Interventional Pain Medicine This Page Intentionally Left Blank Interventional Pain Medicine

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Interventional Pain Medicine This page intentionally left blank Interventional Pain Medicine

Edited by

Anita Gupta , DO , PharmD Assistant Professor of Anesthesiology and Critical Care Hospital of the University of Pennsylvania Philadelphia, PA

1 1 Oxford University Press, Inc., publishes works that further Oxford University’s objective of excellence in research, scholarship, and education. Oxford New York Auckland Cape Town Dar es Salaam Hong Kong Karachi Kuala Lumpur Madrid Melbourne Mexico City Nairobi New Delhi Shanghai Taipei Toronto With offices in Argentina Austria Brazil Chile Czech Republic France Greece Guatemala Hungary Italy Japan Poland Portugal Singapore South Korea Switzerland Thailand Turkey Ukraine Vietnam Copyright © 2012 by Oxford University Press, Inc. Published by Oxford University Press, Inc. 198 Madison Avenue, New York, New York 10016 www.oup.com Oxford is a registered trademark of Oxford University Press All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of Oxford University Press. ______Library of Congress Cataloging-in-Publication Data Interventional pain medicine / edited by Anita Gupta. p. ; cm. Includes bibliographical references and index. ISBN 978-0-19-974060-4 (spiral bound) I. Gupta, Anita. [DNLM: 1. Pain—drug therapy. 2. Analgesics—therapeutic use. 3. Autonomic Nerve Block—methods. 4. Injections, Spinal—methods. WL 704] 616.0472—dc23 2011039717 ______This material is not intended to be, and should not be considered, a substitute for medical or other professional advice. Treatment for the conditions described in this material is highly dependent on the individual circumstances. And, while this material is designed to offer accurate information with respect to the subject matter covered and to be current as of the time it was written, research and knowledge about medical and health issues is constantly evolving and dose schedules for medications are being revised continually, with new side effects recognized and accounted for regularly. Readers must therefore always check the product information and clinical procedures with the most up-to-date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulation. The publisher and the authors make no representations or warranties to readers, express or implied, as to the accuracy or completeness of this material. Without limiting the foregoing, the publisher and the authors make no representations or warranties as to the accuracy or efficacy of the drug dosages mentioned in the material. The authors and the publisher do not accept, and expressly disclaim, any responsibility for any liability, loss or risk that may be claimed or incurred as a consequence of the use and/or application of any of the contents of this material.

9 8 7 6 5 4 3 2 1 Printed in China on acid-free paper To my loving father and mother, Ishwar Saran Pradip and Usha Gupta, for lighting my path of motivation and determination for caring for people and for teaching me that anything is possible.

To my supportive husband and precious sons, Sanjeev M. Srinivas, Shaan R. Srinivas, and Jay R. Srinivas, for being the inspiration and reminding me of what is important in life.

To my prestigious mentors at Georgetown, Penn, Hopkins, and NIH, Jane C. Ballantyne, Lee A. Fleisher, Michael A. Ashburn, Srinivasa N. Raja, Steve P. Cohen, Paul J. Christo, Lance Pohl, Martin Cheatle, Jonathan R. Gavrin, and Russell Wall, for giving me the guidance to become a leader in pain medicine and anesthesiology.

To my cherished family and friends, Kavita Gupta, Sanjay Gupta, and Ayesha Malik, for giving me the support and confidence all through life challenges and reminding me that the best is yet to come. This page intentionally left blank vii Table of Contents

Foreword ix Preface xi Contributors xiii

Section 1: Introduction to Interventional Pain Management 1 1.1 Anatomy of the Spinal Cord for Pain Procedures 3 1.2 Pharmacotherapy for Pain Management 9 1.3 Imaging for Interventional Pain Management 15 1.4 Preparation for Interventional Spine Procedures 31 1.5 Basic Surgical Skills for Interventional Pain Procedures 39

Section 2: Cervical Spinal Injections 53 2.1 Cervical Inter-Laminar Epidural Injections 55 2.2 Cervical Transforaminal Epidural Steroid Injections 65 2.3 Cervical Median Branch Blocks and Radiofrequency Ablation 75

Section 3: Lumbar Spinal Injections 89 3.1 Lumbar Interlaminar Epidural Injections 91 3.2 Lumbar Transforaminal Epidural Injections 105 3.3 Medial Branch Blocks 113 3.4 Lumbar Radiofrequency Ablation 121 3.5 Discography 129 3.6 Biacuplasty 139 3.7 Kyphoplasty 149 3.8 Percutaneous Discectomy 157

Section 4: Pelvic and Sacral Injections 167 4.1 Caudal Epidural Injection 169 4.2 Caudal Adhesiolysis 179 4.3 Sacroiliac Joint Injections and Sacroiliac Joint Denervation Techniques 185 4.4 Sacroiliac Neurotomy 193

Section 5: Sympathetic Blocks 205 5.1 The Stellate Ganglion Block 207 5.2 Lumbar Sympathetic Nerve Block 219 5.3 Superior Hypogastric Plexus Block 225 5.4 Celiac Plexus Blocks and Splanchnic Nerve Blocks 235 viii Section 6: Advanced Neuromodulation Interventions 249 6.1 Spinal Cord Stimulation 251 6.2 Intrathecal Drug Delivery Systems 271

Index 287 Table of Contents ix Foreword

The genesis of this book was the need for a ready reference for new fellows embarking on a course of training in interventional pain management. Its intent was not to be a heavy book that could only be stored on a bookshelf, but a pocket-sized reference that could be carried, easily navigated, and available whenever a conceptual gap compromised the interventionalist’s ability to perform. The editor recognized this need in her own training and practice, and now that she teaches, has taken note of her fellows’ repeated frustration at not having reference book at hand with the answers to questions that arise at the bedside. The fact that Dr Gupta has managed to attract authors who are leaders in the field, including fellowship directors from programs throughout the US, confirms that indeed a need exists for such a book. The book is logically laid out, and each section covers the necessary material in a formulaic way: anatomy, indications, preparation, techniques, complications, clinical notes, and clinical pearls. The focus of the book is on technical aspects, and the book is adequately illustrated with fluoroscopic images and diagrams. The glossary, index, reading lists, and alphabetical contents make it easy to locate unfamiliar material, including where to look for information beyond this small book. Though this book is intended for new trainees in interventional pain management, it should also be noted that even the most seasoned practitioner will sometimes be required to perform an unfamiliar intervention, or will encounter an unusual clinical situation, in which case a ready reference book is invaluable. Thus, this book could well have utility not just for trainees, but for anyone practicing interventional pain management. Jane C . Ballantyne This page intentionally left blank xi Preface

The care of pain patients requires a unique knowledge base and skill set that differs widely from that required for general patient management. The physiology of pain medicine is rapidly changing, with continued advances made on interventions available to treat pain. The aim of this work is to provide, in one source, authoritative information from leaders in pain medicine to guide providers at the point of care for interventional pain therapies. It is intended to provide a rapid and accurate source of information relevant to the impact of the interventional management of pain patients. This handbook is an indispensi- ble resource for a variety of different pain practitioners who provide care to pain patients. This book provides point-of-care guide utilizing contributions of nationally and internationally recognized authors from institutions with advanced pain care practices and centers of excellence. I wish to acknowledge and thank the many outstanding faculty and fellows who contributed to the endeavor. I also want to sincerely thank Andrea Seils and Staci Hou from Oxford University Press for their dedication to this book and for making my vision for this work come to fruition. This page intentionally left blank xiii Contributors

Reginald Ajakwe, MD Steven P. Cohen, MD Fellow, UCLA Pain Management Center Professor of Anesthesiology Department of Anesthesiology Uniformed Services University of the David Geffen School of Medicine at UCLA Health Sciences Los Angeles, CA Director of Pain Research Walter Reed Army Medical Center Neel Amin, MD Washington, DC American Pain Experts and Private Practice Pain Medicine Associate Professor Fort Lauderdale, FL Johns Hopkins School of Medicine Baltimore, MD Aisha Baqai, MD New York Presbyterian Hospital Alexander F. DeBonet, MD Weill Cornell Medical Center Clinical Fellow in Pain Medicine New York, NY Beth Israel Deaconess Medical Center Gaurav Bhatia, MD Harvard Medical School Department of Anesthesia and Critical Care Boston, MA University of Pennsylvania Hospital System Philadelphia, PA Timothy R. Deer, MD President and CEO Richard G. Bowman, MD The Center for Pain Relief Rehabilitation Director and The Center for Pain Relief, Inc. Clinical Professor of Anesthesiology Charleston, WV West Virginia University School of Medicine Jianguo Cheng, MD, PhD Charleston, WV Program Director, Pain Medicine Fellowship Principal Physician Investigator Michael J. DePalma, MD Department of Neurosciences Medical Director Cleveland Clinic Foundation Virginia Commonwealth University Cleveland, OH Spine Center Associate Professor Paul J. Christo, MD, MBA Department of Physical Medicine and Assistant Professor Rehabilitation Director, Multidisciplinary Pain Medicine Virginia Commonwealth University Fellowship Richmond, VA Division of Pain Medicine, Department of Anesthesiology Johns Hopkins University School of Medicine Baltimore, MD xiv Mehul J. Desai, MD, MPH Maged Hamza, MD Director, Pain Medicine & Non-Operative Associate Professor and Director, Pain Spine Services Management Medical Director, GW Outpatient Departments of Anesthesiology, Physical Rehabilitation Center Medicine and Rehabilitation Assistant Professor Virginia Commonwealth University Department of Anesthesiology & Critical Care and Medicine Director, Interventional Pain Program and Department of Neurosurgery Associate Director, VCU Spine Center The George Washington University Medical Center Richmond, VA Washington, DC Matthew Hansen, MD Pradeep Dinakar, MD, MS Clinical Fellow of Pain Medicine Instructor, Department of Anesthesiology, Department of Pain Management

Contributors Perioperative and Pain Medicine Anesthesiology Institute Brigham and Women’s Hospital Cleveland Clinic Foundation Boston, MA Cleveland, OH

Sudhir Diwan, MD, MB, BS Salim Hayek, MD, PhD Director, Division of Pain Medicine Associate Professor, Department of Weill Cornell Medical College Anesthesiology New York, NY Chief, Division of Pain Medicine University Hospitals Benjamin J. Duckles, MD Case Western Reserve University Fellow, Pain Medicine Cleveland, OH University of Pennsylvania Department of Anesthesiology and Critical Care Spencer Heaton, MD Division of Pain Medicine Desert Pain Institute Philadelphia, PA Mesa, AZ

F. Michael Ferrante, MD Robert W. Hurley, MD, PhD Professor of Clinical Anesthesiology and Medicine Chief of Pain Medicine Director, UCLA Pain Management Center Associate Professor Department of Anesthesiology Department of Anesthesiology, David Geffen School of Medicine at UCLA Psychiatry, Orthopaedics Los Angeles, CA and Neurology Director, University of Florida Pain and Spine Rick L. Fisher, DO Center Assistant Professor Director, University of Florida Multidisciplinary Interventional Pain Medicine Pain Fellowship Department of Anesthesiology University of Florida College of Medicine Uniformed Services University Gainesville, FL F. Edward Hébert School of Medicine Bethesda, MD Sergio Lenchig, MD Fellow of Interventional Pain Management Basavana Goudra, MD, FRCA, FCARCSI Division of Pain Medicine Assistant Professor of Clinical Anesthesiology Department of Anesthesia and Critical Care University of Miami Miller School Hospital of the University of Pennsylvania of Medicine Philadelphia, PA Miami, FL xv Imanuel Lerman, MD, MS Jason E. Pope, MD Neurology Resident Partner Department of Neurology Napa Pain Institute Yale New Haven Hospital Napa, CA New Haven, CT and Assistant Professor of Anesthesiology David A. Lindley, DO Vanderbilt University Medical Center Advanced Pain Management Nashville, TN Green Bay, WI Adrian Popescu, MD Edward Michna, MD, JD, RPh Pain Fellow Assistant Professor Department of Anesthesiology and Critical Care Harvard Medical School Hospital of the University of Pennsylvania Director, Pain Trials Center Philadelphia, PA

Department of Anesthesia, Perioperative Contributors and Pain Medicine Kristen Radcliff, MD Brigham and Women’s Hospital Assistant Professor Boston, MA Department of Orthopaedic Surgery Thomas Jefferson University Kacey Montgomery, MD Rothman Institute Department of Anesthesiology Philadelphia, PA University of Florida College of Medicine Gainesville, FL Srinivasa N. Raja, MD Professor, Department of Anesthesiology/Critical Ketan Patel, MD Care Medicine Anesthesiology Resident Director, Pain Research and the Division of Pain Department of Anesthesiology and Critical Care Medicine Medicine Johns Hopkins University School of Medicine Johns Hopkins University School of Medicine Baltimore, MD Baltimore, MD Chitra Ramasubbu, MD Shatabdi Patel, MD Resident in Anesthesiology Department of Neurology Department of Anesthesiology and Critical Care Thomas Jefferson University Hospital Medicine Philadelphia, PA University of Pennsylvania Medical Center Philadelphia, PA Christine Peeters-Asdourian, MD Assistant Professor of Anesthesia Thomas R. Saullo, MD Division of Pain Medicine Interventional Spine Fellow Department of Anesthesia, Critical Care and Pain Clinical Instructor Medicine Department of Physical Medicine and Beth Israel Deaconess Medical Center Rehabilitation Harvard Medical School Virginia Commonwealth University Boston, MA Medical College of Virginia Hospitals Richmond, VA Gregory R. Polston, MD Associate Clinical Professor Nina Singh-Radcliff, MD Department of Anesthesiology Assistant Clinical Professor Division of Pain Medicine Department of Anesthesiology and Critical Care University of California San Diego University of Pennsylvania School of Medicine La Jolla, CA Philadelphia, PA xvi Ashish C. Sinha, MBBS, MD, PhD, DABA Mark S. Wallace, MD Assistant Professor of Anesthesiology and Professor of Clinical Anesthesiology Critical Care Chair, Division of Pain Medicine Assistant Professor of Otorhinolaryngology and Department of Anesthesiology Head and Neck Surgery University of California, San Diego University of Pennsylvania School of Medicine La Jolla, CA Philadelphia, PA Peter K. Yi, MD Dmitri Souzdalnitski, MD, PhD Assistant Professor Clinical Fellow of Pain Medicine Division of Pain Medicine Department of Pain Management Department of Anesthesiology and Cleveland Clinic Critical Care Cleveland, OH University of Pennsylvania School of Medicine

Contributors Lisa M. Tartaglino, MD Philadelphia, PA Associate Professor Division of Neuroradiology Ian Yuan, MD, MEng Department of Radiology Resident in Anesthesiology Thomas Jefferson University and Hospital Department of Anesthesiology and Philadelphia, PA Critical Care Hospital of University of Pennsylvania Bruce Vrooman, MD Philadelphia, PA Staff Physician Department of Pain Management Anesthesiology Institute Cleveland Clinic Cleveland, OH 1

Section 1 Introduction to Interventional Pain Management

1.1 Anatomy of the Spinal Cord for Pain Procedures 3 1.2 Pharmacotherapy for Pain Management 9 1.3 Imaging for Interventional Pain Management 15 1.4 Preparation for Interventional Spine Procedures 31 1.5 Basic Surgical Skills for Interventional Pain Procedures 39 This page intentionally left blank 3

Chapter 1.1 Anatomy of the Spinal Cord for Pain Procedures

Basavana Goudra , Ian Yuan , and Ashish C. Sinha

Spinal Cord 4 Meninges 5 Epidural Space 5 Spinal Nerves 5 Vertebral Column 6 Ligaments and Joints 6 Vertebral Joints 7 Spinal Musculature 7 Summary 7 References 7 4 Introduction A thorough knowledge of spinal anatomy— applied, gross and radiologic— is essential to understand mechanisms of back pain and formulate a plan of care. It is especially important in interventional pain procedures. There are already many established textbooks and handbooks on human anatomy. Anatomic details that help in performing various procedures are explained in-depth, as these are difficult to deci- pher from an anatomy book written by an anatomist. The radiological anatomy is covered under relevant procedures. Spinal Cord The spinal cord is a roughly tubular structure that starts at the lower end of the foramen magnum (also upper border of the atlas). The lower end is variable. Until about 14 weeks post conceptual age, the spinal cord extends its full length with the spinal nerves exiting their respective named foramina. Due, however, to differential growth with the vertebral column and the dura-arachnoid stretching more rapidly, by the end of fifth (post conceptual) month, the lower end of the cord is at the S1 level and by birth 1.1: Anatomy of the Spinal Cord it is at L2. In children, it ends a space lowers than adults and vertebral flexion as in positioning for spinal anesthesia drags it slightly higher. In adults, it usually stops at the junction between the first and second lumbar vertebra. The variation could be as high as the lower third of 12th thoracic vertebra and rarely down to second and third lumbar interspace and it is important to bear this in mind while performing spinal procedures. The upper end of the cord merges with the medulla oblongata and the lower end is a bundle of nerves emanating from the cord and surrounded by various sheaths. The terminal part is made up of fibrous tissues and called filum terminale . Although the spinal cord is tubular of varying thickness, two enlargements stand out. The cervical thickening (C4 through T1) mainly due to the incoming and outgoing nerve bundles to the upper limbs is called cervical enlargement, and the similar thickening at the lumbar level called lumbar enlargement (T9 through T12) is the result of nerves to and from lower limbs. The part between terminal end of the spinal cord and filum terminale is replete with nerve fibers, mainly supplying the lower limbs and is called conus medullaris . The subarachnoid membrane merges with the periosteum at S2 vertebra. The conus medullaris is mainly made up of fibrous tissue, however, and does not contain any nerve fibers. The spinal cord’s surface is marked by an anterior median fissure and a posterior median sulcus. Together they divide the cord into two halves. The anterior spinal artery arises from the vertebral artery and runs in the anterior medial fissure. The two posterior spinal arteries normally originate from the vertebral artery but occasionally from its posterior inferior cerebellar branch. There is significant anasto- mosis between the spinal arteries and segmental branches coming from the vertebral, deep cervical, intercostals, and lumbar arteries. Structurally, spinal cord consists of 12 thoracic segments, 5 lumbar, 5 sacral, and a coccygeal segment— a total of 31 segments. Each segment gives out a pair of spinal nerves. Due to deferential growth of the vertebrae and the cord as mentioned above, the nerves enter their corresponding intervertebral foramina only at the upper cervical level. Below that level, the spinal nerves run varying lengths to ema- nate from their corresponding foramina. (The exception to this is a young fetus, in which the spinal nerves are aligned with their corresponding foramina). The C8 cord segment is approximately at the level of C7 vertebra, T12 at T 9-10 vertebra and L5 segment with T11-12 vertebrae.1,5 As a result, the spinal nerves in general leave the vertebral column at considerable and variable lengths from their corresponding spinal cord segments, a fact to be mindful of while inserting epidural catheters to provide analgesia. Spinal cord has both gray and white matter. The white matter generally forms the outer layer of the spinal cord and is laid out into tracts that are identifiable as a dorsal column, a ventral column, and a pair of lateral columns. The gray matter is made up of neuronal bodies and laid out as nine laminae altogether. In a cross section, however, it is easier to appreciate a pair of dorsal horns, ventral horns, lateral horns and a commissure around the central canal. 5 Meninges The innermost lining of the spinal cord is called pia mater; the layer over the pia is arachnoid mater. Both are in such close proximity, that they are frequently referred to as a single membrane leptomeninx. The layer outside arachnoid is thicker and called pachymeninx. The space outside dura mater is the epidural space, which contains mainly loose areolar tissue, fat, lymphatics, spinal nerve roots, and the internal vertebral venous plexus. Anteriorly, it is bound by posterior longitudinal ligament; the ligamentum flavum and perosteum of the laminae limit it posteriorly. The vertebral pedicles and intervertebral foramina limit it laterally. Epidural Space The epidural space extends from the foramen magnum to sacral hiatus. The existence of an “epidural space” itself was questioned ( 6 ) as it is filled with fat. “Epidural region” might be more appropriate. The distribution of the fat in the epidural space is abundant, predictable, and uneven. It is absent in the cervical area, while in the lumbar region fat in the anterior and posterior aspects forms two unconnected Interventional Pain Medicine structures. Fat cells also are found in the thickness of dural sleeves around spinal roots ( 3 ). There are implications of the amount and distribution of fat in epidural space in health and disease ( 4 ). A recent study, however, concluded that fat is only present in the posterior recess between ligamentum flavum . The presence of posterior midline dural fold, which could be fat, is well known although not apparent in the MRI scans examined by Harrison ( 2 ). The depth of the epidural space from the skin increases from first to the third lumbar space ( 2 ). The depth of the epidural space from the skin is remarkably constant in successive epidurals in about half of 151 pregnant women coming for successive labor epidurals. In about 12 percent, the depth differed by more than 1.5 cm ( 1 ). The clinical implications of these findings are that the depth of the epidural space changes in the same individual’s adult life. The epidural space is also deeper in upper thoracic than in lower thoracic and lumbar sites. The depth with paramedian approach is more than in the standard midline approach ( 7 ). Older and obese patients have a deeper space as well. Unlike epidural space, the subarachnoid space is a continuation of cranial subarachnoid space and extends down to the second sacral vertebra. The pia and arachnoid extend on the spinal roots as they leave the intervertebral foramina to blend with the perineurium of the spinal nerves. Spinal Nerves The spinal nerves are the impulse transmission cables with fibers that carry either sensory information or motor orders. There are 31 pairs of spinal nerves (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal). The first seven of these emerge above their respective vertebrae and the remaining below. The eighth cervical nerve runs between the seventh cervical vertebra and first thoracic vertebra. A series of six to eight rootlets emerge from the spinal cord for each spinal nerve root. A dorsal root (mainly sensory that also bears a ganglion) and a ventral root (mainly motor) emerge from the spinal cord covered by a pia-arachnoid membrane until they pierce the dura, after which they are covered with dural sheath. Due to the differential growth of spinal cord in relation to the vertebral column, the nerve roots lengthen progressively from cranial to caudal, so much so that lumbosacral roots almost all run below the termination of the spinal cord. Majority of the ventral roots are myelinated although there are some non-myelinated autonomic type-C fibers. Dorsal roots are thicker than their ventral counterparts and each fiber represents central process of the dorsal root ganglion. They are sensory and are a mixture of all kinds of fibers. The dorsal root ganglia are made up of pseudounipolar cells with an affrent fiber carrying sensory information and efferent relaying to the spinal cord. Each dorsal root ganglion lies in the intervertebral foramen between articular processes of adjacent vertebrae. The two roots join to form spinal nerves at the distal end of the dorsal root ganglion. While still in the intervertebral foramen, the spinal nerves divide into an anterior (ventral) and a posterior (dorsal) root. The sacral spinal nerves divide in the sacral canal itself. 6 The coccygeal nerves are the smallest and there is no relarion between the size of the foramen and the nerves. The fifth lumbar nerve is the largest, with relatively smaller foramen making it more susceptible to compression. The dorsal rami of each spinal nerve below second cervical divides into a medial and lateral branch. The medial branch frequently provides the articular branch to the facet joints. Many clinicians believe that blocking of the medial branch is better for relieving the back pain arising from the facet joints than injecting the drug (usually mixture of a local anesthetic and steroid) into the joint itself( 8 ). The course and distribution of the remainder of the spinal nerve is beyond the scope of this chapter. A discussion of the microscopic anatomy helpful in clinical practice can be found in ( 9 ). Vertebral Column The primary purpose of bony vertebral column is to support the trunk and protect spinal cord. There are a total of thirty-three vertebrae. This is made up of 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 3 to 4 coccygeal vertebrae. The shape of the vertebral column is a double concave and double convex, both anteriorly and posteriorly. The two forward concavities are called primary curves and the two convexi- 1.1: Anatomy of the Spinal Cord ties are secondary curves. A typical vertebra consists of a body anteriorly with pedicles, articular processes, and laminae all surrounding the spinal cord. The first and second cervical vertebrae are atypical. The size and shape of the vertebrae changes from cranial to caudal becoming larger and thicker in general until they stretch out sideways at the sacral level. In the lumbar area, The bodies are taller ventrally, which explains the lordotic shape. The cervical vertebrae differ from the thoracic and lumbar as they have smaller bodies, bifid spines (C2-C6) and a foramen for the vertebral artery. The size of the vertebral canal is relatively large to accommodate the cervical enlargement. The first cervical vertebra has no vertebral artery foramen (only a groove) and has no body (only two lateral masses connected by two vertebral arches one each in front and back. The seventh cervical vertebra is the most prominent with a long nonbifid spinous process. The second to eighth thoracic vertebrae are called “typical,” each having a broad body, a small and circular vertebral foramen, and pedicles protruding posteriorly from the body. All thoracic vertebrae have lateral facets for rib articulation. The costal facets can be costo-capitular (head of the rib) or costo- tubercular (tubercle of the rib). The spinous processes are more caudally angulated at upper thoracic levels and almost horizontal at L3-L4 and L4-L5. This feature should be kept in mind when inserting the needle between spinous spaces. Ligaments and Joints From a pain practitioner’s point of view, the structures attached to the bony vertebrae are just as important or more important. There are five ligaments holding the vertebrae. Anterior longitudinal ligament extends from the basiocciput to all the way to upper sacrum. The ligament is strongly attached to intervertebral discs and loosely attached to middle of vertebral bodies where it fills up the concavity. The posterior longitudinal ligament extends from C2 to sacrum. It is broader at cervical and thoracic levels than at lumber levels. The ligamentum flavum is the innermost ligament posteriorly and the one immediately adjacent to the epidural space. It is a broad ligament connecting the laminae of neighboring vertebrae. The thickness of the ligament increases cranio-caudally. The ligament is deficient in the middle and if the needle attempt- ing to discover the epidural space is strictly in the midline (often not the case) one might not feel the loss of resistance of this firm ligament. Interspinous ligaments fill the space between spinous processes of the adjacent vertebrae. They are covered by the supraspinous ligaments posterioly and the ligamentum flavum anteriorly. The cervical part of the interspinous ligament is termed nuchal ligament (ligamentum nuche ) and represents thick midline intermuscular septum of the neck posteriorly. The interspinous ligament arises from the upper border of the spinous process and inserts into the adjacent lower border of the upper spinous process. 7 The supraspinous ligaments are firm fibrous structures connecting spinous processes of vertebrae C7-S1. As mentioned above, there are no supraspinous ligaments in the cervical region and there is a single ligamentum nuche taking the space of both supra and interspinous ligaments. Of note is that both interspinous and supraspinous ligaments are a narrow band extending sideways less than a centimeter. The interspinous ligaments are even narrower. When performing epidurals, if the needle is not in the midline, one may not appreciate the resistance offered by both the ligaments. The only resistance could then be of the ligamentum flavum , which is much broader.

Vertebral Joints Each bony vertebra articulates with the corresponding vertebra above and below apart from the first cervical vertebra that articulates with the occiput. They are called intervertebral joints and are symphy- ses and the intervertebral discs are the chief articular surfaces. Each disc has an outer annulus fibrosis and an inner nucleus pulposus. The thickness and extension of the discs varies; in general, the discs are thicker anteriorly. The discs themselves have no blood supply and obtain nutrition from the adjacent vertebrae Interventional Pain Medicine by diffusion. In addition, there are facet joints which are frequent sources of back pain. Facet joints are simple (cervical and thoracic) or complex (lumbar) synovial variety. The nerve supply is by medial branches of the dorsal primary ramus as detailed above that give articular branches. In addition there are cranio vertebral joints, lumbosacral joints and intercoccygeyal joints. The thoracic vertebrae and occasionally the seventh cervical vertebrae also have joints with the corresponding ribs.

Spinal Musculature These are typically arranged in layers. The deeper ones are true back muscles and are innervated by the dorsal rami of spinal nerves. The deepest muscle is multifidus (transvesropinalis ). It arises from dorsal surface of sacrum, mamillary processes of lumbar vertebrae, transverse process of the thoracic vertebrae and articulate processes of C4-C7 vertebrae. The insertion is into the spinous pricess of the vertebrae above its origin. The next layer is semispinalis thoracis, which is only present at upper thoracic levels. Erector spinae (origin from transverse processes of T6-T10 insertion C6-T4 spinous processes) represents next layer covering almost entire spine. Thoracolumbar fascia covers all these muscles, which can be considered as the next layer of transversospinalis group of muscles. Seratus posterior superior and inferior are the next layer and trapezuius above and latissumus dorsi below complete the various layers of back muscles. All the layers of back muscles are innervated by the dorsal primary ramus of the spinal nerves.

Summary The back and the spinal cord have a complicated anatomy. Knowledge of anatomy is the cornerstone for effective diagnosis and treatment of back pain. Pain can arise from any of the structures although facet joints and musculoskeletal structures are most commonly implicated. Knowledge of gross and radiological anatomy is essential in performing a variety of nerve blocks.

References 1. Ranson and Clarke .The Anatomy of the Nervous System: Its Development and Function . Philadelphia, PA: WB Sanders; 1953. 2. Variation in the depth of the epidural space in successive pregnancies. Int J Obstet Anesth . 1992 Jan ; 1 ( 2 ): 69 – 70 . 3. Topographical anatomy of the lumbar epidural region: an in vivo study using computerized axial tomography . Harrison GR . Br J Anesth. 1999 Aug ; 83 ( 2 ): 229 – 234. 8 4. Clinical implications of epidural fat in the spinal canal: a scanning electron microscopic study. Reina MA , Franco CD , López A , Dé Andrés JA , van Zundert A. Acta Anaesthesiol Belg. 2009 ; 60 ( 1 ): 7 – 17. 5. Epidural fat in various diseases: contribution of magnetic resonance imaging and potential implications for neuro axial anesthesia. Reina MA , Pulido P , Castedo J , Villanueva MC , López A , De Andrés JA , Sola RG Rev Esp Anestesiol Reanim. 2007 Mar ; 54 ( 3 ): 173 – 183 . 6. Characteristics and distribution of normal human epidural fat Reina MA , Pulido P , Castedo J , Villanueva MC , López A , Sola RG . 7. The topographical anatomy of the lumbar epidural space . G. Parkin and G. R. Harrison, J. Anat . ( 1985 ), 141 , pp. 211 – 217. 8. The epidural space is deeper in elderly and obese patients in the Japanese population. Adachi Yu , Sanjo Y , Sato S . Acta Anaesthesiol Scand. 2007 Jul ; 51 ( 6 ): 731 – 735 . Epub 2007 April 10. 9. Medial Branch Neurotomy in Management of Chronic Spinal Pain: Systematic Review of the Evidence Manchikanti L , Singh V , Vilims BD , Hansen HC , Schultz DM , Kloth DS . Pain Physician. 2002 Oct ; 5 ( 4 ): 405 – 418 . 10. The somatosensory system, with emphasis on structures important for pain. William D . Willis Jr . Brain Research Reviews . 55 ( 2007 ): pp. 297 – 313 . 1.1: Anatomy of the Spinal Cord 9

Chapter 1.2 Pharmacotherapy for Pain Management

Ashish C. Sinha and Basavana Goudra

Introduction 10 NSAIDs 10 COX-2 Inhibitors 11 Acetaminophen 11 Analgesic Adjuvants 11 Antiepilepsy Agents 11 Antidepressants 11 Local Anesthetics 11 Alpha Adrenergic Agonists 12 Capsaicin 12 NMDA Antagonists 12 Cannabinoids 12 Neuro-immuno Modulatory Agents 12 GABA Agonists 12 Adjuvants for Visceral Pain Syndromes 12 Opioids 12 Pharmacology 13 Opioid Rotation 13 Opioids in Neuropathic Pain 13 Opioids in Elderly 13 References 14 10 Introduction Treatment of pain by a concept of analgesic ladder was first introduced by the World Health Organization more than twenty years ago. These are subdivided into the milder nonopioid analgesics and adjuvants, followed by the stronger opioids. Conceptually, the analgesic ladder is an attempt to match the ceiling effect of pain drugs to the pain. If pain is severe or analgesia is ineffective, an ascent of the ladder is recommended. The ladder’s advantages are in its simplicity, in that only a few common drugs are employed. The technique is applicable to a wide variety of situations and prescribers, as safer drugs are used first. Its emphasis is on multimodal analgesia— the concept that pain is best treated not by a single drug or therapy, but by combinations, which maximize efficacy while minimizing side effects. Its disadvantages include its simplistic means for management of certain types of pain, especially neuropathic pain or other forms of chronic pain. The emphasis in the lower stages is on analgesics, which are taken orally and may occasionally be inappropriate. The evidence base for the efficacy of “weak” opioids (such as codeine, dihydrocodeine, and tramadol) is poor, and certain pain management techniques, such 1.2: Pharmacotherapy for Pain Management as regional or neuraxial blocks, do not fit well into the ladderconcept. Overall, however, the concept of the analgesic ladder is robust and useful, particularly for junior or inexperienced practitioners, and its principles underlie good pain management in many situations. NSAIDs Non-steroidal anti-inflammatory drugs decrease inflammation and in this manner decrease joint and skeletal pain. The mechanism of action is by inhibiting cyclooxygenase (COX) and through that, prostag-

landin PGE2 synthesis. Due to this mechanism of action, the drugs act both peripherally and centrally. The drugs may be divided based on selectivity of COX-2. The non-selective ones are aspirin, ibuprofen, indomethacin, ketoprufen, naproxen, piroxicam, sulindac, and tolmentin. This subgroup is sometimes referred to as the “non-selective” NSAIDs, or NNSAIDs. Different members of these drugs are equally effective in the treatment of back pain.

Opioid for moderate to severe pain

± Non-opioid Pain peristing± or Adjunctant increasing

Opioid for mild to moderate pain ± Non-opioid ± Morphine, Pain peristing Adjunctant or increasing 3 Fentanyl, etc

± N Codeine, ± Adjunctanton-opioid Tramadol, 2 etc Pain Paracetamol, aspirin, or NSAID 1

Figure 1.2.1 WHO Analgesic Ladder. Reprinted with permission from the World Health Organization. Cancer Pain Relief and Palliative Care. World Health Organization 1990. www.who.int/cancer/palliative/painladder . 11 This group of drugs is the first step in the WHO analgesic ladder.( 1 ) Indications and Contraindications: 1. Mild to moderate infl ammatory pain 2. Similar effi cacy across the whole group( 2 ) 3. Choice dependent upon patient factors and drugs’ side effect profi le 4. For severe pain, start NSAID combined with an opioid; “opioid sparing” effect may allow better side effect profi le and better acceptance and tolerance Side Effects: 1. Most common severe side effect relates to the gut: bleeding, ulceration, and even perforation; proportional to dose and length of therapy 2. Risk increases in elderly, patients in poor health, smokers, and in those with increased alcohol consumption 3. Increased bleeding time, even with a single dose 4. Diabetics are especially prone to renal effects. Renal function should be monitored.( 3 )

5. Be alert for over-the-counter NSAID consumption in patients Interventional Pain Medicine COX-2 Inhibitors The COX-2 inhibitors belong to a class of compounds that selectively inhibit the enzyme COX-2, reducing GI toxicity from COX-1 stimulation. These drugs are therefore as effective as NSAIDs in the treatment of rheumatoid arthritis and osteoarthritis, without most of the side effects. Known side effects are insomnia, headache, flatulence, abdominal pain, and diarrhea. COX-2 inhibitor drugs came under a cloud with the increased cardiovascular side effects of myocardial infarction and stroke. (These thrombotic effects are associated with all NSAIDs except naproxen.) Rofecoxib and valdecoxib were withdrawn from the market, but celecoxib continues to be available in the United States. Beginning in June 2005, all NSAIDS containing celecoxib were labeled with a black-box warning for stroke, MI, and gastrointestinal (GI) bleeds. Acetaminophen Acetaminophen is an analgesic and antipyretic; its antipyretic action is probably through one or more of the following: suppress peripheral PGE2 release, block a variant of COX-1, up-regulate central serotoninergic pathway, and or down-regulate interleukin 1β . The analgesic potency of acetaminophen is similar to aspirin. Chronic therapy may adversely affect hepatic or renal function. Analgesic Adjuvants An analgesic adjuvant is a drug that has medical indications other than pain. These are administered along with an analgesic to increase efficacy or decrease dose to mitigate side effects. Recent pain research has shown promise with the following groups: Antiepilepsy Agents Gabapentinoids are primarily antiepilepsy drugs. Gabapentin and pregabalin are well-known compounds to treat neuropathic pain, which act by modulating calcium channels. The treatment of diabetic and cancer neuropathy as well as post herpetic neuralgia responds well to gabapentin. Antidepressants Serotonin and norepinephrine reuptake inhibitors, TCAs such as amitriptyline, nortriptyline, and desipramine, enhance descending inhibition in the central nervous system Several of these have local anesthetic properties as well. Amitriptyline is a more potent Na + channel blocker than bupivacaine. Local Anesthetics These drugs target Na + channels, with examples being lidocaine, mexiletine, carbamazepine, amitriptyline, phenytoin, and doxepin; by frequency dependent blockade of depolarization and also have actions on nociceptive DRG neurons. These drugs affect both spontaneous and evoked pain. Mexiletine has 12 shown some success in neuropathic pain but GI side effects limits use of this oral antiarrhythmic. Both AEDs and TCAs also have local anesthetic properties( 4 ). Alpha Adrenergic Agonists α These drugs, including clonidine and tizanidine, act as agonists at 2 adrenoceptors and inhibit release and ascending spinal pain transmission. Analgesic action of intraspinal opioids is potentiated by clonidine. Tizanidine has been used with some success in the treatment of spasticity. Some success has also been achieved in lessening neuropathic pain.( 5 ) Capsaicin This is a C-fiber neurotoxin that also acts as an agonist at transient response potential vanilloid-1 (TRPV1) receptors. Additionally, it inactivates capsaicin-response nociceptors. NMDA Antagonists These antagonists at N-methyl-D-aspartatereceptors inhibit glutamate-mediated pain transmission and prevent central sensitization. These drugs include D-methadone, dextromethorphan, and ketamine. 1.2: Pharmacotherapy for Pain Management Cannabinoids Drugs in this group, like drobinol, are agonists at cannabinoid receptors and also inhibit transmission at DRG. Neuro-immuno Modulatory Agents These are glucocorticoids receptor agonists, which have been used to blunt pain via their anti-inflammatory factors. The mechanism is through switching off several inflammatory genes, with a reduction in pro-nociceptive mediators like cytokines and prostaglandins. GABA Agonists Drugs that act at GABA-B, like baclofen, enhance intraspinal inhibitory neurons. When combined in low doses with carbamazepine, they help treat trigeminal neuralgia. Baclofen has had some success when used intrathecally to treat neuropathic pain and spasticity. Common side effects are drowsiness, hypotension, and confusion; slow withdrawal is necessary to avoid seizures. Bone metabolism modulators like bisphosphonates are useful in the management of bone related painful conditions like hypercalcemia, osteoporosis, and multiple myeloma. Third-generation bisphosphonates like zoledronic acid and ibandronate are useful in the treatment of pain from metastases, as well as in the treatment of complex regional pain syndrome An associated side effect is osteonecro- sis of the jaw. Similarly, calcitonin has been effectively used in treating bone pain from osseous metastases. Adjuvants for Visceral Pain Syndromes Ketamine, an NMDA antagonist, is known to attenuate visceral pain. Somatostatins, and its octapeptide analog octreotide, are both antinociceptive. Opioids Opioids act as agonists at stereo specific opioid receptors that are normally activated by endogenous ligands called endorphins. These receptors are located in brain stem and spinal cord. Opioid binding to the receptor activates adenylate cyclase and hyperpolarizes neurons, resulting in suppression of spontaneous discharge and evoked potential. Opioids also impede calcium transport as well as the release of acetylcholine, dopamine, norepinephrine, and substance P. The basis of analgesic activity of opioids is the inhibition of the release of acetylcholine from nerve endings. Opioids include tramadol, morphine, meperidine, hydrocodone, oxycodone, oxymorphone, hydromorphone, fentanyl, buprenorphine, and methadone. Morphine has a high affinity for the μ -receptor; oxycodone has additional affinity for κ -receptor. Buprenorphine is a partial μ -agonist and a κ -antagonist. 13 Table 1.2.1 Routes of Opioid Administration Available Preparations

Oral Morphine, hydromorphone, methadone, oxycodone, Hydrocodone, Codeine, Meperidine, Levorphanol Rectal Suppositories with morphine, hydromorphone, oxycodone Sublingual Fentanyl, methadone, buprenorphine Transdermal Fentanyl Intravenous Morphine, hydromorphone, methadone, oxymorphone, meperidine, fentanyl Subcutaneous or intramuscular Morphine, hydromorphone, Methadone, meperidine, levorphanol Epidural or intrathecal Morphine, hydromorphone, methadone, meperidine, fentanyl

Pharmacology Interventional Pain Medicine Tramadol has weak μ -agonist properties but has found good use in neuropathic pain. Morphine is the opioid of reference. Hydrocodone, a μ -agonist is comparable to morphine in its analgesic ability. Oxycodone, a synthetic opioid is frequently combined with acetaminophen or aspirin for effective treatment of mild to moderate pain. Oxymorphone is a semi-synthetic μ -opioid agonist. Oral hydromorphone is four times as potent as morphine. Buprenorphine is a partial μ -opioid high-affinity receptor agonist and a κ -opioid antagonist. Methadone is the cheapest oral opioid. It is an antagonist at the non- competitive NMDA receptor. Opioid related side effects include bowel dysfunction, nausea and vomiting, drowsiness, delirium, hypogonadism, and respiratory depression. These occur because of either opioid receptor pharmacodynamics or opioid metabolites or both. Sedation and respiratory depression are traced to μ -receptor activation. Tolerance to these effects develops rapidly. These can be treated with naloxone. Dysphoria is due to activation of κ -receptors. Activation of δ -receptors results in psychotomimetic and depersonalization issues. Direct stimulation of the CTZ causes nausea and vomiting, and are treated with antiemetics. Intrabiliary pressure is increased secondary to spasm of the sphincter of Oddi. Miscellaneous side effects are constipation, myoclonus and pruritus. Antihistamines sometimes help alleviate the pruritus of opioid administration. Other than constipation and myoclonus, all other side effects diminish over time. Constipation can be treated with peripheral opioid receptor antagonists like alvimopan. In patients with subnormal renal function, morphine metabolites may cause sedation; meperidine metabolites may lower the seizure threshold. Opioid Rotation This is the system of changing one opioid for another, of equianalgesic potency, when treatment limiting toxicity or poor responsiveness develops. This usually leads to a more favorable side-effects-to- analgesia ratio. Opioids in Neuropathic Pain Although neuropathic pain is less responsive to opioids, some degree of analgesia is achievable, usually with a well tolerated dose. Opioids in Elderly Senior patients are more prone to side effects of opioids, either from the coexisting polypharmacy, or just debilitation of age. Pain control can still be achieved, but dose titration has to be done over a longer period of time. Meperidine and propoxyphene should be avoided due to the psychomimetic side effects of their metabolites. Attempt should be made to combine the opioid with non-opioids to decrease side effect issues. 14 References 1. Laird B , Colvin L , Fallon M . Management of cancer pain: basic principles and neuropathic cancer pain . Eur J Cancer 2008 ; 44 : 1078 – 1082 . 2. McNicol E , Strassels SA , Goudas L, et al . NSAIDS or paracetamol, alone or combined with opioids, for cancer pain . Cochrane Database Syst Rev 2005 : CD005180 . 3. Fored CM , Ejerblad E , Lindblad P, et al . Acetaminophen, aspirin, and chronic renal failure . N Engl J Med 2001 ; 345 : 1801 – 1808 . 4. Lai J , Hunter JC , Porreca F . The role of voltage-gated sodium channels in neuropathic pain . Curr Opin Neurobiol 2003 ; 13 : 291 – 297 . 5. Knotkova H , Pappagallo M . Adjuvant analgesics . Med Clin North Am 2007 ; 91 : 113 – 124 . 1.2: Pharmacotherapy for Pain Management 15

Chapter 1.3 Imaging for Interventional Pain Management

Shatabdi Patel and Lisa Tartaglino

Introduction 16 Degenerative Spine Disease 17 Disc Pathology 17 Spinal Stenosis 23 Lesions of the Vertebral Bodies 26 Insufficiency Fractures 27 Malignancy 27 Conclusion 28 References 29 16 Introduction Imaging is critical for the pre-intervention assessment, during spinal intervention, and in follow-up of the procedure. Pre-intervention evaluation of the spine usually incorporates initial evaluation with some combination of plain films, CT, and MRI. Other entities such as nuclear medicine or ultrasound may be used to supplement these primary modalities but will not be covered in this chapter. Both MR and CT are widely used to diagnose, localize, and exclude various disease processes. MR is best at evaluating soft tissue components, the relationship of the disease process to the epidural space, paraspinal spaces, and any associated lesions. It is also the only imaging modality capable of evaluating the spinal cord paren- chyma. By contrast, CT is best at evaluating the bony architecture and areas of calcification and is often complementary to the information on MR. Unlike MR, CT is being used with increasing frequency for guidance during actual interventional procedures. While plain film and fluoroscopy are diagnostically limited compared to CT and MR, they are the mainstay of guidance for interventional spine procedures. Understanding of the spinal anatomy and pathology as it appears on all modalities is critical for correct patient selection, technical mastery, and patient safety. For the purposes of this chapter, we will concen- 1.3: Imaging for Interventional trate on the main disease processes treated with spine interventional procedures and their diagnosis. Complete imaging, techniques, and landmarks of various procedures will be addressed separately in their respective procedural chapters.

BCD Figure 1.3.1 A-D Normal C spine anatomy on CT in multiple planes showing the uncovertebral joint with the uncinate process (black arrows), neural foramina (open white arrow), facet joints (white arrows), pedicle (white arrow heads) and lamina (black arrow heads). In B, the small bilateral transverse foramen are seen where the vertebral artery passes just anterolateral to the pedicles. Note the facet joint in the sagittal plane (C) is bordered by the diamond shaped lateral masses of the adjacent vertebral bodies which have a superior articular facet and an inferior articular facet. On a coronal image (D) the unique anatomy of the base of the skull through C2 is visualized showing the dens (* ) attched to the C2 vertebral body. On either side of the dens, the lateral masses of C1 are identified (black square). Above, the lateral mass of C1 articulates with the occipital condyle to form the atlanto-occipital joint. Inferiorly, the lateral mass of C1 articulates to form the atlanto-axial joint. 17 Interventional Pain Medicine

Figure 1.3.2 Lumbar spine anatomy on Plain film: Note the bilateral L4 pedicles (white arrows) arising from the posterolateral aspect of the vertebral bodies as well as the spinous process (* ) on the AP view. Lateral view shows the L5 pedicle (white arrow) and the L3 neural foramina (open arrow) the space under the L3 pedicle. Unlike the cervical spine, the neural foramina are well seen in the lumbar spine in the lateral/sagittal view. Oblique view shows typical “scotty dog” appearance with the eye representing the pedicle (white arrow), the ear representing the superior articular facet, the front foot representing the inferior articular facet and the neck (arrowheads) representing the pars interarticularis.

Degenerative Spine Disease The majority of the spinal abnormalities that will be encountered by the clinician when evaluating and treating spine pain fall under the broad category of degenerative disease. This spectrum may affect discs, the adjacent endplates, the articular facet and joint, and the spinal ligaments. MRI currently gives the most comprehensive information about degenerative spine disease with its ability to separate disc material, epidural fat, marrow, ligaments, neural foramina, and spinal canal contents. Standard imaging sequences include sagittal and axial T1 and T2 weighted images, each giving different information. T1 images give excellent anatomic information and evaluate the epidural and marrow fat well. T2 images give an excellent “myelographic” affect accentuating the differences between CSF, which is hyperintense and the spinal cord and roots, which are hypointense. In addition, with fat-suppression techniques or with short inversion–time inversion recovery (STIR) sequences there is exquisite sensitivity to edema in the soft tissues. In the setting of the post-operative spine, MR contrast can differentiate recurrent disc herniation from scar tissue [ 1 ], which is critical in assessing treatment for the failed back syndrome. Contrast is also important in suspected malignancy or infection. As mentioned, CT gives more specific bony architectural detail. In the setting of degenerative disease, CT can also give some soft tissue detail about ligaments and disc material especially in the lumbar spine. Disc Pathology The normal appearance of a vertebral disc on T2 imaging has a higher signal centrally in the nucleus and a lower signal peripherally in the annulus reflecting differing fluid content (Figure 1.3.3A ). As a disc degenerates, it loses fluid and begins to lose its structural integrity. On T2-weighted images this is seen as a comparatively decreased signal in the disc and narrowing of the disc space as compared to a normal disc. Annular fissures and tears can develop (Figure 1.3.3C ), which are seen as focal increased signal in the margin of the disc on T2 weighted imaging. Gas may develop, which can be seen on CT, MR, and plain 18

Figure 1.3.3A Normal Disc – T2W axial image through a normal lumbar disc level. Note the centrally brighter nucleus 1.3: Imaging for Interventional pulposis and the darker peripheral annulus fibrosis. T2 weighted images give a myelographic affect with the CSF appearing bright. Normal nerve roots of the cauda equina in cross section appear as small dark dots. The spinal canal has a normal concave margin bordering the anterior thecal sac. Typical T2 images acquired in the spine use fast spin echo techniques and show fat as bright in the neural foramina and muscle planes.

Figure 1.3.3B Bulging Disc - T2W image shows loss of the normal concavity of the thecal sac consistent with a mild disc bulge. Incidentally noted is facet hypertrophy and degeneration though significant neural foraminal stenosis is not seen.

film. Adjacent varying signal changes in the vertebral body endplates begin to occur that may enhance with contrast. Type 1 degenerative endplate changes are the earliest and reflect edema (Figure 1.3.4 ) with hypointense signal on T1 and hyperintense signal on T2 reflecting the increased fluid content. Type 1 changes should not be confused with discitis/osteomyelitis where the disc space is usually brighter on T2 weighted images than the adjacent discs (Figure 1.3.5 ) [ 2 ], and is relatively contraindicated for spine intervention procedures aside from a diagnostic biopsy. Type II changes show hyperintense signal on T1 and T2 reflect fatty replacement of the red bone marrow and are the most common. Finally, type III manifest as hypointense signal on T1 and T2 and reflect subchondral bone sclerosis [ 3 , 4 ]. Description of disc pathology historically has been variable and confusing. In 2001, the North American Spine Society, the American Society of Spine Radiology, and the American Society of Neuroradiology 19

Figure 1.3.3C Protrusion type disc herniation: Note the broad base shallow herniation on this T2W image. Increased Interventional Pain Medicine signal in the herniated disc material reflects an annular tear or fissure. Incidental note is made of facet hypertrophy. developed a standard nomenclature and classification of lumbar disc pathology [ 5 ]. The cervical and thoracic spine have not been as specifically addressed. A disc bulge (DB) (Figure 1.3.3B ) is where the contour of the annulus extends beyond the edges of the disc space— usually less than 3 mm but more than 50 percent in the axial plane and is felt to be related to diffuse laxity of the annulus. A disc herniation (DH) is a more localized extension of disc material beyond the edges of the disc space of less than 50 percent in the axial plane. It may include tissue of the nucleus pulposis, cartilage, or annulus. Though not always possible to differentiate, a disc herniation may be further classified into a disc protrusion or disc extrusion via imaging. A disc protrusion (DP) (Figure 1.3.3C ) is where the defect is a focal relatively shallow defect. A disc extrusion (DE) (Figures 1.3.3D and E ) is where there is a larger extension of disc material into the epidural space but with a narrower waste where it extrudes through the annulus. An extruded disc is further characterized as “sequestered” if a disc fragment is no longer connected to the parent disc and most commonly migrates inferiorly (Figure 1.3.4 ).

Figure 1.3.3D Extrusion Type Disc Herniation : Axial T2W image at the level of L5 - S1 shows a focal herniated disc (red arrow) impinging on the traversing right S1 nerve root (white arrow) in the right subarticular region. The traversing left S1 root surrounded by epidural fat is unaffected as well as the exiting nerve roots (red arrowheads) which have already exited the neural foramina under the L5 pedicles. 20

1.3: Imaging for Interventional Figure 1.3.3E Extrusion Type Disc Herniation: Sagital T2W image shows decreased signal in the L5-S1 disc space compared to the L4-L5 normal appearing disc level. A herniated disc is also seen. Note the narrow neck of disc material (arrowheads) as the disc herniates through the annulus and the proportionately larger extruded disc material beyond the bony margins in the epidural space characteristic of the extrusion type disc herniation.

T1W T1W +C T2W

ABC Figure 1.3.4 A, B, C Sequestered Disc fragment: Sagittal images through the lumbar spine shows a sequestered disc fragment in a subligamentous location behind the body of L4 (Thick arrows). The fragment peripherally enhances on the fat-suppressed post contrast T1W image (B) and is bright on the fat suppressed T2W image (C). Incidental note is made of Type I degenerative endplate changes at L5-S1 (thin arrows). Note that these changes reflect edema which is decreased on T1W (A), decreased on T2W (C) and commonly shows enhancement. These degenerative changes are associated with decreased signal in the degenerated disc space on T2W and should not be confused with discitis which shows increased signal in the disc space (Figure 1.3.5 ). 21 Interventional Pain Medicine

AB Figure 1.3.5 A and B Discitis/osteomyelitis: Note the edema in the adjacent endplates at L3-L4 which is dark on T1W (A) and bright on fat suppressed T2W. However, unlike Type I degenerative endplate changes where the disc is degenerated, in discitis the disc is bright on T2W.

Disc pathology may then be classified by location. One of the more common location classifications in current use was proposed by Wiltse [ 6 ]. Disc herniations were classified on axial imaging as central, subarticular, foraminal, and extra foraminal based on the location of the herniated disc in relation to the medial aspect of the articular facet and pedicle. The use of contrast is generally not indicated in the routine evaluation of degenerated disc disease. In specific circumstances, contrast may be indicated. These include the postoperative spine for evaluation of scar versus. recurrent disc, arachnoiditis, to exclude infection, synovitis, radiculitis, or paraspinal muscle myositis and to differentiate a degenerative process from tumor [ 7 ]. MR with contrast has proven superior to CT scan with contrast for differentiating postoperative scar from recurrent disc herniation in the lumbar spine [ 1 , 8 ] Both scar and disc in the epidural space disrupt the epidural fat and are isointense to disc material. Both may also exhibit a disc defect suggesting disc material on T2W images. Following contrast, however, epidural scar tissue enhances uniformly while disc material and nerve roots in the epidural space usually do not enhance immediately following contrast (Figure 1.3.6 ). If contrast enhancement is seen with a recurrent/residual HD it is usually peripheral. This is also a differentiating point for distinguishing tumor such as a schwannoma from a sequestered fragment (Figure 1.3.4 ). Arachnoiditis is inflammation that causes nerve roots to adhere to themselves and the thecal sac. On T2 weighted images or CT myelography (Figure 1.3.7 ), the most common findings are clumping of nerve roots or a featureless distal sac. Adhesions can also be seen as linear bands and can form loculated arachnoid collections. Enhancement post contrast is variable. Intervertebral discs in the cervical region behave in a similar manner to lumbar disks. It may be harder, however, to distinguish between bulges and small disc herniations on sagittal images. In addition, clear 22

AB Figure 1.3.6 A and B Postoperative scar vs. recurrent disc: figures A and B are fat-suppressed T1W images post contrast in

1.3: Imaging for Interventional two different patients who presented with right sided recurrent back pain approximately 1 year after surgery. Both show enhancement in a right hemilaminectomy defect and both show right epidural enhancement. Figure A has uniform enhancement in the right anterior epidural space (white open arrow) consistent with post-operative scar tissue. Figure B shows a filling defect (white arrow) within the enhancement consistent with a recurrent disc herniation.

BC Figure 1.3.7 A-C Arachnoiditis in a patient presenting with chronic pain years after surgery at L4 and L5: Multiple images from a CT myelogram show clumping of nerve roots (A), band adhesion (B) on axial CT myelogram images. On the sagittal reformatted image (C), the normal conus is seen ending at L1. The caudal roots have a relatively normal appearance superiorly as they leave the conus but adhere together distally (white arrow) at the level of the L4 and L5 laminectomy. 23 distinction of protrusions from extrusions in the axial plane may be difficult. Because of the minimal epidural fat in the cervical region, T2W images or gradient echo (GRE) are more reliable than T1W images for identifying degenerative disc pathology. GRE sequences, in particular, can accentuate small osteophytes and with thin sections can visualize the effects of DH, osteophytes, and facet joints on the spinal canal and neural foramina. It should be noted that the anatomy of the cervical spine makes neural foramina best identified on axial imaging. Since there are eight nerve roots in the cervical spine, nerve roots exit above the pedicle and exit horizontally at the same named level unlike the thoracic and lumbar spine. Therefore, there are no “traversing roots” in the lateral recess. In the thoracic spine, the normal kyphotic curve positions the cord adjacent to the posterior vertebral bodies. Even small herniated discs can cause myelopathic findings clinically. In addition, thoracic herniated discs are more likely to present with myelopathy or referred pain rather than radiculopathy [ 7 ]. In addition, unlike the lumbar spine, herniated thoracic discs are more likely to calcify, and can mimic a tumor on MR [ 9 ]. Spinal Stenosis In spondylosis deformans, osteophytes generally are felt to arise secondary to torn Sharpey’s fibers from Interventional Pain Medicine the attachment along the vertebral body margins. Stress occurs with increased movement; endplate osteophytes form as reaction to this stress [ 7 ]. In the cervical spine, there is a tendency to develop associated osteophytes posterolaterally at the uncovertebral joint (Figure 1.3.8 ). Osteoarthritis is a degenerative arthritis involving the synovial joints of the facets (apophyseal) and also results in bone proliferation and enlargement. Acquired spinal stenosis results from narrowing of the spinal canal, lateral recess or

Figure 1.3.8 Disc Osteophyte Complex Figure 1.3.8A Sagittal T2W image showing a disc osteophyte complex at C4-5. Note the lip of the osteophyte in association with disc material which extends beyond the normal posterior margin of the disc both anteriorly and posteriorly at the endplate of C4-5. Compare this to the appearance of a small herniated disc at C5-6 where disc material alone extends beyond the disc margin. 24

Figure 1.3.8B Axial T2 gradient echo image though the level of C4-5 shows the dark margin of the osteophyte effacing the spinal canal causing central stenosis greater to the left. Also seen is uncovertebral joint hypertrophy laterally causing

1.3: Imaging for Interventional stenosis of the left greater than right neural foramina.

Figure 1.3.8C Axial T2 Gradient echo image through C5-6 showing central HNP causing central stenosis. Note the brighter signal of the soft tissue disc material as compared to the osteophyte in Figure 1.3.3B .

neural foramen from any combination of disc disease, osteophyte formation, facet arthropathy, and ligamentum flavum thickening and occurs most frequently in the lumbar and cervical region. In the cervical spine, this can present with pain, radiculopathy or myelopathy. Classically Lumbar stenosis presents with neurogenic claudication which is worse when standing or walking and absent when recumbent. [ 10 ]. Spondylolisthesis occurs when a vertebral body is displaced in relationship to the vertebral body below it. In the presence of an intact pars interarticularis, degenerative spondylolisthesis is most common at L4-L5 but can be seen throughout the cervical and lumbar spine. The usual cause is facet arthropathy and degeneration with segmental instability (Figure 1.3.9 ) [ 10 ]. Spondylolysis is secondary to a congenital or acquired defect in the pars interarticularis. When acquired, it likely represents a stress fracture of the pars interarticularis [ 11 ], 12], is usually bilateral and most commonly occurs at L5 resulting in an L5-S1 spondylolisthesis. This can be seen as lucency through the neck of the “Scotty dog” with sclerotic margins. On CT (Figure 1.3.10 ) and MR, one can see an “extra facet” sign on axial images as well as the defect with sclerotic margins through the pars interarticularis on sagittal images. The foramen assumes a more horizontal orientation, and compression of the exiting nerve root in the foramen as well as the traversing nerve root in the lateral recess can occur. Characteristically, at the level of the spondylolisthesis, the canal is elongated in the anterior-posterior dimension. 25 Interventional Pain Medicine

AB Figure 1.3.9 A and B Anterolisthesis of L4 in relation to L5 is indicated by arrows on lateral plain film in Figure A. Oblique views in Figure B show widening of the L4-L5 facet joint (arrow).

C Figure 1.3.9 C Axial T2W MR image through a different patient with L4-L5 spondylolisthesis shows severe stenosis centrally. Note the marked facet hypertrophy and degeneration of the facets with associated thickening of the ligamentum flavum (arrow) from the facet arthropathy.

Another disorder secondary to degenerative facet arthropathy that can result in severe stenosis is a synovial cyst (Figure 1.3.11 ). The vast majority occur in the lumbar spine and are best imaged on MRI. The characteristic finding is of a cyst with a low-intensity peripheral wall on T2W images associated with the facet joint. There may be variable enhancement on post contrast T1W images. Signal can vary within the cyst on T1W sequences secondary to abnormal protein or hemorrhage. These cysts can cause a variable degree of central and lateral recess stenosis when associated with the anterior superior aspect of the facet joint in the epidural space. [ 13 ] 26

AB 1.3: Imaging for Interventional Figure 1.3.10 A and B Spondylolysis: Axial (A) and sagittal (B) CT images show defect in the pars interarticularis (white arrows). The right defect on A is just anterior to the facet joint giving an appearance of a “double facet”. Also in A, note the elongated appearance of the central canal characteristic of spondylolysis unlike spondylolisthesis secondary to degenerative facet arthropathy.

Lesions of the Vertebral Bodies Other than pain related to degenerative changes, referrals for treatment of pain related to vertebral body lesions amenable to vertebroplasty or kyphoplasty are probably the second most common entity encountered where imaging is critical for proper management and treatment. These include benign osteoporotic compression (insufficiency) fractures, pathological compression fractures secondary to an underlying metastasis and occasionally aggressive hemangiomas.

A BC Figure 1.3.11 A-C Synovial Cyst: Figure A shows a cystic lesion with characteristic hypointense signal on a T2W image. Figure B shows this lesion immediately adjacent to the left medial facet joint causing severe central and left lateral recess stenosis essentially obliterating the left aspect of the spinal canal. Figure C shows faint rim enhancement on the fat-suppressed T1W post contrast image. 27 Insufficiency Fractures Lifetime risk of all skeletal fractures inclusive of insufficiency fractures is approximately 75 percent in Caucasian women older than age fifty. Plain radiographic evaluation of compression insufficiency fractures may demonstrate a classic “wedge” appearance, which shows loss of anterior vertebral body height with relative preservation of posterior vertebral body height. (The most frequent site of involvement is the thoracolumbar junction, with the second most frequent region being the midthoracic spine. Sagittal alignment typically demonstrates increased segmental kyphosis. Lucas, TS, Einhorn, TA. Osteoporosis: the role of the orthopaedist. J Am Acad Orthop Surg 1 (1993):48–56.) While any benign compression or burst fracture has similar characteristics, the presence of osteoporotic bone predisposes the vertebral body to fracture from less stress and minor trauma. The fracture line is often visible parallel to the disc space and edema preferentially affects the superior aspect of the vertebral body (Figure 1.3.12 ). When retropulsion occurs in the epidural space, it is usually along the superior posterior margin of the vertebral body and is more correctly termed a burst fracture. Posterior element involvement is notably absent. Adjacent soft tissue extension outside of the bony margins may be seen in the acute setting secondary to adjacent edema or hematoma but is usually much more prominent in underlying tumor. Signal intensity Interventional Pain Medicine on MR will show comparatively low signal on T1 and high signal on fat-supressed T2 or STIR sequences consistent with edema in the marrow [ 14 , 15 ]. This can occur in the setting of pain even when plain film and CT are negative indicating pain from a bone bruise or stress fracture. Distinguishing acute from chronic fractures on plain radiographs and CT can be difficult. Features indicating an acute injury include well-demarcated lucent fracture lines without sclerosis or a sharp step-off along the cortex on sagittal views. A more chronic injury is suggested by sclerosis with a well-corticated margin, and osteophytes bordering the fracture site. On MR, chronic healed fractures will no longer exhibit edema and the marrow signal will return to a relatively normal signal on T1 and T2. Malignancy Normal marrow signal on T1-weighted (T1W) images is increased compared to disc spaces reflecting the fat content in the marrow. Tumor replaces the marrow and is seen as hypointense, compared to

A B Figure 1.3.12 A and B Sagittal T1 and fat-suppressed T2 images in the thoracolumbar region shows insufficiency fractures in the two vertebral bodies. Note the classic greater involvement of the superior vertebral bodies. Mild retropulsion seen best on B, shows effacement of the thecal sac along the posterior superior margin of one of the vertebral bodies. 28 normal fatty marrow on T1W images. If contrast is given, fat-suppression techniques are recommended, since enhancement on T1-weighted images could cause the lesions to approach the signal of the normal fatty marrow and obscure the lesion. Discrete lesions that are hyperintense in the marrow on T1 are usually benign and most commonly represent benign hemangiomas. Both benign hemangiomas and tumors may be bright on T2. Distinguishing benign versus malignant lesions is difficult unless associated cord compression or soft tissue is present. When fractures occur, loss of normal marrow signal on T1-weighted images and increased signal intensity on T2-weighted images is sensitive, but not very specific for tumor, as the same findings are seen with insufficiency fractures. Normal marrow intensity on T1 images, however, makes a diagnosis of tumor extremely unlikely. Pathological compression fractures are often associated with extension and replacement of marrow in the posterior elements as well as the whole vertebral body (Figure 1.3.13 ) [ 14 , 15 ]. Use of gadolinium contrast may help show adjacent soft tissue tumor and epidural extension but it is important to remember that both acute and benign compression fractures as well as pathological fractures will exhibit marrow enhancement acutely. Diffusion- weighted magnetic resonance imaging may allow further discrimination between osteoporotic and

1.3: Imaging for Interventional tumor-associated compression fractures. [ 16 ] Conclusion Having discussed the more common causes of patients referred for treatment of spine pain, it should also be noted that even if an abnormality is found, it may not explain the patient’s pain. It has been well described in the literature that disc pathology is often seen in asymptomatic patients. In one study, 52 percent of the subjects had a bulge at least one level, 27 percent had a protrusion, and 1 percent had an extrusion. Of the 98 asymptomatic patients, only 36 percent had normal disks at all levels. [ 17 ] Similar asymptomatic disc pathology, even with cord involvement, has been described in the cervical spine. [ 18 ]

ABC Figure 1.3.13 Pathologic compression fracture - Figures A and B in a patient with breast cancer and new back pain, shows replacement of the marrow signal involving the entire vertebral body with loss of vertical height. In Figure A, there is extension of the marrow replacement into the pedicle, the superior articular facet and the lateral mass. Note the minimal soft tissue encroachment on the fat in the neural foramina beneath the pedicle (open arrow). In Figure B, there is retropulsion which is beginning to compress the spinal cord. An additional metastasis is seen in a more superior vertebral body. Axial post contrast fat-suppressed T1W images (C) show abnormal extension of enhancing soft tissue beyond the bony margins (white arrows) also consistent with underlying tumor. 29 By the same token, pain can be very real even if no abnormalities are seen on imaging. It is clear that imaging can help determine the correct method for treatment of spine pain. It is important to remember, however, that pain is a symptom, that in and of itself, cannot be imaged. It is the clinical exam that ultimately determines which treatment intervention is optimal and where the treatment intervention is best applied for the patient’s pain. References 1. Bundschuh CV , Modic MT , Ross JS , et al . Epidural ﬁ brosis and recurrent disc herniation in the lumbar spine: MR imaging assessment . Am J Neuroradiol . 1988 ; 9 : 169 – 178. 2. Modic MT , Fieglin DH , Pirainao DW , et al . Vertebral osteomyelitis; assessment using MR . Radiology . 1985 ; 157 : 157 – 166. 3. Modic MT , Steinberg PM , Ross JS , et al . Degenerative disk disease: assessment of changes in vertebral body marrow with MR imaging . Radiology . 1988 ; 166 : 193 – 199. 4. Zhang YH , Zhao CQ , Jiang LS , et al . Modic changes: a systemic review of the literature . Eur Spine J .

2008 ; 17 : 1289 – 1299. Interventional Pain Medicine 5. Fardon DF , Milette PC . Combined Task Forces of the North American Spine Society, American Society of Spine Radiology and American Society of Neuroradiology. Nomenclature and classifi cation of lumbar disc pathology. Reccomendation of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology and American Society of Neuroradiology . Spine . 2001 ; 26 ( 5 ): E93 – E113. 6. Wiltse LL , Berger PE , McCulloch JA . A system for reporting the size and location of lesions in the spine . Spine . 1997 ; 22 ( 13 ): 1534 – 1537. 7. Kaplan RT , Czervionke LF , Haughton VM . Degenerative disease of the spine . In: Atlas SW , ed. Magnetic resonance imaging of the brain and spine . Philadelphia, PA : Lippincott Williams & Wlkins ; 2009. 8. Braun IF , Hoffman JC , Davis PC , et al . Contrast enhancement in CT differentiation between recurrent disc herniation and postoperative scar: prospective study . Am J Roentgenol . 1985 ; 6 : 607 – 612. 9. Roosen N , Uwe D , Nicola N , et al . MR imaging of calcifi ed herniated thoracic disc . J Comput Assist Tomogr . 1987 ; 11 : 733 – 735. 10. Modic MT . Degenerative Disorders of the spine . In: Modic MT , Masaryk TJ , Ross JS , eds. Magnetic resonance imaging of the spine . Chicago, IL : Year Book Medical Publishers ; 1989. 11. Jinkins JR , Matthes JC , Sener RN et al . Spondylolysis, pondylolisthesis and associated nerve root entrapment in the lumbosacral spine: MR evaluation . Am J Roentgenol . 1992 ; 159 : 799 – 803. 12. Ross JS , Brant-Zawadzki M , MooreS KR , et al. Part II, section II: Degenerative Disease and infl ammatory arthrititides . In: Diagnostic imaging . Spine . Salt Lake City, UT : Amirsys Inc ; 2004. 1.3 Tillich M , Trummer M , Lindbichler F , Flaschka G . Symptomatic intraspinal synovial cysts of the lumbar spine: correlation of MR and surgical fi ndings . Neuroradiology . 2001 ; 43 : 1070 – 1075. 14. Baur A , Stabler A , Arbogast S , et al . Acute osteoporotic and neoplastic vertebral compression fractures: fl uid sign at MR imaging . Radiology . 2002 ; 225 ( 3 ): 730 – 735. 15. Yuh WTC , Zachar CK , Barloon TJ , et al . Vertebral compression fractures: distinction between benign and malignant causes with MR imaging . Radiology . 1989 ; 172 : 215 – 218. 16. Rupp RE , Ebraheim NA , Coombs RJ . Magnetic resonance imaging differentiation of compression spine fractures or vertebral lesions caused by osteoporosis or tumor . Spine . 1995 ; 20 : 2499 – 2504. 17. Jensen MC , Brant-Zawadski MN , Obuchowski N , et al . Magnetic resonance imaging of the lumbar spine in people without back pain . N Engl J Med . 1994 : 331 ( 2 ); 69 – 73. 18. Teresi LM , Lufkin RB , Reicher MA , et al . Asymptomatic degenerative disc disease and spondylosis of the cervical spine: MR imaging . Radiology . 1987 ; 164 : 83 – 88. This page intentionally left blank 31

Chapter 1.4 Preparation for Interventional Spine Procedures

Thomas R. Saullo and Michael J. DePalma

Patient Selection and Preparation 32 Pre-Procedure 32 Peri-Procedural Medications 33 Medications 33 Patient Positioning 33 Preparing the Sterile Field 34 Equipment 34 Conclusion 36 References 36 32 Patient Selection and Preparation Preparation for interventional spine and pelvic procedures requires several steps. When a patient is examined and determined to have a condition amenable to a minimally invasive percutaneous procedure, the physician must review contraindications, allergies, and current medications with the patient. Patient education must include outcomes, alternatives, and potential risks of the proposed procedure. If the patient is in agreement with the treatment plan, paperwork designating informed consent for the procedure to be performed should be signed by the patient, a witness, and the physician, and placed in the medical record. In patients with severe cardiopulmonary disease or patients who will need to hold anti-coagulant medications prior to the procedure, clearance should be obtained from the appropriate treating physician. A typical regimen is to hold Coumadin (warfarin) for three to five days and Plavix (clopidogrel) for 7 days. ( 1 ) Patients may take an 81 mg aspirin during that period and Coumadin or Plavix may be restarted the evening of the procedure. Aspirin and NSAIDs are not typically held for procedures. ( 1 ) Maintaining the patient on aspirin while holding Plavix and Coumadin is a reasonable plan in patients with established 1.3: Imaging for Interventional Management coronary artery disease. The decision of which aspirin dose to utilize— 81mg versus 325mg— should be made in consultation with the patient’s treating cardiologist. The routine use of sedating medications prior to spinal interventional procedures is not recommended, but patients should be informed about their options for sedation. Most patients experience only mild anxiety prior to spinal injections and sedation is not required, however, if requested, light intravenous sedation is reasonable. Studying patients over a six-month period, Kim, et al., ( 2 ) found that only 25 percent of zygapophysial and epidural injection patients requested sedation. More than 96 percent of those patients received IV sedation. ( 2 ) Pre-Procedure Procedural contraindications, patient allergies, and any changes in the patient’s condition, medical history, or medications should be reviewed prior to executing any planned procedure. When appropriate, such as with patients on blood thinners, pre-procedure labs should be ordered and reviewed. The international normalized ratio (INR) should be within normal limits the day of the procedure. ( 1 ) If conscious sedation is to be used (e.g., vertebroplasty), the patient should be NPO (null per os) for 6 hours prior to the procedure. Vital signs should be monitored and recorded before, during and after the procedure. Patients requiring intravenous (IV) antibiotics, sedatives or pain medication should have a peripheral IV placed. An offi- cial “time out” verifying the patient’s name and birth date, the correct affected side or site, and the proper procedure being performed should be completed prior to the start of the procedure. Supplemental fluids should be readily available in cases involving patients with advanced cardiopulmonary disease, hypotension, vasovagal reactions, or who have been NPO. ( 3 )

The patients’ blood pressure, heart rate, respiratory rate and O2 saturation should be monitored before, during and after the procedure. Supplemental O2 should be administered via nasal cannula to maintain the O2 saturation above 90 percent but used with caution in patients with pulmonary disorders such as COPD. Hypertensive patients should have a systolic pressure below 200 mmHg and a diastolic pressure below 110 mmHg. Caridac monitoring is recommended with more invasive procedures such as intradiscal procedures, spinal cord stimulator implantation, and augmentation procedures, or in patients with a history of myocardial infarction or angina. ( 3 ) In a small study of 12 patients, Gonzalez, et al. ( 4 ) found that epidural steroid injections (ESIs) resulted in a systemic effect with a statistically significant increase in blood sugar levels in diabetic patients. Fasting blood glucose levels rise and peak on the day of the injection ( 4–6 ) with the duration of elevation being dose dependant (2 days to 2 weeks). ( 4–7 ) Postprandial glucose levels increase more and persist longer in diabetic patients compared to non-diabetics. ( 8 ) A direct correlation between percent 33 HBA1c and the magnitude of increase in fasting blood glucose the day of a glucocorticoid injection has been shown, however, finger-stick glucose levels were not found to be predictive. ( 5 ) Ideally, blood glucose levels should be well controlled with an HbA1c <7 percent before instillation of epidural corticosteroid. ( 8 ) Fortunately, reduced insulin sensitivity is unlikely to be clinically relevant in normal individuals. ( 6 ) Transient hyperglycemia is expected with ESIs in diabetic patients, who should be informed of this consequence as part of the consent process. ( 4 ) Diabetic patients require specific advice on the management of their disease after corticosteroid injection with a protocol agreed upon by the his/her managing physician. ( 6 ) Peri-Procedural Medications Intradiscal procedures such as discography, intradiscal injections, IDET, and biaculopasty, carry additional inherent risks. Discitis is a rare but potentially serious complication with intradiscal procedures. One systematic review concluded that when an experienced clinician, with a stiletted two-needle technique, performs lumbar discography, the prophylactic use of antibiotics to prevent discitis is not necessary. ( 9 ) Interventional Pain Medicine Although meticulous sterile technique alone has been shown to be effective, prophylactic antibiotics are routinely used to further reduce the risk of infection. Intravenous Ancef (cefazolin) is recommended at a dosage of 1 gm for patients under 80 kg or 2 gms for patients over 80 kg. ( 10 ) Following the procedure, Keflex (cephalexin) 500mg po four times daily is recommended for seven days. IV and then po Ciprofloxacin may be used for patients with a penicillin allergy. In the more anxious patient, 5 to 10 mg of oral diazepam twenty minutes prior or 5 mg of IV diazepam immediately prior to the procedure appears effective in controlling anxiety. ( 2 ) The administration of narcotics is usually only necessary with percutaneous augmentation or therapeutic intradiscal procedures, with 75–150 mcg of fentanyl being sufficient. Medications Commonly used corticosteroids include triamcinolone (Kenalog), betamethasone (Celestone), and dexamethasone (Decadron) (non-particulate steroid for L3 and cephalad levels involving the nerve root or foramen). Contrast agents utilized to visualize injectate flow include iopamidol (Isovue) or iohexol (Omnipaque). Patients with a contrast allergy can be pretreated with prednisone 20 to 50 mg po, ranitidine 50 mg po, and diphenhydramine 25 to 50 mg po at twelve and two hours prior to the procedure with an additional 25 mg of IV diphenhydramine immediately before the procedure. ( 11 ) Anaphylaxis occurs in up to 2 percent of first-dose administrations of iodinated contrast, and the risk increases to 17 percent to 35 percent with repeated exposure in iodine sensitive patients. ( 12 ) Alternatively, gadolinium may be used in these patients. Gadolinium contrast carries a much lower risk of severe allergic reaction reported to be 0.0003 percent to 0.01 percent. ( 13–15 ) In patients with an allergy to iodinated contrast, gadolinium contrast is an effective, albeit more expensive, alternative for spinal injection procedures under fluoroscopy (including discography). ( 16–18 ) Post discography computed tomography scans should be performed promptly after discography with gadolinium due to a shortened half-life when used intradiscally. ( 18 ) Patients should be monitored for at least thirty minutes after the procedure, as 90 percent of allergic reactions will begin fifteen minutes after administration of contrast dye. ( 19 ) Patient Positioning Optimal positioning of the patient prior to the start of a procedure allows for the best chance of an efficient and technically successful procedure. Proper positioning of the patient should allow for patient comfort, optimal fluoroscopic imaging, and adequate space for the physician to access the target region. 34 The patient is positioned prone with the legs abducted and the feet off the sides of the table (for stability) during S1 transforaminal, caudal, interlaminar, and sacroiliac joint injections. Prone positioning is also used with spinal and pelvic augmentation procedures. The patient is also prone for spinal cord stimulator insertion but with the addition of a pillow under the abdomen to provide an increased thoracolumbar kyphosis, allowing for improved interlaminar access. Patients are positioned prone with hip wedge for a one-quarter to one-third turn during thoracolumbar transforaminal and facet joint injections. A similar position is adopted for discography with the use of a small roll under the dependent side. Cervical injections are carried out with the patient lying on his or her side and the head parallel to the floor with both shoulders depressed. The dependent arm may grip the opposite forearm providing traction on the upper extremity thus allowing for improved visualization of the cervical spine. Preparing the Sterile Field Povidone iodine is used to scrub the target area allowing it to dry for sterilization. Patients allergic to 1.3: Imaging for Interventional Management iodine may be prepped with chlorhexidine and isopropyl alcohol for procedures not invading the epidural space. A triple scrub for 5 minutes including isopropyl alcohol, chlorhexidine, and povidone iodine is recommended for intradiscal procedures and implants. ( 3 ) For most procedures, draping the area surrounding the target region with three or four sterile towels is sufficient (Figure 1.4.1 ). In cases of intradiscal procedures, spinal stimulator implantation and percutaneous augmentation procedures, an additional full length fenestrated sterile drape should be employed (Figure 1.4.2 ). Equipment First and foremost, an interventional procedural suite should have a fluoroscopic C-arm and radiolucent fluoroscopy table. Ideally, the C-arm should have digital subtraction capabilities to provide optimal visualization of intravascular uptake, particularly with transforaminal procedures above L3. The C-arm should be routinely maintained and inspected. ( 3 ) When properly performed, patient radiation exposure is

Figure 1.4.1 Patient positioned prone with skin prepped with betadine and sterile towels in place. C-arm is in position above the patient for an S1 transforaminal ESI. 35 Interventional Pain Medicine

Figure 1.4.2 Patient is in the left lateral oblique position for lumbar discography. The skin is prepped with betadine x3 followed by chlorhexadine, sterile towels, and a fenestrated drape. A sterile barrier is placed over the image intensifier. minimal with fluoroscopic procedures. ( 20–25 ) Staff members in the fluoroscopy suite have a cumulative radiation exposure risk. ( 25 ) Decreasing the amount of radiation to the clinician is a major safety concern for interventionalists. ( 24 ) Pulsed fluoroscopic imaging can reduce overall exposure 20 to 75 percent ( 26 , 27 ). Routinely using colli- mation— the narrowing of the active beam— also reduces the amount of radiation exposure. ( 26 ) The patient’s body serves as the conduit for scattered radiation. ( 28 ) Clinician exposure to scatter radiation depends on distance from the source, overall exposure time, and the use of protective equipment.

Figure 1.4.3 Equipment for a fluoroscopic procedure suite: 1. Lead aprons. 2. Sterile procedure table. 3. Mobile lead barrier shield. 4. Nursing support cart. 5. Adjustable image view screens. 6. Positioning wedge. 7. Radiolucent fluoroscopic table. 36 1.3: Imaging for Interventional Management

Figure 1.4.4 Typical sterile procedural table set up for a vertebroplasty.

Positioning the image intensifier as close to the patient as is practical, also keeping the source further from the table, reduces exposure to scatter. ( 28 ) All personnel in the fluoroscopy suite should use lead aprons, thyroid collars, and radiation badges (both under and over the lead apron and a ring badge if the clinician’s hand is in the field under live fluoroscopy). Interventional clinicians may opt to use additional protection such as leaded barriers, humeral sleeves, gloves and eyewear. Lead drapes can be added to the table for additional protection. ( 25 ) Sterile gloves should be utilized with all procedures. Sterile gowns with accompanying mask and cap are standard with all intradiscal procedures, spinal stimulators, and percutaneous augmentation procedures (Figures 1.4.3 and 1.4.4 ). Conclusion Successful interventional procedures begin with proper patient selection and education assuring that the goals of treatment and patient expectations are mutual and reasonable. Pre-procedure preparation incorporates proper management of the patients’ medical conditions, medications, and allergies. Medical and safety equipment should be well maintained to ensure the safety of the patient as well as the staff. Precise patient positioning allows for a more efficient procedure and will minimize fluoroscopy time. Although infection rates are very low with interventional procedures, the consistent use of meticulous sterile technique is essential. Minimally invasive percutaneous procedures are extremely safe and effective diagnostic and therapeutic tools when adhering to proper methods. References 1. Horlocker TT , Wedel DJ , Benzon H , et al . Regional anesthesia in the anticoagulated patient: deﬁ ning the risks ( the second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation ). Reg Anesth Pain Med . 2003 ; 28 : 172 – 197 . 2. Kim N , Delport E , Cucuzzella T , Marley J , Pruitt C . Is Sedation Indicated Before Spinal Injections? Spine . 2007 ; 32 ( 25 ); 748 – 752 . 3. Windsor RE , Storm S , Sugar R . Prevention and Management of Complications Resulting from Common Spinal Injections . Pain Physician . 2003 ; 6 : 473 – 483 . 4. Gonzalez P , Laker SR , Sullivan W , Harwood JEF , Akuthota V . The Effects of Epidural Betamethasone on Blood Glucose in Patients with Diabetes Mellitus . PMRJ . 2009 ; 1 : 340 – 345 . 37 5. Linn A , Stoller A , Simopoulos T , Peeters-Asdourian C . Changes in Blood Glucose Levels in Diabetics After Epidural Steroid Injection . American Academy of Pain medicine, 24th Annual Meeting Abstract 184 , February 14 , 2008 . 6. Ward A , Watson J , Wood P , Dunne C , Kerr D . Glucocorticoid epidural for sciatica: metabolic and endocrine sequelae . Rheumatology . 2002 ; 41 : 68 – 71 . 7. Spaccarelli KC . Lumbar and caudal epidural corticosteroid injection . Mayo Clin Proc 1996 ; 71 : 169 – 178 . 8. Younes M , Neffati F , Touzi M , Hassen-Zrour S , Fendri Y , Be ´jia I , Amor AB , Bergaoui N , Najjar MF . Systemic effects of epidural and intra-articular glucocorticoid injections in diabetic and non-diabetic patients . J Bone Spine . 2007 ; 74 : 472 – 476 . 9. Willems PC , Jacobs W , Duinkerke ES , De Kleuver M . Lumbar Discography: Should We Use Prophylactic Antibiotics? J Spinal Disord Tech . 2004 ; 17 ( 3 ): 243 – 247 . 10. Forse RA , Karam B , MacLean LD , et al . Antibiotic prophylaxis for surgery in morbidly obese patients . Surgery. 1989 ; 106 : 750 – 756 . 11. Fenton DS , Czervionke LF . Ch 11: Pharmacology for the spine injectionist . In: Image-Guided Spine Intervention Philadelphia, PA : WB Saunders ; 2003 : 287 – 292 .

