRIS, and patients in WASID. Underscoring the power of aggressive management was the observation that SAMMPRIS medical management arm patients had nearly half the risk of stroke and death compared to patients in WASID [30]. Indeed, the Trial of cilOstazol in Symptomatic ICAD 2 (TOSS-2) found that control of hyperlipidemia can prevent progression of ICAD [31]. Therefore the SAMMPRIS aggressive medical management protocol has become de rigueur for patients with atherosclerotic cerebrovascular disease, and has been incorporated into the CREST 2 ­protocol. Medical management of symptomatic ICAD centers on antiplatelet therapy and aggressive control of risk factors such as hyperlipidemia, diabetes, hypertension, and cigarette smoking. Medical therapy is discussed in detail in Chap. 17: Acute Ischemic Stroke. The SAMMPRIS study monitored patients every four months and employed a detailed algorithm for medical management but the essential features of treatment included [32]:

Intracranial angioplasty with or without stenting is an option for patients with symptomatic ICAD. Early reports of angioplasty without stenting were followed by studies of balloon-mounted coronary stents. Angioplasty without stenting was limited by higher restenosis rates, compared to angioplasty and stenting [33], and balloon-­ mounted stents, designed for the coronary arteries, carried a high risk of complications in the intracranial posterior circulation [34]. Major non-randomized studies of intracranial stenting included SSYLVIA (Stenting of Symptomatic Atherosclerotic Lesions in the Vertebral or Intracranial Arteries) [35], which employed the Neurolink balloon-mounted stent, and the Wingspan Trial [36], which used the self-­expanding Wingspan™ Stent System with Gateway™ PTA Balloon Catheter (Stryker Neurovascular, Fremont, CA). Both studies reported relatively favorable results. The Neurolink (a product of the Guidant Corporation, which is now part of Boston Scientific) is no longer available. The SAMMPRIS trial (see below), which began enrollment in 2008, was a randomized trial of patients with 70–99% stenosis comparing aggressive medical management to aggressive medical management plus Wingspan angioplasty and stenting. Enrollment was stopped in April 2011 because of a high rate of periprocedural stroke and death in the stenting group. The VISSIT trial (Vitesse Intracranial Stent Study for Ischemic Stroke Therapy) was a randomized trial comparing the Pharos Vitesse balloon expandable stent (Micrus) to medical therapy for symptomatic ICAD [37]. Enrollment in VISSIT trial was stopped early because of the results of SAMMPRIS. However, the study did find a significantly higher rate of stroke or TIA at one year with stenting compared to medical therapy (36.2% vs 15.1%, p = 0.02). The Pharos Vitesse stent is no longer available either. In the wake of the SAMMPRIS results, many opera-

1. Aspirin 325  mg QD and clopidogrel 75  mg QD for 90 days. 2. Target systolic blood pressure 40 had the worst angiographic results from indirect procedures, leading the authors to conclude that direct procedures (or combined procedures) should be the main treatment option for patients of age >40. (b) Synangiosis procedures work best when there is some degree of hemodynamic stress, as demonstrated by CBF imaging (e.g., PET, or xenon CT or SPECT with acetazolamide challenge) [126]. (c) Elevated CSF bFGF levels may predict the extent of angiogenesis to be expected with indirect revascularization [92].

19.9  Moyamoya Disease and Moyamoya Syndrome

(d) Patients with extensive spontaneous transdural collateral vessels (vault collaterals) should not be considered for synangiosis [209]. 7. Surgical results (a) Pediatric moyamoya disease: A review of 57 studies of revascularization surgery for pediatric moyamoya found the following [224]: (i) Indirect procedures are the most commonly reported (73% of cases) and combined direct and indirect was next (23%). (ii) In 87% of cases the patients were reported to derive symptomatic benefit. (iii) Overall rates of perioperative stroke and reversible deficit were 4.4% and 6.1%, respectively. (b) Adult ischemic moyamoya: Several series have reported clinical improvement in most adults undergoing revascularization procedures [209, 210, 226, 228, 229]. (i) Two North American retrospective series have reported a benefit with revascularization: • Chiu [209]: The 5-year risk of ipsilateral stroke after indirect revascularization was 15%, compared with 20% for medical treatment. • Hallemeier [210]: The 5-year risk of perioperative or subsequent ipsilateral stroke or death for surgical patients was 17%, compared with 65% for patients not having surgery. (c) Cheiro-oral syndrome (i) Cheiro-oral syndrome (pronounced chiro-oral, as in chiropractor) consists of sensory disturbances around the corner of the mouth and the hand without significant motor impairment [230]. Transient cheiro-oral syndrome occurs in 22.9% of patients undergoing bypass surgery for moyamoya disease [231]. This may occur because of

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a transient reduction in flow through lenticulostriate vessels after surgery. 8. Hemorrhagic moyamoya disease. The role of bypass surgery in patients with hemorrhagic moyamoya was assessed in the Japan Adult Moyamoya Trial.

Japan Adult Moyamoya Trial (JAM) Eighty adult patients with moyamoya disease and a history of hemorrhage within the previous year were randomized to bilateral direct STA-MCA bypass (42 patients) or nonsurgical management (38 patients) [232]. Primary endpoint was any adverse event during a mean follow-up period of 4.32 years. Patients assigned to the bypass group underwent surgery on both sides (each side within 3 months of enrollment). 1. All adverse events, Kaplan-Meier survival analysis: (a) 3.2% per year in the surgery group (b) 8.2% per year in the nonsurgical group (p = 0.048) 2. Rebleeding, Kaplan-Meier survival analysis: (a) 2.7% per year in the surgery group (b) 7.6% per year in the nonsurgical group (p = 0.042) 3. Perioperative complications occurred in eight patients having surgery, but only one (2.4%) was permanent. No permanent severe disability was observed. Commentary: This relatively small study, with statistically marginal results, suggests that direct bypass surgery is protective against recurrent hemorrhage. However, a larger study will be needed to confirm this finding. In addition, the study focused on outcome within five years; and recurrent bleeding may occur >10 years after the initial hemorrhage [134]. Also, although the surgical results appeared to be very good (and therefore may not be applied to surgeons with less expertise in bypass surgery), neither of the endpoints included surgical complications, which results in bias in favor of surgery [233].

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Intracranial Angioplasty Several cases of intracranial angioplasty with or without stenting for ischemic moyamoya disease have been reported [53, 234]. In two small series of endovascular treatment in this setting, the rates of recurrence of symptoms were high, occurring in the majority of patients [235, 236]. Based on a systematic review including this data [237], successful prevention of recurrent stenosis or recurrent stroke was only achieved in 25% of treated patients. Hemorrhage occurred in 7%. There is no indication that angioplasty and stenting is a durable treatment for moyamoya disease.

Pregnancy and Moyamoya A review of 30 reported cases of patients with moyamoya disease and pregnancy found that good outcomes were achieved for both mother and child in all but one case [238]. The one poor outcome occurred in a woman with hemorrhagic moyamoya disease. The authors concluded that pregnancy can be managed successfully in patients with moyamoya disease. Furthermore, they surmised that the presence of moyamoya disease should not determine the method of delivery, as successful deliveries have been obtained with both vaginal delivery and cesarean section.

19.10 Kids Korner: ACTA2 Mutation and Cerebrovascular Disease: “Moyamoya-like Syndrome?” Congenital mutations of the ACTA2 gene can be associated with smooth muscle dysfunction manifesting as thoracic aortic aneurysms, dissections,

19  Intracranial Cerebrovascular Occlusive Disease

premature coronary artery disease, and stroke [239, 240]. They can often have dilated pupils from iris hypoplasia, patent ductus arteriosus, and a very characteristic markedly dysplastic, dolichoectatic petrous internal carotid with relatively small supraclinoid carotid and middle cerebral arteries and abnormal, straight middle cerebral branches with corkscrew-like distal branches (Fig.  19.5). The syndrome is seen with both the Arg179 and Arg 258 mutations of this gene [241]. These finding were originally described as “moyamoya-like syndrome” [242]. Histologically, the ACTA2 patients showed distinct differences from moyamoya which displays attenuation of the media and small vessel collateral proliferation, whereas ACTA2 displays distinctive vessel wall thickening with smooth muscle proliferation, and medial fibrosis that may explain the characteristic straight small distal branches [243]. The transition between the dilated petrous and more normal distal internal carotid are thought to be related to the transition between a predominantly elastic and muscular vessel wall [241]. There have been a number of reports of associated occlusive disease of the terminal carotid and proximal middle cerebral similar to moyamoya associated with these mutations [240, 241, 244]. Typical small vessel basal moyamoya collaterals usually seen in moyamoya are not a feature of ACTA2 vasculopathy, and the widespread vasculopathy and carotid dolichoectasia of ACTA2 vasculopathy are not a feature of moyamoya [241]. There have been isolated case reports of treatment by surgical bypass for occlusive changes in patients with this disease [242].