12. Dreyer SJ . Commonly used medications in pain procedures . In: Lennard TA , ed. Pain Procedures in Clinical Interventional Pain Medicine Practice . Philadelphia, PA : Hanley & Belfus ; 2000 : 1 – 9 . 13. Murphy JM , O’Hare NJ , Smiddy P , et al . Gadopentetate dimeglumine as a contrast agent in peripheral angioplasty report . Acta Radiol . 1998 ; 39 : 576 – 578 . 14. Murphy KJ , Brunberg JA , Cohan RH . Adverse reactions to gadolinium contrast media: A review of 36 cases . AJR Am J Roentgenol . 1996 ; 167 : 847 – 849 . 15. Murphy KP , Szopinski KT , Cohan RH , et al . Occurrence of adverse reactions to gadolinium-based contrast material and management of patients at increased risk: A survey of the American Society of Neuroradiology Fellowship Directors . Acad Radiol . 1999 ; 6 : 656 – 664 . 16. Falco FJE , Rubbani M . Visualization of Spinal Injection Procedures Using Gadolinium Contrast . Spine . 2003 ; 28 ( 23 ): 496 – 498 . 17. Falco FJE , Moran JG . Lumbar Discography Using Gadolinium in Patients with Iodine Contrast Allergy Followed by Postdiscography Computed Tomography Scan . Spine . 2003 ; 28 ( 1 ): 1 – 4 . 18. Slipman CW , Rogers DP , Lipetz JS , et al . MRI discography with intradiscal gadolinium in patients with severe anaphylactoid reaction to iodinated contrast material . J Pain . 2001 ; 2S : 9 . 19. Granger RG . Annotation: Radiological contrast media . Clin Radiol . 1987 ; 38 : 3 – 5 . 20. Botwin KP , Thomas S , Gruber RD et al . Radiation exposure of the spinal interventionalist performing fl uoroscopically guided lumbar transforaminal epidural steroid injections . Arch Phys Med Rehabil . 2002 ; 83 : 697 – 701 . 21. Manchikanti L . Transforaminal lumbar epidural steroid injections . Pain Physician . 2000 ; 3 : 374 – 398 . 22. Botwin KP , Freeman ED , Gruber RD, et al . Radiation exposure to the physician performing fl uoroscopically guided caudal epidural steroid injections . Pain Physician . 2001 ; 4 : 343 – 348 . 23. Manchikanti L , Pampati V . Research designs in interventional pain management: Is randomization superior, desirable or essential? Pain Physician . 2002 ; 5 : 275 – 284 . 24. Manchikanti LM , Cash KA , Moss TL et al . Radiation exposure to the physician in interventional pain management . Pain Physician 2002 ; 5 : 385 – 393 . 25. Manchikanti L , Cash K , Moss T , Pampati V . Effectiveness of protective measures in reducing risk of radiation exposure in interventional pain management: A prospective evaluation . Pain Physician . 2003 ; 6 : 301 – 306 . 26. Hernandez RJ , Goodsitt MM . Reduction of radiation dose in pediatric patients using pulsed fl uoroscopy . Am J Roentgerol . 1996 ; 167 : 1247 – 1253 . 27. Adelstein SJ . Uncertainty and relative risks of radiation exposure . JAMA . 1987 ; 258 : 655 – 657 . 28. Fishman SM , Smith H , Meleger A et al . Radiation safety in pain medicine . Reg Anesth Pain Med . 2002 ; 27 : 296 – 305 . This page intentionally left blank 39 Chapter 1.5 Basic Surgical Skills for Interventional Pain Procedures

Kristen Radcliff and Nina Singh-Radcliff

Incidence of infection 40 Aseptic Technique 40 Surgical Handwashing 40 Surgical Site Prep 41 Surgical Prep Solution 41 Preoperative Hair Removal 41 Antibiotics 41 Sterile Field Principles 42 Sterile Gloves 42 Universal Protocol and Time-Out 42 Conduct a Pre-Procedure Verification Process 43 Mark the Procedure Site 43 Perform a Time-Out 44 Relevant Surgical Instruments 44 Needle Drivers 44 Bovie/Electrocautery/Unipolar and Bipolar (Pictures) 45 Tissue adhesives 47 Surgical Preparation Skills 47 Surgical Gown 50 References 50 40 Incidence of infection The Centers for Disease Control and Prevention (CDC) estimates that over 27 million surgical procedures are performed in the United States each year.1 Surgical site infections (SSIs) are the third most common nosocomial (hospital-acquired) infection and are responsible for longer hospital stays and increased costs to the patient and hospital. 2 Resultantly, SSIs are now recognized as a “never event” measure of the quality of patient care by physicians, infection control practitioners, health planners, and the public. 3 Under provisions of Section 5001(c) of the Deficit Reduction Act of 2005, the Centers for Medicare and Medicaid Services (CMS) will no longer render payment to hospitals for cases in which SSI have occurred.4 Although percutaneous pain procedures are commonly perceived to have a reduced risk of infection, infections of the spine have been reported after nearly every spinal injection. Indeed, a recent meta- analysis found that the most common complication of sacroiliac joint, facet, and trigger point injections is infection. 5 The source of the infection can derive from external sources, skin contamination, hematogenous sources, or post-procedure seeding. Bacteria may be inoculated either through skin flora, needle 1.5: Basic Surgical Skills contamination, or contaminated medications. Additionally, bacteria may be inadequately cleansed from the skin during preparation or migrate hematogenously to the injection site and cause an infection from localized bleeding or a steroid-suppressed local immune response. With the growing number of interventional pain management procedures being performed in the United States, both in the operating room and physicians’ offices, it is imperative that the physician has a thorough understanding of aseptic technique. This chapter will review the recent literature and the practices to prevent nosocomial infection after procedures relevant to the pain physician. Aseptic Technique Aseptic technique is a set of specific practices and procedures performed under carefully controlled conditions with the goal of asepsis— the absence of pathogenic organisms in a clinical setting. This differs from practices that clean (remove dirt and other impurities), sanitize (reduce the number of microorganisms to safe levels), or disinfect (remove most microorganisms but not highly resistant ones). Cleaning, sanitizing, and disinfecting are not sufficient to prevent infection. Components of aseptic technique include applying bacteriocidal agents to the operative surface, establishing a barrier to separate sterile from nonsterile, and preventing contamination during or after the procedure. Surgical Handwashing Presurgical hand scrubbing with an antimicrobial solution is an important intervention in maintaining surgical asepsis and preventing the spread of nosocomial infections. An effective scrub also involves donning and changing gloves without contamination of the surgical field. Traditionally, scrubbing involves mechanical removal of debris and bacteria, using a solvent brush over the hands and forearms for ten minutes. Several detergent agents are available for optimization of surgical scrub. Iodine-based detergent agents have the longest record of use and are the “gold standard” against which other agents are compared. Limitations of iodine include minimal persistence and that its bacteriocidal action results not from direct contact, but from the process of the solution drying. Chlorexadine gluconate (CHG) is a chemical antiseptic that is often formulated with isopropyl alcohol in varying concentrations; trade names include Chloraprep, Avagard, and Hibiclens. CHG is responsible for the bacteriostatic effects (limiting growth and reproduction of bacteria without killing) and the alcohol is responsible for the rapid bactericidal (kills bacteria) action to gram-positive and gram-negative microbes. Potential benefits include immediate bactericidal effects, compared with iodine, as well as persistence of bacteriostatic effect for up to forty-eight hours, compared to two hours for iodine.6 Additionally, it has been suggested that unlike iodine, the formulation remains active in the presence of blood, serum, and other protein-rich biomaterials. 7 41 Several studies have shown that iodine and CHG brush applications can be abrasive and cause skin damage, resulting in excessive shedding of the superficial layers and microscopic cuts on the skin’s surface. Such damaged skin can harbor microbes and contribute to the spread of infections. Additionally, damaged skin can potentially lead to undesirable changes in colonizing skin flora, such as increased colonization with gram-negative bacteria and candida species. Studies have suggested that surgical hand rubbing with aqueous alcoholic solutions may be as effective as surgical hand scrubbing8 and involves relatively shorter application time (average two to three minutes compared with six to ten minutes for the scrub) and may optimize staff time and hospital resources as well as improve staff compliance. 9 Pain physicians should consider a traditional scrub for the first scrub of the day to remove any gross debris or after using the restroom, eating, or patient contact. A brushless scrub may be an acceptable alternative for subsequent scrubs. Surgical Site Prep Pre-procedure bathing or showering with an antiseptic skin wash product is a well-accepted procedure for reducing skin bacteria. A meta-analysis of 10,007 patients, however, demonstrated no clear evidence of benefit for preoperative cleansing with chlorhexidine over other wash products to reduce surgical site Interventional Pain Medicine infection.10 Surgical Prep Solution For pain procedures, the ideal prep solution agent would be rapidly bactericidal, persistent, and safe around the spine. A recent study of 849 patients undergoing clean-contaminated surgery showed that the overall rate of SSI was significantly lower in patients who received skin cleansing with chlorhexidine-alcohol compared to the povidine-iodine group.11 Several other studies have shown similar findings. 12 , 13 , 14 Specifically regarding pain procedures, Yentur, et al., looked at patients undergoing epidural catheter placement for surgery who were prepped with iodine. Their findings demonstrated that skin surface cultures had a 3.5 percent colonization, epidural needles 34.6 percent colonization, and catheters 45.8 percent colonization.15 In another study comparing catheter colonization in patients with povidone-iodine versus chlorhexidine, however, minimal or no difference was seen. 16 Preoperative Hair Removal Whether to remove hair as well as how to do so has been looked at extensively. In a meta-analysis by Tanner, et al., of several thousand patients, it was concluded that there was no evidence of a difference in SSIs among patients who have had hair removed prior to surgery and those who have not. Their findings also led them to suggest that when hair removal was deemed necessary, electric clipping and depilatory creams were preferable, as they resulted in less SSIs.17 As opposed to shaving these also had the additional benefit of potentially reducing the introduction of foreign bodies in a wound or injection site. Shaving can result in microscopic and visible injury. There is the risk for bacterial liberation and growth after razor injury as well.18 If clipping is chosen, moderate evidence exists to recommend removal of hair as close as possible to the time of the surgical procedure. Seropian, et al., looked at 1,013 patients in a randomized study and found that when clipping was performed the evening before surgery, infection rates were double.18 A literature search did not demonstrate any convincing differences in the incidence of postoperative SSIs between electric clipping, depilation, or no hair removal. Antibiotics The majority of pain procedures are considered “clean procedures,” meaning they do not involve entrance into the gastrointestinal, gynecologic, or respiratory tracts.19 Thus, trigger point, epidural steroid, sacroiliac joint, and facet joint injections are considered clean surgical procedures and do not necessarily warrant antibiotic prophylaxis. The decision to administer prophylactic antibiotics is deemed appropriate, however, if the pain physician is implanting a foreign body such as a device or pump. 42 Table 1.5.1 Sterile Field Principles - All items in the sterile field must be sterile and sterile drapes are used to establish an aseptic barrier. - Sterile packages or fields are opened or created as close as possible to time of actual use. - Contaminated items must be removed immediately from the sterile field. - Gowns are considered sterile only in the front, from chest to waist and from the hands to slightly above the elbow. - Tables are considered sterile only at or above the level of the table. - Nonsterile items should not cross above a sterile field. - There should be no laughing, coughing, or sneezing across a sterile field. - Personnel with colds should avoid working while ill or apply a double mask. - Edges of sterile areas or fields (generally the outer inch) are not considered sterile. - When in doubt about sterility, discard the potentially contaminated item and begin again. - A safe space or margin of safety is maintained between sterile and nonsterile objects and areas. - When pouring fluids, only the lip and inner cap of the pouring container is considered sterile; the pouring container should not touch the receiving container, and splashing should be avoided.

1.5: Basic Surgical Skills - Tears in barriers and expired sterilization dates are considered breaks in sterility.

Additionally, the risk of infection in the patient, based on their general health, should be balanced against the risk of a nosocomial infection. Patients with diabetes, malnutrition, active neoplastic disease, or other immunocompromised states (myeloproliferative disorders, low neutrophil counts, etc.), may particularly benefit from antibiotics20 . When antibiotic prophylaxis is chosen, it should be aimed at usual skin flora, typically gram positive staphylococcus aureus. A cephalosporin such as cefazolin is appropriate. If the patient has a penicillin allergy, vancomycin may be chosen. Sterile Field Principles After skin preparation, an impermeable barrier is established to maintain the sterility of the local microenvironment. Sterile Gloves Following appropriate hand scrubbing or rubbing, intact, sterile gloves need to be donned. Not only do they protect the surgical site from microorganisms on the skin of the physician, they also protect the physician from bloodborne pathogens. Unfortunately, glove perforation is fairly common, with puncture rates being reported as high as 61 percent.21 The index finger of the nondominant hand of the physician seems to be the most prone part of the glove to be punctured or torn.22 This is likely due to holding the instrument in the dominant hand and the tissue with the nondominant hand. The needle holder is usually in the right hand, and the needle may accidentally puncture the glove of the opposite hand.21 Additionally, duration of procedure has also been associated with increased perforation. 23 The color indicator double-gloving system has been developed for early recognition of glove perforation. 24 In a study by Naver, et al., blood contamination of the hands decreases from 13 percent to 2 percent with the use of double gloves.25 The loss of sensitivity and dexterity, however, has been cited by several health care works as a drawback. Risks versus benefits of protecting oneself versus loss of sensitivity, which has been shown to diminish fairly quickly, need to be balanced. Universal Protocol and Time-Out The Universal Protocol was introduced in 2004 by the Joint Commissions to prevent wrong-person, wrong-site, and wrong procedure events. Office-based and out-of-OR procedures have increased in wrong-site events.26 A recent study identified a total of thirteen wrong-site cases from approximately 48,941 collective pain management procedures (52 percent were deemed to be “at risk” for occurrence, 43 or unilateral procedures). Root-cause analysis revealed that in only one case was the Universal Protocol completely followed, and in nine procedures, multiples lapses in protocol occurred.27 Thus, the Universal Protocol is not limited to OR or surgical procedures; rather, it is relevant to all settings where surgical and non-surgical invasive procedures are performed. It is imperative that physicians performing regionnal blockade and invasive pain therapies correctly apply the components of the Universal Protocol to enhance patient safety. The Universal Protocol is delineated by The Joint Commissions in the following manner28 : Conduct a Pre-Procedure Verification Process - Verify the correct procedure, for the correct patient, at the correct site. - When possible, involve the patient in the verification process. - Identify the items that must be available for the procedure. - Use a standardized list to verify the availability of items for the procedure. (It is not necessary to document that the list was used for each patient.) At a minimum, these items include:

- relevant documentation Interventional Pain Medicine Examples: history and physical, signed consent form, pre-anesthesia assessment - labeled diagnostic and radiology test results that are properly displayed Examples: radiology images and scans, pathology reports, biopsy reports - any required blood products, implants, devices, special equipment - Match the items that are to be available in the procedure area to the patient. Mark the Procedure Site - The site does not need to be marked for bilateral structures. Examples: tonsils, ovaries - For spinal procedures: Mark the general spinal region on the skin. Special intraoperative imaging techniques may be used to locate and mark the exact vertebral level. - Mark the site before the procedure is performed. - If possible, involve the patient in the site-marking process. - The site is marked by a licensed independent practitioner who is ultimately accountable for the procedure and will be present when the procedure is performed. * - Ultimately, the licensed independent practitioner is accountable for the procedure— even when delegating site marking. * In limited circumstances, site marking may be delegated to some medical residents, physicians assistants (P.A.), or advanced practice registered nurses (A.P.R.N.). - The mark is unambiguous and is used consistently throughout the organization. - The mark is made at or near the procedure site. - The mark is sufficiently permanent to be visible after skin preparation and draping. - Adhesive markers are not the sole means of marking the site. - For patients who refuse site marking or when it is technically or anatomically impossible or impracti- cal to mark the site (see examples below): Use your organization’s written, alternative process to ensure that the correct site is operated on. Examples of situations that involve alternative processes: - mucosal surfaces or perineum - minimal access procedures treating a lateralized internal organ, whether percutaneous or through a natural orifice - interventional procedure cases for which the catheter or instrument insertion site is not predetermined Examples: cardiac catheterization, pacemaker insertion 44 - teeth - premature infants, for whom the mark may cause a permanent tattoo Perform a Time-Out - Conduct a time-out immediately before starting the invasive procedure or making the incision. - A designated member of the team starts the time-out. - The time-out is standardized. - The time-out involves the immediate members of the procedure team: the individual performing the procedure, anesthesia provider(s), circulating nurse, operating room technician, and other active participants who will be participating in the procedure from the outset. - All relevant members of the procedure team actively communicate during the time-out. - During the time-out, the team members agree, at a minimum, on the following: - correct patient identity - correct site 1.5: Basic Surgical Skills - procedure to be done - When the same patient has two or more procedures: If the person performing the procedure changes, another time-out needs to be performed before the start of each procedure. - Document the completion of the time-out. The organization determines the amount and type of documentation. Institutions have varied timing and location of the pre-procedure verification and site marking based on what works best for their unique circumstances and practices. Relevant Surgical Instruments Needle Drivers 1. The needle holder must be an appropriate-sized instrument for the size needle selected. 2. Needles should be grasped in an area about 1/3 to ½ of the distance from the swaged area to the point. Avoid placement on or near the swaged area. 3. The needle should be placed securely in the tip of the needle holder jaws. 4. When placing the needle in tissue, any force applied should be in the direction following the curve of the needle. 5. Do not take excessively large bites of tissue with small needles. 6. Do not force or twist the needle in an effort to bring the point out through the tissue; instead, withdraw the needle and replace tissue. 7. Do not force a dull needle through tissue— obtain a new one. 8. When the needle holder with needle is passed to the surgeon, the needle should be pointing in the right direction in which it will start to be used, without need for readjustments.

Figures 1.5.1 45

Figures 1.5.2 Interventional Pain Medicine

Figures 1.5.3

Figures 1.5.4

Bovie/Electrocautery/Unipolar and Bipolar (Pictures) Needles and Sutures Needles come in a variety of sizes that are appropriate for the diameter of the suture attached to the needle. The main difference that is relevant for pain physicians is that some needles have sharpened edges to pass more easily through large bites of tissue. These needles are considered “cutting.” Other needles are tapered and do not cut adjacent tissue. Although cutting needles are technically easier to pass, they may damage integrity of the tissue and thereby weaken the closure. Needles may be permanently swaged to the suture or may be designed to come off the suture with a sharp straight tug. These “pop-offs” are commonly used for interrupted sutures, where each suture is only passed once and then tied. 46 Sutures are commonly classified as either absorbable or non-absorbable depending on whether the body will naturally degrade and absorb the suture material over time. Absorbable suture materials are degraded by the body’s enzymatic pathways via hydrolysis and proteolytic degradation.29 Phagocytes attack and destroy the stitch material in the same manner that it would a foreign particle. The process can last from ten days to eight weeks. Sutures are intended to be used in internal body tissues to hold the body tissues together long enough to allow healing, but will disintegrate so that they do not leave foreign material or require further procedures. 30 They are not intended to be used on the surface of the skin; however, they can be used to close skin in a subcuticular or completely buried pattern. Occasionally, absorbable sutures can cause inflammation and be rejected by the body rather than be absorbed. 31 Types of self-dissolving sutures are listed below. * Vicryl (Polyglactin, Ethicon): Synthetic braided polymer made of glycolytic acid. Dissolves at a slower rate than catgut, but causes less of a reaction on implantation. Used below the surface of the skin. This is a very pliable suture material and is easy to knot.

1.5: Basic Surgical Skills * Monocryl : Absorbable, monofilament suture. The least reactive substance of this group, and should leave least scarring. The suture is less pliable and requires more knots. Non-absorbable sutures are typically used to close skin, and should be removed after wound healing is complete. They are made of special silk or the synthetics polypropylene, polyester, or nylon. They are fine/thin, unlikely to leave marks or scars (they provoke less immune response), and unlikely to get infected. 31 , 32 Additionally, they are usually colored blue or black to make them more visible against the blood red of a wound. Their smooth surface allows them to be removed easily.33 Suture Sizes The United States Pharmacopeia (U.S.P.) defines suture sizes. By convention, suture diameter increases as the number increases (e.g., a #1 suture is smaller in diameter than a #4). The deep fascia requires a strong layer of closure, typically with a #1 absorbable suture. If a large subcutaneous fat layer needs closure, it may be loosely reapproximated with a #1 absorbable suture in order to close down dead space. The subcutaneous dermal closure is a critical layer, as it actually heals and seals the wound. Meticulous closure should be performed, and can be done with either a 2–0 vicryl or monocryl. The epidermis may be reapproximated with either a 4–0 monocryl in a running subcuticular fashion, a 3–0 nylon in an interrupted fashion, or a topical skin adhesive. The epidermal suture layer is designed to take pressure off the dermal closure and further seal the wound. Suture Techniques Many different techniques for suturing exist. The most common is the simple interrupted stitch; it is considered the simplest to perform and is called “interrupted” because the suture thread is cut between each individual stitch. The vertical and horizontal mattress stitches are also interrupted but are more complex and specialized for everting the skin and distributing tension. The running or continuous stitch is quicker but risks failing if the suture is cut in just one place. When performing wound closure, sutures should bring together the wound edges, but should not cause indenting or blanching of the skin, since the blood supply may be impeded and thus increase infection and scarring. Sutured skin should roll slightly outward from the wound (eversion), and the depth and width of the sutured flesh should be roughly equal. Placement varies based on the location, but the distance between each suture generally should be equal to the distance from the suture to the wound edge. 47 Removal While some sutures are intended to be permanent, and (in specialized cases) others may be kept in place for an extended period of many weeks, as a rule sutures are a short-term device to allow healing of a trauma or wound. Different parts of the body heal at different intervals; the trunk of the body usually heals in seven to ten days. Tissue adhesives In recent years, “liquid stitches,” or topical cyanoacrylate adhesives, have been used in combination with, or as an alternative to, sutures in wound closure. The adhesive remains liquid until exposed to water or water-containing substances/tissue, after which it cures (polymerizes) and forms a flexible film that bonds to the underlying surface. The tissue adhesive has been shown to act as a barrier to microbial penetration as long as the adhesive film remains intact. There exists a mild learning curve on correct usage. Liquid stitches also may have the benefit of causing less irritation.32 The drying time allows for an opportunity to manipulate skin position and juxtaposition. If used as the sole means to close a wound, tissue adhesives provide the benefit of avoiding suture Interventional Pain Medicine removal. This is not always an option, however: it cannot be used in areas where excess motion may be seen, because the motion may cause it to peel too soon.35 It also is not as effective in moist areas. Surgical Preparation Skills To open sterile gloves, do the following: 1. Open the outer package of gloves. 2. Open the inner sterile package on a ﬂ at surface.

Figures 1.5.5 Figures 1.5.6 48 1.5: Basic Surgical Skills

Figures 1.5.7 Figures 1.5.8

Figures 1.5.9 Figures 1.5.10 49 Interventional Pain Medicine

Figures 1.5.11 Figures 1.5.12

3. Fold the lower edge of the inner package underneath so the package remains open.

Figures 1.5.13 50 To don sterile gloves, do the following: 1. With the hands still inside the gown’s sleeves, pick up a glove by the cuff and push your hand into the opening, lining up your thumb to the glove’s thumb. 2. As the hand enters the glove, you should let your hand come out of the sleeve so that your ﬁ ngers enter the ﬁ nger spaces of the glove 3. Repeat with the second glove. 1.5: Basic Surgical Skills

Figures 1.5.14

Surgical Gown 1. Open the outer package of the gown. 2. Pick up the gown, holding it only by the inside. 3. Slip your arms into the sleeves, but do not push your hands out of the sleeves at this time. 4. If someone is available, have them connect the snap at the neck and tie the inner tie string at the waist. Studies have not shown a difference in contamination and infection of the surgical site between fabric and non-fabric scrubs.36 References 1. Center for Disease Control and Prevention , Department of Health and Human Services. Surgical Site Infection (SSI) . Reviewed December 17 , 2008 . www.cdc.gov . 2. Scott , RD . The Direct Medical Costs of Healthcare-Associated Infections in U.S. Hospitals and the Benefi ts of Prevention . Division of Healthcare Quality Promotion National Center for Preparedness, Detection, and Control of Infectious Diseases Coordinating Center for Infectious Diseases Center for Disease Control and Prevention . March 2009 . www.cdc.gov . 3. The Centers for Medicare and Medicaid Services . Hospital-acquired conditions (present on admission indicator) , 2009 . www.cms.hhs.gov/HospitalAcqCond/ . 4. The Centers for Medicare and Medicaid Services . Defi cit Reduction Act of 2005 All CMS Provisions As of February 28 , 2006 . www.cms.gov/legislativeupdate/downloads . 5. Cheng J , Abdi S . Complications of joint, tendon, and muscle injections . Tech Reg Anesth Pain Manag . 2007 ; 11 ( 3 ): 141 – 147 . 6. Garcia R , Mulberry G , Brady A , Hibbard JS . Comparison of Chloraprep and Betadine as preoperative skin preparation antiseptics . Poster Presentation at 40th Annual Meeting of the Infectious Disease Society of America . October 25 , 2002 . 51 7. Denton GW . Chlorhexadine . In: Block SS , ed. Disinfection, Sterilization, and Preservation . Philadelphia, PA : Lippincott Williams & Wilkins ; 2001 : 321 – 336 . 8. Parienti JJ , Thibon P , Heller R , Le Roux Y , von Theobald P , Bensadoun H , Bouvet A , Lemarchand F , Le Coutour X . Hand-rubbing with an aqueous alcoholic solution vs traditional surgical hand-scrubbing and 30-day surgical site infection rates . JAMA . 2002 ; 6 ( 288 ): 722 – 727 . 9. Tavolacci MP , Pitrou I , Merie V , Haghighat S , Thillard D , Czernichow P . Surgical hand rubbing compared with surgical hand scrubbing, comparison of effi cacy and cost . J Hosp Infect . 2006 ; 63 ( 1 ): 55 – 59 . 10. Webster J , Osborne S . Preoperative bathing or showering with skin antiseptics to prevent surgical site infection . Cochrane Database Syst Rev. 2007 ; ( 2 ):C D004985 . 11. Darouiche RO , Wall MJ Jr , Itani KM , Otterson MF , Webb AL , Carrick MM , et al. Chlorhexidine-alcohol versus povidone-iodine for surgical-site antisepsis . N Engl J Med . 2010 ; 362 ( 1 ): 18 – 26. 12. Johnson AJ , Daley JA , Zywiel MG , Delanois RE , Mont MA . Preoperative Chlorhexidine preparation and the incidence of surgical site infections after hip arthroplasty . J Arthroplasty . 2010; May 28 . 13. Zywiel MG , Daley JA , Delanois RE , Naziri Q , Johnson AJ , Mont MA . Advance pre-operative chlorhexidine reduces the incidence of surgical site infections in knee arthroplasty . Int Orthop . 2010; June 20 .

14. Hemani ML , Lepor H . Skin preparation for the prevention of surgical site infection: which agent is best? Interventional Pain Medicine Rev Urol . 2009 ; 11 ( 4 ): 190 – 195. 15. Yentur EA , Luleci N , Topcu I , Degerli K , Surucuoglu S . Is skin disinfection with 10% povidone iodine suffi cient to prevent epidural needle and catheter contamination? Reg Anesth Pain Med . 2003 ; 28 ( 5 ): 389 – 393 . 16. Kasuda H , Fukuda H , Togashi H , Hotta K , Hirai Y , Hayashi M . Skin disinfection before epidural catheterization: comparative study of povidone-iodine versus chlorhexidine ethanol . Dermatology . 2002 ; 204. Suppl 1 : 42 – 46 . 17. Tanner J , Woodings D , Moncaster K . Preoperative hair removal to reduce surgical site infection . Cochrane Database Syst Rev. 2006 ; 3 : CD004122 . 18. Seropian R , Reynolds BM . Wound infections after preoperative depilatory versus razor preparation . Am J Surg . 1971 ; 121 ( 3 ): 251 – 254 . 19. Ozgun H , Ertugrul BM , Soyder A , Ozturk B , Aydemir M . Peri-operative antibiotic prophylaxis: adherence to guidelines and effects of educational intervention . Int J Surg . 2010 ; 8 ( 2 ): 159 – 163 . 20. The Department of Surgical Education . Antibiotic Prophylaxis in Surgery . www.surgicalcriticalcare.net . Last accessed July 4 , 2010 . 21. Laine T , Aarnio P . How often does glove perforation occur in surgery? Comparison between single gloves and a double-gloving system . Am J Surg . 2001 ; 181 ( 6 ): 564 – 566 . 22. Palmer JD , Rickett JW . The mechanisms and risks of surgical glove perforation . J Hosp Infect . 1992 ; 22 ( 4 ): 279 – 286 . 23. Partecke LI , Goerdt AM , Langner I , Jaeger B , Assadian O , Heidecke CD , et al. Incidence of microperforation for surgical gloves depends on duration of wear . Infect Control Hosp Epidemiol . 2009 ; 30 ( 5 ): 409 – 414 . 24. Tanner J , Parkinson H . Double gloving to reduce surgical cross-infection . Cochrane Database Syst Rev. 2006 ; 3 : CD003087 . 25. Naver LP , Gottrup F . Incidence of glove perforations in gastrointestinal surgery and the protective effect of double gloves: a prospective, randomized controlled study . Eur J Surg . 2000 ; 166 ( 4 ): 292 – 295 . 26. Neily J , Mills PD , Eldridge N , Dunn EJ , Samples C , Turner JR , et al. Incorrect surgical procedures within and outside of the operating room . Arch Surg . 2009 ; 144 ( 11 ): 1028 – 1034 . 27. Cohen SP , Hayek SM , Datta S , Bajwa ZH , Larkin TM , Griffi th S , et al. Incidence and root cause analysis of wrong-site pain management procedures: a multicenter study . Anesthesiology . 2010 ; 112 ( 3 ): 771 – 718 . 28. The Joint Commission . The 2010 Universal Protocol Speak Up Program . www.jointcommission.org . Accessed July 4, 2010 . 29. Firestone DE , Lauder AJ . Chemistry and mechanics of commonly used sutures and needles . J Hand Surg Am . 2010 ; 35 ( 3 ): 486 – 488 . 30. Lin KY , Farinholt HM , Reddy VR, Edlich RF , Rodeheaver GT . The scientifi c basis for selecting surgical sutures . J Long Term Eff Med Implants . 2001 ; 11 ( 1–2 ): 29 – 40 . 31. Meyer RD , Antonini CJ . A review of suture materials, Part II . Compendium. 1989 ; 10 ( 6 ): 360 – 362 . 32. Tritle NM , Haller JR , Gray SD . Aesthetic comparison of wound closure techniques in a porcine model . Laryngoscope . 2001 ; 111 ( 11 Pt 1): 1949 – 1951 52 33. Swanson NA , Tromovitch TA . Suture materials, 1980s: properties, uses, and abuses . Int J Dermat . 1982 ; 21 ( 7 ): 373 – 378 . 34. U.S. Pharmacopeia . www.usp.org . Accessed July 4 , 2010 . 35. Coulthard P , Esposito M , Worthington HV , van der Elst M , van Waes OJ , Darcey J . Tissue adhesives for closure of surgical incisions . Cochrane Database Syst Rev 2010 ; 5 : CD004287 . 36. Burgatti JC , Lacerda RA . Systematic review of surgical gowns in the control of contamination/surgical site infection . Rev Esc Enferm USP. 2009 ; 43 ( 1 ): 237 – 244 . 1.5: Basic Surgical Skills 53

Section 2 Cervical Spinal Injections

2.1 Cervical Inter-Laminar Epidural Injections 55 2.2 Cervical Transforaminal Epidural Steroid Injections 65 2.3 Cervical Median Branch Blocks and Radiofrequency Ablation 75 This page intentionally left blank 55

Chapter 2.1 Cervical Inter-Laminar Epidural Injections

Gaurav Bhatia and Anita Gupta

Introduction 56 Indications 56 Contraindications 58 Functional Anatomy 58 Equipment and Preparation 60 Medications 60 Technique 60 Complications 62 Summary 62 Clinical Pearl 64

References 64 56 Introduction In the United States, lifetime prevalence of neck pain in adults has been reported to be 26 to 71 percent with 12-month prevalence estimates ranging from 30 to 50 percent.[ 1 ] Similar to low back pain, neck pain is also associated with significant economic, societal, and health impact, though not to the same extent as low back pain. There are multiple structures that can cause neck and upper extremity pain. The list includes cervical intervertebral disc, cervical facet joints, atlanto-axial and atlanto-occipital joints, ligaments, fascia, muscles, and nerve root dura, which are capable of transmitting pain.[ 2 ] An epidural injection for managing chronic neck pain is one of the most commonly performed interventions in the United States. [ 3 ] In 1933, Professor A. Dogliotti first described the cervical epidural block and was also the first to describe the loss of resistance technique with identifying epidural space.[ 4 ] In 1953, the French team of Lievre, et al., reported the first use of epidural steroids for the relief of back pain and sciatica.[ 5 ] Since that time, numerous investigators have pioneered the technique of safely and effectively administering steroids into the epidural space, ranging from cervical to caudal epidural space. There are two major portals 2.1: Cervical Interlaminar Epidural that are available for delivery of medication into the epidural space: inter-laminar and transforaminal. The choice of which approach to use is commonly made by assessing the patient’s structural pathology, one’s skill in performing each procedure, and then weighing the advantages versus the risk associated with the particular technique.[ 6 ] The transforaminal approach is considered technically difficult and owes to greater complications including intravascular penetration, nerve root puncture, and pain provocation.[ 6 ] For this reason, only the interlaminar approach will be discussed in this chapter. The loss of resistance technique to correctly identify needle placement into the cervical epidural space may be inadequate due to various anatomical and structural variations in individuals. Therefore, fluoroscopy-guided techniques have become popular and are now considered the standard of care when placing cervical epidural steroid injections. Fluoroscopy increases the procedure precision and helps confirm correct needle placement into the epidural space.[ 7 ] The placement can be easily confirmed by injecting a small volume of contrast material and performing epidurogram under real-time fluoroscopy. Indications The most common indication for performing cervical epidural injection is cervical radiculitis, which approximately affects 83 per 100,000 population per year. The most common causes of cervical radiculitis are spondylosis and herniated disk.[ 8 , 9 ] Initial treatment usually consists of conservative measures such as activity modification, NSAIDs, and physical therapy. Occasionally, narcotic analgesics may be needed to treat pain adequately. A cervical orthosis may provide comfort for some patients during the acute phase.[ 10 ] If the improvement is not satisfactory with conservative treatment or symptoms are debilitating, a cervical epidural injection is indicated. These injections are usually given as a series of 3 injections, 2 weeks apart in a 6-month period. Cervical epidural injections have been used to treat radicular pain from herniated discs, spinal stenosis, chronic pain secondary to post-cervical surgery syndrome, and chronic neck pain of discogenic origin.[ 2 ] Furthermore, cervical epidural nerve block with local anesthetics have been used as a diagnostic tool to perform a differential neural blockade on an anatomic basis in the evaluation of head, neck, face, shoulder, and upper extremity pain. This technique can also be utilized acutely in the management of postoperative pain as well as pain secondary to trauma. The administration of local anesthetics and steroids/opioids via the cervical approach to the epidural space have also been utilized to treat cervicalgia, phantom limb pain, tension-type headaches, chemotherapy-related peripheral neuropathy, post-herpetic neuralgia, chronic regional pain syndrome, and palliation of cancer-related pain of head, face, neck, shoulder, upper extremity, and upper trunk.[ 11 ] 57 Interventional Pain Medicine

Figure 2.1.1 A 62-year-old male patient with bilateral neck and shoulder pain of 2 years duration. A T-2 weighted saggital MR image showing diffuse bulging discs at C5-6 and C6-7 levels and ligamentum flavum hypertrophy.

Figure 2.1.2 A 35-year-old female patient with posterior neck pain of 8 month’s duration. A T-2 weighted saggital MR image showing intervertebral disc herniation at the C5-6 level. 58 Contraindications There are several contraindications for performing epidural injections, which include both absolute and relative. The foremost absolute contraindication is patient refusal. The potential for hematogenous spread via Baston’s plexus makes local infection and sepsis an absolute contraindication to the cervical approach to the epidural space.[ 12 ] Moreover, anticoagulation and coagulopathy represent absolute contraindications to cervical epidural nerve block because of the risk of epidural hematoma. Other absolute contraindications include known hypersensitivity to agents, local malignancy, and increased intracranial pressure. Relative contraindications include hypovolemia, psychological instability, uncontrolled diabetes mellitus, and congestive heart failure.[ 12 ] In addition, caution must be used in pregnant women when doing injections under fluoroscopic guidance to avoid exposing the fetus to ionizing radiation. Functional Anatomy Understanding of the cervical spine anatomy as well as the anatomy of the epidural space is imperative to

2.1: Cervical Interlaminar Epidural the interventionalist performing the procedure. The cervical spine begins at the base of the skull and has seven vertebrae abbreviated as C1-C7. There are eight pairs of cervical nerves abbreviated as C1-C8, which exit via intervertebral neural foramen. The epidural space exists outside the dural sac but within the vertebral canal. Anteriorly, cervical epidural space is bounded by posterior longitudinal ligament, vertebral bodies, and intervertebral discs. Posteriorly, it is bounded by the vertebral laminae and ligamentum flavum . The vertebral pedicles and intervertebral foramina form the lateral limits of the epidural space. The superior boundary of the cervical epidural space is the fusion of the periosteal and spinal layers of the dura at the foramen magnum.[ 10 , 11 , 12 ] The epidural space continues inferiorly to the sacrococcygeal membrane and contains fat, venous plexus, radicular arteries, lymphatics, and connective tissue.[ 11 ] (Figure 2.1.3 .) When performing an interlaminar cervical epidural block, the following structures are encountered in a specific order, which include skin, subcutaneous tissue, ligamentum nuchae or supraspinous ligament, interspinous ligament, ligamentum flavum , and epidural space (Figures 2.1.4 and 2.1.5 ).[ 11 ] A significant

Ligamentum flavum Spinal dura Interspinous ligament Posterior longitudinal ligament Supraspinous ligament Venous plexus Epidural fat

Figure 2.1.3 59

Ligamentum nuchae

C2 Interspinous ligament

C3 Ligamentum flavum

Epidural space C6 Interventional Pain Medicine

Supraspinous ligament C7

Spinal dura mater Figure 2.1.4

Needle in supraspinous ligament/ligamentum nuchae Spinous process Needle in interspinous ligament

Needle in ligamentum flavum Needle in epidural space

Sup. articular process Post. ramus

Ant. ramus

Vertebral a. Vertebral body Spinal ganglion Figure 2.1.5 60 increase in resistance in needle advancement signals that the needle tip is impinging on the dense ligamentum flavum . The dense ligamentum flavum is made up of elastin fibers, which results in continuous increase in resistance as the needle traverses the ligamentum flavum.[ 11 ] A sudden loss of resistance occurs as the needle tip enters the epidural space. Specifically to the cervical region, there is a space between interspinous ligament and ligamentum flavum that may be perceived as a “false” loss of resistance by the interventionalist. In some individuals, at the level of the cervical region, there is also minimal to absent interspinous ligament, and ligamentum flavum is unfused in the midline.[ 13 ] In these individuals, entry into the epidural space could be achieved without passage through either interspinous ligament or ligamentum flavum and therefore without loss of resistance. This factor, combined with shallow posterior compartment, and phenomenon of “false” loss of resistance makes epidural needle placement especially challenging at cervical levels above C7-T1.[ 10 , 13 ] Equipment and Preparation The procedure is safely performed in an operating room or surgical suite under sterile conditions and 2.1: Cervical Interlaminar Epidural with just local anesthesia. Patients with procedural anxiety can be premedicated with oral benzodi- azepines. Heavy sedation is avoided to allow patient communication if direct needle impingement of the nerve root is encountered.[ 12 ] A pulse oximeter, or blood pressure cuff with or without electrocardiogram leads is appropriate for patient monitoring. A block tray with sterile- prep solution, sterile drape, 1 percent lidocaine for skin infiltration, 23- and 25-gauge syringe needles, a skin marker pen, sterile saline solution, glass or plastic syringe to check for loss of resistance, and 20- to 22-gauge Tuohy needle is sufficient. A contract solution of 5 cc of non-ionic (omnipaque) is drawn up separately in a sterile syringe. Medications The injectant mixture is comprised of 2cc of 0.25 percent bupivacaine with 2cc of methylprednisolone acetate (40mg/cc) suspension or 2cc of triamcinolone hexacetonide (20mg/cc) suspension in a 1:1 ratio. The mixture of local anesthetic and corticosteroids has additional benefits beyond the direct anesthetic affect. The anti-inflammatory affect of corticosteroids is attributed to as the primary reason for long- term relief from epidural steroid injections.[ 10 , 12 , 14 ] Extracts from herniated discs have been found to contain twenty to ten thousand times more phospholipase activity which plays a major role in inflammation of the nerve root and can be neurotoxic. Epidural steroids have been shown to inhibit phospholipase A2 activity and thus prevent prostaglandin generation.[ 15 ] Additionally, prostaglandins have been found to cause hyperalgesia. Corticosteroids also affect cell-mediated activity and cytokines, which may be involved in the pathogenesis of radicular pain. Corticosteroids stabilize nerve membranes inhibiting ectopic impulses,[ 16 ] inhibit ion conductance,[ 14 ] hyperpolarize spinal neurons,[ 14 ] and inhibit C fiber transmission.[ 17 ] The advantages of epidural steroid injections include deposition of drug directly into the affected area and requiring a much smaller dose to achieve the desired result with lower risk of side effect, and longer duration of relief.[ 12 ] Technique Cervical epidural blocks can be safely administered in the sitting, prone, and lateral decubitus positions, with or without the assistance of fluoroscopic guidance.[ 11 ] Additionally, confirmation of entrance into the epidural space can be achieved by loss or resistance approach, “hanging drop technique,” or administration of contrast medium yielding an epidurogram.[ 12 ] The rate of success to safely perform this injection depends on the familiarity and experience of the practitioner with a particular approach. The prone position with the help of fluoroscopy is now considered the gold standard for performing this procedure. [ 18 ] The patient is placed in a prone position on the fluoroscopy table with arms either up in a diver’s position or by the side against the hips. A bed strap is placed around the patient to ensure safety. The neck is 61 flexed with forehead resting on a folded blanked or foam pillow. The neck is prepped and draped in the usual sterile manner and sterile technique is utilized throughout the procedure. Under fluoroscopy, AP view of the neck is obtained to identify the C7-T1 interspace. A mark is made with the skin marker pen at the site of entry of the needle. Next, 3 to 5 cc of 1 percent lidocaine is administered to the skin, subcutaneous and interspinous structures at this level. A Tuohy needle is introduced midline with a tunnel view parallel to the trajectory of the spinous processes and advanced until it is firmly seated in the interspinous ligament.[ 10 ] At this point, based on user’s preference, “loss of resistance” or “hanging drop” technique can be utilized to identify entrance into the epidural space. To use the “hanging drop” technique, the stylet of the needle is removed and saline is used to fill the needle until a drop of saline sits above the hub of the needle. The needle is stabilized by holding at the wings and advanced slowly until the drop of saline is drawn into the epidural space upon entry due to the negative pressure within the space.[ 12 ] To use the “loss of resistance” technique, the stylet is removed and a syringe containing normal saline is attached at the hub of the needle. Maintaining the same trajectory, the needle is advanced slowly holding it firmly at the wings and loss of resistance is checked by gently tapping on the syringe plunger. Once loss of resistance occurs, needle advancement should be stopped. With either technique, position of the needle is Interventional Pain Medicine checked in both the AP and lateral plane to ensure the needle is midline and at or only slightly beyond the spinolaminar line. A check for negative aspiration for blood or cerebrospinal fluid is performed. During the procedure, if patient develops pain or parathesias, advancement of needle is stopped and the needle is withdrawn and redirected appropriately.[ 19 ] Whichever technique is utilized to enter the epidural space, a small volume of non-ionic contrast material is utilized to confirm needle placement. Next, 2 to 5 cc of omnipaque contrast solution is injected under live fluoroscopy in AP view and lateral view to perform an epidurogram to ensure epidural flow and no vascular pattern (Figures 2.1.6 and 2.1.7 ).[ 23 ] If a venous vascular pattern occurs, needle is withdrawn and repositioned. If an arterial vascular pattern occurs or myelographic pattern is obtained indicating subarachanoid injection, the procedure should be abandoned.[ 19 , 20 ] With confirmation of entry into the cervical epidural space based on the flow of the contrast, the injectant mixture of local anesthetic and corticosteroids is slowly infused. The stylet is reinserted into the needle and needle is withdrawn slowly. The prepped area is cleaned with sterile gauge and dressing is applied at the needle entry site.

Figure 2.1.6 Anteroposterior view of an epidural injection performed at the C6-7 interspace. Contrast dye spreads bilaterally from the C3 to T1 (black arrows). 62 2.1: Cervical Interlaminar Epidural

Figure 2.1.7 Lateral view of an epidural injection performed at the C6-7 interspace. Contrast dye spreads in the dorsal and ventral epidural space from the C3 to T1 (black arrows).

Complications The complications from a cervical epidural injection are rare and most commonly a result of technical error. Mild complications such as needle trauma to epidural veins may result in self limited bleeding, which may cause post-procedure pain.[ 12 ] Discomfort at the needle insertion site can present as myalgias or burning sensation few hours after the procedure. Direct impingement on the nerve roots by the needle causes discomfort and can also cause neural trauma if needle is not repositioned immediately. Post- dural puncture headache is a potential complication from any spinal procedure. Other complications such as neck pain, non-positional headaches, insomnia the night of the injection, vasovagal reactions, transient parathesias, and facial flushing have also been reported.[ 10 ] Serious and life-threatening complications can result from performing this procedure and include spinal cord trauma, epidural hematoma formation,[ 21 ] subarachanoid or subdural injections, and intravascular injection. In immunocompromised and immunocompetent patients, several cases of epidural abscess [ 22 ] have also been reported. Early detection of these complications is crucial to avoid potentially life-threatening sequelae.[ 12 ] Summary The most common indication for performing cervical epidural injection is cervical radiculitis. The most common causes of cervical radiculitis are spondylosis and herniated disk. Initial treatment usually consists of conservative measures such as activity modification, NSAIDs, and physical therapy. Cervical epidural injections are effective and safe in providing significant pain relief if careful attention is paid to technique. Cervical epidural injections have been used to treat radicular pain from herniated discs, spinal stenosis, chronic pain secondary to post-cervical surgery syndrome, and chronic neck pain of discogenic origin. Patient refusal, chronic anticoagulation, known hypersensitivity to agents, local malignancy, and increased intracranial pressure are absolute contraindications to performing epidural steroid injections.[ 12 ] Understanding of the cervical spine anatomy as well as the anatomy of the epidural space is imperative to the interventionalist performing the procedure. There are two major portals which are available for delivery of medication into the epidural space: interlaminar and transforaminal. The choice of which approach to use is commonly made by assessing the patient’s structural pathology, one’s skill in 63

Figure 2.1.8 Cervical epidural injection, lateral view. Interventional Pain Medicine

performing each procedure, and then weighing the advantages versus the risk associated with the particular technique. Fluoroscopy-guided techniques have become popular and are now considered the standard of care when placing cervical epidural steroid injections. Fluoroscopy increases the procedure precision and helps confirm correct needle placement into the epidural space. The placement can be easily confirmed by injecting a small volume of contrast material and performing epidurography under live fluoroscopy. The mixture of local anesthetic and corticosteroids has additional benefits beyond the direct anesthetic affect. The mechanism by which epidural steroid injections provide relief is an anti-inflammatory mechanism secondary to inhibition of phospholipase A2 with resultant blockade of prostaglandin and leukot- riene synthesis. The advantages of epidural steroid injections include deposition of drug directly into the affected area and requiring a much smaller dose to achieve the desired result with lower risk of side effect, and longer duration of relief. These injections are usually given as a series of 3 injections, 2 weeks apart in a 6 month period. Failure to accurately identify the location of needle placement and lack of familiarity with potential aberrancies in cervical anatomy increases the risk of complications. The early detection of complications is crucial to avoid potentially life-threatening sequelae.

AB Figure 2.1.9A and B Cervical epidural injection, lateral view. 64 Clinical Pearl The routine use of sedation or general anesthesia should be avoided because it will compromise the ability of the patient to provide accurate verbal feedback should needle misplacement occur, and also jeop- ardizes the ability of early detection of a potential life-threatening complication. References 1. Hogg-Johnson S , van der Velde G , Carroll LJ , et al . Bone and Joint Decade 2000–2010. Task Force on Neck Pain and Its Associated Disorders. The burden and determinants of neck pain in the general population . Spine . 2008 ; 33 : S39 – S51. 2. Benyamin R , Singh V , Parr AT , Conn A , Diwan S , Abdi S . Systematic review of the effectiveness of cervical epidurals in the management of chronic neck pain . Pain Physician 2009 ; 12 : 137 – 157. 3. Peloso PMJ , Gross A , Haines T , Trinh K , Goldsmith CH , Burnie SJ . Cervical overview group: Medicinal and injection therapies for mechanical neck disorders . Cochrane Database of Systemic Reviews . 2007 ;Issue 3 . Art number: CD000319.

2.1: Cervical Interlaminar Epidural 4. Dogliotti AM . Segmental peridural anesthesia . Am J Surg . 1933 ; 20 : 107 – 118. 5. Lievre JA , Bloch-Michel H , Pean G , et al . L’hydrocortisone en injection locale . Rev Rhum Mal Osteoartic . 1953 ; 20 : 3 10 – 11. 6. Derby R , Sang-Heon L , Byung-Jo K , Chen Y , Sik Seo K . Complications following cervical epidural steroid injections by expert interventionalists in 2003 . Pain Physician . 2004 ; 7 : 445– 449. 7. Silbergleit R , Mehta B , Sanders W , Talati S . Imaging-guided injection techniques with fl uoroscopy and CT for spinal pain management . Radiographics . 2001 ; 21 : 927 – 939. 8. Sampath P , Bendebba M , Davis J , Ducker T . Outcome in patients with cervical radiculopathy . Prospective, multicenter study with independent clinical review. Spine . 1999 ; 24 ( 6 ): 591 – 597. 9. Heckmann J , Lang C , Zobelein I , et al . Herniated cervical intervertebral discs with radiculopathy: an outcome study of conservatively or surgically treated patients . J Spinal Disord. 1999 ; 12 : 396 – 401. 10. Huston C . Cervical epidural steroid injections in the management of cervical radiculitis: interlaminar vs transforaminal . Curr RevMusculoskeletal Med . 2009 ; 2 : 30 – 42. 11. Waldman S . Cervical Epidural Block: Translaminar Approach . In: Waldman , S . Atlas of Interventional Pain Management. 2 nd ed . Philadelphia, PA : Saunders ; 2004 : 129 – 135 , 343. 12. DeSio J . Epidural Steroid Injections . In: Warfi eld C , Bajwa Z . Principles and Practice of Pain Medicine. 2 nd ed . New York : McGraw-Hill Medical ; 2004 : 665 – 661. 13. Hogan Q . Epidural anatomy examined by cryomicrotone section . Reg Anesth. 1996 ; 21 : 395 – 406. 14. Hall E . Glucocorticoid effect on central nervous excitability and synaptic transmission . Int. Rev. Neurobiol. 1982 ; 23 : 165 – 195. 15. Lee H , Weinstein J , Meller S , Hayashi N . The role of steroids and their effects on phospholipase A2: an animal model of radiculopathy . Spine . 1998 ; 23 : 1191 – 1196. 16. Devor M , Govrin-Lippmann R , Raber P . Corticosteroids suppress ectopic neural discharge originating in experimental neuromas . Pain . 1985 ; 22 : 127 – 137. 17. Johansson A , Hao J, Sjolund B . Local corticosteroid application blocks transmission in normal nociceptive C-fi bers . Acta Anaesthesiol Scand. 1990 ; 34 : 335 – 338. 18. Kwon J , Lee J , Kim S , et al . Cervical interlaminar epidural steroid injection for neck pain and cervical radiculopathy: effect and prognostic factors . Skeletal Radiol . 2007 ; 36 : 431 – 436. 19. Derby R . Point of view: cervical epidural steroid injection with intrinsic spinal cord damage: two case reports . Spine 1998 ; 23 : 2141 – 2142. 20. Chakravorty BG . Arterial supply of the cervical spinal cord . Anat Rec. 1971 ; 170 : 311 – 330. 21. Williams KN , Jackowski A , Evans PJD . Epidural haematoma requiring surgical decompression following repeated cervical epidural steroid injections for chronic pain . Pain . 1990 ; 42 : 197 – 199. 22. Huang RC , Shapiro GS , Lim M , Sandhu HS , et al . Cervical epidural abscess after epidural steroid injection . Spine . 2003 ; 29 : E7 – 9. 23. Kim K , Shin S , Kim T , Jeong C , Yoon M , Choi J . Fluoroscopically guided cervical interlaminar epidural injections using the midline approach: an analysis of epidurography contrast patterns . Anesth Analg . 2009 ; 108 : 1658 – 1651. 65

Chapter 2.2 Cervical Transforaminal Epidural Steroid Injections

Alexander F. DeBonet and Christine Peeters-Asdourian

Introduction 66 Diagnosis 66 Causes and Epidemiology 66 Treatment Options 67 Anatomy of the Intervertebral Foramen and Injection Technique 67 Therapeutic Benefit of Cervical Transforaminal Injections 68 Vascular anatomy and Complications 69 Risk Reduction 71 Conclusion 72 References 72 66 Introduction Cervical radiculopathy is a painful condition involving the disturbance and dysfunction of a cervical spinal nerve and its roots. It typically presents with pain in the neck with a radiating pain to the shoulders and arms and is usually unilateral. Commonly, there are associated symptoms of sensory impairment and varying degrees of weakened motor function in the affected nerve-root distribution. The incidence is approximately four cases per 100,000 per year consistent with herniation of the nucleus pulposus (20–25 percent) and/or with intervertebral foraminal stenosis and degenerative spondylosis (70–75 percent). Diagnosis There is no formal standardization for the criteria in the diagnosis of cervical radiculopathy. Generally, the patient history and physical examination are adequate to establish a working diagnosis. Patients can present with varying degrees of neck and arm pain and have associated sensory disturbances, including aching and paresthesias, which typically follow a dermatomal distribution. They may report an abrupt or

2.2: Cervical Transforaminal Epidural gradual onset of constant or episodic pain. The pain, sensory, and motor symptoms may have progressed or even intermittently improved since onset. Patients frequently describe the pain as having a “pins and needles” quality, numbness, or a sensation as if their limb has “fallen asleep.” On physical exam, decreased sensation to light touch, pin point, and vibration may be appreciated in a dermatomal distribution. Motor weakness may occur in the involved root distribution, and diminished or absent deep tendon reflexes may be appreciated. As several serious conditions can mimic cervical radiculopathy, it is crucial for the clinician to specifically pursue a line of questioning about the presence of alarming factors (red flags) in the patient’s history including fevers, chills, unexplained weight loss, and persistent nighttime pain, as well as a history of immunosuppression or malignancy. These findings should alert physicians to the possibility of a more serious disease path such as tumor or perineural infections, which would require further more specific work-up.( 1 ) Causes and Epidemiology Radiculopathy, whether cervical or at other spinal levels, frequently has an underlying anatomic and mechanical process as the initial cause of development. In 70 to 75 percent of cases, cervical radiculopathy is initiated by progressive narrowing of the neural foramen, which causes disturbance of the exiting spinal nerve. This is generally due to a combination of factors referred to as cervical spondylosis. This may include degenerative disc disease or dessication leading to decreased intervertebral disc height. The spondylotic process typically also involves varying degrees of degenerative changes of the uncovertebral joints at the anterior aspect of the foramen and of the zygapophyseal (facet) joints at the posterior border of the foramen. Radhakrishan, et al., conducted an epidemiological survey of cervical radiculopathy in Rochester, Minnesota, from 1976 to 1990 of 561 patients (332 males and 229 females) with ages ranging from 13 to 91. A history of physical exertion or trauma preceded the onset of symptoms in only 14.8 percent of cases. Isolated radiculopathy involving C7 nerve root was the most frequent, followed by C6. A confirmed disc protrusion was responsible for cervical radiculopathy in only 21.9 percent of patients; 68.4 percent were related to spondylosis, disc disease, or both. This study suggested that cervical radiculopathy has an annual incidence rate of 107.3 per 100,000 for men and 63.5 per 100,000 for women, with a peak at 50 to 54 years of age.( 2 ) The specific mechanisms responsible for the translation of the anatomic interference of an exiting nerve root into radicular pain are not well described and are most likely multifactorial. It has been demonstrated that isolated nerve-root compression by itself does not always lead to pain unless the dorsal- root ganglion is also crowded or compressed to some extent, as can occur with foraminal stenosis.( 3 ) Additionally, there is evidence demonstrating that specific inflammatory mediators including prostaglandins, interleukins, and nitric oxide are released by cervical intervertebral disks that have extruded 67 contents posteriorly into the vicinity of neural structures. These inflammatory mediators may aggravate neural and perineural structures leading to localized edema potentially worsening the underlying nerve compression.( 4 , 5 ) Presumably this supports the use of anti-inflammatory agents such as localized steroids as a means of ameliorating the underlying inflammatory component of the process leading to radiculopathy. Systemic anti-inflammatory medications including a steroid taper may be beneficial early on. ( 6 ) Although there are no specific guidelines detailing when to obtain radiologic studies, imaging is appropriate for cervical radiculopathy when successive histories and examinations offer findings that demonstrate progressive sensory or motor deficits. If there is concern for infection or involvement of possible malignancy imaging obviously becomes more urgent. When the clinician has made the decision to obtain such studies to clarify a diagnosis of cervical radiculopathy, MRI is the appropriate modality. It is important for the clinician to make the decision to obtain imaging with the understanding that there are a high frequency of abnormalities detected even in asymptomatic adults, including disk herniation or bulging (57 percent of cases), spinal cord impingement (26 percent), and cord compression (7 percent).( 7 , 8 ) Correlation between the imaging findings and the patient’s clinical presentation is of utmost importance for a good outcome. Interventional Pain Medicine Treatment Options Treatment options for cervical radiculopathy consist of surgical interventions and varying degrees of conservative nonsurgical treatments. Surgery for the management of cervical radiculopathy typically is indicated when there is clinical and radiographic evidence of spinal cord impingement as this can lead to potentially irreversible neurologic deficits over time if not definitively treated. Other commonly accepted surgical indications include critical cervical root compression demonstrated by imaging studies with a corresponding progressive motor deficit, as well as the progression of pain and neurologic deficit despite nonsurgical treatment for at least twelve weeks. Nonsurgical therapies include oral medications, such as non-steroidal anti-inflammatory agents (NSAIDs), oral steroids, muscle relaxants, neuropathic agents, targeted physical therapies, and nonsurgical interventional pain management techniques including injection therapy. Conservative care of cervical radiculopathy can include epidural administration of corticosteroids and local anesthetics. Epidural injection may be classified as being interlaminar or transforaminal, depending upon the approach taken to the epidural space. Prospective and retrospective studies have reported positive results with interlaminar and transforaminal epidural injections of corticosteroids, with up to 60 percent of patients reporting long-term relief of radicular and neck pain together with improved funtionality.( 9 ) The transforaminal technique involves the placement of a needle in the posterolateral aspect of the intervertebral foramen and depositing a small volume of injectate close to the dorsal root ganglion. This allows the delivery of medication at a high concentration adjacent to the affected spinal nerve at the site of inflammation. Theoretically, in comparison to the interlaminar approach, this provides improved delivery to the anterior portion of the epidural space where a disc-neural interface may be inflamed.( 10 ) Initial cohort studies of cervical transforaminal epidural steroid injections (CTFESI) demonstrated improvements in radicular symptoms with no reported injection-related neurologic injuries.( 11 ) Anatomy of the Intervertebral Foramen and Injection Technique A clear understanding of the boundaries and contents of the intervertebral foramen is clearly essential for safe needle placement. The intervertebral foramen is the exit pathway for spinal nerves that are formed from the union of ventral and dorsal rami that descend in the spinal canal. The foramen is formed by the juxtoposition of the postero-lateral structures of two articulating vertebrae. Anteriorly, the intervertebral foramen is bound by the inferior portion of the upper vertebral body and a portion of the intervertebral disc immediately below. The superior articular process (SAP) of the lower vertebra and 68 the inferior articular process (IAP) from the upper vertebra, together forming the zygapophyseal (facet) joint, form the posterior boundary of the foramen. Superiorly and inferiorly, the foramen is bound by the pedicles of the vertebrae above and below the foramen. A dural sleeve and arachnoid mater accompany the exiting nerve root from the epidural space to the foramen and then thins to form the epineurium of the spinal nerve.( 12 ) The CTFESI can be performed with the patient in the supine or lateral decubitus position and should enable fluoroscopic views of the intervertebral foramen in the anterior-posterior (AP), lateral, and oblique axis. Starting from an AP view with the end plates of the vertebral body “squared off”— that is, where parallax is minimized as much as possible— an optimal oblique view of the open foramen is attained. After local infiltration of the skin over the identified target, the needle is placed in the neck and directed toward the superior articular process (SAP), the posterior border of the intervertebral foramen. After the needle approaches the SAP, it is then redirected to enter the posterior edge of the foramen. An AP view is then taken to assess the medial depth of the needle tip. Caution must be taken to not advance the needle beyond the medial half of the SAP in the AP view to prevent placement too deep into

2.2: Cervical Transforaminal Epidural the foramen. A small volume of nonionic contrast dye is used to ensure the correct placement of the needle. This is done under real-time fluoroscopy and digital substraction technique is used when available. The aim is to display a characteristic outline of the exiting nerve root and confirm spread to the epidural space. The spread of contrast needs to demonstrate that there is no vascular uptake or breach of the dura with spread of the contrast agent to the cerebro spinal fluid (CSF). Negative aspiration is not always a reliable method, especially with small-gauge needles. Following proper spread of the contrast material, a small volume of local anesthetic and corticosteroid is deposited near the exiting root.( 13 , 14 ) Therapeutic Benefit of Cervical Transforaminal Injections Several studies provide support for the efficacy of CTFESI though none of them are prospective randomized clinical trials comparing injections with conservative management or comparing interlaminar and transforaminal injections. In a prospective cohort study, Bush and Hillier treated sixty-eight patients with cervical radiculopathy using a sequence of procedures including transforaminal injections of corticosteroids. Those who failed to respond to transforaminal injection then received an interlaminar injection of steroids. Though it is not clear from their study what portion of the study group was relieved specifically by transforaminal injections they reported that 76 percent of patients achieved complete relief of arm pain.( 11 ) In a retrospective study, Slipman, et al., performed transforaminal injection of steroids in twenty patients with cervical radicular pain due to cervical spondylosis with evidence of nerve root involvement due to foraminal stenosis. At follow-up after an average of twenty-two months, they reported reduced pain, a reduction in analgesic use, and satisfaction with treatment in 60 percent of patients. Most patients received two injections.( 9 ) Vallee, et al., in a prospective cohort study, performed transforaminal injection of steroids in thirty patients with cervical radicular pain lasting longer than two months with radiographic evidence of foraminal stenosis. After an average of 1.3 injections, at 3 months, 29 percent of patients had complete relief, a proportion that decreased to 20 percent at 12 months; another 29 percent reported at least 50 percent relief of their pain, which at 12 months fell to 18 percent. When the group was assessed at 6 months, they reported in more than 50 percent of subjects greater than 75 percent improvement or even total relief.( 15 ) There is no agreement as to optimal amount of steroids, the volume of local anesthetic or normal saline, the volume of non-ionic contrast, and the frequency of injections. A large volume of injectate may have a mass effect and account for some of the complications. There are currently no prospective studies comparing the effectiveness of CTFESI versus interlaminar cervical epidural injections in the management of cervical radiculopathy secondary to disc herniation or to spondylosis. With the understanding that findings from studies performed at the lumbar level cannot 69 necessarily be extrapolated to the cervical level, it is interesting to consider that, in a randomized controlled trial, selective nerve root injection or perineural injection in the lumbar spine was found to be superior to inter-laminar epidural injection in patients with radiculopathy from lumbar disk herniation. Kraemer, et al., described a trial composed of two controlled studies on 182 patients. One arm compared prospectively randomized patients with lumbar radicular complaints: forty-seven received epidural perineural injections and forty received interlaminar epidural injections. As a control group, forty-six patients received paravertebral local anesthetic. Epidural perineural injections were more effective than conventional interlaminar epidural injections and both epidural groups had better overall results than the paravertebral local injection group. The second arm in a double-blind study compared perineural epidural injections using triamcinolone 10mg in one group of twenty-five patients with a control group of twenty-four patients receiving only perineural saline plus IM steroid to control for a potential systemic steroid effect. Epidural perineural injections with steroids were more effective than saline alone.( 16 ) In a prospective, randomized, double-blind study, Thomas, et al., compared the efficacy of transforaminal versus interlaminar epidural corticosteroid injections in patients with radiculopathy from disc herniation. Thirty-one patients with radicular pain for three months or shorter duration were rand- Interventional Pain Medicine omized to receive either fluoroscopically-guided transforaminal or blindly performed interlaminar epidural corticosteroid injections. Outcomes were evaluated at six and thirty days clinically, and then at six months by mailed survey. At days six and thirty as well as on the six-month survey, pain relief and overall functionality was significantly better in the transforaminal group.( 17 ) Vascular anatomy and Complications Despite the possible benefits of cervical transforaminal epidural steroid injections at the cervical level, potentially devastating complications have been reported and must be taken into consideration by the clinician in an assessment of risks versus benefit. The most serious complications include infarction occurring in the distribution of the posterior cerebral circulation supplying brain stem and cerebellum, resulting in varying degrees of disabling paralysis, paraplegia or quadriplegia from spinal cord infarction, coma, or death. Scanlon, et al., presented a case series with the objective to survey pain physicians about neurologic complications following CTFESI. Anonymous surveys were sent to members of the American Pain Society. Respondents were asked about details of complications including use of fluoroscopy and contrast, local anesthetic, corticosteroid, doses, and radiologic and autopsy findings. Their study reported on a total of 78 complications, including 16 vertebrobasilar brain infarcts, 12 cervical spinal cord infarcts, and 2 combined brain/spinal cord infarcts. Brain infarcts consistently involved the cerebellum, brain stem, or posterior cerebral artery territory. Thirteen cases resulted in a fatal outcome: 5 with brain infarcts, 1 with combined brain/spinal cord infarcts, 1 following high spinal anesthesia, 1 associated with a seizure, and 5 with unspecified etiology. Of all the case reports, the ones with injection of steroids alone (methylprednisolone) without saline or local anesthetic resulted in brain infarction, and 3 out of 4 were fatal.( 18 ) There has been extensive discussion about the potential mechanisms of these complications, which have cited potential explanations such as suboptimal needle placement leading to vascular injury or vasospasm, intravascular injection resulting in embolization of particulate steroids leading to occlusion of downstream vulnerable vessels, or even a correctly placed bolus injection into a constricted foramen resulting in the compression of a critical vessel. In a comparative study by Kim, et al., the incidence of intravascular injection during transforaminal epidural injections at the lumbar and cervical levels were compared. After ideal needle placement was confirmed by biplanar fluoroscopy a 3 ml mixture of nonionic contrast and saline were injected. Of a total of 182 injections, 56 (30.8 percent) showed intravascular injection. Of 111 lumbar transforaminal injections 11 (9.9 percent) revealed either pure intravascular or mixed perineural and intravascular spread. Whereas of 71 cervical transforaminal injections, 45 (63.4 percent) injections showed either pure 70 intravascular or mixed perineural and intravascular spread. This study highlights the significantly increased risk of intravascular injection at the cervical level.( 19 ) Anterior spinal artery syndrome and cerebellar ischemia are devastating complications of CTFESI. It is widely suspected that, by any of several potential mechanisms including vasospasm, direct needle trauma, or particluate embolization, cervical transforaminal injections can compromise a radicular artery that provides a critical portion of total blood supply to the anterior spinal artery, or the posterior spinal artery.( 20 ) The ascending cervical and deep cervical arteries are branches of the thyrocervical and cos- tocervical trunks, respectively, that ultimately arise from the proximal subclavian artery. They commonly have branches that anastomose with branches from the vertebral artery or sprout radicular arterial perforating vessels that provide blood supply, at times critical flow, to the anterior spinal and posterior spinal arteries. The anterior spinal artery is often interrupted and is susceptible to decreased perfusion if its reinforcing radicular arteries are compromised.( 21 ) To investigate the potential causes of injury during CTFESI, an anatomic study was conducted by Huntoon in 2004 in which embalmed cadavers underwent meticulous dissection of the vasculature

2.2: Cervical Transforaminal Epidural approximating the intervertebral foramen. Significant variability was found in the anastomoses between the vertebral and cervical arteries demonstrating that critical arteries may potentially be located in the posterior aspect of the intervertebral foramen and may be vulnerable to injection or injury during optimally performed transforaminal epidural steroid injection.( 22 ) In 2001, Paul J.A.M. Brouwers, et al., described vividly a devastating injury that occurred during a right- sided diagnostic C6 transforaminal injection. A forty-eight-year-old male presented with chronic right- sided cervical radiculopathy, who had demonstrated some benefit from a previous right sided C7 transforminal injection. After fluoroscopic placement of a 22-gauge needle in the posterior caudal quadrant of the foramen and following a negative aspiration, contrast dye confirmed epidural spread and appropriate needle placement. Thereafter 0.5ml of 0.5 percent bupivacaine with 0.5 ml triamcinolon- hexacetonide 2 percent was injected. Upon conclusion of the procedur,e the patient developed an acute flaccid paralysis with respiratory distress requiring intubation. MRI revealed extensive spinal cord infarction, which resulted in persistent paralysis. The patient course was complicated by multiple pneumonias and other complications that ultimately lead to the patient’s death.( 23 ) In 2002, Baker et al., reported on a near-miss involving a transforaminal cervical injection. During routine injection under live fluoroscopy, after appropriate needle placement, contrast medium filled a radicular artery that passed to the spinal cord. The procedure was immediately aborted and the patient fortunately suffered no injury. This early report demonstrated that despite the use of careful technique, it is possible to accidentally access and inject a radicular artery. The use of digital subtraction prior to injection of particulate steroid is emphasized after this close call.( 20 ) A commonly discussed mechanism of injury involved in the performance of transforaminal epidural injections at the cervical level is the intravascular injection of particulate material. As demonstrated by Huntoon’s anatomic demonstration and Baker’s report, there may be considerable risk of the intravascular injection of particulate steroid into a cervical radicular artery, thereby obstructing critical blood supply to the anterior spinal artery, or embolization into and direct obstruction of the anterior spinal artery itself. There is also the equally catastrophic risk of injection into the vertebral arteries allowing particulate embolization into the basalar and posterior cerebral circulations. To investigate more thoroughly the line of particulate embolization as a source of potential harm Benzon, et al., in 2007 performed a comparison of several commercially available and compoundable steroid preparations in microscopic analysis. This study was prompted by a case report by Tiso, describ- ing a cerbellar infarct following a CTFESI of the right C6. Tiso examined the size of the different particles of depot steroid preparations under a microscope. Benzon’s group compared the sizes of the steroids methylprednisolone acetate, triamcinolone acetonide, dexamethosone sodium phosphate, and betamethasone phosphate/betamethasone acetate. Using laser scanning confocal microscopy, they examined samples in diluted and undiluted form and performed measurements of particulate sizes. Dexamethasone 71 and betamethasone sodium phosphate were purely non-particulate. They found a significantly greater degree of large particle aggregates in the methylprednisolone and compounded betamethasone groups than in the commercially available betamethasone. There was no significant difference between the commercially available betamethasone and triamcinolone particle sizes though betamethasone had a lower percentage of large particles. Interestingly, they reported that saline dilution of methylprednisolone 80mg/ml, a very common practice, increased the percentatage of large particles and the dilution of compounded betamethasone with lidocaine decreased the proportion of large particles. As long-term data is not available about the routine use of dexamethasone, the authors recommended commercial betamethasone if a nonsoluble steroid is desired.( 24 , 25 ) In 2008, Okubadejo, et al., reported on a study comparing the effect on the spinal cord and central nervous system of intravascular injection at the cervical level of particulate steroid and non-particulate steroid preparations. They performed an animal study using 11 pigs under general anesthesia in which direct intravascular injection was delivered into the vertebral arteries under fluoroscopic guidance. They used particulate injection in 4 pigs using methylprednisolone acetate and nonparticulate injection in the remaining 7 pigs; 4 received dexamethasone and 3 received prednisolone. Post injection, the physical Interventional Pain Medicine activity of the animals was directly observed, MRI assessment was performed, and histopathologic analysis was performed on brain and spinal cord samples of killed animals. In the non-particulate groups, no behavioral signs of neurologic harm were observed and there was no MRI or histologic evidence of hypoxic neurologic injury. In the particulate steroid group, however, all 4 animals failed to regain consciousness. MRI study revealed upper cervical spinal cord and brain stem edema and histologic study showed evidence of ischemic damage and necrosis. This study clearly suggests the importance of further investigation of non-particulate steroid formulations as the accidental intravascular injection of particulate preparations clearly can be devastating.( 26 ) Recently, a case report describes yet another type of injury associated with CTFESI, direct trauma to the cord caused by injection of air and contrast material resulting in incomplete tetraplegia.( 27 ) Risk Reduction Several basic methods should routinely be employed and documented to reduce the potential for intravascular injection of steroid. The data may be scarce to demonstrate the overall reduction in morbidity and mortality that these techniques offer. Clinicians should routinely perform an aspiration to check for blood or cerebrospinal fluid prior to injection of contrast and steroid medications to help minimize the risk of intravascular and intrathecal needle placement with the understanding that a negative aspiration does not necessarily rule out errant needle placement. Consideration should be given to the overall volume of injectate, as increased volume may be associated with increased risk of neural and vascular compression in a stenotic foramen. Likewise, increased dose of particulate material in the injectate mixture may increase the risk of particulate embolization if violation of a vessel wall does occur. The use of live fluoroscopy during contrast injection may allow real-time visualization of vascularized contrast whereas a static fluoroscopic image may not capture the intravascular contrast before it is flushed away. The use of extension tubing, the so called “imobile needle” technique may help minimize the risk of accidental needle movement during injection. Digital subtraction is a very useful tool to identify potential intravascular injection that may be missed with plain fluoroscopic images. Unfortunately, the ability to use digital subtraction is far from universal and is therefore not yet standard of care. The process involves injection of contrast under live fluoroscopy while at the same time digitally removing the pre-injection components of the image. Specifically by subtraction of pixels of an initial baseline image from subsequently acquired live fluoroscopy images, only the contrast that is being actively injected will be revealed, and if there is intravascular spread a distinct vascular pattern would be demonstrated. Disadvantages of digital subtraction include the added expense for a device with the ability as well as the increased overall dose of radiation administered to patients and personnel during the subtraction study.( 28 ) 72 Many injections are performed under various degrees of sedation. One case reviewed by the senior author involved a cord infarct following a CTFESI at C5 under propofol sedation. Feedback from the patient during the injection is extremely important, as reports from severe radicular pain or numbness during advancement of the needle warrants prompt withdrawal of the needle. Repositioning of the needle and injection of contrast preferably under digital substraction technique should not be attempted unless symptoms have subsided. If the patient remains symptomatic, the procedure should be aborted.( 29 ) Conclusion In light of a growing body of evidence that demonstrates significant risk involved in the performance of transforaminal epidural steroid injections at the cervical level due to anatomical, technical, and pharmacologic factors, the clinician must perform a thorough risk-benefit assessment prior to recommending this course of therapy to patients. Even after conservative measures such as medications, physical therapy, and interlaminar cervical steroid injections, the potential catastrophic results of an even technically 2.2: Cervical Transforaminal Epidural optimally performed CTFESI may outweigh the potential benefit offered by the procedure. Prior to obtaining consent, patients must be fully informed about the risks associated with the procedure to ensure they feel the therapeutic benefit warrants its potential hazards. Despite the abundant evidence of injury, this procedure is still very commonly being performed in many private and academic pain management centers in the United States. In 2004, in an editorial following the first few published reports of devastating complications associated with CTFESI, Rathmell stated “a randomized trial of transforaminal injections of steroids versus alternate therapy (conservative treatment, surgical decompression, or interlaminar route) appears to be warranted.” To this date, no such study has been published.( 30 ) In the meantime, the French authorities for the safety of medications, the Agence Française de Sécurité Sanitaire des Produits de Santé (Afssaps), has recommended strongly against the use of particulate steroids for CTFESI.( 31 ) References 1. Carette S , M.D. , M. Phil. , and Fehlings, M.G. M.D., Ph.D . Cervical Radiculopathy. Engl J Med . 2005 ; 353 : 392 – 399 . 2. Radhakrishan K , Litchy WJ , O’Fallon WM , Kurland LT . Epidemiology of cervical radiculopathy: a population- based study from Rochester, Minnesota, 1976 through 1990 . Brain . 1994 ; 117 : 325 – 335 . 3. Sugawara O , Atsuta Y , Iwahara T , Muramoto T , Watakabe M , Takemitsu Y . The effects of mechanical compression and hypoxia on nerve root and dorsal root ganglia: an analysis of ectopic fi ring using an in vitro model . Spine . 1996 ; 21 : 2089– 2094 . 4. Kang JD , Georgescu HI , McIntyre-Larkin L , Stefanovic-Racic M , Evans CH . Herniated cervical intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6 and prostaglandin E2 . Spine . 1995 ; 20 : 2373 – 2378 . 5. Kang JD , Stefanovic-Racic M , McIntyre LA , Georgescu HI , Evans CH . Toward a biochemical understanding of human intervertebral disc degeneration and herniation: contributions of nitric oxide, interleukins, prostaglandin E2, and matrix metalloproteinases . Spine . 1997 ; 22 : 1065 – 1073 . 6. Miyamoto H , Saura R , Doita M , Kurosaka M , Mizuno K . The role of cyclooxygenase-2 in lumbar disc herniation . Spine . 2002 ; 27 : 2477 – 2483 . 7. Boden SD , McCowin PR , Davis DO , et al . Abnormal magnetic-resonance scans of the cervical spine in asymptomatic subjects . A prospective investigation. J Bone Joint Surg Am . Sep 1990 ; 72 ( 8 ): 1178 – 1184. 8. Teresi LM , Lufkin RB , Reicher MA , et al . Asymptomatic degenerative disk disease and spondylosis of the cervical spine: MR imaging . Radiology . 1987 ; 164 : 83 – 88 . 9. Slipman CW , Lipetz JS , Jackson HB , Rogers DP , Vresilovic EJ . Therapeutic selective nerve root block in the nonsurgical treatment of atraumatic cervical spondylotic radicular pain: a retrospective analysis with independent clinical review . Arch Phys Med Rehabil . 2000 ; 81 : 741 – 746 . 10. Jasper JF . Lumbar retrodiscal transforaminal injection . Pain Physician . May 2007 ; 10 ( 3 ): 501 – 510 . 11. Bush K , Hillier S . Outcome of cervical radiculopathy treated with periradicular/epidural corticosteroid injections: a prospective study with independent clinical review . Eur Spine J . 1996 ; 5 : 319 – 325 . 73 12. Netter Frank H . Atlas of Human Anatomy, Fifth Edition. Saunders Publishing. 13. Rathmell JP , Aprill C , Bogduk N . Cervical transforaminal injection of steroids . Anesthesiology . 2004 ; 100 : 1595 – 1600 . 14. Verrills , Paul ; Nowesenitz , Gillian ; Barnard , Adele : Case report–penetration of a cervical radicular artery during a transforaminal epidural injection . Pain Medicine . 2010 ; 11 : 229 – 231 . 15. Vallee JN , Feydy A , Carlier RY , Mutschler C , Mompoint D , Vallee CA . Chronic cervical radiculopathy: lateral- approach periradicular corticosteroid injection . Radiology . 2001 ; 218 : 886 – 892 . 16. Kraemer J , Ludwig J , Bickert U , Owczarek V , Traupe M . Lumbar epidural perineural injection: a new technique . Eur Spine J . 1997 ; 6 ( 5 ): 357 – 361 . 17. Thomas E , Cyteval C , Abiad L , Picot MC , Taourel P , Blotman F. Effi cacy of transforaminal versus interspinous corticosteroid injectionin discal radiculalgia— a prospective, randomized, double-blind study . Clin Rheumatol . Oct 2003 ; 22 ( 4–5 ): 299 – 304 . 18. Scanlon G C ; Moeller-Bertram T, Romanowsky SM, Wallace MS. Cervical Transforaminal Epidural Steroid Injections : More Dangerous Than We Think? Spine . May 2007; 32(1 1); 1249 – 1256 . 19. Kim DW , Kyung RH , Chan K , Yun JC . Intravascular fl ow patterns in transforaminal epidural injections: a

comparative study of the cervical and lumbar vertebral segments anesthesia and analgesia. Jul 2009; 109 ( 1 ). Interventional Pain Medicine 20. Baker R , Dreyfuss P , Mercer S , Bogduk N : Cervical transforaminal injection of corticosteroids into a radicular artery: A possible mechanism for spinal cord injury . Pain . 2002 ; 103 : 211 – 215 . 21. Gillian , L. A. : The arterial blood supply of the human spinal cord . J. Comp. Neurol . 1958; 110 : 75 . 22. Huntoon MA . Anatomy of the cervical intervertebral foramina: vulnerable arteries and ischemic neurologic injuries after transforaminal epidural injections . Pain . Sep 2005 ; 117 ( 1–2 ): 104 – 111 . 23. Brouwers P JAM , Kottnick E JBL , Simon MAM , Prevo RL . A cervical anterior spinal artery syndrome after diagnostic blockade of the right C6-nerve root . Pain . 2001;91 : 397 – 399 . 24. Benzon HT , Chew TL , McCarthy RJ , Benzon HA , Walega DR . Comparison of the particle sizes of different steroids and the effect of dilution: a review of the relative neurotoxicities of the steroids . Anesthesiology . Feb 2007 ; 106 (2 ): 331 – 338 . 25. Tiso R L, Cutler T; Catania J A ; Whalen K. Case studies— adverse central nervous system sequelae after selective transforaminal block: the role of corticosteroids . The Spine Journal. 2004 ; 4 : 468 – 474 . 26. Okubadejo GO , Talcott MR , Schmidt RE , Sharma A , Patel AA , Mackey RB , Guarino AH , Moran CJ , Riew KD J : Perils of intravascular methylprednisolone injection into the vertebral artery . An animal study . Bone Joint Surg Am . Sep 2008 ; 90 ( 9 ): 1932 . 27. Lee JH , Lee JK , Seo BR , et al . Spinal cord injury produced by direct damage during cervical transforaminal epidural injection . Reg Anesth Pain Med. 2008 ; 33 : 377 – 379 . 28. Jasper JF . Role of digital subtraction ﬂ uoroscopic imaging in detecting intravascular injections . Pain Physician . 2003 ; 6 : 369 – 372 . 29. Bromage PR , Benumof JL . Paraplegia following in-tracord injection during attempted epidural anethesia under general anesthesia . Reg Anesth Pain Med . 1998 ; 23 : 104 – 107 . 30. Rathmell , JP . Benzon H T . Transforaminal injection of steroids: should we continue? Reg Anesth Pain Med . 2004 ; 29 :( 5 ) 397– 399 . 31. Le Meur , N.; Benkritly , A . Information importante de pharmacovigilance relative aux cas rapportés de paraplégie/ tétraplégie au cours d’injection radioguidée de glucocorticoıïdes aux rachis lombaire et cervical . Jul 2010. http:www. afssaps.fr/var/afssaps_site/storage/original/application/ab6de4eceefb6b2645865f74256fbaeb.pdf This page intentionally left blank 75

Chapter 2.3 Cervical Median Branch Blocks and Radiofrequency Ablation

Mark Wallace and Greg Polston

Introduction 76 Patient Selection 76 Medications for Diagnostic Block 77 Medications for Radiofrequency Procedures 77 Monitoring 77 Sedation 77 Needles for Diagnostic Blocks 78 Absolute Contraindications 78 Relative 78 Diagnostic Procedure 78 Post-Procedural Evaluation 80 Cervical Radiofrequency 80 Contraindication for RF 83 Absolute 83 Relative 83 Patient Position for Radiofrequency 83 Anatomy 84 Complications 86 References 86 76 Introduction Cervical medial branch radiofrequency ablation is a therapy applied to the nerves that innervate cervical zygapophysial joints because they are thought to play a role in chronic neck pain.1–5 Pain transmitted through these nerves can also present as headaches when the third occipital nerve and the upper cervical facets are affected. 6 Because clinical history, examination, and diagnostic imaging do not clearly identify this syndrome, it is necessary to first perform diagnostic medial branch blocks in order to make this diagnosis. If there is a positive response to this procedure, only then should radiofrequency be considered. The following chapter will describe how to safely and accurately perform diagnostic and radiofrequency procedures to the cervical medial branches. Intra-articular cervical facet joint injections were originally used to treat pain that was thought to originate from these synovial joints. Unfortunately, long-term relief with this procedure was rare.7 Therapeutic medial branch blocks and radiofrequency neurotomy of the cervical medial branch have clinical evidence for both short- and long-term improvement of chronic neck pain. 8 The dorsal medial branch is blocked with a small amount of local anesthetic to confirm a diagnosis.9 , 10 Using this procedure 2.3: Cervical Median Branch Blocks is supported by studies that show distention of the cervical facet joints with saline, and electrical stimulation of the medial branch in normal controls have consistent and reproducible segmental referral patterns that correlate with chronic neck pain. 1 , 4 , 11 The sensitivity and specificity of diagnostic cervical medial branch blocks is greatest when the block is repeated with different medications on separate occasions.12 , 13 The medications injected can include a short-acting local anesthetic, a long-acting local anesthetic, and normal saline as a placebo. Using local anesthetics with different lengths of anesthesia (or saline with none) enables the amount of time of pain reduction (or the absence of pain reduction) to be used as a variable in establishing the diagnosis. If lidocaine is used as the short-acting agent, the expected length of relief in the patient would be approximately four hours. If bupivacaine is used as the long-acting agent, the expected length of relief would be approximately six hours. In clinical practice, placebo injections are generally contraindicated for both ethical and financial considerations. The reason to do more than one block is to identify false-positive responses. 14 Further, it is believed that the placebo effect and other clinical variables will be reduced or eliminated by subjecting the patient to repetitive tests at the same level and obtaining results that are concordant and consistent with the medication injected. Current guidelines recommend pain reduction of 80 percent on two occasions in order to call the response positive and proceed with radiofrequency.8 , 12 , 15 , 16 Patient Selection Patients with headaches, neck pain, and shoulder pain all potentially can have pain referred from the cervical facets. The syndrome can present unilaterally or bilaterally. It is a common diagnosis after whiplash injuries and high-speed motor vehicle accidents. Clinical examination shows provocation of pain with palpation or movement with these joints. Pain referral patterns also help to suggest affective cervical levels (Figure 2.3.1 ). Unfortunately, there are no clinical maneuvers or tests to clearly identify patients who should undergo this procedure. Imaging studies including plain films, CT scans, and MRIs have also not been proven to confirm this diagnosis. Nevertheless, a full medical workup should be performed to rule out other diagnoses and select potential candidates for this procedure. In general, this procedure should not be used for acute pain because many patients will recover without intervention. Because patients must be able to note differences in their pain before and after the procedure, patients must fully understand the procedure and be able to report the differences in their pain before and after the diagnostic procedure. Pain distal to the shoulders and cervical radicular symptoms are not caused by cervical facet pathology; therefore, this form of treatment should not be used to treat these problems. Nevertheless, patients can still have cervical facets pathology coexisting with these other symptoms, and treatment of the cervical medial branches may reduce part of the patient’s pain. 77

C2/3 C3/4 C4/5

C5/6 C6/7 Interventional Pain Medicine

Figure 2.3.1 Typical distribution of pain referred from each cervical facet joint when injected in normal volunteers. Source: The International Spinal Intervention Society.

Medications for Diagnostic Block Lidocaine 1 percent, 2 percent, or 4 percent Bupivacaine 0.25 percent, 0.5 percent, or 0.75 percent Ropivicaine 0.2 percent, 0.5 percent, 0.75 percent or 1 percent Volume 0.25 to 0.3 ml per injection Radiopaque contrast can be used to ensure proper placement of needles and prevent intravascular or intrathecal injection. The addition of steroids does not improve the diagnostic accuracy of the procedure. It will alter length of relief provided and should be considered when evaluating the results. Further, the use of steroid can increase the risk of side effects and complications. Medications for Radiofrequency Procedures For high-temperature radiofrequency (RF), 0.5 ml of one of the above local anesthetics is injected at least one minute before the lesion in order to provide pain reduction during the heating of the tissue. After the lesion is complete, a small amount of steroid is given in order to reduce pain after the procedure. For pulsed RF procedures, a similar amount of local anesthetic and steroid is not given until after the lesion because this treatment is not as painful as high-temperature RF and giving this before the treatment may blunt the response to the treatment with pulsed RF. Monitoring Standard monitoring includes pulse oximetry, blood pressure, and EKG. Resuscitate equipment must also be immediately available. Sedation Oral or IV sedation is not recommended for diagnostic procedures because it can alter the patient’s postoperative pain. Separating which amount is from the procedure and which is due to the sedation is difficult to determine and can lead to false positives. Its use is acceptable for radiofrequency procedures 78 as long as the patient remains cooperative, maintains the ability to provide feedback, and is properly monitored. Needles for Diagnostic Blocks 25- or 27-g 1.25- to 1.5-inch needles for lateral approaches to the medial branch 25-g 3.5-inch needles for a posterior approach to the medial branch Absolute Contraindications Infection (at the site or systemic) Bleeding disorder Relative Pregnancy Allergy to contrast or local anesthetic Inability to cooperate or report changes in pain Severe cardiopulmonary disease 2.3: Cervical Median Branch Blocks Unable to proceed with RF Acute onset Anticoagulant Therapy that cannot be stopped Diagnostic Procedure Before the procedure, the patient should be properly informed and give consent. A “time-out” with the patient and surgical team is preformed to confirm the intended procedure. Standard vital sign monitors should be applied and closely monitored. Sterile skin prep should be used and sterile drapes applied. A C-arm is used for fluoroscopic imaging. Position of the patient for diagnostic blocks is based on patient comfort and practitioner preference. Target distance from skin to nerve is the shortest in a lateral approach, which may be an advantage because, in general, the patient experiences less procedural pain. This can give a clearer postoperative interpretation of pain reduction. The lateral approach can be performed with the patient supine, prone, or lateral decubitus with a swimmer’s position for their arms. This approach is limited when the patient has high riding shoulders that obstruct the view of the lower cervical levels on fluoroscopic views. The other potential difficulty or hazard that can occur with this approach is that the needle can be inad- vertently advanced into the neuroforamen and cause complication with vascular, dural, or intrathecal injection. The patient is placed in a prone position with posterior approach. This has the advantage of decreasing the obstruction caused by the shoulders. The disadvantage of this approach is that the distance from the skin to the target site is greater, which can lead to greater procedural pain. Whichever approach is chosen, the targeted end point will be the same. And with both approaches, care must be taken to view needle position in multiple planes, listen to feedback provided by the patient, and have the experience and skill to clearly identify the targeted position on fluoroscopy. Proficiency in efficiently performing the procedure using both lateral and posterior approaches is necessary to maximize the number of patients who can receive safe and accurate diagnosis. Because small volumes of local anesthetic are used, the point of injection must be precise. Before starting, the location and path of the targeted dorsal medial branch or third occipital nerve needs to be clearly understood. This will provide maximum prognostic capabilities. Properly aligned fluoroscopic images are also required to establish the precise injection point. In a true lateral fluoroscopic image, the ipsilateral and contralateral facet joints are superimposed at the targeted level and will be located in the center of the field. This means that the ventral, dorsal, rostral, and caudal boarders of the articular pillars aligned with the opposite side. This will create a diamond or trapezoid shape. (Figures 2.3.2 A and 2.3.2 B) The correct AP view will show the concaved lateral surface of the articular pillar. Obtaining these at each level will ensure accuracy and safety when performing this procedure. Before all injections aspiration 79

Figure 2.3.2A Fluoroscopic image of lateral cervical spine with ipsilateral and contralateral lateral masses superimposed. Interventional Pain Medicine The center of each lateral mass is marked by the X.

Figure 2.3.2B Fluoroscopic image of a/p cervical spine with needle touching the lateral mass at C3, C4, and C5. should be negative and contrast material can be injected to see proper spread over the articular pillar and not into the joint, neuroforamen, or a vascular structure. The third occipital nerve is blocked at the level of the C2–3 joint. This nerve is larger than the medial branches. It is recommended that this be anesthetized in three locations with 0.3 mLs (0.25–0.5 mL) of local anesthetic. These spots are located just superior, inferior, and at the level of the joint in the cephlo- caudal direction and in the ventral-dorsal direction halfway between the medial and lateral boundaries of the joint itself. (Figure 2.3.5 ) Care must be taken not to enter the joint itself, especially when directly over the joint. The dorsal medial branches of C3-6 are anesthetized at the center of the articular pillars at the respective levels. (Figure 2.3.3 ) As described above, the center of the articular pillar is seen on the lateral fluoroscopic image by aligning the edges of the articular pillars to create a diamond or trapezoid figure. The intersection of the diagonals created by this figure is the targeted point. On the AP image, the needle should be located in the apex or midpoint of the concave lateral surface at each cervical level. 80

2.3: Cervical Median Branch Blocks Figure 2.3.3 The coronal illustrations (sagittal, pillar view under fluoroscopy) on the left demonstrates the significant variability of the TON. The initial RF lesion is typically cephlad. The position where the dorsal medial branch blocks at C7 and -8 are performed is unique compared to the higher levels. The C7 nerve can have a variable anatomy and may require more than one block to ensure success. The first target is the apex of the superior articular process. Extreme care must be used to ensure that from a lateral approach the needle does not enter the neuroforamen. This can best be checked by an AP view showing that the needle is against the lateral boarder of the articular pillar and not medial to this point. The second injection is recommended because the dorsal medial branch nerve can be displaced laterally by the semispinalis capitis. This can be performed easily by simply pulling the needle back laterally from the periosteum. Both injections should be 0.3 mL of local anesthetic. The dorsal medial branch block at C8 is performed on the transverse process of T1. The targeted area is just medial to the superior lateral portion of the transverse process. Injection of contrast material the needle position will show spread along the path of the transverse process. The same 0.3 mL injection of local anesthetic should be used. Post-Procedural Evaluation The patient’s pre-procedural visual analog scale (VAS) should be compared to their post-procedural VAS approximately ten to fifteen minutes after the injection. In addition, any change in range of motion or other signs and symptoms should be evaluated and commented on in the record. Some have suggested that the person performing this evaluation be blinded to the procedure and medication used. The patient should also be asked to complete a post-procedural pain log with frequent recordings during the first six to twelve hours. A positive diagnostic block is 80 percent pain reduction in the targeted area without the use of sedation during the procedure. Because of a high false-positive rate, repeating this procedure on a second visit may provide a more certain diagnosis. Only when the initial and repeat procedures show concordant pain reduction can the diagnosis be made and radiofrequency be recommended. If the decision is made to proceed with radiofrequency, the patient may be scheduled for the next procedure at discharge. If there is question of the effectiveness of the procedure, the patient can be rescheduled to return to the clinic or interviewed by phone at a later date. Some patients may have minor postoperative pain with this procedure. This can be treated with conservative measures including ice, heat, rest, and small amounts of oral analgesics. Cervical Radiofrequency Percutaneous radiofrequency cervical medial branch neurotomy is performed after positive diagnostic cervical medial branch block or the third occipital nerve. Before proceeding with this, however, 81 a thorough understanding of how radiofrequency works and the additional equipment required must be obtained. Several different radiofrequency generators are available commercially with numerous options including continuous high-temperature radiofrequency, pulsed radiofrequency, and cooled radiofrequency along with options to treat multiple levels simultaneously. All generators at a minimum will include dis- plays of impedance (Ω ), voltage (V), current (Amp), wattage (W) and temperature (∞C), a sensory and motor nerve stimulator, and ability to deliver radiofrequency. Familiarity with its use is required before performing these procedures. The generator passes current through the needle into the patient, which is dispersed through a grounding pad on the patient. (Figure 2.3.4 ) Care must be taken to ensure that when the pad is applied, it is in full contact with the patient skin, free of air bubbles, and away from metal objects in the patient, as electrical arching can cause significant harm to the patient. (As with all electrical devices, strict electrical safety protocols should also be followed.) Electrical impedance measurement ensures a continuous electrical circuit and can give an indication of the location of the needle. In general, impedance ranges from greater than 1,000 Ω in spinal tissue, less Interventional Pain Medicine than 200 Ω in vertebral disc, and between 300 Ω and 600 Ω in extradural tissue. Impedance should be between 250 Ω and 400 Ω when lesioning. The nerve stimulator can be used to detect proximity to the targeted nerve with sensory stimulation at 50 Hz and also proximity to motor nerves with stimulation at 2 Hz. With sensory stimulation, voltage is increased slowly and the patient reports when stimulation in the painful area is perceived. When sensory stimulation is felt at or below 0.5V, the needle is felt to be located close enough to the nerve for radiofrequency stimulation to have a positive effect. If no sensations are felt or sensation occurs at greater than 0.5V, the proximity of the needle to the nerve is called into question and the needle should be repositioned. Motor stimulation is used to determine the proximity of needle to motor fibers. Performed at 2 Hz, slowly increasing voltage to either three times the sensory voltage threshold or 1.5 V should not cause movement in the shoulder or arm. If motor stimulation is seen in the distal shoulder or arm, permanent nerve damage could occur with high-temperature lesions. It must be remembered that motor stimulation can still be seen with proper placement because the medial branch innervates the multifidus and interspinales muscles. Stimulation of these muscles will cause contractions in the neck but not in the arm. If motor stimulation is in question, it is better to reposition the needle or consider pulsed radiofrequency ablation. Sensory and motor stimulation testing for all patients have recently been called into question.15 , 16 Reasons include sensory thresholds in pathologic states may be altered, which would change the relationship of voltage and distance from the nerve, accurate reporting of sensory stimulation can be difficult for some patients, pulsed radiofrequency does not result in a neurolytic lesion, radiological landmarks provides sufficient precision for these treatments, and no published studies have shown improvement when motor and sensory stimulation is performed. Application of radiofrequency causes electrolytes in tissue to vibrate, which leads to friction and the production of heat. Neural destruction occurs within 20 seconds when temperatures greater than 45 to 50 °C are applied. 17 When this temperature is reached, a neurolytic lesion will have occurred if the area heated contains the nerve. The higher the temperature, the more tissue damaged; studies show a linear relationship between temperatures measured at the tip of the needle and the size the lesion created. This relationship decreases when temperature approaches 100° C. At these temperatures, plasma starts to boil and the disrupted plasma proteins begin to adhere to the electrode, which increases impedance and causes a rapid fall in effective tissue heating.18 The optimal temperature for heating with continuous RF has been recommended at 80° C to limit the accumulation of proteins on the needle but still maximize the size of the lesion. The recommended temperature for pulsed radiofrequency is set below 45° C and thus below the neurolytic threshold. 82

RF generator 2.3: Cervical Median Branch Blocks

Figure 2.3.4 Four basic elements are required to complete the radiofrequency (RF) circuit the RF generator, the active electrode (insulated needle cannula and RF probe), the dispersive electrode (grounding pad), and the patient’s body. The arrows indicate the direction of current flow and the dashed lines symbolize passage of the current through the patient’s body. With kind permission from Springer Science+ Business Media: FM Ahadian. Pulsed radiofrequency neurotomy: advances in pain medicine. Current Pain and Headache Reports . 2004;8(1):34–40.

The lesion created by continuous high-temperature RF physically disrupts the transmission of a pain signal. Pulsed RF is different from continuous RF because temperatures stay below neurolytic thresholds. Pulsed RF mode delivers 500,000 Hz RF current for 20 milliseconds twice per second. During the off cycle, the heat decreases and thus prevents irreversible thermal damage to the nerve. It is recommended that the temperature is set at between 42° and 45° C with pulsed RF. How this decreases pain is still uncertain, but short 20 ms (millisecond) bursts create temperature spikes with thermal lesions. In addition, non-thermal effects occur with this application leading to neuromodulation of the pain fibers.19–21 Temperature is monitored through a thermocouple at the tip of the needle. This gives a reflection of temperature of the tissue being heated, which then allows the machine to alter its parameters to maintain a set temperature at the target. The actual temperature in the tissue will vary not only by the amount of energy delivered by the machine, but also by the characteristics of the tissue at the site of treatment. The temperature is altered by the varying heat conductivity of different tissues such as bone and muscle and also by the amount of blood flow in the tissue. These factors create a variable heat sink and can greatly affect the amount of heat that is applied to the nerve. In order to compensate for this, the machine monitors the temperature of the tissue through the thermocouple and varies the amount of power delivered to keep the temperature constant at the tip of the needle. This keeps the lesion consistent and predictable. The diameter of the needle and the length of the active tip on the needle also affect the size of the lesion. A larger gauge needle and a longer active tip will create a larger lesion. In general, the most common size for cervical radiofrequency is 22-gauge with a 5- or 10-mm active (un-insulated) tip. The amount of time that the radiofrequency is applied also affects the size of the lesion. The size of the lesion does not increase significantly after 45 to 90 seconds at neurolytic temperatures. This is why it is recommended to treat for approximately 60 seconds with high temperature RF at lesion. 83 The problem does not apply to pulse RF and the recommend time of treatment at each lesion is 2 to 6 minutes. Another way to increase size of the lesion is to move the needle slightly and treat again. This movement can be done by rotating a curved needle or moving it one needle’s width more medial or lateral. This will expose more of the nerve to the radiofrequency, help account for slight variations in individual anatomy, and should therefore improve results. In general, two or three lesions are recommended at each level. Because continuous RF lesions are painful, it is recommended that 0.5 to 1cc of local anesthetic be given approximately one minute before lesioning either through the RF needle or a second, specially placed block needle. In order to prevent post-operative inflammation and pain, a small amount of steroid can also be injected after the procedure at each level. Because pulsed RF is not painful and local anesthetic may interfere with this type of lesion, local anesthetic and steroid are not given until after a pulsed RF procedure. The lesions made by continuous high-temperature RF tend not to extend much past the distal tip of the needle but rather surround the long axis of the un-insulated needle tip. The electrical field created by Interventional Pain Medicine pulsed RF is more distal to the needle tip and this has been theorized as to where the greatest biological affect occurs.22–24 Using this information, a posterior approach (parallel to the course of the nerve) is recommended for continuous RF and a lateral approach (perpendicular to the course of the nerve) is recommended for pulsed RF. Contraindication for RF Absolute Patient unwilling or unable to sign consent Untreated infection systemically or at the surgical site Bleeding diathesis Unstable patient Indeterminate results of diagnostic block Pregnancy Anticoagulation medication that can’t be stopped Relative Pacemaker, ACD, spinal cord stimulator or other device that uses RF energy Inability to undergo procedure due to cardiac or respiratory illness Immunosuppression Unrealistic expectations Difﬁ cult anatomy, which makes landmarks difﬁ cult to identify Uncooperative patient Poor or short live response to prior radiofrequency treatments Patient Position for Radiofrequency Like the diagnostic block, patient position can be supine, prone, or lateral decubitus based on patient comfort and physician preference. Unlike the diagnostic block, consideration of how the needle comes in contact with the nerve should also be considered. If the radiofrequency current is to be applied parallel to the nerve, the patient is placed in the prone position and the needle enters from the dorsal aspect of the neck. If the current is to be applied to the nerve in a perpendicular direction, the patient is placed in a supine or prone position and the needle is directed from the lateral side of the neck. Again, the advantage of a lateral approach is less tissue and muscle need to be crossed, which reduces discomfort. There is also a theoretical advantage for application of pulsed radiofrequency in this direction. (The disadvantage of placing the needle from a lateral position is that the needle can more easily enter the neuroforamen, 84 which increases the risk of nerve root or spinal cord injury.) In addition, the lateral approach becomes more difficult and almost impossible in some patients for the lower cervical medial branches because high-riding shoulders obscure visualizations. The main advantage of a dorsal parasagittal approach for radiofrequency is that the long axis of the needle will be placed parallel to the path of the nerve on the lateral mass. This will create a larger lesion and theoretically result in a more effective treatment. In addition, because the needle is inserted deeper into the tissue, the needle is held more stable when compared to a much more superficial lateral approach. With the patient in position after informed consent, standard monitors should be applied. If sedation is to be used, consciousness and patient cooperation must be maintained. The patient must be able to follow directions and answer questions to ensure safety and allow feedback for placement of the needles. Resuscitative equipment and drugs should be available. The skin is prepped and drapes are placed around the site. Fluoroscopy is used to identify the target sites. If the lateral approach is chosen, the fluoroscope is placed in the lateral position and the right and left lateral masses are aligned. Next, the C2 vertebral body is identified by its unique shape in the lateral

2.3: Cervical Median Branch Blocks position. This is often used as a reference point in labeling the other cervical levels. In order to visualize the lower cervical medial branch nerve targets occasionally the patient’s arms will need be pulled carefully in a caudal direction by an assistant so that the shoulder does not block visualization. As stated above, the lateral view will have the targeted lateral mass aligned to form a trapezoidal shape with the corresponding opposite lateral mass. The course of the nerve travels across the lateral mass near the center of an X formed by drawing two lines from each of its four counters. The exact position varies at each level. A radiopaque pointer is used to identify the starting point on the skin and a small amount of local anesthetic is placed over this area. An insulated RF needle is then used for this approach. Radiofrequency needles come curved, straight, sharp and blunt. The lengths are 5, 10, 15 and 20 cm but 5 cm are best for a lateral approach. The 10 cm length is commonly used for the dorsal approach. The gauges range from 18 to 22, with a 22-gauge most often used in the neck. The larger the gauge, the larger the treated area but this comes at the expense of more procedural pain. The active tip of the insulated needle also varies in size with 2 mm, 5 mm and 10 mm available. An increase in size also increases treatment-area size but reduces precision of the lesion. When choosing needles make certain that the radiofrequency electrodes are compatible with the needle and the generator used. Care must be used when inserting and removing the electrodes so that the needle is not moved and that the connections between the electrode and wires are not damaged. Anatomy The successful application of radiofrequency waves occurs when the needle is placed in close proximity to these nerves. Like the diagnostic medial branch blocks, the path of the nerves over the articular pillars and the shape of the articular pillars must be understood in order to effectively and safely use this technique. At each level, the radiofrequency needle is placed along the path of the nerve to maximize exposure of the nerve to the active tip of needle. This will create the largest lesion of the nerves and will provide the greatest pain reduction and longest duration of effect. The final position of the needle before lesioning must be seen in multiple fluoroscopic projections for obvious safety reasons. In the lateral fluoroscopic view, the “diamond-shaped” articular pillars are the targeted sites. As already described the path of the medial branch nerve is unique at each level. At the C3 level, two nerves are located on the articular pillar. The more cephlad is the third occipital nerve. This nerve is located either just cephlad, just caudal, or at the level of the C2-3 zygapophysial joint. (Figure 2.3.5 ) The second nerve at this level is the C3 dorsal medial branch and is located just cephlad to the center of the diamond shaped lateral mass. The C4 and C5 medial branches travel more in the center of articular pillar. The C6 medial branch is again slightly more cephlad on the articular pillar and the C7 medial branch is located even more cephlad 85

T∞

AB Figure 2.3.5 Sketches of the consecutive appearance of the electrode placements for third occipital neurotomy. (A) Lateral view of the oblique pass. The tips of the electrodes lie over the anterior third of the superior articular process of C3. (B) PA view of the oblique pass. The tips of the electrodes project just medial to the lateral silhouette of the C2 superior articular process. Interventional Pain Medicine on the proximal superior articular process. Last the C8 medial branch is targeted over the lateral superior portion the transverse process at the C7 level. In the AP view, the nerves are in the concavity of each articular pillar (Figure 2.3.5 ). In the lateral view, the articular pillars have a concave groove that travels caudally and posteriorly. In order to best place the needle along this groove, it should be angled parallel to zygapophysial joint. Steeper or shallower needle approaches are not desirable because the needle will deflect laterally away from the nerve and prevent optimal treatment (Figure 2.3.6 ). In the sagittal plane, the articular pillar is convex (Figure 2.3.7 ). This means that only a small target on this arc will come in contact with the nerve. Using two approaches with different obliquity and using a curved radiofrequency needle will increase the

Flange obstructs Flange obstructs path path Inserted path of electrode

Inserted path of electrode AB

CD Figure 2.3.6 A: If an electrode is aimed at a nerve (a) running across the upper half of an articular pillar but is inserted directly posterior, its passage will be obstructed by the flange of the zygapophyseal joint. If the anatomy is view in the plane of the zygapohpyseal joint (block arrow) the appearance is that shown in B. B: An oblique view shows how the target nerve lies below the flange of the zygapophyseal joint, which obstructs the passage of the electrode. Moreover if the electrode were to contact the flange, it would lie too far laterally from the nerve. C: If the electrode is inserted parallel to the plane of the zygapophyseal joint, it passes under the flange of the joint. D: As a result, the electrode (e) lies in close apposition, parallel to the nerve (a). 86

OBL

SAG

Figure 2.3.7 Sketch of the top view of a cervical veterbra showing the course of the medial branch (mb) and the

2.3: Cervical Median Branch Blocks oroentation of electrode placed along the sagittal path (SAG), and an oblique path (OBL), to coagulate the nerve.

amount of the nerve exposed to the treatment. When increasing the obliquity, care needs to be taken to ensure that the needle does not travel too far medial and enter the neuroforamen. This can be prevented on the lateral view by keeping the tip of the needle posterior to the ventral boarder of the articular pillar. On the AP image the needle will be no further than the lateral boarder of the vertebral column. Negative motor stimulation provides further confirmation. Last, because of individual variation in the exact location of these nerves, more than one lesion is recommended. This is thought to more likely increase the chances of a successful outcome. In general, the needle can be moved one needle’s breadth more cephlad, one needle’s breadth more caudal, or rotating a curved needle will alter its position. Complications Like all percutaneous procedures, bleeding and infection are possible. The vertebral artery, spinal nerves, radicular arteries, and the spinal cord are in proximity to the targeted sites and are theoretical sites of complications. Electrical burns have been reported due to improper placement of the grounding pad. Complications unique to using radiofrequency include neuritis, numbness, and dysaesthesia.15 The sided effects for conventional RF to the third occipital nerve have been reported to have a higher incidence and include ataxia, numbness, and dysaesthesia. 25 Though these problems have been reported to be short lived, self-resolving, and not disabling but should be anticipated. References 1. Fukui S , Ohseto K , Shiotani M , Ohno K , Karasawa H , Naganuma Y , Yuda Y . Referred pain distribution of the cervical zygapophyseal joints and cevical dorsal rami . Pain . 1996 ; 68 : 79 – 83. 2. Dwyer A , Aprill C , Bogduk N . Cervical Zygapopyseal joint pain patterns: a study in normal volunteers . Spine . 1990 ; 15 : 453 – 457. 3. Pawl R . Headache, cervical spondylosis, and cervical fusion . Surg Ann . 1977 ; 9 : 391 – 498. 4. Windsor R , Nagula D , Storm S . Electrical stimulation induced cervical medial branch referral patterns . Pain Physician . 2003 ; 6 : 411 – 418. 5. Bogduk N , Marsland A . The cervical zygapophyseal joints as a source of neck pain . Spine . 1988 ; 13 : 610 – 617. 6. Bogduk N , Marsland A . On the concept of third occipital headache . J Neurol Neurosurg Psychiat . 1986 ; 49 : 775 – 780. 87 7. Barnsley L , Lord S , Wallis B , Bogduk N . Lack of effect of intra-articular corticosteroids for chronic pain in the cervical zygapophyseal joints . N Engl J Med . 1994 ; 330 : 1047 – 1050. 8. Falco F , Erhart S , Wargo B , et al. Systematic review of diagnostic utility and therapeutic effectiveness of cervical facet joint interventions . Pain Physician . 2009 ; 12 : 323 – 344. 9. Bogduk N . The clinical anatomy of the cervical dorsal rami . Spine . 1982 ; 7 : 319 – 330. 10. Barnsley L , Bogduk N . Medial branch blocks are speciﬁ c for the diagnosis of cervical zygapophyseal joint pain . Reg Anes . 1993; 18 : 343. 11. Aprill C , Dwyer A , Bogduk N : Cervical zygapophyseal joint pain patterns II: A clinical evaluation . Spine . 1990 ; 15 : 458 – 461. 12. Barnsley L , Lord S , Bogduk N : Comparative local anesthetic blocks in the diagnosis of cervical zygapophyseal joints pain . Pain . 1993 ; 55 : 99 – 106. 13. Lord S , Barnsley L , Bogduk N : The utility of comparative local anesthetic blocks versus placebo-controlled blocks for the diagnosis of cervical zygapophyseal joint pain . Clin J Pain . 1995 ; 11 : 208 – 213. 14. Manchukonda K , Manchikanti K , Cash K , Pampati V , Manchikanti L . Facet joint pain in chronic spinal pain: An evaluation of prevalence and false-positive rate a diagnostic blocks . J Spinal Disord Tech . 2007 ; 20 :

539 – 545. Interventional Pain Medicine 15. Bogduk N . Practice guidelines for spinal diagnostic and treatment procedures , Interventional Spinal Intervention Society , 2004. 16. Raj P , Lou P , Erdine S , et al. Interventional Pain Management: Image-Guided Procedures , 2 nd Edition . Philadelphia , PA: WB Saunders ; 2008. 17. Cosman EJ , Cosman ES . Electrical and thermal ﬁ eld effects in tissue around radiofrequency electrodes . Pain Med . 2005 ; 6 : 405 – 424. 18. Nath S , Barber M . Update on the biophysics and thermodyanmics of radiofrequency ablation . Cardiac Electrophysiol Review . 1997 ; 4 : 407 – 411. 19. Erdine S , Bilir A , Cosman E , Cosman EJ . Ultrastrural changes in axons following exposure to pulsed radiofrequency ﬁ elds . Pain Pract . 2009 ; 9 : 407 – 417. 20. Sluijter M . Radiofrequency ablation in the management of spinal pain: controversies and consensus in imaging and intervention ( serial online ), 2006. 4(1) 21. Edrine S , Yucel A , Cimen A , Aydin A , Sav A , Brlir A . Effects of pulsed versus conventional radiofrequency lesions at 42 degrees C to rat dorsal root ganglion and sciatic nerve . Spine . 2005; 30 : 1008 – 1013. 22. Bogduk N . Letter to the Editor . Pain Med . 2007 ; 8 : 390 – 391. 23. Sluijter M . Radiofrequency, Part 1 . Meggen, Switzerland : Filvopress ; 2001. 24. Gaucci C . Manual of RF Techniques . Meggen, Switzerland : Filvopress ; 2004. 25. Govind J , King W , Bailey B , Bogduk N . Radiofrequency neurotomy for the treatment of third occipital headache . J Neurol Neurosurg Psychiat . 2003 ; 74 : 88 – 93. This page intentionally left blank 89

Section 3 Lumbar Spinal Injections

3.1 Lumbar Interlaminar Epidural Injections 91 3.2 Lumbar Transforaminal Epidural Injections 105 3.3 Medial Branch Blocks 113 3.4 Lumbar Radiofrequency Ablation 121 3.5 Discography 129 3.6 Biacuplasty 139 3.7 Kyphoplasty 149 3.8 Percutaneous Discectomy 157 This page intentionally left blank 91

Chapter 3.1 Lumbar Interlaminar Epidural Injections

Imaneul Lerman , Matthew Hansen , Dmitri Souzdalnitski

Introduction 92 Indications 92 Contraindications 92 Functional Anatomy 93 Equipment and Preparation 94 Medications 94 Technique 95 Complications 99 Summary 99 Clinical Pearls 100 References 100 92 Introduction Since the early 1900s, physicians have performed epidural steroid injections. Prior to that time, the differentiation between dural or epidural medicinal administration was unclear.( 1 ) The first attempt to deliver medication into the epidural (initially termed “extradural”) space was reported in 1901 by Sicard, et al., who injected cocaine into the caudal epidural space in an attempt to treat acute back pain and sciatica.( 2 ) Shortly after the discovery of the anti-inflammatory effects of steroids, Robecchi and Capra (1952) are credited with using epidural steroids to treat spinal-related disorders.( 3 ) Goebert and colleagues (1961) carried out a prospective study of 113 patients with back pain, and reported improvement after caudal epidural steroid injection in two-thirds of the treated patients.( 4 ) Since that time, epidural steroid injections have developed into an integral part of the pain physician’s practice. There have been many published studies supporting the efficacy of lumbar epidural steroid injections in reducing short-term radiculopathic lower back pain. ( 5–7 ) Lumbar epidural steroids are extensively used to treat patients with radicular lower back pain secondary to either herniated or extruded disc material. In addition, steroids may be effective in the treatment of other syndromes associated with radiculopathic lower back pain, including intervertebral 3.1: Lumbar Interlaminar Epidural Injections disc degeneration without disc herniation, spinal stenosis in isolation, degenerative spondylothesis with spinal stenosis, and failed lumbar back surgery syndrome.( 8 ) Lower back pain can be attributed to many structural and non-structural injuries to the fascia, musculature, ligaments, facet joints, discs, nerve roots, and dura.( 9 ) Radiculopathic lower back pain can occur without structural nerve impingement( 8 , 10 ) and, in fact, is thought to be multifactorial in origin, stemming from 1) mechanical structural nerve compression and dysfunction, 2) vascular compromise, and 3) inflammatory and immune mediated mechanisms.( 10 ) Recent studies have shown that the contents of the nucleus pulposus activate an inflammatory cascade through the initial attraction of leukocytes, increasing local vascular permeability and the production of inflammatory factors.( 11–13 ) In discogenic injury, Phospholipase A-2 (PLA2), which is thought to play a key role in perpetuating the inflammatory cascade that leads to radiculopathic pain, is released from the nucleus pulposus. PLA2 triggers the arachidonic acid cascade, increasing local inflammation and edema through the action of both prostaglandins and leukotrienes.( 14–16 ) Potent inflammatory factors, IL-6, IL-8, and TNF-alpha are also thought to play a critical role in radiculopathic pain. ( 17–22 ) The activation of multiple inflammatory cascades can culminate in an edematous and inflamed nerve or nerve root, which in turn, may impair its own blood flow and nutritional support.( 22 ) Prolonged nerve edema can lead to intraneural fibrosis, pathological nerve fiber growth, and further nerve irritation, resulting in worsened radiculopathic pain. Epidural steroids decrease this pain by inhibiting and modulating this inflammatory cascade. Indications Lumbar epidural steroid injections are primarily used to treat radiculopathic lower back pain arising from inflamed and irritated nerve or nerve roots. A complete history and physical, review of pharmacotherapy, and review of the imaging data will focus on key facts and findings which should either include or exclude a patient from undergoing a lumbar epidural steroid injection. The patient most likely to benefit from a lumbar interlaminar steroid injection will demonstrate a clinically characteristic radiculopathic pain pattern (Table 3.1.1 ) with concordant structural abnormalities seen on imaging (Table 3.1.2 ). If the patient has both radiculopathic pain and evidence of structural finding on imaging associated with that dermatomal distribution, it is likely that this patient will gain significant pain relief from an epidural steroid injection. Contraindications Lumbar epidural steroid injections are safe and result in significant pain relief when the correct patient population is selected and experienced physicians trained in fluoroscopic neuraxial interventions perform the procedure. Interlaminar lumbar epidural injections should be avoided in some patients, 93 Table 3.1.1 Radicular pain signs and symptoms Radicular Pain signs and symptoms

Sharp sudden shooting pain Low back pain radiating below the knee Increased pain with coughing or sneezing or straining Pain occurring with onset of heavy lifting

however, even if they are likely to gain relief from the procedure, due to an undesirable risk/benefit ratio. Contraindications for epidural steroid injection are the following: - Patient unwilling to consent to the procedure

- Infection at the site of injection Interventional Pain Medicine - Sepsis - INR > 1.5 or platelets <100000 - Pregnancy - Conditions associated with increased intracranial pressure - Allergy to the local anesthetic, corticosteroid, or contrast agent Functional Anatomy Radiculopathic pain can arise from structural and subsequent inflammatory abnormalities of the spine. Imaging of the spinal anatomy can provide a clear illustration of the patient’s underlying pathophysiology, aid in detecting those structural abnormalities, and guiding the treatment plan. Plain films, MRI, CT, and CT myelogram, all offer a wealth of information to the consulting pain physician, such as estimating the distance from the skin to the epidural space. In 80 percent of the population, the skin to epidural distance commonly averages 4–6 cm in depth.( 23 ) The pain physician should review all imaging studies and be cognizant of this measurement in order to prevent unintended penetration of the dura, or inadvertent injury to neural and vascular structures. The posterior epidural space normally measures 5–6 mm at the L2-L4 region and decreases cephalad toward the cervical vertebra. Failed back surgery syndrome, a common indication for the epidural steroid injections, may be associated with significant distortion of the anatomy secondary to scarring and adhesions. In this category of patients, caudal epidural steroid injection with a navigable catheter may be a better choice, as this approach decreases the chance of dural puncture or nerve damage.( 23 , 24 ) The thickness of the ligamentum flavum in the mid-lumbar region is 5–6 mm. In some patients, however, there are known gaps in the ligamentum flavum at certain lumbar levels. These gaps are

Table 3.1.2 Indications for epidural steroid injection Indications for Epidural Steroid Injection

Disc degeneration or herniation Spinal nerve root compression and or inflammation-traumatic Spinal nerve root inflammation, associated with certain infectious (e.g., acute or subacute herpes zoster, postherpetic neuralgia) Spinal stenosis Failed back syndrome 94 uncommon below L4, but are seen in 22 percent of patients between L1 and L2 and 11 percent of patients between L2-L3 and L3-L4.( 25 ) If a patient has a large enough gap at the L2-L3 level he or she might not obtain adequate pain relief secondary to impaired spread of the steroid at that level. Equipment and Preparation Tuohy epidural needles 18- and 20-gauge, 3.5 inch (Figure 3.1.1 ) Needle, 25-gauge, 1.5 inch (subcutaneous local anesthetic) Syringe 10 ml (subcutaneous local anesthetic) Syringe 10 ml glass (glass provides smooth plunger movement and improved tactile for “loss of resistance” technique) Sterile gloves, drapes, towels, gauze, gown Betadine/chlorhexidine prep Adhesive bandages Lead apron, hat, mask 3.1: Lumbar Interlaminar Epidural Injections Flouroscopy, C-arm Medications As previously mentioned, interlaminar steroid injections are thought to improve radiculopathic pain through multiple pathways. First it has been shown that corticosteroids directly inhibit PLA2, thereby decreasing the production of inflammatory factors involved in the arachidonic acid cascade, prostaglandins, and leukotrienes. Furthermore, corticosteroid administration has been shown to significantly decrease the inflammatory cytokine, IL-6.( 26 ) Corticosteroids also directly inhibit the production of edematous fluid and likely reduce vascular permeability. Corticosteroids have been shown to reversibly inhibit C fiber neurons while leaving AB fibers unaffected.( 27 ) Moreover, it is likely that corticosteroids activate norepinephrine and 5-hydroxytrpitpamine receptors found in the dorsal root ganglion, which are both known to be involved in modulation of pain pathways.( 28 , 29 ) The following steroid preparations are commonly used for epidural steroid injections (Table 3.1.3 ). In addition, the following medications are required for an interlaminer epidural steroid injection (Table 3.1.4 ). Patients with allergies to iodinated contrast agents can alternatively undergo epidurography with Gadolinium or Magnevist.( 30 , 31 ) While nephrogenic systemic fibrosis has been associated with the administration of Gadolinium, most cases are associated in patients with underlying renal failure and with higher doses of Gadolinium contrast than that used for epidurography.( 32 )

Figure 3.1.1 This is a Tuohy epidural needle. The black areas demarcating 1-cm intervals are noted while inserting the epidural needle. 95 Table 3.1.3 Steroid formulations used for epidural steroid injection Steroid, Concentration, Manufacturer Dosage

Triamcinolone diacetate, 25mg/ml, 40mg/ml (Kenalog (Bristol-Myers Squibb, (50–80 mg for New York, NY), interlaminar injection) Methylprednisone acetate injectable suspension 40mg/ml (Depo-medrol (Pfizer, (40–80 mg for New York, NY) interlaminar injection) Betamethasone sodium phosphate and betamethasone acetate injectable suspension (6–12 mg for 6mg/ml (Celestone (Schering, Kenilworth, NJ) interlaminar injection) Dexamethasone injectable suspension 4mg/ml, 10mg/ml Decadron (Merck, Whitehouse (4–10 mg for Station, NJ) interlaminar injection)

Technique Interventional Pain Medicine Before starting the procedure, it is imperative that the risks and benefits of the procedure be explained to the patient, that all questions are answered, and that an informed consent is signed. In order to perform the procedure, position the patient prone on the fluoroscopic table with the head turned to one side and arms placed above the head. We recommend placing a small pillow under the patient’s mid to lower abdomen to further open the lumbar interlaminar space, in addition to increasing the distance between the contiguous spinous processes. The C-arm should then be rotated 15 to 20 degrees caudad to ensure adequate visualization of the target interlaminar space. After the patient and C- arm is appropriately positioned, the interlaminar space should be identified under fluoroscopic guidance. Two approaches to the interlaminar space— the median and paramedian— have been described. The paramedian approach avoids bony and ligamentous structures, which could be variable in the elderly and patients with failed back syndrome.( 33 ) The paramedian is faster and has less associated complications, such as dural puncture and paresthesias.( 34 , 35 ) An imaginary line connecting the superior pedicle and the area lateral to the spinous process demarcates the best paramedian insertion site( 36 ) (Figures 3.1.2 and 3.1.2 b). The median approach site will be located directly between the spinous processes.

Table 3.1.4 Medications used for epidural steroid injections Medication Dosage

Lidocaine hydrochloride 1 percent preservative free (Xylocaine) 2–5 ml (for subcutaneous (SC) (APP Pharmaceuticals, Schaumberg, IL) injection) Saline sterile (preservative free) 5 ml (for loss or resistance (APP Pharmaceuticals, Schaumberg, IL) technique and diluent) Non-ionic iodinated myelographic contrast agent (Omnipaque, Iohexol) 2–3 ml (for epidurography) (Amersham Health, Princeton, NJ) Non diluted gadopentate dimeglumine (Magnevist, Berlex, Wayne, NJ) 1–3 ml (for epidurography) Lidocaine hydrochloride 1 percent preservative free (Xylocaine) 5–10 ml (for interlaminar injection) (APP Pharmaceuticals, Schaumberg, IL) Bupivacaine 0.25 percent preservative free (Sensorcaine) (5 + ml for interlaminar injection) (APP Pharmaceuticals, Schaumberg, IL) 96 3.1: Lumbar Interlaminar Epidural Injections A B Figure 3.1.2 Panel A shows the needle position in the median approach. Panel B shows the needle position in the paramedian approach.

Prep the skin over the target site (median or paramedian) with povidone-iodine three or more times. Alternatively, the skin can be prepped once with chlorhexadine-alcohol.( 37 ) Drape the site in sterile fashion before proceeding with the intervention. The loss of resistance technique (LOR) is used extensively by anesthesiologist to identify the epidural space and carry out epidural anesthesia with out fluoroscopy. The current literature shows that combined LOR technique with fluoroscopic guidance and epidurography significantly improves epidural steroid injection efficacy.( 37 , 38 ) It is widely accepted that the most common culprit for epidural steroid injection treatment failure is inappropriate needle placement. Incorrect needle placement has been noted to occur 25 to 40 percent of the time when the LOR technique is undergone without fluoroscopy. ( 39 , 40 ) In a study involving more than 5,000 patients, Johnson, et al., showed that potential complications of inaccurate injection of corticosteroids could be avoided when using the LOR with fluoroscopic guidance.( 41 ) A recent study by Taenzer, et al., found significantly decreased mal-positioned needle placement (1.6 percent) for epidural catheter placement in children when using fluoroscopy and epidurography, which speaks to the advantages of combining LOR technique with fluoroscopy and epidurography.( 42 ) After appropriate cleansing and draping, the overlying skin should be anesthetized with 2–5 ml of 1 percent lidocaine in a 10 ml syringe attached to a 25-gauge 1.5-inch needle. A 20-gauge Tuohy epidural needle is advanced until adequate alignment and depth are perceived and then a 10-ml glass syringe is attached. The needle is slowly advanced by the LOR technique, described below (Figures 3.1.3 a and 3.1.3 b). 1. 10-ml glass syringe fi lled with air or sterile saline is attached to the Tuohy epidural needle. 2. The non-dominant hand will grasp the needle base at the skin surface. 3. The dominant hand thumb will hold pressure over the syringe plunger. 4. The needle is slowly advanced with either constant pressure or the ballottement technique by 1–2 mm at a time. During this advancement, repeat fl uoroscopic images should be taken at intervals of every 0.5–1.0 cm of needle advancement. 5. As the needle passes through the ligamentum fl avum and enters the epidural space, a loss of resistance occurs, allowing for the easy injection of the contents in the syringe. After successful injection of air or normal saline into the epidural space, the 10 ml syringe is removed. At this point, an AP fluoroscopic image should be performed in order to again verify correct epidural needle placement between the laminae (Figure 3.1.4 ). Next, the 3-ml syringe containing 2 ml of 97 Interventional Pain Medicine A B Figure 3.1.3 Panel A. Initial insertion of the Tuohy epidural needle using the double-hand stabilization technique, with intermittent flouroscopy. Panel B. Insertion of the epidural needle using the non-dominant hand to stabilize the needle base, the right dominant hand uses a ballotement technique to obtain a loss of resistance.

omnipaque is connected to the Tuohy needle with tubing, and aspirated to evaluate for the presence of blood or cerebral spinal fluid (Figure 3.1.5 ). After injection of 2–3 ml of contrast, vascular uptake should be suspected if a washout of contrast is seen under continuous fluoroscopy. If washout occurs, the needle should be repositioned and the injection of contrast can be reevaluated. We find it helpful to use both the AP and lateral fluoroscopic view to verify correct needle position and identify the anterior and posterior epidural space with epidurography (Figures 3.1.6 a and 3.1.6 b).

Figure 3.1.4 Image of Tuohy needle. The needle is placed in the paramedian approach lateral to the spinous process and below the pedicle. 98 3.1: Lumbar Interlaminar Epidural Injections

Figure 3.1.5 The syringe containing a contrast agent (Omnipaque) is attached to the Tuohy needle. First, the needle is aspirated to ensure the absence of cerebral spinal fluid or blood.

After confirmation of successful needle placement with epidurography, the practitioner can inject the steroid solution in small 0.5-ml increments, which avoids pain associated with the injection of fluid into a tight space. After the injection is completed the patient should be monitored for thirty minutes to observe for new motor or sensory deficits, allergic reaction, and increased pain, which could be an early sign of epidural hematoma.

AB Figure 3.1.6 Panel A. Spread of contrast below the spinous process indicating that the contrast is in the epidural space. Panel B. A lateral view that demarcates the epidural space outlined with contrast abutting the anterior and posterior longitudinal ligaments. 99 Complications Complications of epidural steroid injection arise from either needle placement technique or the effects of the administered medication. Needle placement may result in tenderness at the insertion site and patients should be notified about this frequent complication. Dural puncture, the most common complication, is associated with incorrect needle placement technique or variant patient anatomy, which is not always possible to detect. An aberrant dural puncture may result in a positional headache. MacDonald estimated the incidence of dural puncture and subsequent headache following 5,685 lumbar epidural injections was 0.33 percent, or less than 1 percent for all lumbar epidural injections.( 43 ) Postdural puncture headache typically is more severe in younger patients, when compared to elderly patients. Initial management for these headaches should be conservative. If pain persists for more than twenty-four to forty-eight hours or greatly is impacting the patient’s functionality, however, an epidural blood patch may be performed. Unintentional dural puncture with loss of resistance technique may result in pneumocephalus, manifested by a sudden acute severe headache.( 44 , 45 ) Interventional Pain Medicine Nerve injury may result in transient paresthesias or permanent nerve damage. Nerve root injury and spinal cord injury can occur with epidural needle placement or from the formation of an epidural hematoma or an epidural abscess. Immediate low back pain and lower extremity weakness can be a sign of lumbar epidural hematoma formation. In contrast, delayed lower extremity weakness and lower back pain over a period of three days to three weeks is more likely a sign of epidural abscess formation.( 46 ) The patient with an epidural abscess usually presents with fever, spinal pain, radicular pain, or progressive neurological deficit. Molloyand Gaul independently reviewed the reported cases of epidural abscess formation from 1984–2000, and both found that the most common pathogen identified was Staphylococci aureus .( 46 , 47 ) In both series, patients who were immunocompromised or had uncontrolled diabetes were found to have an increased risk for epidural abscess formation.( 46 , 47 ) When compared to cervical and thoracic epidural steroid injections, lumbar epidural steroid injections are most commonly associated with epidural abscess formation.( 48 ) ESR and CRP may be elevated in patients with epidural abscess. Diagnosis is confirmed by MRI imaging. The complications of lumbar interlaminar epidural injection related to medication effects can occur from either the local anesthetic or the injected steroid. Local anesthetic injection can lead to allergic reaction or, if injected intravascularly or intrathecally, seizures, hypotension, cardiac arrhythmia, or weakness from a motor block.( 46 , 47 , 49 ) Steroid injection have been associated with cushingoid signs and symptoms, hyperglycemia, hypertension, congestive heart failure, avascular necrosis, osteoporosis, oste- openia, steroid induced myopathy, cataract formation, and epidural lipomatosis.( 48–51 ) Arachnoiditis, however, has not been associated with epidural steroid injection when there is no evidence of dural puncture.( 44 ) Epidural hematoma formation is a relatively uncommon complication (1/150,000) associated with interlaminar epidural steroid injections. There is, however a significant risk in patients receiving anticoagulant medications.( 52–53 ) The American Society of Regional Anesthesia’s recently published recommendations to reduce the risk of epidural hematoma in patients undergoing epidural steroid injetions (Table 3.1.5 ). Even strict adherence to these guidelines may still result in unfortunate epidural hematoma formation as seen in two recent case reports.( 54 , 55 ) Summary Lower back pain is a very common patient complaint and costs the American health care system 100 billion dollars a year.( 56 ) Non-surgical treatments continue to be a cornerstone of low back pain management. The recent literature continues to show that there is significant short-term pain relief with the use of lumbar epidural steroid injections.( 5–7 ) When performed in an appropriately selected patient 100 Table 3.1.5 ASRA recommendations for use of anticoagulation medications and epidural steroid injections Medication ASRA guidelines

Tissue plasmino- Avoid these medications for ten days after epidural steroid injection. ASRA recommends against gen activator neuraxial blockade in any patient who has recently received a thrombolytic medication. (TPA), Streptokinase, and Urokinase Warfarin Stop Warfarin and bridge with Low Molecular Weight Heparin (LMWH) four to five days prior to epidural steroid injection. No guidelines on when to restart Warfarin. Low Molecular Hold LMWH twenty-four hours prior to epidural steroid injection. If the patient is on LMWH twice Weight Heparin daily, change his or her dosage interval to once daily prior to the procedure. If a traumatic injection (LMWH) occurs and or blood is encountered during needle manipulation, LMWH should be reinitiated no less than twenty-four hours later. Heparin Not contraindicated. In this patient population, however, a CBC should be evaluated to ensure (Low-Dose absence of Heparin Induced Thrombocytopenia, (HIT), and adequate platelet counts. 3.1: Lumbar Interlaminar Epidural Injections Subcutaneous) Non-Steroidal When used alone and not combined with other anti-coagulant medications, are considered safe Anti- for continued use in patients undergoing epidural steroid injections. Inflammatory (NSAIDS) Ticlodipine Discontinue ticlopidine fourteen days prior to epidural steroid injection. Clopidogrel Disontinue Clopidogrel seven days prior to epidural steroid injection.

population and by physicians who are appropriately trained in fluoroscopic neuraxial interventions, lumbar epidural steroid injections are a safe and effective treatment of low back pain. Clinical Pearls Epidural steroid injection is an invaluable tool to decrease the frequency and intensity of a patient’s lower back pain, thereby allowing for adequate physical rehabilitation, a reduction in opiate consumption, and promotion of greater functionality and return to work. - Diabetic patients with poorly controlled blood sugars should undergo consultation with their PCP prior to intervention to discuss the systemic effects of steroids. - Diabetic, immunosuppressed, and AIDS patients are at increased risk of epidural abscess formation. Consider prophylactic antibiotic treatment for S. Aureus in this patient population. - Patients with significant renal failure should be closely monitored in situations where renally cleared medications, including Gadolinium, are used. - Patients allergic to omnipaque iodinated contrast agent can substitute with Gadolinium for epidurography when renal function is adequate. References 1. Corning JL . Spinal anesthesia and local medication of the cord . NY State Med J . 1885 ; 42 : 483485. 2. Sicard MA . Les injections médicamenteuses extradurales par voie sacrococcygienne . C R Soc Dev Biol . 1901 ; 53 : 396 – 398 . 3. Robecchi A , Capra R , Robecchi A . Hydrocortisone (compound F); fi rst clinical experiments in the fi eld of rheumatology. Minerva Med . 1952 ; 43 ( 98 ): 1259 – 1263 . 4. Goebert HW , Jallo SJ , Gardner WJ , Wasmuth CE , Goebert HW . Painful radiculopathy treated with epidural injections of procaine and hydrocortisone acetate: results in 113 patients . Anesth Analg . 1961 ; 40 : 130 – 134 . 101 5. Arden NK , Price C , Reading I , et al . A multicentre randomized controlled trial of epidural corticosteroid injections for sciatica: the WEST study . British Journal of Rheumatology . 2005 ; 44 ( 11 ): 1399 – 1406 . 6. Wilson-MacDonald J , Burt G , Griffi n D , Glynn C , Wilson-MacDonald J . Epidural steroid injection for nerve root compression . A randomized, controled trial. Journal of Bone & Joint Surgery, British Volume . 2005 ; 87 ( 3 ): 352 – 355 . 7. Carette S , Leclaire R , Marcoux S , et al . Epidural corticosteroid injections for sciatica due to herniated nucleus pulposus . N Engl J Med . 1997 ; 336 ( 23 ): 1634 – 1640 . Chan ST , Leung S , Chan ST . Spinal epidural abscess following steroid injection for sciatica . Case report. Spine . 1989 ; 14 ( 1 ): 106 – 108 . 8. Parr AT , Diwan S , Abdi S . Lumbar interlaminar epidural injections in managing chronic low back and lower extremity pain: a systematic review . Pain Physician . 2009 ; 12 ( 1 ): 163 – 188 . 9. Kuslich SD , Ulstrom CL , Michael CJ . The tissue origin of low back pain and sciatica: a report of pain response to tissue stimulation during operations on the lumbar spine using local anesthesia . Orthop Clin North Am . 1991 ; 22 ( 2): 181 – 187 . 10. Wheeler AH , Murrey DB . Chronic lumbar spine and radicular pain: pathophysiology and treatment . Curr Pain Headache Rep . 2002 ; 6 ( 2 ): 97 – 105 .

11. Olmarker K , Nordborg C , Larsson K , Rydevik B . Ultrastructural Changes in Spinal Nerve Roots Induced by Interventional Pain Medicine Autologous Nucleus Pulposus . Spine . 1996 ; 21 ( 4 ). 12. McCarron RF , Wimpee MW , Hudkins PG , Laros Gerald S . The infl ammatory effect of nucleus pulposus: a possible element in the pathogenesis of low-back pain . Spine . 1987 ; 12 ( 8 ): 760 –764. 13. Iwabuchi M , Rydevik B , Kikuchi S , Olmarker K . Effects of anulus fi brosus and experimentally degenerated nucleus pulposus on nerve root conduction velocity: relevance of previous experimental investigations using normal nucleus pulposus . Spine . 2001 ; 26 ( 15 ). 14. Saal JS , Franson RC , Dobrow R , et al . High levels of infl ammatory phospholipase A2 activity in lumbar disc herniations . Spine . 1990 ; 15 ( 7 ): 674 – 678 . 15. Vishwanath BS , Fawzy AA , Franson RC , Vishwanath BS . Edema-inducing activity of phospholipase A2 purifi ed from human synovial fl uid and inhibition by aristolochic acid . Infl ammation . 1988 ; 12( 6 ): 549 – 561 . 16. Chen C , Cavanaugh JM , Ozaktay AC , Kallakuri S , King I , Chen C . Effects of phospholipase A2 on lumbar nerve root structure and function . Spine . 1997 ; 22 ( 10 ): 1057 – 1064 . 17. Kang JD , Georgescu HI , McIntyre-Larkin L , Stefanovic-Racic M , Donaldson WFI , II , Evans CH . Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2 . Spine . 1996 ; 21 ( 3 ). 18. Norimoto M, Ohtori S , Yamashita M , et al . Direct application of the TNF-alpha inhibitor, etanercept, does not affect CGRP expression and phenotypic change of DRG neurons following application of nucleus pulposus onto injured sciatic nerves in rats . Spine . 2008 ; 33 ( 22 ): 2403 – 2408 . 19. Yamashita M , Ohtori S , Koshi T , et al . Tumor necrosis factor-alpha in the nucleus pulposus mediates radicular pain, but not increase of infl ammatory peptide, associated with nerve damage in mice . Spine . 2008 ; 33 ( 17 ): 1836 – 1842 . 20. Wagner R , Myers RR . Endoneurial injection of TNF-[alpha] produces neuropathic pain behaviors . Neuroreport . 1996 ; 7 ( 18 ). 21. Burke JG , Watson RW , McCormack D , et al . Intervertebral discs which cause low back pain secrete high levels of proinfl ammatory mediators . Journal of Bone & Joint Surgery, British Volume . 2002 ; 84 ( 2 ): 196 – 201 . 22. Tonkovich-Quaranta LA , Winkler SR , Tonkovich-Quaranta LA . Use of epidural corticosteroids in low back pain . Ann Pharmacotherapy . 2000 ; 34 ( 10 ): 1165 – 1172 . 23. Hogan QH . Epidural anatomy examined by cryomicrotome section: infl uence of age, vertebral level, and disease . Regional Anesthesia & Pain Medicine . 1996 ; 21 ( 5 ): 395 – 406 . 24. Bevacqua BKMD , Haas TRN , Brand FRN , M.S.N . A clinical measure of the posterior epidural space depth . Regional Anesthesia & Pain Medicine . 1996 ; 21 ( 5 ): 456 – 460 . 25. Lirk P , Moriggl B , Colvin J , et al . The incidence of lumbar ligamentum fl avum midline gaps . Anesth Analg . 2004 ; 98 ( 4 ): 1178 – contents . 26. Reikeras O , Helle A , Krohn CD , Brox JI . Effects of high-dose corticosteroids on post-traumatic infl ammatory mediators . Infl amm Res . 2009 ; 58 ( 12 ): 891 – 897 . 27. Johansson A , Hao J , Sjolund B . Local corticosteroid application blocks transmission in normal nociceptive C-fi bres . Acta Anaesthesiol Scand . 1990 ; 34 ( 5 ): 335 – 338 . 102 28. Fuxe K , Harfstrand AC , Okret S , et al . Mapping of glucocorticoid receptor immunoreactive neurons in the rattel- and diencephalon using a monoclonal antibody against rat liver glucocorticoid receptor . Endocrinol . 1985 ; 117 ( 5 ): 1803 – 1812. 29. Hua SY , Chen YZ. Membrane receptor-mediated electrophysiological effects of glucocorticoid on mammalian neurons . Endocrinol . 1989 ; 124 ( 2 ): 687 – 691 . 30. Safriel Y , Ali M , Hayt M , Ang R , Safriel Y . Gadolinium use in spine procedures for patients with allergy to iodinated contrast— experience of 127 procedures . Am J Neuroradiol . 2006 ; 27 ( 6 ): 1194 –1197 . 31. Shetty SK , Nelson EN , Lawrimore TM , Palmer WE , Shetty SK . Use of gadolinium chelate to confi rm epidural needle placement in patients with an iodinated contrast reaction . Skeletal Radiol . 2007 ; 36 ( 4 ): 301 – 307 . 32. Kallen AJ , Jhung MA , Cheng S , et al . Gadolinium-containing magnetic resonance imaging contrast and nephrogenic systemic fi brosis: a case-control study . Am J Kidney Dis . 2008 ; 51 ( 6 ): 966 – 975 . 33. Rabinowitz A , Bourdet B , Minville V , et al . The paramedian technique: a superior initial approach to continuous spinal anesthesia in the elderly . Anesth Analg. 2007 ; 105 ( 6 ): 1855 – contents . 34. Blomberg RG , Jaanivald A , Walther S . Advantages of the paramedian approach for lumbar epidural analgesia with catheter technique . A clinical comparison between midline and paramedian approaches. Anesthesia . 1989 ; 44 ( 9 ): 742 – 746 . 3.1: Lumbar Interlaminar Epidural Injections 35. Leeda M , Stienstra R , Arbous MS , et al . Lumbar epidural catheter insertion: the midline vs . the paramedian approach. Eur J Anaesthesiol . 2005 ; 22 ( 11 ): 839 – 842 . 36. Ranson MT , Deer TR . Epidural injections for the treatment of spine-related pain syndromes . In: Golovac S , ed. Image-Guided Spine Interventions. New York : Springer ; 2010 : 157 – 110 . 1007/978–1-4419–0352-5_8 . 37. Mehta M , Salmon N . Extradural block . Confi rmation of the injection site by X-ray monitoring. Anesthesia . 1985 ; 40 ( 10 ): 1009 – 1012 . 38. Renfrew DL , Moore TE , Kathol MH , et al . Correct placement of epidural steroid injections: fl uoroscopic guidance and contrast administration . Am J Neuroradiol . 1991 ; 12 ( 5 ): 1003 – 1007 . 39. White AH , Derby R , Wynne G , White AH . Epidural injections for the diagnosis and treatment of low-back pain . Spine . 1980 ; 5 ( 1 ): 78 – 86 . 40. Bartynski WS , Grahovac SZ , Rothfus WE . Incorrect needle position during lumbar epidural steroid administration: inaccuracy of loss of air pressure resistance and requirement of fl uoroscopy and epidurography during needle insertion . Am J Neuroradiol . 2005 ; 26 ( 3 ): 502 – 505 . 41. Johnson BA , Schellhas KP , Pollei SR , Johnson BA . Epidurography and therapeutic epidural injections: technical considerations and experience with 5334 cases . Am J Neuroradiol . 1999 ; 20 ( 4 ): 697 – 705 . 42. Taenzer AH , Clark CV , Kovarik WD . Experience with 724 epidurograms for epidural catheter placement in pediatric anesthesia . Regional Anesthesia & Pain Medicine . 2010 ; 35 ( 5 ): 432 – 435 . 43. MacDonald R . Dr Doughty’s technique for the location of the epidural space . Anesthesia . 1983 ; 38 ( 1 ): 71 – 72 . 44. Abram SE , O’Connor TC . Complications associated with epidural steroid injections . Regional Anesthesia & Pain Medicine . 1996 ; 21 ( 2 ): 149 – 162 . 45. Simopoulos T , Peeters-Asdourian C . Pneumocephalus. After cervical epidural steroid injection . Anesthesia & Analgesia . 2001 ; 92 ( 6 ): 1576 – 1577 . 46. Molloy R , Benzon H . Interlaminar epidural steroid injections for lumbosacral radiculopathy . In: Benzon S. ed. Essentials of Pain Medicine and Regional Anesthesia . New York : Elsevier Churchill Livingstone ; 2005: 331 – 340 . 10.0443066515. 47. Gaul C , Neundorfer B , Winterholler M , Gaul C . Iatrogenic (para-) spinal abscesses and meningitis following injection therapy for low back pain . Pain Suppl . 2005 ; 116 ( 3 ): 407 – 410 .22. 48. Abram SE , Complications associated with epidural, facet joint, and sacroiliac joint injections . In: Complications in Regional Anesthesia and Pain Medicine . Saunders ; 2010 : 247 – 265 . 10.1416023925 . 49. Sitzman TB , Epidural injections . In: Fenton S , ed. Image-Guided Spine Inervention . Saunders ; 2003 : 99 – 138 . 10.0721600212 . 50. Sandberg DI , Lavyne MH , Sandberg DI . Symptomatic spinal epidural lipomatosis after local epidural corticosteroid injections: case report . Neurosurg . 1999 ; 45 ( 1 ): 162 – 165 . 51. McCullen GM , Spurling GR , Webster JS , McCullen GM . Epidural lipomatosis complicating lumbar steroid injections . J Spinal Disord . 1999 ; 12 ( 6 ): 526 – 529 . 52. Horlocker TT , Wedel DJ , Benzon H , et al. Regional anesthesia in the anticoagulated patient: Defi ning the risks (the second ASRA consensus conference on neuraxial anesthesia and anticoagulation) . Reg Anesth Pain Med . Jan 2003; 28 ( 3 ): 172 – 197 . 103 53. Horlocker TT , Wedel DJ , Rowlingson JC , Enneking FK , American College of CP, Horlocker TT. Regional anesthesia in the patient receiving antithrombotic or thrombolytic therapy: American society of regional anesthesia and pain medicine evidence-based guidelines (third edition) . Reg Anesth Pain Med . Jan 2010 ; 35 ( 1 ): 102 – 105 . 54. Ain RJ , Vance MB , Ain RJ . Epidural hematoma after epidural steroid injection in a patient withholding enoxaparin per guidelines . Anaesthesiology . 2005 ; 102 ( 3 ): 701 – 703 . 55. Xu R , Bydon M , Gokaslan ZL , et al . Epidural steroid injection resulting in epidural hematoma in a patient despite strict adherence to anticoagulation guidelines . J Neurosurg Spine . 2009 ; 11 ( 3 ): 358– 364 . 56. Katz J . Lumbar disc disorders and low-back pain: socioeconomic factors and consequences . J Bone Joint Surg (Br) . 2006 ; 88; Suppl 2 : 21 – 24 . Interventional Pain Medicine This page intentionally left blank 105

Chapter 3.2 Lumbar Transforaminal Epidural Injections

Adrian Popescu and Anita Gupta

Introduction 106 Indications 107 Contraindications 107 Equipment and preparation 107 Medications 108 Technique 108 Complications 108 Summary 110 References 111 106 Introduction Lumbar transforaminal epidural steroid injections (LTFESI) can be employed as part of the non-surgical management to improve the lower limb radicular symptoms. In general, the LTFESI can be added to the non-surgical therapy once the patient fails to have significant improvement in symptoms with physical therapy, analgesics and changes in his or her work and activity ergonomics. Some experts recommend initiation of interventions to facilitate the active conservative therapy, more specifically the physical therapy exercises. It is the general consensus that the lower-limb radicular symptoms result from an inflammatory mileu within the proximal vicinity of a nerve root in the lumbar spine. This inflammatory process can induce changes in the neurophysiology of the nerve resulting in radicular symptoms, which can consist of sensory, motor, or sensory-motor changes. Physical findings include sensory loss in a specific nerve root dermatome, weakness and atrophy of the muscle supplied by that nerve root, and muscle stretch (also improperly termed “deep tendon reflex”) reflex changes corresponding to the specific nerve root. Diagnosis is usually sustained by one or several 3.2: Lumbar Transforaminal Epidural corroborative tests, the most frequently used of which are MRI, CT, myelography, and electrodiagnostic studies (including nerve conduction studies (NCS) and electromyography (EMG)).[ 1 ] The spinal stenosis, foraminal stenosis, space-occupying lesions, as well as the herniated inter-vertebral disc can induce the inflammatory changes and spinal nerve irritation.[ 2, 3 ] There are numerous studies that associate the presence of inflammation in the spinal nerve with radicular symptoms and nerve membrane instability and irritability.[ 4–9 ] The inflammatory theory and the evidence of inflammatory markers in radicular pain make the use of anti-inflammatory medications, particularly corticosteroids, the logical choice to reduce the inflammation and possible relief of nerve irritation and pain. Injections of steroids, particularly in the epidural space, have been used as a complement to conservative non-operative therapy for the treatment of lumbar radicular pain. The method of delivering the epidural steroids and the technique used are part of a wider debate about their efficacy and safety. Interlaminar epidural steroid injections (ILESI) failed to show in several studies the superiority to normal saline injections.[ 10, 11 ] Caudal epidural steroid injections were employed as a safe alternative for patients with radicular symptoms, especially for patients who underwent spine surgery and have extensive scar tissue and hardware in the lumbar region. Some of the studies failed to show superiority of steroid injectate as compared to local anesthetic alone.[ 12 ] Of note, the flaws in study designs and the limited reproducibility in similar studies preclude us to generalize the aforementioned results. Some studies showed the superiority of lumbar TFESI compared to lumbar interlaminal ESI with respect to pain relief.[ 13 ] Other studies showed no significant increased benefit of transforaminal epidural steroid injections versus transforaminal epidural injection of local anesthetic alone for radicular pain.[ 14–16 ] To assess their efficacy, however, these studies reported mean values of scores for pain and other outcomes and compared them. When evaluated using mean values of a group response, treatments emerge as significantly more effective only if all patients consistently benefit to some degree, or if a substantial majority of patients benefit to at least a moderate degree.[ 17 ] Group data can hide good responses when they occur in a subgroup of patients, however. Furthermore, the less good outcomes of the other patients statistically cancel the good responders of the subgroup.[ 17 ] Of note, in a seminal series of articles, Riew, et al, demonstrated the possible sparing-surgery effect and its maintance of efficacy at five years after transforaminal epidural steroid injections.[ 18 , 19 ] More recently, Ghahreman, et al., demonstrated the uncontested efficacy of lumbar TFESI in patients with radicular lower limb pain.[ 17 ] Transforaminal injection of steroids was compared with transforaminal injection of local anesthetic, to test for a local anesthetic effect; with transforaminal injection of normal saline, to test for an irrigation effect; with intramuscular injection of steroids, to test for a systemic effect; and with intramuscular injection of normal saline, to test for nonspecific (placebo) effects of an elaborate injection. 107 The rationale for transforaminal injections is that the medication is injected in a periradicular fashion, in the anterior aspect of the spinal canal where the nerve root resides, so the medication will cover better the nerve root and the perineural tissue. In theory, the medication is delivered close to the site of nerve-related mechanical and inflammatory irritation which is often in the anterior aspect of the spinal canal. Indications Transforaminal injection of steroids (LTFESI) is effective only in a proportion of patients. Its superiority over other injections is obscured when group data are compared but emerges when categorical outcomes are calculated.[ 17 ] Over time, it appears that the proportion of patients maintaining the benefit of steroid injections diminishes. In essence, transforaminal injection of steroids is a viable alternative to surgery for lumbar radicular pain due to disc herniation. Its immediate yield is substantial, and is not simply a placebo effect. For long- term efficacy, proof beyond reasonable doubt would require very large studies.[ 17 ] Generally speaking, there is no role of a series of LTFESI unless the patient received some benefit with the first intervention, Interventional Pain Medicine assuming the correct level was selected based on clinical and imaging parameters. For patients who received some benefit from the initial injection, the possibility that a second, “booster” injection might increase the yield of positive results. The studies with somewhat negative results all used only one injection,[ 14–16 , 20 ] whereas those with better results used up to three injections, with an average of about two.[ 18 , 19 , 21–23 ] The evidence for LTFESI for axial low back pain is very limited and not supported by scientifically designed studies. The interventionalist and the patient should be well aware about the potential catastrophic scenarios that a spinal injection, particularly a LTFESI can lead to.[ 24 , 25 ] There are numerous reports in the literature regarding reported complications.[ 26 , 27 ] Of note, those might be just a fraction of the real number since some of the events are never reported to a medical journal. Even though the incidence of complications in lumbar TFESI is generally very low, careful preparation and execution of the injection must be employed every single time. Contraindications Absolute: a) Patient is unwilling to consent to the procedure b) True allergy to the local anesthetic, corticosteroid or contrast agent c) Bleeding diathesis: anticoagulant medications, bleeding disorder d) Pregnancy (due to teratogenic effect due to radiation) e) Bacterial or viral infection (localized at the site of injection or generalized). For example, for patient with zoster active infection the practitioner should wait for the lesions to heal and get clearance from a dermatologist that the lesions are no longer infectious. Relative: a) Remote questionable allergy to different components of the injectate. For patients with allergy to IV contrast, the practitioner should consider using an alternative contrast dye (if patient is allergic to IV Omipaque, one could consider using Gadolinium solution to conﬁ rm the epidural spread). b) NSAIDs, aspirin, or other antiplatelet agens c) Hyperglicemia, adrenal disorder, congestive heart failure, severe immune compromise Equipment and preparation Scrub hat, mask, sterile gloves Betadine or chlorhexidine for sterile skin preparation Sterile plastic drape or towels 108 Fluoroscope C-arm (better if has digital substraction capabilities) Skin marker and connection tubing 27-gauge 1.5-inch needle (skin anesthesia) 22-gauge 3.5-, 5- or 7-inch spinal needle (based on patient’s body habitus) Medications 1 percent lidocaine for skin anesthesia, 0.25–0.5 percent bupivacaine (for mixture with steroid) Corticosteroid: Dexamethasone (non-particulate steroid— author’s preference), Bethametasone (Celestone 6–12 mg), triamcinolone hexacetonide Radiographic contrast medium (Isovue, Omnipaque or Gadolinium) Resuscitation equipment and medications immediately available Technique

3.2: Lumbar Transforaminal Epidural Lumbar transforaminal epidural steroid injections should only be performed using fluoroscopic guidance and contrast dye to assess for needle placement and epidural/perinerve contrast spread as well as to rule out any vascular uptake under live fluoroscopy. The purpose of the LTFESI is to inject the mix of steroid and local anesthetic around the spinal nerve root and in the anterior aspect of the epidural space. Generally, there are two approaches used for a LTFESI: AP technique and oblique technique. The most commonly used is the oblique technique, described here. The patient is placed in a prone position on the fluoroscopic table. The vertebral level is identified counting down from T12 level (identified as rib-bearing), then the ipsilateral pedicle of the corresponding vertebral body is identified. The fluoroscope (with the image intensifier above the patient) is rotated in an ipsilateral oblique fashion 25–35 degrees for a better visualization of the subpedicular space. The apex of the superior articular process (SAP) of the inferior vertebra should be under the pedicle when there is enough obliquity of the image. The target for the needle tip is superior, lateral and anterior aspect of the neuroforamen. A slight cephalad-caudad tilt (image intensifier caudad) can be employed to maximize the fluoroscopic anatomy opening of the neuroforamen. The needle is inserted and advanced under intermittent fluoroscopic guidance toward the aforementioned target. The final advancement should be made under lateral and AP view. The needle should never pass the six o’clock position beneath the vertebral pedicle in the AP view (danger view) or the dura can be penetrated accidentally. The operator should gently aspirate for blood or CSF return after final needle positioning. Then 0.5–0.75cc of contrast dye is injected under AP live fluoroscopy and a careful assessment for intravascular or subdural uptake is performed. Using digital subtraction technique (although rare in real clinical practice) helps in differentiating difficult-to-interpret imaging. After obtaining a satisfactory epidurogram/nervogram, the injectate solution is injected slowly. Using non-particulate steroids might be warranted for higher upper lumbar segments where the radicular area can enter the spinal cord through one of the neuroforaminae. The S-1 transforaminal injection is performed in a similar manner, identifying the S-1 foramen under AP view. The fluoroscope can be slightly rotated 5 to 10 degrees in an ipsilateral fashion with a slight cranio-caudal tilt. The spinal needle is inserted under intermittent fluoroscopy into the S-1 neuroforamen. The final advancements should be made under lateral and AP view. In a similar manner with LTFESI, after negative aspiration for blood or CSF, a total of 0.5–0.75cc of contrast dye is injected under live fluoroscopy under AP visualization to assess for vascular uptake and epidural/periradicular contrast spread. After negative vascular uptake and satisfactory contrast dye pattern, the steroid mix is injected slowly. Complications Transforaminal injections are potentially the most hazardous of all spinal diagnostic and treatment procedures. There are several reasons: the needle is placed close to the nerve root sleeves of the dural 109 sac and can potentially pierce the nerve itself; the needle may engage a reinforcing radicular artery in its traject; the needle can penetrate the dural sac and the injection can potentially be delivered intrathecally instead; the needle can damage a vein and in a patient with coagulation problems can generate a spinal hematoma. The complications associated with LTFESI can range from increased pain at the injection site and increased discomfort in a radicular pattern after injection to the more catastrophic events like spinal cord ischemia and paraplegia. The latter are more often associated with injection of the steroid mix into a radicular artery resulting in severe vasospasm and/or occlusion. Some of the complications associated with Lumbar transforaminal epidural injections are well known secondary to reports in the medical literature, and some are potential complications associated with any procedure but not necessarily reported in association with LTFESI. Some of the more common complications are infection, bleeding, allergic reaction, or worsening of back or leg pain post procedure. Infection is a complication associated with any invasive procedure. It is estimated that 13 percent of complications associated with any spinal procedure are infections.[ 28 ] Reports of epidural abscess after transforaminal epidural steroid injection have occurred.[ 29 ] Interventional Pain Medicine Minor complications occur in about 9 percent of lumbar transforaminal injections.[ 25 ] In descending rank order of prevalence, these include transient headaches (3 percent), increased back pain (2 percent), facial flushing (1 percent), increased leg pain (0.6 percent), and vasovagal reaction with dizziness and light-headedness post procedure(0.3 percent).[ 30 ] Major complications involve the radicular artery known as the artery of Adamkiewicz. Although this artery typically arises at the lower thoracic levels, it can arise as low as L-2 in about 1 percent of people, and more rarely at even lower levels.[ 31 ] In those people, it is a hazard while performing lumbar transforaminal epidural injections. There have been several reports of complications potentially involving this vessel. Unfortunately, there is no way in predicting which patients have the anatomic variant. One report described three patients (in two cases the injections were performed at L3-4, the third the injection was at S1 TFESI) who developed paraplegia after transforaminal injections.[ 32 ] In all cases, MRI demonstrated increased signal intensity of the thoracic spinal cord. Another case reported T12 paraplegia, which resulted after a CT-guided LTFESI at L2-3 level without use of contrast dye.[ 33 ] Another report involved an L4-5 transforaminal epidural steroid injection of hydrocortisone with immediate onset of T12 paraplegia, but without subsequent MRI changes, despite clinical picture of paraplegia.[ 34 ] A spinal cord infarction, consistent with a vascular injury, was reported after a T12-L1 transforaminal injection.[ 27 ] In this specific case, apparently, the injections were performed under lateral fluoroscopic imaging and with the needle at the upper end of the screen. Both factors limit the ability of the interventionalist to ideally visualize an artery passing medially and upward to the spinal cord and identify radicular flow. More recently, another two cases of paraplegia following Lumbar TFESI were reported: one after a fluoroscopically guided, left L3-L4, transforaminal injection of betamethasone (Celestone Soluspan) and the other after a CT-guided, right L3-L4, transforaminal injection of methylprednisolone (DepoMedrol).[ 24 ] Both patients developed bilateral lower extremity paralysis, with neurogenic bowel and bladder, immediately after the procedures. MRI scans were consistent with spinal cord infarction. There was no evidence of intraspinal mass or hematoma.[ 24 ] Several cases of paraplegia following lumbar transforaminal injection of particulate steroids are known to some experts in the field but remained sub judice.[ 30 ] A potential complication is unique to sacral transforaminal injections. The needle can be advanced too far through the anterior foramen and into the pelvis, with the risk of penetration of pelvic viscera, large or small bowel, and the subsequent potential complications arising from it. Sometimes the LTFESI have been complicated by intrathecal injections. Local anesthetic may produce protracted and unwanted anesthesia, and hypotension. Corticosteroid preparations could precipitate arachnoiditis and its sequelae. Such complications can be avoided if subdural or intrathecal injection is recognized during live fluoroscopy time during the administration of the test dose of contrast medium venous puncture can result in epidural or spinal hematoma. 110 Using International Spine Injection Society (ISIS) guidelines along with treating each and every intervention with the outmost respect will reduce the unwanted complications to a minimum. We advise that knowing the fluoroscopic anatomy and the “danger views” and potential complications are prerequisites before any needle insertion. Ideal views of the target region should be obtained before inserting needles. Needles should be placed accurately onto target points in the ideal manner and should not be allowed to enter into hazardous areas. The intelligent use of real-time fluoroscopy while injecting contrast dye can uncover dangerous patterns. These patterns should be immediately identified, recognized, and interpreted by the interventionalist. As one of the foremost leaders in the field recognized, “Abandoning a procedure that has become compromised should not be viewed as an indictment of skill. Procedures are abandoned in the interests of the patient. Rescheduling is only an inconvenience. A complication can be a catastrophe.”[ 30 ] Summary Lumbar transforaminal injection of steroids is a viable alternative to surgery for lumbar radicular pain due 3.2: Lumbar Transforaminal Epidural to disc herniation and nerve irritation. Precise patient selection, applying an algorithmic approach and performing judicious interventional spine injections may certainly improve clinical outcomes.

Figure 3.2.1 Left L4-L5 transforaminal epidural injection, AP view.

Figure 3.2.2 Right S-1 transforaminal epidural injection, lateral view. 111

A B

Figure 3.2.3 A and B Right L-4 transforaminal epidural injection, AP view. Interventional Pain Medicine

AB Figure 3.2.4 A and B S-1 transforaminal epidural injection. A: right, B: left.