19.10  Kids Korner: ACTA2 Mutation and Cerebrovascular Disease: “Moyamoya-like Syndrome?”

a

b

c

d

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f e

Fig. 19.5  ACTA2 mutation and typical cerebrovascular findings. Right carotid arteriogram, Anteroposterior (a), and Lateral views (b). There is fusiform enlargement of distal cervical and petrous carotid with straightening of the supraclinoid carotid and anterior and middle cerebral branches. Distal branches show some corkscrew-like tortuosity. Left carotid arteriogram, Anteroposterior view (c), and magnified Lateral

view (d). Similar dilatation of petrous carotid and general straight course of middle and fetal origin posterior cerebral arteries. A1 segment of anterior cerebral is hypoplastic. Distal branches show some corkscrew-like tortuosity. Left vertebral arteriogram, Anteroposterior view (d) and magnified Lateral view (e). Straight proximal vessels and the abnormal distal corkscrew loops that may be mistaken as aneurysms (f)

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Spinal Vascular Lesions

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Several classification schemes for spinal vascular lesions have been described; the following four-­ type system is the most commonly used, with several other spinal vascular lesions added for completeness: • Type I: Dural arteriovenous fistula (dAVF) • Type II: Intramedullary arteriovenous malformation (AVM) • Type III: Juvenile AVM • Type IV: Intradural perimedullary AVF • Epidural arteriovenous fistulas • Sacral arteriovenous fistulas • Spinal cord aneurysms • Intramedullary cavernous malformations • Vascular spinal tumors • Spinal cord infarction • Cerebrospinal fluid-venous fistulas

20.1 Type I: Dural Arteriovenous Fistula Type I lesions (aka angioma racemosum, angioma racemosum venosum, intradural dorsal AVF, long dorsal AVF, dorsal extramedullary AVF) consist of an abnormal communication between the radicular artery in the nerve root sleeve and the intradural venous system, causing venous hypertension

Fig. 20.1  Type I dural arteriovenous fistula (dAVF). There is a direct connection between a radicular artery (A) and a radicular vein (V) in the dura of the nerve root sleeve. Arterialization of the coronal venous plexus causes engorgement and congestion of the veins. Note that the contralateral radicular vein (VV) in this depiction is small; impairment of alternative routes of venous drainage is thought to contribute to the development of venous hypertensive myelopathy

(Fig. 20.1). They can be subclassified into type I-A and type I-B lesions, depending on whether there is one or more radicular feeding arteries [1].

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 M. R. Harrigan, J. P. Deveikis, Handbook of Cerebrovascular Disease and Neurointerventional Technique, Contemporary Medical Imaging, https://doi.org/10.1007/978-3-031-45598-8_20

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Epidemiology and Clinical Features 1. Type I dAVFs are the most common spinal vascular lesion, representing approximately 70% of spinal vascular malformations [2]. 2. More common in males (male/female ratio is 5:1) [3]. 3. Mean age at presentation is 60; range is 28–83 years [3, 4]. 4. Mean duration of symptoms prior to diagnosis: 23 months [3]. 5. The majority of type I lesions are located in the thoracolumbar spine, with T7, 8, and 9 being the most common levels; 85% of lesions are below T6, and 100% of lesions are below T3 [5]. 6. Presentation: (a) Symptoms are typically progressive and may be exacerbated by physical activity [6]. (b) Motor symptoms are present in 78–100% of cases [3, 7]. (c) Upper or lower motor neurons may be involved; flaccid paresis is about as common as spastic paresis [8]. (d) Sensory symptoms are present in 69–90% of cases [6, 8]. (e) Paresthesias, and sensory and gait abnormalities are common. (f) Pain is a complaint in more than half of cases [6, 8]. (g) Patients may report worsening of symptoms with exertion (neurogenic claudication) or with certain postural changes [5]. 7. Imaging: (a) MRI is the screening procedure of choice for spinal dAVFs [7]. Spinal cord hyperintensity on T2-weighted images and post-gadolinium enhancement on T1-weighted images are the most common findings [2]. Cord signal changes usually extend for six or seven vertebral levels [2]. (i) Cord edema is seen in up to 74% of cases [8]. (ii) The coronal venous plexus has a characteristically nodular, shaggy,