References 1. Durning RP , Murphy ML. Lumbar disk disease. Clinical presentation, diagnosis, and treatment . Postgrad Med ., 1986 ; 79 ( 5 ): 54 – 74 . 2. McCarron RF , et al ., The infl ammatory effect of nucleus pulposus: a possible element in the pathogenesis of low-back pain . Spine . 1987 : 12 ( 8 ): 760 – 764 . 3. Olmarker K , Rydevik B , Nordborg C . Autologous nucleus pulposus induces neurophysiologic and histologic changes in porcine cauda equina nerve roots . Spine . 1993 ; 18 ( 11 ): 1425 – 1432 . 4. Omarker K, Myers RR . Pathogenesis of sciatic pain: role of herniated nucleus pulposus and deformation of spinal nerve root and dorsal root ganglion . Pain . 1998 ; 78 ( 2 ): 99 – 105 . 5. Murata Y , et al . The role of tumor necrosis factor-alpha in apoptosis of dorsal root ganglion cells induced by herniated nucleus pulposus in rats . Spine . 2008 ; 33 ( 2 ): 155 – 162 . 6. Byrod G , et al ., Early effects of nucleus pulposus application on spinal nerve root morphology and function . Eur Spine J . 1998 ; 7 ( 6 ): 445 – 449 . 7. Brisby H , et al ., Proinfl ammatory cytokines in cerebrospinal fl uid and serum in patients with disc herniation and sciatica . Eur Spine J . 2002 ; 11 ( 1 ) 62 – 66 . 112 8. Murata Y , et al . Nucleus pulposus-induced apoptosis in dorsal root ganglion following experimental disc herniation in rats . Spine . 2006 ; 31 ( 4 ): 382 – 390 . 9. Kobayashi S , et al . Effect of mechanical compression on the lumbar nerve root: localization and changes of intraradicular infl ammatory cytokines, nitric oxide, and cyclooxygenase . Spine . 2005 ; 30 ( 15 ): 1699 – 1705 . 10. Carette S , et al . Epidural corticosteroid injections for sciatica due to herniated nucleus pulposus . N Engl J Med . 1997 ; 336 ( 23 ): 1634 – 1640 . 11. Valat , J.P. , et al . Epidural corticosteroid injections for sciatica: a randomized, double-blind, controlled clinical trial . Ann Rheum Dis . 2003 ; 62 ( 7 ): 639 – 643 . 12. Bush K, Hillier S . A controlled study of caudal epidural injections of triamcinolone plus procaine for the management of intractable sciatica . Spine . 1991 ; 16 ( 5 ): 572 – 575 . 13. Thomas E ., et al. Effi cacy of transforaminal versus interspinous corticosteroid injectionin discal radiculalgia— a prospective, randomized, double-blind study . Clin Rheumatol . 2003 ; 22 ( 4–5 ): 299 – 304 . 14. Karppinen J , et al , Periradicular infi ltration for sciatica: a randomized controlled trial . Spine . 2001 ; 26 ( 9 ): 1059 – 1067 . 15. Ng L , Chaudhary N , Sell P. The effi cacy of corticosteroids in periradicular infi ltration for chronic radicular pain: a randomized, double-blind, controlled trial . Spine . 2005 ; 30 ( 8): 857 – 862 . 16. Tafazal S , et al . Corticosteroids in periradicular infi ltration for radicular pain: a randomized, double-blind, 3.2: Lumbar Transforaminal Epidural controlled trial. One-year results and subgroup analysis . Eur Spine J . 2009 ; 18 ( 8 ): 1220 – 1225 . 17. Ghahreman A , Ferch R , Bogduk N.The effi cacy of transforaminal injection of steroids for the treatment of lumbar radicular pain . Pain Med . 2010 . 11 ( 8 ): 1149 – 1168 . 18. Riew KD , et al . The effect of nerve-root injections on the need for operative treatment of lumbar radicular pain. A prospective, randomized, controlled, double-blind study . J Bone Joint Surg Am . 2000 ; 82 -A( 11 ): 1589 – 1593 . 19. Riew KD , et al. Nerve root blocks in the treatment of lumbar radicular pain. A minimum fi ve-year follow-up . J Bone Joint Surg Am . 2006 ; 88 ( 8 ): 1722 – 1725 . 20. Karppinen J , et al. Cost effectiveness of periradicular infi ltration for sciatica: subgroup analysis of a randomized controlled trial . Spine . 2001 ; 26 ( 23 ): 2587 – 2595 . 21. Lutz GE , Vad VB , Wisneski RJ. Fluoroscopic transforaminal lumbar epidural steroids: an outcome study . Arch Phys Med Rehabil . 1998 ; 79 ( 11 ): 1362 – 1366 . 22. Cooper G , et al . Effectiveness of transforaminal epidural steroid injections in patients with degenerative lumbar scoliotic stenosis and radiculopathy . Pain Physician . 2004 ; 7 ( 3 ): 311 – 317 . 23. Vad , VB , et al . Transforaminal epidural steroid injections in lumbosacral radiculopathy: a prospective randomized study. Spine . 2002 ; 27 ( 1 ): 11 – 16 . 24. Kennedy DJ , et al . Paraplegia following image-guided transforaminal lumbar spine epidural steroid injection: two case reports . Pain Med . 2009 ; 10 ( 8 ): 1389 – 1394 . 25. Botwin KP , et al . Complications of fl uoroscopically guided transforaminal lumbar epidural injections . Arch Phys Med Rehabil . 2000 ; 81 ( 8 ): 1045 – 1050 . 26. Glaser SE, Shah RV. Root-cause analysis of paraplegia following transforaminal epidural steroid injections: the “unsafe” triangle . Pain Physician . 2010 . 13 ( 3 ): 237 – 244 . 27. Glaser SE, Falco F. Paraplegia following a thoracolumbar transforaminal epidural steroid injection . Pain Physician . 2005 ; 8 ( 3 ): 309 – 314 . 28. Fitzgibbon DR , et al . Chronic pain management: American Society of Anesthesiologists closed claims project . Anesthesiology . 2004 ; 100 ( 1 ): 98 – 105 . 29. Kabbara A , Rosenberg SK , Untal C Methicillin-resistant staphylococcus aureus epidural abscess after transforaminal epidural steroid injection . Pain Physician . 2004 ; 7 ( 2 ): 269 – 272 . 30. Bogduk N , et al . Complications of spinal diagnostic and treatment procedures . Pain Medicine . 2008 ; 9 (S 1 ): S11 – S34 . 31. Lo D , et al . Unusual origin of the artery of Adamkiewicz from the fourth lumbar artery. Neuroradiology . 2002 ; 44 ( 2 ): 153 – 157 . 32. Houten , JK, Errico TJ .Paraplegia after lumbosacral nerve root block: report of three cases . Spine . , 2002 ; 2 ( 1 ): 70 – 75 . 33. Somayaji, HS , et al . Spinal cord infarction following therapeutic computed tomography-guided left L-2 nerve root injection . Spine . 2005 ; 30 ( 4 ): E106 – 108 . 34. Quintero N , et al . [Transforaminal epidural steroid injection and paraplegia: case report and bibliographic review] . Ann Readapt Med Phys . 2006 ; 49 ( 5 ): 242 – 247 . 113

Chapter 3.3 Medial Branch Blocks

Benjamin Duckles and Peter K. Yi

Introduction 114 Indications 115 Contraindications 115 Functional Anatomy 116 Equipment and Preparation 116 Medications 117 Techniques 117 Lumbar Medial Branch Block (MBB) 117 Radiofrequency Ablation of Medial Branch Nerve 117 Intra-Articular Facet Injection (Lumbar) 118 Complications 119 Summary 119 Clinical Pearls 119 References 119 114 Introduction The facet joints (zygapophysial joints) of the spine serve important structural and functional capacities. Their orientation allows them to both guide extension and prevent excessive axial rotation of the vertebral column. As a consequence of the aging process, the burden of axial weight bearing is shifted from the degenerating intervertebral discs to the facet joints themselves. This can increase the shear forces placed on the facet joints, subjecting them to the same degenerative changes that define arthritis seen in larger joints: synovitis, articular cartilage wear, and osteophyte formation. Typically the patient describes gradual onset of dull, achy axial pain that may radiate to surrounding areas. The referral patterns for cervical and lumbar facet joint pain are predictable but nonspecific (Figures 3.3.1 and 3.3.2 ). Performing coupled maneuvers (ipsilateral lateral bending, rotation, and extension) on exam can provoke facet joint pain. If the history and/or physical exam elicit a neurologic deficit or a radiculopathy, imaging should be obtained to investigate the possibility of a disc protrusion compressing neural structures. Despite the recognition that facet joint dysfunction is a common cause of axial low back pain, there is 3.3: Medial Branch Blocks controversy regarding the efficacy of interventional procedures targeting the facet joint. This is mostly due to a lack of large, prospective randomized trials evaluating these interventions. In one recent study of 60 patients with chronic low back pain due to facet joint dysfunction, 85 percent of patients reported less

C2–3

C3–4 C4–5 C5–6 C6–7

C2/3, C3 C2/3, C3/4, C3 C3/4, C4/5, C4 C4/5, C5/6, C4, C5 C6/7, C6, C7 C4/5, C5/6, C4 C0/1, C1/2, C2/3

C7/Th1, C7

B Figure 3.3.1 A) A composite map of the results in all volunteers, depicting the characteristic distribution of pain from zygapophyseal joints at segments C2-3 to C-67. B) Main referred pain distributions for the zygapophyseal joints from C0-1 to C7-T1 and the dorsal rami C3-7. This was ﬁ gure published in Benzon H, Rathmell JP, Wu CL, Turk DC, and Argoff CE. Raj’s Practical Management of Pain, 4th edition . Copyright Elsevier 2008. 115

1 6 2 3

4 5

B Interventional Pain Medicine

A Normal Abnormal Figure 3.3.2 A) Pain referral patterns produced by intra-articular injections of hypertonic saline in asymptomatic (normal) and symptomatic (abnormal) patients. The more darkly shaded areas show the most common referral detected, and the lighter shades indicate the less common patterns. B) Referred pain distribution: 1, lumbar spinal region; 2, gluteal region; 3, trochanter region; 4, lateral thigh region; 5, posterior thigh region; 6, groin region. This was ﬁ gure published in Benzon H, Rathmell JP, Wu CL, Turk DC, and Argoff CE. Raj’s Practical Management of Pain, 4th edition . Copyright Elsevier 2008.

than 50 percent pain relief at 12 months and 78 percent of patients had significant functional improvement following a series of medial branch blocks with local anesthetic and steroid. Similar results were observed in the comparison group given medial branch blocks with local anesthetic alone. Several randomized trials have shown significant improvement in pain scores in individuals with chronic low back pain following radiofrequency neurotomy of medial branch nerves. Indications An intra-articular facet joint injection or medial branch block is indicated when it is believed that a patient’s pain is being generated by pathology at the facet joint. Intra-articular injections are most often performed for acute onset of pain where a single facet joint is known to be the pain generator. After a successful diagnostic medial branch block (less than 50 percent reduction in pain for duration of local anesthetic used), longer periods of relief may be gained by radiofrequency ablation of the medial branch nerve. Contraindications As with any invasive procedure, this block should not be performed on an individual who is anticoagulated. Particularly for cervical medial branch blocks, fasting guidelines should be observed due to the potential complication of intravascular or intrathecal injection, which could compromise the airway. 116 Functional Anatomy The zygapophysial joint is located at the posterolateral aspect of the vertebrae and is comprised of the inferior articular process and the superior articular process of adjacent vertebrae. In the lumbar spine, this joint forms the posterior aspect of the neural foramen. The joint is a true joint in that it contains a synovial lining and the articular surfaces are cartilaginous. The innervation of the facet joint is from the medial branch of the posterior ramus of the spinal nerve root from the segment above and at the level the joint itself. For example, the L4-L5 facet joint receives innervation from the medial branch of L4 and L5 nerve root. (Figure 3.3.3 ) Equipment and Preparation - Scrub hat, mask, sterile gloves - Betadine or chlorhexidine skin preparation - Sterile plastic drape or towels 3.3: Medial Branch Blocks - 25-gauge 2-inch needle (skin anesthesia) - 25-gauge 3.5-inch spinal needle (one needle for each medial branch nerve to be blocked) - 1 percent lidocaine - 0.5 percent bupivacaine (for diagnostic medial branch block) - 80 mg Depo-medrol (for intra-articular facet injections, to be divided among all joints to be injected) - Fluoroscope C-arm - Resuscitation equipment immediately available

mb a p d

Figure 3.3.3 A (top): This oblique drawing of the lumbar spine shows the course of the medial branch. (a): the presence of the mammilla-accessory ligament; (mb): the trajectory of the medial branch under this structure. The “eye” (c) is marked with a black dot, which is the target for the needle for facet block and neurolysis. After the medial branch crosses under the mammilla-accessory ligament (a), it divides into distal (d) and proximal (p) zygapophyseal branches. B (bottom): Anteroposterior drawing of the lumbar spine showing the course of the medial branches in the lumbar region from L1-2 and from L5 -S1. The trajectory of the medial branch of L5 can also be appreciated as it crosses along the groove between the ala of the sacrum and the base of the superior articular process, which should be the target for block or denervation at this level. This was ﬁ gure published in Benzon H, Rathmell JP, Wu CL, Turk DC, and Argoff CE. Raj’s Practical Management of Pain, 4th edition . Copyright Elsevier 2008. 117 Medications - 1 percent lidocaine is used to anesthetize skin and subcutaneous tissue overlying the intended path of the spinal needle. - For diagnostic medial branch blocks, 0.5 percent bupivacaine is injected through the spinal needle once it is in proper position. - For intra-articular facet joint injection, 80 mg methlprednisolone acetate is divided among all joints to be injected. A 1:1 mixture of steroid and 0.5 percent bupivacaine may be used to provide immediate pain relief via local anesthetic. Techniques Lumbar Medial Branch Block (MBB) The patient is placed prone on the fluoroscopy table and the lumbar region is prepped and draped in a sterile fashion (Figure 3.3.4 ). The C-arm is positioned over the lumbar region and rotated in the oblique plane approximately 25 to 35 degrees to allow visualization of the facet joints and the junction Interventional Pain Medicine between the transverse process and the superior articular process. The skin and subcutaneous tissue are anesthetized with 1–2 ml 1 percent lidocaine. A 22-gauge, 3.5-inch spinal needle is advanced coaxially with the fluoroscope beam until the needle tip contacts bone at the junction between the base of the transverse process and the superior articular process of the intended targets (Figures 3.3.5 and 3.3.6 ). A small amount of local anesthetic (0.5 ml of 2 percent lidocaine or 0.5 percent bupivacaine) is injected through each needle. Since this is primarily a diagnostic procedure, the patient is instructed to evaluate the degree of pain relief in the hours following the injection. Radiofrequency Ablation of Medial Branch Nerve The positioning and technique is similar to that of diagnostic MBB, however with RFA it is important to angle the C-arm approximately 25 to 35 degrees caudal to the axial plane so that the active portion of the needle tip will lie parallel to the medial branch nerve as it traverses the groove between the transverse process and superior articular process.

Figure 3.3.4 Position for intra-articular lumbar facet joint injection. The patient is placed prone with the head turned to one side. The C-arm is angled 25 to 35 degrees from the sagittal plane parallel to the axial plane. 118 3.3: Medial Branch Blocks

Figure 3.3.5 An oblique view of the needles in place for a medial branch block at the lumbar levels. The needles are positioned at the “eye of the Scottie dog.”

Intra-Articular Facet Injection (Lumbar) The patient is placed prone on fluoroscopy table with head turned to one side and the lumbar region is prepped and draped in a sterile fashion. The C-arm is positioned over the lumbar region and is rotated in the oblique plane 25 to 35 degrees to allow visualization of the facet joints. The skin and subcutaneous tissue are anesthetized with 1–2 ml 1 percent lidocaine. A 22-gauge, 3.5-inch spinal needle is advanced coaxially with the fluoroscope beam until the needle tip engages in the joint space. Steroid + /- local anesthetic is then deposited in the joint, with each joint accommodating approximately 1.5 ml of injectate.

Figure 3.3.6 An AP view of the needles in place for a medial branch block. 119

Figure 3.3.7 Bilateral median branch blocks L3, L4 of lumbar spine. A. Left AP view B. Right AP view Interventional Pain Medicine

Complications The most common complaint following facet joint injections is exacerbation of pain symptoms, which is typically transient. Infection has been documented following facet joint injections, though it is rare. Summary Facet joint pathology is implicated in up to 50 percent of individuals who suffer from chronic axial low back pain. This is due to the age-related degeneration of the weight-bearing structures of the lumbar spine, which in turn places added stress on these joints. Injections of the facet joint or medial branch blocks should be considered in these individuals due to their low risk and potential great benefit in pain relief and improved function. Clinical Pearls Placement of the needle for medial branch blocks is often described as aiming for the “eye of the Scottie dog.” The “eye of the Scottie dog” is at the junction between the transverse process and pedicle (see Figure 3.3.5 ). Although at first this can be difficult to visualize, once the landmarks for the Scottie dog are recognized, it can be useful as a general guide to placing the needle. References 1. Benzon H , Rathmell JP , Wu CL , Turk DC , Argoff CE . Raj’s Practical Management of Pain . New York : Elsevier Mosby; 2008 . 2. Rathmell JP . Atlas of Image-guided Intervention in Regional Anesthesia and Pain Medicine . Baltimore, MD : Lippincott Williams & Wilkins; 2005. 3. Slipman CW, et al . A critical review of the evidence for the use of zygapophyseal injections and radiofrequency denervation in the treatment of low back pain . Spine . 2003 ; 3 : 310 – 316. 4. Manchikanti L, et al . Lumbar facet joint nerve blocks in managing chronic facet joint pain: one year follow-up of a randomized, double-blind controlled trial: clinical trial NCT00355914 . Pain Physician . 2008 ; 11 : 121 – 132. 5. Ackerman WE, et al . Pain relief with intra-articular or medial branch nerve blocks in patients with positive lumbar facet joint SPECT imaging: a 12-week outcome study . Southern Medical Journal . Sept 2008; 101:9. 6. Gallagher J, et al . Radiofrequency facet joint denervation in the treatment of low back pain: a prospective controlled double-blind study to assess its efﬁ cacy . Pain Clin . 1994 ; 7 : 193 – 198 . 7. Van Kleef M, et al . Randomized trial of radiofrequency lumbar facet joint denervation for chronic low back pain . Spine . 1999 ; 24 : 1937 – 1942. This page intentionally left blank 121

Chapter 3.4 Lumbar Radiofrequency Ablation

Chitra Ramasubbu and Anita Gupta

Introduction 122 Radiofrequency Lesion Generator System 122 Mechanism of Action 122 Continuous Versus Pulse Radiofrequency Ablation 122 Indications 123 Contraindications 124 Absolute Contraindications 124 Relative Contraindications 124 Functional Anatomy 124 Equipment and Preparation 124 Medications 125 Technique 125 Radiofrequency Ablation of the Lumbar Zygopophyseal Joint 125 Radiofrequency Ablation to the Dorsal Root Ganglion 126 Complications 126 Summary 126 Clinical Pearls 127 References 127 122 Introduction The annual incidence of low back pain is 18.6 percent[ 1 ] in the adult population, out of which 62 percent of the patients with low back pain still experience pain after 12 months.[ 2 ] There are very few interventions that provide long-term pain relief. Some causes of low back pain include herniated disks, spondylolisthesis, diskitis, and fractures. Major structures that cause low back pain include lumbar facet joints, intervertebral disks, and sacroiliac joints. In adults patients with low back pain, the prevalence of facet joint pain is 15–32 percent.[ 3 ] The diagnosis is confirmed by at least a 50 percent reduction in pain after a diagnostic local anesthetic nerve block of the dorsal ramus of the lumbar spine. The three nonsurgical ablative techniques that can potentially provide long-term pain relief are the use of neurolytic agents like alcohol, phenol, extreme cold (cryoanalgesia) and high temperature (radiofrequency ablation).[ 4 ] Radiofrequency is a complex process, which interferes with both the afferent action potential propagation as well as the efferent peripheral nerve functions. Shealy introduced a fluoroscopically guided radiofrequency technique for facet denervation in 1974.[ 5 ] Since 3.4: Lumbar Radiofrequency Ablation then, radiofrequency ablation has been used widely and its rate of success has improved. Reports of success rate have varied over a wide range from 17 percent to 83 percent. [ 6 , 7 ] Radiofrequency treatment of low back pain is most frequently used and most often described. [ 16 ] Radiofrequency Lesion Generator System A modern RF-lesion generator has the following functions:[ 14 ] - Continuous online impedance measurement - A nerve stimulator - Monitoring of voltage, current during RF procedure - Temperature monitoring - Pulsed current delivery mode Mechanism of Action Radiofrequency ablation works on the concept of differential selection even though definite evidence is lacking.[ 8 ] It stops the nociceptive Aδ and C fibers input to the central nervous system without a destructive effect on the motor or sensory fibers. The RF electrode tip produces heat up to a temperature of 47 °C secondary to a radio-wave frequency. Frequently, a lesion is formed if the temperature within the neuronal tissue exceeds 47° C. Several factors influence the success of RFA and include the duration of the RF application, current intensity and length of the electrode.[ 4 ] The lesion initially demonstates acute inflammatory changes followed by cell necrosis with fibrosis and collagen fiber deposition. This process takes approximately three weeks to complete. Most important, the basal lamina of the Schwann cells are preserved after RFA, allowing future regeneration.[ 9 ] Continuous Versus Pulse Radiofrequency Ablation In the continuous form, the generator establishes a voltage gradient between the electrode and the ground plate. The body tissues complete the circuit and RF current flows through the tissue, resulting in an alternating electric field.[ 14 ] The electric field causes ionic movement in the tissue, resulting in tissue heating. The tip temperature determines the size of the lesion. Heat is removed from the lesion by conductive heat loss and blood circulation. Hence blood vessels close to the dorsal root ganglion may have considerable heat washout compared to bone.[ 15 ] Pulsed radiofrequency (PRF)) is based on the dual effect of exposure of the tissue to RF fields.[ 14 ] Along with the thermal effect, there is a non-thermal effect that can modify neuronal structures. This has a mild ablative effect affecting the thin nerve fibers. 123 Interventional Pain Medicine

Figure 3.4.1 Radiofrequency monitor.

Indications - Other causes of back pain including malignancy, infection, vascular disease are ruled out - Identification of the painful joint and localizing the nerve supply to the targeted joints using diagnostic blocks - Appropriate relief at the site of pain after diagnostic local anesthetic block - FR neurotomy is an effective but temporary management of lumbar facet pain - Discogenic pain can be treated by heating the annulus fibrosis - Patient population should be carefully selected paying attention to somatic and psychosocial factors

AB Figure 3.4.2A and B Electrodes with cables 124 Contraindications Absolute Contraindications - Bleeding diasthesis - Systemic infection or local infection at the site - Patients with no response to diagnostic blocks - Pregnancy Relative Contraindications - Surgical/congenital changes to the spine - Anticoagulated patients - Defibrillator, pacemaker Functional Anatomy 3.4: Lumbar Radiofrequency Ablation The potential pain generators of the lumbar spine include the annulus, the posterior longitudinal ligament, portions of the dural lining, face joints, the spinal nerve roots, dorsal root ganglia, the sacroiliac joint, ligaments, and its associated musculature.[ 10 ] RF techniques can be used to treat pain arising from facet joints, nerve roots, annulus fibrosis, and sacroiliac joints. Since the lumbar facet joints receive innervations from multiple levels, two levels must be lesioned to properly denervate the site.[ 7 ] Equipment and Preparation - Scrub hat, mask, and sterile gloves - Betadine or chlorhexidine skin preparation - Sterile plastic drape or towels - 25-gauge 2-inch needle (skin anesthesia)

Figure 3.4.3 Radiofrequency ablation of the facet joint. 125 - 25-gauge 3.5-inch spinal needle - Syringes for local anesthetic injection - Low volume extension tubing - C-arm fluoroscopy - Radiofrequency generator - Radiofrequency cannula and matching thermocouple— a 10–15-cm cannula with a 10-mm exposed tip - Grounding pad - Monitoring devices including EKG, pulse oximetry, and blood pressure - Resuscitation equipment immediately available Medications - 2 percent lidocaine to anesthetize skin Interventional Pain Medicine - 0.5 percent bupivacaine injected through the spinal needle once in proper position. - Contrast dye Technique Radiofrequency Ablation of the Lumbar Zygopophyseal Joint Patient is in prone position on the fluoroscopic table. Physiological lumbar lordosis is reduced by placing a pillow under the abdomen. An initial AP projection is obtained. Care is taken to make sure no double contours of the caudal end plate of the middle vertebra are present. This is done by rotating cranially or caudally. The levels of vertebra that are to be treated are used as a reference point. The C-arm is angled at approximately 15° oblique view until the spinous processes are projecting over the midline but well inside the contralateral facet joint. The junction of the superior articular process and the transverse process is marked as the target point. A diagnostic block is initially performed by injecting 1 percent lidocaine into the skin. Needle is inserted 1 mm under the target junction to avoid unwanted spreading of the local anesthetic to the segmental nerves, which can cause false positives. Position is checked in lateral view and should be at the level of the inferior part of the intervertebral foremen in line with the facet joint. After a negative aspiration, 1 ml of local anesthetic is injected when accurate position is confirmed. Radiofrequency lesioning of the medial branch is performed by initially making bone contact with the needle tip. After contact, the needle is redirected cephalad until bone contact is lost. The needle is advanced 1–2 mm farther anteriorly over the superior margin of the transverse process. Lateral view of C-arm should show the needle tip in line with the facet line column and at the level of the inferior part of the intervertebral foramina and about 1 mm dorsal to the level of the line connecting posterior aspects of the intervertebral foramina. It should be slightly deeper and more cranial than the needle position for a diagnostic block. Once positioning is confirmed, 50 Hz stimulated is conducted. The patient should feel pressure or tingling in the back at less than 0.5 volt. If the sensations are felt in the ipsilateral extremity, the needle is close to the segmental nerve and should be withdrawn slightly. Subsequent stimulation at 2 Hz is then performed. The patient should experience localized contractions of the multifidus muscles but not muscles of the leg. After proper needle positioning and negative aspiration test, 1 ml of local anesthetic is injected following by RF lesioning at 67° for 60 seconds. The L5-S1 facet joint has different anatomy than the other lumbar levels. The L5 median branch lies at the junction between the superior sacral articular process and the upper border of the sacrum. The C-arm is rotated at a 15° oblique angle with the target point being the round curved transition. In lateral view, the tip must project over the posterior border of the facet column. 126 Radiofrequency Ablation to the Dorsal Root Ganglion Percutaneous radio frequency ablation of the dorsal root ganglion was developed as an alternative to surgical rhizotomy for refractory pain. The goal is to create a minimal lesion near the dorsal root ganglion for treating nerve root pain without causing sensory and motor deficits. A 10 cm electrode is placed in the dorsal cranial quadrant of the intervertebral foramen in the lateral view. The 22-gauge, 5-mm active tip electrode is placed between one-third and approximately halfway across the midfacetal column in the AP projection. Sensory and motor stimulation is applied at 50 Hz and 2 Hz. The electrode position is adjusted to reach a sensory stimulation threshold between 0.5 and 1 volt. Motor stimulation threshold is required to be at least 1.5 times the sensory threshold. The electrode position is confirmed by injecting radiopaque dye to visualize the nerve ganglion. Local anesthetic is then injected, and RF ablation is performed at 65–67° C for 90 seconds. Complications

3.4: Lumbar Radiofrequency Ablation Transient numbness of the ipsilateral extremity may occur because of overflow of local anesthetic into the intervertebral foremen. One of the common complaints is exacerbation of pain symptoms, which appear to be transient. There was a 1 percent incidence of minor complication per lesion site in a retrospective analysis on the incidence of complications related to radiofrequency ablations. Of the 616 RF ablations, three had localized pain lasting greater than two weeks; three had neuritic pain lasting less than two weeks. There were no cases of infection, new motor deficits, or new sensory deficits.[ 11 ] Summary There has been a remarkable evolution in radiofrequency treatments for chronic pain syndromes. When performed in well-selected patients who suffer pain refractory to conventional methods, the degree of pain relief can be higher than with conventional treatment. A systemic review of six randomized controlled trials studying the efficacy of radiofrequency procedures for the treatment of spinal pain showed that there was moderate evidence that RF lumbar facet denervation was more effective for chronic low back pain

Figure 3.4.4 RFA of lumbar zygopophyseal joint. This ﬁ gure was published in Van Kleef M, Sluijter M, Van Zundert J. Radiofrequency Treatment. Raj’s Practical Management of Pain, 4th edition, Edited by Benson . Philadelphia PA: Mosby Elsevier; 2008. 127 Interventional Pain Medicine

Figure 3.4.5 RFA of the DRG. This ﬁ gure was published in Van Kleef M, Sluijter M, Van Zundert J. Radiofrequency Treatment. Raj’s Practical Management of Pain, 4th edition, Edited by Benson . Philadelphia PA: Mosby Elsevier; 2008.

than placebo.[ 12 ] The Cochrane review included six studies of 275 randomized patients, which concluded that radiofrequency denervation offered short-term relief for chronic neck pain. The evidence was conflicting, however, on the short-term effect of radiofrequency lesioning in chronic low back pain of zygapophyseal joint origin and limited evidence that intradiscal radiofrequency thermocoagulation was not effective for chronic discogenic low back pain.[ 13 ] In conclusion, the application of RF in the management of chronic pain may be a useful tool in patients where conservative treatment failed as long as the appropriate population is targeted and is safely done by a well-trained physician. Clinical Pearls A RF lesion generator has many functions to enhance the generation of the lesion. Recording of voltage, current power, temperature, time and electrode type for each lesion should be noted. The temperature meter should read body temperature at about 37° C to ensure it is functioning properly.[ 7 ] Insulation on the electrode should be checked for cracks or breaks before each procedure. One of the common problems with equipment problems during RF lesioning is from damaged cables. Switching to the impedance monitor instantly checks for cable and electrode continuity. To prevent skin burns, a large area dispersive electrode of at least 150 cm2 is recommended.[ 7 ] A minimal value of the stimulation threshold is 0.4 V to avoid denervation. A < 0.05 V ultra-low thresholds are avoided as it may reflect intraneural electrode placement.[ 8 ] References 1. Cassidy JD , Cote P , Carroll LJ , Kristman V . Incidence and course of low back pain episodes in the general population . Spine . 2005 ; 30 ( 24 ): 2817 – 2823 . 2. Hestbaek L , Leboeuf-Yde C , Manniche C . Low back pain: What is the long-term course? A review of studies of general patient populations . Eur Spine J . 2003 ; 12 ( 2 ): 149 – 165 . 3. Revel ME , Listrat VM , Chevalier XJ , et al . Facet joint block for low back pain: identifying predictors of a good response . Arch Phys Med Rehabil . 1992 ; 73 ( 9 ): 824 – 828 . 128 4. Kapural L , Mekhail N . Radiofrequency ablation for chronic pain control . Current Pain and Headache Reports . 2001 ; 5 : 517 – 525 . 5. Shealy CN , Maurer D. Transcutaneous nerve stimulation for control of pain: a preliminary technical note . Surg Neurol . Jan 1974 ; 2 ( 1 ): 45 – 47 . 6. Anderson K.H , Mosdal C. , Vaernet K . Percutaneous radiofrequency facet denervation in low-back and extremity pain , Acta. Neurochir . 1987 ; 87 : 48 – 51 . 7. Kine MT , Yin W . Radiofrequency techniques in clinical practice . Interventional Pain Management , Edited by Waldman S . Philadelphia, PA: W.B. Saunders ; 2001 ; 243 – 293 . 8. Raj PP . Interventional Pain Management: Image-guided procedures. 2nd edition . Philadelphia, PA : Sounders Elsevier . 2008 . 9. Smith HP , McWhorter JM , Challa VR , Radiofrequency neurolysis in a clinical model . neuropathological correlation . J Neurosurg . 1981 ; 55 : 246 – 253 . 10. Bogduk N , Twomey LT. Clinical Anatomy of the Lumbar Spine . Edinburgh , Scotland : Churchill Livingston , 1987 . 11. Kornick C , Kramarich SS , Lamer TJ , Todd S . Complications of lumbar facet radiofrequency devervation . Spine . 2004 ; 29 ( 12 ): 1352 – 1354 . 12. Geurts J , Van Wijik RM , Stolker R , Groen GJ. Efﬁ cacy of radiofrequency procedures for the treatment of 3.4: Lumbar Radiofrequency Ablation spinal pain: A systemic review of randomized clinical trials . Reg Anesth Pain Med . 2001 ; 26 ( 5 ): 394 – 400 . 13. Nienisto L , Kalso E , Malmivaara A. et al . Radiofrequency denervation of neck and back pain: a systemic review within the frame work of the Cochrane Collaboration Back Review Group . Spine . 2003 ; 28 ( 16 ): 1877 – 1888 . 14. Van Kleef M , Sluijter M, Van Zundert J . Radiofrequency Treatment. Raj’s Practical Management of Pain, 4th edition, Edited by Benson . Philadelphia PA : Mosby Elsevier ; 2008 . 15. Cosman EJ , Cosman ES . Electric and thermal ﬁ eld effects in tissue around radiofrequency electrodes . Pain Med . 2005 ; 6 ( 6 ): 405 – 424 . 16. Geurits JW , Lou L , Gauci CA , et al : Radiofrequency treatments in low back pain . Pain Pract 2 . 2002 ; 226 – 234 . 129

Chapter 3.5 Discography

Mehul Desai

Introduction 130 Indications 130 Contraindications 130 Complications 130 Infection 130 Bleeding 131 Nerve damage 131 Aggravation of Pain 131 Accelerated Disk Degeneration 131 Nucleus Pulposus Pulmonary Embolism 131 Functional Anatomy 131 Equipment and Preparation 132 Technique 132 Patient Position 132 Disc Puncture 133 Provocation 133 Interpretation 135 Controversies 136 Summary 137 References 137 130 Introduction Discography was first developed in the late 1940s for the purposes of diagnosing herniation of the lumbar intervertebral discs; it was originally described as a “diagnostic disc puncture with injection of opaque medium that demonstrate(d) disc rupture and protrusions.”( 1 ) With the advent of less invasive imaging modalities, the role of discography evolved toward an extension of the clinical examination as both an imaging modality as well as a provocation maneuver. In its most contemporary incarnation, lumbar provocation discography is undertaken as a dynamic confirmatory procedure for the diagnosis of internal disc disruption resulting in discogenic pain. Modern discographic practice utilizes pain provocation in combination with imaging to select patients for various intradiscal therapies.( 2 ) Indications Discography is typically not the first diagnostic study of choice and is performed strictly to obtain information after other imaging modalities fail to provide diagnostic relevance. The Executive Committee

3.5: Discography of the North American Spine Society announced its Position statement on Discography first in 1988( 3 ) and again in 1995.( 4 ) Indications for discography are as follows: ( 3 , 4 , 5 ) 1. Evaluation of patients with unremitting spinal pain of greater than four months and who has been unresponsive to all appropriate methods of conservative therapy. 2. Patients should have undergone investigations with other modalities, which have failed to explain the source of pain. 3. Preoperative planning for lumbar discectomy and fusion surgery. 4. Evaluation of failed back surgery to distinguish between psuedoarthrosis and annular pathology at an adjacent level. The purpose of provocation discography is the collection of further information regarding the intervertebral disc. Specifically determining whether the studied disc is symptomatic in the setting of normal asymptomatic controls allows for targeted therapies. Contraindications Congenital abnormalities of the vertebrae or nerve roots and postoperative spinal abnormalities may constitute relative contraindications to discography. Furthermore, the following includes a list of relative and absolute contraindications:( 5 ) 1. Patients with a known bleeding disorder or anticoagulation therapy 2. Pregnancy 3. Systemic infection or infection of skin over proposed puncture site 4. Severe allergic reaction to injectate 5. Previously operated disc 6. Fusion that does not allow access to disc 7. Spinal cord compromise at disc level to be investigated Complications The major complications of lumbar discography include infection; specifically, discitis and neural injury. Other complications include bleeding, aggravation of pain, spinal cord injury, cord compression or myelopathy, urticaria, retroperitoneal hemorrhage, nausea, convulsions, headache, and aggravation of pain. Accelerated disc degeneration has been suggested. Infection As with all invasive procedures, discography poses a threat of disc space infection or discitis. Fraser, et al., showed that using a two-needle coaxial tech decreases infection rates from 2.7 percent to 0.7 percent. 131 This was thought to be because the inner needle that entered the nucleus pulposus did not come in contact with skin.( 6 ) Skin should be prepared with betadine or chlorhexadine and sterile technique should be employed at all times. Intravenous and intradiscal antibiotics are additional methods for reducing risk of infection.( 7 ) Bleeding All patients should be screened for any known bleeding diasthesis or use of anticoagulation therapy. All coagulation abnormalities should be corrected if discography is being considered. Nerve damage Because of the close proximity of the needle to the spinal nerve, the possibility of potential nerve damage exists.

Aggravation of Pain Interventional Pain Medicine Patients may experience an amplification of their typical discogenic pain after the procedure. Lehmer et al. describes patients with a delayed onset of discogenic pain two to twelve hours after the procedure. This is proposed to occur when contrast injected into the disc space leaks through annular tears and come in contact with nerve endings in the outer third of the annulus fibrosis.( 8 ) Accelerated Disk Degeneration Carragee, et al., recently concluded a ten-year cohort study suggesting that discography could result in accelerated disc degeneration, disc herniation and loss of disc height compared to controls.( 9 ) Certainly, careful consideration should be taken with weighing of risks and benefits before discography is performed. Nucleus Pulposus Pulmonary Embolism A single case report by Shreck, et al., comments on this phenomenon. The account concludes that a fragment of nucleus entered vertebral marrow sinusoids subsequently flowing into the anterior external vertebral plexus causing a pulmonary embolism.( 10 ) Functional Anatomy The intervertebral unit consists of two adjacent vertebral bodies with the intervertebral disc (IVD) in between. The IVD is a complex structure that consists of the nucleus pulposus (NP), annulus fibrosus (AF), and the cartilaginous vertebral endplates (VE). Specifically, the IVD consists of a thick outer ring of fibrous cartilage, the annulus fibrosis, which surrounds a gelatinous core known as the nucleus pulposus. The annulus is made up of fifteen to twenty-five concentric lamellae with collagen fibers lying parallel to individual lamella. Elastin fibers lie between the lamellae, allowing the discs to return to their original configuration after flexion or extension.( 11 ) The IVD’s primary functions are to transmit pressure and allow movement between vertebral bodies. The nucleus pulposus and annulus fibrosis allow for pressure dispersal when external forces transmit axial loads to the spine. Axial loads cause the gelatinous nucleus pulposus to expand radially and exert pressure on the annulus fibrosus. The annulus fibrosis also restrains excessive movements and stabilizes the vertebral joint, acting as a ligament.( 12 ) The VEs are a layer of cartilage that covers the area of the vertebral body encircled by the ring apophysis.( 12 ) Although they cover the NP entirely, they do not cover the entire AF.( 12 ) This structure is crucial to the diffusion of nutrients from the marrow spaces of the vertebral bodies.( 12 ) The concentration of proteoglycans present within the nucleus pulposus is primarily responsible for the water-binding properties of the IVD. The nucleus pulposus is 70 to 90 percent water while the 132 annulus fibrosis is 60 to 70 percent water. Over time, the disc degenerates and the water-binding properties of the disc change with variations in its constituents. As the entire structure becomes less fluid, vertical stresses upon the disc are altered in their distribution and tearing of the annulus fibrosis may occur.( 13 ) These tears are often oriented in a radial orientation and most commonly involve the posterior annulus. The lumbar intervertebral discs are supplied by two extensive plexi that include the sinuvertebral nerves and the gray rami communicantes. The posterior outer third of the annulus, ventral aspect of the dura matter, the posterior portion of the vertebral body and the posterior longitudinal ligament are innervated by the sinuvertebral nerves, which are formed by the confluence of a somatic root from the ventral ramus and an autonomic root from the gray rami communicantes. The anterior aspect of the disc receives innervation from the anterior branches from the rami communicantes and the branches of the sympathetic trunk. Lateral innervation is also present as provided by the branches of the gray rami communicantes but is less pronounced. The anterior longitudinal ligament is innervated by recurrent branches of rami communicantes.( 14 )

3.5: Discography Theoretically, only innervated tissues are capable of generating pain. In a normal human lumbar disc, nerve endings can be found only in the periphery of the outer annulus, at a depth of a few millimeters. The perianular connective tissues are the most densely innervated structures in a normal disc. In degenerated discs, nerves may penetrate farther into the disc and quite possibly contact the nucleus pulposus, which despite its significant load-bearing properties is significantly pro-inflammatory. Conversely, the nucleus pulposus can herniate into the periphery of the disc or chemical pain mediators may reach the peripheral as a result of annular disruption and be a source of biochemical pain generators.( 15 ) Mechanical and inflammatory changes in degenerated discs may lead to internal disc disruption and, consequently, discogenic pain. As weight-bearing and pressure distribution is shifted toward the AF in the degenerated disc, breakdown of normal load bearing occurs. This, combined with torsional loads, may lead to both injury to the VE and annular tears, which subsequently further compromise the annulus’ ability to function. The diminished integrity of the VE may also lead to the activity of inflammatory cytokines and neuropeptides within the NP. This process ultimately leads to further disc degeneration and spur the process of neoneuralization characterized by ingrowth of peripheral sensory nerves toward the nucleus pulposus particularly in the presence of annular tears. This, combined with changes in the VE, leads to further and more accelerated degeneration. Equipment and Preparation Allergies to contrast, latex, iodine, or the need for prophylactic medications such as diphenhydramine and a steroid for allergy management should be considered before the procedure.( 17 ) Options for patients with severe iodine contrast allergy include Gadolinium contrast followed by post-procedural MRI.( 17 ) Our protocol includes the use of a peri-operative antibiotic (Ancef, Clindamycin) as well an antibiotic/contrast mixture of intradiscal injection. Additionally, pain medications including anti-inflammatory drugs, sedatives, opioids, and any medication that may alter the patient’s perception to pain should be minimized or discontinued on the day of the procedure to minimize any potential compromise of results. Furthermore, the patient’s anesthesia plan of care should take into account his or her active participation. Our protocol involves monitored anesthesia care without opioid use. Previous imaging studies should be reviewed before the procedure to evaluate disc morphology and to identify at least one normal control. Technique Patient Position The patient lies in a prone position on a radiolucent table. Often a folded towel, pillow, or soft wedge may be placed under the patient’s abdomen to reduce lordotic curvature. In some instances, elevating 133 Interventional Pain Medicine

Figure 3.5.1 L3-L4 discographic approach.

the target side approximately 15° may facilitate disc puncture particularly in fluoroscopes that do not counter-rotate beyond 35 to 40° , furthermore radiation scatter may be reduced in this position. The skin overlying the lumbar spine is widely prepped and draped. Disc Puncture Entry into the disc may be achieved via a double- or single-needle technique. Needle side of disc entry is a debated topic; no consensus on this issue currently exists. We utilize a single-needle, right sided entry with a 15–20° curved spinal needle for all patients. Between the L1-L4 levels, a standardized approach is undertaken. Typically a cephalo-caudad tilt is utilized to “square-off” the superior endplate of the verter- bral body immediately below the disc to be studied. This is usually achieved with a minimal angulation of 5–10 °. Then the fluoroscope is rotated to an oblique view of 30–45° until the superior articular process (SAP) bisects the disc space (Figures 3.5.1 – 2 ). The skin entry site is typically immediately lateral to the SAP. Once the needle passes the SAP and encounters the disc, alternating AP and lateral views are undertaken to position the needle tip in the middle of the disc (Figure 3.5.3 ). Care must be taken to avoid nerve root puncture and endplate penetration. Technically, disc puncture at L5-S1 is more challenging. Combined with a greater coronal footprint of the lumbar facets, high-riding iliac crests can prove difficult to navigate. Often, this will require a greater cephalad tilt in order to “move” the iliac crest from the expected needle path. The inverse triangle formed by the inferior endplate of the L5 vertebral body, the SAP, and the iliac crest is the target (Figure 3.5.4 ). Provocation Once the needles are appropriately positioned in the center of the discs, our protocol involves awakening and orienting the patient. A non-ionic contrast medium mixed with antibiotic is then injected using a graded-manometry device with a digital meter. The amount of contrast agent injected into the nucleus pulposus and resistance encountered during injection should be carefully recorded. The normal lumbar disc may hold up to 1.5 mL of contrast agent. A degenerated lumbar disc will usually take up a volume up to 3.5 mL. The injection is stopped when high resistance is encountered of if severe pain is produced.( 19 , 20 ) Pain provocation is the most useful and important aspect of discography. The individual patient’s response is subjective; therefore, it is important to avoid introducing bias during the procedure. Patients should instead be told before the start of the procedure and subsequently reminded to immediately 134 3.5: Discography

Figure 3.5.2 L4-L5 discographic approach.

inform the practitioner when he or she experiences any new or increasing pain. Leading questions should be avoided. During injection, the location and character of the pain should be noted and recorded. The pain response can be classified into the following categories: 1. No pain 2. Pain different from the usual painful symptoms (discordant) 3. Pain similar to some of the usual painful symptoms (partially concordant) 4. Pain identical to the usual painful symptoms (concordant)

Figure 3.5.3 Central needle position 135 Interventional Pain Medicine

Figure 3.5.4 L5-S1 discographic approach.

Measuring and recording pressures during disc stimulation may be useful with regards to clinical decision making and has been linked to surgical outcomes (Table 3.5.1 ).( 21 ) Furthermore, parameters for assessment including a maximal pressure of 100 psi may provide an objective measure of disc sensitization. Interpretation Disc morphology is determined on evaluation of anteroposterior (AP) and lateral radiographs obtained after intradiscal contrast injection. A normal disc maintains a normal height on both AP and lateral radiographs. Injected contrast agent remains in the nucleus pulposus, and may be unilobular (“cotton ball”) or bilobular (“hamburger bun”) in shape. Further morphological findings may include fissured or degenerated patterns. A Schmorl’s node is seen as focal protrusion of injected contrast agent into the adjacent vertebral endplate.( 22 ) In degenerated discs, discography shows a reduced disc height, and complex or multiple irregular fissures in the annulus fibrosis, with or without contrast leakage through annular tears. A bulging disc is often associated with degeneration, and is characterized by circumferential, diffuse and symmetrical annular bulging. Discography may show annular fissures with an intact peripheral annulus. Disc protrusion refers to focal, often asymmetrical central or posterolateral protrusion of disc material within an intact posterior longitudinal ligament. On discography, a single annular fissure is often seen. The nuclear material may migrate superiorly or inferiorly. We routinely obtain post-discography CT to augment diagnostic yield. For those patients with true contrast allergies, gadolinium contrast injection followed by magnetic resonance imaging has been reported.( 31 ) CT images obtained following discography provides good anatomical details in the axial plane. The Dallas discogram description is based on CT appearances and was originally classified into grades 0 to 3,( 21 ) later expanded as the Modified Dallas discogram scale (Table 3.5.2 ).( 23 ) It is important to interpret discography with morphological and pain provocation results. A study by Calhoun showed that 89 percent of 137 subjects with positive discography had clinical benefit from subsequent operation.( 24 ) 136 Table 3.5.1 Interpretation of Disc Stimulation Disc Classiﬁ cation Intradiscal Pressure at Pain Provocation Pain Pain Type Ruling Severity

Chemical Immediate onset of pain occurring as ≥ 6/10 Concordant Positive <1mL of contrast is visualized reaching the outer annulus, or pain provocation at <15 PSI above opening pressure Mechanical Between 15 and 50 PSI above opening pressure ≥ 6/10 Concordant Positive (but other pain generators may exist) Indeterminate Between 51 and 90 PSI ≥ 6/10 Concordant Further Normal > 90 PSI No pain investigation Negative 3.5: Discography Reprinted with permission from Derby R, Howard MW, et al. The ability of pressure-controlled discography to predict surgical and nonsurgical outcomes. Spine . 1999; 24( 4 ):364–71.

Controversies Carragee recently published a prospective match-cohort study of disc degeneration progression over ten years with and without baseline discography.( 9 ) The study objective was to compare progression of degeneration between lumbar discs injected ten years earlier with those same disc levels in subjects not exposed to discography. The study found that discs that had been exposed to discography had greater progression of disc degeneration compared to control (p = 0.03). The study concluded that discography resulted in accelerated disc degeneration, disc herniation and loss of disc height.( 9 ) Despite the long- term follow up during this study and the careful stratification undertaken by the authors, inherently radiographic changes on magnetic resonance imaging are a case of n=1 in that the pace and trajectory of the degenerative cascade in the lumbar spine is truly a unique process to the individual, one that can not be easily predicted even with careful study design. Furthermore, despite its inadequacies, it remains our best means for assessing discogenic pain.

Table 3.5.2 Modified Dallas Discogram Scale Modiﬁ ed Dallas Discogram Scale Grade Description

0 Contrast agent confined to within normal nucleus pulposus 1 Contrast agent extends radially along fissure involving the inner 1/3 of annulus 2 Contrast agent extends into the middle 1/3 of annulus 3 Contrast agent extends into the outer 1/3 of annulus, either focally or radially, to an extend not > 30 ° of disc circumference 4 Contrast agent extends into the outer 1/3 of annulus, dissecting radially to involve > 30 ° of disc circumference 5 Full thickness tear, either focal or circumferential with extension of contrast outside of annulus

Reprinted with permission from Sachs BL, Vanharanta H, Spivey MA, et al. Dallas discogram description. A new classiﬁ cation of CT/discography in low-back disorders. Spine 1987;12:287–294. 137 The risk of false-positive lumbar provocation discography has also been controversial. There is significant debate regarding the lack of relative sensitivity of the examination, furthermore fairly variable techniques have contributed to these findings. False-positive rates ranging from 37 to 40 percent have been reported.( 25 , 26 ) Certainly undiagnosed pathology of adjacent anatomic sources may contribute. Translation of pressures during discography to adjacent levels may also contribute to false-positive rates. False-negative rates have also been problematic. A study by Yasuma, et al., studied lower 181 thoracic and lumbar cadaver discs discographically and histologically. The findings showed 32 true-positive, 15 false-positive, 122 true-negative, and 12 false-negative discograms. Discograms were designated as false positive when the injected contrast was noted to extend beyond the peripheral vertebral margin, by histological sectioning of the disc was negative for protrusion. In the same study 77 discography patients were analyzed retrospectively who were found to have herniated disc during surgical exploration. The discograms were falsely interpreted as negative in 32 percent of the 59 patients with a protruding disc and 56 percent of the 18 patients with a prolapse.( 27 )

The predictive value of provocative discography on surgical outcome has also been questioned. Interventional Pain Medicine Madan, et al., performed a study involving seventy-three patients with chronic back pain. Thirty-two patients underwent spinal fusion based on pain provocation during discography, with 41 patients having surgery without discography. In the discography group, 75.6 percent of patients had satisfactory outcomes at 2-year follow-up versus 81.2 percent in the group who did not have preoperative discography. ( 28 ) Multiple studies have failed to unequivocally determine whether preoperative discography improves surgical outcomes in patients with discogenic low back pain.( 29 ) The role of analgesic discography including functional analgesic discography is also an area of considerable debate. This technique utilizes pain relief following intradiscal injection of local anesthetic in lieu of or in addition to traditional provocation discography. Certainly, further research to compare these techniques is needed to determine their utility and use. The advent and popularity of radiofrequency-based intradiscal therapies have generated a renewed interest in lumbar provocation discography amongst practitioners. Although the success rates and outcomes have been variable, these procedures utilize discography as a screening mechanism.( 30 , 31 ) Summary Lumbar provocation discography is widely used for the evaluation of discogenic pain in the lumbar spine. Techniques to further refine this modality including analgesic discography are on the horizon. Although controversy regarding optimal technique and long-term sequelae of performing the procedure persist, when performed with a standardized technique it remain a value tool in the diagnosis of internal disc disruption and an adjuvant to the clinical examination of the patient. References 1. Lindblom K . Diagnostic puncture of the intervertebral disc in sciatica , Acta Orthop Scandinivia . 1948 ; 17 : 213 – 239 . 2. Shah RV , Everett CR , Mckenzie-Brown AM , Sehgal N . Discography as a diagnostic test for spinal pain: a systematic and narrative review . Pain Physician . 2005 ; 8 : 187 – 209 . 3. North American Spine Society : Position statement on discography . The Executive Committee of the North American Spine Society . Spine . 1988 ; 13 : 1343 . 4. Guyer RD , Ohnmiess DD . Lumbar discography: Position statement from the North American Spine Society Diagnostic and Therapeutic Committee . Spine . 1995 : 20 : 2048 – 2059 . 5. Anderson MW . Lumbar discography: an update . Seminars in Roentgenology . 2004 ; 39 ( 1 ): 52 – 67 . 6. Fraser RD , Osti OL , Vernon-Roberts B . Discitis after discography . J Bone Joint Surg . 1987 ; 69-B : 26 – 35 . 7. Osti OL , Fraser RD , Vernon-Roberts B : Discitis after discography. The role of prophylactic antibiotics . J Bone Joint Surg . 1990 ; 72 -B: 271 – 274 . 138 8. Lehmer SM , Dawson MHO , O’Brien JP . Delayed pain response after lumbar discography . European Spine Journal . 1994 : 3 : 28 – 31 . 9. Carragee EJ , Don AS , et al . Does discography cause accelerated progression of degeneration changes in the lumbar disc ? Spine . 2009 : 34 : 2338 – 2345 . 10. Schreck RI , Manion WL , Kambin P : Nucleus pulposus pulmonary embolism: a case report . Spine . 1995 : 22 : 2463 – 2466 . 11. Marchand F , Ahmed AM . Investigation of the laminate structure of lumbar disc annulus fi brosus . Spine. 1990 ; 15 : 402 – 410 . 12. Bogduk N , Twomey LT . Clinical anatomy of the lumbar spine . 2nd edition. London : Churchill Livingstone ; 1991 . 13. Saboeiro GR . Lumbar Discography . Radiology Clinical North America . 2009 : 47 : 421 – 433 . 14. Bogduk N , Tynan W , Wilson AS . The nerve supply to the human lumbar intervertebral discs . Journal of Anatomy . 1981 : 132 ( Pt1 ): 39 – 56 . 15. Hurri H , Karppinen J . Discogenic pain . International Association for the Study of Pain , 2004 . 16. Sachs BL , Vanharanta H , Spivey MA , et al. Dallas discogram description : a new classifi cation of CT/ discography in low-back disorders. Spine . 1987 : 12 ( 3 ): 287 – 294 . 3.5: Discography 17. Walker J , Isaac Z , Muzin S . Discography in practice: a clinical and historical review . Current Review Musculoskeletal Med . 2008 : 1 : 60 – 8 3 . 18. Falco FJ , Moran JG . Lumbar discography using gadolinium in patients with iodine contrast allergy followed by postdiscography computed tomography scan . Spine . 2003 ; 28 : E1 – 4 . 19. Tehranzadeh J . Discography . Radiological Clinical of North America . 1998 ; 36 : 463 – 495 . 20. Fenton , DS , Czervionke LF . Discography . In: Fenton DS , Czervionke LF (eds) Image-guided spine intervention . Philadelphia, PA: W.B . Saunders 1996 ; 227 – 255 . 21. Derby R , Howard MW , Grant JM , Lettice JJ , Van Peteghem PK , Ryan DP . The ability of pressure-controlled discography to predict surgical and nonsurgical outcomes . Spine . Feb 1999 ; 15 ; 24 ( 4 ): 364 – 371 . 22. Brightbill TC , Pile N , Eichelberger RP et al . Normal magnetic resonance imaging and abnormal discography in lumbar disc disruption . Spine . 1994 ; 19 : 1075 – 1077 . 23. Sachs BL , Vanharanta H , Spivey MA, et al . Dallas discogram description: a new classifi cation of CT discography in low-back disorders . Spine . 1987 ; 12 : 287 – 294 . 24. Calhoun E , McCall IW , Williams L et al . Provocation discography as a guide to planning operations on the spine . Journal of Bone and Joint Surgery (Br) . 1988 ; 70 : 267 – 271 . 25. Holt EP . The question of lumbar discography. J Bone Joint Surg (Am) . 1968; 50 : 720 – 726 . 26. Caragee EJ , Alamin TF , Miller J , Grafe M . Provocative discography in volunteer subjects with mild persistent low back pain . Spine . 2002; 2 : 25 – 34 . 27. Yasuma T , Ohno R , Yamauchi Y . False-negative discograms . Journal of Bone and Joint Surgery . 1989 ; 70A : 1279 – 1290 . 28. Madan S , Gundanna M , Harley JM , Boeree NR , Sampson M . Does provocative discography screening of discogenic back pain improve surgical outcomes? Journal of Spinal Disorders and Techniques . 2002 ; 15 : 245 – 251 . 29. Gibson JN , Waddell G , Grant IC . Surgery for degenerative lumbar spondylosis . Cochrane Database of Systemic Reviews . 2000 ; 2 : CD001352 . 30. Helm S , Hayek SM , Benyamin RM , Manchikanti L . Systematic review of the effectiveness of thermal annular procedures in treating discogenic low back pain . Pain Physician . Jan–Feb 2009 ; 12 ( 1 ): 207 – 232 . 31. Kallewaard JW , Terheggen MA , Groen GJ , et al. Discogenic Low Back Pain . Pain Pract . Sept 2010 . [Epub ahead of print]. 32. Slipman CW , Rogers DP , Isaac Z , et al. MR lumbar discography with intradiscal gadolinium in patients with severe anaphylactoid reaction to iodinated contrast material . Pain Med . Mar 2002 ; 3 ( 1 ): 23 – 29 . 139

Chapter 3.6 Biacuplasty

Dmitri Souzdalnitski , Bruce Vrooman , Jianguo Cheng

IIntroduction 140 Indications 141 Contraindications 141 Functional Anatomy 142 Equipment and Preparation 142 General Equipment 142 Special Equipment (Kimberly-Clark TransDiscal system for Biacuplasty Procedure) 143 Medications 144 Techniques 144 Complications 146 Summary 147 Clinical Pearls 147 References 148 140 Introduction A large proportion (> 40 percent) of lower back pain can be attributed to degenerative changes in intervertebral discs. This pain, termed “discogenic,” is produced by the sensitization of nociceptors, mainly in the outer posterior portion of the annulus. It occurs secondary to inflammatory response to disc microtraumatization and degeneration.( 1 ) Biacuplasty is the latest of a variety of minimally invasive outer posterior annulus interventional techniques. The term biacuplasty is derived by combining the following words: two (“bi”) needles (“acu”) are used to transform (“plasty”) the intervertebral disc into a state of decreased nociceptor firing. The probes are placed percutaneously, which is why biacuplasty is considered a minimally invasive intervention. During biacuplasty, the probes are introduced to the opposite posterolateral sides of the annulus fibrosus in order to coagulate commonly fractured disc material. Coagulation is achieved by heating the proteins comprising the outer portion of the disc through radiofrequency energy delivered from the biacuplasty needles.( 2 , 3 ) The procedure leads to the ablation of the nerve endings innervating this portion of the disc. It may 3.6: Biacuplasty also simultaneously decompress the disc and relieve pressure on the nerve endings, providing additional means of pain relief.( 1–4 ) Similar to other minimally invasive interventional techniques, biacuplasty heats and decompresses the outer posterior portion of the intervertebral disc. Biacuplasty differs from other techniques in that: 1) It provides relatively even heating over a larger area of the posterior annulus by concentrating radiofrequency current between the tips of two straight probes (Figure 3.6.1 ). This is achieved by regulating the temperature of the probes through an embedded cooling system. 2) It is technically less challenging as compared with similar techniques, e.g., electrothermal therapy, as it allows easy placement with no need to steer the probe. 3) The use of two probes (rather than one probe, as with other techniques) helps avoid creating artiﬁ cial concentric ﬁ ssures by navigating the unipolar probe within the disc. 4) Consequently, it requires a shorter recovery time in comparison with other minimally invasive techniques. Cooled radiofrequency electrodes may increase the lesion size and facilitate ablation compared with traditional radiofrequency ablation electrodes. They are used in cardiac electrophysiology and

Figure 3.6.1 It demonstrated that biacuplasty provides relatively even heating over a larger area of the posterior annulus of the disc by concentrating radiofrequency current (colored) between the tips of two straight probes. Courtesy of Kimberly-Clark, used with permission. 141 tumor ablation. The TransDiscal 17 G electrodes (Kimberly-Clark TransDiscal system for biacuplasty procedure) are FDA-approved devices for intradiscal biacuplasty.( 5 , 6 ) As randomized controlled studies of biacuplasty are currently being conducted, there is not yet sufficient evidence to extrapolate the efficacy and/or safety of the procedure outside of the treatment applied in published research data.( 1 ) Case reports and case series suggest that biacuplasty appears to be a safe and relatively effective procedure for patients with discogenic pain. These studies demonstrated no complications during the procedure or during follow-up. Within the first month after the procedure, most patients reported greatly reduced pain and much better functional capacity. At six months, median opioid use decreased, median pain scores had fell, and functional capacity and quality-of-life measures also improved significantly. Most of the treated patients had minimal or no pain and some had the same amount of pain as before the procedure, but not worse.( 6–10 ) Indications Patients with chronic discogenic pain, originating from annular fissures or contained disc herniation, who Interventional Pain Medicine have failed to respond to treatments with medications, injections, and other conservative measures, may be candidates for biacuplasty. Despite the fact that discogenic pain is commonly characterized by a typical set of clinical signs, a clinical diagnosis is usually not sufficient to make a decision to apply biacuplasty. A pressure-controlled provocative discography is needed to confirm concordant discogenic pain. (Discography is discussed in details elsewhere in this book.) To proceed with biacuplasty, a positive discogram is required. It should reproduce the patient’s typical pain at an intensity of > 6/10 at a pressure of < 15 psi above opening pressure and at a volume less than 3.0 mL. A special pressure-monitoring device (manometer) should be used for discography. The slow injection rate of 0.05 mL/s should be applied to minimize false-positive results associated with high dynamic pressures.( 1 ) Table 3.6.1 summarizes the criteria for biacuplasty. Contraindications The following general conditions are considered to be absolute contraindications for biacuplasty: - Pregnancy - Systemic or localized infection at the anticipated introducer entry site - Systemic anticoagulation - History of coagulopathy or unexplained bleeding

Table 3.6.1 Criteria for biacuplasty Criteria for Biacuplasty (All criteria should be met)

– patient’s age should be greater than eighteen years – history of predominant axial/mechanical pain chronic back pain (more than six months) – evidence of discogenic pain on physical examination (discogenic antalgic postion, pain on provocative maneuvers, ex. Flexion, and other) – demonstration of positive concordant pain of intensity > 6/10 during provocative lumbar discography at one or two disc levels at low pressures (<50 psi) with negative control disc at one and preferably two adjacent levels and sham pressurization – at least 50 percent preserved disc height on as evidenced by imaging studies – failure to achieve adequate improvement with comprehensive non – other possible causes of low back pain have been ruled out e.g., failure to obtain prolonged improvement (> fourteen days) from lumbar medium branch blocks followed by radiofrequency ablations, sacroiliac joint injections and other applicable interventions 142 In addition, the following specific conditions would preclude the procedure: - intervertebral disc herniations greater than 4 mm - extruded or sequestered intervertebral disc herniations - structural spinal pathology that may impede recovery, e.g., spina bifida occulta, spondylolisthesis at the painful segmental level, or scoliosis - moderate to severe foraminal or central canal stenosis - existing endplate damage - significant annular tear (greater than grade 4 on modified Dallas Grading) Biacuplasty is relatively contraindicated in obese patients, in patients with significant psychological barriers to recovery, prior lumbar spine surgery or any other surgery within last three months, radiculopathy, immunodeficiency, (e,g., AIDS, diabetes mellitus) or immune suppression (e.g., organ transplant patients, patients with cancer being treated with chemotherapy or radiation).( 1 , 6–10 )

3.6: Biacuplasty Functional Anatomy The nucleus pulposus and the annulus fibrosus are two major components of the discus intervertebralis. The vertebral bodies lie above and below the discus, and are connected with the discs. The anterior portion of the disc is stronger and not supported by any additional structures. The posterior side is supported by two facet joints, providing support and stability of the spine and spinal canal. A normal disc does not contain blood vessels. The exchange of nutrients and metabolic product washing out rely on a diffusion process.( 1 ) Aging and microtraumatization lead to degenerative changes in the disc. The common radiologic sign that the disc is beginning to degenerate is decrease in disc height, which closely correlates with dehydration of the nucleus pulposus. Disc dehydration may lead to circumferential and/or radial tear, mainly present in the outer posterior portion of the annulus fibrosus. This process subsequently stimulates the growth of blood vessels and accompanying nerve endings into the annulus. Chronic inflammation is associated with the sensitization of nociceptors and neuroplastic changes that can produce chronic discogenic pain. In fact, these changes in discus intervertebralis are considered to be the most common cause of lower back pain, occurring in about 40 percent of cases.( 1 ) Sensory innervation of the discus intervertebralis occurs via branches of the truncus sympathicus . The dorsal part of the discus annulus is innervated via branches of the nervi sinuvertebrales (or recurrentes meningei ), which derives from rami communicantes. There are multiple left-right and cranio-caudal alli- ances. This may explain the fact that searching for the pain generator is not an easy task, as the pain could be a symptom of a distant structural problem (right vs. left or up vs. down). This is the main reason a biacuplasty can only be performed when the pain generator is localized by discography, a functional anatomic study. Equipment and Preparation General Equipment - Needle, 25-gauge, 1.5 inch (subcutaneous local anesthetic) - Syringe 5–10 mL (subcutaneous local anesthetic) - Sterile gloves - Towels - Gauze - Gown - Hat - Mask - Betadine/chlorhexidine preparation 143 - Sterile drapes - Adhesive bandage - Fluoroscopy, C-arm - Lead apron Special Equipment (Kimberly-Clark TransDiscal system for Biacuplasty Procedure) - TransDiscal Probe. The probe used to heat the intervertebral disc tissue. Each probe has two temperature sensors placed 3 mm apart at the distal end of the electrode. These sensors measure temperature and provide control of radiofrequency energy delivery throughout the procedure. Each probe includes a 4-foot cable and tubing extension to reach out of the sterile fi eld (Figure 3.6.2 A). - TransDiscal Introducer. Two introducers are required for the procedure. An introducer is comprised of a fully-insulated cannula and a sharp trocar-tipped stylet. An optional introducer is equipped with a cable connected to the stylet which allows impedance monitoring by the generator and can be used as an aid in placement. The 17-gauge introducer allows for accurate placement of the probe

(Figure 3.6.2 A). Interventional Pain Medicine - Pain Management Generator. This is a radiofrequency generator which automatically controls the pump unit (cooling system) and the delivery of radiofrequency energy (Figure 3.6.2 B). - Pain Management Pump Unit, with two peristaltic pump heads to circulate sterile water through the TransDiscal Probes, and two closed-loop fluid circuits. Sterile water is circulated within the electrode

Figure 3.6.2 Kimberly-Clark TransDiscal system for biacuplasty procedure. It demonstrates TransDiscal Probe (Figure A, top ). The probe used to heat the intervertebral disc tissue. Each probe has two temperature sensors placed 3 mm apart at the distal end of the electrode. Figure A demonstrates the TransDiscal Introducer (in the bottom of the Figure A). Figure B demonstrates the Pain Management Generator. This is a radiofrequency generator that automatically controls the pump unit (cooling system) and the delivery of radiofrequency energy. Figure C shows Pain Management Pump Unit. Sterile water is circulated within the electrode during the procedure, keeping the surface cool. Figure D demonstrates the Pain Management Tube Kit. The Tube Kit is comprised of medical-grade tubing and a burette for holding sterile water. Each is used to circulate sterile water through the TransDiscal Probes in order to cool the electrodes. The Pain Management Pump Unit peristaltically pumps water through the tube kits. Courtesy of Kimberly-Clark, used with permission. 144 during the procedure, keeping the surface cool. The sterile water is contained and does not contact patient tissue (Figure 3.6.2 C). - Pain Management Tube Kit. The Tube Kit is comprised of medical-grade tubing and a burette for holding sterile water. Each is used to circulate sterile water through the TransDiscal Probes in order to cool the electrodes. The Pain Management Pump Unit peristaltically pumps water through the tube kits (Figure 3.6.2 D). Medications - Lidocaine Hydrochloride, 1 percent 5–10 mL (for subcutaneous (SC) injection) - Midazolam 2–6 mg for intravenous sedation. - Intravenous preparation of Cefazolin 1 gm (or Vancomycin 1 gm, or Clindamycin 900 mg if the patient reports allergy to Cephalosporins, or severe anaphylactic allergic reaction to penicillins).

3.6: Biacuplasty Techniques The patient should provide informed consent for the procedure. Intravenous access should be obtained prior to the procedure. Cefazolin 1 gm IV (or other antibiotic) administered for prophylaxis, typically 30 minutes prior to the procedure. The patient is brought to the fluoroscopy suite, and positioned prone on the fluoroscopy table, with the head turned to one side or faced forward, and arms placed above the head. A pillow may be placed under the patient’s mid- to lower abdomen to optimize the imaging. A roll can be placed under the patient’s ankles for comfort during the procedure. Continuous hemodynamic monitoring should be initiated, including blood pressure, EKG, and pulse oximetry. Intravenous sedation is administered incrementally to allow the patient to remain comfortable and conversant throughout the procedure. The skin at the site of intervention is prepped with prep solution and draped with sterile technique. The targeted discs are identified by fluoroscopy, and the skin and subcutaneous tissues overlying the needle insertion points are anesthetized using 5 mL of 1 percent lidocaine. The C-arm is then adjusted to

Figure 3.6.3 This figure shows a 17-gauge 150-mm introducer advanced into the posterior annulus of the targeted discs, identified by fluoroscopy (left side, white arrow). Kimberly-Clark TransDiscal system for biacuplasty procedure, used with permission. 145 Interventional Pain Medicine

Figure 3.6.4 It shows the next step, when the second 17-gauge 150-mm introducer advanced into the posterior annulus of the targeted disc on the contralateral side, and identified by fluoroscopy (right side–yellow arrow, left side–white arrow). ensure adequate visualization of the target intervertebral space. Under fluoroscopic guidance, a 17-gauge 150 mm introducer (6 mm active tip)— TransDiscal Introducer— is slowly advanced into the disc at the posterior annulus (Figure 3.6.3 ). The same procedure is repeated on the contralateral side (Figure 3.6.4 ). The distance between the tips of the two introducers is approximately 2.5–3 cm. The position of the needles is confirmed using oblique, anterior-posterior, and lateral fluoroscopic imaging (Figure 3.6.5 ). A TransDiscal Probe is inserted through each introducer into the posterior intervertebral disc on each side (Figure 3.6.6 ). Once the probes are in place, radiofrequency energy is delivered between the

Figure 3.6.5 The figure demonstrates the fluoroscopic image of the targeted disc with two 17-gauge 150-mm introducers in place (left side— white arrow, right side— yellow arrow). Kimberly-Clark TransDiscal system for biacuplasty procedure, used with permission. 146 3.6: Biacuplasty

Figure 3.6.6 This figure demonstrates the fluoroscopic image of the targeted discs, with two Trans-Discal probes (white and yellow arrows) advanced into the disc at the posterior annulus, with corresponding lateral fluoroscopic view. Kimberly-Clark TransDiscal system for biacuplasty procedure, used with permission.

two electrodes in the disc, heating the area between and immediately around these electrodes. Bipolar heating is used at 50 degrees Celsius for fifteen minutes at each level. In addition, monopolar heating may be performed at 60 degrees Celsius for 150 seconds each side. Radiofrequency energy is used to heat the tissue while the internally circulating water cools the tissue in close proximity to the electrodes. This combination creates an adequate heating profile across the posterior disc without excessive heating. It allows denervation of nociceptors in the disc in a controlled fashion. Throughout this process, the patient should be awake and able to communicate with the medical team. The needles are removed and sterile dressing applied. Patients may be discharged home the same day. It is important to provide patients with detailed verbal and written instructions at the time of discharge.( 11 ) Complications Any minimally invasive interventional pain procedure is associated with risks of infection, bleeding or nerve injury, worsened pain, and complications associated with anesthesia administration. Having the patient in a state of conscious sedation, which allows for verbal communication of any unwanted sensations, reduces the risk of these potential adverse events. Potential complications related to disc biacuplasty should be similar to those of other interventional disc procedures. In rare cases, biacuplasty procedures have caused burns at the introducer needle insertion site. Due to the rarity of these cases, it is believed that such events may be caused by practitioner’s inaccuracy.( 9 , 11 ) Cautions should be taken to prevent complications of biacuplasty. Prior to the procedure, certain steps should be taken in order to prepare the patient. The patient should be questioned as to the presence of any infections, known medical conditions, allergies to medication (e.g., anesthetics or antibiotics), or other contraindications.( 1 , 7–9 ) - Patients should discontinue NSAIDs at least one week prior to the procedure. - Anticoagulants should be discontinued according to guidelines of American Society of Regional Anesthesia - Other medications may be continued at the discretion of the physician. 147 Summary Biacuplasty is a minimally invasive percutaneous intervention that uses internally cooled radiofrequency probes to denervate nociceptors in the posterior portion of the intervertebral disc. This procedure is reported to be effective for chronic discogenic back pain generated by nociceptors located in the annular fissures or contained disc herniations. Patients with chronic lower back discogenic pain, who have failed to respond to pain medications and other conservative treatments may be considered as candidates for biacuplasty. Published data are limited to case reports and case series reports that suggest biacuplasty is effective and safe. Clinical Pearls Appropriate patient selection is one of the most important factors affecting the outcomes of biacuplasty. Properly placed probes allow the current to concentrate between the two probes during biacuplasty to create a dumbbell-shaped lesion covering the posterior and posterolateral annulus fibrosus. This allows

for the preservation of other tissues from heating and prevention of potential side effects. Interventional Pain Medicine Patients should be notified that they may experience tenderness and inflammation of the treatment area due to the insertion of the introducers and the generation of heat in the disc. This pain usually subsides within seven to fourteen days after the procedure. The detailed printed discharge instructions are critical for post procedural care. Patients should avoid strenuous activity for a period of six weeks after biacuplasty. Physical activity should be increased gradu- ally, and a brace should be used for 6–8 weeks after the procedure. The detailed instructions are listed in Table 3.6.2 .

Table 3.6.2 Discharge Instructions (adapted from 11 ).

General Discharge Instructions, Activity in Daily Living, Back-to-Work Recommendations – Patients should not drive or operate machinery. – Patients should not engage in any strenuous activity. – Patients should wear a lumbar back brace for six to eight weeks, except when showering or in bed. – Patients may shower but should avoid soaking in the bathtub. – Patients should resume a regular diet. – Patients may remove bandages the day following the procedure. – Patients may use an ice pack on the site of the insertion the day of the procedure and warm, moist heat the following day if they experience discomfort when the local anesthetic wears off. – Rest for one to three days after the procedure in a comfortable position (i.e., lying down or reclining). – Limit sitting or walking to ten to twenty minutes at a time. – Limit to 30–45 minutes at a time for the first 6 weeks in a chair with good support. – Patients should avoid sitting on soft couches or chairs. – Patients should stand and walk about for short breaks between sitting periods. – If a patient’s work is sedentary they may return to work in roughly two weeks. – For other jobs, especially physically demanding jobs, the decision should be made on a case by case basis. Driving – Patients should not drive for the first 1–5 days after the procedure, and driving should be limited to 20–30 minutes for the first 6 weeks. – Vehicles should be equipped with proper lumbar support. – As a passenger, patients should recline the seat and try to limit driving duration to less than forty-five minutes for the first six weeks. – It is okay for patients to recline or lie down in the back seat and be driven home the day of the procedure. 148 Table 3.6.2. Cont’d.

Patient Should Call the Ofﬁ ce If: – There is a severe headache or severe pain at the injection site with swelling and redness. – If their pain increases or if they experience fever or chills. – If there is sudden onset of weakness of lower extremities of bladder incontinence. – He or she experiences shortness of breath or chest pain.

References 1. Kallewaard JW , Terheggen MA , Groen GJ , et al . 15. Discogenic Low Back Pain . Pain Pract . 2010 : 560 - 579 . 2. Helm S , Hayek SM , Benyamin RM , Manchikanti L . Systematic review of the effectiveness of thermal annular procedures in treating discogenic low back pain . Pain Physician . 2009 ; 12 ( 1) : 207 – 232 . 3. Pauza K . Cadaveric intervertebral disc temperature mapping during disc biacuplasty . Pain Physician . 3.6: Biacuplasty 2008 ; 11 ( 5) : 669 – 676 . 4. Petersohn JD , Conquergood LR , Leung M . Acute histologic effects and thermal distribution proﬁ le of disc biacuplasty using a novel water-cooled bipolar electrode system in an in vivo porcine model . Pain Med . 2008 ; 9 ( 1) : 26 – 32 . 5. Kapural L , Mekhail N , Hicks D , et al . Histological changes and temperature distribution studies of a novel bipolar radiofrequency heating system in degenerated and nondegenerated human cadaver lumbar discs . Pain Med . 2008 ; 9 ( 1) : 68 – 75 . 6. Kapural L . Intervertebral disk cooled bipolar radiofrequency (intradiskal biacuplasty) for the treatment of lumbar diskogenic pain: a 12-month follow-up of the pilot study . Pain Med . 2008 ; 9 ( 4) : 407 – 408 . 7. Kapural L , Cata JP , Narouze S . Successful treatment of lumbar discogenic pain using intradiscal biacuplasty in previously discectomized disc . Pain Pract . 2009 ; 9 ( 2) : 130 – 134 . 8. Kapural L , Mekhail N . Novel intradiscal biacuplasty (IDB) for the treatment of lumbar discogenic pain . Pain Pract . 2007 ; 7 ( 2) : 130 – 134 . 9. Kapural L , Ng A , Dalton J , et al . Intervertebral disc biacuplasty for the treatment of lumbar discogenic pain: results of a six-month follow-up . Pain Med . 2008 ; 9 ( 1) : 60 – 67 . 10. Kapural L , Sakic K , Boutwell K . Intradiscal biacuplasty (IDB) for the treatment of thoracic discogenic pain . Clin J Pain . 2010 ; 26( 4) : 354 – 357 . 11. http://www.rfpainmanagement.com . Last assessed 09/15/2010 . 149

Chapter 3.7 Kyphoplasty

Kacey Montgomery , Neel Amin , and Robert W. Hurley

Introduction 150 Anatomy and Physiology 150 Risk Factors 151 Indications 152 Contraindications 152 The Procedure 152 Efficacy 154 Complications 154 References 155 150 Introduction Every year, 1.4 million vertebral body compression fractures become clinically apparent.[ 1 ] Fractures can result from a loss of mineral content, reduction in bone mass, or trabecular disconnectivity.[ 2 ] These fractures occur in the thoracic and lumbar spine, and can lead to loss of height and kyphosis, resulting in chest cavity compression. Decreased pulmonary function may ensue, with up to a 9 percent loss in predicted forced vital capacity.[ 1 , 3 , 4 ], [ 5–7 ] The outcome of these events is pain, disability, a decrease in quality of life [ 1 , 2 , 4 ], and, ultimately, a reduction in life expectancy.[ 5 ] As a result of altered spine biomechanics, one compression fracture can subsequently produce up to a five-fold increase in adjacent vertebral body fractures.[ 1 , 8 , 9 ] Vertebral compression fractures represent a significant morbidity in elderly patients, and patients with thoracic or lumbar fractures have a four- to five-year mortality rate that exceeds that of hip fracture patients.[ 10–12 ] Treatment of vertebral fractures covers a wide spectrum of options, depending upon the individual patient’s comorbidities and prognosis. These range from a conservative multimodal approach to either minimally invasive procedures or open surgical repairs. Analgesic control, bed rest, back bracing, and 3.7: Kyphoplasty physical therapy are often first-line treatments.[ 1 ] Bed rest, although used in the conservative treatment of osteoporotic lesions, actually results in an accelerated decrease in bone density.[ 13 ] When the patient’s pain is unresponsive to conservative treatment, an interventional procedure is usually indicated. Vertebroplasty and kyphoplasty will both stabilize a fracture and allow for pain relief and improved physical mobility.[ 2 , 4 , 9 , 13–16 ] Vertebroplasty was originally developed for the treatment of hemangiomas, but was therapeutically expanded to treat compression fractures, osteolytic tumors, and bone metastasis.[ 17 ] The primary difference between these minimally invasive techniques is that, with kyphoplasty, a cavity is created within the fractured vertebral body to allow the instillation of viscous cement. Also, balloon kyphoplasty may correct the vertebral body deformity, whereas this is not possible with percutaneous vertebroplasty.[ 2 ] Open surgical repairs are usually reserved for patients with neurological impairment resulting from the fracture.[ 1 ] Anatomy and Physiology The vertebrae are composed of two components: the vertebral body and the vertebral arch (Figure 3.7.1 ). The vertebral body is the anterior and largest part of the vertebrae. Generally, it is cylindrical in shape, and increases in size from the cervical to the lumbar spine. The vertebral bodies stack up on one another, creating the vertebral column. In between the vertebrae are discs whose primary functions are shock absorption and cushioning (Figure 3.7.2 ). They are also part of the structures that make up the spaces through which the spinal cord travels, in addition to the exiting spinal nerves.

Superior articular process

Transt: Proc. Pedicle Body Spin: Proc. Infer. Artic.Proc.

Figure 3.7.1 Lateral view of lumbar vertebra. 151 Interventional Pain Medicine

Figure 3.7.2 Normal vertebra with normal vertebral height (in contrast to the illustration with vertebral compression fracture). Risk Factors There are many factors that increase the risk for vertebral compression fractures (VCF). These include a preexisting VCF, age, sex, bone mineral density, and drugs that affect bone (i.e., steroids). There are multiple studies showing that a prior VCF is one of the most significant predictors of future VCFs. In any given year, independent of bone density, the risk of fractures is higher for women than for men. The center of the body’s gravity applies forces that pull the spine to the front; the forces of the back muscles that pull the spine posteriorly counterbalance this action. In a healthy individual, these two forces equal each other to keep the spine upright and balanced. A VCF affects the body’s center of gravity force, pulling the spine forward and inferiorly. This shift generates an imbalance in the spine, causing kyphosis, a condition that imposes increased stress on the anterior portion of the vertebral bodies (Figure 3.7.3 ). Kyphosis also fatigues the patient by making him

Kyphosis

Figure 3.7.3 Physical changes in stature with vertebral compression fractures leading to kyphosis. 152 or her work harder to maintain spine alignment. The combination of these two factors leads to a higher fracture rate in vertebral bodies as well as negatively impacting the patient’s quality of life. Balloon kyphoplasty is an excellent tool for the treatment of VCF. This procedure improves the saggital alignment of the injured vertebral body, and, thereby, more balanced spinal biomechanics. This reduces kyphosis of the spine and ultimately decreases the incidence of subsequent adjacent fractures. The question, “Can bone cement cause adjacent fractures in the future?” is often raised. The concern is that the cement will increase the stiffness of the vertebral body, and, consequently, will produce fractures in the levels above and below the affected part. Simply stated, biomechanical studies show little evidence that this will occur for two main reasons. First, bone cement does not increase the stiffness of the vertebral body beyond that of the pre-fracture state. Second, it is the intervertebral discs, not the vertebral bodies, that determine the stress load absorbed by the individual’s spine. The mechanism of pain relief is not yet understood, but may be secondary to stabilization of the microfractures with cement and the “exothermic reaction produced by polymerization process as polymethylmethacrylate (PMMA) hardens.”[ 18 ] Thus, the “mechanical, vascular, chemical and thermal effects of cement might account for

3.7: Kyphoplasty the destruction of nerve endings.”[ 18–20 ] It is hypothesized that PV has a higher incidence of extravasation secondary to using a lower viscosity of PMMA. Indications Compression fractures secondary to osteoporosis, multiple myeloma, metastatic cancer, or chronic steroid use as seen in transplant patients, result in loss of vertebral height, along with symptomatic pain and decreased function and quality of life.[ 1 , 2 , 4 , 21 ] Contraindications Absolute contraindications to kyphoplasty include those with a bleeding disorder, infection, and cement allergy, in addition to those in whom the vertebral level that is generating the pain has not yet been identified [ 22 , 23 ]. Relative contraindications involve fractures associated with the posterior wall [ 22 ], considered to be secondary to a theoretical probability that the balloon will cause retropulsion of the posterior cortical wall into the spinal canal [ 2 , 24 ]. The inability to lie prone for the duration of the procedure also serves as a relative contraindication [ 22 ]. Multiple back surgeries may obscure the pathology and, thereby, could impede the performance of a successful procedure. The Procedure Kyphoplasty generally is performed under local anesthesia, monitored anesthetic care, or general anesthesia. It is recommended to give a dose of antibiotics prior to skin incision. The patient should be positioned prone, with a slight hyperlordosis of the lower thoracic and lumbar spine. The procedure can be performed with a single C-arm machine, or two C-arm machines can be used for biplanar fluoroscopy (Figure 3.7.4 ). The vertebral body is cannulated with an 11-gauge needle, most often using an extrapedicular approach for the thoracic spine and a transpedicular approach for the lumbar spine (Figure 3.7.5 a). The ultimate target of the needle’s trajectory on lateral view is the lower, anterior quadrant of the vertebral body. Approximately 5 mm anterior to the dorsal wall of the vertebral body, the working cannula is positioned (Figure 3.7.5 b). A tamp is next used to create a channel after the obturator is removed. Next, the kyphoplasty balloon is placed into the newly fashioned channel and is inflated with contrast medium; the flow of contrast is controlled under balloon pressure and fluoroscopic guidance (Figure 3.7.5 c). Balloon inflation typically is terminated when one of the cortical walls is reached or when the pressure rises to 350 psi. After the balloon is removed, PMMA is injected through the cannula, with the goal of packing the cement as tightly as possible (Figure 3.7.5 d, e). Special attention must be paid for cement leaks outside the fractured vertebra. 153

Fractured vertebra Interventional Pain Medicine Cavity

4 AFTER THE PROCEDURE

Stabilized vertebra

Figure 3.7.4 Steps in balloon kyphoplasty: 1) approach to vertebral body 2) balloon restoration of vertebral height 3) cement placement 4) stabilized vertebra status/post balloon kyphoplasty 154

A BC 3.7: Kyphoplasty

DE Figure 3.7.5 Balloon kyphoplasty: a) Interventional approach b) Position for balloon inﬂ ation c ) Balloon deployed d ) Lateral view of cement placement e ) A/P view of stabilized vertebral body s/p balloon kyphoplasty

Efficacy The Fracture Reduction Evaluation (FREE) trial revealed statistically significant improvement in physical component summary scores over those of conservative treatment, specifically when following up patients in the immediate postoperative period to one-month post procedure.[ 1 ] The difference in pain, quality of life, and movement diminished at twelve months post randomization secondary to fracture healing in the conservative group.[ 1 , 4 ] Reduction in visual analog scale (VAS) scores is one of the benefits of balloon kyphoplasty.[ 4 , 18 ] A reduction in VAS scores by 79 percent has been reported by Pflugmacher and colleagues, in addition to improvement in disability scores [ 17 ]. There is a reported 40 to 60 percent incidence of kyphotic deformity correction with balloon kyphoplasty[ 2 , 4 , 8 ]; however, the ability of kyphoplasty to have a positive impact on pulmonary restrictive disease has yet to be shown.[ 2 ] Complications As with any invasive procedure, balloon kyphoplasty is not without risk. Bleeding and infection are two problems to consider, as would be the case with any procedure that violates skin integrity. Nerve root contusion can also occur in the first part of the procedure as the practitioner is approaching the vertebra, causing transient radicular paresis.[ 2 ] 155

A BC Interventional Pain Medicine

D E Figure 3.7.6 a) transpedicular approach b) posterior cement extravasation c) anterior cement extravasation d) epidural cement extravasation e) intradiscal extravasation of cement

Polymethyl methacrylate, a substance used in balloon kyphoplasty, may extravasate into the epidural space and lead to neurological deficits, which may require open surgery for evacuation [ 2 ] (Figure 3.7.6 ). A study by Stoffel and colleagues showed a 28 percent occurrence of asymptomatic extravertebral leakage. Typically reported is a leakage incidence of 2.7 to 10 percent, although 33 percent has also been described. [ 2 ] Extravasation has been shown to be linked with cement viscosity and volume used. [ 2 , 4 ] References 1. Wardlaw D , Cummings SR , Van Meirhaeghe J , et al . Effi cacy and safety of balloon kyphoplasty compared with non-surgical care for vertebral compression fracture (FREE): a randomized controlled trial . Lancet . 2009 ; 373 : 1016 – 1024 . 2. Stoffel M , Wolf I , Ringel F , et al . Treatment of painful osteoporotic compression and burst fractures using kyphoplasty: a prospective observational design . J Neurosurg Spine . 2007 ; 6 : 313 319 . 3. Brunton S , Carmichael B , Gold D , et al . Vertebral compression fractures in primary care: recommendations from a consensus panel . The Journal of Family Practice . 2005 ; 54 : 781 – 788 . 4. Pfl ugmacher R , Kandziora F , Schroeder RJ , et al . Percutaneous balloon kyphoplasty in the treatment of pathological vertebral body fracture and deformity in multiple myeloma: a one-year follow-up . Acta Radiol . 2006 ; 47 : 369 – 376 . 5. Kado D , Browner W , Palermo L , et al . Vertebral fractures and mortality in older women: a prospective study . Archives of Internal Medicine . 1999 ; 159 : 1215 . 156 6. Leech JA , Dulberg C , Kellie S , et al . Relationship of lung function to severity of osteoporosis in women . Am Rev Respir Dis . 1990 ; 141 : 68 – 71 . 7. Schlaich C , Minne , HW , Bruckner T , et al . Reduced pulmonary function in patients with spinal osteoporotic fractures . Osteoporos Int . 1998 ; 8 : 261 – 267 . 8. Atalay B , Caner H , Gokce C , et al . Kyphoplasty: 2 years of experience in a neurosurgery department . Surg Neurol . 2005 ; 64 Suppl 2 : S72 – 76 . 9. Barr , JD , Barr , MS , Lemley , TJ , et al . Percutaneous vertebroplasty for pain relief and spinal stabilization . Spine . 2000 ; 25 : 923 – 928 . 10. Garfi n SR , Buckley RA , and Ledlie J. Balloon kyphoplasty for symptomatic vertebral body compression fractures results in rapid, signifi cant, and sustained improvements in back pain, function, and quality of life for elderly patients . Spine . 2006 ; 31 : 2213 – 2220 . 11. Cooper C , Atkinson , EJ , Jacobsen SJ , et al . Population-based study of survival after osteoporotic fractures . Am J Epidemiol . 1993 ; 137 : 1001 – 1005 . 12. Johnell O , Kanis , JA , Oden , A , et al .: Mortality after osteoporotic fractures . Osteoporos Int . 2004 ; 15 : 38 – 42 . 13. Garfi n SR , Yuan HA , and Reiley MA. New technologies in spine: kyphoplasty and vertebroplasty for the treatment of painful osteoporotic compression fractures . Spine . 2001 ; 26 : 1511 – 1515 . 3.7: Kyphoplasty 14. Amar AP , Larsen DW , Esnaashari N. Percutaneous transpedicular polymethylmethacrylate vertebroplasty for the treatment of spinal compression fractures . Neurosurgery . 2001 ; 49 : 1105 – 1114 ; discussion 1114–5 . 15. Cortet B , Cotten A , Boutry N , et al . Percutaneous vertebroplasty in the treatment of osteoporotic vertebral compression fractures: an open prospective study . J Rheumatol . 1999 ; 26 : 2222 – 2228 . 16. Lieberman IH , Dudeney S , Reinhardt MK , et al . Initial outcome and effi cacy of “kyphoplasty” in the treatment of painful osteoporotic vertebral compression fractures . Spine . 2001 ; 26 : 1631 – 1638 . 17. Pfl ugmacher R , Beth P , Schroeder RJ , et al . Balloon kyphoplasty for the treatment of pathological fractures in the thoracic and lumbar spine caused by metastasis: one-year follow-up . Acta Radiol . 2007 ; 48 : 89 – 95 . 18. De Negri P , Tirri T , Paternoster G , et al . Treatment of painful osteoporotic or traumatic vertebral compression fractures by percutaneous vertebral augmentation procedures: a nonrandomized comparison between vertebroplasty and kyphoplasty . Clin J Pain . 2007 ; 23 : 425– 430 . 19. Cotten A , Boutry N , Cortet B , et al . Percutaneous vertebroplasty: state of the art . Radiographics . 1998 ; 18 : 311 – 320 ; discussion 320–3 . 20. Hardouin P , Fayada P , Leclet H , et al . Kyphoplasty . Joint Bone Spine . 2002 ; 69 : 256 – 261 . 21. Deen HG , Aranda-Michel J , Reimer R , et al . Balloon kyphoplasty for vertebral compression fractures in solid organ transplant recipients: results of treatment and comparison with primary osteoporotic vertebral compression fractures . Spine . 2006 ; 6 : 494 – 499 . 22. Peh WC and Gilula LA. Percutaneous vertebroplasty: indications, contraindications, and technique . Br J Radiol . 2003 ; 76 : 69 – 75 . 23. Gangi A , Guth S , Imbert JP , et al . Percutaneous vertebroplasty: indications, technique, and results . Radiographics . 2003 ; 23 : e10 . 24. Ledlie JT and Renfro M. Balloon kyphoplasty: one-year outcomes in vertebral body height restoration, chronic pain, and activity levels . J Neurosurg . 2003 ; 98 : 36 – 42 . 157

Chapter 3.8 Percutaneous Discectomy

Salim Hayek

Introduction 158 Percutaneous Laser Disc Decompression (PLDD) 161 Historical Perspective 158 Procedure 162 Operative Versus Non-Operative Treatment 158 Evidence of Efficacy 162 Evolution of Minimally Invasive Disc Radiofrequency Coblation® Procedures 159 (Plasma Disc Decompression (PDD)/Nucleoplasty) 162 Minimally Invasive Percutaneous Disc Procedures 159 Procedure 162 Percutaneous Disc Decompression 159 Evidence of Efficacy 162 Percutaneous Endoscopic Discectomy (PED) 159 Mechanical Disc Decompression 163 Functional Anatomy 160 Procedure 163 Patient Selection 160 Evidence of Efficacy 163 Indications 160 Post-Procedural Care 163 Contraindications 161 Complications 163 Automated Percutaneous Lumbar Clinical Pearls 164 Discectomy (APLD) 161 Conclusion 164 Procedure 161 References 164 Evidence of Efficacy 161 158 Introduction The lifetime prevalence of low back pain (LBP) has been reported as between 54% and 80 percent.1 LBP is one of the most common reasons for visits to internists and the second most common reason for disability in the United States. 2 , 3 The prevalence of chronic low back pain ranges from 15 to 45 percent, with a median point prevalence of 30 percent. 1 It is the most significant source of spine-related pain and is associated with significant economic, societal, and health implications. The impact of low back pain on the U.S. economy can be gauged from the fact that spine-related health care expenditure reached around $86 billion for the year 2005, increasing 65 percent since 1997.4 The increase in health care utilization among those with LBP is multifactorial, including an increased prevalence of acute and chronic LBP, increased prevalence of those with chronic LBP who seek care, increased per-user health care cost, and innovation in interventional techniques.4–6 There are three structures that are considered to be most important causes of chronic LBP with best available scientific evidence and proven diagnostic techniques. 6 They are the intervertebral discs, facet joints, and the sacroiliac joint. By employing controlled diagnostic injections, the relative contribution 3.8: Percutaneous Discectomy of these structures as a source of chronic LBP has been estimated at 39 percent,7 15 percent, 8 and 19 percent 9 respectively. Lumbar disc prolapse accounts for less than 5 percent of all low back problems, yet is the most common cause of the radicular symptoms.10 Given the incomplete understanding of the exact natural history of disc herniation, clinicians are often faced with the dilemma of treatment options; namely surgical versus non-surgical care. Historical Perspective In 1934, William Jason Mixter, a neurosurgeon, and Joseph Barr, an orthopedic surgeon, published a land- mark article in the New England Journal of Medicine establishing a link between the interveterbral disc and sciatica. 11 They concluded in their paper that previously described “enchondromas,” “Schmorl’s nod- ules” and “ruptured intervertebral discs” as nothing more than intervertebral disc pathology associated with classic signs and symptoms of sciatica. Their work led to a paradigm shift from conservative to surgical management of sciatica. This, in turn, spurred innovations in diagnostic and surgical techniques to minimize the trauma of therapeutic interventions. Operative Versus Non-Operative Treatment A review of the literature shows the pendulum has swung back and forth between operative and non- operative treatment with no single modality proven superior in long-term studies. Saal and Saal, in their well-known retrospective study, have shown a resolution of pain in more than 90 percent of subjects treated non-operatively.12 This is comparable to the outcome of the non-operative arm of another land- mark study by Henrik Weber at four years. 13 Weber’s ten-year follow-up study concluded that although surgically treated patients fared better in the short term (at one year); no significant difference was noted after four years. On the other hand, as-treated four year analysis of a large multicenter trial (Spine Patient Outcomes Research Trial: SPORT) continued to show beneficial effect of surgery over non-operative care. 14 Methodological flaws in both trials, including significant crossover between operative and non- operative arms of the treatment, weaken the conclusions that can be drawn. Hence, in light of the favorable natural history of disc herniation, one could argue in favor of non- operative modalities— including epidural steroid injections— as the mainstay of the treatment in the majority of the patients with lumbar disc herniation associated with radiculopathy. Clear exceptions to this would include progressive neurologic deficits and cauda equina syndrome. Relative advantages for surgical decompression, meanwhile, include rapid pain relief and functional improvement in those who have failed conservative management. 159 Evolution of Minimally Invasive Disc Procedures Historically, conventional discectomy has been the “gold standard” treatment for sciatica refractory to conservative management. With the introduction of surgical microscopes in the 1970s, comparable results could be achieved with “microdiscectomy”; the advantages being a smaller surgical incision and enhanced operative field view.10 This notion of “less is more” allowed comparable outcomes while minimizing tissue damage. Dating back to the 1960s, three decades after Mixter and Barr’s publication, once again there was a paradigm shift to a minimally invasive approach to lumbar disc disease. Lyman Smith was the first to perform percutaneous injection of chymopapain (a proteolytic enzyme) for unrelenting sciatica, a technique he called chemonucleolysis (CNL).15 In 1975, Japanese orthopedic surgeon Hijikata introduced “Percutaneous Manual Nucleotomy” and decompressed the disc by fenestration of the annulus and partial resection of nuclear material.16 Subsequently, CNL and percutaneous manual nucleotomy fell out of favor due to fatal enzymatic complications and technical limitations, respectively.17 Clinicians’ desire for minimally invasive Interventional Pain Medicine therapies in spine surgery techniques continues to lead to breakthroughs in percutaneous intradiscal therapies. Minimally Invasive Percutaneous Disc Procedures Understandably, minimally invasive procedures are associated with smaller surgical scars, rapid convales- cence, less post-operative analgesic consumption, lower cost, and less spinal instability. Gibson and Waddell, in an updated Cochrane review, concluded that surgical discectomy procedures, in general, are superior to chemonucleolysis and other forms of percutaneous discectomy.10 In several trials, most of them non-randomized and uncontrolled, however, the success rate of percutaneous disc decompression ranges from 50 to 90 percent. 18–20 Percutaneous disc procedures can be classified as follows: Percutaneous Disc Decompression The postulated mechanism of indirect decompression techniques entails the excision or degradation of a portion of the central nucleus results in intradiscal pressure reduction and prolapsed disc retraction, thus allowing indirect nerve decompression and, potentially, resolution of radicular pain.21 Understandably, appropriate patient selection with specific disc pathology would be a key to successful outcomes of the chosen percutaneous disc decompression technique. Carragee and others have demonstrated prognostic significance of clinical (symptom duration, litigation status), demographic (age), morphometric (disc size and shape evident on MRI/CT scans) and intraoperative (type of disc herniation) variables in terms of treatment outcomes.22 , 23 Small (<6 mm) and contained disc protrusions (intact outer annulus and posterior longitudinal ligament) are less likely to resorb spontaneously and are associated with fair to worse surgical outcomes after discectomy.22–24 Percutaneous decompression can be accomplished through several techniques including chemical (chemonucleolysis, Ozone), thermal (Radiofrequency Coblation ® , Acutherm ® and laser) and mechanical (Automated Percutaneous Lumbar Discectomy and Dekompressor ® ) means. Each technique has its limitations, however, and full efficacy is unknown due to a paucity of high-quality evidence. Chemonucleolysis was the most thoroughly studied technique in several clinical trials. Systemic reviews of non-randomized clinical trials showed it to be certainly inferior to discectomy but superior to placebo.10 Percutaneous Endoscopic Discectomy (PED) Traditional open discectomy and less invasive microdiscectomy entail the excision of actual herniated portion of the disc, thus allowing the decompression of the nerve. Historically, Parviz Kambin performed the first endoscopic (arthroscopic) disc procedure refining Hijikata’s technique of percutaneous manual 160 neucleotomy.25 Non-working channel arthroscope was used intermittently through the working cannula using uniportal approach to visualize the annulus and periannular structures during the mechanical disc removal. Innovations in techniques led to the emergence of working multi-channel endoscope for the first time in the late 1990s, which allowed constant, real-time visualization while simultaneously removing the disc using uniportal approach.26 PED, unlike the percutaneous disc decompression techniques, not only allows excision of tissue at the center of nucleus, but also removes far lateral migrated disc fragments under direct endoscopic visualization. 25 The learning curve of endoscopic techniques is steep and can result in comparable outcomes to traditional microdiscectomy in experienced surgical hands with the benefits of less spinal instability, less surgical scaring, shorter length of hospital stay, and earlier return to work. Functional Anatomy For any percutaneous disc procedure, access to the intervertebral disc is achieved using an extrapedicular posterolateral approach under oblique fluoroscopic guidance through a working triangular zone 3.8: Percutaneous Discectomy called Kambin Triangle.27 The exiting nerve root or spinal nerve makes the hypotenuse of the triangle delineating its superolateral margin. The longer side of triangle is defined inferiorly by superior endplate of distal vertebra. The shorter leg of triangle is defined medially by superior articular facet of distal vertebra. Further fluoroscopic maneuvers are performed to access disc as follows: 1. An oblique view of the target disc is obtained, whereby superior articular process of the facet joint (SAP) of the target segment lies against the mid-point of the intervertebral disc. 2. A puncture point is identifi ed over the target point at the mid-height of target disc and ventral to the SAP projection. The introducer (Trocar) entry in a coaxial fashion at this insertion point should avoid the spinal nerve as it passes superolateral to this needle trajectory. 3. The fi nal position of introducer needle is confi rmed in AP and lateral projection of fl uoroscopy preferably halfway between superior and inferior end-plates. Fine adjustments are made in accordance with the specifi cs of the procedure. Patient Selection Radiologic identification of disc herniation concordant with patient’s history and physical examination is the mandatory step before contemplating a percutaneous disc procedure. Magnetic resonance imaging has been both sensitive and specific in diagnosing lumbar disc herniations with reasonable reliability.28 Additionally, MRI findings (size of disc herniation and containment) have been found to have significant impact on the surgical outcomes as mentioned before. Recently, in a prospective study, MRI was found to be 70 percent accurate in detecting containment status of lumbar disc herniation. 29 The other important prerequisite is the demonstration of patient’s symptoms emanating from the disc level of proposed target decompression. In case of multi-level disc morphologic changes evident on MRI, one way to identify the culprit level is to perform selective nerve-root block commensurate with the resolution of patient’s pain symptoms. In case of equivocal findings on MRI or lack of pain relief to selective nerve root block, provocative discography is warranted to find the symptomatic disc and to assess its containment. 30 Indications 30 1) Radicular pain > back pain lasting more than 6 months 2) Failure of conservative treatment 3) Small, contained disc herniation evident on MRI or CT discography 4) Involved disc should have more than 50 percent of residual disc height 161 Contraindications30 In addition to the usual contraindications for any neuraxial interventions (such as systemic infection, local infection, coagulopathy, and patient refusal), the other ones that are particular to percutaneous disc decompression are: 1. Severe disc degeneration as evidenced by <50 percent of disc height on imaging 2. Large disc herniation occupying greater than one third of spinal canal 3. Extruded or sequestered nucleus pulposus at affected level 4. Previous lumbar back surgery (laminectomy, discectomy, or fusion) at the affected level 5. Progressive neurologic defi cit 6. Structural deformities such as spondylolisthesis, spinal canal stenosis, scoliosis, tumor, fracture Automated Percutaneous Lumbar discectomy, Laser discectomy, Radiofrequency Coblation ® and Disc Dekompressor` are four current applications of percutaneous disc decompression discussed below. Interventional Pain Medicine Automated Percutaneous Lumbar Discectomy (APLD) After the demise of “percutaneous manual nucleotomy” and diminishing use of CNL due to adverse effects, refinements in surgical techniques led to the emergence of Automated Percutaneous Lumbar Discectomy in 1984. To overcome the inherent limitations of manual nucleotomy with large cannula size (5–8 mm in diameter) and cumbersome manual removal of nucleus pulposus, Onik, et al., developed a new and smaller 2-mm probe with single side port which potentially reduces the risk of nerve root injury and facilitates easier removal of the tissue with all-in-one suction cutting device.31

Procedure After adequate preparation, the aspiration probe is placed through the 2.5-mm size cannula previously positioned against the annulus over the affected side of protrusion using posterolateral approach under fluoroscopic guidance as mentioned above. The aspiration probe is a sharpened cannula which is pneu- matically driven and fitted through an outer needle. Using suction, disc fragments are aspirated, along with irrigation, through inner cannula to a collection bottle. Procedure is discontinued when aspiration ceases significantly. Patient is then recovered and discharged home the same day.

Evidence of Efficacy Clinical studies reported conflicting evidence and thus its effectiveness is yet to be determined. Initial prospective evaluations and case series reported promising outcomes on the order of 75 to 85 percent success rate.32 , 33 Later randomized trials, however, reported lower success rates of 29 to 37 percent and inferiority of APLD to other techniques such as surgical discectomy and CNL, respectively.34 , 35 Subsequently, Revel’s study, however, was criticized due to inappropriate patient selection. Hirsh and coworkers in their systemic review identified four RCT and reported modest evidence for APLD in properly selected populations with contained disc herniation. 35

Percutaneous Laser Disc Decompression (PLDD) Declining popularity of chemonucleolysis and APLD led to the emergence of alternative techniques employing thermal energy devices such as LASER (light amplification by stimulated emission of radiation) and Radiofrequency Nucleotomy. Arguably, the advantage of thermal techniques is combination of mechanical decompression along with modification of intradiscal biochemical milieu resulting into reduction in both neuropathic (radiculopathic) and nociceptive pain, respectively.21 , 37 162 Procedure The first clinical application of PLDD was witnessed in 1986.38 Since then, various types of laser have been described in the literature— those close to infrared region (ND:YAG, Ho:YAG, diode laser); and with visible green radiation (potassium-titanyl-phosphate KTP laser).39 The working principle of PLDD is similar to other decompression techniques— access to intervertebral disc is achieved as mentioned above with smaller diameter needle (18-gauge needle) followed by introduction of 400 μ m optical fiber for transmission of laser energy . Fiberoptic channel is often combined for visualization (LASE ® Endoscopic discectomy). If endoscope is utilized for visualization, dilators are advanced over the guide needle for introduction of endoscope. Different protocols have been reported in the literature as to the type of laser, duration of the treatment and impulsion energy to achieve decompression. Gangi and coworkers40 reported application of 1064-nm Nd:YAG in short pulses of 0.5 to 1 s with pauses of 4–10 s; while Choy and coworkers 41 reported 1064 nm Nd:YAG in short pulses of 1 s and pauses of 1 s with favorable outcomes. The patient is recovered and discharged home same day.

3.8: Percutaneous Discectomy Evidence of Efficacy To date, most observational studies reported favorable outcomes. Tassi, Choy, and coworkers reported a 70 to 89 percent success rate based on experiences from multiple centers and approximately 20,000 procedures. Complication rate, mainly discitis, ranged from 0.3 to 1.0 percent with recurrence rate of 4 to 5 percent over 23 years follow-up.19 Singh, et al., in their systemic review encompassing 14 observational studies only reported modest evidence for short- and long-term pain relief on the order of a 56 to 87 percent success rate. 42 Lack of well-designed randomized clinical trials and methodological flaws in current studies question its validity. Radiofrequency Coblation ® (Plasma Disc Decompression (PDD)/Nucleoplasty) PDD uses bipolar radiofrequency energy working on the principle of ArthroCare Corp (Sunnyvale, CA, USA) patented Coblation ® (controlled ablation) technology. This results into formation of precisely focused plasma field of high-energy ionized particles close to tip of RF electrode (SpineWand™ ) causing dissolution and vaporization of neighboring nucleus tissue.43 As opposed to Laser discectomy with its thermal effects, plasma-based disc ablation works at lower range of temperature (40–70° C) potentially resulting into minimal tissue charring and collateral tissue damage.44 Procedure After adequate preparation, appropriate intervertebral disc is accessed using extrapedicular posterolateral approach as mentioned above with 17-guage obturator stylet. SpineWand™ device is advanced through the introducer needle and pathway is established between anterior and posterior annular margins setting up the proximal and distal limits of excursion. Thereafter, Coblation is commenced, which typically consists of six alternative cycles of ablation and coagulation causing excavation of cavity and volumetric reduction of approximately 1 ml of nuclear tissue.45 During ablation mode, SpineWand is advanced, creating plasma field and causing a molecular dissociation process converting tissue into gas, which exits through the introducer needle. During coagulation mode, SpineWand is retracted along the same pathway inducing collagen shrinkage thereby consolidating the ablation process. The patient is sent to recovery and later discharged home the same day. Evidence of Efficacy Despite the favorable results from pre-clinical and observational studies in terms of safety profile and clinical outcomes, paucity of well designed methodologically sound clinical trials makes this modality 163 questionable. Gerges, et al., reported modest evidence in a pooled analysis of 14 publications (one randomized trial and 13 observational studies) for various outcome measures of pain and function, and the median percentage of improvement was 62.1 percent with a range of 6.25 percent to 84 percent.46 One trial reporting outlying data of 6.25 percent improvement was criticized for inappropriate patient selection including ones with moderately degenerated disc and non-contained disc herniation. 47 Mechanical Disc Decompression Advancements in automated discectomy led to the new addition to the armamentarium of mechanical decompression in the form of Dekompressor (Stryker Corporation, Kalamazoo, MI, USA) with a smaller profile introduced in 2002. This is comprised of a disposable, battery-operated, hand-held rotational motor device attached to a helical probe. The outer cannula measures 1.5 mm with an inner rotating probe. Additional benefits of Dekompressor are to provide disc sample for biopsy and to avoid the thermal damage to neural structures.

Procedure Interventional Pain Medicine The system is deployed into the disc of interest on the affected side through a 17-guage introducer needle previously positioned under fluoroscopic guidance as mentioned above. When fully advanced, the base of the probe locks onto the hub of introducer needle so that at least one full thread of the probe tip extends beyond the end of cannula. The probe is activated and advanced slowly ( ≈ 1cm/10s) under fluoroscopic guidance, which draws out tissue based on the Archimedes screw pump principle. Approximately 0.5 to 2 cc of nucleus pulposus is removed.15 The patient is recovered and sent home the same day. Evidence of Efficacy Scientific evidence is very limited. Two observation studies reported favorable outcomes on the order of 65 to 80 percent for short- and long-term pain relief.48 , 49 Post-Procedural Care 30 Post-procedural rehabilitation protocols vary according to procedure. 1 Generally sitting, bending, twisting, and lifting more than ten pounds are limited for the fi rst week or so. 2 Patients may experience fl are-up of back pain for several days, especially with thermal ablation. Analgesics can be prescribed according to patient needs. Patients may use an ice pack on the site of the insertion the day of the procedure and warm, moist heat the following day if he or she experiences discomfort when the local anesthetic wears off. 3 Activity restriction: generally prophylactic in nature to prevent reherniation. Return to activity varies on case by case. Many patients resume work and daily activities within one week after mechanical disc decompression. On average, with thermal ablation such as Laser: a Sedentary activity at one to two weeks after the procedure b Light duty at two to four weeks depending upon activity c Resumption of full duty at six to ten weeks Complications The complication rate in general appears to be low with the percutaneous disc decompression procedure itself. Rather, the most common complications are those due to needle placement that arise from all intradiscal therapies: 1. Transient paresthesiae and exacerbation of back pain in the fi rst several days are the most common complications requiring supplemental analgesics. 164 2. Superfi cial skin infection 3. Paraspinal abscess 4. Discitis Potential complications due to intradiscal procedures are: 1. Refl ex sympathetic dystrophy or causalgia 2. Vascular injury 3. Abdominal perforation50 4. Aseptic spondylodiscitis (presumably from heat damage to disc or adjacent vertebral endplate) 5. Cauda equina syndrome 50 6. Epidural fi brosis after Coblation51 7. Breakage of probe needle Clinical Pearls 1. At any time during the procedure, if patient reports any lower extremity sensation (radicular pain 3.8: Percutaneous Discectomy or burning foot), procedure should be stopped. The position of the trocar or probe should be assessed using AP and lateral fl uoroscopic views, and repositioned as necessary. 2. Like all intradiscal procedures, multiplanar fl uoroscopy should be used for confi rmation of needle and probe placement. Sedation should be optimal to maintain meaningful communication between the operator and patient. 3. If back pain occurs during PLDD, it may be due to heating of adjacent vertebral endplates or increased pressure within disc from trapped gas. In such cases, the position of the optical fi ber should be checked (away from endplates) and interval between the pulses increased. Aspiration could also be applied through the side arm fi tting to avoid gas trapping. 4. If no aspirated material is present on the Dekompressor probe after three minutes of activation, discontinue the procedure. Conclusion The quest for successful, minimally invasive techniques for the treatment of disc herniation associated with lumbar radiculopathy continues to drive innovation in intradiscal techniques. Like in all of pain medicine, improved patient selection and robust, blinded clinical trials are needed to properly evaluate the efficacy of these techniques and establish their place in the paradigm of LBP treatment. Given the inconsistent and considerable risks of the open surgical alternatives, viable minimally invasive percutaneous disc procedure would seem to be the next reasonable option in appropriately selected population. In the authors’ opinion, endoscopic techniques will be the predominant technique of future spine procedures. 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Clinical outcomes after lumbar discectomy for sciatica: the effects of fragment type and anular competence . J.Bone Joint Surg.Am . 2003 ; 85-A :102 – 108. 24. Saal JA , Saal JS , Herzog RJ . The natural history of lumbar intervertebral disc extrusions treated nonoperatively . Spine . 1990 ; 15 : 683 – 686. 25. Kambin P . Arthroscopic microdiscectomy . Arthroscopy . 1992 ; 8 : 287 – 295. 26. Yeung AT . The evolution of percutaneous spinal endoscopy and discectomy: state of the art . Mt.Sinai J.Med . 2000 ; 67 : 327 – 332. 27. Kambin P , Brager MD. Percutaneous posterolateral discectomy . Anatomy and mechanism. Clin.Orthop.Relat Res . 1987 ; 145 – 154. 28. Jackson RP , Cain JE Jr , Jacobs RR , Cooper BR , McManus GE . The neuroradiographic diagnosis of lumbar herniated nucleus pulposus: II . A comparison of computed tomography (CT), myelography, CT-myelography, and magnetic resonance imaging. Spine. 1989 ; 14 : 1362 – 1367. 29. Weiner BK , Patel R . The accuracy of MRI in the detection of lumbar disc containment . J.Orthop.Surg.Res . 2008 ; 3 : 46. 30. Pomerantz SR , Hirsch JA . Intradiscal therapies for discogenic pain . Semin.Musculoskelet.Radiol . 2006 ; 10 : 125 – 135. 31. Onik G , Helms CA , Ginsburg L , Hoaglund FT , Morris J . Percutaneous lumbar diskectomy using a new aspiration probe . AJR Am.J.Roentgenol . 1985 ; 144 : 1137 – 1140. 166 32. Davis GW , Onik G , Helms C . Automated percutaneous discectomy . Spine . 1991 ; 16 : 359 – 363. 33. Onik G , Mooney V , Maroon JC , et al. Automated percutaneous discectomy: a prospective multi-institutional study . Neurosurgery . 1990 ; 26 : 228 – 232. 34. Chatterjee S , Foy PM , Findlay GF . Report of a controlled clinical trial comparing automated percutaneous lumbar discectomy and microdiscectomy in the treatment of contained lumbar disc herniation . Spine . 1995 ; 20 : 734 – 738. 35. Revel M , Payan C , Vallee C , et al. Automated percutaneous lumbar discectomy versus chemonucleolysis in the treatment of sciatica . A randomized multicenter trial. Spine . 1993 ; 18 : 1 – 7. 36. Hirsch JA , Singh V , Falco FJ , Benyamin RM , Manchikanti L . Automated percutaneous lumbar discectomy for the contained herniated lumbar disc: a systematic assessment of evidence . Pain Physician . 2009 ; 12 : 601 – 620. 37. O’Neill CW , Liu JJ , Leibenberg E , et al. Percutaneous plasma decompression alters cytokine expression in injured porcine intervertebral discs . Spine . 2004 ; 4 : 88 – 98. 38. Choy DS , Case RB , Fielding W , Hughes J , Liebler W , Ascher P . Percutaneous laser nucleolysis of lumbar disks . N.Engl.J.Med . 1987 ; 317 : 771 – 772. 39. Goupille P , Mulleman D , Mammou S , Griffoul I , Valat JP . Percutaneous laser disc decompression for the treatment of lumbar disc herniation: a review . Semin.Arthritis Rheum . 2007 ; 37 : 20 – 30. 3.8: Percutaneous Discectomy 40. Gangi A , Dietemann JL , Ide C , Brunner P , Klinkert A , Warter JM . Percutaneous laser disk decompression under CT and fl uoroscopic guidance: indications, technique, and clinical experience . Radiographics . 1996 ; 16 : 89 – 96. 41. Choy DS , Ascher PW , Ranu HS , et al. Percutaneous laser disc decompression . A new therapeutic modality. Spine . 1992 ; 17 : 949 – 956. 42. Singh V , Manchikanti L , Benyamin RM , Helm S , Hirsch JA . Percutaneous lumbar laser disc decompression: a systematic review of current evidence . Pain Physician . 2009 ; 12 : 573 – 588. 43. Kenneth R, Stalder R., et al . Electrosurgical plasmas. Journal of Physics D: Applied Physics . 2005 ; 38: ( 11 ); 1728 . Ref Type: Abstract. 44. Chen YC , Lee SH , Saenz Y , Lehman NL . Histologic fi ndings of disc, end plate and neural elements after coblation of nucleus pulposus: an experimental nucleoplasty study . Spine . 2003 ; 3 : 466 – 470. 45. Singh V , Piryani C , Liao K , Nieschulz S . Percutaneous disc decompression using coblation (nucleoplasty) in the treatment of chronic discogenic pain . Pain Physician . 2002 ; 5 : 250 – 259. 46. Gerges FJ , Lipsitz SR , Nedeljkovic SS . A systematic review on the effectiveness of the Nucleoplasty procedure for discogenic pain . Pain Physician . 2010 ; 13 : 117 – 132. 47. Cohen SP , Williams S , Kurihara C , Griffi th S, Larkin TM . Nucleoplasty with or without intradiscal electrothermal therapy (IDET) as a treatment for lumbar herniated disc . J.Spinal Disord.Tech . 2005 ; 18 Suppl: S119 – S124. 48. Alo KM , Wright RE , Sutcliffe J , Brandt SA . Percutaneous lumbar discectomy: one-year follow-up in an initial cohort of fi fty consecutive patients with chronic radicular pain . Pain Pract . 2005 ; 5 : 116 – 124. 49. Lierz P , Alo KM , Felleiter P . Percutaneous lumbar discectomy using the Dekompressor system under CT-control . Pain Pract . 2009 ; 9 : 216 – 220. 50. Quigley MR . Percutaneous laser discectomy . Neurosurg.Clin.N.Am . 1996 ; 7 : 37– 42. 51. Smuck M , Benny B , Han A , Levin J . Epidural fi brosis following percutaneous disc decompression with coblation technology . Pain Physician . 2007 ; 10 : 691 – 696. 167

Section 4 Pelvic and Sacral Injections

4.1 Caudal Epidural Injection 169 4.2 Caudal Adhesiolysis 179 4.3 Sacroiliac Joint Injections and Sacroiliac Joint Denervation Techniques 185 4.4 Sacroiliac Neurotomy 193 This page intentionally left blank 169

Chapter 4.1 Caudal Epidural Injection

Spencer Heaton and Srinivasa Raja

Introduction and Indications 170 Disc Herniation and Radiculitis 170 Spinal Stenosis 170 Post-Lumbar Surgery Syndrome 171 Discogenic Pain 171 Anatomy 171 Technique 172 Complications 174 Summary 175 References 176 170 Introduction and Indications Caudal epidural injections (CEI) are indicated for the short and long term management of chronic low back and lower extremity radicular pain in patients without predominant facet-mediated or sacroiliac joint pain [ 1 , 2 ]. Specifically CEIs have been shown to be effective for both short- and long-term management of lumbar disc herniation and radiculitis, post-lumbar surgery syndrome, lumbar spinal stenosis and discogenic pain as summarized in a systematic review by Conn, et al, (see Table 4.1.1 ) [ 23 ]. Other reviews that appropriately evaluate CEIs separately from transforaminal and interlaminar epidural injection techniques conclude that there is moderate evidence for the management of chronic low back pain and radiculopathy [ 1 , 2 , 23 , 24 ].

Table 4.1.1 Grading of recommendations for caudal epidural steroid injections for management of short and long term pain

4.1: Caudal Epidural Injections Diagnosis Associated with Pain Complaint Level of Recommendation

Lumbar disc herniation with or without radiculitis 1A or 1B Discogenic pain without disc herniation or radiculitis 1A or 1B Post lumbar laminectomy syndrome 1B or 1C Lumbar Spinal Stenosis 1B or 1C

1A: Strong recommendation, high-quality evidence. 1B: Strong recommendation, high-quality evidence. 1C: Strong recommendation, low-quality or very low-quality evidence. Source: Guyatt, G., et al. Grading strength of recommendations and quality of evidence in clinical guidelines: report from an american college of chest physicians task force. Chest . 2006;129(1):174–81.

Disc Herniation and Radiculitis There are two randomized trials using fluoroscopic guidance for CEIs in the management of lumbar disc herniation with or without radiculitis. Dashfield, et al. compared CEI with epidural endoscopy targeted steroid placement, reporting significant differences in visual analog scale (VAS) at 6 weeks, 3 months, and 6 months in both groups compared to pretreatment values.[ 15 ] Manchikanti, et al., prospectively evaluated CEIs for short term ( six months) pain management in patients with disc herniation with or without radiculitis. Patients received repeat injections as needed with an average of three to four injections per year. At one-year follow-up, approximately 80 percent of patients reported > 50 percent pain reduction and improved functional status as defined by a 40 percent or greater reduction in Oswestry Disability Index (ODI) scores.[ 9 ] Spinal Stenosis Barre, et al., retrospectively evaluated the long term efficacy of an average of 1.6 fluoroscopically guided CEIs for lumbar spinal stenosis with a mean follow-up of thirty-two months. A significant pain reduction of > 50 percent VAS was seen in 35 percent of patients with no difference in outcome between patients with primarily low back versus lower extremity pain.[ 12 ] In the only prospective, randomized study evaluating fluoroscopically guided CEIs for lumbar spinal stenosis, Manchikanti, et al., demonstrated pain reduction of > 50 percent that was sustained at 1-year follow-up in 55 to 65 percent of patients with > 40 percent ODI reduction in 55 to 80 percent of patients as well as decreased opioid consumption. Patients received repeat injections as needed during the study with an average of three to four injections per year.[ 11 ] Botwin, et al., demonstrated in a prospective study a > 50 percent pain reduction at 6 weeks in 65 percent of the patients with lumbar spinal stenosis accompanied by lower extremity pain in whom an average of 2.2 CEIs were performed. The pain relief was sustained at 6 months in 62 percent of patients and in 54 percent of patients at 12 months.[ 13 ] Lee, et al., reported improved patient satisfaction 171 and pain rated as “much improved” or “no pain” lasting over four months in approximately half of patients following CEI for the treatment of lumbar spinal stenosis.[ 16 ] Post-Lumbar Surgery Syndrome In the only study evaluating the treatment of post-lumbar surgery syndrome with fluoroscopically guided caudal epidural injections, Manchikanti, et al., reported pain relief of > 50 percent in 60 to 65 percent of patients in association with a > 40 percent reduction in ODI in 55 to 70 percent of patients at 1-year follow-up. Similar results were seen in short-term follow-up. During the study, patients received between three to four CEIs. Previous studies that did not use fluoroscopic guidance support the evidence for the effectiveness of CEIs for the treatment of post-lumbar surgery syndrome.[ 25 , 26 ] Discogenic Pain Caudal epidural injections repeated as needed 4 to 5 times per year for discogenic pain in patients with negative diagnostic facet and sacroiliac blocks have been shown to decrease VAS by > 50 percent in more than 70 percent of patients and decrease ODI in 81 percent of patients at both short- and long-term

follow-up.[ 8 ] In a prospective evaluation of patients with either discogram positive or negative pain, Interventional Pain Medicine Manchikanti, et al., reported similar improvement in pain relief and decrease ODI in > 60 percent of patients in both groups at six-month follow-up. This was accompanied by decreased opioid intake and increased employment. Thus provocative discography may not adequately predict pain reduction following CEI in the setting of discogenic pain.[ 17 ] In addition to the common indications above, caudal epidural injections have been used to treat diabetic polyneuropathy, postherpetic neuralgia, complex regional pain syndrome, vertebral compression fractures, and pelvic pain syndromes.[ 27 ] Anatomy Identification of the sacral hiatus (SH) is essential for successful needle placement. The SH is formed by an incomplete fusion of the fifth sacral lamina, forming a triangular-shaped opening that allows access to the epidural space (Figure 4.1.1 ). Superiorly, the apex of the SH is formed by partial laminar fusion at S4,

Posterior Sacroiliac Ligament

Median Sacral Crest

Intermediate Sacral Crest

Lateral Sacral Crest Sacrospinous Ligament

Posterior Sacral Foramen Sacrotuberous Ligament

Sacral Hiatus Superficial Posterior Sacral Cornu Sacrocococcygeal Ligament Deep Posterior Sacrococcygeal Coccyx

Figure 4.1.1 Sacral Anatomy. Adapted with permission from Manchikanti L, et al., Evaluation of ﬂ uoroscopically guided caudal epidural injections. Pain Physician . 2004;7(1):81–92. 172 but may also extend in a cephalad direction as high as S1.28] Bound on each side by the sacral cornua, the hiatus has an approximate width of 4–15 mm. The anterior-posterior dimension at the apex of the SH is typically 4–7 mm but can be as narrow as <2 mm and the length of the SH is typically 10–40mm.[ 28–31 ] The sacrococcygeal ligament overlies the entire SH and is the only barrier to the sacral canal and epidural space besides subcutaneous tissue and skin. Within the sacral canal the dura terminates at S1 (8 percent), S2 (84 percent) or S3 (8 percent) and the epidural venous plexus, which is predominantly in the anterior epidural space, extends to S4. [ 29 , 32 ] Technique Correct needle placement for caudal epidural injections performed based on palpating anatomic landmarks is subject to a failure rate of 23 to 36 percent even in experienced hands. [ 20 , 33 , 34 ] Fluoroscopy is recommended for confirmation of the needle in the epidural space as well as to reduce the risk of aspiration-negative intravascular or intrathecal injection. [ 34 , 35 ] With the patient in a prone position, the epidural space is seen in a lateral fluoroscopic projection as a radiolucency between the 4.1: Caudal Epidural Injections posterior border of the sacral vertebral bodies and the posterior sacral wall with the sacral hiatus visible as the angled termination of the lucency typically at S4-S5 (Figure 4.1.2 ). The overlying skin is prepped and draped in a sterile fashion and local anesthetic is infiltrated carefully at the anticipated midline needle entry site to avoid premature epidural injection. At an angle of approximately 30 degrees, the needle is advanced toward the center of the sacral hiatus. After passing through overlying skin and subcutaneous tissue, the only barrier to entry into the sacral canal is the sacrococcygeal ligament, which is identified by tactile resistance followed by a notable loss of resistance with needle advancement into the epidural space. Intermittent fluoroscopy serves to guide needle depth, which should not exceed 5mm in the epidural space to avoid dural puncture.[ 29 , 31 ] After negative aspiration, injection of radiopaque contrast will provide a confirmatory epidurogram (Figure 4.1.3 ). Classically contrast as viewed in an anterior posterior projection is described as having an irregular margin with heterogeneous small filling defects (Figure 4.1.4 ). Intrathecal injection of contrast results in a myelogram, described as having homogeneous opacity and smooth margins as well as ventral layering on a lateral projection.[ 16 ] Real-time fluoroscopy

Figure 4.1.2 Lateral fluoroscopic view of caudal epidural needle placement. A) sacral hiatus B) posterior sacral wall C) posterior border of sacral vertebral bodies. Note the needle tip advanced past the sacral hiatus into the epidural space. 173 Interventional Pain Medicine

Figure 4.1.3 Lateral fluoroscopic view of caudal epidural contrast injection Arrows: Contrast ﬁ lling the epidural space

Figure 4.1.4 Anterior posterior fluoroscopic view of caudal epidural contrast injection Arrowheads: Contrast indicating ﬂ ow through the anterior sacral foramina. Arrows: Heterogeneous ﬁ lling defects characteristic of epidural contrast during contrast injection is advocated to maximize the potential to recognize intravascular needle placement.[ 35 ] Since contrast will flow in the direction of least resistance, epidural scarring and adhesions will appear as filling defects within the epidural space or nerve sheaths. Preferential fluid flow through the low resistance anterior sacral foramina is expected; nevertheless 10–15 ml of injectate will typically ascend to at least L4 with filling of the dorsal epidural space in nearly all patients and the ventral epidural space in two-thirds of patients.[ 32 , 34 , 36 ] Because of the unpredictable cephalad spread of injectate above the 174 level of L4, CEIs are most suited for pathology at or caudad to the level of L4, especially in a setting of multilevel or bilateral involvement. Most commonly a combination of preservative-free normal saline, local anesthetic, and corticosteroid (methylprednisolone 20–80mg, triamcinolone 20–80mg or betamethasone 6–12mg) is injected with a total volume of 10–15 ml. Corticosteroids have been shown to increase the magnitude and reduce the onset time of pain relief compared to saline alone via epidural injection. Corticosteroids inhibit phospholipase A2 activity, thus reducing local inflammation, in addition to their action as a transient local anesthetic. Membrane stabilization, suppression of dorsal horn sensitization and inhibition of neuronal discharge activity are possible alternative mechanisms of analgesia.[ 21 ] Some studies comparing local anesthetic alone to local anesthetic with corticosteroid via CEI have shown that both groups have similarly positive outcomes.[ 1 ] Complications Complications related to CEI are rare but when they occur they are either due to needle placement or 4.1: Caudal Epidural Injections injectate. Without fluoroscopy CEI is subject to an inaccurate needle placement rate of 23% -36% with a reported 14 percent rate of intravascular needle placement.[ 20 , 33 , 34 ] However, even with fluoroscopic guidance the potential for intravascular injection is not adequately reduced unless real time imaging during contrast injection is used to identify partial intravascular injections. Ergin, et al., using an 18g Tuohy needle reported 1/10 patients with easily identifiable intravenous contrast uptake using intermittent fluoroscopy. This number increased to 4/10 patients with identifiable intravascular uptake when using live fluoroscopy.[ 35 ] Needle placement in the epidural space may potentially be complicated by dural puncture; however, this risk is reduced by using a caudal epidural injection approach. Studies of CEIs report a dural puncture incidence of 0.2 to 0.9 percent without fluoroscopic guidance and no identifiable incidence of dural puncture with fluoroscopic guidance.[ 27 ] Although not designed to quantify complications, studies evaluating the efficacy of caudal epidural injections with fluoroscopic guidance also report no incidence of dural puncture.[ 21 , 27 , 34 ] Nevertheless, a needle in the caudal epidural space should not be advanced more than 5mm beyond the sacrococcygeal ligament and certainly not beyond the level of S3 to minimize the risk of dural puncture. Botwin, et al., in an evaluation of 139 patients who underwent 257 fluoroscopically guided CEIs, reported no major complications and an incidence of 15.6 percent of minor complications as follows: insomnia the night of injection (4.7 percent), transient nonpositional headache resolving within 24 hours (3.5 percent), increased back pain (3.1 percent), facial flushing (2.3 percent), vasovagal reaction (0.8 percent), nausea (0.8 percent), and increased leg pain (0.4 percent). No dural punctures were noted.[ 27 ] Rare complications known to occur with percutaneous epidural access but with unknown incidences in CEIs include epidural abscess, epidural hematoma, discitis, nerve injury, retinal hemorrhage, transient blindness, meningitis, transient paralysis and extradural abscess.[ 37–46 ] The incidence of severe adverse reaction to nonionic radiocontrast media is 0.04 percent.[ 47 ] When administered systemically corticosteroids have many side effects including Cushing’s syndrome, immunosuppression, hyperglycemia, suppression of the pituitary-adrenal axis, bony avascular necrosis, myopathy, epidural lipomatosis, weight gain, osteoporosis, fluid retention, euphoria, depression, mood swings, insomnia, facial flushing, nausea and rash; however intermittent epidural administration of corticosteroids is felt to have a reduced side effect profile.[ 2 , 27 ] Gonzalez, et al., reported a 106 mg/dl average increase in blood glucose the evening following an epidural corticosteroid injection, with elevated blood glucose persisting until post-injection day two.[ 48 ] Ward, et al. demonstrated a decrease in insulin sensitivity that resolved within one week in individuals with normal glucose tolerance test after CEI with triamcinolone. While unlikely to be clinically relevant in patients without a predisposition to hyperglycemia, it is prudent to provide education to diabetic patients regarding the potential for an unpredictable 175 response to a stable insulin regimen.[ 49 ] Studies examining the adrenal response to epidural corticosteroids have reported no measurable absorption of corticosteroid in the systemic circulation; nevertheless, a three-week decrease in plasma cortisol levels has been reported, possibly due to central glucocorticoid receptor occupancy [ 49 , 50 ]. Summary Caudal epidural injections provide the benefit of simple and safe access to the epidural space with minimal risk of serious complication when performed with a conscientious technique using fluoroscopic guidance. Moderate evidence supports the use of CEIs for the treatment of discogenic pain, disc herniation with radicular pain, spinal stenosis and post lumbar surgery syndrome. CEIs may be considered the interventional procedure of choice for these conditions when the pathology is at or inferior to the level of L4, multilevel in presentation or bilateral. Interventional Pain Medicine

Figure 4.1.5 Caudal epidural injection, AP view.

A B Figure 4.1.6 Caudal epidural injection. A. Lateral view B. AP view 176

4.1: Caudal Epidural Injections Figure 4.1.7 Cervical epidural steroid injection, AP view.

AB Figure 4.1.8 Caudal epidural injection A. Lateral view B. AP anterior posterior view

References 1. Manchikanti L , et al . Comprehensive review of therapeutic interventions in managing chronic spinal pain . Pain Physician . 2009 ; 12 ( 4 ): E123 – 198 . 2. Abdi S , et al . Epidural steroids in the management of chronic spinal pain: a systematic review . Pain Physician . 2007 ; 10 ( 1 ): 185 – 212 . 3. Yousef AA , El-Deen AS , Al-Deeb AE , The Role of Adding Hyaluronidase to Fluoroscopically Guided Caudal Steroid and Hypertonic Saline Injection in Patients with Failed Back Surgery Syndrome: A Prospective, Double- Blinded, Randomized Study. Pain Pract . 2010 . Nov-Dec; 10 ( 6 ): 548 - 53 . 4. Mohamed MM , Ahmed M , Chaudary, M . Caudal epidural injection for L4–5 versus L5-S1 disc prolapse: is there any difference in the outcome? J Spinal Disord Tech . 2007 ; 20 ( 1 ): 49 – 52. 5. Manchikanti L , et al . The preliminary results of a comparative effectiveness evaluation of adhesiolysis and caudal epidural injections in managing chronic low back pain secondary to spinal stenosis: a randomized, equivalence controlled trial . Pain Physician . 2009 ; 12 ( 6 ): E341 – 354 . 6. Dincer U , et al . Caudal epidural injection versus non-steroidal anti-infl ammatory drugs in the treatment of low back pain accompanied with radicular pain. Joint Bone Spine . 2007 ;74 ( 5 ): 467 – 471 . 7. Bush K, Hillier, S . A controlled study of caudal epidural injections of triamcinolone plus procaine for the management of intractable sciatica . Spine . 1991 ; 16 ( 5 ): 572 – 575 . 177 8. Manchikanti L , et al . Preliminary results of a randomized, equivalence trial of fl uoroscopic caudal epidural injections in managing chronic low back pain: Part 1— Discogenic pain without disc herniation or radiculitis . Pain Physician . 2008 ; 11 ( 6 ): 785 – 800 . 9. Manchikanti L , et al . Preliminary results of a randomized, equivalence trial of fl uoroscopic caudal epidural injections in managing chronic low back pain: Part 2— Disc herniation and radiculitis . Pain Physician . 2008 ; 11 ( 6 ): 801 – 815 . 10. Manchikanti L , et al . Preliminary results of a randomized, equivalence trial of fl uoroscopic caudal epidural injections in managing chronic low back pain: Part 3— Post surgery syndrome . Pain Physician . 2008 ; 11 ( 6 ): 817 – 831 . 11. Manchikanti , L , et al . Preliminary results of a randomized, equivalence trial of fl uoroscopic caudal epidural injections in managing chronic low back pain: Part 4— Spinal stenosis . Pain Physician . 2008 ; 11 ( 6 ): 833 – 848 . 12. Barre L , et al . Fluoroscopically guided caudal epidural steroid injections for lumbar spinal stenosis: a restrospective evaluation of long term effi cacy . Pain Physician . 2004 ;7 ( 2 ): 187 – 193 . 13. Botwin K , et al . Fluoroscopically guided caudal epidural steroid injections in degenerative lumbar spine stenosis . Pain Physician . 2007 ; 10 ( 4 ): 547 – 558 .

14. Changulani M, Shaju A. Evaluation of responsiveness of Oswestry low back pain disability index . Arch Orthop Interventional Pain Medicine Trauma Surg . 2009 ; 129 ( 5 ): 691 – 694 . 15. Dashfi eld AK , et al . Comparison of caudal steroid epidural with targeted steroid placement during spinal endoscopy for chronic sciatica: a prospective, randomized, double-blind trial . Br J Anaesth . 2005 ; 94 ( 4 ): 514 – 519 . 16. Lee JW , et al . Fluoroscopically guided caudal epidural steroid injection for management of degenerative lumbar spinal stenosis: short-term and long-term results . Skeletal Radiol . 2010 ; 39 ( 7 ): 691 – 699 . 17. Manchikanti , L. , et al ., Effectiveness of caudal epidural injections in discogram positive and negative chronic low back pain. Pain Physician , 2002 . 5 ( 1 ): p. 18 – 29 . 18. Manchikanti L , et al . A comparative effectiveness evaluation of percutaneous adhesiolysis and epidural steroid injections in managing post-lumbar surgery syndrome: a randomized, equivalence controlled trial . Pain Physician . 2009 ; 12 ( 6 ): E355 – 368 . 19. Mendoza-Lattes S , et al . Comparable effectiveness of caudal vs. trans-foraminal epidural steroid injections . Iowa Orthop J . 2009 ; 29 : 91 – 96 . 20. Price CM , et al . Comparison of the caudal and lumbar approaches to the epidural space. Ann Rheum Dis . 2000 ; 59 ( 11 ): 879 – 882 . 21. Sayegh FE , et al . Effi cacy of steroid and non-steroid caudal epidural injections for low back pain and sciatica: a prospective, randomized, double-blind clinical trial . Spine . 2009 ; 34 ( 14 ): 1441 – 1447 . 22. Southern D , et al . Are fl uoroscopic caudal epidural steroid injections effective for managing chronic low back pain? Pain Physician . 2003 ; 6 ( 2 ): 167 – 172 . 23. Conn A , et al . Systematic review of caudal epidural injections in the management of chronic low back pain . Pain Physician . 2009 ; 12 ( 1 ): 109 – 135 . 24. Boswell MV , et al . Interventional techniques: evidence-based practice guidelines in the management of chronic spinal pain . Pain Physician . 2007 ; 10 ( 1 ): 7 – 111 . 25. Revel M , et al . Forceful epidural injections for the treatment of lumbosciatic pain with post-operative lumbar spinal fi brosis . Rev Rhum Engl Ed . 1996 ; 63 ( 4 ): 270 – 277 . 26. Hesla E, Breivik , H . Epidural analgesia and epidural steroid injection for treatment of chronic low back pain and sciatica . Tidsskr Nor Laegeforen . 1979 ; 99 ( 19–21 ): 936 – 939 . 27. Botwin KP , et al . Complications of fl uoroscopically guided caudal epidural injections . Am J Phys Med Rehabil . 2001 ; 80 ( 6 ): 416 – 424 . 28. Sekiguchi M , et al . An anatomic study of the sacral hiatus: a basis for successful caudal epidural block . Clin J Pain . 2004 ; 20 ( 1 ): 51 – 54 . 29. Aggarwal A , et al . Anatomic consideration of caudal epidural space: a cadaver study . Clin Anat . 2009 ; 22 ( 6 ): 730 – 737 . 30. Aggarwal A , Harjeet K , Sahni , D . Morphometry of sacral hiatus and its clinical relevance in caudal epidural block . Surg Radiol Anat. 2009 . 31 :793 – 800 . 31. Senoglu N , et al . Landmarks of the sacral hiatus for caudal epidural block: an anatomical study . Br J Anaesth . 2005 ; 95 ( 5 ): 692 – 695 . 178 32. Ogoke BA . Caudal epidural steroid injections . Pain Physician . 2000 ; 3 ( 3 ): 305 – 312 . 33. Stitz MY, Sommer , HM . Accuracy of blind versus fl uoroscopically guided caudal epidural injection . Spine . 1999 ; 24 ( 13 ): 1371 – 1376 . 34. Manchikanti L , et al . Evaluation of fl uoroscopically guided caudal epidural injections . Pain Physician . 2004 ;7 ( 1 ): 81 – 92 . 35. Ergin A , et al . Accuracy of caudal epidural injection: the importance of real-time imaging . Pain Pract . 2005 ; 5 ( 3 ): 251 – 254 . 36. Kim KM , et al . Cephalic spreading levels after volumetric caudal epidural injections in chronic low back pain . J Korean Med Sci . 2001 ; 16 ( 2 ): 193 – 197 . 37. Nelson DA, Landau , WM . Intraspinal steroids: history, effi cacy, accidentality, and controversy with review of United States Food and Drug Administration reports. J Neurol Neurosurg Psychiatry . 2001 ; 70 ( 4 ): 433 – 443 . 38. Markham JW , Lynge , HN , Stahlman , GE . The syndrome of spontaneous spinal epidural hematoma . Report of three cases. J Neurosurg . 1967 ; 26 ( 3 ): 334 – 342 . 39. Kushner FH, Olson , JC . Retinal hemorrhage as a consequence of epidural steroid injection . Arch Ophthalmol . 1995 ; 113 ( 3 ): 309 – 313 . 40. Dougherty Jr JH , Fraser , RA . Complications following intraspinal injections of steroids . Report of two cases. 4.1: Caudal Epidural Injections J Neurosurg . 1978 ; 48 ( 6 ): 1023 – 1025 . 41. Shealy C.N . Dangers of spinal injections without proper diagnosis . JAMA . 1966 ; 197 ( 13 ): 1104 – 1106 . 42. Goucke CR, and Graziotti , P . Extradural abscess following local anaesthetic and steroid injection for chronic low back pain . Br J Anaesth . 1990 ; 65 ( 3 ): 427 – 429 . 43. Young WF . Transient blindness after lumbar epidural steroid injection: a case report and literature review . Spine . 2002 ; 27 ( 21 ): E476 – 477 . 44. Yue WM, Tan , SB . Distant skip level discitis and vertebral osteomyelitis after caudal epidural injection: a case report of a rare complication of epidural injections . Spine . 2003 ; 28 ( 11 ): E209 – 211 . 45. Hooten WM , Kinney MO , Huntoon , MA . Epidural abscess and meningitis after epidural corticosteroid injection . Mayo Clin Proc . 2004 ; 79 ( 5 ): 682 – 686 . 46. McLain RF , Fry M , Hecht , ST . Transient paralysis associated with epidural steroid injection . J Spinal Disord . 1997 ; 10 ( 5 ): 441 – 444 . 47. Katayama H , et al . Adverse reactions to ionic and nonionic contrast media . 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Chapter 4.2 Caudal Adhesiolysis

Sergio Lenchig and David Lindley

Introduction 180 Procedure 180 Comparable Efficacy of Hyaluronidase and Hypertonic Versus Normal Saline 181 Indications 182 Adverse Effects and Complications 182 Contraindications 182 References 182 180 Introduction Caudal adhesiolysis is an interventional pain management technique developed by Dr. Gabor Racz in the late 1980s, as a treatment to manage chronic low back pain that has not responded to conservative treatment. Caudal adhesiolyis also known as percutaneous epidural adhesiolysis, lysis of epidural adhesions, percutaneous neuroplasty, or epidural neurolysis. The indications include refractory pain due to the development of epidural adhesions as a result of most commonly caused by hemorrhage into the epidural space after a surgical spine intervention, diskogenic leakage into the epidural space, or inflammatory response.1 , 3 , 9 , 16 , 17 During caudal adhesiolyis, a catheter is placed into the epidural space and directed to the area of pathology. The rationale of the procedure is simple and has been described by many. The phenomenon of inflammation, edema, fibrosis, and venous congestion create a mechanical pressure in the area of the posterior longitudinal ligaments, annulus fibrosus, and spinal nerves. This is proposed to create a diminished nourishment of the spinal nerve and/or nerve roots.27 , 28 Nerves that are surrounded by scar tissue are 3.2 times more likely to produce pain. 25 Most back surgery failures were reported to be caused by 4.2: Caudal Adhesiolysis epidural fibrosis by Fritsh et al.,26 however, fibrosis in the spinal canal can also develop without any surgical intervention. Examples of this include infections, hematomas, annular tears, and even intrathecal contrast. 24 Therefore, it has been reasonably suggested that catheter directed delivery of anti-inflammatory medications such as corticosteroids, edema-reducing agents such as hypertonic saline, and fibrolytic agents such as hyaluronidase would be effective treatment of such injury.15 , 22 , 23 Procedure The procedure requires a fluoroscopy suite. The patient is placed in the prone position and he/she may receive intravenous sedation. The site is prepped under sterile technique.6 Interlaminar, transforaminal, and sacral hiatus (caudal) approaches have been described. Although this chapter addresses mainly the caudal adhesiolysis approach, thoracic and cervical interlaminar approaches have also been described. The transforaminal and hiatal approach can both be used to reach the lumbar region. An advantage to the sacral hiatus approach is ease of access. It has been proposed that the transforaminal approach more effectively targets the intervertebral foramen and anterior epidural space.10 , 24 Epidural needles and adhesiolysis catheters are commercially available. The needles used are typically modified with a dulled bevel to allow safer catheter passage. The hub rotates to assist in directing the catheter for during proper placement. Once fluoroscopic verification of proper needle tip placement in the epidural space is confirmed, the adhesiolysis catheter is passed through the needle. The catheter is advanced using fluoroscopic guidance. Once the cathter tip reaches the level of pathology, contrast is injected to confirm intimate contact with the adhesions.1 , 10 At this point, the technique can be differentiated into the classic Racz technique or the modified Racz procedure. In the classic Racz technique, a mixture of local anesthetic, triamcinolone, hyaluronidase, and 10 percent sodium chloride (hypertonic saline) is injected through the Racz catheter. This is followed by either an infusion or intermittent doses of hypertonic saline on session day one. The catheter is left in place and secured. The procedure is repeated again, but without steroids or hyaluronidase in single sessions on days two and three. 4 The patient is then discharged home after removal of the catheter. The modified Racz method is done in a single day session, and the catheter is not left in place. A mixture of local anesthetic and steroid is injected, followed by injection of hypertonic saline solution. Hyaluronidase may be omitted. Manchikanti has proposed this approach to reduce cost and risk, while maintaining efficacy. 3 , 4 Both the classic and modified Racz techniques have been shown to be cost effective. 14 Most cases require multiple interventions. Some evidence suggests that the intervention can be performed every six to eight weeks. Guidelines issued in 2003 by the American Society of Interventional Pain 181 Physicians indicates the classic Racz procedure may be performed twice per year and the modified Racz procedure may be performed up to four times per year.10 , 13 Another variation on the procedure is endoscopic adhesiolysis. Those who have endorsed this variation have proposed that a three-dimensional view allows direct application of the medication at the site of pathology. 6 Comparable Efficacy of Hyaluronidase and Hypertonic Versus Normal Saline The use of hyaluronidase and hypertonic verus normal saline was examined in prospective studies.2 , 9 There was no demonstration of superiority of treatment with the addition of hyaluronidase.9 Use of hypertonic saline, as compared to normal saline, was correlated with decreased need for future repeated procedures. 2 , 9 Interventional Pain Medicine

Figure 4.2.1 Video-Guided Assembly by Myelotec® A. Fiber-optic access port B. Guidewire/Instrumentation access port C. Steering mechanism D. Flexible tip with two working 1-mm channels; ﬁ ber-optic scope ends here E. Injection port F. Injection port Used with permission from Myelotec, Inc.

Figure 4.2.2 Racz Catheter by Epimed® . Used with permission from Epimed International, Inc. 182 Indications The suggested indications after appropriate diagnostic evaluation and failure of conservative modalities include the following: - Post-laminectomy syndrome - Documented epidural adhesions - Vertebral body compression fracture - Disk disruption - Radiculopathy - Resistant multilevel degenerative arthritis - Spinal stenosis11 Adverse Effects and Complications

4.2: Caudal Adhesiolysis Although rare, complications of the Racz procedure may at times be serious. Rapid infusion into the epidural space may cause increased intraspinal pressure, decreased spinal perfusion, cerebral hemorrhage, visual disturbance, and headache. Hypertonic saline infusion may carry a higher risk than other infusion agents used in the epidural space. The transforaminal approach likely carries a higher risk of intravascular penetration and neural trauma as compared to the interlaminar or caudal approaches.15 , 18–21 Puncture and leakage of anesthetic and/or hypertonic saline into the subarachnoid space can cause serious adverse effects such as cardiac arrhythmias, myelopathy, and paralysis. 10 Catheter shear has been reported. In most of the cases reported, the remaining portions of the sheared catheter have been left inside the epidural space with no major consequences. 2 , 4 Contraindications Contraindications include coagulopathy, pregnancy, renal insufficiency, liver dysfunction, history of gastrointestinal bleeding or ulcers, urinary sphincter dysfunction, chronic obstructive pulmonary disease, coronary artery disease, or known allergies to the medications infused as well as any entity that can cause increased intracranial pressure such as intracranial tumors. The patient should have the ability to achieve the desired positioning for the procedure as well as to be able to understand the informed consent. The procedure should never be performed under general anesthesia.10 , 15 References 1. Racz GB , et al . Percutaneous epidural neuroplasty: prospective one-year follow-up. ” Pain Digest . 1999 ; 9 : 97 – 102 . 2. Manchikanti L , et al . One-day lumbar epidural adhesiolysis and hypertonic saline neurolysis in treatment of chronic low back pain: a randomized, double-blind trial. Pain Physician . 2004 ; 7 : 177 – 186 . 3. Manchikanti L , et al . Role of adhesiolysis and hypertonic saline neurolysis in management of low back pain: evaluation of modiﬁ cation of the Racz Protocol. Pain Digest . 1999 ; 9 : 91 – 96 . 4. Manchikanti L , et al , Role of one-day epidural adhesiolysis in management of chronic low back pain: a randomized clinical trial. Pain Physician . 2001b ; 4 ( 2 ): 153 – 166 . 5. American Medical Association (AMA) . Current Procedural Terminology, CPT 2003 . Chicago, Illinois : AMA Press ; 2003 . 6. Manchikanti L , Staats PS , Singh V , et al. Evidence-Based Practice Guidelines for Interventional Techniques in the Management of Chronic Spinal Pain. Pain Physician . 2003 ; 6 ( 1 ): 3 – 81 . 7. Devulder J , et al. “ Relevance of epidurography and epidural adhesiolysis in chronic failed back surgery patients. ” Clinical Journal of Pain . 1995 ; 11 : 147 – 150 . 8. German Medical Association and the National Association of Statutory Health Insurance Physicians. Minimal invasive Wirbelsaülen-Kathetertechnik nach Racz . Joint Policy Statement . March 2003 . 9. Heavner JE , et al . Percutaneous epidural neuroplasty: prospective evaluation of 0.9% NaCl versus 10% NaCl with or without hyaluronidase. Regional Anesthesia and Pain Medicine . 1999 ; 24 ( 3 ): 202 – 207 . 183 10. Manchikanti L, Bakhit C . Percutaneous lysis of epidural adhesions. Pain Physician . 2000 ; 3 ( 1 ): 46 – 64 . 11. Manchikanti L , et al . Effectiveness of percutaneous adhesiolysis with hypertonic saline neurolysis in refractory spinal stenosis. Pain Physician. 2001a ; 4 ( 4 ): 366 – 373 . 12. Manchikanti L , Pakanti R , Pampati V , Fellows B . The value and safety of epidural endoscopic adhesiolysis. Am J Anesthesiol . 2000 ; 27 ( 6S ): 275 – 279 . 13. Manchikanti L , Singh V . “ Epidural lysis of adhesions and myeloscopy.” Current Pain and Headache Reports . 2002 ; 6 : 427 – 435 . 14. Manchikanti L , Pampati V , Bakhit CE etal . “ Non-endoscopic and endoscopic adhesiolysis in post lumbar laminaectomy syndrome. A one-year outcome study and cost effective analysis. ” Pain Physician. 1999 ; 2 : 52 – 58 . 15. Manchikanti L , Pampati V , Cash K . Protocol for evaluation of the comparative effectiveness of percutaneous adhesiolysis and caudal epidural steroid injections in low back and/or lower extremity pain without post- surgery syndrome or spinal stenosis . Pain Physician . 2010 ; 13 : E91 - E110. 16. Epter RS , Helm S , Hayek SM , Benyamin RM , Smith HS , Abdi S . Systematic review of percutaneous adehesiolysis and management of chronic low back pain inpost lumbar surgery syndrome . Pain Physician . 2009 ; 12 : 361 – 378 .

17. Veilhelmann A , Devens C , Trouiller H , Birkenmaier C , Gerdesmeyer L , Refi or HJ . Epidural neuroplasty versus Interventional Pain Medicine physiotherapy to relieve pain in patients with sciatica: a prospective randomized blinded clinical trial. J Orthop Science . 2006 ; 11 : 365 – 369 . 18. Lewandowski EM . The effi cacy of solutions used in caudal neuroplasty. ” Pain Digest . 1997 ; 7 : 323 – 330 . 19. Aldrete JA , Zapata JC , Ghaly R . Arachnoiditis following epidural adhesiolysis with hypertonic saline, report of two cases. Pain Digest . 1996 ; 6 : 368 – 370 . 20. Manchikanti L , Bakhit CE . Removal of torn Racz catheter from lumbar epidural space. Reg Anesth . 1997 ; 22 : 579 – 581 . 21. Kim RC , Porter RW , Choi BH , Kim SW . Myelopathy after intrathecal administration of hypertonic saline. Neurosurgery . 1988 ; 22 : 942 – 944 . 22. Manchikanti L . Role of neuraxial steroids in interventional pain management. Pain Physician . 2002 ; 5 : 182 – 199 . 23. Byrod G, Otani K , Brisby H , Rydevik B , Olmarker K . Methylprednisolone reduces the early vascular permeability increase in spinal nerve roots induced by epidural nucleus pulposus application. J Orthop Res . 2000 ; 18 : 983 – 987 . 24. Racz G , Heavner J , Trescot A . “ Percutaneous lysis of adhesions— evidence for safety and effi cacy. Pain Practice . 2008 ; 8 : 277 – 286 . 25. Ross JS , Robertson JT , Frederickson RC . Association between peridural scar and recurrent radicular pain after lumbar discectomy: magnetic resonance evaluation. Neurosurgery . 1996 ; 28 : 855 – 861 . 26. Fritsch EW , Heisel J , Rupp S. The failed back surgery syndrome. Reasons, intraoperative fi nds, and long term results: a report of 182 operative treatments. Spine . 1996 ; 21 : 626 – 633 . 27. Holyland JA , Fremont AJ , Jayson MI . Intervertebral foramen venous obstruction: a cause of periradicular fi brosis? Spine . 1989 ; 14 : 558 – 568 . 28. Olmaker K , Rydevik B . Pathophysiology of the spinal nerve roots as related to sciatica and disc herniation. In: Herkowitz et al . The Spine . Philadelphia, PA : W.B. Saunders ; 1999 : 159 – 172 . 29. Veihelmann A , Devens C , Trouiller H , Birkenmaier C , Gerdesmeyer L , Refi or HJ . Epidural neuroplasty versus physiotherapy to relieve pain in patients with sciatica: a prospective randomized blinded clinical trial. J Orthop Sci . 2006 ; 11 : 5 – 369 . 30. Talu GK , Erdine S . Complications of epidural neuroplasty: a retrospective evaluation. Neuromodulation . 2003 ; 6 : 237 – 347 . 31. Perkins WJ , David DH , Huntoon MA , Horlocker TT . A retained Racz catheter fragment after epidural neurolysis: implications during magnetic resonance imaging. Anesth Analg. 2003 ; 96 : 1717 – 1719 . 32. Akbas M , Karlsi B . Caudal epidural neuroplasty. Agri . 2005 ; 17 : 40 – 43 . This page intentionally left blank 185 Chapter 4.3 Sacroiliac Joint Injections and Sacroiliac Joint Denervation Techniques

Reginald Ajakwe and F. Michael Ferrante

Introduction 186 Functional Anatomy 186 Patient Selection 186 Indications for SI Joint Infections 187 Contraindications 187 Equipment and Preparation 187 Medications 187 Techniques 188 Diagnostic SI joint Injection with Local Anesthetics and Steroids 188 Radiofrequency (RF) Strip Lesioning of SI Joint 188 Lateral Branch Denervation of SI Joint 190 Complications 190 Clinical Pearls 191 References 192 186 Introduction Sacroiliac joint pain is a challenging condition affecting 15 to 25 percent of patients with axial low back pain. 1 , 2 Sacroiliac (SI) joint pain is often difficult to distinguish from other causes of pain at the lumbosacral junction. It usually presents as pain overlying the sacrum or upper buttock over the SI joint. SI joint pain may refer to the posterior thigh. Pain extending below the knee is unusual, but SI joint pain can refer to the calf, as does facet disease. The most consistent factor for identifying patients with SI joint pain is unilateral pain (unless both joints are involved) localized predominantly below the L5 spinous process.1 , 2 , 3 There are numerous etiologies for SI joint pain. Cohen et al classified these etiologies into intra- articular and extra-articular sources 1 . Examples of intra-articular sources include infection and arthritis. Examples of extra-articular sources include enthesopathy, fractures, and ligamentous injury. There are several factors that predispose a person to SI joint pain. These include true and apparent leg length discrepancy, gait abnormalities, prolonged vigorous exercise, scoliosis, trauma, pregnancy, and spinal fusion to the sacrum. Intra-articular injection of the SI joint with local anesthetic and steroid provides short-term relief of 4.3: Sacroiliac Joint Injections SI joint pain and can help diagnostically in establishing the source of pain. Radiofrequency treatments of SI joint related pain are modestly effective in a fraction of treated patients. 2 Functional Anatomy The SI joints are the largest axial joints in the body. These joints are paired structures formed by the sacrum medially and the ilium of the pelvis laterally. They are large auricular-shaped, diarthrodial synovial joints. They are designed primarily for stability. Their functions include the transmission and dissipation of truncal loads to the lower extremity, limiting x-axis rotation, and facilitating parturition.1 , 2 , 3 Only the anterior third of the interface between the sacrum and ilium is a true synovial joint. The rest of this interface is comprised of an intricate network of ligamentous connections. There is a small portion of the synovial joint space that extends to the posterior-inferior most extent of this interface between the sacrum and ilium. It is from this point that access for intra-articular injection is gained. The superior extent of the joint is difficult to access, as it lies anterior to the iliac crest 1 , 2 , 3 . The SI joint is also supported by a network of muscles that help to deliver regional muscle forces to the pelvic bones. Some of the major muscles that are attached to the SI joint include the gluteus maximus, gluteus medius, lattisimus dorsi, multifidus, biceps femoris, psoas, piriformis, obliquus, and transverse abdomi- nus . The purpose of these muscles is to confer stability for loading and unloading forces produced by walking and running. There is much debate as to the exact innervation of the SI joint. Most authors cite the innervations of the posterior joint to arise from the lateral branches of the L3-S3 dorsal rami. The anterior joint is innervated by L2-S2 ventral rami and may also be innervated by the obturator, superior gluteal nerve and lumbosacral trunk. 1 , 2 , 3 Patient Selection As noted above, patients with SI joint pain are difficult to distinguish from those with other causes of axial spinal pain who report pain over the SI joint or near the lumbosacral junction. Unfortunately, medical history, physical examination, and imaging studies perform very poorly in identifying the dysfunctional SI joint as a pain generator. The most consistent factor for identifying patients with SI joint pain is unilateral pain (unless both joints are affected) localized predominantly below the L5 spinous process.1 , 2 , 3 Point- specific tenderness over the sacral sulcus and posterior sacroiliac spine is another consistent physical finding with SI joint dysfunction. There are several SI joint pain provocation tests that have been developed to detect SI joint dysfunction. Some of the more commonly used tests include FABER (also known as Patrick’s test), Gaenslen’s test, POSH test, READ test, Yeoman’s test, and pelvic rock (these tests are described under the Clinical Pearls section below). Broadhurst, et al., 4 found the combination of FABER 187 (Flexion, Abduction and External Rotation), POSH (Posterior shear), and READ (Resisted Abduction) tests had high predictive value in identifying patients with SI joint dysfunction. This combination of provocation tests demonstrated a sensitivity of 70 to 80 percent and a specificity of 100 percent. Degenerative changes of the joint on standard X-ray roentgenography are uncommon and nonspecific, as most patients with SI joints dysfunction have normal-appearing joints on roentgenography. Other imaging modalities such as CT scan, bone scintigraphy, and MRI also do not play a major role in the selection of patients with SI joint dysfunction. Essentially, resolution of axial back pain following intra- articular injection of local anesthetic under fluoroscopic or computed topography (CT) guidance is the best available diagnostic tool. 5 , 6 Indications for SI Joint Infections 1. Diagnostically to determine if pain is arising from the SI joint. 2. Radiofrequency neurotomy/lesioning is indicated after conservative measures have been exhausted in a patient with SI joint dysfunction diagnosed by concordant response to a diagnostic injection7 . Interventional Pain Medicine Contraindications 1. Absolute a. Patient refusal to give informed consent b. Bacterial infection, systemic or localized in the region of the intended block to be performed c. Bleeding diathesis due to hematologic disease or anticoagulation d. Possible pregnancy 2. Relative a. Allergy to contrast media— may require pre-treatment with H1 and H2 antagonist b. Allergy to local anesthetics, which may require identiﬁ cation and use of local anesthetics of a different class (amide versus ester) c. Co-morbid conditions that may be aggravated by use of corticosteroids, such as poorly controlled diabetes and hypertension; in which case, injection may have to be performed without concomitant use of steroids Equipment and Preparation 1. Fluoroscopy, preferably C-arm ﬂ uoroscope 2. Radiofrequency lesion generator (For RF neurotomy/strip lesioning) 3. Radiofrequency probes, 20-gauge 100mm or 22-gauge 100mm 4. Needles: 3.5-inch 22- or 25-gauge spinal needles 5. Syringes: 3- or 5-ml syringes 6. Gowns, drapes, and gloves 7. Minimal volume extension tubing 8. For prepping, we use chlorhexidine or an iodine-based solution Medications 1. Any conventional local anesthetic is appropriate. Most commonly used include a. Bupivacaine 0.5 percent b. Bupivacaine 0.25 percent c. Lidocaine 2 percent 2. Corticosteroids. There are several options, including: a. Triamcinolone acetonide (10 and 40mg/ml) b. Methylprednisolone acetate (20, 40, or 80 mg/ml 188 c. Betamethasone sodium phosphate (6mg/ml)/betamethasone acetate suspension (3mg/ml) (Celestone Soluspan) 3. Radiographic Contrast Medium: a. Iohexol (Omnipaque 180 or 300). This is an ionic iodine-based contrast. b. Gadodiamide (Omniscan). This is non-iodine based. Omniscan is a formulation of the gadolinium complex of diethylenetriamine pentaacetic acid bismethylamide. Techniques Diagnostic SI joint Injection with Local Anesthetics and Steroids Physical Exam The patient’s lower back should be examined for SI joint tenderness. Four SI joint provocation tests should be performed and the results documented. At our institution, we test for Patrick’s, Gaenslen’s, Yeoman’s and pelvic rock. The same tests should be repeated after the injection, and the results

4.3: Sacroiliac Joint Injections documented. Positioning The patient is positioned prone on a fluoroscopy table. The C-arm is rotated 25 to 35 degrees caudally from the axial plane to place the posterior superior iliac spine and iliac crest cephalad along the line of the SI joint. The c-arm is then rotated obliquely 0 to 30 degrees until the posterior-inferior aspect of the SI joint is clearly visible, and until the anterior and posterior margins of the joint are aligned if possible. Technique The area of the lumbar spine and upper buttocks should be prepped with chlorhexidine (or iodine solution) and draped with sterile towels. The inferior margin of the joint is identified and marked. The skin and subcutaneous tissue overlying the mark is anesthetized with 1 to 2 ml of 1 percent lidocaine. A 3.5-inch, 22-gauge spinal needle is placed through the skin and advanced until it is seated in the tissues in a coaxial plane with the x-axis of the X-ray beam. The needle is adjusted to remain coaxial, or occasionally angled in a slightly cephalad direction, while being directed in incremental steps toward the inferior aspect of the joint using repeated AP fluoroscopic images. Once the surface of the joint space is contacted, the needle is advanced slightly, penetrating the posterior joint capsule. (As the needle enters the joint capsule the needle normally curves slightly in the direction of the joint contour.) A contrast of 1ml may be injected in order to obtain an SI arthrogram and confirm needle placement. After negative aspiration, 4ml of a 1:1 solution of 0.25 percent bupivacaine and 40mg of methylprednisolone (or equiva- lent) may be injected. (The total volume of the SI joint is 4mL.) The needle should then be removed with a 1 percent lidocaine flush. The patient’s back can then be cleaned off with water, and bandages placed over the needle insertion sites. A post-up exam utilizing SI joint provocation test should be repeated in the recovery room area after the injection. Radiofrequency (RF) Strip Lesioning of SI Joint Position The patient is positioned prone on a fluoroscopy table. A pillow should be placed under the lower abdomen to tilt the pelvis backward and swing the iliac crest posteriorly away from the lumbosacral junction. The C-arm is rotated 25 to 35 degrees caudally from the axial plane to place the posterior superior iliac spine and iliac crest cephalad along the line of the SI joint. The C-arm is then rotated obliquely 0 to 30 degrees until the posterior-inferior aspect of the SI joint is clearly visible, and until the anterior and posterior margins of the joint are aligned if possible. Technique At our institution, we typically perform these with mild intravenous sedation. Standard monitors should be placed, and vital signs monitored throughout the procedure. 189

Figure 4.3.1 Anterior-posterior radiogragh of the SI joint during intra-articular SI joint injection following contrast injection.