and tortuous appearance on MRI and MRA. (iii) Dilated veins on the dorsal surface of the cord can be distinguished from CSF pulsation artifact by a typical salt and pepper appearance on post-contrast T1-weighted images [8]. (iv) Several MRI techniques can localize difficult-to-find spinal dAVFs prior to catheter angiography: • Volumetric myelographic MRI can help localize difficult-to-find spinal dAVFs [9]. • Contrast-enhanced time-resolved spinal MRA [10]. • Heavily T2-weighted volumetric MRI sequence (3D sampling perfection with application-­ optimized contrasts using different flip-angle evolutions [SPACE]) [11]. (b) Catheter angiography is the gold standard for the workup of spinal dAVFs [7]. (i) Scour the spine MRI/MRA for clues to the source of the feeding artery. (ii) Do selective injection of the thoracic and lumbar spinal arteries first, since the majority of dAVFs are located in those regions. (iii) A single feeding artery is present in 98% of cases [12]. (iv) When the artery of Adamkiewicz is found, imaging of the venous phase of the angiogram will fail to show normal filling of spinal cord veins in most cases of spinal dAVF [13]. This is evidence of the severe venous hypertension in the cord. (v) In some 10% of cases, the sacral arteries are involved [14, 15]. (vi) Rarely, intracranial dural AVFs may drain inferiorly and mimic spinal dural AVFs clinically and on MRI [15].

20.1  Type I: Dural Arteriovenous Fistula

With intracranial fistulas draining to spinal cord veins, angiography of the artery of ­ Adamkiewicz may show normal appearance of spinal cord veins in the venous phase [16]. Thus, if a fistula is not found during spinal angiography, angiography of the cerebral vessels should be done. (vii) Dilated, tortuous veins draining a dAVF are characteristic findings, predominantly along the posterior surface of the spinal cord. (viii) When a fistula is found, the adjacent levels should be imaged as well, because of the possibility of multiple radicular feeding arteries. (ix) It has been reported that placement of a platinum coil in the major feeding artery can facilitate intraoperative fluoroscopic localization of the fistula [17]. (c) Myelography is very accurate in identifying spinal dAVFs, showing tortuous filling defects in up to 100% of cases [2, 6]. These abnormal vessels are always located on the dorsal surface of the cord, and may also be present on the ventral surface in some 10% of cases [6].

Pathophysiology 1. Normal radicular veins have a constriction at the point where the vein passes through the dura, which prevents the transmission of arterial pressure into the valveless coronal venous plexus. Fistulas are usually located at this point or within the nerve root sleeve. The fistula is usually supplied by a meningoradicular branch of a segmental artery, although any artery supplying the dura may be involved [7]. The intrathecal spinal venous system is valveless, and therefore, arterial pressure is transmitted via the corresponding radicular vein into the perimedullary and spinal veins, causing venous hypertension, congestion and impairment of the spinal cord and nerve root

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microcirculation. Direct measurement of the coronal venous pressure during surgery found that the spinal cord venous pressure averages 74% of the simultaneous mean systemic venous pressure [18]. 2. The etiology of spinal dAVFs is not understood. Notably, in contrast to cranial dAVFs, in which venous sinus thrombosis is believed to contribute to the development of those lesions, prothrombotic conditions are not associated with spinal dAVFs [19]. 3. Spinal dAVFs have been associated with infection [20], syringomyelia [21], spine trauma [22], and spine surgery [23].

Management The natural history of untreated spinal dAVFs is generally thought to be abysmal. An early study found that 50% of untreated patients became severely disabled (wheel-chair-bound) within 3 years of the onset of lower extremity weakness [24].

Surgery Vs Embolization? 1. Both surgery and endovascular treatment can be effective for treatment of type I lesions. Although surgery is more likely to be curative, embolization is less invasive and some operators favor an attempt at embolization prior to surgery. 2. In a systematic review of 35 studies, initial definitive fistula occlusion was reported in 96.6% of surgery patients vs 72.2% of endovascular patients (p