A 22-gauge spinal needle is in position in the posterior-inferior aspect of the left SI joint, and 1.5 ml of radiographic contrast Interventional Pain Medicine (iohexol 180 mg per ml) has been injected. Note that contrast extends to the superior portion of the joint.

We usually perform 6 lesions per joint using 20- or 22-gauge 100mm radiofrequency probes. The area of the lumbar spine and upper buttocks should be prepped with chlorhexidine (or iodine solution) and draped with sterile towels. The inferior most aspect of the SI joint is identified and marked. The skin and subcutaneous tissue overlying the mark is anesthetized with 1 to 2 ml of 1 percent lidocaine. One 22-gauge 100mm radiofrequency probe is placed through the skin and advanced until it is seated in the tissues in a coaxial plane with the x-axis of the X-ray beam. The needle is advanced toward the target using repeated AP fluoroscopic images. Once the surface of the joint space is contacted, the needle is advanced slightly penetrating the posterior joint capsule. After negative aspiration 1 ml of contrast is injected to confirm placement. A second RF probe is placed about 0.5-1cm above the first in the joint space. After negative aspiration, 4ml of a 1:1 solution of 0.25 percent bupivacaine and Triamcinolone (40mg/ml) is injected through each cannula. A bipolar lesion is performed for 60 to 90 seconds at 80 to

Figure 4.3.2 Technique for RF Denervation Strip Lesioning of SI Joint. Starting at the inferior margin of the joint, two electrodes are inserted in the joint and a bipolar lesion is made at 90 degrees for 90 seconds. A third electrode is place more cephalad in the joint at a distance of less than 1cm from the next inferior electrode (as viewed fluoroscopically). Sequentially, more cephalad lesions are made using this “leapfrog” approach. Typically five lesions are made. 190 90 degrees centigrade. The procedure is repeated, ascending cephalad in the joint until 6 lesions are completed (thus the “strip” lesion). All needles should be removed with a 1 percent lidocaine flush.

Lateral Branch Denervation of SI Joint Position The patient is positioned prone on a fluoroscopy table. AP fluoroscopy with a 25- to 30-degree caudal tilt is used to visualize the junction between the medial superior border of the transverse process and superior articular process (Barton’s point) from L3 to L5. A 2-5 to 30-degree caudal angulation to the axial plane is used for this procedure so that the active tip of the radiofrequency probe will be parallel to the medial branch nerve. (Caudal tilt is unnecessary if employing pulsed radiofrequency neurotomy. See #8 in Clinical Pearls section.) Technique At our institution we typically perform this technique with mild intravenous sedation. Standard monitors

4.3: Sacroiliac Joint Injections should be placed, and vital signs monitored throughout the procedure. The area of the lumbar spine and upper buttocks should be prepped with chlorhexidine (or iodine solution) and draped with sterile towels. AP fluoroscopy (with caudal tilt) is used to identify Barton’s points at L3 to L5 levels. The skin and subcutaneous tissues in these identified areas are anesthetized with 1 percent lidocaine. A 20- or 22-gauge, 100mm radiofrequency probe is advanced towards each of these points under fluoroscopic guidance. Once bone is contacted, negative aspiration is confirmed. Next, the sacral ala and the two o’clock position of the right S1, S2 and S3 foraminae (or the 10 o’clock position of the left S1, S2 and S3 foraminae) are identified and marked. The skin and subcutaneous tissues in these identified areas are anesthetized with 1 percent lidocaine. A 20- or 22-gauge, 100mm radiofrequency probe is advanced toward each of these points under fluoroscopic guidance. Once bone is contacted, negative aspiration is confirmed. As this point, a lateral fluoroscopic view must be obtained to verify that the sacral RF probes are not in the sacral foramina. Next, sensory and motor testing is done. Sensory stimulation is performed at 50 Hertz and at less than 0.5 volts; the patient should usually report a pressure sensation, pain, or tingling during stimulation. Motor testing is done at 2 Hertz and less than 3 times the voltage threshold for sensory stimulation. The patient should have no stimulation to the affected myotome of the lower extremity. Prior to lesioning each level is anesthetized with 1ml of 1 percent lidocaine to reduce thermal pain. Lesions can be created at 80 to 90 degrees centigrade for 60 to 90 seconds. Once lesioning is complete, 1 ml of a 1:1 solution of triamcinolone 40mg/ml and 0.25 percent bupivacaine is injected through each cannula to prophylax against neuritis, dysesthesia, and neuroma formation. Each needle is removed with a 1 percent lidocaine flush. The patient’s back is cleaned, and bandages may be applied to the needle insertion sites. Complications SI Joint Injections Complications 1. An exacerbation of pain can occur in the days following the resolution of the local anesthetic effect. 2. Infection, leading to abscess in the presacral musculature, can occur but is uncommon. 3. Bleeding complications are exceeding low. Strip Lesioning and Lateral Branch Denervation Complications 1. Commonly, a post-procedure pain fl are may occur, resulting in exacerbation of the patient’s typical pain for several days to a week. This can normally be treated with NSAIDs. Occasionally, patients may require a methylprednisolone (medrol) dose pack. 2. Following lateral branch denervation, uncomfortable dysesthesia may occur in a small group of patients. This is usually in the form of a sunburned feeling of the skin at the level of treatment often 191 accompanied by allodynia. Methylprednisolone (medrol) dose pack should be administered to prevent neuritis or neuroma formation. This usually subsides over weeks. 3. Injury to spinal nerve root with new onset radiculopathy has been reported but should be extremely rare when nerve monitor testing (see above) is employed prior to lesioning. 4. Infection, leading to abscess in the presacral musculature, can occur but is uncommon. 5. Bleeding complications are exceeding low. Clinical Pearls 1. For SI joint injection, consider gently bending the needle tip 20 to 30 degrees away from the bevel. This should not be for done for radiofrequency procedures. 2. Do not use alcohol-based solutions to prep for SI joint procedures, as these can drip onto and burn the anal or vaginal mucosa when used to prep the buttock area. 3. In some older patients, it may be impossible to obtain an adequate SI joint arthrogram with contrast due to formation of ubiquitous erosions and plaques. In these cases, the periarticular injection of steroid and local anesthetic may be acceptable. Signifi cant pain relief after both Interventional Pain Medicine intra-articular and periarticular SI joint injection have been demonstrated.5 , 6 4. If using steroids for the injection, do not forget to discuss the possible adverse reactions associated with steroid when obtaining informed consent. 5. Synvisc (Hyalan GF 20) has been used for a case series by Srejic, et al8 . The dose is 8mg/ml per SI joint. This may be repeated twice at two-week intervals. There are no randomized studies showing the effi cacy of Synvisc in the treatment of SI joint dysfunction. 6. For patients with iodine allergy, consider using the non-iodine contrast omniscan. 7. Contrast may be iodine based or non-iodine based. The iodine based radio-contrast medium may be ionic (urograffi n) or non-ionic (Omnipaque). Omnipaque (iohexol) is the agent used most exclusively in pain medicine. 8. Multiple authors have using pulsed radiofrequency neurotomy to reduce maximum temperatures and risk of adjacent tissue destruction9 , 10 . Consequently, pulsed radiofrequency neurotomy does not produce tissue damage, post procedure fl are is uncommon (but does occur), and painful dysesthesias and other consequences of nerve injury are uncommon (but do occur).

AB Figure 4.3.3 Left sacroiliac joint injection. A. AP view B. Lateral view 192 9. Gaenslen’s test is performed with the patient in the supine position. The hip and knee are maximally ﬂ exed toward the trunk and the opposite leg extended. A positive test is deﬁ ned as pain felt across the SI joint. 10. The pelvic rock test is performed with the patient in the prone position. Place the hands on the iliac crests and the thumbs on the anterior superior iliac spines and then forcibly compress the pelvis toward the midline. A positive test is indicated by the production of pain at the sacroiliac joint. 11. Yeoman’s test is performed in the prone position. It stresses the sacroiliac joint by extending the leg and rotating the ilium. A positive test produces pain at the sacroiliac joint. References 1. Cohen SP . Sacroiliac joint pain: A comprehensive review of anatomy, diagnosis, and treatment . Anesth Analg. 2005 ; 101 ( 5 ): 1440 – 1453. 2. Foley BS , Buschbacher RM . Sacroiliac joint pain: Anatomy, biomechanics, diagnosis, and treatment . Am J Phys

4.3: Sacroiliac Joint Injections Med Rehabil . 2006 ; 85 ( 12 ): 997 – 1006. 3. Hansen HC . Sacroiliac joint interventions: a systematic review . Pain Physician . 2007 ; 10 ( 1 ): 165 – 184. 4. Broadhurst N , Bond M . Pain provocative tests for the assessment of sacroiliac joint dysfunction . J Spinal Disord . 1998 ; 11 : 341 – 345. 5. Maugars Y, et al . Assessment of the efﬁ cacy of sacroiliac corticosteroid injection in spondyarthropathies: a double-blinded study . Br J Rheumatol . 1996 : 35 : 767 – 770. 6. Braun J, et al . Computed topography guided corticosteroid injection of the sacroiliac joint in patients with spondyarthropathy with sacroiliitis: clinical outcome and follow up by dynamic magnetic resonance imaging . J Rheumato. 1996 ; 23 : 659 – 664. 7. Ferrante FM , King LF , Roche AE et al . Radiofrequency sacroiliac joint denervation for sacroiliac syndrome . Reg Anesth Pain Med . 2001 ; 26 ( 2 ): 137 – 142. 8. Srejic U , Calvillo O , Kabakjbou K . Viscosupplementation: a new concept in the treatment of sacroiliac joint syndrome: a preliminary report of four cases . Reg Anesth Pain Med . 1999 ; 24( 1 ): 84 – 88. 9. Muhlner SB . Review article: radiofrequency neurotomy for the treatment of sacroiliac joint syndrome . Musculoskeletal Medicine . 2009 ; 10 – 17. 10. Vallejo R , Benyamin R , Kramer J et al . Pulsed radiofrequency denervation for the treatment of sacroiliac joint syndrome . Pain Med . 2006 ; 7 : 429 – 434. 193

Chapter 4.4 Sacroiliac Neurotomy

Rick L. Fisher and Steven P. Cohen

Introduction 194 Functional Anatomy 194 Indications 194 Contraindications 196 Techniques 196 Conventional Radiofrequency Ablation 196 Cooled Radiofrequency 197 Intra-Articular Ablation 198 Bipolar Radiofrequnecy 198 Combination Ligamentous and Neural RFA 200 Intra-Articular Phenol 200 Cryoanalgesia 200 Pulsed Radiofrequency 200 Equipment and Preparation 200 Complications 200 Summary 200 Clinical Pearls 201 References 201 194 Introduction Axial low back pain has many potential etiologies. Traditionally, the facet joints, intevertebral discs, and soft tissues have been implicated as principal causes, with the sacroiliac joint (SI joint) contribution being underappreciated.1 The SI joint, the largest axial joint in the body,2 has been implicated as a primary cause of symptoms in 15 to 25 percent of all patients presenting with axial low back pain. 3 , 4 , 5 Understanding sacroiliac functional anatomy and innervation, clinical presentation, and treatment options are critical in offering appropriate interventional therapies to properly selected patients. Functional Anatomy The average surface area of the SI joint in adults is 17.5 cm2 , though there is inter-individual variability with respect to joint shape, size, and contour.2 The joint is primarily designed for weight-bearing and stabilization, but it’s design is essential in allowing small degrees of multi-planar movement (up to 3 degrees of rotation and 2mm of translation) within the sacroiliac complex.6 , 7 A robust network of

4.4: Sacroiliac Neurotomy ligamentous structures provides anterior and posterior support. (Figures 4.4.1 and 4.4.2 ) Muscular stabilization and joint mobility occur with contributions from the biceps femoris, gluteus maximus , piriformis , and latissimus dorsi via the thoracolumbar fascia and erector spinae. The sacroiliac complex has both intra-articular as well as extra-articular nociceptors with capsular distention and ligamentous stimulation provoking pain in asymptomatic individuals.8 , 9 , 10 , 11 , 12 , 13 Understanding the nerve supply to the sacroiliac region is important to the interventional pain practitioner. The primary innervation of the posterior SI joint arises from the S1-S3 dorsal rami, with a significant percentage of persons receiving contribution from L5.3 , 14 , 15 , 16 , 17 In one recent study, > 50 percent of cadaveric specimens were found to have a contribution from S4 to the long posterior sacroiliac ligament.18 Older reports citing contributions from L4, the obturator nerve and the superior gluteal nerve are non-definitive. Innervation of the ventral joint has not been well-elucidated and is not clinically amenable to denervation. Indications The diagnosis of SI joint pain is challenging and difficult to distinguish from other sources of low back pain (LBP). For this reason, a thorough history and physical exam will give etiologic clues and determine the

Anterior longitudinal ligament Iliolumbar ligament

Anterior sacroiliac ligament

Anterior & lateral sacrococcygeal Greater sciatic foramen ligaments Sacrospinous ligament Iliofemoral ligament

Sacrotuberous ligament Pubofemoral Sacrospinous ligament ligament Public symphysis Acurate pubic ligament

Figure 4.4.1 Anterior view of the sacroiliac joint and surrounding structures. Drawing by Jee Hyun Kim. Reprinted with permission from Cohen SP. Sacroiliac joint pain: a comprehensive review of anatomy, diagnosis, and treatment. Anesth Analg . 2005;101:1440–1453. 195

Supraspinous ligament

Long and short posterior sacroiliac ligaments

Greater sicatic foramen Ischiofemoral ligament Sacrospinous ligament Interventional Pain Medicine Lateral Sacrotuberous sacrococcygeal ligament ligament Deep posterior Superficial posterior sacrococcygeal ligament sacrococcygeal ligament

Figure 4.4.2 Posterior view of the sacroiliac joint and surrounding structures. Drawing by Jee Hyun Kim. Reprinted with permission from Cohen SP. Sacroiliac joint pain: a comprehensive review of anatomy, diagnosis, and treatment. Anesth Analg . 2005;101:1440–1453. need for further work-up. Single historical or physical exam maneuvers have not been shown to reliably identify the SI joint as the pain generator.13 , 19 , 20 Batteries of provocative maneuvers, however, may help in distinguishing SI joint from other sources of chronic low back pain.9 , 21 , 22 Leg length discrepancy and pelvic asymmetry are risk factors for LBP in general, and specifically SI joint pain. 23 Variable presentation seems to be a consistent feature of the disorder. Symptoms arising from the SI joint can present as LBP, leg pain, buttock pain, or pelvic pain. Referral patterns vary significantly, 24 and may extend to the buttock, lower lumbar area, inner thigh, groin, abdomen, lower leg and occasionally the foot.1 , 25 In comparison to other causes of mechanical LBP (e.g., myofascial, facetogenic, discogenic) SI joint pain is usually unilateral in presentation and more commonly associated with trauma (i.e., motor vehicle crash, fall etc.) cumulative stress (e.g., running), unilateral loading sports (e.g., throwing) and pregnancy.1 , 19 , 26 Two indicators used to select patients for procedural interventions are unilateral pain below the fifth lumbar vertebrae spinous process that is exacerbated with rising from a seated position11 , 13 , 19 , 25 and overlying joint tenderness. Radionuclide bone scans and computed tomography are poor screening exams for SI joint dysfunction, as they are characterized by low sensitivity. 27 , 28 , 29 Sacroiliac neurotomy should be considered in properly selected patients who have responded positively but with short-term relief to low-volume diagnostic blocks done with local anesthetic. Whereas most observational studies evaluating SI joint RF denervation used response to intra-articular screening blocks as the primary selection criteria, a recent study by Dreyfuss et al., 12 determined that lateral branch blocks are more effective at blocking afferent input from extra-articular structures than capsular distension, suggesting that extra-articular ligamentous injections may be a superior selection tool. Controlled studies have also demonstrated that extra-articular blocks can provide intermediate-term benefit.30 Similar to the paradigm used for facet joint RF lesioning, some investigators have employed “prognostic” lateral branch blocks before SI joint denervation.31 , 32 Some investigators have sought to examine selection criteria prior to RF denervation. Several studies found no difference in effectiveness when comparing patients who received 50 percent pain relief after diagnostic blocks versus those experiencing > 80 percent pain relief. 1 , 33 A recent randomized, comparative cost-effectiveness study found that the double-block paradigm prior to RF lumbar facet joint 196 denervation was associated with the lowest overall success rate and highest cost per successful procedure.34 The downside of using double-blocks to select patients for RF denervation include not only higher costs, but also a higher dropout rate and a significant false-negative rate.35 Contraindications Absolute contraindications to neuroablative procedures include patient refusal, and infection involving the SI joint or overlying soft tissue structures. Patients with suspected SI joint pathology that fail to respond to prognostic injections should not have subsequent neuroablative procedures performed, as the negative predictive value of prognostic injections are generally higher than the positive predictive value. It is recommended that the guidelines of the American Society of Regional Anesthesia and Pain Medicine for neuraxial procedures 36 be implemented when considering procedures in the anticoagulated patient. Ultimately, the decision to proceed in the presence of known or suspected bleeding diathesis or in the presence of anticoagulant medication is the decision of the attending physician.

4.4: Sacroiliac Neurotomy Techniques In patients with injection-confirmed SI joint pain who fail to obtain persistent relief from blocks, RF denervation can be employed to provide prolonged pain relief. Described RF techniques address targeting the nerves supplying the SI joint,14 , 31 , 37 lesioning the joint proper— results of which have not been favorable,38 , 39 and a combination of ligamentous and nerve lesioning.40 Two-thirds of patients report significant pain relief following RF lesioning targeting the nerve supply of the SI joint. For purposes of discussion, conventional radiofrequency lesioning is performed as follows: Proper electrode placement is confirmed by achieving electrostimulation at 50Hz with concordant sensation at < 0.5 V, with absence of distal motor stimulation at 2Hz up to 2 volts or three times the sensory threshold. An alternative approach is to place small 25-gauge “finder” needles inside each of the relevant foramina, and strategically insert the electrodes in a half circle around the lateral border. Following confirmation of needle placement, 0.5 to 1.0 ml of local anesthetic and steroid solution is injected before RF lesioning is performed for 90 seconds at 80° C. Conventional radiofrequency lesioning creates a lesion 3 to 4 mm in diameter along the length of the active tip tapering at either end. Various approaches are subsequently described. Conventional Radiofrequency Ablation Extra-articular ablation addresses the nerves supplying the joint and is referred to as lateral branch RF denervation. The L5 dorsal ramus is included since this nerve innervates the SI joint in a majority of individuals. Since some people receive a contribution from L4, and because many people have a concurrent facetogenic pain component to their back pain, some investigators routinely target L4 as well. Because S4 innervates the posterior SI joint ligaments in more than 50 percent of individuals, it is our practice to include S4 when the foramen is parallel or cephalad to the inferior plane of the SI joint. To optimize visualization of the foramina, either an AP or slightly cephalad angulation of the image intensifier is utilized. At S1, an ipsilateral oblique view can sometimes further facilitate discerning the posterior foraminal opening from the surrounding bone. To confirm identification of the foramina, 25 gauge “finder” needles are often placed into the foramen and withdrawn to the bony cortex. Conventional electrodes are inserted 3 to 5 mm from the lateral aspect of the designated foramen. Although sometimes difficult on the irregular sacral surface, inserting the electrode so that the active tip lies in a slight cephalo-caudad plane at each location is optimal. Our practice is to use the following positions refer- enced to the face of a clock: right-sided S1 and S2, electrodes at 2:00, 3:30, and 5:00. At S3 on the right, needles are placed at 1:30 and 3:00, but can be varied depending on the relationship of the foramen to the lower edge of the joint. Analogous left-sided targets for S1 and S2 are 7:00, 8:30, and 10:00; at S3, the corresponding location points are 10:30 and 9:00. If targeted, S4 electrode sites should be decided based on the relationship to the inferior joint (Figure 4.4.3 ). Pre-procedure bowel preparation may be useful in helping to visualize the sacral foramina in obese patients and those on high dose opioids.1 197

Figure 4.4.3 Schematic drawing (left image) demonstrating needle placement at approximately 2:00, 3:30, and 5:00 positions on the face of a clock for right S1 lateral-branch RF denervation with anticipated continuous strip lesion (right image).

Drawing by Cherry Crooks. Reprinted with permission from Cohen SP, Strassels SA, Kurihara C, et al. Outcome predictors for sacroiliac Interventional Pain Medicine joint (lateral branch) radiofrequency denervation. Reg Anesth Pain Med . 2009;34;206–214.

Provided concordant sensation is elicited at 0.5 volts or less, sensory stimulation is only performed for the first needle insertion at each level. Electrodes are placed and stimulated at contiguous levels before local anesthetic is administered so as to prevent interference with stimulation from inadvertent spread. Before lesioning, 1 ml of local anesthetic and steroid is injected to prevent coagulation-related pain, enhance lesion size, and reduce the incidence of neuritis.41 , 42 Cooled Radiofrequency Cooled-probe radiofrequency ablation utilizes relatively new technology which heats the target tissue to 75 ° C while maintaining the adjacent tissue at 60° C through internally cooled electrodes, thereby reducing the ability of tissue charring to limit lesion size. The result is a lesion between 8 and 10 mm in diameter that unlike conventional RF, extends significantly distal to the tip.43 Because the lesion volume is eight times greater than with conventional RF, higher success rates should theoretically result from greater area of tissue ablation (Figure 4.4.4 ).

Figure 4.4.4 Difference in lesion size between cooled (A) and conventional (B) radiofrequency probes in chicken meat. Each small line represents a distance of 1mm. Reprinted with permission from Cohen SP, Hurley RW, et al. Randomized, placebo-controlled study evaluating lateral branch radiofrequency denervation for sacroiliac joint pain. Anesthesiology . 2008;109:279–288. 198 Given the eightfold increase in lesion size and the fact that the tip of the electrode resides 2 mm proximal to bone, some practitioners elect not to perform sensory testing. In view of the aggressive lesion created with cooled RF, probe tips must be kept at least 7 mm lateral from the foraminal opening to ensure that temperatures within the foramen are kept <45° C. Probe tip placement is similar to conventional RF (Figure 4.4.5 ), but are placed in a perpendicular, rather than a parallel trajectory. Since the stylet is 2mm longer than the electrode, the tip of the electrode lies 2mm off the bony cortex, which ensures that a three dimensional lesion is created. In a study by Cohen, et al., the authors found a trend for higher success rates when cooled RF was employed than for conventional denervation.1 Disadvantages include an increased risk of bleeding due to the larger probe diameter, and longer lesion times (150 seconds). The use of cooled electrodes is not currently recommended for lumbar medial branch radiofrequency. 43 Intra-Articular Ablation Intra-articular RF denervates the posterior-inferior third of the joint by “leapfrogging” electrodes in the part of the joint accessible to needle penetration (Figure 4.4.6 ). Either unipolar, or preferably bipolar, 4.4: Sacroiliac Neurotomy lesions can be created by this method. In the largest study evaluating intra-articular bipolar RF ablation, Ferrante, et al., reported that 36.4 percent of 33 patients obtained > 50 % pain relief lasting at least 6 months.38 The main limitation to this technique is that it only denervates a small portion of the largest joint in the spinal region. Bipolar Radiofrequnecy Conventional RF lesioning utilizes a monopolar electrode, which limits the lesion size. In a small series of nine patients in which bipolar strip lesions were created between four sequentially placed electrodes, Burnham and Yasui reported that two-thirds of patients continued to experience excellent relief one year post-treatment.32 The advantage of bipolar lesioning is that it reduces the likelihood of missing nerve

Figure 4.4.5 Schematic diagram: (A) Target points for right-sided conventional RF of L4 and L5 (note “X” on L5 transverse process and sacral ala) and cooled-probe S1-S3 (points 1–8) radiofrequency denervation. (B) Anticipated lesions at each of the target points. Reprinted with permission from Cohen SP, Hurley RW, et al. Randomized, placebo-controlled study evaluating lateral branch radiofrequency denervation for sacroiliac joint pain. Anesthesiology . 2008;109:279–288. 199

Figure 4.4.6 Intra-articular technique of SI joint RF denervation. Reprinted with permission from Ferrante FM, King LF, Roche EA, et al. Radiofrequency sacroiliac joint denervation for sacroiliac Interventional Pain Medicine syndrome. Reg Anesth Pain Med . 2001;26:137–142.

tissue. Highly variable tissue impedance, however, may lead to unpredictable results from asymmetric and non-confluent lesions. Bipolar RF can also be accomplished using a single “lead” containing multiple electrodes. One system entails inserting a long, thick, flexible probe in a cephalad direction along the contour of the sacrum so that the length of the 63mm 3-electrode lead contacts bone lateral to the S1-3 foramina (Figure 4.4.7 ). This technique employs both monopolar RF ablation circumferentially around the individual electrodes, and bipolar lesions in between the three electrodes. A separate lesion using a monopolar electrode is generally created at L5 and sometimes L4. Advantages of this technique include a single insertion site, and when the electrode is placed appropriately, a continuous strip lesion that is likely to encompass all nociceptive input into the posterior foramina. The main limitation is that placement can be challenging in patients with aberrant anatomy (i.e., an unusually angled or shaped sacrum), in whom obtaining bony contact along the entire length of the lead can be difficult.

Figure 4.4.7 AP radiograph demonstrating single electrode placement for S1-3 lateral branch radiofrequency denervation. Also pictured is a separate electrode for L5 dorsal ramus lesioning. 200 Combination Ligamentous and Neural RFA CT-guided RF lesioning of the L5 dorsal ramus and sacroiliac posterior interosseous ligaments has been described, with 65 percent of 38 patients reporting substantial pain relief lasting at least 3 months.40 The principal shortcomings of this approach are that it leaves most of the neural structures intact, and there is a dubious conceptual basis for creating RF lesions in soft-tissue structures. In addition, even if ligamentous RF is effective, only a small portion of ligamentous framework is lesioned. Intra-Articular Phenol Intra-articular injections of neurodestructive substances, by bathing the entire joint, should theoretically denervate the entire joint, to include the capsule and anterior portion. Unfortunately, the integrity of the joint capsule is frequently compromised, and spread to the sacral nerve roots is not uncommon with intra-articular injections. 19 , 20 Therefore, this technique is not recommended as a first-line treatment as devastating neurological sequalae can occur. Cryoanalgesia 44 4.4: Sacroiliac Neurotomy Cryoanalgesia is an alternative technique to conventional RF of the SI joint. By cooling the nervous structures, ice crystal formation damages the vasonervorum, leading to severe endoneurial edema. The main advantages of cryoanalgesia in comparison to conventional RF are the larger lesions afforded by the comparatively larger probes, and the fact that it leaves the perineurium intact. Disadvantages include a relatively shorter duration of benefit and a possibly higher risk of bleeding and nerve injury. Pulsed Radiofrequency This technique employs short pulses of high voltage applied to the neural tissues. Since significant rises in temperature are avoided, the neurolytic threshold (45° C) is not reached. Because such a large elec- tromagnetic field is created, the affected area may be greater compared to conventional RF. There is a paucity of evidence supporting the efficacy of pulsed RF for nociceptive pain, and the evidence that does exist suggests that any benefit may be shorter in duration compared to conventional RF. Equipment and Preparation Various manufactures provide quality radiofrequency generators. Important considerations are the ability to lesion several locations simultaneously, which can significantly reduce procedure time. If lesioning based on sensory stimulation is anticipated, the patient should be informed ahead of time what to expect. Because of the need for multiple lesions with large-gauge electrodes, we generally insert an IV to administer sedation. Although RF may be associated with a lower infectious risk than diagnostic blocks, adherence to sterile technique is essential. Complications Common complications from neuroablative procedures range from traumatic post-procedure related pain (several days) to post-denervation neuritis. The latter can last several weeks and may be attenuated by the application of small volume of corticosteroid administered prior to lesioning.41 , 42 In less than 10 percent of patients, numbness or tingling is noted. Infection, superficial, and deep bleeding are risks of any percutaneous procedure, although the incidence is very low. In the event of misguided electrodes, damage to neighboring nervous structures may occur, resulting in incontinence, worsening pain or lower extremity weakness. Allergic reactions to the injectate (local anesthetic and contrast dyes in diagnostic blocks) are rare, but should be included in the informed consent. If intravenous agents are administered, sedation protocols should be implemented. Summary The SI joint is a common, yet frequently overlooked, cause of axial low back pain. RF denervation may provide relief in properly selected patients that respond favorably to a low-volume intra- or 201 extra-articular diagnostic block. Several approaches have been described, but the current evidence favors lateral branch denervation as the most conceptually appealing and effective. Lack of randomized comparative trials precludes definitive statements regarding superiority of one technique over another. Clinical Pearls - The sacroiliac joint is a pain contributor in up to 25 percent of axial low-back-pain patients, often with a variable pain referral pattern. - Patients with a history of trauma, participation in repetitive impact (e.g., running), or unilateral loading sports (e.g., throwing), and pregnancy may be predisposed to SI joint dysfunction. - No single historical item or physical exam finding is pathognomonic for SI joint pain . Patients with a suggestive history, unilateral back pain below L5 (may be bilateral) that is worse with rising from a seated position, and a positive battery of provocative tests should be considered for diagnostic blocks.

- Patients with greater than 50 percent pain relief after diagnostic blocks that lasts less than two months Interventional Pain Medicine should be considered for lateral branch radiofrequency treatment. - Multiple modalities to disrupt the neural input to the SI joint are available. Current evidence suggests that the optimal approach is radiofrequency lesioning of the L5-S3 dorsal rami branches. References 1. Cohen SP , Strassels SA , Kurihara C , et al . Outcome predictors for sacroiliac joint (lateral branch) radiofrequency denervation . Reg Anesth Pain Med . 2009 ; 34 ; 206 – 214 . 2. Bernard TN , Cassidy JD . The sacroiliac syndrome: pathophysiology, diagnosis and management . In: Frymoyer JW , ed. The Adult Spine: Principles and Practice . New York : Raven , 1991 ; 2107 – 2130 . 3. Cohen SP . Sacroiliac joint pain: a comprehensive review of anatomy, diagnosis, and treatment . Anesth Analg . 2005 ; 101 : 1440 – 1453 . 4. Dreyfuss P , Dreyer SJ , Cole A , Mayo K . Sacroiliac joint pain . J Am Acad Orthop Surg . 2004 ; 12 : 255 – 265 . 5. Rupert MP , Lee M , Manchikanti L , Datta S , Cohen SP . Evaluation of sacroiliac joint interventions: a systematic appraisal of the literature . Pain Physician . Mar–Apr 2009 ; 12 ( 2 ): 399 – 418 . 6. Egund N , Olsson TH , Schmid H , Selvik G . Movements in the sacroiliac joints demonstrated with roentgen stereophotogrammetric analysis . Acta Radiol Diagn . 1978 ; 19 : 833 – 845 . 7. Jacob H , Kissling R . The mobility of the sacroiliac joints in healthy volunteers between 20 and 50 years of age . Clin Biomech . 1995 ; 10 : 352 – 361 . 8. Sakamoto N , Yamashita T , Takebayashi T , et al. An electrophysiologic study of mechanoreceptors in the sacroiliac joint and adjacent tissues . Spine . 2001 ; 26 : E468 – 471 . 9. Szadek KM , van der Wurff P , van Tulder MW , Zuurmond WW , Perez RR . Diagnostic validity of criteria for sacroiliac joint pain: a systematic review . J Pain . 2009 ; 10 : 354 – 368 . 10. Fortin JD , Dwyer AP , West S , Pier J . Sacroiliac joint: pain referral maps upon applying a new injection/ arthrography technique. Part I: asymptomatic volunteers . Spine . 1994 ; 19 : 1475 – 1482 . 11. Fortin JD , Aprill CN , Ponthieux B , Pier J . Sacroiliac joint: pain referral maps upon applying a new injection/ arthrography technique. Part II: clinical evaluation . Spine . 1994 ; 19 : 1483 – 1489 . 12. Dreyfuss P , Snyder BD , Park K , Willard F , Carreiro J , Bogduk N . The ability of single site, single depth sacral lateral branch blocks to anesthetize the sacroiliac joint complex . Pain Med . 2008 ; 9 : 844 – 850. 13. Dreyfuss P , Michaelsen M , Pauza K , et al . The value of medical history and physical examination in diagnosing sacroiliac joint pain . Spine . 1996 ; 21 : 2594 – 2602 . 14. Yin W , Willard F , Carreiro J , Dreyfuss P . Sensory stimulation guided sacroiliac joint radiofrequency neurotomy: technique based on neuroanatomy of the dorsal sacral plexus . Spine . 2003 ; 28 : 2419 – 2425 . 15. Grob KR , Neuhuber WL , Kissling RO . Innervation of the sacroiliac joint in humans [in German] . Z Rheumatol . 1995 ; 54 : 117 – 122 . 16. Ikeda R . Innervation of the sacroiliac joint: macroscopic and histological studies . J Nippon Med Sch. 1991 ; 58 : 587 – 596 . 202 17. Fortin JD , Kissling RO , O’Connor BL , Vilensky JA . Sacroiliac joint innervation and pain . Am J Orthop . 1999 ; 28 : 68 – 90 . 18. McGrath MC , Zhang M . Lateral branches of dorsal sacral nerve plexus and the long posterior sacroiliac ligament . Surg Radiol Anat . 2005 ; 27 : 327 – 330 . 19. Schwarzer AC , Aprill CN , Bogduk N . The sacroiliac joint in chronic low back pain . Spine . 1995 ; 20 : 31 – 37 . 20. Maigne JY , Aivakiklis A , Pfefer F . Results of sacroiliac joint double block and value of sacroiliac pain provocation test in 54 patients with low back pain . Spine . 1996 ; 21 : 1889 – 1892 . 21. Laslett M , Williams M . The reliability of selected pain provocation tests for sacroiliac joint pathology . Spine . 1994 ; 19 : 1243 – 1249 . 22. Berthelot JM , Labat JJ , Le Goff B , Gouin F , Maugars Y . Provocative sacroiliac joint maneuvers and sacroiliac joint block are unreliable for diagnosing sacroiliac joint pain . Joint Bone Spine . 2006 ; 73 : 17 – 23 . 23. Prather H , Hunt D . Conservative management of low back pain , part I . Sacroiliac joint pain . Dis Mon . 2004 ; 50 : 670 – 683 . 24. Norman GF : Sacroiliac disease and its relationship to lower abdominal pain . Am J Surg . 1968 ; 116 : 54 – 56 . 25. Slipman CW , Jackson HB , Lipetz JS , et al . Sacroiliac joint pain referral zones . Arch Phys Med Rehabil . 2000 ; 81 : 334 – 338 . 4.4: Sacroiliac Neurotomy 26. Chou LH , Slipman CW , Bhagia SM , et al . Inciting events initiating injection-proven sacroiliac joint syndrome . Pain Med . 2004 ; 5 : 26 – 32 . 27. Maigne JY , Boulahdour H , Chatellier G . Value of quantitative radionuclide bone scanning in the diagnosis of sacroiliac joint syndrome in 32 patients with low back pain . Eur Spine J . 1998 ; 7 : 328 – 331 . 28. Slipman CW , Sterenfeld EB , Chou LH , et al . The value of radionuclide imaging in the diagnosis of sacroiliac joint syndrome . Spine . 1996 ; 21 : 2251 – 2254 . 29. Elgafy H , Semaan HB , Ebraheim NA , Coombs RJ . Computed tomography fi ndings in patients with sacroiliac pain . Clin Orthop . 2001 ; 382 : 112 – 118 . 30. Luukkainen R , Wennerstrand PV , Kautiainen HH , et al . Effi cacy of periarticular corticosteroid treatment of the sacroiliac joint in non-spondyloarthropathic patients with chronic low back pain in the region of the sacroiliac joint . Clin Exp Rheumatol . 2002 ; 20 : 52 – 54 . 31. Cohen SP , Abdi S . Lateral branch blocks as a treatment for sacroiliac joint pain: a pilot study . Reg Anesth Pain Med . 2003 ; 28 : 113 – 119 . 32. Burnham RS , Yasui Y . An alternate method of radiofrequency neurotomy of the sacroiliac joint: A pilot study of the effect on pain, function and satisfaction . Reg Anesth Pain Med . 2007 ; 32 : 12 – 19 . 33. Cohen SP , Stojanovic MP , Crooks M , et al. Lumbar zygapophysial (facet) joint radiofrequency denervation success as a function of pain relief during diagnostic medial branch blocks: a multi-center analysis . Spine . 2008 ; 8 : 498 –504 . 34. Cohen SP , Williams KA , Kurihara C , et al. Randomized, comparative cost-effectiveness study comparing 0, 1 and 2 medial branch blocks before lumbar facet radiofrequency denervation. Accepted to Anesthesiology Feb 2010 . 35. Lord SM , Barnsley L , Bogduk N . The utility of comparative local anesthetic blocks versus placebo-controlled blocks for the diagnosis of cervical zygapophysial joint pain . Clin J Pain . 1995 ; 11 : 208 – 213 . 36. Horlocker TT, Wedel DJ, Benzon H, et al. Regional anesthesia in the anticoagulated patient: defi ning the risks (the second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation) . RAPM . May–June 2003; 28 ( 3 ) 172 – 197 . 37. Buijs EJ, Kamphuis ET , Groen GJ . Radiofrequency treatment of sacroiliac joint-related pain aimed at the fi rst three sacral dorsal rami: a minimal approach . Pain Clinic . 2004 ; 16 : 139 – 146 . 38. Ferrante FM , King LF , Roche EA , et al . Radiofrequency sacroiliac joint denervation for sacroiliac syndrome . Reg Anesth Pain Med . 2001 ; 26 : 137 – 142 . 39. Sanders M , Zuurmond WW . Percutaneous intra-articular lumbar facet joint denervation in the treatment of low back pain: a comparison with percutaneous extra-articular lumbar facet denervation . Pain Clinic . 1999 ; 11 : 329 – 335 . 40. Gevargez A , Groenemeyer D , Schirp S , Braun M . CT-guided percutaneous radiofrequency denervation of the sacroiliac joint . Eur Radiol . 2002 ; 12 : 1360 – 1365 . 41. Dobrogowski J , Wrzosek A , Wordliczek J . Radiofrequency denervation with or without addition of pentoxifylline or methylprednisolone for chronic lumbar zygapophysial joint pain . Pharmacol Rep . 2005 ; 57 : 475 – 480. 203 42. Bruners P , Müller H , Günther RW , Schmitz-Rode T , Mahnken AH . Fluid-modulated bipolar radiofrequency ablation: an ex-vivo evaluation study . Acta Radiol . 2008 ; 49 : 258 – 266 . 43. Cohen SP , Hurley RW , Buckenmaier CC 3rd , Kurihara C , Morlando B , Dragovich A . Randomized, placebo- controlled study evaluating lateral branch radiofrequency denervation for sacroiliac joint pain . Anesthesiology . 2008 ; 109 : 279 – 288 . 44. Trescot AM . Cryoanalgesia in interventional pain management . Pain Physician . Jul 2003 ; 6 ( 3 ):345 – 360 . Interventional Pain Medicine This page intentionally left blank 205

Section 5 Sympathetic Blocks

5.1 The Stellate Ganglion Block 207 5.2 Lumbar Sympathetic Nerve Block 219 5.3 Superior Hypogastric Plexus Block 225 5.4 Celiac Plexus Blocks and Splanchnic Nerve Blocks 235 This page intentionally left blank 207

Chapter 5.1 The Stellate Ganglion Block

Sudhir Diwan and Aisha Baqai

Introduction 208 Anatomy 208 Indications 209 Contraindications 210 Techniques 210 Anterior Paratracheal Approach 210 Lateral/Anterolateral Approach 211 Posterior/Paravertebral Approach 211 Approaches Using Fluoroscopy and Ultrasound 212 Permanent Lesion Techniques 213 Evidence of Successful Sympathetic Blockade 213 Complications 214 Conclusion 215 References 216 208 Introduction The Stellate Ganglion is also known as the cervicothoracic sympathetic block1 . It was first used in the mid-1930s by Leriche, and was further developed by Findley and Patzer 2 . The stellate ganglion block is well known as the standard treatment for complex regional pain syndrome, or CPRS, of the upper extremity 3 , 4 , however is it also used for the diagnosis and treatment of other pain-provoking conditions related to sympathetic dysfunction of the head, neck, and upper extremities.5 This chapter will review the anatomy of the cervical and thoracic sympathetic chain, indications, contraindications, various techniques and approaches to performing the block, methods for verifying the effectiveness of sympathetic blockade, and potential complications of stellate ganglion blockade. Anatomy The cervical sympathetic chain consists of four ganglia, the superior, middle, intermediate, and inferior cervical ganglia.6 In 80 percent of individuals, the first thoracic ganglion and the lowest cervical ganglion

5.1: The Stellate Ganglion Block are fused to form the cervicothoracic, or the stellate ganglion. If these two ganglion are not fused, the first thoracic ganglion is considered the stellate ganglion.7 The stellate ganglion is an oval mass, with dimensions of 2.5 cm in length, 1 cm in width, and 0.5 cm in depth. The stellate ganglion is bordered anteriorly by the subclavian artery near the branching point of the vertebral artery, posteriorly by the neck of the first rib and the transverse process of the C7 vertebra, medially by the longus colli muscle lying over the vertebral column, laterally by the scalenus muscle mass, and inferiorly by the posterior aspect of the pleura. Loose areolar and adipose tissue separating the ganglion from the bony structures below it facilitate the spread of anesthetic solutions used in the blocks 1 . A diagram of the cervical sympathetic chain and surrounding anatomy is depicted in Figure 5.1.1 . Blockade of the stellate ganglion has the potential to interrupt sympathetic and visceral pathways to the head, neck, upper limbs, and thoracic viscera depending on the volume of anesthetic solution used.1 A study by Feigl, et al., looked at the spread of 5, 10, and 20 mL of injectate volumes used for stellate ganglion block in cadaveric models with the use of CT scan to observe the spread of contrast. The group injected with 5 mL of contrast showed a constant spread from C4 to T2-T3, without dissemination to ventral or lateral regions; 10 mL of contrast showed spread from C4- T3 with ventral and lateral spread in one third of the specimens; 20 mL of contrast resulted in spread from C3 to T4-T5, with additional spread to ventral, lateral, and posterior regions of the neck8 .

2 Superior Cervical Ganglion

3 Longus Colli Muscle 4

Middle Cervical Ganglion 6

Vertebral Artery 7 Intermediate Cervical Ganglion

First Rib Stellate Ganglion Esophagus Subclavian Artery Trachea Clavicle Sternothyroid Common Carotid Artery Sternohyoid Sternocleidomastoid Figure 5.1.1 Cervical Sympathetic Chain and Surrounding Anatomy. 209 Generally, all the sympathetic nerves that supply the head and neck, and most of the nerves that supply the upper limb, travel through the stellate ganglion, allowing stellate ganglion blockade to provide sympathetic denervation to these areas.1 . The stellate ganglion may be thought of as a relay station between the paravertebral sympathetic chain and the cervical trunks of the brachial plexus.9 A short review of the anatomy of the cervical and thoracic sympathetic chain illustrates how the stellate ganglion functions as a neural relay center. The cervical ganglia receive preganglionic fibers from the lateral gray column of the spinal cord. Nerve fibers from the upper thoracic spinal cord emerge from the ventral spinal root, and join the spinal nerves at the start of the ventral rami. These nerve fibers leave the spinal nerve through white rami communicantes, which may then enter corresponding thoracic ganglia and ascend into the neck. Primarily the upper three thoracic spinal nerves give off preganglionic fibers for the head and neck, which ascend in the sympathetic trunk to synapse in cervical ganglia. The thoracic segments T2-T6 give rise to preganglionic fibers that supply the upper limb, which ascend the sympathetic trunk to synapse in the stellate ganglion, where postganglionic fibers may continue on to the brachial plexus. The white ramus to the stellate ganglion contains many of the preganglionic fibers that supply the head and neck, which continue up the sympathetic trunk to the superior cervical ganglion where post- Interventional Pain Medicine ganglionic branches may supply vasoconstrictor and sudomotor nerves to the face and neck, the dilator pupillae, non-striated muscle of the eyelid and orbitalis, and secretory fibers to the salivary glands. The stellate ganglion also sends gray ramus communicantes to the C7, C8, and T1 nerves, which give off branches to nearby vessels, the heart, and the vagus nerve. 7 In a significant number of individuals, alternate pathways known as Kuntz’s nerves may bypass the stellate ganglion so that blockade may result in incomplete sympathetic denervation of the upper limb. For instance, an intrathoracic somatic nerve branch may arise from the T2 spinal nerve and join the T1 spinal nerve, which contributes to the brachial plexus. This intrathoracic branch is commonly joined by gray rami communicantes that carry postganglionic fibers that arise from cell bodies in the T2 sympathetic ganglion and possibly lower ganglia. The same situation may exist with a second intrathoracic nerve, which contains postganglionic sympathetic fibers that arise from the T3 ganglion. In these cases, an additional block of the T2 and T3 ganglia may be necessary to completely denervate the upper limb. 1 Indications While the stellate ganglion block may be most notable for the treatment of CPRS, there are many more potential uses for this block. The indications for stellate ganglion block include treatment of: CPRS I (formerly reflex sympathetic dystrophy), CPRS II (formerly causalgia), post-amputation pain syndromes including phantom and stump pain, peripheral vascular disease, acute vascular disease, thrombophlebitis, Raynaud’s disease, cold injuries, chronic occlusive arterial disease, acute myocardial infarction, angina pectoris, pulmonary embolism, cardiac arrhythmias, acute herpes zoster, postherpetic neuralgia, cancer pain, myofascial pain syndromes, orofacial pain, glaucoma, optic neuritis, tinnitus, and vascular headache.1 , 2 , 7 , 9 , 10 , 11 More recently, stellate ganglion blockade has found more innovative uses, including the treatment of intractable postherpetic itching, hot flashes in breast cancer patients, and even symptoms of panic and anxiety in patients with post-traumatic stress disorder12 , 13 , 14 . A more comprehensive list of indications for stellate ganglion blockade is included in Table 5.1.1 . Sympathetic blockade resulting in improved collateral vessel blood flow and decreased risk for continued ischemic damage is one mechanism by which stellate ganglion block may be helpful in treating vascular diseases1 . The efficacy of stellate ganglion blockade in the treatment of CPRS I was recently evaluated by Yucel et al. This study considered patient groups with short and long symptom onset-to-treatment intervals, and compared pain intensity and range of motion of the wrist joint before and 2 weeks after treatment. Stellate ganglion block resulted in a significant difference in wrist range of motion for all patients, as well as a significant difference in pain as measured by visual analog score (VAS). It was notable that the patient group with short symptom onset-to-treatment interval (less than 29 weeks) had a greater decrease in VAS score compared to the group that initiated treatment after 29 weeks. 15 210 Table 5.1.1. Indications and Uses for S tellate Ganglion Blockade1 , 2 , 7 , 9 , 10 , 11 - CPRS I - Thrombophlebitis - CPRS II - Post-amputation pain syndromes - Head: migraine, tension headache, cluster - phantom pain headache, cerebral angiospasm, cerebral - stump pain thrombosis - Peripheral vascular disease - Face: Bell’s palsy, Hunt’s syndrome, - Acute vascular disease atypical facial hair, masticatory muscle - Posttraumatic vasospasm syndrome, orofacial pain, temporoman- - Vasoconstriction from intra-arterial injection of irritating substances dibular arthrosis - Acute arterial occlusion from thrombosis, embolism, or direct - Eye: retinal vascular occlusion, retinal pig- injury ment degeneration, uveitis, optic neuritis, - macular edema, corneal herpes, corneal Acute venous thrombosis - ulcer, allergic conjunctivitis, glaucoma Cold injuries - - Ear/Nose/Throat: allergic rhinitis, nasal Chronic occlusive arterial disease

5.1: The Stellate Ganglion Block polyps, acute or chronic sinusitis, sudden - Raynaud’s disease deafness, Meniere’s disease, benign - Acrocyanosis paroxysmal positional vertigo - Livedo reticularis - Cardiac: arrhythmias, acute myocardial - Acute herpes zoster infarction, angina pectoris - Postherpetic neuralgia - Pulmonary embolism - itching - Neck/Shoulder: neck-shoulder-arm - Cancer pain syndrome, traumatic cervical extremity - Myofascial pain syndromes syndrome, thoracic outlet syndrome, - scapulohumeral periarthritis, postopera- Hot flashes - tive edema, tennis elbow, hyperhidrosis, Panic and anxiety shoulder stiffness - Quinine poisoning

Contraindications Contraindications to performing stellate ganglion blockade include bleeding diatheses, anticoagulant therapy, patient refusal, infection at the site of injection, contralateral pneumothorax or pneumonec- tomy, and performing stellate ganglion block in the presence of unilateral recurrent nerve or phrenic nerve palsy on the side opposite the nerve defect. Bilateral stellate ganglion blockade should be avoided because the compromise of both phrenic or both recurrent laryngeal nerves can result in possible airway obstruction and respiratory embarrassment. Glaucoma and certain heart blocks are relative contraindications to stellate ganglion blockade.11 , 16 Techniques More than sixteen approaches for performing the stellate ganglion block have been described, with the most common being the original anterior paratracheal technique, which was first performed by Leriche.17 Other techniques described include the lateral, anterolateral, superior, and posterior approaches. For all approaches, intravenous access should be started, and standard resuscitative equipment should be available. 7 Classically, techniques were performed blindly. It is, however, becoming more common for stellate ganglion blockade to be performed under the guidance of ultrasound, MRI, or fluoroscopy.11 Anterior Paratracheal Approach For the anterior paratracheal approach, the patient should be supine with the head lifted forward slightly and tilted backwards. The mouth may be held slightly open to help relax the muscles of the neck. 211 The cricoid cartilage is palpated to identify the level of the C6 transverse process. The Chassaignac’s tubercle, or the anterior tubercle of the transverse process of C6, is found in most individuals at approximately 3 cm cephalad to the sternoclavicular joint at the medial border of the sternocleidomastoid muscle. The second and third fingers of the non-dominant hand should placed around the medial edge of the sternocleidomastoid muscle, between the muscle and the trachea. The sternocleidomastoid muscle and the underlying carotid sheath are retracted laterally. Using a 22-gauge, 4- or 5-cm needle, the needle is advance downward, perpendicular to the table plane, until it touches either the C6 tubercle, or the junction between the C6 vertebral body and the tubercle. After touching bone, retract the needle 2 to 5mm to place the bevel anterior to the fascia of the longus colli muscle. Injection of local anesthetic solution into this space allows diffusion cephalad, caudad, and laterally to block the stellate ganglion and surrounding sympathetic chain. Aspiration should be performed before injecting any local anesthetic. A test dose of 0.5 to 1 mL should be slowly injected to look for signs of intravascular injection such as loss of consciousness or seizure. Magnetic resonance imaging, computed tomography, ultrasound, radionuclide tracers, and fluoroscopy may be used to confirm needle placement. One to 2 mL of contrast is generally sufficient to see the characteristic spread of contrast. Lack of visualization of contrast may indicate that Interventional Pain Medicine the injection has entered the intravascular, intrathecal, epidural, or intrapleural space.1 , 7 A modified ver- sion of this block can be performed by entering at the level of C7. Because C7 has a vestigial tubercle, the C7 transverse process is located one fingerbreadth caudal to the C6 tubercle. This technique may require less volume to achieve sympathetic blockade. The close proximity of the C7 transverse process to the vertebral artery and the dome of the lung increases the risk of arterial puncture and pneumothorax, respectively 7 . Lateral/Anterolateral Approach The lateral or anterolateral approach to stellate ganglion blockade begins laterally above the clavicle, passing posterolaterally to the carotid sheath, above the subclavian artery and apex of the lung. The reference point of this block is the anterior tubercle of the sixth cervical transverse process. The soft structures of the neck are displaced to the opposite side of the neck, and the needle is introduced in an anteroposterior direction toward the base of the transverse process. As pressure on the neck is released, the needle assumes a lateral position. Anesthetic solution is then injected into the prevertebral muscles and into the loose fascia in front of them. Because the needle is directed toward the intervertebral foramina, accidental intrathecal injection has occurred more commonly with this technique compared to others. Pneumothorax may also occur.18 Posterior/Paravertebral Approach The posterior or paravertebral approach involves passing through the mass of the paravertebral muscles, then between the vertebral transverse processes close to the emerging spinal nerve. The needle is guided along the side of the body of the vertebra toward the region of the head of the rib. For this technique the patient is positioned with his or her legs drawn up, with the head flexed and supported to eliminate any lateral curvature of the spine. A 10-cm needle is inserted 4 cm lateral to the tip of C7, and T1-T3. The needle is inserted perpendicular to the skin until the transverse process or the articulating portion of the rib is contacted at about 2 to 5 cm in depth. The needle should then be directed caudad until it touches the lower border of the transverse process. The needle should be angled about 20 degrees with the median sagittal plane. The side of the vertebral body should then be contacted at a further depth of 3 cm. Aspiration and a test dose of local anesthetic should be used before injection a full dose of local anesthetic or alcohol. Caution should be taken with this technique, as it involves placing the needle very close to the mediastinal pleural.18 A slight variation on this technique involves inserting the needle 2 to 4 cm lateral to the T1-T3 thoracic spinous processes adjacent to the body of the vertebra. Using a 22-gauge, 8- to 10-cm needle, the lamina is contacted, and the needle is moved laterally off the lamina, parallel to the sagittal plane, until it passes through the costotransverse ligament at a depth of about 2cm beyond the lamina. A loss of resistance technique may be used, or contrast may be injected to 212 document the area of spread.7 Aspiration and a test dose of local anesthetic should be given prior to injecting a full dose of local anesthetic solution. Approaches Using Fluoroscopy and Ultrasound The accuracy of stellate ganglion blockade using fluoroscopy may be greater than techniques performed blindly, and may also require smaller volumes of local anesthetic solution.19 Abdi, et al., described a modified anterior cervical approach for stellate ganglion blockade which involves the use of fluoroscopy in the oblique view to visualize the C5-C6 disc space. With the patient supine with the neck slightly extended and head rotated away from the side being blocked, an anteroposterior image is initially taken. The fluoroscopic beam is then rotated ipsilateral to the side to be blocked, to allow visualization of the neural foramina. A skin wheal is raised on the skin at the point where the uncinate process and the vertebral body join on the fluoroscopy image. Under real-time imaging, a 25-gauge spinal needle is inserted through skin to contact bone, with the tip of the needle tip resting at the junction between the uncinate process and vertebral body. One to 2 mL of radio-opaque contrast should be injected to visualize the longus colli muscle. A 0.5 mL test dose of local anesthetic may be given to rule out intraarterial injection, 5.1: The Stellate Ganglion Block followed by 3 to 5 mL of local anesthetic to block the stellate ganglion.19 Vallejo, et al., described a similar technique using fluoroscopy to obtain an oblique view of the C7 uncinate process and intervertebral foramen to block the stellate ganglion using the insertion of a catheter. After numbing the skin with the 25-gauge needle and lidocaine, an 18-gauge Tuouy needle is advanced in a tunnel view toward the uncinate process. After contact with the uncinate process, the bevel of the needle is turned caudally, and after confirming negative aspiration of blood or cerebrospinal fluid, a 21-gauge radio-opaque epidural catheter is advanced under intermittent fluoroscopic imaging until the catheter tip is at the junction of T2/T3. Contrast is injected to confirm spread, and following a test dose of 0.5 mL, not more than 7 mL of local anesthetic solution is injected. 20 Ultrasound may also be useful when performing stellate ganglion blockade. Compared to fluoroscopy, which reliably identifies bony structures, ultrasounds may help visualize the vertebral vessels, the thyroid gland and vessels, the longus colli muscle, nerve roots, and the esophagus.6 Nakagawa, et al., compared the blind anterior paratracheal approach at C6 with ultrasound guided stellate ganglion blockade using an 8–5 MHz curved array transducer to inject along the longus colli muscle at C6 by the out of plane technique. Using difference in skin temperature and the development of Horner’s syndrome to confirm block efficacy, no significant difference in block efficacy was noted between the two groups.21 More studies are needed to determine which imaging techniques and approaches are most efficacious in performing stellate ganglion blockade. The success rate of the stellate ganglion block is reported to be anywhere between 16% -100% . The rate is so variable because it may be difficult to evaluate the success of the block, and improper placement of the needle can also occur despite confirmatory tests. For example, radiographic contrast injected into the muscle may spread linearly along the transverse process, which would lead the prac- tioner to believe that the needle is correctly placed. Placement of the needle tip within the longus colli muscle, however, results in an ineffective block.22 Variability between the anatomy and dimensions of the bony and muscular landmarks involved with the stellate ganglion block can also account for unsuccessful blockade. Janik, et al., studied the distance from the lateral margin of the cricoid cartilage, to Chassaignac’s tubercle. This distance ranged from 3 mm to 22 mm lateral to the cricoid cartilage, and the depth of the tubercle ranged from 10 mm to 33 mm from the surface of the skin.17 Ates, et al., looked at the thickness of the longus colli muscle, as the anterior paratracheal approach involves withdrawing the needle 2 to 5mm to allow injection anterior to the muscle fascia. Using measurements on cadavers and using MRI, the thickness of the longus colli muscle was found to range between 5 and 10 mm at C6 and C7 on cadavers, and between 8 and 10 mm as measured by MRI. This study suggests that the needle tip may need to be drawn back 8 mm at the C6 level, and 10 mm at the C7 level to avoid intramuscular injection 22 . 213

Thyroid gland Sternohyoid Sternothyroid Trachea Sternocleidomastoid Esophagus Carotid sheath Common Omohyoid carotid artery Stellate Ganglion Internal jugular vein C6 Vagus nerve Anterior scalene muscle

Vertebral Longus colli muscle artery and vein

Figure 5.1.2 Cross-sectional anatomy of the neck at C6 while performing the paratracheal approach. This ﬁ gure was published in Raja SN, Cohen SP, Benzon H, et al. Essentials of Pain Medicine and Regional Anesthesia, 2nd Edition , pp. 687–689. Copyright Elsevier 2004. Interventional Pain Medicine

Permanent Lesion Techniques Permanent blockade of the stellate ganglion may be useful in situations where repeated blockade has successfully treated sympathetically mediated pain, or in situations where a recurrent pathology was initially responsive to sympathetic blockade. Invasive techniques such as open surgery and endoscopic thoracic sympathectomy have been used for stellate sympathectomy. Numerous nonsurgical techniques including thermal and lytic lesioning have also been described. Radiofrequency lesion produces a thermal lesion to the neural structure by generating heat in the tissue around the electrode where radiofrequency current has passed. Multiple lesions may be required to achieve a wider sympathectomy, as performing smaller lesions numerous times may help avoid injury to the nearby arteries and nerves. It is recommended to use a temperature of 80–90° Celsius to avoid boiling the nearby tissue. 11 Lesion size may be determined by several variables, including tissue temperature, duration of the lesion, and electrode size. It should be noted that when performing radiofrequency lesion of the stellate ganglion, no stimulation response can be elicited. Proper localization of the electrode is confirmed by the injection of contrast. Motor stimulation may be performed to ensure a safe distance from the brachial plexus. The procedure is performed with the patient in the supine position. Using two fingers to keep the large vessels aside, a radiofrequency cannula is inserted to contact the base of the transverse process of C6 or C7. Position of the cannula should be confirmed with the injection of 1 mL of contrast. One mL of 2 percent Xylocaine should be injected after motor stimulation, and radiofrequency may be performed.23 Radiofrequency neurolysis under CT guidance has also been used to visualize soft tissues, bone, vessels, and nerves. 24 Forouzanfar, et al., looked at 86 radiofrequency lesion procedures of the stellate ganglion to evaluate the outcome of this therapy for various chronic pain syndromes. About 41 percent of patients having this procedure noted a greater than 50 percent reduction in pain, 55 percent reported no effect on pain, and 4 percent showed worsening of pain, which is consistent with the literature on other stellate ganglion blockade procedures. The study also noted that radiofrequency lesion of the stellate ganglion may be most beneficial in patients suffering from CPRS type 2, ischemic pain, cervicobrachialgia, and post-thoracotomy pain. 9 Evidence of Successful Sympathetic Blockade Correctly performed stellate ganglion blockade may prove difficult to assess on routine examination. Horner’s syndrome may accompany stellate ganglion blockade, and is characterized by miosis (pinpoint pupils), ptosis (drooping of the upper eyelid), enophthalmos (recession of the eyeball within the orbit), along with conjunctival injection, nasal congestion, and facial anhydrosis. The presence of Horner’s 214 syndrome does not necessarily infer complete sympathetic blockade to the upper extremity.11 Additional methods for assessing the completeness of sympathetic interruption include measuring the skin conductance response, or the sympathogalvanic reflex, sweat tests, including the Ninhydrin, cobalt blue, and intravenous starch tests, thermography, skin plethysmography, and measuring a change in pulse amplitude. An increase in pulse amplitude and temperature can occur with a partial sympathetic blockade, so complete sympathetic blockade must be confirmed with the abolition of sweating and the sympathogalvanic response. 1 , 11 , 22 Schurmann, et al., used laser Doppler flowmetry to assess sympathetic nervous function via the vasoconstrictor response to sympathetic stimuli in thirty-three patients with CPRS I following stellate ganglion blockade. Thermography, pain relief using the visual analog scale, and the development of Horner’s syndrome were also monitored. Seventy-nine percent of patients developed Horner’s syndrome, 70 percent showed signs of sympathicolysis with a greater than 1.5° C increase in temperature in the treated hand, and 52 percent had a greater than 50 percent reduction in pain. In the twenty-three patients who did have sympathicolysis, laser Doppler flowmetry showed undisturbed sympathetic nervous function in 48 percent of the patients, and in the 10 patients who did not show

5.1: The Stellate Ganglion Block sympathicolysis, 4 patients still had pain relief greater than 50 percent, suggesting a placebo effect. Only seven patients with pain relief demonstrated both clinical sympathicolysis and extinguished sympathetic nervous function. 25 Thus, despite the numerous methods available to assess sympathetic blockade following stellate ganglion block, it may still prove difficult to establish that a block will prove to be effective and successful. Complications The potential complications of the stellate ganglion block are not few. A list of complications related to stellate ganglion block are listed in Table 5.1.2 . Technical complications can include injury to nearby nerves and viscera including the brachial plexus, trachea, esophagus, pleura, and lung. Injury to be trachea and esophagus may result in mediastinal emphysema, and injury to the pleura and lung can cause

Table 5.1.2. Potential Complications of Stellate Ganglion Blockade11 , 16 , 18 , 26 , 27 , 28 - Injury to the brachial plexus, trachea, esophagus, pleura, lung - Mediastinal emphysema - Pneumothorax - Hemothorax - Compression of the airway - Vasovagal attacks - Air embolism - Local abscess - Cellulitis - Osteitis of the vertebral body and transverse process - Hoarseness - Laryngeal and phrenic nerve paralysis - Brachial plexus blockade - Intra-arterial injection into the vertebral artery or nearby vessels - Seizure - Epidural or intrathecal injection - Bradyarrhythmias - Hypotension - Hypertension - Prolonged Horner’s syndrome 215 pneumothorax and hemothorax requiring chest tube insertion. Local bleeding and hematoma may cause compression of the airway, and vasovagal attacks may also occur. The possible injection of air into a vessel may also result in air embolism. Infectious complications can include local abscess formation, cellulitis, and osteitis of the vertebral body and transverse process. Additional side effects can occur from the use of local anesthetics. Hoarseness, as well as laryngeal and phrenic nerve paralysis may occur, and brachial plexus blockade can also result. Intra-arterial injection into the vertebral artery may cause seizure.11 , 18 Huntoon recently suggested that the ascending and deep cervical arteries, which can be situated anterior to the surface of the C6 and C7 transverse processes, may also be targets for vascular complications during stellate ganglion blockade. 26 Inadvertent injection into the epidural or intrathecal space may also occur, possibly leading to a high spinal and loss of cardioaccelerator activity, resulting in bradyarrhythmias and hypotension. Additional rare and unexpected side effects have also been reported as complications of stellate ganglion block, including a reported case of iatrogenic Horner’s syndrome which lasted nearly one year and transient locked-in syndrome possibly related to intraarterial injection.16 , 27 , 28 Severe hypertension with systolic blood pressures greater than 200 mm Hg has also been noted in several patients following stellate ganglion blockade, possibly from the diffusion of local anesthetic along Interventional Pain Medicine the carotid sheath causing vagal blockade resulting in unopposed sympathetic activity as a result of attenuation of the baroreceptor reflex29 . Conclusion The stellate ganglion block has found many uses beyond the treatment of CRPS over the years. While the anterior paratracheal approach has been the most commonly used technique to perform the stellate ganglion block, the increasing use of imaging guidance such as MRI, ultrasound, and fluoroscopy has allowed a variety of different techniques to be safely employed. Permanent lesioning techniques have also proven useful in situations where repeated blocks have been effective, or where a block has been successful for the treatment of a recurrent pathology. Many studies have been performed to study the efficacy of the stellate ganglion block for various pathologies, as well as identify which techniques and approaches may result in the most successful block, however, there is a need for larger and more comprehensive studies to identify those patients who may benefit the most from stellate ganglion blockade.

Figure 5.1.3 Right stellate ganglion block, AP view. 216 References 1. Loeser JD , Butler SH , Chapman RC , Turk DC. Bonica’s Management of Pain, Third Edition. In: Block of the Sympathetic Nervous System . 2001 :855-856 Philadelphia, PA . Lippincott Williams and Wilkins . 2. Gofeld M , Bhatia A , Abbas , S , et al . Development and validation of a new technique for ultra-sound guided stellate ganglion block . Regional Anesthesia and Pain Medicine . 2009 ; 34 ( 5 ): 475 – 479 . 3. Brown DL . Atlas of Regional Anesthesia, Second Edition. Philadelphia: W.B . Saunders . 1994 ; 189 – 193 . 4. Cepeda MS , Lau J , Carr DB . Defi ning the therapeutic role of local anesthetic sympathetic blockade in complex regional pain syndrome: a narrative and systematic review. The Clinical Journal of Pain . 2002 ; 18 : 216 – 233 . 5. Chaturvedi A , Dash HH . Sympathetic blockade for the relief of chronic pain . Journal of Indian Medical Association . Dec 2001; 99 ( 12 ): 698 – 703 . 6. Narouze S , Vydyanathan A , Patel N . Ultrasound-guided stellate ganglion block successfully prevented esophageal puncture . Pain Physician . 2007 ; 10 : 747 – 752 . 7. Raja SN , Cohen SP , Benzon H , et al . Essentials of Pain Medicine and Regional Anesthesia, Second Edition. In: Peripheral Sympathetic Blocks . 2004 ; 687 – 689 . 5.1: The Stellate Ganglion Block 8. Feigl GC , Rosmarin W , Stelzl A , et al . Comparison of different injectate volumes for stellate ganglion block: an anatomic and radiologic study . Regional Anesthesia and Pain Medicine . May–Jun 2007 ; 32 ( 3 ): 203 – 208 . 9. Forouzanfar T , van Kleef M , Weber WEJ . Radiofrequency lesions of the stellate ganglion in chronic pain syndromes: retrospective analysis of the clinical effi cacy in 86 patients . Clinical Journal of Pain . 2000 ; 16 ( 2 ): 164 – 168 . 10. Salvaggio I , Adducci E , Dell’Aquila L , et al . Facial pain: a possible therapy with stellate ganglion block . Pain Medicine . Oct 2008 ; 9 ( 7 ): 958 – 962 . 11. Elias , Mazin . Cervical sympathetic and stellate ganglion blocks . Pain Physician . 2000 . 3 ( 3 ): 294 – 304 . 12. Peterson RC , Patel L , Cubert K , et al . Serial stellate ganglion blocks for intractable postherpetic itching in a pediatric patient: a case report . Pain Physician . May–Jun 2009 ; 12 ( 3 ): 629 – 632 . 13. Pachman DR , Barton D , Carns PE . Pilot evaluation of a stellate ganglion block for the treatment of hot fl ashes . Support Care Cancer. May 2010 ; 23 ( Epub ahead of print ). 14. Mulvaney SW , McLean B , de Leeuw . The use of stellate ganglion block in the treatment of panic/anxiety symptoms with combat-related post-traumatic stress disorder; preliminary results of long-term follow-up: a case series . Pain Practice . Jul 2010 ; 10 ( 4 ): 359 – 365 . 15. Yucel I , Demiraran Y , Ozturan K , et al . Complex regional pain syndrome type I: effi cacy of stellate ganglion blockade . Journal of Orthopaedics and Traumatology . 2009 ; 10 : 179 – 183 . 16. Lake APJ , Puvanachandra K . A complication of stellate ganglion block? Pain Practice . 2004 ; 4 ( 2 ): 130 – 131 . 17. Janik JE , Hoeft MA , Ajar AH , et al . Variable osteology of the sixth cervical vertebra in relation to the stellate ganglion block . Regional Anesthesia and Pain Medicine. Mar–April 2008 ; 33 ( 2): 102 – 108 . 18. Walls , WKJ . The anatomical approach in stellate ganglion injection . British Journal of Anaesthesia . 1955 ; 27 : 616 – 621 . 19. Abdi S , Zhou Y , Patel N , et al . A new and easy technique to block the stellate ganglion . Pain Physician . 2004 ; 7 : 327 – 331 . 20. Vallejo R , Plancarte R , Benyamin RM , et al . Anterior cervical approach for stellate ganglion and T2 to T3 sympathetic blocks: a novel technique . Pain Practice . 2005 ; 5 ( 3 ): 244 – 148 . 21. Nakagawa M, Hayashi M , Houki S , et al . Ultrasound guided T2 intercostal nerve block: a comparison with stellate ganglion block under the blind technique and ultrasound guided technique . Masui . May 2010 ; 59 ( 5 ): 604 – 609 . 22. Ates Y , Asik I , Ozgencil E , et al . Evaluation of the longus colli muscle in relation to the stellate ganglion block . Regional Anesthesia and Pain Medicine . May–June 2009 ; 34 ( 3 ): 219 – 223 . 23. Manchikanti L . The role of radiofrequency in the management of complex regional pain syndrome . Current Review of Pain . 2000 ; 4 : 437 – 444 . 24. Kastler B , Michalakis D , Clair CH , et al . Stellate ganglion radiofrequency neurolysis under CT guidance . Preliminary study. JBR-BTR . 2001 ; 84 ( 5 ): 191 – 194 . 25. Schurmann M , Gradl G , Wizgal I , et al . Clinical and physiologic evaluation of stellate ganglion blockade for complex regional pain syndrome type I . Clinical Journal of Pain . 2001 ; 17 : 94 – 100 . 217 26. Huntoon , MA . The vertebral artery is unlikely to be the sole source of vascular complications occurring during stellate ganglion block. Pain Practice . 2010 ; 10 ( 1 ): 25 – 30 . 27. Tuz M , Erodlu F , Dodru H , et al . Transient locked-in syndrome resulting from stellate ganglion block in the treatment of patients with sudden hearing loss . Acta Anaesthesiologica Scandinavia . Apr 200 3; 47 ( 4 ): 485 – 487 . 28. Dukes RR , Alexander LA . Transient locked-in syndrome after vascular injection during stellate ganglion block . Regional Anesthesia . Nov–Dec 1993 ; 18 ( 6 ): 378 – 380 . 29. Kimura T , Nishiwaki K , Yokota S, et al . British Journal of Anaesthesia . Jun 2005 ; 94 ( 6 ): 840 – 842 . Interventional Pain Medicine This page intentionally left blank 219

Chapter 5.2 Lumbar Sympathetic Nerve Block

Pradeep Dinakar and Edward Michna

Introduction 220 Clinical Anatomy of the Lumbar Sympathetic Nervous System 220 Indications 220 Technical Considerations 220 Testing the Efficacy of the Lumbar Sympathetic Block 223 Complications 223 Nerve Injury 223 Vascular Injury 223 Infections 223 Medication-Related Complications 224 References 224 220 Introduction Lumbar sympathetic blocks (LSB) are the mainstay in the diagnosis and treatment of various sympathetically mediated conditions, including many abdominal/pelvic and lower extremity neuropathic pain conditions and vascular insufficiency disorders of the lower extremities. In the early twentieth century, LSB was predominantly used to treat lower extremity ischemia from peripheral vascular disease, a technique introduced by Felix Mandl in 1924.1 This technique was improvised with the use of X-ray guidance and contrast over the next couple of decades. When patients respond to sympathetic blocks, long-term pain relief can be achieved with repeating the blocks or using neurolytic agents or cryoneurolysis or radiofrequency lesioning of the sympathetic chain. The blockade of the lumbar sympathetic trunks diagnostically helps differentiate somatic pain from sympathetically mediated pain. Therapeutically interruption of these pain pathways gives dramatic pain relief in conditions that are refractory to other modalities of pain relief, including opioids, neuropathic agents, minimally invasive pain procedures or surgeries. It breaks the vicious pain cycle, thus preventing long term neurodegenerative changes from the central sensitization process due to exposure to 5.2: Lumbar Sympathetic Nerve Block chronic pain. Clinical Anatomy of the Lumbar Sympathetic Nervous System The sympathetic nervous system originates from the descending projections from the hypothalamus, locus ceruleus , nucleus of the solitary tract, reticular formation, amygdala, hippocampus, and olfactory cortex, which synapse with cell bodies of the preganglionic nerve fibers of the sympathetic nervous system in the intermediolateral cell column from T1 through L2. These preganglionic fibers exit along with the ventral nerve root and synapse with the post ganglionic sympathetic fibers at the sympathetic ganglia located either paravertebrally, known as the sympathetic chain or at ganglia located more distantly like the celiac and hypogastric plexus through the splanchnic nerves. The sympathetic ganglia are located between L1-L5 vertebral bodies, three ganglia on each side.2 The neurotransmitter at the sympathetic ganglia is acetylcholine; postganglionic fibers use norepinephrine. The lumbar sympathetic chain is located anterior to the vertebral body, separated from the somatic nerves by the psoas muscles compared to the more dorsal location of the thoracic and cervical chains. Indications Lumbar sympathetic blocks are indicated in a variety of chronic neuropathic pain conditions of the abdominal viscera, pelvis, kidneys, ureters, genitalia, and lower extremities and vascular insufficiency conditions of the lower extremities. The various pain syndromes that benefit from LSB include complex regional pain syndrome (CRPS), phantom limb pain, peripheral neuropathies, acute herpes zoster and post herpetic neuralgia and chronic pain from renal colics. The lower extremity circulatory conditions where LSB serves more a palliative role include atherosclerosis, claudication, rest pain, arteritis, chronic ulcers from vascular insufficiency, and diabetes and following vascular reconstructive surgeries to maintain adequate blood flow. The less common indications include hyperhydrosis. A successful LSB has a positive predictive value in the success of spinal cord stimulator implantation for various neuropathic conditions. See Table 5.2.1 for the indications of lumbar sympathetic blocks. Technical Considerations The objective of this block is to inject local anesthetic over the ipsilateral lumbar sympathetic chain, which is located anterior to the L1-L5 verterbal bodies. The patient is placed in the prone position with a pillow under the abdomen to correct for the lumbar lordosis. The level of block is identified, the spinous process above and below the level is marked and vertebral bodies squared using fluoroscopy. A wide area in the lower back is prepped and draped in the usual sterile fashion with either cholraprep 221 Table 5.2.1 Lumbar sympathetic block indications Neuropathic Pain Syndromes Vascular Insufﬁ cency Other Complex regional pain syndrome(I or II) Atherosclerosis Hyperhidrosis Acute herpes zoster Buerger’s disease Postherpetic neuralgia Vascular ulcers Phantom limb pain Vascular reconstructive surgeries Kidney/ureter colic Vasospasm Frostbite Occlusive and embolic vascular Peripheral neuropathies disease Neuralgia and neuropathies Arteritis from CTD (connective tissue disorder) Diabetic ulcer/gangrene

or Betadine. Using 0.5 percent lidocaine mixed with bicarbonate, a subcutaneous skin wheal is created Interventional Pain Medicine three inches lateral to the interspinous space on the ipsilateral side. Using live fluoroscopy or CT guidance, a 22G 3.5 or 5-inch needle is inserted at a 45-degree angle to the skin and not too deep to avoid the kidney but not too shallow to be in the erector spinae muscle, which could cause painful spasms. The needle should touch the anterolateral border of the upper vertebral body at about two inches. If bony contact is made prior to this, it is most likely the transverse process. A cephalad redirection of the needle is then required. The needle is then walked off anteriorly on the body of the vertebrae till bony contact is lost. The needle is now close to or in the psoas muscle as characterized by some difficulty with injection. Once needle tip is anterior to the psoas muscle, aspirate for blood or CSF. A small amount of contrast should be injected and visualized on fluoroscopy as a longitudinal spread. A single injection of 10–15 ml of 0.25 percent bupivacaine at this level blocks most of the lumbar sympathetic ganglia.3 The role of addition of corticosteroids along with the local anesthetic is controversial.

Kidney Kidney Colon L2

Liver Stomach

Abdominal aorta Inf. vena cava Sympathetic trunk Figure 5.2.1 Line diagram showing a right lumbar sympathetic block. Patient in prone position and the needle entry point is 3 inches lateral to the lumbar spinous process. Care must be taken to avoid the kidney and perforating the peritoneum. 222 5.2: Lumbar Sympathetic Nerve Block

Figure 5.2.2 AP fluoroscopy image of a right lumbar sympathetic block showing the needle approaching the lateral border of the vertebral body. This ﬁ gure was published in Waldman SD. Atlas of Interventional Pain Management, 2nd Edition . Copyright Elsevier 2003.

Figure 5.2.3 Lateral fluoroscopy image of a lumbar sympathetic block with the needle tip anterior to the vertebral body. Contrast lines the sympathetic trunk without any peritoneal or epidural spread. This ﬁ gure was published in Waldman SD. Atlas of Interventional Pain Management, 2nd Edition . Copyright Elsevier 2003.

Chemical neurolysis of the lumbar sympathetic chain is done in a similar fashion except that either 6–10 percent phenol or 50–95 percent alcohol mixed with contrast is injected instead of the local anesthetic. This results in a long-term relief of the sympathetically mediated pain from destruction of the neurons and cell bodies. The lumbar sympathetic ganglion radiofrequency lesioning is done with the needle in similar position followed by a trial sensory stimulation at 50 Hz at 1 volt is tested. Stimulating the sympathetic chain results in localized back pain as opposed to groin and leg pain that is secondary to somatic nerve stimulation. Motor stimulation with 2 Hz at 3 volts should be negative before lesioning the nerves at 80 ° C for 60 seconds. 223 Testing the Efficacy of the Lumbar Sympathetic Block Patients immediately rate a significant reduction in pain with increased activity and range of motion of the affected area. The skin temperature of the lower extremities should increase by 1 to 2 ° C following the block. In vaso-occlusive conditions along with pain reduction and increased temperature improved claudication distance and increase blood flow on a Doppler study is seen. Psychogalvanic response or sweat testing should show no sweat on the blocked lower extremity. Complications The complications following the LSB have significantly reduced with the widespread use of fluoroscopy. A good understanding of the clinical anatomy and technical details of the procedure is also essential in reducing the incidence complications.4 Nerve Injury

Direct mechanical injury to the somatic nerves is more common with cervical and thoracic sympathetic Interventional Pain Medicine block and less with the LSB due to the lumbar sympathetic chain anatomy as described above. Sometimes, persistent paresthesia from somatic nerve injury occurs and this could be debilitating. Accidental epidural, intrathecal, or intraspinal injections are rare given the widespread use of fluoroscopy and contrast. Post-dural headaches can be associated with such accidental spinal or nerve root injuries. Vascular Injury Injury to the radicular artery of Adamkiewicz, which can arise as low as L2, can result in spinal cord infarcts. Incidence of other major subcutaneous or retroperitoneal bleeds with due to LSB is minimal in patients without coagulaopathy. Bleeding from the IVC or aorta can be significant but is usually self limited. Infections Risks for subcutaneous and deeper infections after LSB is minimal if standard antiseptic precautions are followed. Routine antibiotics are not required. Rarely accidental injury to the disc could also result in discitis.

AB Figure 5.2.4 Right lumbar sympathetic block. A. Lateral view B. AP view 224 Medication-Related Complications Intravascular injection of the local anesthetic into the IVC or the aorta can cause seizures and/or cardiovascular collapse. Using epinephrine in the local anesthetic would cause heart rate changes, which would be helpful indicator for intravascular injections. Otherwise following routine precautions of aspiration prior to injection, using contrast and fluoroscopy and slower injection are essential. References 1. Mandl F. Die parvertibrale injection . Vienna : J Springer , 1926 . 2. Rocco AG , Palombi D , Racke D . Anatomy of the lumbar sympathetic chain . Reg Anesth . 1995 ; 20 : 13. 3. Hatangdi WS , Boas RA . Lumbar sympathectomy: a single needle technique . Br J Anaesth . 1985 ; 57 : 285. 4. Neal JM , Rathmell JP . Complications in Regional Anesthesia and Pain Medicine . Philadelphia : Saunders Elsevier ; 2006 . 5.2: Lumbar Sympathetic Nerve Block 225

Chapter 5.3 Superior Hypogastric Plexus Block

Ketan Patel and Paul J. Christo

Introduction 226 Indications 226 Contraindications 227 Functional Anatomy 227 Equipment and Preparation 227 Agents 228 Techniques 229 Posterior Approach 229 Transdiscal Approach 230 Anterior Approach 231 Complications 231 Clinical Pearls 231 Summary 231 References 232 226 Introduction The introduction to any procedure is best served with a discussion of the events that led to its discovery and use. It has been long known that interruption of the sympathetic fibers to the pelvis has resulted in analgesia. At the turn of the twentieth century, Jaboulay and Ruggi first described the pelvic sympathectomy.1 , 2 Then in 1913, Leriche performed the first internal iliac periarterial sympathectomy.3 It was not until the 1920s that Cotte delineated the analgesic benefit of removing the superior hypogastric plexus (SHP) in a systematic manner. 4 Over the next few decades, pelvic pain, including dysmennorhea, was treated with surgical sympathec- tomies. 5–9 With surgical advancement in the 1980s, there was a transition toward laparoscopic sympathetic removal.10–12 Over time, the trend toward less invasive techniques continued. For instance, neurolysis began to be performed under laparoscopy. Finally, the first attempt at the SHP block was reported by Plancarte in 1990.13 It was found that this approach proved difficult and therefore, newer approaches, including the transdiscal, transvaginal and anterior methods were discovered. These initial blocks were performed with fluoroscopy and subsequently, computed tomography (CT) guidance and 5.3: Superior Hypogastric Plexus Block ultrasound were implemented. The SHP innervates the bladder, prostate, testes, uterus, ovaries, vagina, transverse colon, descending colon, sigmoid colon, and rectum. Indications The indications for the SHP block are debated in the medical community; however, it is thought that it is a useful therapy for pelvic pain when utilized as part of a multi-modal approach to analgesia. An approach to incorporating the SHP block focuses on determining the etiology of the pelvic pain. For those with non-malignant pain, the utility of the SHP block is controversial because the value of repeated neurolytic blocks that are designed to provide sustained relief is unknown. Neurolysis carries risks including excessive neurological injury, non-neurologic damage, and possible incomplete relief secondary to scar tissue formation. Once the effect of the neurolytic dissipates, the pain can return in a similar form, or less likely, worse. Because of these adverse effects, neurolysis is questioned in those with non-malignant pain. Traditionally, it is felt that local anesthetics do not provide long-term benefit; however, they may produce a prolonged effect by altering central sensitization and sympatheticially mediated pain. Interestingly, Rosenberg demonstrated prolonged pain relief with the SHP block using steroid and local anesthetic for non-malignant penile pain in 1998.14 There have been no further studies that demonstrate prolonged relief for non-malignant pain without the use of neurolysis, however. Patients with cancer of the pelvis may benefit from the SHP block. The World Health Organization (WHO) analgesic ladder is reported to manage cancer pain in a majority of patients. There is a cohort of patients who cannot achieve adequate analgesia or tolerate the side effects of recommended medications, which lead to a poor quality of life. In these patients, a multi-modal approach that includes nerve blocks can provide pain relief and reduce adverse effects. In neoplasms of the pelvis, especially in those with advanced cancer, some believe that pelvic pain may display a more somatic component than pain in the abdominal distribution of the celiac plexus, such as pancreatic cancer. 15 Therefore, some authors suggest that a visceral nerve block such as the SHP block be used as an adjunct only to a well-rounded oral analgesic regimen.16 , 17 On the contrary, there is also evidence that given the relative ease of performance, potential for added analgesia, and preferable side effect profile, the SHP may be a reasonable treatment option to utilize earlier than traditionally thought.18–20 One last indication under recent discussion is the use of the SHP block for acute pain. Specifically, the utilization of the anterior approach of the SHP block has been shown to improve pain control in patients undergoing outpatient uterine artery embolization. 21 Although more studies are needed prior to recommending this as routine practice, it does provide another indication for this procedure beyond the scope of chronic pain management. 227 Apart from its therapeutic treatment for pelvic pain, there is also diagnostic utility for the block.22 That is, the SHP block is useful in differentiating between low back pain from pelvic pathology and low back pain from a primary lumbar pathology. Contraindications There are few absolute contraindications. These include patient refusal, local infection, and sepsis. There are many relative contraindications. These include inability of patient to cooperate, untreated psychiatric illness, coagulopathy, and pregnancy. For the posterior approach specifically, coexisting neuropathy and osteophytic overgrowth can be considered relative contraindications. For the transdiscal approach, disc replacement or fusion at L5-S1 can be considered a relative contraindication. Functional Anatomy The SHP is a web-like convergence in the retroperitoneal space that contains both sympathetic and para-

sympathetic fibers. It forms in the midline, anterior to the L5-S1 vertebrae, just below the aortic bifurca- Interventional Pain Medicine tion (Figure 5.3.1 ). There is a slight leftward predominance of the plexus. The SHP is formed from the continuation of the inferior mesenteric plexus, while the continuation is two hypogastric nerves that supply the pelvic viscera (Figures 5.3.2 a and 5.3.2 b). The pelvic viscera receive neurons from both the sympathetic and parasympathetic nervous systems. Visceral afferent fibers traveling in the sympathetic trunk contain their cell bodies in the dorsal root ganglia between T10-L2. Similarly, visceral afferent parasympathetic fibers contain their cell bodies in the dorsal root ganglia arising from S2-S4. These form the neuronal network of the SHP. A recent cadaveric study that evaluated the SHP anatomy in thirty-five patients showed a large degree of variance.23 There was a single nerve in 17.14 percent, reticular formation in 28.57 percent, nerve trunk with connective tissue in 22.85 percent, and two distinct nerves in 31.44 percent of patients. Although these anatomic variances exist, there is no clear difference in clinical outcome with the SHP block and neurolysis. When performing any procedure, it is important to understand the proximity of critical structures. For example, the posterior border of the SHP is the L5-S1 vertebral body. The ureters travel near the anterolateral aspect of the L5 vertebral body. Cephalad to the SHP is the aortic bifurcation. Lateral to the SHP are the iliac vessels, and just posterior to these vessels is the psoas muscle. Anterior to the SHP is the peritoneal lining. In those with neoplasms, both pelvic anatomy and the SHP may be distorted due to tumor invasion. Equipment and Preparation The SHP block is best tolerated with intravenous conscious sedation using midazolam and/or fentanyl. It is important for the patient to be comfortable and cooperative during the procedure, and alert enough to communicate with the practitioner. An oxygen source should be available along with standard American Society of Anesthesiologists recommended monitors. Below is a list of equipment utilized by the authors for the transdiscal approach to the SHP block. 1) Agents as mentioned below. 2) Antibiotic of choice (typically intravenous cefazolin 1–2grams, or clindamycin 600–900 milligrams if a true penicillin allergy is present). 3) Sterile fi eld: 2 percent chlorhexidine, sterile towels, sterile gloves. 4) One 7-inch, 22-gauge short beveled needle, one 1.5-inch, 25-gauge needle for local anesthetic skin infi ltration. 5) Sterile syringes: one 20 ml (analgesic medication), one 10 ml (local anesthestic) and one 3 ml syringe (contrast) are suffi cient. 6) Fluoroscopy machine. 228

Sacrum L1 L2 L3 L4 L5

Bifurcation of iliac vessels

Superior hypogastric Psoas major plexus muscle Superior hypogastric plexus 5.3: Superior Hypogastric Plexus Block Superior Psoas major muscle rectal artery

Internal iliac artery and vein

External iliac artery and vein

Figure 5.3.1 Superior hypogastric plexus block in relation to relevant surround anatomy. Reprinted with permission from Cousins MJ, Bridenbaugh PO. Neural Blockade, 3rd ed . Philadelphia, PA: Lippincott Williams & Wilkins 1998.

Agents There is a great paucity of data comparing the various agents that may be utilized in the SHP block. The suggestions here are based on data from treating cancer pain, and experience of the authors. Contrast: Two commonly used agents are iohexol and gadopentetate dimeglumine (for those with iodine allergies). Local agent: Typically an equal mixture of 10ml of bupivacaine 0.5 percent and 10 ml of Lidocaine 2 percent. Neurolytic agent: Ethanol and phenol at varied concentrations are the most commonly used neurolytic agents. Phenol has been shown to possess local anesthetic properties. As a result, it may be preferred due to its inherent analgesic effect. 229 Interventional Pain Medicine

AB Figures 5.3.2a and b Fluoroscopic images of the bilateral needle approach to the superior hypogastric plexus block shown with appropriate spread of contrast in the AP and lateral projections. In the lateral projection, the needle tips can clearly be seen at the L5-S1 junction.

Techniques Three different approaches to the SHP block are discussed. The transvaginal and surgical approaches are not covered here given that they are not typically utilized by the pain physician. The authors routinely perform the transdiscal approach given the ease of technique compared to the other two approaches. More studies comparing these approaches are needed.24 Posterior Approach Pros: First described approach with the most evidence for its support. Cons: Technically more difficult to perform when compared to the other approaches. For the posterior approach, the patient should be placed prone with a pillow beneath the pelvis to reduce the lumbar lordosis. The L4-L5 interspace is identified using the iliac crests as an anatomic guide. In the two needle technique, after standard aseptic preparation, areas 5 to 7 cm lateral to the L4-L5 spinous process are anesthetized with local anesthetic. Using fluoroscopy, a 7-inch, 22-gauge beveled needle is then inserted towards midline, roughly 30 degrees caudad and 45 degrees medially. The needle tip should ultimately be positioned 1cm beyond the anterior aspect of the L5 vertebral body. Occasionally one may feel a loss of resistance as the needle tip exits the anterior fascial boundary of the psoas muscle. If vertebral body or transverse process is encountered, the needle may be redirected and “walked-off” with the bevel facing the bony structure to facilitate this maneuver. Once the needle tip is just beyond the anterolateral border of L5-S1, 3 to 4 ml of radio-opaque contrast is injected to verify position. In the AP projection, there is medial spread, while in lateral projection there is cephalad and caudad spread of the dye just anterior to the vertebral body (Figure 5.3.3 ). After verification of position, 15 to 20 ml of the local anesthetic of choice, typically bupivacaine 0.25 percent, or a mixture of bupivacaine and lidocaine, is injected incrementally. For neurolysis, 5 to 8ml of 10 percent aqueous phenol is injected, 13 , 25 although 15 to 30ml of 100 percent ethanol has also proven to be efficacious.19 There is difference of opinion regarding the use of two needles versus one needle for the posterior approach to the SHP block. 26 Currently, there is some evidence that suggests a single needle approach may be as efficacious as the two needle approach when combined with computed tomography.27 This may be particularly advantageous in patients with significant tumor burden. 28 230 5.3: Superior Hypogastric Plexus Block

Figure 5.3.3 Fluoroscopic images of the transdiscal, single-needle approach to the superior hypogastric plexus block. The top images show appropriate initial contrast spread in the AP and lateral projections, while the two bottom images show the further appropriate spread and dilution with local anesthetic injection.

Transdiscal Approach Pros: Ease of technique. Typically shorter procedural time compared to posterior approach. Cons: Theoretical risk of discitis or disc rupture. This approach is an adaptation described by Erdine.29 The patient is placed prone with a pillow underneath the pelvis to reduce the lumbar lordosis. Using fluoroscopy, the scope is angled 15 to 20 degrees cephalad. A 7-inch, 22-gauge needle is then inserted approximately 5 to 7 cm from the midline after infiltration with local anesthetic. The needle is advanced intradiscally, then verified with 0.5 ml of radio- opaque contrast in the AP and lateral positions. Finally, the needle is advanced through the disc into the retroperitoneal space utilizing a loss of resistance technique. 3ml of radio-opaque contrast is then injected to verify position and spread under imaging. A total of 15 to 20ml of local anesthetic is injected, typically 0.25 percent bupivacaine or a mixture of bupivacaine and lidocaine. For neurolysis, 5 ml of 10 percent phenol is injected. Alternatively, 15 to 30 ml of 80 to 100 percent ethanol is proven to be as efficacious. Prior to withdrawing the needle, 0.5ml of air or saline is injected to prevent intradiscal neurolytic spread. Some suggest that prophylactic antibiotics, systemic as well as intradiscal, may be indicated to prevent discitis. In one study, there was no evidence of disk complications when systemic ceftriaxone was administered prior to the procedure, although many traditionally use cephazolin.30 231 Anterior Approach Pros: Useful in cancer patients who may not be able to lie prone. Useful when posterior approach is contraindicated or difficult such as those with existing radiculopathy, disc disease, or osteophytic overgrowth. Cons: Greater concern for infection. Greater risk for bowel or ureteral injury. The anterior approach was first described by Kanazi in 1999.31 It has been described utilizing both fluoroscopy 24 as well as CT guidance. 22 , 28 , 32 For the fluoroscopic approach, the patient is placed in the supine position with 15 degree of Trendelenburg. An area 2 to 5 cm inferior to the umbilicus is infiltrated with local anesthetic. A 22-gauge, 6-inch needle is then inserted toward the inferior two-thirds of the L5 vertebral body. The angle of approach is typically perpendicular to the floor. Incremental aspiration may help one identify possible bowel or ureteral insertion. Once bony contact is made, the needle is aspirated to rule out intravascular placement. Location is confirmed with both AP and lateral projections after a small amount of radio-opaque contrast is injected. After confirmation, 20 to 30ml of local anesthetic, typically 0.25 percent bupivacaine, or bupivacaine and lidocaine mixture, is injected incrementally. Subsequently, neurolysis may be performed with phenol or ethanol as described in the previous two Interventional Pain Medicine approaches. When performing the procedure under CT guidance, the needle insertion site is halfway between the umbilicus and the symphysis pubis, aimed toward the left iliac vein. The risk of bowel perforation and infection has deterred many from utilizing the anterior approach. Complications The SHP block is a relatively safe procedure. In a large randomized controlled trial, there were no complications seen. As with any procedure, a thorough discussion of the possible complications is necessary. Most known complications are transient or resolved with minimal intervention. Cerebrospinal fluid leak, intrathecal, or epidural injection are rare complications;33.34 however, the consequences associated with neurolytic agents can be severe. There have also been reports of transient bowel, bladder and sexual dysfunction. It is this author’s opinion that these risks should specifically be discussed with the patient given the added psychosocial consequences of damage to these organs. With the transdiscal approach, the literature quotes <5 percent rate of discitis,24 however there have been no reported cases of discitis in those that received prophylactic antibiotics. Bladder and ureteral trauma are possible with the posterior approach; however, this risk is greater with the anterior approach. Given the proximity of vascular structures, direct damage as well as hematoma formation are possibili- ties, particularly with the posterior approach. Clinical Pearls 1) Bowel evacuation prior to the block can help minimize gas content and improve fl uoroscopic images. 2) Placement of a pillow below the pelvis helps to reduce lumbar lordosis and facilitate the posterior approach because it opens the intervertebral spaces. 3) CT guidance is suggested when tumor burden is likely infi ltrating the SHP or otherwise signifi cantly distorting relevant pelvic structures. Summary A discussion of the efficacy of the SHP block is a necessity. To date, there are few studies that have attempted to determine the effectiveness of this procedure. Much of the literature is limited due to of a lack of universally acceptable outcome measures. The greatest markers utilized for efficacy are a decrease in the Visual Analog Scale (VAS) as well as mean opioid consumption. Although these are valid endpoints, more studies are needed to determine the length of follow up necessary for the SHP block to prove most meaningful. 232 Many of the studies that are currently available have limited power and deficiencies in their design methods. 35 One of the first studies was performed by Plancarte in 1990, which showed a benefit of the SHP block on sympathetically mediated cancer pain with no serious complications.11 In 1993, de Leon- Casasola demonstrated moderate efficacy in 69 percent of pain patients measured by a decrease in the VAS scores as well as opioid consumption for a total of six months after the procedure. 26 It was felt that some of the non-responders may have responded to larger volumes of neurolytic agent. Both of these studies were limited by small group sizes, but showed a trend toward efficacy. In 1997, Plancarte and de Leon-Casasola studied a larger group of 227 patients with pelvic cancer. 36 They were able to demonstrate significant decreases in pain scores as well as opioid consumption in 72 percent of patients for up to three months. Those who were minimal or non-responders tended to have more extensive disease that involved the SHP. Mercadante showed in 2002 that patients with pelvic pain tend to demonstrate greater neuropathic components to their symptomatology. 15 This may explain why pelvic pain can be more recalcitrant to the SHP block compared to abdominal pain treated by blockade and neurolysis of the celiac plexus.

5.3: Superior Hypogastric Plexus Block Because of the variability in the data, two strategies have emerged for the application of the SHP: early and later use. Early users highlight the benefit in VAS scores and advocate a more aggressive, initial treatment plan, particularly in cancer patients. Others, however, argue that better evidence should dictate whether the SHP should be regarded as first line therapy. De Oliveira examined the efficacy of performing various sympathetic blocks with neurolysis as an early intervention for cancer pain; a technique that challenges current WHO protocol. 19 The groups that received the neurolytic blocks reported better pain scores as well as quality of life scores than the group that did not receive the blocks; an outcome that has been similarly reported with the celiac plexus block.17 , 37 The eight week follow up reflects a limitation of the study; however early procedural intervention challenges the traditional pharmacotherapeutic approach to analgesia for those with cancer pain. Future studies should stratify patients based on specific criteria to ensure the greatest chance of success. For example, investigations in rat models have discovered a difference in the response to sympathetic neurolysis based on age. 38 Ultimately, the SHP block should be considered for cancer and non-cancer pelvic pain, and represents a tool in the armamentarium of pain interventions for the specialist. References 1. Jaboulay M . Le traitement de la nevralgie pelvienne par la paralysie du sympathetique sacre . Lyon Med . 1899 ; 90 : 102 . 2. Ruggi G . Della sympathectomy mia al collo ed ale abdome . Policlinico . 1899 ; 103 . 3. Leriche , R . Periarterial sympathectomy of internal iliac arteries for patient with pelvic neuralgia . Annals of Surgery . 1921 ; 39 : 471 . 4. Cotte G . La sympathectomie hypogastrique peri-arterielle ou la section du nerf . Lyon Med . 1925 ; 56 : 153 . 5. Greenhill JP . Sympathectomy for the relief of pelvic pain in women . J Mt Sinai Hosp N Y. 1947 ; 14 ( 3 ): 363 – 368 . 6. Wetherell FS . Resection of the superior hypogastric plexus; modiﬁ cation of the technique to prevent regeneration . Am J Obstet Gynecol . 1951 ; 61 ( 4 ): 738 – 742 . 7. Guixa HM , Otturi JE . Resection of the superior hypogastric plexus in pelvic pain . Obstet Ginecol Lat Am . 1952 ; 10 ( 3–4 ): 107 – 115 . 8. Dailey HR , Tafel RE . Superior hypogastric sympathectomy for the relief of pain associated with endometriosis . Am J Obstet Gynecol . 1952 ; 64 ( 3 ): 650 – 654 . 9. Schockaert JA . Extensive resection of the superior and inferior hypogastric plexuses in painful forms of pelvic neurodystonia . Brux Med . 1956 ; 36 ( 46 ): 2195 – 2211. 10. Lee RB , Stone K , Magelssen D , Belts RP , Benson WL . Presacral neurectomy for chronic pelvic pain . Obstet Gynecol . 1986 ; 68 ( 4 ): 517 – 521 . 11. Perez JJ . Laparoscopic presacral neurectomy. Results of the ﬁ rst 25 cases . J Reprod Med . 1990 ; 35 ( 6 ): 625 – 630 . 12. Chen FP . Laparoscopic presacral neurectomy for chronic pelvic pain . Chang Gung Med J . 2000 ; 23 ( 1 ): 1 – 7 . 233 13. Plancarte R , Amescua C , Patt RB , Aldrete JA . Superior hypogastric plexus block for pelvic cancer pain . Anesthesiology . 1990 ; 73 ( 2 ): 236 – 239 . 14. Rosenberg SK , Tewari R , Boswell MV , Thompson GA , Seftel AD . Superior hypogastric plexus block successfully treats severe penile pain after transurethral resection of the prostate . Reg Anesth Pain Med . 1998 ; 23 ( 6 ): 618 – 620 . 15. Mercadante S , Fulfaro F , Casuccio A . Pain mechanisms involved and outcome in advanced cancer patients with possible indications for celiac plexus block and superior hypogastric plexus block . Tumori . 2002; 88 ( 3 ): 243 – 245 . 16. de Leon-Casasola OA . Critical evaluation of chemical neurolysis of the sympathetic axis for cancer pain . Cancer Control . 2000 ; 7 ( 2 ): 142 – 148 . 17. Plancarte R , de Leon-Casasola OA , El-Helaly M , Allende S , Lema MJ . Neurolytic superior hypogastric plexus block for chronic pelvic pain associated with cancer . Reg Anesth . 1997 ; 22 ( 6 ): 562 – 568 . 18. Patt RB , Reddy SK , Black RG . Neural blockade for abdominopelvic pain of oncologic origin . Int Anesthesiol Clin . 1998 ; 36 ( 3): 87 – 104 . 19. de Oliveira R , dos Reis MP , Prado WA . The effects of early or late neurolytic sympathetic plexus block on

the management of abdominal or pelvic cancer pain . Pain . 2004 ; 110 ( 1–2 ): 400 – 408 . Interventional Pain Medicine 20. Nagaro T , Tsubota S . Cancer pain treatment with nerve blocks and neuroablative procedures . Nippon Rinsho . 2007 ; 65 ( 1 ): 103 – 108 . 21. Rasuli P , Jolly EE , Hammond I , et al . Superior hypogastric nerve block for pain control in outpatient uterine artery embolization . J Vasc Interv Radiol . 2004 ; 15 ( 12 ): 1423 – 1429 . 22. Wechsler RJ , Maurer PM , Halpern EJ , Frank ED . Superior hypogastric plexus block for chronic pelvic pain in the presence of endometriosis: CT techniques and results . Radiology . 1995 ; 196 ( 1 ): 103 – 106 . 23. Paraskevas G , Tsitsopoulos P , Papaziogas B , et al . Variability in superior hypogastric plexus morphology and its clinical applications: a cadaveric study . Surg Radiol Anat . 2008 ; 30 ( 6 ): 481 – 488 . Epub May 2008 . 24. Erdine S , Yucel A , Celik M , Talu GK . Transdiscal approach for hypogastric plexus block . Reg Anesth Pain Med . 2003 ; 28( 4 ): 304 – 308 . 25. Mauroy B , Demondion X , Drizenko A , et al . The inferior hypogastric plexus (pelvic plexus): its importance in neural preservation techniques . Surg. Radiol. Anat . 2003 ; 25 ( 1 ): 6 – 15 . 26. de Leon-Casasola OA , Kent E , Lema MJ. Neurolytic superior hypogastric plexus block for chronic pelvic pain associated with cancer . Pain . 1993 ; 54 ( 2 ): 145 – 151 . 27. Waldman SD , Wilson WL , Kreps RD . Superior hypogastric plexus block using a single needle and computed tomography guidance: description of a modiﬁ ed technique . Reg Anesth . 1991 ; 16 ( 5): 286 – 287 . 28. Cariati M , De Martini G , Pretolesi F , Roy MT . CT-guided superior hypogastric plexus block . J Comput Assist Tomogr . 2002 ; 26 ( 3 ): 428 – 431 . 29. Erdine S , Ozyalcin S. Pelvic Sympathetic Blocks . In: Raj , P. et al . (Ed) Interventional Pain Management: Image- Guided Procedures . 2008 . 30. Gamal G , Helaly M , Labib YM . Superior hypogastric block: transdiscal versus classic posterior approach in pelvic cancer pain . Clin J Pain . 2006 ; 22 ( 6 ): 544 – 547 . 31. Kanazi GE , Perkins FM , Thakur R , Dotson E . New technique for superior hypogastric plexus block . Reg Anesth Pain Med . 1999 ; 24 ( 5 ): 473 – 476 . 32. Michalek P , Dutka J . Computed tomography-guided anterior approach to the superior hypogastric plexus for noncancer pelvic pain: a report of two cases . Clin J Pain . 2005 ; 21 ( 6 ): 553 – 556 . 33. Chan WS , Peh WC , Ng KF , Tsui SL , Yang JC . Computed tomography scan-guided neurolytic superior hypogastric block complicated by somatic nerve damage in a severely kyphoscoliotic patient . Anesthesiology . 1997 ; 86 ( 6 ): 1429– 1430 . 34. Dutka J , Michalek P . Neurological complications in neurolytic blocks in the visceral and pelvic regions . Int. Monitor. Reg. Anesth . 2002 ; 14 : 69 . 35. Schmidt AP , Schmidt SR , Ribeiro SM . Is superior hypogastric plexus block effective for treatment of chronic pelvic pain? Rev Bras Anestesiol . 2005 ; 55 ( 6 ): 669 – 679. 36. Plancarte R , de Leon-Casasola OA , El-Helaly M , Allende S , Lema MJ . Neurolytic superior hypogastric plexus block for chronic pelvic pain associated with cancer . Reg Anesth . 1997 ; 22 ( 6 ): 562 – 568 . 37. Mercadante , S . Celiac plexus block versus analgesics in pancreatic cancer pain . Pain . 1993 ; 52 ( 2 ): 187 – 192 . 38. Jaatinen P , Hervonen A . Reactions of rat sympathetic neurons to ethanol exposure are age-dependent . Neurobiol Aging . 1994 ; 15 ( 4 ): 419 – 428 . This page intentionally left blank 235

Chapter 5.4 Celiac Plexus Blocks and Splanchnic Nerve Blocks

Nina Singh-Radcliff

Anatomy 236 Indications 238 Preparation 239 Technique 239 Retrocrural Splanchnic Nerve Block 243 Antecrural Splanchnic Nerve Block 244 Anterior Approach 244 Radiofrequency Lesioning 245 Complications 245 Hypotension 245 Nerve injury/paraplegia 245 Diarrhea 246 Pneumothorax 246 Failed Block 246 Local Anesthetic/Neurolytic Agents 246 Clinical Pearls 246 References 247 236 Anatomy Plexus is Latin for “braid” and is the term used to describe a complex network of nerves. Appropriately named, the celiac plexus is an aggregate of ganglia and a dense network of nerve fibers uniting, crossing through, and surrounding the ganglia. It innervates most of the digestive tract. The celiac plexus is located in the abdomen, at approximately the L1 level, anterior to the aorta, and below the crus of the diaphragm. Like a spider web, it surrounds the celiac artery and root of the superior mesenteric artery. Figures 5.4.1 – 5.4.3 demonstrates the location of the celiac plexus as below the diaphragm, anterior to aorta, and spider web like around the arteries and also abdominal anatomy related to function of the celiac plexus. The plexus has several ganglia components, or relay stations similar to a command base, that have the appearance of lymph nodes. The celiac ganglia comprise the “middle” of the plexus, and vary in number ( 1–5 ), as well as size (0.5 to 4.5cm) and position relative to the vertebral column (bottom of T12 to middle of L2).( 1 ) The upper portions of the celiac ganglia are joined by the greater splanchnic nerves (sympathetic chains) after they pierce through the diaphragmatic crura, while the lower portions receive the 5.4: Celiac Plexus Blocks lesser splanchnic nerves.( 2 ) In addition to sympathetic fibers, it also receives some fibers from the right vagal nerve (parasympathetic).

Hepatic Diaphragmatic artery ganglion Suprarenal gland Left celiac ganglion Superior mesenteric artery Greater Greater splanchnic nerve splanchnic Lesser splanchnic nerve nerve Right celiac ganglion Aorticorenal ganglion

Aorticorenal ganglion Lowest splanchnic nerve Renal artery

Renal artery Superior mesenteric Sympathetic ganglion trunk

Communicating branch

Branch to aortic plexus

Sympathetic trunk

Branch to aortic plexus

Inferior mesenteric artery

Inferior mesenteric ganglion

Sacrovertebral angle Common iliac vein Common iliac artery

Figure 5.4.1 Abdominal anatomy. III Ciliary Midbrain Eye Sphenopalatine 237 VII VII Lacrimal gland Submaxillary Mucous mem. Medulla IX nose and palate Submaxillary gland X Sublingual gland IC. Otic Mucous mem. mouth Sup. cerv. g. Parotid gland

Heart

IT. Larynx

Trachea Bronchi Great splan chnic Celiac Esophagus nic nch Stomach la p s Bloodves. of abd. ll a m S Liver and ducts Interventional Pain Medicine Superior Pancreas mesenteric gang. IL. Adrenal

Inferior Small intestine mesenteric gang.

IS. Large intestine

Pelvic nerve Rectum Kidney

Bladder

Sexual organs

External genitalia

Figure 5.4.2 Abdominal anatomy.

AORTA

Retrocrural spread

DIAPHRAGM L1 Celiac plexus

Anterocrural Ao spread

SPLANCHNIC NERVES

Diaphragmatic crus

Figure 5.4.3 Retrocrural and antecrural blocks. 238 The celiac plexus is also unique in that it has a multitude of secondary plexuses that arise from or connect with the celiac plexus: phrenic, hepatic, lineal, superior gastric, suprarenal, renal, superior mesenteric, abdominal aortic, inferior mesenteric. The term solar plexus is sometimes used to refer to this plexus as it, aptly, describes the widely radiating incoming and outgoing nerves and ganglia that link the celiac ganglia, much like the sun’s rays. Indications Several visceral organs— pancreas, liver, gallbladder, omentum, mesentery, and alimentary tract from the stomach to the transverse portion of the large colon— have afferent pain fibers that are routed through the celiac plexus. Hence, pain originating from these structures can potentially be alleviated from a celiac plexus block or splanchnic nerve block. Pancreatic cancer remains the most common indication for CPB. Tumor of the pancreas can cause pain by invasion or stretching of nerves, involvement of viscrera or organs, as well as blockage of the pancreatic ducts.( 3 ) ( 4 ) The characteristics of pancreatic cancer— limited therapeutic options, short life 5.4: Celiac Plexus Blocks expectancy, opioid limitations— make CPB a potentially attractive and effective component of a multimodal treatment regimen. Average life expectancy at the time of pancreatic cancer diagnosis is six months.( 5 ) Diagnosis is oftentimes delayed because symptoms usually do not present until the tumor is metastatic; hence, pancreatic cancer is often unresectable, and poorly responsive to chemotherapy or radiation. With limited treatment options, palliative care becomes the focus.( 6 ) Eighty-five percent of patients attain good to complete pain relief within one week of the procedure;( 7 ) 50 to 90 percent of patients report continued relief at three months.( 8 ) The duration of the neurolytic block is hindered by the aggressiveness of the tumor and invasion into peritoneum and organs as well as regeneration of new pain pathways. However, because of the dismal life expectancy, the neurolysis may equal or exceed patient survival. Additionally, although long-term complete pain relief has not been attained, short-term relief may allow some patients to gain coping skills and learn to manage their pain.( 9 ) Prior World Health Organization recommendations (1996) advocated a pain treatment ladder with acetaminophen, opioids, and CPB only after it was demonstrated that patients were unresponsive to these standard analgesic medications. Several large studies, however, have shown potential advantages of implementing CPB earlier in the treatment of pancreatic cancer,( 10 ) ( 11 ) including improved pain control, reduced opioid use and side effects, as well as quality of life. Narcotic analgesia administration can be limited by its side effects: drowsiness, constipation, nausea, and respiratory depression. Additionally, there is evidence suggesting that opioid analgesia can cause measurable suppression of the activity of natural killer cells, which are thought to scavenge tumor cells.( 12 ) The immunosuppressive effects of analgesis opioids may be the reason that Lillemoe and colleagues not only found a significant reduction or prevention of pain after chemical splanchnicectomy, but also significant improvement in survival when compared with controls. Improved pain control may also have resulted in less nausea and vomiting, allowing for better oral intake and nutrition. Of note, neurolysis has been shown to be more effective in cases with tumor involving the head of the pancreas. Patients with advanced tumor proliferation and metastasis showed less favorable results regardless of technique or imaging modality.( 13 ) Other abdominal malignances such as gastric, esophageal, colorectal, and gallbladder cancer, as well as liver metastasis and cholangiocarcinoma ( 14 ) may be indications for a CPB. Patients often demonstrate good immediate pain relief.( 7 ) As with pancreatic cancer, however, new pain pathways or growing tumors can limit long-term efficacy. The most frequent indication for CPB with benign disease is pain from chronic pancreatitis. This indication is controversial, with opponents stating that the lack of long-term pain reduction, and potential 239 adverse effects (see Complications) limit its use.( 15 ) Advocates however, assert that general impairment of the patient can be ameliorated, such as food intolerance, weight loss, opioid usage, and hence, improved quality of life, even if only temporary. Acute pancreatitis, which often requires hospitalization for bowel rest, antibiotics, and pain control, may be a potentially attractive indication. In addition to the single-shot technique (with local anesthetic), intermittent or continuous unilateral CPB with local anesthetic can offer an effective alternative treatment for pain in acute pancreatitis, especially in patients with a history of alcoholic pancreatitis or opioid addiction, in whom conventional methods may fail to give proper pain relief.( 16 ) Preparation Informed consent for the SNB and CPB need to be attained. Details of the procedure, its potential benefits and risks (See Complications) need to be discussed with the patient and family. Oftentimes the prone position is utilized and patients appreciate being informed of this ahead of time, as well what measures will be taken to improve their comfort. IV access needs to be attained for potential pre-operative hydration, administration of sedation and narcotic, as well for treatment of complications (hypotension, Interventional Pain Medicine local anesthetic toxicity, etc). Technique There are two principal techniques that are performed via the posterior approach: the deep splanchnic nerve block (SNB) or true celiac plexus block (CPB). Although the CPB and SNB are anatomically different procedures, their clinical effect and potential complications are virtually indistinguishable.( 17 ) Figures 5.4.4 – 5.4.13 demonstrate both the fluoroscopic and CT-guided procedures. Both approaches utilize introduction of percutaneous needles typically at the T12 level, however they vary depending on the location of the needle tip in relation to the diaphragmatic crura. Hence, the term retrocrural (behind the crura) is oftentimes used exchangeably with the SNB, while the antecrural (front of the crura) block refers to the CPB. We will also briefly discuss the anterior approach, which some practitioners perform with the assistance of CT guidance.

Figures 5.4.4 Flouroscopic guided placement of needles for celiac plexus block. 240 5.4: Celiac Plexus Blocks Figures 5.4.5

Figures 5.4.6

Figures 5.4.7 241 Interventional Pain Medicine

Figures 5.4.8

Figures 5.4.9 CT-guided placement of needles for celiac plexus block.

Figures 5.4.10 242 5.4: Celiac Plexus Blocks Figures 5.4.11

Figures 5.4.12

Figures 5.4.13 243 The decision between which posterior technique should be used may depend on the indication for the block, and potential for complications. Compared with a CPB, the SNB may be more useful for visceral abdominal pain secondary to pancreatic masses where the celiac plexus anatomy may be distorted,( 18 ) thus making successful neurolysis less likely (reference). The retrocrural approach to the SNB, however, may predispose to complications including paraplegia, resulting from diffusion of neurolytic agents to the nerve roots, as well as puncture of the lungs, liver or kidney,( 19 ) Once the patient is placed prone on the procedure room, lordosis of the lumbar spine can be reduced by placing a pillow under the abdomen. Standard American Society of Anesthesiology monitoring should be utilized (pulse oximetry, non-invasive blood pressure cuff, continuous electrocardiogram), and if sed- ative or opioid administration is given, supplemental oxygen such as a nasal cannula or facemask should be applied. The patient should not be oversedated and unable to communicate effectively; it is imperative that the effectiveness of the local anesthetic injection be able to be ascertained prior to neurolysis. Also, respiratory depression and hypoxia in the prone position may be especially difficult to manage.

Retrocrural Splanchnic Nerve Block Interventional Pain Medicine Historically, the anatomical approach, or classic technique, was used for the splanchnic nerve block. It was described as early as 1914 by Max Kappin and was modified in 1964 by Bridenbaugh. The classic technique and surgical splanchnicectomy were used for several years. The classic technique involved identifying the T12 and L1 spinous processes. From the midline, lines were drawn in the cephalo-caudal direction 7 to 8 cm from the midline, bilaterally. The twelfth ribs were identified bilaterally and markings made on the lower border of the rib; finally a straight line was drawn between these two marks to complete the triangle. Percutaneous needles were inserted at a 45-degree angle and were advanced until contact with the L1 vertebral body was made (typically 7 to 9 cm). The needle was then withdrawn to skin level, and the angle increased, from the table, to allow the needle to “walk off” the lateral border of the vertebral body. On the left, or aortic side, final needle insertion was more shallow than the right. Aspiration was conducted to rule out blood, urine, and CSF before injectate was administered.( 6 ) Today, radiologic guidance is considered standard of care, and is most frequently performed with X-ray, fluoroscopy, or CT assistance. Some practitioners have advocated for ultrasound or MRI guidance, however, that is beyond the scope of this chapter. The purpose of this section will be to familiarize the reader with the anatomy, and not to advocate for one technique over another. X-ray and fluoroscopy allow for the physician to identify the needle tip location as it is advanced, as well as assess final needle position with radiocontrast before injection of neurolytic material. Studies have shown improved success as well as a reduction in complications when compared to the anatomical approach.( 20 ) Additionally, both X-ray and fluoroscopy are easily available in most procedure rooms and operating suites today. 1. Identify the L1 spinous process. 2. Mark points 7 to 8 cm from the midline bilaterally 3. Make a skin wheal with local anesthetic using a 30-gauge needle. The SNB typically requires left and right needle insertion (the CPB is often performed unilaterally). 4. Begin on one side by inserting a 20-gauge or 22-gauge 10–15-cm needle at a 45–60 degree angle from the table. 5. Imaging should be performed as needed to determine if the trajectory will allow for eventual needle tip position anterior to the body of L1. Unlike the anatomical approach, the “walk off” technique from the vertebral body is not desired. Fluoroscopy may have the added benefi t of allowing for dynamic monitoring of needle advancement compared to X-ray. 6. In the lateral view fi lm, the fi nal needle position should demonstrate the tip anterior to the body of L1. In the anterorposterior view, the needle tip should be close to the midline, overlying the same vertebral body. 244 7. A test with radiocontrast is often performed to confi rm appropriate positioning on the radiograph. 8. The needles should still be aspirated before injection of local anesthetic or neurolytic agent to rule out blood, urine, and CSF. There have been several advocates for computer tomography (CT) guidance as a superior method for successful performance of the retrocrural block. Yang, et al., have suggested that CT imaging improved needle placement accuracy, increased patient tolerance, and reduced the possibility of complications such as hematuria, intravascular injection, and pneumothorax compared to fluoroscopy (Y). CT allows for improved visualization of the anatomic structures that lie in close proximity to the target site during neurolytic CPB. In patients who are increased risk for failure or complications, CT may theoretically be of advantage. However, routine CT guided imaging for SNB may not be feasible given limited availability, increased cost and potential procedure length. Antecrural Splanchnic Nerve Block The antecrural, or true celiac plexus block, involves needle placement anterior to the diaphragmatic 5.4: Celiac Plexus Blocks crura. Theoretical advantages of this technique are that it can be done unilaterally, requires less total neurolytic injectate, and minimizes neurologic complications by limiting the spread of neurolytic agent (exclusive preaortic spread), although this has not been proven in studies. The anatomical approach for the antecrural technique has not been advocated historically, except when using the transaortic approach. The transaortic approach utilized blood return and cessation to determine entrance into the posterior wall of the aorta and passage through the anterior wall, respectively. Radiographic imaging has always been advocated, particularly from the right, because unlike the ligamentum flavum , which has a pathognomonic “tough” feel as the needle passes through it, the diaphragmatic crura does not. Thus, it may not be possible to confidently assume that one is in the antecrural space. Radiography, fluoroscopy, and CT imaging allow the antecrural approach to be performed on either side. Practitioners, however, may prefer the right side to avoid aortic involvement, as the celiac plexus lies anterior to it. The CPB involves: 1. Identify the L1 spinous process. 2. Create a skin wheal on one side 5 to 6 cm from the midline. If one desires to avoid the aorta, then the right is chosen. 3. Insert a 20- or 22-gauge 10–15-cm needle at a 45- to 60-degree angle from the table. Imaging is used to identify the tip of the needle as it advances, and to make changes to the trajectory to allow fi nal needle placement anterior to the vertebral bodies. This typically involves 10–13 cm of needle insertion. 4. Aspirate to rule out CSF, urine, and blood. 5. Inject radiocontrast dye to confi rm fi nal needle tip location before local anesthetic or neurolytic is administered. Anterior Approach The anterior approach is utilized by surgeons when performing open splanchnicetomies. Additionally, it has been performed percutaneously with CT, MRI, and ultrasound imaging modalities using “skinny needles.” Thin, small-gauge needles are used to provide minimal injury to the abdominal wall, stomach, intestines, and pancreas. Several techniques have been described. Some advocate that the optimal puncture site and needle path should be chosen to avoid, whenever possible, the liver, stomach, colon, or pancreas.( 7 ) Because organ puncture is not always avoidable, the transhepatic and transpancreatic routes, have been advocated by others. Advocates of the anterior approach cite a low complication rate ( 7 ) and the avoidance of the prone position. Thus, this technique may be attractive in patients who have undergone abdominal surgery recently, have pulmonary compromise from ascites, or their pain 245 precludes lying on their stomach for an extended period of time. Similar to the posterior antecrural approach, the anterior approach has the advantage of one puncture, potentially resulting in less discomfort to the patient, reduced procedure time, and use of a smaller volume of neurolytic agent.( 21 ) Potential disadvantages include damage to the visceral organs that the needle passes through, peritonitis, and intra-abdominal abscess, hemorrhage and fistula formation.( 22 ) Coagulation profile and prophylactic antibiotics should be considered.( 21 ) Radiofrequency Lesioning This technique is a “neurodestructive” procedure that lesions the nerve plexus with temperatures that exceed 45 degrees Celsius.( 9 ) Advocates state the radiofrequency lesioning has the benefit of a circum- scribed and controlled lesion, compared to neurolysis. The proximal and distal spread of the lesion beyond the uninsulated tip of the probe is only 1mm, with the cross-sectional lesion diameter 5 to 6 mm. There is little or no possibility of nerve root damage or destructive damage of the epidural and subarachnoid structures.( 23 ) Sensory and motor stimulation are often performed, in order to ensure that there is no break in the insulation.( 24 ) Interventional Pain Medicine Complications Being well-versed in the potential complications of SNBs and CPBs allows the physician to balance the potential risks with the benefits of the procedure, enhancing optimal patient selection. Understanding the risks also allow the physician to make attempts to reduce the incidence of complications, should they occur, as well as maintain a high index of suspicion. As mentioned in the Techniques section, there may be an increased risk of pneumothorax and damage to the somatic nerve roots when performing a SNB (Reference). Hypotension Blocking the celiac plexus causes a sympatholysis of the splanchnic vasculature. Pooling of blood in this large capacitance, vascular bed can cause hypotension. It is relatively common, and typically transient. Thus, prophylaxis, appropriate monitoring, and a management strategy should hypotension occur, need to be addressed and performed. Intravenous prehydration with 500 to 1,000 mL of a crystalloid solution may reduce the incidence of hypotension. The patient should have their vital signs monitored after the block in the procedure room and the post-operative holding area. Patients may also demonstrate ortho- static hypotension, and demonstrate a drop in blood pressure with a change in position (supine to sitting, sitting to standing), due to impaired vasoconstrictor, or sympathetic compensation. Elderly, debilitated, and chronically or acutely dehydrated patients may be at a greater risk for hypotension.( 9 ) Nerve injury/paraplegia Neurological injury may occur from the spread of neurolytic agent to somatic nerves,( 6 ) spinal cord ischemia due to radicular artery spasm,( 25 ) or needle injury to the spinal cord. Manifestations are multi- tudinous, transient and permanent, and of varying severity (loss of sensation over anterior abdominal wall to paraplegia). Large studies of neurological complications from CPB and SNB have shown an incidence of less than 1 percent to 12 percent ( 6 , 25 )). Fortunately, it appears that minor complications are the most frequent neurologic injury observed (numbness or pain over the anterior thigh, lower abdominal wall, or anterior thigh).( 9 ) However, although infrequent, major neurologic complications (paraplegia) are devastating outcomes. Injury to somatic nerves from neurolytic agent may have a higher risk when SNB are performed. Theoretically, SNB require larger volumes of neurolytic agent, have a limited spread due to the diaphragm, and are in proximity to the spinal cord.( 26 ) Studies have also demonstrated that ethanol or phenol can cause concentration-dependent contractions in vascular smooth muscle, or spasm of lumbar radicular arteries.( 6 ) 246 Diarrhea Diarrhea is a side effect that results from unopposed parasympathetic activity (sympathetic block). However, many patients experience constipation from opioid use, and these patients often experience an improvement in bowel habit. Up to 60 percent of patients encounter self-limited diarrhea for thirty- six to forty-eight hours.( 9 ) In patients who encounter occasional severe and persistent hypermotility, it may be life-threatening. Pneumothorax Passing percutaneous needles through the pleura of the lungs can cause pneumothorax. Some studies have shown that pneumothorax occurs in 1/100 CPBs.( 27 ) The physician should have a high index of suspicion in patients who demonstrate a reduced pulse oximetry, dyspnea, or tachypnea. Use of radiologic imaging may reduce the occurrence by reducing the incidence of high needle insertion. Failed Block A failed block may result from poor placement of the needle, alternative pain pathways, anatomic

5.4: Celiac Plexus Blocks variations, insufficient volume of neurolytic agent, or inability to inject the agent because of tumor or scar tissue encasement of the aorta in the region of the celiac plexus. Additionally, distorted anatomical relationships (ascites, organomegaly, tumor bulk, obesity), post-radiation changes, post-surgical changes, peritoneal seeding, and surgical clip interference may also reduce successful neurolysis. Long term failure may be seen when local extension of the tumor involves structures with other pain fiber pathways( 21 ) Local Anesthetic/Neurolytic Agents Prior to neurolysis with permanent agents, a local anesthetic block is performed for diagnostic and prognostic purposes to confirm that the pain is part of a viscerally mediated pathway, as well as possibly reduce neurologic injury. Most practitioners perform this in two stages on the same day, without moving the confirmed needle placement. Both lidocaine 0.5 to 2 percent (10–15 mL) and bupivacaine 0.125 to 0.25 percent (10–15 mL) can be used. The main neurolytic substances used for the SNB and CPB are alcohol and phenol. Studies with impact factor have not been conducted to suggest the benefit of one substance over another. Alcohol’s mechanism of action is the extraction of cholesterol and phospholipid from neural membrane and the precipi- tation of lipoproteins and mucoproteins.( 28 ) The concentrations of alcohol range from 50 to 100 percent. On injection, alcohol may produce severe, transient pain. Advocates for this state it has more intense nerve destruction than phenol. Additionally, it is possible to add local anesthetic to the alcohol solution to reduce the discomfort. Phenol in water produces protein coagulation and necrosis of the neural structures; phenol comes in 6 to 10 percent concentrations. Phenol has the potential benefit of painless on injection, as it has an immediate local anesthetic effect. Although painless, it seems to have a slightly slower onset of action, less efficacy, and a shorter duration. Additionally, phenol is viscous, particularly at 10 percent and makes it difficult to inject; thus, 6 percent is often preferred.( 29 ) The volume needing to be injected depends on the localization of the needle and ease of flow in the injected area. Anywhere between 16 mL to 80 mL has been used. The volume of injectate is usually 25 mL through each needle, or 50 mL if a single needle technique is used.( 30 ) A smaller injectate is indicated (15–30 mL) when the needle is placed directly into the celiac plexus (anterior approach) or when the needles are specifically placed on splanchnic nerves.( 31 ) Clinical Pearls - The celiac plexus is an aggregate of ganglia and a dense network of nerve fi bers uniting, crossing through, and surrounding the ganglia that innervates most of the digestive tract. 247 - The two principal techniques performed via the posterior approach are the deep splanchnic nerve block (SNB) or true celiac plexus block (CPB). Although the CPB and SNB are anatomically different procedures, their clinical effect and potential complications are virtually indistinguishable - Although historically the anatomic approach was utilized, today it is considered standard of care to utilize some form of radiological guidance, typically X-ray and fluoroscopy. These imaging modalities allow for the physician to identify the needle tip location as it is advanced, as well as assess final needle position with radiocontrast before injection of neurolytic material. - The antecrural, or true celiac plexus block, involves needle placement anterior to the diaphragmatic crura. Theoretical advantages of this technique are that it can be done unilaterally, requires less total neurolytic injectate, and minimizes neurologic complications by limiting the spread of neurolytic agent (exclusive preaortic spread), although this has not been proven in studies. - It is imperative that the physician understands potential complications in order to balance the potential risks with the benefits of the procedure, enhance optimal patient selection, reduce the incidence of complications as well as maintain a high index of suspicion should they occur. Risks include hypotension, nerve injury, diarrhea, and pneomothorax. Interventional Pain Medicine - Alcohol and phenol are commonly used neurolytic agents. Studies have not shown a strong benefit of one over the other in clinical practice. References 1. Ward EM , Rorie DK , Nauss LA , Bahn RC . The celiac ganglia in man: normal anatomic variations . Anesth Analgesia. 1979 ; 58 ( 6 ): 461 – 465 . 2. Erdine S . Celiac ganglion block . Agri. 2005 ; 17 ( 1 ): 14 – 22 . 3. World Health Organization . Cancer Pain Relief . Second Edition 1996 . 4. Nakagawa T , Mori K , Nakano T , et al . Perineural invasion of carcinoma of the pancreas and biliary tract . Br J Surg. 1993 : 80 ( 5 ): 619 – 621 . 5. Saltzburg D , Foley KM . Management of pain in pancreatic cancer . Surg Clin North Am . 1989 ; 69 ( 3 ): 629 – 649 . 6. Wong GY , Brown DL . Celiac plexus block for cancer pain . Techniques in Regional Anesthesia and Pain Management . 1997 ; 1 ( 1 ): 18 – 26 . 7. Mercadante S . Celiac plexus block: a reappraisal . Reg Anesth Pain Med . 1998 ; 23 ( 1 ): 37 – 48 . 8. Firdousi FH , Sharma D , Raina VK . Palliation of celiac plexus block for upper abdominal visceral cancer pain . Trop Doct . 2002 ;32 ( 4 ): 224 – 226 . 9. Raj PP. Celiac plexus/splanchnic nerve blocks . Techniques in Regional Anesthesia and Pain Management . 2001 ;( 5 ) 3 : 102 – 115 . 10. Akhan O , Ozmen MN , Basgun N , et al. Long-term results of celiac ganglia block: correlation of grade of tumoral invasion and pain relief . AJR Am J Roentgenol . 2004 ; 182 ( 4 ): 891 – 896 . 11. Yan BM , Myers RP . Neurolytic celiac plexus block for pain control in unresectable pancreatic cancer . Am J Gastroenterol. 2007 ; 102 ( 2 ): 430 – 438 . 12. Yeager MP , Colacchio TA , Yu CT , et al. Morphine inhibits spontaneous and cytokine-enhanced natural killer cell cytotoxicity in volunteers . Anesthesiology . 1995 ; 83 ( 3 ): 500 – 508 . 13. Rykowski JJ , Hilgier M . Effi cacy of neurolytic celiac plexus block in varying locations of pancreatic cancer: infl uence of pain relief . Anesthesiology . 2000 ; 92 ( 2 ): 347 – 354 . 14. Eisenberg E , Carr DB , Chalmers TC . Neurolytic celiac plexus block for treatment of cancer pain: a meta-analysis . Anesth Analg. 1995 ; 80 ( 2 ): 290 – 295 . 15. Olaf S . Long-term effi cacy of neurolytic celiac plexus block in patients with chronic pancreatitis or other non-malignant abdominal disease . Journal of Chinese Clinical Medicine. 2007 ; 2 ( 3 ): 457 – 162 . 16. Rykowski JJ , Hilgier M . Continous celiac plexus block in acute pancreatitis . Reg Anesth . 1995 ; 20 ( 6 ): 528 – 532 . 17. Rosenthal JA . Diaphragmatic paralysis complicating alcohol splanchnic nerve block . Anesth Analg. 1998 ; 86 ( 4 ): 845 – 846 . 18. Eggleston ST , Lush LW . Understanding allergic reactions to local anesthetics . Ann Pharmacother . 1996 ; 30 ( 7–8 ): 851 – 857 . 248 19. Reisfi eld GM , Wilson GR . Blocks of the sympathetic axis for visceral pain . J Palliat Med . 2004 ; 7 ( 1 ): 75 – 76 . 20. Raj PP. Radiographic imaging for regional anesthesia and pain management . In: Raj PP , Lou L , Erdine S , Staats PS , Waldman SD , eds. 1 st ed. New York : Churchill Livingston ; 2003 ; 164 – 174 . 21. Romanelli DF , Beckmann CF , Heiss FW . Celiac plexus block: effi cacy and safety of the anterior approach . AJR Am J Roentgenol . 1993 ; 160 ( 3 ): 497 – 500. 22. Navarro-Martinez J , Montes A , Comps O , Sitges-Serra A . Retroperitoneal abscess after neurolytic celiac plexus block from the anterior approach . Reg Anesth Pain Med . 2003 ; 28 ( 6 ): 528 – 530 . 23. Brennan L , Fitzgerald J , McCrory C . The use of pulsed radiofrequency treatment for chronic benign pancreatitis pain . Pain Pract . 2009 ; 9 ( 2 ): 135 – 140 . 24. Markman JD , Philip A . Interventional approaches to pain management . Med Clin North Am . 2007 ; 91 ( 2 ): 271 – 286 . 25. Wong GY , Brown DL . Transient paraplegia following alcohol celiac plexus block . Reg Anesthesia . 1995 ; 20 ( 4 ): 352 – 355 . 26. De Cicco M , Matovic M , Bortolussi R , et al. Celiac plexus block: injectate spread and pain relief in patients with regional anatomic distortion . Anesthesiology . 2001 ; 94 ( 4 ): 561 – 565 . 27. Brown DL , Bulley CK , Quiel EL . Neurolytic celiac plexus block for pancreatic cancer pain . Anesthesia Analg . 5.4: Celiac Plexus Blocks 1987 ; 66 ( 9 ): 869 – 873 . 28. Raj PP . Neurolytic Agents . In: Raj PP , ed. Clinical Practice of Regional Anesthesia , 1 st edition. New York : Churchill Livingston , 1991 . pp 207 – 213 29. Patt RB . Peripheral neurolysis . In: Patt RB , ed. Cancer Pain , 1 st edition. Philadelphia, PA: J.B . Lippincott , 1993 : 359 – 337 . 30. Moore DC . Celiac (splanchnic) plexus block with alcohol for cancer pain of the upper intra-abdominal viscera . In: Bonica JJ , Ventafridda V , eds. Advances in pain research and therapy , 2 nd edition. New York : Raven Press , 1979 : 357 – 371 . 31. Fujita Y . CT-guided neurolytic splanchnic nerve block with alcohol . Pain . 1993 : 55( 3 ): 363 – 366 . 249

Section 6 Advanced Neuromodulation Interventions

6.1 Spinal Cord Stimulation 251 6.2 Intrathecal Drug Delivery Systems 271 This page intentionally left blank 251

Chapter 6.1 Spinal Cord Stimulation

Jason E. Pope , Richard G. Bowman , Timothy R. Deer

Introduction 252 Gross Anatomy 252 Circuit Review 256 Mechanism of Action 258 Technology 258 Indications and Patient Selection 259 Trial Procedure 260 Permanent Procedure 261 Stimulator Lead Orientation 262 Programming 263 Complications 263 Long-Term Management 265 Efficacy 265 Failed Back Surgery Syndrome 265 Complex Regional Pain Syndrome (CRPS) 266 Conclusions 267 References 267 252 Introduction Spinal Cord Stimulation (SCS) has had an amazing evolution since it was first introduced more four decades ago. In the 1960s, the Gate Control Theory developed, which gave rise to an interest in using electrical current to modify the nervous system.[ 1 ] In 1967, with this interest peaking, Norman Shealy described the use of intrathecal dorsal column stimulation to treat severe neuropathic pain.[ 2 ] Since that time, neurostimulation has evolved and its applications have exploded, with advances in spinal, nerve root, peripheral nerve, and brain stimulation. This chapter will focus on use in the spine, and key points to success with this therapy. SCS has become an essential part of the armamentarium for interventional pain physicians. Traditionally, neurosurgical treatments employed for pain are anatomic, ablative or augmentative. As only augmentative strategies are reversible and there exists good evidence based and comparative effectiveness research support, these therapies have gained popularity. Our focus is on stimulation of the spinal cord with pulsed electrical energy to control pain. Before we discuss the spinal cord stimulation procedure, we need to begin with a review of neuro- 6.1: Spinal Cord Stimulation anatomy and basic circuitry, as this knowledge is essential for optimized use of spinal cord stimulation. Gross Anatomy Most commonly, the spinal cord extends through the foramen magnum caudally to L1-2 in the adult population and L2-3 in the pediatric population, although 30 percent of adults may have the terminal portion at T12, while 10 percent may be as far as L3. Not surprisingly, dural sack extends to S1 in adults and S3 in children.[3]. There are predicatively two enlargements in the cervical and thoracic regions, between C4-T1 and T9-12, respectively. The terminal portion of the spinal cord is called the conus medullaris , while the collection of spinal nerves below L1-2 is termed the cauda equina . Spinal nerves exit their respective foramina bilaterally below the same numbered thoracic and lumbar vertebrae and above for the cervical vertebrae (as there are 8 cervical nerves). The DRG of each nerve root is just medial to the corresponding ipsilateral pedicle. Entry into the epidural space requires penetration (from superficial to deep) of the skin, supraspinatus ligament (from sacrum to T7) and the ligamentum nuche (from T7 to the occipital protuberance), interspinous ligament, and the ligamentum flavum . The ligamentum flavum is a wedge-shaped structure

Table 6.1.1 Neurosurgical Therapies for Pain Anatomic Ablative Augmentative

Correction of Structure Neurectomy Stimulation Sympathectomy Peripheral nerve Ganglionectomy Spinal cord Rhizotomy Thalamus Spinal DREZ lesion Motor cortex Cordotomy Myelotomy Nucleus Caudalis DREZ lesion Neuroaxial Drug Infusion Trigeminal tractotomy epidural Mesencephalotomy intrathecal Thalamotomy intraventricular Cingulotomy Hypophysectomy

This ﬁ gure was published in Benzon H, Rathmell JP, Wu CL, Turk DC, and Argoff CE. Raj’s Practical Management of Pain, 4th Edition . Copyright Elsevier 2008. 253 with bilateral portions that span adjacent vertebral bodies, although it is not continuous. Additionally, the meninges, from superficial to deep, include the dural mater, the arachnoid mater, and the pia mater. The cerebral spinal fluid is contained between the arachnoid mater and the pia mater in the subarachnoid space, although typical puncture of the dura also punctures the subarachnoid membrane as they are in such close proximity. The epidural space is reliably larger in the lumbar region and decreases in the anterior/posterior direction as one moves in the cephalad direction. Furthermore, the ligamentum flavum is thicker, and more reliably fused at the midline in the lumbar region and is thinner and unreliably fused in the cervical and thoracic region.[ 4 , 5 ] The architecture of the spinal cord can be topographically arranged. Importantly, the ascending nociceptive pathways include the spinothalamic tract (STT), the postsynaptic dorsal column (PSDC), the spinore- ticular tract, and the spinohypothalamic, along with the limbic and cortical interconnections. Primarily, myelinated A delta and unmyelinated C fibers transmit nociceptive information, with the first order neuron located in the dorsal root ganglia and terminating in the dorsal horn, the second order neuron crossing traveling to the thalamus, and the third order from the thalamus to the cortex. The dorsal horn has been characterized histologically and described topographically by Rexed as 10 laminae. Commonly, cells receiv- Interventional Pain Medicine ing C-fiber somatic noxious stimuli in the STT terminate in the ipsilateral dorsal horn (laminae I and II) and may ascend or descend a few spinal levels before crossing the midline via the anterior white commissure and ascending in the STT and to the thalamus (ventral posterolateral nucleus) and to the somatosensory cortex, where somatotopic encoding provides for specific localization (Figure 6.1.1 ).

Sensory cortex

Thalamus

Periaqueductal gray Afferent Sensory Reticular Pathways formation

Spinothalamic tract

Specialized sensory Dorsal horn receptors laminae I marginal II gelatinosa III IV nucleus C V proprius A delta A VI & C fibers Free nerve endings. Anterolateral Nociceptive neurons fasciculus Figure 6.1.1 Afferent sensory pathways. 254

Postsynaptic dorsal column pathway Dorsal root ganglia

Lateral PSDC STT

Ventral Somatic afferents Spinothalamic tracts 6.1: Spinal Cord Stimulation Visceral afferents

Figure 6.1.2 PSDC pathway.

Cutaneous A-delta nociceptors mostly terminate in the ipsilateral Rexed laminae I and V of the dorsal horn. Comparatively, the visceral nociceptive afferents again have first order neurons located in the dorsal root ganglia, however, may extend for more than five vertebral body segments before terminating in the ipsilateral dorsal horn before continuing on in the ipsilateral post-synatpic dorsal column (PSDC) pathway and STT bilaterally. The visceral nociceptors are widely distributed in laminae I, II, V, X, and laminae III and X contralaterally. The face and head are wired a bit differently. The trigeminal nucleus caudalis is responsible for the pain sensation of the face and can extend caudally to the C2 or C3 level, as demonstrated by Goadsby, and is termed the trigeminocervical complex.[ 7 ] The primary afferent has its cell body in the trigeminal ganglion, which synapses in the ipsilateral trigeminal nucleus caudalis, then cross and ascend in the STT to terminate in the VPN(ventral posteriomedial nucleus) of the thalamus. The trigeminocervical complex, and its reciprocal nature, has been implicated in a variety of primary and secondary headaches.[ 4 ] Regardless of the type of nociception, the ascending signal intensity can be altered by descending, efferent nociceptive modulating pathways, collectively described as the bulbospinal tracts, and involve the periaqueductal gray (PAG), rostroventromedulla (RVM), the nucleus raphe magnus (NRM), and the anterior pretectal nucleus. The dorsal columns have complex design and function. Exclusive to the visceral nociceptive ascending pathway, the dorsal columns are more commonly known for their role in touch, pressure, vibration, and proprioception. Although nociceptive input from A-beta fibers may terminate in laminae III and IV in the ipsilateral dorsal horn, the majority of the fibers ascend ipsilaterally in the dorsal columns, the gracile tract and the cuneate tract (more lateral), and terminate in the gracile nucleus and cuneate nucleus, respectively. These fibers then decuss at the level of the medulla to form the medial lemniscus ascend to the thalamus, whereby the third order neuron travels in the internal capsule and terminates in the cortex. It is this PCML pathway that is exploited in spinal cord stimulation (Figure 6.1.3 ). 255 (A) (B) Cerebrum

Primary somatic sensory cortex

Ventral posterior Ventral posterior lateral nucleus of medial nucleus of thalamus Midbrain the thalamus

Medial Trigeminothalamic leminiscus tract (trigeminal lemniscus) Trigeminal ganglion Mid-pons

Medial Interventional Pain Medicine Medial lemniscus lemniscus Principal Mechano- nucleus of sensory trigeminal receptors Rostral complex from face medulla Gracile nucleus (pathways from lower body) Internal arcuate Cuneate nucleus fibers (pathways from upper body) Caudal medulla Gracile tract Cuneate tract

Mechanosensory Cervical receptors from spinal cord upper body

Mechanosensory Lumbar receptors from spinal cord lower body

3a 3b

S L Th c

s 4a L 1a Th c 2b 2a c Th L s 5a 2b 4b

1b 2d 5b 6 2c

Figure 6.1.4 Axial view of the spinal cord. 256 Table 6.1.2 Ohm’s Law

I = E (or V)/R (or Z) E = electromotive force(measured in Volts) I = Current (conventional measured in SI unit A = Amperes (A). # R = resistance (measured in ohms)@

# also in coulombs/second where one coulomb is 6.25 x 1018 electrons @ a form of resistance is impedance, z.

An axial representation of the spinal cord may help construct the spatial arrangement of the aforementioned tracts. Circuit Review 6.1: Spinal Cord Stimulation Like any circuit, the biologic systems are governed by Ohm’s Law, where current is directly proportional to the voltage and inversely proportional to the resistance of the circuit (I = V/R). Appropriate electrical nomenclature describes current as the flow of a hypothetical positive charge and flows from positive to negative, while electrons flow from negative to positive and, by definition, flow in the opposite direction. Resistance is better represented by impendence, Z, which is dependent on frequency of the altering current, directly proportional to inductance, and inversely proportional to capacitance. (See Figure 6.1.5 .) Resistance (impedance) for the circuit (or system) to perform neuromodulation is governed by the inherent properties of the biologic tissues and the distance to the target (dorsal columns). Knowledge of the conductivity of the elements is therefore important. Biologic cells can be thought of as uneven capacitors. Capacitors consist of any parallel conductors separated by an insulator, has the ability to store a charge, and is logically measured by capacitance, the ability of a substance of store a charge. As one can now see, neural membranes are exactly that, capacitors, as they are barriers that separate a charge; and can be oversimplified by the Nernst equation. Sodium, potassium, and calcium channels contribute to the membrane resting potential (where potassium is the most important). Nerve transmission for myelinated axons proceeds via salutatory conduction. The subsequent voltage gated ion channel temporal relationship after an action potential is generated include sodium channels (extracellular to intracellular movement), potassium channel (intracellular to extracellular), and calcium (extracellular to intracellular) activation. Of particular interest is the effect of an electrical field on the membrane ionic environment. An electrical current flowing through two electrodes on a given node will stimulate the nerve at the cathode

R 1

Flow of positive charge Flow of electrons + V IIR – 2

R 3 Figure 6.1.5 Relationship between current and electron flow. 257

––––––– v Capacitor Plates Insulator +++++++

Figure 6.1.6 Capacitor model.

Action Myelinated potential –– axon – – + Node of – – + ++ + Ranvier + + ++ ++ ++ + + + ––

– – – Interventional Pain Medicine – – – –– – + Myelin Spread of + sheath depolarization

Cell body – – –– + + + + + (soma) + – + + + + – – + + + + + – – – – – – – – – – + + + – – + + + Action potential

Unmyelinated

Figure 6.1.7 Saltatory conduction.

(negative electrode) and resist excitation at the anode (positive electrode). Intracellular and extracellular ions move toward the cathode, resulting in membrane depolarization and producing an action potential. The figure describes the four “conventional currents” created when a cathode/anode system is placed near a neural membrane. Not illustrated, however, is the effect of electrode proximity (either cathode/ cathode or cathode/anode) on subsequent depolarization, and although beyond the scope of this introductory chapter, is relevant in stimulator lead design and configuration.

Electric Nomenclature and Variables Longitudinal stimulation>transverse stimulation. Four “conventional currents”; uneven capacitor

ANODE (+) CATHODE (–) Extracellular

Membrane ––––––––– +++++++

Intracellular

Figure 6.1.8 Electrical nomenclature. 258 This obviously is an oversimplification, as complex models and equations govern nerve excitation models, namely the Frankenauser-Huxley (FH) or the Hodgkin-Huxley (HH) equations. It does, however, provide a framework for the interventional pain physician to understand some of the methodology behind cathode/anode arrays in spinal cord stimulation. Mechanism of Action The mechanism of action for SCS is undetermined, but many theories have been postulated. The Gate Control Theory proposed by Melzack and Wall postulated that low-threshold stimulation of A-beta fibers in the dorsal columns inhibits the responses of nociceptive input from the C, A-delta fibers, and wide dynamic range (WDR) neurons in the substantia gelatinosa of the dorsal horn. This is not the whole story, however, as numerous mechanisms have been offered. Neurophysiologic explanations include inhibitory control on the abnormally active WDR, antidromic stimulation of the dorsal horn may produce presynatpic inhibition of neurons responsible for hyperexcitiability and central sensitization, and post synaptic inhibition of the afferent neuropathic pain signal[ 9 , 10 ]. Neurochemical mechanisms include 6.1: Spinal Cord Stimulation activation of gamma-aminobutyric acid (GABA) B receptors, which are metabotrophic G protein linked complex receptors located with greatest abundance in the dorsal horn and associated with potassium ionophore, with activation inducing potassium influx and inhibition of calcium channels with subsequent inhibition of adenylate cyclase (in contrast to GABA A that is a ligand gated ion channel, increasing chloride influx). Other postulated mechanisms include increasing oxygen delivery to the spinal by reducing sympathetic tone or ephaptic release of vasodilatory neurotransmitters.[ 11 ] Technology Currently, there are three major neuromodulation companies with variances in the same technology. The stimulator system components include the electrodes (sometimes requiring adapters or extensions) and a power source (either externalized as an RF or implanted as a rechargeable or non rechargeable IPG). Electrodes can be classified by their mode of entry, the number of electrodes and their shape: for example, quad (4) versus octrode (8) percutaneous (cylindrical) or laminectomy (paddle). Percutaneous leads are narrow cylindrical leads that pass through either 14-gauge or 17-gauge needles; laminectomy leads are rectangular, thin profile electrodes that resemble a boat paddle. Traditionally, and as suggested by the name, laminectomy leads require a lamina surgical disturbance for placement in the epidural space, and are therefore more invasive than percutaneous leads. These “paddle” leads deliver unidirec- tional current versus percutaneous leads that disperse current in 360 degrees. Electrodes are available in

Table 6.1.3 Conductivity of Intraspinal Elements Tissue Conductivity

Gray Matter 0.23 White Matter Longitudinal 0.6 Transverse 0.08 CSF 1.7 Epidural fat 0.04 Dura mater 0.03 Vertebral bone 0.02 Electrode insulation 0.002

Reprinted with permission from Oakley JC, Prager JP. Spinal cord stimulation: mechanisms of action. Spine . 2002;27(22):2574–2583. 259 Table 6.1.4 Recommended Lead choices Percutaneous Lead Paddle Lead

Less Invasive + + + + Patient awake *$ + + + + Lead Migration + + + + + Ease of revision + + + +

*conversant to conﬁ rm paresthesia during device placement. $ Some recent reports of MAC with paddle lead placement[12]. different lengths, with different numbers of contacts, different size and shape of contacts, and different contact spacing. Spinal cord stimulator trials are performed most often via a percutaneous lead placement. Lead choice for the permanent implanted device is surrounded in controversy and is greatly supported by anecdotal evidence and opinion. Some considerations are described in the following table. Interventional Pain Medicine Generators are of three primary types. Conventional generators include a non-rechargeable battery and computer circuitry. Rechargeable generators offer computer circuitry and a battery that accepts transcutaneous current, which recharges the IPG. Radiofrequency generators have computer circuitry and a receiver that requires an externalized power source to be held on the skin to transcutaneously power the active system. Nonrechargeble IPGs offer minimal user maintenance but are limited in utility by their finite battery source and may not be ideal for those with high electrical current demands. Rechargeable generators offer the benefit of a renewable power source that may accommodate higher current demands, but require the user to recharge it intermittently. Radiofrequency units accommodate individuals with very high current demands, but require the patient to wear a cumbersome external battery pack whenever it is in use. Most commonly, nonrechargeable and rechargeable IPGs are implanted. The depth, “battery life,” mode of recharging, programmability, and survivability (of the IPG if not recharged) differ with each neuromodulation company and the reader is directed to each specific company for information. Indications and Patient Selection The FDA indications for spinal cord stimulation are neuropathic pain of the trunk and limbs. This includes both radicular pain syndromes and ischemic pain of the limbs. Disease states that are often noted to have a potential for successful treatment with SCS include post-herpetic neuralgia, intercostal neuralgia, postlaminectomy pain (failed back surgery syndrome), complex regional pain syndrome, phantom limb pain,

Table 6.1.5 SCS Indications - Failed Back Syndrome (FBSS) or low back syndrome or failed back - Radicular pain syndrome or radiculopathios resulting in pain secondary to FBSS or herminated disk - Post-laminectomy pain - Multiple back operations - Unsuccessful disk surgery - Degenerative Disk Disease (DDD)/herminated disk pain refractory to conservative and surgical interventions - Peripheral causalgia - Epidural fibrosis - Arachnoiditis or lumbar adhesive arachnoiditis - Complex Regional Pain Syndrome (CRPS), Reflex Sympathetic Dystrophy (RSD), or causalgia

Source: Medtronic, Inc. 2009. 260 angina, painful peripheral neuropathy, focal peripheral neuropathies, ischemic limb pain, and radiculitis/ radiculopathy.[ 13 ] It has been well established that certain comorbid psychiatric illness reduces the success of procedural intervention [ 14 ]. Because 20 to 45 percent of patients have pain and psychopathology,[ 15 ] it is important to concomitantly treat or exclude these patients from spinal cord stimulation. Instruments to help identify the presence of clinically significant psychopathology include the Minnesota Multiphasic Personality Inventory (MMPI-2), which has a length of 566 items, or the Symptom Checklist 90 Revised (SCL-90-R), which is much shorter. It is important to utilize SCS appropriately in the treatment algorithm for a given diagnosis. Although some advocate exhausting all medical therapy and other conservative therapies before proceeding to stimulation, this treatment algorithm paradigm innately prohibits appropriate treatment access and may increase patient cormobidities associated with escalating polypharmacy and reduction in function. Several cost analysis comparisons between polypharmacy and SCS have been performed and are surrounded by controversy, however, if appropriate patient selection and technique are employed, earlier

6.1: Spinal Cord Stimulation intervention seems cost effective. Estimated times to “cost neutrality” are immediate in patients who would otherwise have received a coronary artery bypass surgery (CABG) for symptomatic relief of angina, one year for patients with angina who are not candidates for CABG, and three years for patients with failed back surgery and CRPS.[ 16 ] This contention to introduce neuromodulation via SCS is becoming more popular, and supported by Simpson.[ 17 ] Paramount to this argument is the trialing of the device. Percutaneous trialing is a reversible procedure. Objectively, a successful trial is generally described as one where the patient has at least 50 percent reduction of the neuropathic pain being addressed during the trial, significant functional improvement, and/or reduction in opioid consumption. Functional improvement instruments that are commonly employed and provide appropriate insight into pain-associated disability include the PDI (Patient Disability Index) and ODI (Oswestry Disability Index). Subjectively, a successful trial should be one in which the patient can appreciate a reduction in pain, an improvement in their functional status and quality of life, weighed against the subsequent the burden of an operation and device implantation maintenance. Trial Procedure The patient is positioned prone with lumbar support to minimize lumbar lordosis. The area is prepped in sterile fashion and draped appropriately. Monitored anesthesia care is performed to ensure appropriate, intelligent, patient communication and comprehension. The skin is then localized with 1 percent lidocaine (with or without epinephrine). The 14-gauge needle is then introduced in an acute angle (from the skin) to allow for gradual entry into the epidural space using a paramedian approach, lessening the “turn” the lead has to make in the posterior epidural space. There are many techniques to ensure appropriate needle trajectory and some of the most common include starting percutaneous entry at the medial border of the pedicle at one to two vertebral bodies below the desired entry site and advancing under intermittent fluoroscopy in the AP projection with the needle at a 30 degree or more shallow angle, while others utilize a image intensifier caudal to “open up” the interlaminar space and using the very commonly employed “gun barrel technique.” The epidural access is achieved by utilizing the “loss of resistance” technique with air or saline. A lateral fluoroscopic image may be helpful in suggesting the depth of the epidural space, acknowledging parallax may introduce some error if the image is not a true lateral (superimpose pedicles). If there is a question of the loss of resistance, one may use the provided guide wire to apply gentle pressure to investigate epidural entry: if the wire does not advance easily then the introducer needle is not in the epidural space. Once reliable entry is achieved, the lead is introduced and advanced under intermittent or live fluoroscopy. The lead is more easily “driven” when it is being slowly advanced. Most advocate advancing 261 with non-dominant hand and “driving” the stylet with the operator’s dominant hand. To aid in placement, different stylets exists: standard curved, straight, or rigid (and experience guides their use). Once the lead is in position, stimulation testing is performed. Of note, radiographic midline may not necessarily correlate with physiologic midline, as determined by the stimulation parestheisa distribution. If a second lead is chosen for the trial, it can be placed in either the same ipsilateral interlaminar interspace, the same contralateral interspace, or in an adjacent interlaminar interspace (most commonly ipsilaterally). To aid in lead placement, sometimes it may be beneficial to move the lead during the timeframe that it is being stimulated during the procedure, while exercising careful communication with the device representative and the patient. This technique can ensure ideal placement of the lead with emphasis on generating paresthesias in the desired painful locations and minimizing paresthesias felt by the patient outside of the areas that hurt. Once the testing is complete, the stylets are removed and the leads are secured (either by suture, adhesive bandage, or via the supplied anchors), with frequent fluoroscopic confirmation that the leads have not migrated. Some advocate tunneling the leads to minimize infection and increase lead stability. Once in the recovery room, the external IPG is connected and the patient is instructed to continue his/her daily activities. Trials are commonly three to Interventional Pain Medicine seven days. A variant of the aforementioned percutaneous trial is the implanted percutaneous lead trial. The difference from the aforementioned percutaneous trial is that the leads are secured and closed internally. It is connected to a temporary extension that is tunneled and externalized to the IPG. If the trial is successful, then the incision is opened, the lead is disconnected to the extension, and the temporary extension is pulled from the externalized site and discarded, leaving the sterile implanted lead. Advantages to this include reduced operative time for the implant and assurance that the trail stimulation is the same as the permanent stimulation. The disadvantage includes a second trip to the operating room to remove the surgical lead for a failed trail and the slightly higher risk of infection for the implant.[ 18 ] Permanent Procedure The permanent procedure is the same for placement of the electrodes as the aforementioned percutaneous trial, excluding the externalization of the leads. Once stimulation is achieved that overlies the appropriate painful area, the leads are secured using the anchor and nylon suture. First, an incision is created along the location overlying the needle entry through the fascia. Careful dissection down to the needle entry through the fascia is performed. Hemostasis is achieved and sutures are placed through the fascia for the purpose of securing the anchors. This may be performed before or after needle removal. An anchor is applied to each electrode. With regard to anchor choice, only the length of the anchor has been proven to reduce lead migration, and as described in Kumar,[ 19 ] the nose of the anchor should be buried within the supraspinous fascia. Furthermore, stress loops (generally of diameter of 1 inch or larger) are typically created near the anchors and an additional stress loop is placed also underneath the implanted battery to reduce lead migration and fracture. The IPG implantation site varies. The advantage of implanting in the buttock or posterior flank is the ability to perform the entire operation with the patient in the prone position. IPG placement in the upper chest wall, the abdomen, and the axilla have also been described in the literature. It is vitally important to assess the IPG implant site prior to the operation while the patient is lucid and able to consent to the desired location. It is then that the site should be marked. The chosen site should be one away from bony surfaces. Furthermore, the IPG pocket should be created adjacent to the pocket incision site so the suture line does not overlay the IPG, promoting healing and reducing stress on the suture line. Hemostasis should be carefully maintained to promote rapid healing. One is reminded that incisions should be performed parallel to the normal stress vectors of the skin, to minimize the chance of wound dehiscence and layered closure is recommended, ensuring the minimization of dead space, with absorbable suture deep and nonabsorbable superficially. Skin may be closed via staples, subcuticular stitches, or dermabond adhesives. 262

(A) Anchor end pushed through fascia Skin surface Lumbodorsal fascia

Cable conductor lead resistant to kinking Epidural space

(B) Anchor away from puncture through fasica

Skin surface

Lumbodorsal fascia

Kink location Cable conductor lead susceptible to kinking Epidural space 6.1: Spinal Cord Stimulation

Figure 6.1.9 (A) Cable conductor lead resistant to kinking. (B) Cable conductor lead susceptible to kinking. Reprinted with permission from Kumar K, Buchser E, et al. Avoiding complications from spinal cord stimulation: practical management recommendations from an international panel of experts. Neuromodulation . 2007;10:24–33.

Normal post-operative care is recommended, which includes keeping the incision site clean and dry for the first five to seven days after the procedure and avoidance of excessive twisting or bending for two to four weeks. Stimulator Lead Orientation Barolat et al., in 1993 mapped dorsal column cathodal stimulation positions to the body surface areas of perceived paresthesias in 106 patients and devised formula to measure effectiveness of the stimulation

Table 6.1.6 Electrode positioning suggestions Pain Location (dermatome) Verbal Level (center bipole placement)

Anterior Shoulder (C4-5 fibers) C3 (range C3-S) External Arm (C5 fibers) C4 (range C2-T3) Radial Forearm (C6 fibers) C5 (range C2-T3) Median Hands (C6-7 fibers) C6 (range C2-T3) Ulnar Hand (C8 fibers) C7 (range C2-T2) Ulnar forearm (T1 fibers) C7 (range C4-T3) Internal Arm (T2 fibers) T1 (range C5-T3) Chest (T2-6 fibers) T2 (range T1-T7) Buttock through LE (L2-S1 fibers) T9-T10 (range T11-L1) Low back (T9-L1 fibers) T9 (range T8-11) Abdomen (T9-L1 fibers) T8 (range T6-T11) Anterior thigh (L2-L3 fibers) T11 (range T11-T12) Anterior Leg (L4-5 fibers) T12 (range T12-L1) Posterior Leg (S1-S2 fibers) L1 (range T11-L1) Posterior thigh (S1-S2 fibers) L1 (range T11-L1) Foot (L5-S1 fibers) L1 (range T11-L1) 263

ymax Amplitude

ymin

0 D.TT2T+D.T T+D.T 2T3T 2T+D.T Time Figure 6.1.10 Pulse width, amplitude, and frequency measurements. position (effectiveness = number of combinations at the spine level eliciting paresthesias x 100/total number of combinations at the spine level).[ 20 ] This experiment provides target foundations to guide lead placement. Interventional Pain Medicine Programming After placement of the epidural lead, the electrical stimulation parameters that can be manipulated include amplitude, pulse width and rate.[ 21 ] Amplitude is the strength of the stimulation measured in volts. Pulse width is the duration in microseconds of the duration of the amplitude application. Rate (or frequency) is measured in cycles per second (or Hertz). (See Figure 6.1.11 ). Common values are indicated in Table 6.1.7 . Generally, the cathode is the target of stimulation and positioned over the target area in the middle of the lead, large pulse widths typically expand dermatomal coverage, while lower frequencies produce more thumping and higher frequencies produce more buzzing paresthesias. Impedance testing is used routinely to confirm terminal placement of the spinal cord lead. Low impedance values suggest intrathecal or subarachnoid (subdural) placement. Tsui et al., in a series of published reports, described electrical stimulation characteristics for intrathecal, subarachnoid, and proximal nerve root electrode positions, and requires current of 0.2mA, 0.3mA, and 0.5mA, using a frequency of 1Hz and pulse width of 200 microseconds.[ 22–25 ] As the physical antero-posterior (AP) position of the spinal cord stimulator is dependent on patient recumbence, so, too, is the impedance and resultant stimulation paresthesias. Abejon and Feler investigated posture related epidural impedance differences in seventy patients with spinal cord stimulation. The mean thoracic impedance was described to be 487.23 ohms prone, with a standard deviation of 259.67 ohms, where the perception threshold current mean was 4.3mA, with a standard deviation of 2.75mA.[ 26 ] Complications The overall incidence of spinal cord stimulation varies, and has been estimated to be 17 to 43 percent.[ 27 ] Spinal cord stimulator complications can be broadly divided into those that are technical or those that

Table 6.1.7 Common programming stimulation capture values Typical Values

Amplitude 1–10 volts Current 1.5–7.5 mA Pulse width 100–400 μ s Impedance 200–600 Ω Rate 20–120 Hz 264 Table 6.1.8 Potential Complications and Preventative Measures Complication Frequency Preventative Measures

TECHNICAL Lead migration requiring 11 percent[ 28 ], Appropriate anchoring, stress loop, use of nylon (avoidance of silk), revision 13.2 percent[ 46 ] placing “nose of anchor through fascia.” Battery placement Lead integrity violation 6 percent[ 28 ], Stress loop, avoid acute angles, proper anchoring requiring revision 9 percent[ 46 ] Hardware malfunction 2.9 percent[ 46 ] Appropriate preoperative testing Battery failure 1.6 percent[ 46 ] Appropriate preoperative testing BIOLOGIC Infection 5 percent [ 28 ], Appropriate prep and sterile technique, preoperative antibiotics 3.4 percent[ 46 ] within 30 minutes of incision Epidural hematoma 0.3 percent[ 19 ], Follow ASRA guidelines Dural puncture/CSF leak 2 percent[ 13 ], Shallow angle, appropriate loss of resistance technique 6.1: Spinal Cord Stimulation 0.3 percent [ 19 ] Seroma 2.5 percent [ 29 ] Limit aggressive blunt dissection, dead space closure, avoidance of shear forces, abdominal binder Pain over device 0.9 percent[ 19 ] Ensure appropriate placement away from bony structures, battery placement consensus with patient before placement Skin erosion 0.2 percent[ 19 ] Avoid placing suture line overlying device, pocket sufficient size to minimize wound tension.

are biologic/surgical in nature. The consequences of these complications can range from the mundane to the devastating. Please refer to Table 6.1.8 . Devastating complications associated with spinal cord stimulation are thankfully in the minority, but have been reported, and include paralysis, epidural abscess, and death (from methicillin resistant staphylococcus aureus infection).[ 30–33 ] Interestingly, Kumar, et al.[ 19 ] reported that complications requiring revisions were approximately 25 to 33 percent, and furthermore, only approximately 12 percent of reoperation patients were satisfied with the results.[ 34 ] If an infection is suspected, infectious disease consultation is highly recommended, to guide appropriate, geographical conscientious antibiotic therapy. Spinal hematomas incidence is largely unknown, although it has been estimated to be near 1/150,000 epidurals and 1/222,000 spinal anesthetics.[ 35 ] Although a review of the American Society of Regional Anesthesia (ASRA) 2010 guidelines for neuroaxial interventions in patients receiving anticoagulation therapy is beyond the scope of this chapter, it is vital the reader employ the guidelines.[ 35 ] Treatment is contingent on hematoma evacuation within eight hours of neurologic deficit.[ 36 ] Immediate neurosurgical consultation is paramount. Post-operative symptoms that may suggest epidural hematoma or other spinal compression associated with the SCS procedure include excess pain along the lead in the spine, weakness or numbness in distal dermatomes, or parethesias present even when the SCS device is not turned on. Fluoroscopy and electric testing of the lead can be used to investigate SCS lead misplacement. Anterior lead placement is suggested by muscle contraction of adjacent or distal spinal nerves and painful stimulation (within the normal aforementioned stimulation parameters). Intrathecal lead placement is suggested by very low impedance testing, while the hallmark of subdural stimulation is segmental, low amplitude stimulation that is often uncomfortable to the patient.[ 37 ] Recommendations to avoid complications associated with the surgery include an avoidance of steep needle trajectory when entering into the epidural space and appropriate bevel orientation with the cutting edge directed posteriorly to avoid dural tear, placement of anchor noses into the supraspinous fascia, suturing the anchor with nylon (not silk), creating strain loops, and placing the battery after 265 discussion with the patient prior to the operation to determine the optimal position (as choices include the buttocks, mid flank, abdominal wall, or the infraclavicular regions). Regarding seroma, the incidence is approximately 2.5 percent and can be attributed to shear forces between abdominal layers and lack of immobilization in patients undergoing abdominoplasty.[ 29 ] Additionally, aggressive blunt dissection should be avoided and dead space should be closed to reduce the chance of seroma formation. Infections can be mitigated by appropriate sterile technique, hemostasis control prior to closure, good patient hygiene, preoperative antibiotics, intraoperative irrigation prior to closure, appropriate post-op care (keeping incision clean, dry), and limited to no excessive movement/twisting/bending for 2–4 weeks after procedure to minimize tension along the suture line and reduce the propensity for wound dehiscence. Furthermore, infections and skin erosions can be minimized by a careful layered closure and avoiding suture lines on top of the newly implanted device. Although postoperative antibiotics for coverage of gram-positive skin flora are commonly given for a seven- to ten-day course, no evidence supports its routine use.

Long-Term Management Interventional Pain Medicine Patients undergoing spinal cord stimulator placement require long-term management for device programming and troubleshooting to ensure optimal treatment outcomes. Most patients undergoing SCS placement will need their IPG reprogrammed periodically. Impedance variability can result from subtle lead orientation changes within the epidural space, correlating with patient movement. Alternatively, scar tissue development (or adhesions) can increase the circuit resistance. These problems can often be addressed via reprogramming of the IPG so that the pain relieving paresthesias can be recaptured. SCS interrogation may also provide insight into problems with communication between the handheld pro- grammer and the IPG, along with recharging difficulty. When paresthesias cannot be recaptured or when electrode impedances appear to have increased significantly, X-rays assessing lead position can be obtained to investigate lead migration, fracture, or a disconnect from the IPG. Revisions can be necessary for a variety of reasons in long-term implant patients: including lead migration, lead fracture, and IPG power depletion, to name a few. Development of extensive epidural fibrosis along the electrode contacts may necessitate revision and placement of laminectomy leads. Indolent infections and autoimmune rejection may present as long as six months post-operatively and may require explanation. In certain cases where the allergy can be identified as exclusively due to the IPG metal, a Dacron pouch utilized in the generator pocket shielding the IPG can be considered. In rare cases, new infection of hardware can be seeded to SCS devices from systemic infections in patients, resulting in device infection presenting years after implantation. As a general rule, in all cases where infection of a SCS device is identified, all hardware, sutures, and anchors should be explanted. A post-operative MRI of the spine should be obtained (CT if the patient is not a candidate for a MRI) to assess for epidural abscess. Neurosurgical and infectious disease specialists should be consulted as appropriate. If re-implantation is desirable, this should not be considered until the patient is infection-free and medically stable for at least twelve weeks. Efficacy The efficacy of SCS in the United States centers on clinical investigation and the post-marketing data regarding SCS is voluminous. Although there are many proposed indications, SCS is predominately used for neuropathic pain from failed back surgery syndrome and CRPS. In Europe, the major indication is for management of ischemic pain. To adequately discuss efficacy, we will discuss outcomes for each of the United States indications. Failed Back Surgery Syndrome North, et al., published prospective, randomized crossover study of patients with failed back surgery syndrome who were between reoperation and SCS and allowed to cross over at six months. 266 Twenty-seven patients participated. Of the patients who underwent reoperation, 67 percent crossed over to SCS, while 17 percent crossed over from SCS to reoperation, suggesting that SCS is better at treating pain than reoperation.[ 38 ] North again demonstrated the long-term success rate at 2.9 years + /− 1.1 years of SCS for FBSS versus reoperation was 47 percent versus 12 percent reoperation.[ 35 ] Other studies have refuted reoperation, as patients that undergo multiple surgical interventions fair worse, regardless of the initial treatment.[ 39 ] Furthermore, the benefits of SCS for FBSS have been supported by other prospective studies.[ 40 , 41 ] Kumar, et al., compared SCS to conventional medical management in patients with primarily radicular neuropathic pain secondary to FBSS and demonstrated that 48 percent of the SCS group had 50 percent pain reduction at 12 months, compared to 9 percent of the conventional management. At twenty-four months, this trend continued and the authors concluded that pain, quality of life, functional capacity, and satisfaction with SCS were superior to medical management. [ 42 , 43 ] A recent guidelines review suggested Level II-1 or II-2 evidence and class 1B or 1C recommendation level for SCS in managing patients with FBSS.[ 44 ] Complex Regional Pain Syndrome (CRPS) 6.1: Spinal Cord Stimulation There is a paucity of research for SCS managing CRPS, when compared to FBSS. Kemler, et al., performed a randomized controlled trial of SCS for treatment of CRPS in the Netherlands from 1997–98. He randomized patients who had upper extremity CRPS for at least six months to either SCS and physical therapy or physical therapy alone and assessed pain, functionality, quality of life, and complications at six months.[ 45 ] Patients were then allowed to cross over, and were followed for twenty-four months. [ 46 ] At six months, the patients who received the SCS and PT had improvements in pain control and satisfaction, but no statistical difference was appreciated regarding improvement in functionality. At twenty-four months, the pain improvement from six months was maintained, along with a statistically significant improvement in health related quality of life. These results are further supported by multiple case series and retrospective reviews.[ 47 , 48 , 51 ] Interestingly, Bennett, et al., compared effectiveness of different lead configuration and program features, and concluded that adequate analgesia required high frequency stimulation of greater than 250 Hz.[ 48 ] Stanton-Hicks, et al., in 2002 commented on the multidisciplinary approach to treatment of CRPS, integrating psychological, physical, and interventional pain therapy to optimize patient outcome.[ 49 ] They concluded that early, aggressive pain therapy, including SCS, should be instituted in patients that fail to progress through rehabilitation alone. This was a change from the 1998 CRPS treatment guidelines.[ 50 ]

AB Figure 6.1.11 Spinal cord stimulation A. AP view B. Lateral view 267 Taylor, et al., performed a systematic review of literature up to 2002 for determine the clinical and cost effectiveness of spinal cord stimulation for treatment of CRPS. They conclude that there is level-A evidence for type I and Level D evidence for type II treatment of CRPS with SCS. Furthermore, they predicted a lifetime cost savings of $60,800 when SCS was used in conjunction with physical therapy as compared to physical therapy alone.[ 30 ] Conclusions Spinal Cord Stimulation provides an excellent addition to the pain management physician’s armamentarium. Treatment successes hinge on appropriate patient selection and technique. As we continue to practice in times focused on cost containment, it is paramount to advocate this therapy for appropriate patients to ensure its accessibility and affordability. References 1. Melzack R , Wall PD . Pain mechanisms: a new theory . Science . 1965 ; 150 : 971 – 979 . Interventional Pain Medicine 2. Shealy CN , Mortimer JT , Reswick JB . Electrical inhibition of pain by stimulaton of the dorsal columns: preliminary clinical report . Anesth Analg . 1967 ; 46 ( 4 ): 489 – 491 . 3. Boonpirak N , Apinhasmit W . Length and caudal level of termination of the spinal cord in Thai adults . Acta Anatominca . 1994 ; 149 : 74 – 78 . 4. Anthony M . Headache and the greater occiptial nerve . Clinical Neurology and Neurosurgery . 1992 ; 94 ( 4 ): 297 – 301 . 5. Zarzur E . Anatomic studies of the human lumbar ligamentum fl avum . Anesth Analg . 1984; 63 : 499 – 502 . 6. Oakley J , Prager J . Spinal cord stimulation: mechanism of action . Spine . 2002 ; 27 ( 22 ): 2574 – 2583 7. Goadsby PJ , Hoskin KL . The distribution of trigeminovascular afferents in the nonhuman primate brain Macaca nemestrina: a c-fos immunocytochemical study . J Anat . Apr 199 7; 190 (Pt 3): 367 – 375 . 8. Purves D , Fitzpatrick D , Williams SM , et al. In: Chapter 9. Neuroscience , Second Edition. Victoria, Australia: 2001 . 9. Linderoth B , Foreman RD . Physiology of spinal cord stimulation: review and update . Neuromodulation . 1999 ; 2 : 150 – 164 . 10. Roberts MHT , Rees H . Physiological basis of spinal cord stimulation . Pain Rev . 1994 ; 1 : 184 – 198 . 11. Kunnumpurath S , Srinivasagopalan R , Vadivelu N . Spinal cord stimulation: principles of past, present and future practice: a review . Journal of Clinical Monitoring and Computing . 2009 ; 23 : 333 – 339 . 12. Harned ME , Owen RD , Steyn PG , Hatton KW . Novel use of intraoperative Dexmedetomodine infusion for sedation during spinal cord stimulator lead placement via surgical laminectomy . Pain Physician . Jan 2010 ; 13( 1 ): 19 – 22 . 13. Pinzon EG . Spinal cord stimulation . Practical Pain Management . May/Jun 2005 . 14. Fishbain D , Goldberg M , Meagher BR , et al . Male and female chronic pain patients characterized by DSMIII psychiatric diagnostic criteria . Pain . 1986 ; 26 : 81 – 197 . 15. Gallagher R . Primary care and pain medicine: a community solution to the public health problem of chronic pain . Med Clin North Am . 1999 ; 83 : 555 – 583 . 16. North RB , Shipley J , Taylor RS . In: chapter 26: The Cost Effectiveness of Spinal Cord Stimulation . Neuromodulation , Volume II; 355–376. New York : Elsevier ; 2009 . 17. Simpson BA . The role of neurostimulation: the neurosurgical perspective . J Pain Symptom Manage . 2006 ;S 4 : S3 – S5. 18. May MS , Banks C , Thomson SJ . A retrospective, long-term, third party follow-up of patients considered for spinal cord stimulation . Neuromodulation . 2002 ; 3: 137 – 144 . 19. Kumar K , Buchser E , Linderoth B , Meglio M , Van Buyten JP . Avoiding complications from spinal cord stimulation: practical management recommendations from an international panel of experts . Neuromodulation . 2007 ;Volume 10 , 24 – 33 . 20. Barolat G, Massoro F , He J , Zeme S , Ketcik B . Mapping sensory responses to epidural stimulation of the intrapsinal neural structures in man . J Neurosurg . 1993 ; 78 : 233 – 239 . 21. Alfano S , Darwin J , Picullel B . Programming Principles in Spinal Cord Stimulation: Patient Management Guidelines for Clinicians . Minneapolis : Medtronic ; 2001 : 27 – 33 . 268 22. Tsui BC , Wagner AM , Cunningham K , Perry S , Desai S , Seal R . Threshold current of an insulated needle in the intrathecal space in pediatric patients . Anesth Analg . 2005 ; 100 ( 3 ): 662 – 665. 23. Tsui BC , Gupta S , Finucane B . Detection of subarachnoid and intravascular epidural catheter placement . Can J Anaesth . 1999 ; 46 ( 7 ): 675 – 678 . 24. Tsui BC , Gupta S , Emery D , Finucane B . Detection of subdural placement of epidural catheter using nerve stimulation . Can J Anaesth . 2000 ;47 ( 5 ): 471 – 473 . 25. Tsui BC , Guenther C , Emery D , Finucane B . Determining epidural catheter location using nerve stimulation with radiological confi rmation . Reg Anesth Pain Med . 2000 ; 25 ( 3 ): 306 – 309 . 26. Abejon D , Feler C . Is impedance a parameter to be taken into account in spinal cord stimulation? Pain Physician . 2007 ; 10 ( 4 ): 533 – 540. 27. Eldrige JS , Weingarten TN , Rho RH . Management of cerebral spinal fl uid leak complicating spinal cord stimulator implantation . Pain Practice . 2006 ; 6 ( 4 ): 285 –288 . 28. Sarubbi F , Vasquez J . Spinal epidural abscess associated with the use of temporary epidural catheters: Report of two cases and review . Clin Infect Dis . 1997 ; 25 : 1155 – 1158 . 29. Beer GM , Wallner H . Prevention of seroma after abdominoplasty . Aesthetic Surgery Journal . 2010; 30 ( 3 ): 414 – 417 . 6.1: Spinal Cord Stimulation 30. Taylor RS , Van Buyten JP , Buchser E . Spinal cord stimulation for complex regional pain syndrome: a systematic review of the clinical and cost-effectiveness literature an assessment of prognostic factors . Eur J Pain . Feb 2006 ; 10 ( 2 ): 91 – 101 . 31. Taylor RS , Van Buyten JP , Buchser E . Spinal cord stimulation for chronic back and leg pain and failed back surgery syndrome: a systematic review and analysis of prognostic factors . Spine . 2005 ; 30 : 152 – 160 . 32. Torrens K , Stanely PJ , Ragunathan PL , Bush DJ . Risk of infection with electrical spinal cord stimulation . Lancet . 1997 ; 349 : 729 . 33. Meglio M , Cioni B , Rossi GF . Spinal cord stimulation in management of chronic pain : a 9-year experience. J Neurosurg . 1989 ; 70 : 519 – 524 . 34. North RB , Kidd DH , Farrokhi F , Piantadosi SA . Spinal cord stimulation versus repeated lumbosacral spine surgery for chronic pain: a randomized, controlled trial . Neurosurgery . 2005 ; 56 : 98 – 107 . 35. Horlocker TT , Rowlingson JC , Enneking FK , et al. Regional Anesthesia in the Patient Receiving Antithrombotic or Thrombolytic Therapy: American Society of Regional Anesthesia and Pain Medicine Evidence–Based Guidelines (Third Edition) . Regional Anesthesia and Pain Medicine . 2010; 35 ( 1 ): 64 – 101 . 36. Vandermeulen EP , Van Aken H , Vermylen J . Anticoagulants and spinal-epidural anesthesia . Anesth Analg . 1994 ; 79 : 1165 – 1177 . 37. Pope JE, Stanton-Hicks M . Accidental subdural spinal cord stimulator lead placement and stimulation. Neuromodulation : Technology at the Neural Interface. 2010 ; prior to print . 38. North RB , Kidd DH , Piantadosi S . Spinal cord stimulation versus reoperation for failed back surgery syndrome: a prospective, randomized study design . Acta Neurchir Suppl . 1995; 64 : 106 – 108 . 39. Chang Y , Singer DE , Wu YA , Keller RB , Atlas SJ . The effect of surgical and nonsurgical treatment on longitudinal outcomes of lumbar spinal stenosis over 10 years . J Am Geriatr Soc . May 2005 ; 53 ( 5 ): 785 – 792 . 40. Borolat G , Oakley J , Law J . Epidural spinal cord stimulation with multiple electrode paddle lead is effective in treating low back pain . Neuromodulation . 2001 ; 2 : 59 – 66 . 41. Bruchiel KJ , Anderson VC , Brown FD . Prospective, multicenter study of spinal cord stimulaton for the relief of chronic back and extremity pain . Spine . 1996 ; 21 : 2786 – 2794 . 42. Kumar K , Taylor RS , Jacques L , et al. Spinal cord stimulation versus conventional medical management for neuropathic pain: a multicentre randomized controlled trial in patients with failed back surgery syndrome . Pain . 2007 ; 132 : 179 – 188 . 43. Kumar K , Taylor RS , Jacques L , et al. The effects of spinal cord stimulation in neuropathic pain are sustained: a 24-month follow-up of the prospective randomized controlled multicenter trial of the effectiveness of spinal cord stimulation . Neurosurgery . 2008 ; 63 : 762 – 770 . 44. Manchikanti , L , Boswell MV , Singh V , et al. Comprehensive evidence-based guidelines for interventional techniques in the management of chronic spinal pain . Pain Physician . 2009 ; 12 : 699 – 802 . 45. Kemler MA , Reulen JP , Barendse GA , van Kleef M , de Vet HC , van den Wildenberg FA . Impact of spinal cord stimulation on sensory characteristics in complex regional pain syndrome type I: a randomized trial . Anesthesiology . 2001 ; 95 : 72 – 80 . 269 46. Kemler MA , De Vet HCW , Barendse GAM , Van Den Wildenberg FAJM , Van Kleef M . The effect of spinal cord stimulation in patients with chronic refl ex sympathetic dystrophy: two years follow-up of the randomized controlled trial . Ann Neurol . 2004 ; 55 : 13 – 18 . 47. Oakley JC . Spinal cord stimulation for the relief of pain: proceedings of a symposium during the 4th International Congress of the International Neuromodulation Society, September 16–20, 1998, Lucerne, Switzerland . Neuromodulation . 1999 ; 2 : 184 – 187 . 48. Bennett D , Alo K , Oakley J et al . Spinal cord stimulation for complex regional pain syndrome I (RSD): a retrospective multicenter experience from 1995–1998 of 101 patients . Neuromodulation . 1999 ; 3 : 202 – 210 . 49. Stanton-Hicks MD , Burton AW , Bruehl SP , et al. An updated interdisciplinary clinical pathway for CRPS: report of an expert panel . Pain Pract . Mar 2002 ; 2 ( 1 ): 1 – 16 . 50. Stanton-Hicks M , Baron R , Boas R , et al . Complex regional pain syndromes: guidelines for therapy . Clin J Pain . 1998 ; 14 : 155 – 166 . 51. Shrivastav M , Musley S . Spinal cord stimulation for complex regional pain syndrome . Conf Proc IEEE Eng Med Biol Soc. 2009 ; 2033 – 2036 . Interventional Pain Medicine This page intentionally left blank 271

Chapter 6.2 Intrathecal Drug Delivery Systems

Maged Hamza

Introduction 272 Physiology 272 Indications 272 Contraindications for the Use of IDDS 273 Are Drug Delivery Systems Efficacious? 273 Are IDDS Cost-Effective? 273 Patient Selection/Patient Education 274 Psychological Screening 274 Intrathecal Trials 274 Implantation of Drug Delivery System 275 Clinical Pearls of Intrathecal Placement 281 Postoperative Complications 283 Pharmacologic Complications 283 System-Related Complications 284 Summary 284 References 284 272 Introduction The use of intrathecal medications to alleviate pain associated with childbirth, trauma, and surgery is well understood. Physiologically, the administration of opioids to bring about pain reduction was documented in 1976. Intrathecally-delivered opioids produced a significant inhibition of the stimulus-induced spinal nociceptive neuronal discharge, resulting in a significant elevation of the pain threshold that was what was written and with models. Opioids are known to bind high-affinity to Mu receptors and the substantia gelatinosa . That in turn leads to the inhibition of the transmission of nociceptives which in turn results in reduction of pain transmission.( 1 ) In the early 1980s, the use of intrathecal drug delivery system (IDDS) to administer opioids in the spinal fluid compartment for the treatment of pain was introduced.( 2 ) For the treatment of chronic severe pain, and spasticity, the FDA currently approves the use of drug delivery system with delivery of morphine and baclofen, respectively. The use of drug delivery system delivery for administration of chemotherapy for cancer is also FDA approved. Currently, FDA-approved medications for the continuous intrathecal delivery are principally morphine, clonidine, baclofen, and ziconotide. 6.2: Intrathecal Drug Delivery Systems Over the last three decades, the use of drug delivery systems for alleviation of chronic pain and spasticity has been increasing. More agents are being used, though with no FDA approval, and are making their place as commonly used medications. Examples of that are local anesthetics such as bupivacaine, and opioids such as hydromorphone, and fentanyl. In current practice, drug delivery system for alleviation of chronic pain is becoming an increasingly important tool used by many physicians to alleviate the chronic, intractable suffering of many patients. Physiology Opioids administered neuraxially act at receptors in the substantia gelatinosa of the spinal cord dorsal horn to yield dose-dependent analgesia.( 3 , 4 ). Opioids may act through multiple mechanisms, including inhibition of presynaptic neurotransmitter release from primary afferents via presynaptic inhibition of calcium channels.( 5 , 6 , 7 ) Furthermore, opening of G-proteingates, K+ channels in the central nervous system (G-protein-regulated inwardly rectifying K+ channels [GIRKs]) may lead to postsynaptic neuronal yperpolarization.( 4 ) The MOR-expressing neurons in the dorsal horn of the spinal cord appear to be significantly involved in spinal opioid analgesia.( 8 ) a They activate opioid receptors at the central terminals of C-ﬁ bers in the spinal cord. b They activate opioid receptors on the second-order pain transmission cells, thus inhibiting ascending transmission of the pain signal. c Systemically administered morphine leads to an opioid-induced increase in spinal acetylcholine (Ach), and the opioid-induced spinal Ach— via activation of the spinal cholinergic system— contributes to opioid-mediated antinociception.( 9 ) Upregulation of mu opioid receptors in the dorsal root ganglion may increase the antinociceptive potency of IT morphine more than five times.( 10 ) Finally, it is conceivable that some of the analgesia from IT morphine may be due to IT morphine causing spinal release of adenosine and subsequent spinal adenosine A1 receptor activation.( 11 ) A variety of analgesic/co-analgesic agents have been utilized to provide spinal analgesia. The long-term spinal administration of agents to alleviate refractory persistent pain, the classic initial class of analgesics has been opioids. Indications Drug delivery systems are used for the alleviation of chronic severe intractable pain. Commonly specific diseases include radiculitis, discogenic pain, epidural fibrosis, adhesive arachnoiditis, postlaminectomy syndrome, spondylolisthesis, spondylosis, and spinal stenosis. If these states involve neurologic damage, 273 intrathecal therapy might be used to treat pain and spasticity, meaning a combination of morphine and baclofen. Other disease states that have been associated with pain in which alleviation of pain has been reported with implantable pumps include systemic lupus, neurofibromatosis, peripheral neuropathy, chronic vascular disease, and phantom pain. Drug delivery systems have been generally used for the following conditions: 1. Severe chronic intractable pain. 2. In patients where less invasive lines of therapy have not been able to produce adequate sustained pain relief. 3. In patients with opioid responsive disease; however, adverse events have limited the advancement of dose to adequate relief More recently over the last decade or so, there have been better, well defined indications for the use and utilization of drug delivery systems for treatment of chronic pain.( 12 , 13 )

Contraindications for the Use of IDDS Interventional Pain Medicine Absolute Contraindications 1. Local systemic untreated infections. 2. Poorly controlled or untreated coagulopathies. 3. Cranial processes that may lead to cerebral herniation with any cerebrospinal ﬂ uid leaks and loss. 4. Psychological barriers that would render the patient an inappropriate candidate, most notably borderline personality disorders. 5. Patient refusal to the utilization of therapy. Relative Contraindications: 1. Life expectancy of less than three months. 2. Untreated psychiatric disorder such as signiﬁ cant depression and anxiety. 3. Diminished mental capacity. 4. Poorly treated or untreated substance abuse. Are Drug Delivery Systems Efficacious? Multiple publications have reported efficacy and the effectiveness of drug delivery systems on the alleviation of chronic pain. In the Interventional Technique Evidence/Lines in the Management of Chronic Spine Pain, it was concluded that evidence for implantable intrathecal infusion systems is strong for short term improvement in pain of malignancy of neuropathic pain whereas it was moderate for long term management of chronic pain.( 14 , 15 ) Are IDDS Cost-Effective? Two studies have documented the cost-effectiveness of intrathecal therapy for chronic pain. In one study, estimated annual cost over five years has been $16,579.00/year in a post-laminectomy syndrome patient. These were defined as patients who have received spinal surgery and continued to have pain. The studies compared the average cost annualized over five years for conventional medical therapy versus intra-spinal therapy; intra-spinal therapy was considered cost-effective. The studies did not account for the intangible cost of alleviating pain and suffering. As seen in the efficacy section, pain reduction is one of the aspects of evaluating intra-spinal therapy. Increased quality of life and improved function, however, have been also repeatedly reported, as mentioned earlier. The intangible cost of alleviating pain and suffering and allowing for better function was not reported on these two studies. The cost-effectiveness studies also did not account for the more expensive recently developed and introduced medications that would add to the cost of conventional comprehensive medical therapy. 274 All considered will further highlight and emphasize the cost-effectiveness of intra-spinal therapy over comprehensive medical care for chronic pain.( 16 , 17 ) To be taken into account that the average allowable reimbursement associated with the cost of intraspinal therapy (professional and facility fees associated with IDDS implants) remained unchanged, as per the CMS guidelines. That further adds to the cost-effectiveness of intra-spinal therapy compared to conventional medical management. Patient Selection/Patient Education Perhaps the most important factor in determining short as well as long-term success and outcome following intrathecal therapy would be considered patient selection and patient education. Choosing the appropriate patient with the right indications and providing patient with adequate information, knowledge, and education as well as setting appropriate realistic patient’s expectations of the therapy is of crucial importance to ensure satisfactory outcome. The following is the general patient selection criteria considered to be most acceptable: 6.2: Intrathecal Drug Delivery Systems 1. Chronic severe intractable pain with structural etiology. 2. Failed less invasive, more conservative lines of therapy that includes medications of various classes and various combinations of appropriate doses, minimally interventional procedures namely nerve blocks, patient understanding of the procedure with realistic expectations. 3. Lack of indications and successful pre-procedural psychological screening. 4. Successful trial prior to implant. Psychological Screening The psychological screening in preparing patients for intrathecal therapy aims to delineate and elucidate any major barriers toward improvement. It has been shown that screening and counseling may improve the outcome of factors such as uncontrolled depression, uncontrolled anxiety, drug addiction, and some personality disorders.( 18 ) Psychological screening should not be considered as the pass/fail litmus test. It should be considered as an added tool to ensure adequate patient selection, and understanding of the therapy. Also confirm realistic expectations on patient’s behalf as well as optimize any uncontrolled and uncorrected factors, all aiming to improve and optimize patient’s outcome. Intrathecal Trials It is considered as an important step in selecting patients for intrathecal therapy to have performed a trial of delivering opioids neuraxially and documenting outcome prior to considering drug delivery system implantation. Multiple methods of performing trials have been reported. Anecdotal reports have proposed the superiority of one method over the other. There has not been a definitive study to suggest a clear-cut best method of trial. Recently, nineteen authors discussed the proper method of trialing. The group has concluded that trialing using a method that limits permanent implant is logical. Relevant factors to consider in trialing include delivery site, delivery modality, and rate infusion.( 19 ) A recent survey in multicenter design physicians were asked to qualify patient primary pain, trialing data was collected in terms of single shot boluses and continuous infusion. A twelve-month analysis of the data there was no difference in the nociceptive group regardless of whether an epidural or intrathecal route was used. In trialing for neuropathic syndromes, the initial success of trialing was significantly better if a continuous infusion method was used. There was no difference in outcome between trialing through epidural compared to intrathecal route. Epidural delivered opioid or intrathecally delivered opioid. In both, this can be achieved by a single dose injection or multi-boluses or continuous infusion. Documenting the success and outcome of trial 275 should be in terms of pain reduction, functional improvement with improved activity, and reduction in the use of oral opioid. Recently there has been increasing interest in weaning patients off or at least reducing their total dose of oral opioid prior to trial to further emphasize and demonstrate the success of the trial in reducing pain, increasing activity, and decreasing the dependence and the utilization of orally administered opioid.( 20 ) Since there has not been one method proven superior and/or best trial of method it is important to consider multiple factors in selecting a trialing technique; Available local ancillary support (nursing, physical therapy, etc.), level of expertise of the implanting physician and the trialing physician are not to be ignored, especially in today’s managed care requirement and expectations of the pair source of trial methods, which can have geographic variation. Implantation of Drug Delivery System After ensuring all section criteria has been met, patient is then prepared for drug delivery system implantation. Preoperatively Interventional Pain Medicine 1. Including CBC with differential, PT, PTT, urinalysis, ECG, and chest X-ray are done based on indication/need. For example, it is essential to assess PT and PTT with patients on anticoagulants or with bleeding disorders or bleeding tendencies. 2. Adequate control of preexisting concomitant medical problems such as hypertension, diabetes with euglycemic and hemoglobin A1C, patients are strongly encouraged to cease smoking preoperatively as smoking has been shown to impair healing. 3. Medication to be infused in the pump has been already predetermined and selected based on the results of the trialing phase. 4. Discussion and counseling with the patient for selection of the site of pump implantation to avoid bony prominences, avoid belt lines to avoid chronic wound site/incision site irritation and possible infection. Day of Surgery 1. Preoperative consent discussed with patient and family involved. 2. Mark implant site (Figure 6.2.1 ).

Figure 6.2.1 Anterior site marking for intrathecal pump device. 276 Intraoperative Preparation 1. Preoperative sepsis prophylaxis. It is generally advised to follow the local established standards of care by other surgeons in the area. However, evidence suggests that IV antibiotics thirty to sixty minutes prior to skin incision have been shown to reduce infections. 2. Prepare for equipment ensuring that representative/vendor/manufacturer is present with all preferred equipment arranged and discussed prior to the case. Also, prearrange and coordinate/ order the medicine to be infused in the pump prior to the case. 3. Positioning. Commonly used position is lateral decubitus with hips slightly fl exed; knees slightly bent and ensure adequate padding of all pressure points, especially using a bean bag (Figure 6.2.2 ). 4. For skin prep and drape, it is generally advised to follow the locally established guidelines. 5. Under fl uoroscopic guidance establish access into the intra-thecal compartment with a paramedian shallow approach. The intrathecal access is obtained below the level of L2 to avoid injury of the cord since the cord ends at the L1-2 interspace. Remove the stylet. There should be free fl ow of the CSF (Figures 6.2.3 and 6.2.4 ). 6.2: Intrathecal Drug Delivery Systems

Figure 6.2.2 Flourscopic and surgical setup for pain procedures in operating room.

Figure 6.2.3 Needle placement for intrathecal catheter placement in lumbar spine. 277 Interventional Pain Medicine

Figure 6.2.4 Needle placement for intrathecal catheter placement in lumbar spine.

Figure 6.2.5 Intrathecal catheter placement via lumbar spinal needle.

6. The catheter should be placed through the needle under ﬂ uoroscopic guidance. Catheter tip is usually at the site of the pain generator (Figure 6.2.5 ). Recent discussions considering intrathecal tip granuloma, however, has shown reduced incidence by placing catheter tip at the L1 level. 7. Make an incision around the needle down to the level of the spinal ligament and fascia (Figure 6.2.6 ). 8. Purse string suture is placed around the Tuohy needle. Needle is then removed ensuring catheter tip has not migrated or changed. Purse string suture is tightened around the catheter. 278 6.2: Intrathecal Drug Delivery Systems

Figure 6.2.6 Intrathecal catheter placement via lumbar spinal needle with exposure of fascia.

J-wire is removed out of the catheter and at this point there should be spontaneous free ﬂ ow of CSF through the catheter (Figure 6.2.7 ) 9. Anchor the catheter to the fascia (Figures 6.2.8 and 6.2.9 ). Make sure an adequate loop of catheter is left in the back incision (Figure 6.2.10 ). 10. Location of the pocket has already been preselected, discussed with the patient, and marked on the skin. Pocket is made by making a transverse incision deepened about 1½ inches from the skin; the skin is then undermined to create a pocket or a pouch (Figure 6.2.11 ). Tunnel from the front to the back; the catheter is then passed through the tunnel. The pump is then prepared as per manufacturer guidelines and reﬁ lled with the medicine to be infused (Figure 6.2.12 ).

Figure 6.2.7 Closeup of intrathecal catheter placement via lumbar spinal needel with exposure of fascia. 279 Interventional Pain Medicine

Figure 6.2.8 Intrathecal catheter placement after removal of lumbar spinal needle and sutures.

Figure 6.2.9 Intrathecal catheter secured with wings and sutures.

11. Attach the catheter to the side port of the pump. 12. Place the pump in the pocket; secure the pump in place with a four-point attachment to avoid migration and ﬂ ipping. The use of a Dacron pouch is controversial, as it might be a factor increasing the risk of infection (Figures 6.2.13 and 6.2.14 ). 13. Thorough irrigation, and hemostasis. It is recommended after placing the pump in the pocket to aspirate through the side port. Readily aspirating CSF would ensure adequate connectivity between all components and lack of any signiﬁ cant obstructions (Figure 6.2.15 ). 14. Close both incisions with a running absorbable suture for fascis. Skin may be approximated with staples or a subcuticular suture. 280 6.2: Intrathecal Drug Delivery Systems

Figure 6.2.10 Lumbar incision with intrathecal catheter.

Figure 6.2.11 Lumbar incision site for intrathecal pump device.

15. Apply sterile, dry clean dressing. Abdominal binder is placed and the patient is transported to the recovery room. Postoperative Care 1. Postoperatively, patient and caregiver should be educated on wound healing, dressing changes if indicated as instructed by the physician, and possible warning signs for local infection or distant infection to report to the physician immediately. Operation might be on an outpatient basis or might be followed by twenty-three-hour overnight observation. Generally, we observe patients for twenty-three hours and discharge the next day. The patient is then seen in the ofﬁ ce ten to 281 Interventional Pain Medicine

Figure 6.2.12 Anterior site for intrathecal pump device.

Figure 6.2.13 Anterior site for intrathecal pump device and sutures placement.

twelve days postoperatively. Pump is programmed to start infusion in the recovery room. The dose is determined by the preoperative opioid level as well as the doses used during the trial. Clinical Pearls of Intrathecal Placement 1. When you trim the catheter, make sure you measure the trimmed portion as proper documentation of the exact catheter length. This is crucial for programming of the pump. 2. Ensure adequate smooth redundancy catheter curves in the back incision and in the pocket behind the pump and of loops, to avoid kinks and obstruction of catheter and possible impedance of future drug delivery. 282 6.2: Intrathecal Drug Delivery Systems

Figure 6.2.14 Intrathecal pump device with suture placement.

Figure 6.2.15 Anterior site for intrathecal pump device with pocket exposure technique.

3. The use of cautery should be done with caution, as excessive cauterization can result in necrotic tissue and predispose to infection. 4. All anchoring stitches are non-absorbable. 5. Avoid using any toothed instrumented in handling catheter as that might puncture the catheter and the tubing. 6. Avoid placing incisions over hardware, meaning ensure that the pump is caudal to the incision in the front as that might interfere with healing. 283 Postoperative Complications 1. Infection. In implants, infections are defi ned as any infection at the operation site or remotely happening within thirty days after procedure. Warning signs are fever of 38.5 degrees Celsius or higher, chills, or any meningeal signs. Treatment of infection will depend on the time of presentation as well as the severity of the presentation. Any suspected infection should be managed with clinical surveillance as well as biochemical surveillance. Clinical surveillance includes serially examining the patient’s incision, monitoring vital signs most importantly temperature, local inspection with erythema, tenderness, or discharge. Chemical surveillance includes CBC with differential, C-reactive protein, and erythrocyte sedimentation rate. Of note, C-reactive protein and erythrocyte sedimentation rate are very sensitive but not specifi c tests. However, repeat serial assessment will provide good insight in the progression of an infection and/or the response to treatment. Early onset cellulitis might be treated with antibiotics provided there is receding erythema, there is improving fever, white cell count normalizing. If any of the aforementioned signs are not present, then it is probably a more serious infection and serious observation and possible Interventional Pain Medicine explanation is warranted.( 21 , 22 , 23 ) 2. Bleeding. Bleeding can happen in the immediate postop phase due to inappropriate hemostasis or delayed hematoma collection and bleeding due to trauma. Hematoma/bleeding in the absence of any sign of infection may be managed conservatively. If there is any sign of infection, however, follow the protocol for infection management. 3. The accumulation of bleeding and/or hematoma in the epidural space is a serious complication. It is not clinically easily observed and requires a high index of suspicion with worsening back pain progressing to sensory changes and motor changes, and eventually cauda equine syndrome. An epidural hematoma gives a very small window for intervention and that might require imaging and neurosurgical decompression to avoid further serious sequelae. 4. Loss of CSF can be minor and asymptomatic, however a symptomatic CSF leak will manifest as a Post Dural Puncture Headache (PDPH). Clinically, this severe headache improves with lying down fl at and is worsened by sitting up. Management can be conservative with analgesia and hydration. If not successful, an epidural blood patch should be considered. Placing a purse string suture after catheter insertion will minimize CSF leak.( 24 , 25 ) 5. Seroma is the accumulation of serous fl uid in one or both incisions, usually in the pocket where the pump is placed. Binder application usually resolves the condition; if infection is occurs, it should be managed according to the infection protocol. Pharmacologic Complications 1. Side effects reported with opioids: Constipation, nausea, lethargy, pruritis, diaphoresis mental status change, urinary hesitancy, and peripheral edema 2. Side effects reported with local anesthetics: Sensory changes (numbness and tingling), muscle weakness ( 26 , 27 ) 3. Drug overdose presents with respiratory depression and seizures. Refi lling of pumps is done under the supervision and direction of the prescribing physician. Initiate therapy at a small dose, and increase dose in small increments. Closely observe patients following therapy initiation and dose increases. Local experience is two persons double-checking the prescription provided and two persons double-checking the programming of the pump to ensure adequate delivery of the exact prescribed medication. It is also essential to have local resources providing 24/7 coverage in case adverse events, side effects, misprogramming, or a wrong prescription is inserted. Caregivers and patients should be thoroughly educated in early warning signs. In the case of any of the aforementioned adverse events, they are encouraged and required to promptly report to the physician in charge. 284 System-Related Complications Catheter-related complications Obstruction, occlusion, or kinking Migration or dislodgment Tear, break, or puncture 1. Pump-related complications Pump failure Flipping, torsion, and occlusion Summary Drug delivery systems are important tools in the management of chronic severe intractable pain. Selecting patients with the right indications, providing them with adequate education and counseling about all aspects of the process is a key component to ensure successful outcome. Often physicians are weaning

6.2: Intrathecal Drug Delivery Systems patients of oral opioids prior to implant for potential improved outcomes in terms of pain relief and functional improvement. Efficay and cost-effectiveness are supported by evidence base medicine. The most common complication is catheter malfunction. Future advances of intrathecal therapy will include new catheter and pump technology to reduce catheter failure and produce smaller pumps, and new drugs will expand indications for the therapy. References 1. Wang JK , Nauss LA , Thomas JE . Wang JK, Nauss LA, Thomas JE . Pain relief by intrathecally applied morphine in man. Anesthesiology 1979;50:149–151 . 2. Coombs DW , Saunders RL , Gaylor MS , Block AR, et al . Releif of continuous chronic pain by intraspinal; narcotics infusion via an implanted reservior . JAMA . 1983 ; 250 : 2336 – 2339 . 3. Pert CB , Snyder S . Opiate receptor: Demonstration in nervous tissue . Science . 1973 ; 179 : 1011 – 1014 . 4. Terenius L . Characteristics of the “receptor” for narcotic analgesics in synaptic plasma membrane fractions from rat brain . Acta Pharmacol Toxicol . 1973 ; 33 : 377 – 384 . 5. Brescia FJ . An overview of pain and symptom management in advanced cancer . Pain Symptom Management . 1987 ; 2 : S7 – S11 . 6. Foley KM . Treatment of cancer pain . N Engl J Med . 1985 ; 313 : 84 – 95 . 7. Krames ES , Lanning RM . Intrathecal infusional analgesia for nonmalignant pain : Analgesic effi cacy of intrathecal opioid with our without bupivacaine . J Pain Symptom Manage . 1993 ; 8 : 539 – 548 . 8. Kline R , Wiley R . Postsynaptic spinal mu opioid receptor-expressing neurons are required for morphine anti-hyperalgesia . J Pain . 2007 ; 8 : S1 . 9. Nallu R , Radhakrishnan R . Spinal release of acetylcholine in response to morphine . J Pain . 2007 ; 8 : S19 . 10. Gu Y , Xu Y , Li GW , Huang LY . Remote nerve injection of mu opioid receptor adeno-associated viral vector increases antinociception of intrathecal morphine . J Pain . 2005 ; 6 : 447 – 454 . 11. Zhang Y , Conklin DR , Li X , Eisenach JC . Intrathecal morphine reduces allodynia after peripheral nerve injury in rats via activation of a spinal A1 adenosine receptor . Anesthesiology . 2005 ; 102 : 416 – 420 . 12. Eisenback JC , Zhang Y , Dufl o F . Alph2-adrenoreceptors inhibit the intracellular Ca2+ response to electrical stimulation in normal and injured sensory neurons, with increased inhibition of calcitonin gene related peptide expressing neurons after injury . Neuroscience . 2005 ; 131 : 189 – 197. 13. Milijanich GP . Ziconatide : neuronal calcium channel blocker for treating severe chronic pain . Curr Med Chem . 2004 ; 11 : 3029 – 3040 . 14. Boswell MV , Shah RV , Everett CR , Sehgal N , McKenzie-Brown AM, et al . Interventional techniques in the management of chronic spinal pain: evidence-based practice guidelines . Pain Physician . 2005 ; 8 : 1 – 47 15. Boswell MV , Trescot AM , Datta S , Schultz DM , Hansen HC , Abdi S et al . Interventional techniques: evidence-based practiceguidelines for the management of chronic spinal pain . Pain Physician . 2007 ; 10 : 7 – 111. 16. Muller-Schwefe G , Hassenbusch SJ , Reig E . Cost-effectiveness of intrathecal therapy for pain . Neuromodulation . 1999 ; 2 : 77 – 84. 285 17. de Lissovoy G , Brown RF , Halpern M , Hassenbusch SJ , Ross E . Cost-effectiveness of long-term intrathecal morphine therapy for pain associated with failed back surgery syndrome . Clin Ther . 1997 ; 19 : 96 – 112. 18. Brown J , Klapow J , Doleys D , Lowery D , Tutak U . Disease specifi c and generic health outcomes: a model for the evaluation of long term intrathecal opioid therapy in non-cancer low back pain patients , Clin J Pain . 1999 ; 15 : 122 – 131. 19. Hassenbusch SJ , Portenoy RK , Cousins M , et al . Polyanalgesic consensus conference 2003: an update on the management of pain by intraspinal drug delivery: report of an expert panel. J Pain Sympt Management. 2003; 27 ;6 : 540 – 563. 20. Deer T , Chapple I , Calssen A , et al . Intrathecal drug delivery for treatment of chronic low back pain: report from the national outcome registry for low back pain . Pain Med . 2004 ; 5 : 6 – 13 . 21. Turner JA , Sears JM , Loeser JD . Programmable intrathecal opioid delivery systems for chronic non-cancer pain: a systematic review of effectiveness and complications . Clin J Pain . 2007 ; 23 : 180 – 195 . 22. Follett KA , Boortz-Marx RL , Drake JM , et al . Prevention and management of intrathecal drug delivery and spinal cord stimulation system infections . Anesthesiology . 2004 ; 100 : 1582 – 1594 . 23. Naumann C , Erdine S , Koulousakis A , et al . Drug adverse events and system complications of intrathecal

opioid delivery for pain: origins, detection, manifestations, and management . Neuromodulation. 1999 ; 2 : 92 – 107 . Interventional Pain Medicine 24. Naumann C , Erdine S , Koulousakis A , et al . Drug adverse events and system complications of intrathecal opioid delivery for pain: Origins, detection, manifestations, and management . Neuromodulation. 1999 ; 2 : 92 – 107 . 25. SynchroMed® II Programmable Infusion System Clinical Reference Guide, Surgical Procedures . Minneapolis, MN : Medtronic, Inc .; 2007 . 26. Infumorph (preservative-free morphine sulfate sterile solution) package insert . Baxter Healthcare Corp ., Deerﬁ eld, Ill .; 2003 . 27. Anderson VC , Burchiel KJ . A prospective study of long-term intrathecal morphine in the management of chronic nonmalignant pain . Neurosurgery . 1999 ; 44 : 289 – 300 . This page intentionally left blank 287 Index

abdominal malignancies 238 for SCS 252–56, 253 f , 254 f , 255 f AB fiber neurons, corticosteroids and 94 for SHP block 227 , 228 f ablation. See radiofrequency ablation of SI joints 186 , 194 , 194 f , 195 f abscess. See epidural abscess spinal 3 acetaminophen 11 CT of 16 f Aδ fibers, RFA and 122 epidural space 5 , 58–60 , 58 f , 59 f , 93 adhesiolysis. See caudal adhesiolysis ligaments and joints 6–7 adhesives, tissue 47 meninges 5 adjuvants. See analgesic adjuvants musculature 7 AF. See annulus fibrosis nerves 5–6 alcohol. See ethanol plain film of 17f allergic reaction, to contrast 33 spinal cord 4 alpha adrenergic agonists 12 vertebral column 6 American Society of Regional Anesthesia vertebral joints 7 (ASRA), anticoagulation and ESI for stellate ganglion block 208–9, 208 f recommendations of 99 , 100 t vascular 69–71 amitriptyline 11 of VE 131–32 analgesic adjuvants 11–12 of vertebrae 150 , 150 f , 151 f analgesic discography 137 of vertebral arch 150 , 150 f , 151 f analgesic ladder 10 , 10 f of vertebral body 150 , 150 f , 151 f anatomy Ancef. See cefazolin of AF 131 , 142 anesthetics. See local anesthetics for biacuplasty 142 annular pathology, discography for 130 for CEI 171–72, 171 f annulus fibrosis (AF) for cervical inter-laminar ESIs 58–60 , 58 f , 59 f anatomy of 131 , 142 for cervical median branch blocks and in biacuplasty 140 RFA 84–86 , 85 f , 86 f lumbar RFA of 123 for cervical transforaminal ESIs 67–68 antecrural SNB 244 for CPB and SNB 236–38, 236 f , 237 f anterior approach of disc 131–32, 142 , 150 , 150 f , 151 f for CPB and SNB 244–45 for discography 131–32 for SHP block 231 of facet joints 116 , 116 f anterior paratracheal approach, for stellate for kyphoplasty 150 , 150 f , 151 f ganglion block 210–11, 213 f for LSB 220 anterior spinal artery syndrome 70 for lumbar interlaminar epidural anterolateral approach, for stellate ganglion injections 93–94 block 211 for lumbar RFA 124 , 124 f antibiotic prophylaxis 33 for MBBs 116 , 116 f for aseptic technique 41–42 of NP 131–32, 142 for IDDS implantation 276 for percutaneous discectomy 160 for SHP block 230 288 anti-coagulants 32 , 58 biacuplasty 139–48 ASRA recommendations on 99 , 100 t clinical pearls for 147 , 147 t –148 t biacuplasty and 146 complications of 146 MBB and 115 contraindications for 141–42 antidepressants 11 discharge instructions for 147 , 147 t –148 t antiepilepsy agents 11 equipment and preparation for 142–44 APLD. See automated percutaneous lumbar functional anatomy for 142 discectomy general equipment for 142–43 AP technique, for transforaminal epidural indications for 141 , 141 t injections 107 medications for 144 arachnoiditis 21 , 22 f other technique differences with 140 , 140 f artery of Adamkiewicz, transforaminal epidural special equipment for 143–44, 143 f injections and 109 techniques for 144–46, 144 f , 145 f , 146 f aseptic technique bipolar needles and sutures 44–47 , 44 f , 45 f

Index antibiotic prophylaxis 41–42 bipolar radiofrequency, for sacroiliac preoperative hair removal 41 neurotomy 198–99, 199 f sterile field principles 42 , 42 t bisphosphonates 12 surgical handwashing 40–41 bleeding surgical prep solution 41 with discography 131 surgical site prep 41 after IDDS implantation 283 aspirin 10 , 32 bleeding diathesis, lumbar transforaminal ASRA. See American Society of Regional epidural injections and 107 Anesthesia blocks automated percutaneous lumbar discectomy cervical median branch 75 (APLD), 161 anatomy for 84–86, 85 f , 86 f axial low back pain complications of 86 facet joints and 114–15, 122 contraindications for 78 , 83 SI joints in 194 diagnostic procedure for 78–80 , 79 f , 80 f transforaminal epidural injections for 107 medications for 77 monitoring for 77 back pain. See axial low back pain; low back pain; needles for 78 radiculopathic lower back pain patient selection for 76 , 77 f baclofen 12 , 272–73 post-procedural evaluation for 80 balloon kyphoplasty 149 RF technique for 80–84 , 82 f anatomy and physiology for 150 , sedation for 77–78 150 f , 151 f CPB and SNB 235 complications of 154–55, 155 f anatomy for 236–38, 236 f , 237 f contraindications for 152 antecrural 244 efficacy of 154 anterior approach to 244–45 FREE trial and 154 clinical pearls for 246–47 indications for 152 complications of 245–46 procedure for 152 , 153 f , 154 f indications for 238–39 VAS and 154 local anesthetics and neurolytic agents for VCF 152 for 246 vertebroplasty compared with 150 preparation for 239 benzodiazepine 60 retrocrural 243–44 betamethasone (Celestone) 33 RF lesioning after 245 betamethasone acetate 70–71 technique for 239–43, 239 f , 240 f , betamethasone phosphate 70–71 241 f , 242 f 289 blocks (cont.) calcitonin 12 LSB 219 cancer. See malignancy anatomy for 220 cannabinoids 12 complications of 223–24 capsaicin 12 indications for 220 , 221 t carbamazepine 11 , 12 medications for 221 , 224 cauda equina 252 technical considerations for 220–22, 221 f , caudal adhesiolysis 179–82 222f , 223 f adverse effects and complications of 182 testing of efficacy of 223 contraindications for 182 MBB 113–14 hyaluronidase and hypertonic compared with clinical pearls for 118f , 119 normal saline 181 complications of 119 indications for 182 contraindications for 115 procedure for 180–81, 181 f equipment and preparation for 116 caudal epidural injection (CEI) 169–76,

functional anatomy for 116 , 116 f 175f , 176 f Index indications for 115 anatomy for 171–72, 171 f medications for 117 complications of 174–75 techniques for 117–18, 117 f , indications for 170–71, 170 t 118f , 119 f disc herniation and radiculitis 170 , 170 t SHP 225 discogenic pain 170t , 171 agents for 228 post-lumbar surgery syndrome anatomy for 227 , 228 f 170t , 171 clinical pearls for 231 spinal stenosis 170–71, 170 t complications of 231 summary of 175 , 175 f , 176 f contraindications for 227 technique for 172–74, 172 f , 173 f efficacy of 231–32 cefazolin (Ancef ) 33 , 42 equipment and preparation for 227 ceftriaxone 230 indications for 226–27 CEI. See caudal epidural injection summary of 231–32 celecoxib 11 techniques for 229–31, 229 f , 230 f Celestone. See betamethasone stellate ganglion 207 celiac plexus block (CPB), 235 anatomy for 208–9 , 208 f anatomy for 236–38, 236 f , 237 f complications of 214–15, 214 t antecrural SNB and 244 contraindications for 210 anterior approach to 244–45 evidence of success in 213–14 clinical pearls for 246–47 indications for 209 , 210 t complications of 245–46 techniques for 210–13, 213 f , 215 f indications for 238–39 bone cement, fractures and 152 local anesthetics and neurolytic agents Bovie needles and sutures 44–47 , 44 f , 45 f for 246 brain infarct, after cervical transforaminal preparation for 239 ESI 69 retrocrural SNB and 243–44 bulging disc 18 f , 19 , 57 f , 135 RF lesioning after 245 bupivacaine 60 technique for 239–43, 239 f , 240 f , 241 f , 242 f for cervical median branch blocks 77 cephalexin (Keflex), 33 for CPB and SNB 246 cephalosporin 42 intrathecal delivery of 272 cephazolin 230 for LSB 221 cerebellar ischemia, after cervical transforaminal for SHP block 228 ESI 70 buprenorphine 12–13, 13 t cervical facet pathology 76 , 77 f 290 cervical inter-laminar ESIs 55 , 68–69 codeine 13 t anatomy for 58–60 , 58 f , 59 f complex regional pain syndrome (CRPS) clinical pearl for 64 SCS for 266–67 complications of 62 stellate ganglion block for 208–9 contraindications for 58 computed tomography (CT), 16 , 16 f equipment and preparation for 60 of degenerative spine disease indications for 56 , 57 f disc pathology 17–23 , 18 f , 19 f , 20 f , medications for 60 21 f , 22 f summary of 62–63, 63 f spinal stenosis 23–25 , 23 f , 24 f , technique for 60–61 , 61 f , 62 f 25 f , 26 f cervical median branch blocks and RFA 75 for retrocrural SNB 244 anatomy for 84–86 , 85 f , 86 f of vertebral body lesions 26 complications of 86 insufficiency fractures 27 , 27 f contraindications for 78 , 83 malignancy 27–28 , 28 f

Index diagnostic procedure for 78–80 , 79 f , 80 f continuous RFA, pulse compared with 122 medications for 77 contrast allergy 33 monitoring for 77 conus medullaris 4 , 252 needles for 78 cooled RFA, for sacroiliac neurotomy 197–98, patient selection for 76 , 77 f 197 f , 198 f post-procedural evaluation for 80 corticosteroids 33 RF technique for 80–84 , 82 f for cervical inter-laminar ESIs 60 sedation for 77–78 for cervical transforaminal ESIs 70–71 cervical radiculitis, inter-laminar ESI for 56 phospholipase A-2 and 94 cervical radiculopathy 66–67 Coumadin. See warfarin causes and epidemiology of 66–67 COX-2 inhibitors 11 diagnosis of 66 CPB. See celiac plexus block treatment of 67 CRPS. See complex regional pain syndrome cervical sympathetic chain 208–9 , 208 f cryoanalgesia, for sacroiliac neurotomy 200 cervical transforaminal ESIs 56 , 65 CT. See computed tomography anatomy and technique for 67–68 complications of 69–71 Dallas discogram 135 diagnosis for 66 Decadron. See dexamethasone indications for 66–67 degenerative spine disease 17–26. See also disc risk reduction for 71–72 degeneration therapeutic benefit of 68–69 disc pathology 17–23 , 18 f , 19 f , 20 f , 21 f , 22 f cervicothoracic sympathetic block. See stellate spinal stenosis 23–25, 23 f , 24 f , 25 f , 26 f ganglion block desipramine 11 C fiber neurons dexamethasone (Decadron), 33 corticosteroids and 94 dexamethasone sodium phosphate 70–71 RFA and 122 dextromethorphan 12 chemonucleolysis (CNL), 159 diabetes, ESIs in patients with 32–33 chlorhexidine gluconate (CHG), 40–41 diarrhea, after CPB and SNB 246 chronic pain, IDDS use in 272–73 diazepam 33 ciprofloxacin 33 digital subtraction, for cervical transforaminal circuit, for SCS 256–58, 256 f , 256 t , 257 f , 258 t ESIs 71 clonidine 12 , 272 diphenhydramine 33 clopidogrel (Plavix), 32 disc CNL. See chemonucleolysis anatomy of 131–32, 142 , 150 , 150 f , 151 f Coblation. See plasma disc decompression bulging 18 f , 19 , 57 f , 135 291 disc (cont.) disc pathology, imaging of 17–23 , 18 f , 19 f , 20 f , LBP and 158 21 f , 22 f low back pain and 122 arachnoiditis 21 , 22 f primary functions of 131 bulging disc 18 f , 19 disc decompression extruding disc herniation 19 , 19 f , 20 f mechanical 163 herniated disc 19 , 19 f , 20 f , 21 , 22 f PDD 162–63 normal disc 18 f percutaneous 159 protruding disc herniation 19 , 19 f PLDD 161–62 disc protrusion 135 disc degeneration disc puncture, for discography 133 , 133 f , bulging disc and 135 134f , 135 f discogenic pain and 132 D-methadone 12 discography and 135 dorsal root ganglion, RFA of 126, 127 f acceleration of 131 , 136 doxepin 11

facet joints 114 dronabinol 12 Index lower back pain and 140 dural puncture, with lumbar interlaminar water-binding properties and 131–32 epidural injections 99 discectomy. See percutaneous discectomy dural sac, transforaminal epidural injections disc herniation. See herniated disc and 109 discitis 33 imaging of 21f elderly, opioids in 13 after SHP block 230–31 electrocautery needles and sutures 44–47 , discogenic pain 44 f , 45 f CEI for 170t , 171 electrodes, for SCS 258–63, 259 t , 262 t disc degeneration and 132 epidural abscess discography 129–37 with interlaminar epidural injections 99 analgesic 137 with transforaminal epidural for biacuplasty 141–42 injections 109 complications of 130–31 epidural hematoma accelerated disc degeneration 131 , 136 with lumbar interlaminar epidural bleeding 131 injections 99 infection 130–31 with transforaminal epidural nerve damage 131 injections 109 nucleus pulposus pulmonary embolism 131 epidural injection. See caudal epidural pain aggravation 131 injection contraindications for 130 epidural space, anatomy of 5 , 58–60 , 58 f , controversies over 136–37 59 f , 93 equipment and preparation for 132–35 epidural steroid injections (ESIs). See also disc puncture 133 , 133 f , 134 f , 135 f lumbar ESIs interpretation 135 , 136 t cervical inter-laminar 55 , 68–69 patient position 132–33 anatomy for 58–60 , 58 f , 59 f provocation 133–35, 136 t clinical pearl for 64 false-negative 137 complications of 62 false-positive 137 contraindications for 58 functional anatomy for 131–32 equipment and preparation for 60 indications for 130 indications for 56 , 57 f North American Spine Society Position medications for 60 Statement on 130 summary of 62–63 , 63 f predictive value of 137 technique for 60–61, 61 f , 62 f 292 epidural steroid injections (cont.) pain referral patterns 114 , 114 f , 115 f cervical transforaminal 56 , 65 RFA of 124 f , 125 , 126 f anatomy and technique for 67–68 failed back surgery complications of 69–71 discography for 130 diagnosis for 66 ESIs for 93 indications for 66–67 failed back surgery syndrome, SCS for 265–66 risk reduction for 71–72 failed block, after CPB and SNB 246 therapeutic benefit of 68–69 fentanyl 12 , 13 t , 33 in diabetic patients 32–33 intrathecal delivery of 272 formulations for 94 , 95 t for SHP block 227 indications for 93 t fluoroscopy medications for 94 , 95 t for CEI 172–73, 172 f , 173 f epidurography, for lumbar interlaminar epidural of cervical inter-laminar ESIs 56 , 61 , 61 f , 62 f , injections 96 63 , 63 f

Index equipment for cervical median branch blocks and for biacuplasty 142–44, 143 f RFA 78 , 79 f for cervical inter-laminar ESIs 60 for interlaminar epidural injections 96 for cervical median branch blocks and for LSB 221, 222 f , 223 f RFA 78 for retrocrural SNB 243 for discography 132–35, 133 f , 134 f , for stellate ganglion block 212 , 215 f 135 f , 136 t for transforaminal epidural injections 107 for lumbar interlaminar epidural Fracture Reduction Evaluation (FREE) trial 154 injections 94 , 94 f fractures. See also vertebral compression for lumbar RFA 123 f , 124–25 fractures for lumbar transforaminal epidural bone cement and 152 injections 107–8 imaging of 27 , 27 f for MBBs 116 FREE trial. See Fracture Reduction Evaluation needle drivers 44 trial needles and sutures 44–47 , 44 f , 45 f , 78 fusion surgery, discography for 130 preparation of 34–36 , 35 f , 36 f for sacroiliac neurotomy 200 GABA agonists 12 for SCS 258–59, 259 t gabapentin 11 for SI joint injections 187 gadolinium contrast 33 , 94 ESIs. See epidural steroid injections gadopentetate dimeglumine 228 ethanol gate control theory 258 for CPB and SNB 246 gloves. See sterile gloves for lumbar sympathetic neurolysis 222 gown. See surgical gown for SHP neurolysis 228 Gray rami communicantes 132 Ethicon sutures. See Vicryl sutures extruding disc herniation 19 , 19 f , 20 f hair removal, preoperative 41 eye of Scottie dog 118 f , 119 handwashing, surgical 40–41 hanging drop technique 61 facet injection, intra-articular 118 hematoma. See also epidural hematoma facet joints after IDDS implantation 283 anatomy of 116 , 116 f after SCS 264 axial low back pain and 114–15, 122 with transforaminal epidural injections 109 cervical pathology of 76 , 77 f herniated disc 19 , 19 f , 20 f , 21 , 22 f , 57 f function of 114 CEI for 170 , 170 t LBP and 158 hydrocodone 12–13 , 13 t 293 hydromorphone 12–13 , 13 t , 272 intervertebral foramen 67–68 hypotension, after CPB and SNB 245 intervertebral unit 131 intra-articular ablation 198 , 199 f ibandronate 12 intra-articular facet injection 118 ibuprofen 10 intra-articular phenol, for sacroiliac IDDS. See intrathecal drug delivery system neurotomy 200 IL-6. See interleukin 6 intraoperative preparation, for IDDS imaging 15–29, 16f , 17f . See also specific implantation 276–80, 276 f , 277 f , 278 f , 279 f , modalities 280f , 281 f , 282 f of degenerative spine disease intrathecal drug delivery system (IDDS), 271 disc pathology 17–23 , 18 f , 19 f , 20 f , clinical pearls for placement of 281–82 21f , 22 f complications of 283–84 spinal stenosis 23–25 , 23 f , 24 f , 25 f , 26 f contraindications for 273 for interlaminar lumbar epidural steroid cost-effectiveness of 273–74

injections 93–94 efficacy of 273 Index of vertebral body lesions 26 implantation of 275–81, 275 f , 276 f , 277 f , 278 f , insufficiency fractures 27 , 27f 279f , 280 f , 281 f , 282 f malignancy 27–28 , 28 f indications for 272–73 implantation, of IDDS 275–81, 275 f , 276 f , 277 f , intrathecal trials for 274–75 278f , 279 f , 280 f , 281 f , 282 f medications used in 272 , 283 indomethacin 10 patient selection and education for 274 infarct, after cervical transforaminal ESI 69 physiology of 272 infection psychological screening for 274 with discography 130–31 summary of 284 after IDDS implantation 283 intrathecal injections, with transforaminal incidence of 40 epidural injections 109 after LSB 223 intrathecal trials, for IDDS use 274–75 of SI joints 187 intravascular injection with transforaminal epidural injections 109 during cervical transforaminal ESI 69–71 insufficiency fractures, imaging of 27 , 27 f after LSB 224 inter-laminar approach. See cervical iodinated contrast 33 inter-laminar ESIs iodine-based detergents 40–41 interlaminar epidural injections, iohexol (Omnipaque), 33 , 228 lumbar 91–100 iopamidol (Isovue), 33 clinical pearls of 100 ischemic limb pain, SCS for 259–60, 259 t complications of 99 , 100 t ISIS. See International Spine Injection Society contraindications for 92–93 Isovue. See iopamidol equipment and preparation for 94 , 94 f functional anatomy for 93–94 joints history of 92 facet indications for 92 , 93 t anatomy of 116 , 116 f medications for 94 , 95 f axial low back pain and 114–15 , 122 technique for 95–98 , 96 f , 97 f , 98 f cervical pathology of 76 , 77 f transforaminal compared with 106 function of 114 interleukin 6 (IL-6), corticosteroids and 94 LBP and 158 International Spine Injection Society (ISIS), pain referral patterns 114 , 114 f , 115 f guidelines for transforaminal epidural RFA of 124f , 125 , 126 f injections 110 spinal 6–7 intervertebral disc. See disc vertebral 7 294 Kambin Triangle 160 operative compared with non-operative Keflex. See cephalexin treatment for 158 Kenalog. See triamcinolone prevalence of 158 ketamine 12 SI joints and 122 , 158 , 194 ketoprofen 10 lower-limb radicular symptoms 106 Kimberly-Clark TransDiscal system LSB. See lumbar sympathetic block 143–44, 143 f lumbar discectomy, discography for 130 kyphoplasty 149 lumbar disc prolapse, LBP and 158 anatomy and physiology for 150 , 150 f , 151 f lumbar ESIs complications of 154–55, 155 f interlaminar contraindications for 152 clinical pearls of 100 efficacy of 154 complications of 99 , 100 t FREE trial and 154 contraindications for 92–93 indications for 152 equipment and preparation for 94 , 94 f

Index procedure for 152 , 153 f , 154 f functional anatomy for 93–94 VAS and 154 history of 92 for VCF 152 indications for 92 , 93 t vertebroplasty compared with 150 medications for 94 , 95 f kyphosis 151–52, 151 f technique for 95–98 , 96 f , 97 f , 98 f transforaminal compared with 106 lateral approach, for stellate ganglion block 211 transforaminal 105–11 lateral branch denervation, of SI joints 190 complications with 108–10 LBP. See low back pain contraindications for 107 leads. See electrodes efficacy of 106 levorphanol 13 t equipment and preparation for 107–8 lidocaine 11 indications for 107 for cervical median branch blocks 77 interlaminar compared with 106 for CPB and SNB 246 medications for 108 for SHP block 228 technique for 108 , 110 f , 111 f ligaments, spinal 6–7 lumbar medial branch block 117 , 117 f , 118 f , ligamentum flavum 6–7 , 58–60 , 58 f , 59 f , 93 , 119 f 252–53 lumbar radicular pain ligamentum nuche 6–7 cause of 106 liquid stitches. See tissue adhesives transforaminal epidural injections for 107 local anesthetics 11–12 lumbar RFA 121 for cervical inter-laminar epidural clinical pearls 127 injections 60 complications of 126 for cervical median branch blocks 77 contraindications for 124 for CPB and SNB 246 equipment and preparation for 123 f , for intrathecal drug delivery 283 124–25 for LSB 221 , 224 functional anatomy for 124 , 124 f with transforaminal epidural injections 109 indications for 123 loss of resistance technique (LOR) 56 , 60–61 , mechanism of action of 122 96 , 260 medications for 125 low back pain (LBP), 92. See also radiculopathic radiofrequency lesion generator system lower back pain for 122 causes of 122 , 140 technique for 125–26 historical perspective on 158 of dorsal root ganglion 126 , 127 f incidence of 122 of lumbar facet joints 124 f , 125 , 126 f 295 lumbar spinal injections 89–90 methadone 12–13, 13 t biacuplasty 139–48 methylprednisolone acetate 60 , 70–71 discography 129–37 mexiletine 11 interlaminar epidural 91–100 microdiscectomy 159 kyphoplasty 149–55 midazolam 227 lumbar RFA 121–27 Modified Dallas discogram scale 135 , 136 t medial branch blocks 113–19 Monocryl sutures 46 percutaneous discectomy 157–64 morphine 12–13 , 13 t transforaminal epidural 105–11 intrathecal delivery of 272–73 lumbar sympathetic block (LSB), 219 MR. See magnetic resonance anatomy for 220 musculature, spinal 7 complications of 223–24 indications for 220 , 221 t naproxen 10–11 medications for 221 , 224 neck pain 56, 76, 77f . See also cervical

technical considerations for 220–22, 221 f , radiculopathy Index 222f , 223 f needle drivers 44 testing of efficacy of 223 needles 44–47, 44f , 45 f for cervical median branch blocks 78 magnetic resonance (MR) 16 Tuohy epidural 94 , 94 f of degenerative spine disease nerve block. See blocks disc pathology 17–23 , 18 f , 19 f , 20 f , 21 f , 22 f nerve injury spinal stenosis 23–25 , 23 f , 24 f , 25 f , 26 f after CPB and SNB 245 of vertebral body lesions 26 with discography 131 insufficiency fractures 27 , 27 f after LSB 223 malignancy 27–28 , 28 f nerve root injury, with lumbar interlaminar malignancy epidural injections 99 abdominal 238 nerves, spinal 5–6 imaging of 27–28 , 28 f nerve stimulation. See spinal cord stimulation pancreatic 238 nervi sinuvertebrales 142 marking, of procedure site 43–44 neuro-immuno modulatory agents 12 MBB. See medial branch blocks neurolytic agents mechanical disc decompression 163 for CPB and SNB 246 medial branch blocks (MBB) 113–14 for lumbar sympathetic neurolysis 222 clinical pearls for 118f , 119 for sacroiliac neurotomy 200 complications of 119 for SHP neurolysis 228 contraindications for 115 neuropathic pain equipment and preparation for 116 LSB for 220 , 221 t functional anatomy for 116 , 116 f opioids in 13 indications for 115 SCS for 259–60, 259 t medications for 117 neurosurgical pain treatments 252 , 252 t techniques for 117–18 neurotomy. See sacroiliac neurotomy intra-articular facet injection 118 NMDA antagonists 12 lumbar medial branch block 117 , 117 f , non-selective NSAIDs (NNSAIDs), 10 118f , 119 f non-steroidal anti-inflammatory drugs RFA of medial branch nerve 117 (NSAIDs) , 10–11 , 146 median approach, to lumbar interlaminar North American Spine Society Position epidural injections 95–98 , 96 f , 97 f , 98 f Statement on Discography 130 meninges 5 nortriptyline 11 meperidine 12–13 , 13 t NP. See nucleus pulposus 296 NSAIDs. See non-steroidal anti-inflammatory preparation of 32 drugs selection of 32 nucleus pulposus (NP) for cervical median branch blocks and anatomy of 131–32, 142 RFA 76 , 77 f pulmonary embolism of, with for IDDS use 274 discography 131 for percutaneous discectomy 160 in radiculopathic lower back pain 92 for SCS 259–60, 259 t for SI joint injections 186–87 oblique technique, for transforaminal epidural PCML pathway. See posterior column medial injections 107 lemniscus pathway octreotide 12 PDD. See plasma disc decompression Ohm's law 256 , 256 t PDPH. See post dural puncture headache older adult. See elderly PED. See percutaneous endoscopic discectomy Omnipaque. See iohexol pelvic pain, SHP block for 226–27

Index opioids 12–13 , 13 t percutaneous disc decompression 159 in elderly 13 percutaneous discectomy 157–64 intrathecal delivery of 272 , 283 APLD 161 in neuropathic pain 13 clinical pearls for 164 for pancreatic cancer 238 complications with 163–64 pharmacology of 13 contraindications for 161 rotation of 13 functional anatomy for 160 osteomyelitis, imaging of 21 f indications for 160 osteophytes 23 , 23 f , 24 f mechanical disc decompression 163 oxycodone 12–13 , 13 t minimally invasive procedures 159–60 oxymorphone 12–13 , 13 t evolution of 159 percutaneous disc decompression 159 pain aggravation, with discography 131 percutaneous endoscopic Pain Management Generator 143 , 143 f discectomy 159–60 Pain Management Pump Unit 143–44, 143 f patient selection for 160 Pain Management Tube Kit 143 f , 144 PDD 162–63 pain provocation, for discography PLDD 161–62 133–35, 136 t post-procedural care for 163 pancreatic cancer, CPB and SNB for 238 percutaneous endoscopic discectomy pancreatitis, CPB and SNB for 238–39 (PED) 159–60 paramedian approach, to lumbar interlaminar percutaneous laser disc decompression epidural injections 95–98 , 96 f , 97 f , 98 f (PLDD) 161–62 paraplegia percutaneous manual nucleotomy 159 after CPB and SNB 245 periannular connective tissues 132 with transforaminal epidural peri-procedural medications 33 injections 109 permanent lesion techniques, for stellate paravertebral approach, for stellate ganglion ganglion block 213 block 211–12 pharmacotherapy 9. See also specific patient medications education of 32 , 274 for biacuplasty 144 positioning of 33–34 for cervical inter-laminar ESIs 60 for cervical median branch blocks and for cervical median branch blocks and RFA 78–80, 79 f , 80 f , 83–84 RFA 77 for discography 132–33 for CPB and SNB 246 297 for ESIs 94 , 95 t post-lumbar surgery syndrome, CEI for for intrathecal drug delivery 272 , 283 170t , 171 for LSB 221 , 224 postoperative care, for IDDS for lumbar interlaminar epidural implantation 280–81 injections 94 , 95 f postoperative scarring, imaging of 21 , 22 f for lumbar RFA 125 postsynaptic dorsal column (PSDC), for lumbar transforaminal epidural 253–54, 254 f injections 108 prednisone 33 for MBBs 117 pregabalin 11 peri-procedural 33 preoperative hair removal 41 pre-procedure 32–33 preoperative preparation, for IDDS for SHP block 228 implantation 275 , 275 f for SI joint injections 187–88 pre-procedure preparation 32–33 phenol pre-procedure verification process 43

for CPB and SNB 246 PRF. See pulsed radiofrequency Index for lumbar sympathetic neurolysis 222 prophylactic antibiotics 33 for sacroiliac neurotomy 200 for aseptic technique 41–42 for SHP neurolysis 228 for IDDS implantation 276 phenytoin 11 for SHP block 230 phospholipase A-2 (PLA2) propoxyphene 13 corticosteroids and 94 protruding disc herniation 19 , 19 f in radiculopathic lower back pain 92 PSDC. See postsynaptic dorsal column piroxicam 10 pseudoarthrosis, discography for 130 PLA2. See phospholipase A- 2 psychological screening, for IDDS use 274 plain films 16 , 17 f pulmonary embolism, of nucleus pulposus, with of degenerative spine disease discography 131 disc pathology 17–23 , 18 f , 19 f , 20 f , pulsed radiofrequency (PRF) 21f , 22 f continuous compared with 122 spinal stenosis 23–25 , 23 f , 24 f , 25 f , 26 f for sacroiliac neurotomy 200 for retrocrural SNB 243 of vertebral body lesions 26 Racz technique, for caudal adhesiolysis insufficiency fractures 27 , 27 f 180–81, 181 f malignancy 27–28 , 28 f radiation exposure 34–36 plasma disc decompression (PDD), 162–63 radicular artery, transforaminal epidural Plavix. See clopidogrel injections and 109 PLDD. See percutaneous laser disc radicular pain decompression cervical 66–67 pneumocephalus, with lumbar interlaminar lumbar 106–7 epidural injections 99 SCS for 259–60, 259 t pneumothorax, after CPB and SNB 246 signs and symptoms of 93t Polyglactin sutures. See Vicryl sutures radicular paresis, kyphoplasty and 154 post dural puncture headache (PDPH), after radiculitis IDDS implantation 283 CEI for 170 , 170 t posterior approach cervical, inter-laminar epidural injection for 56 for SHP block 229 , 229 f radiculopathic lower back pain 92 for stellate ganglion block 211–12 radiofrequency ablation (RFA) posterior column medial lemniscus (PCML) bipolar 198–99, 199 f pathway 254 , 255 f of celiac plexus and splanchnic nerve 245 298 radiofrequency ablation (RFA) (cont.) injections for cervical median branch 75 clinical pearls for 191–92, 191 f anatomy for 84–86 , 85 f , 86 f complications with 190–91 complications of 86 contraindications for 187 contraindications for 78 , 83 diagnostic 188 , 189 f diagnostic procedure for 78–80 , 79 f , 80 f equipment and preparation for 187 medications for 77 medications for 187–88 monitoring for 77 patient selection for 186–87 needles for 78 technique for 188–90 patient selection for 76 , 77 f lateral branch denervation of 190 post-procedural evaluation for 80 LBP and 122 , 158 , 194 RF technique for 80–84 , 82 f pain in 186 sedation for 77–78 RF strip lesioning of 188–90, 189 f combination ligamentous and neural 200 sacroiliac neurotomy 193–201

Index continuous compared with pulse 122 clinical pearls for 201 cooled 197–98, 197 f , 198 f complications of 200 of dorsal root ganglion 126 , 127 f equipment and preparation for 200 of facet joints 124f , 125 , 126 f indications for 194–96 intra-articular 198 , 199 f summary of 200–201 lesion generator system for 122 techniques for 196–200 lumbar 121 bipolar radiofrequency 198–99, 199 f clinical pearls for 127 combination ligamentous and neural complications of 126 RFA 200 contraindications for 124 conventional RFA 196–97, 197 f equipment and preparation for 123 f , cooled RFA 197–98, 197 f , 198 f 124–25 cryoanalgesia 200 functional anatomy for 124 , 124 f intra-articular ablation 198 , 199 f indications for 123 intra-articular phenol 200 medications for 125 pulsed radiofrequency 200 technique for 125–26 Scottie dog, eye of 118 f , 119 mechanism of action of 122 SCS. See spinal cord stimulation of medial branch nerve 115 , 117 sedation 32–33 pulsed 200 for cervical inter-laminar ESIs 60 , 64 for sacroiliac neurotomy 196–200, 197 f , for cervical median branch blocks and 198 f , 199 f RFA 77–78 radiofrequency strip lesioning, of SI for cervical transforaminal ESIs 71 joints 188–90, 189 f for SHP block 227 radiography. See plain films sequestered disc fragment 19 , 20 f ranitidine 33 seroma recurrentes meningei 142 after IDDS implantation 283 retrocrural SNB 243–44 after SCS 265 RFA. See radiofrequency ablation serotonin and norepinephrine reuptake rofecoxib 11 inhibitors 11 ropivacaine 77 severe chronic pain, IDDS use in 272–73 rotation, of opioids 13 SHP block. See superior hypogastric plexus block sacroiliac (SI) joints SI joints. See sacroiliac joints functional anatomy of 186 , 194 , 194 f , 195 f sinuvertebral nerves 132 infections of 187 SNB. See splanchnic nerve block 299 somatostatins 12 anterior approach to 244–45 spinal anatomy 3 clinical pearls for 246–47 CT of 16 f complications of 245–46 epidural space 5 , 58–60 , 58 f , 59 f , 93 indications for 238–39 ligaments and joints 6–7 local anesthetics and neurolytic agents meninges 5 for 246 musculature 7 preparation for 239 nerves 5–6 retrocrural 243–44 plain film of 17f RF lesioning after 245 spinal cord 4 technique for 239–43, 239 f , 240 f , 241 f , 242 f vertebral column 6 spondylolisthesis 24 , 25 f vertebral joints 7 spondylolysis 24 , 26 f spinal cord infarct, after cervical transforaminal SPORT. See Spine Patient Outcomes ESI 69 Research Trial spinal cord injury, with lumbar interlaminar SSIs. See surgical site infections Index epidural injections 99 Staphylococcus aureus , with lumbar interlaminar spinal cord stimulation (SCS) 251 , 252 t epidural injections 99 anatomy for 252–56, 253 f , 254 f , 255 f stellate ganglion block 207 circuit review for 256–58, 256 f , 256 t , anatomy for 208–9 , 208 f 257f , 258 t complications of 214–15, 214t complications of 263–65, 264 t contraindications for 210 efficacy of 265–67, 266 f evidence of success in 213–14 indications and patient selection for indications for 209 , 210 t 259–60, 259 t techniques for 210–13, 213 f , 215 f lead orientation for 262–63, 262 t stenosis. See spinal stenosis long-term management of 265 sterile field mechanism of action of 258 preparation of 34 , 34 f , 35 f permanent procedure for 261–62, 262 f principles of 42 , 42 t programming for 263 , 263 f , 263 t sterile gloves 42 , 47–50 technology for 258–59, 259 t steroids. See also corticosteroids trial procedure for 260–61 for cervical median branch blocks 77 spinal hematoma, with transforaminal epidural for ESIs 94 , 95 t injections 109 particulates in 70–71 spinal injections. See lumbar spinal injections stimulation. See spinal cord stimulation spinal pain, discography for 130 STT. See spinothalamic tract spinal stenosis sulindac 10 CEI for 170–71, 170 t superior hypogastric plexus (SHP) block 225 imaging of 23–25 , 23 f , 24 f , 25 f , 26 f agents for 228 osteophytes 23 , 23 f , 24 f anatomy for 227 , 228 f spondylolisthesis 24 , 25 f clinical pearls for 231 spondylolysis 24 , 26 f complications of 231 synovial cyst 25 , 26 f contraindications for 227 Spine Patient Outcomes Research Trial efficacy of 231–32 (SPORT), 158 equipment and preparation for 227 SpineWand. See plasma disc decompression indications for 226–27 spinothalamic tract (STT), 253–54 , 253 f summary of 231–32 splanchnic nerve block (SNB), 235 techniques for 229–31, 229 f , 230 f anatomy for 236–38, 236 f , 237 f surgical gown 50 antecrural 244 surgical handwashing 40–41 300 surgical prep solution 41 trigeminocervical complex 254 surgical site truncus sympathicus 142 marking of 43–44 Tuohy epidural needle 94 , 94 f preparation of 41 tissue adhesive use 47 ultrasound, for stellate ganglion block 212 surgical site infections (SSIs) 40 unipolar needles and sutures 44–47 , 44 f , 45 f surgical skills 39 universal protocol 42 aseptic technique 40–42 , 42 t pre-procedure verification 43 infection and 40 procedure site marking 43–44 instrument use 44 time-out 44 Bovie/electrocautery/unipolar and bipolar needles and sutures 44–47 , 44 f , 45 f valdecoxib 11 needle drivers 44 vancomycin 42 preparation skills 47–50 , 47 f , 48 f , 49 f , 50 f VAS. See visual analog scale

Index sterile glove use 47–50 vascular anatomy, cervical transforaminal ESI surgical gown use 50 complications and 69–71 time-out 44 vascular injury, after LSB 223 universal protocol 42–44 vascular insufficiency, LSB for 220 , 221 t sutures 44–47 , 44 f , 45 f VCF. See vertebral compression fractures removal of 47 VE. See vertebral endplate sizes of 46 verification, pre-procedure 43 techniques for 46 vertebrae 150 , 150 f , 151 f synovial cyst 25 , 26 f vertebral arch 150 , 150 f , 151 f vertebral body 26 , 150 , 150 f , 151 f third occipital nerve block 79 , 84–85 , 85 f insufficiency fractures of 27 , 27 f time-out 44 malignancy of 27–28 , 28 f tissue adhesives 47 vertebral column 6 tizanidine 12 vertebral compression fractures (VCF) tolmetin 10 prevalence of 150 tramadol 12–13 risk factors for 151–52, 151 f transdiscal approach, for SHP block 230 , 230 f treatment of 150 TransDiscal Introducer 143 , 143 f vertebral endplate (VE), 131–32 TransDiscal Probe 143 , 143 f vertebral joints 7 transforaminal approach. See cervical vertebroplasty, kyphoplasty compared transforaminal ESIs with 150 transforaminal epidural injections, Vicryl (Polyglactin, Ethicon) sutures 46 lumbar 105–11 visceral pain complications with 108–10 adjuvants for 12 contraindications for 107 CPB and SNB for 238–39 efficacy of 106 visual analog scale (VAS), balloon kyphoplasty equipment and preparation for 107–8 and 154 indications for 107 interlaminar compared with 106 warfarin (Coumadin), 32 medications for 108 World Health Organization (WHO), analgesic technique for 108 , 110 f , 111 f ladder of 10 , 10 f triamcinolone (Kenalog), 33 triamcinolone acetonide 70–71 ziconotide, intrathecal delivery of 272 triamcinolone hexacetonide 60 zoledronic acid 12 tricyclic antidepressants 11 zygapophysial joints. See facet joints