Pain Procedures in Clinical Practice: Expert Consult: Online and Print

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Pain Procedures in Clinical Practice: Expert Consult: Online and Print

PAIN PROCEDURES in CLINICAL PRACTICE 3RD EDITION Ted A. Lennard, MD Clinical Assistant Professor Department of Physical

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Ted A. Lennard, MD Clinical Assistant Professor Department of Physical Medicine and Rehabilitation University of Arkansas Little Rock, Arkansas Springfield Neurological and Spine Institute Cox Health Systems Springfield, Missouri

Stevan Walkowski, DO Ohio University College of Osteopathic Medicine Athens, Ohio

Aneesh K. Singla, MD, MPH Instructor Harvard Medical School Department of Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts

David G. Vivian, MM, BS, FAFMM Medical Director Metro Pain Clinics Metro Spinal Clinic Clinical Intelligence Victoria, Australia

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

ISBN: 978-1-4160-3779-8

PAIN PROCEDURES IN CLINICAL PRACTICE Copyright © 2011, 2000 by Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without ­permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data Pain procedures in clinical practice / Ted A. Lennard … [et al.]. -- 3rd ed. p. ; cm. Includes bibliographical references and index. ISBN 978-1-4160-3779-8 (hardcover : alk. paper) 1. Medicine, Physical. 2. Medical rehabilitation. I. Lennard, Ted A., 1961[DNLM: 1. Pain—therapy. 2. Pain—prevention & control. 3. Rehabilitation—methods. WL 704] RM700.P46 2011 616’.0472—dc22 2011004326

Acquisitions Editor: Daniel Pepper Senior Developmental Editor: Deidre Simpson Publishing Services Manager: Patricia Tannian Team Manager: Radhika Pallamparthy Senior Project Manager: Sharon Corell Project Manager: Joanna Dhanabalan Design Direction: Louis Forgione

Printed in China Last digit is the print number:  9  8  7  6  5  4  3  2  1 

To my wife, Suzanne, and our four daughters, Selby, Claire, Julia, and Maura. Ted A. Lennard

TRIBUTE We were saddened to hear of the death of Jay Govind, MBChB, DPH, MMed, FAFOM, on June 20, 2009. Dr. Govind was extensively involved in the content of the “Spine” section of this edition. He served in many capacities throughout his professional career, most recently as the senior specialist and director of the Pain Management Unit at Canberra Hospital. He was the past president of The Australian Faculty of Musculoskeletal Medicine. He also was a board member of the International Spinal Intervention Society and served as chairman of the Standards Committee. Dr. Govind lectured extensively and had a special interest in neck and back pain. He made a significant contribution to pain services, influenced attitudes toward pain, and brought new ideas to the management of chronic pain. He was a prolific writer, clinician, researcher, teacher, and a compassionate and kind man. We were also saddened to learn of the death of Peter Huijbregts, PT, MSc, MHSc, DPT, OCS, FAAOMPT, FCAMT, on November 6, 2010. Dr. ­Huijbregts enthusiastically accepted the task of authoring the chapter on “Manual Therapy.” His passion and expertise were in the field of orthopedic and manual physical therapy. He wrote many book chapters and research papers and co-authored many texts. Dr. Huijbregts practiced in Victoria, British-Columbia, Canada, but was originally trained in The Netherlands. He completed two separate research master’s degrees and a doctorate in physical therapy. He was well known for his generosity, sense of humor, and humility. Each of these men will be missed by all who knew them. Ted A. Lennard, MD



Shihab Ahmed, MD, MPH

Medical Director Massachusetts General Hospital Pain Clinic Lowell General Hospital Lowell, Massachusetts Emerson Hospital Concord, Massachusetts

Steven T. Akeson, PsyD

Neuropsychological Association of Southwest Missouri, PC Springfield, Missouri

Alvin K. Antony, MD FABPMR

Director Physical Medicine and Rehabilitation Carolina Sports and Spine, PA Rocky Mount, North Carolina

Charles N. Aprill, MD

Interventional Spine Specialists Kenner, Louisiana

Robert Baker, DO

Resident PGY-1 New York College of Osteopathic Medicine Department of Osteopathic Manipulative Medicine St. Barnabas Hospital Bronx, New York

Joel Jay Baumgartner, MD

CAQ Sports Medicine, Rejuv Medical Sartell, Minnesota

William Jeremy Beckworth, MD

James MackIntosh Borowczyk, BSc, MB, ChB, MMed (Pain), DMM, FRCP (Edin), FAFMM Musculoskeletal Medicine Senior Clinical Lecturer Academic Coordinator of Postgraduate Musculoskeletal and Pain Studies Department of Orthopaedics and Musculoskeletal Medicine University of Otago Christchurch School of Medicine and Health Sciences Senior Clinical Lecturer Department of Orthopaedics and Musculoskeletal Medicine Christchurch Hospital Christchurch, New Zealand

Kenneth Botwin, MD Fellowship Director Florida Spine Institute Clearwater, Florida

Gerry Catapang, PT, DPT, MGS

Physical Therapy Care Manual Physical Therapy and Industrial Rehabilitation Center, PC Springfield, Missouri

Lalaine Madlansacay Catapang, PT

Physical Therapy Care Manual Physical Therapy and Industrial Rehabilitation Center, PC Springfield, Missouri

Philip Ceraulo, DO

Florida Spine Institute Clearwater, Florida

Assistant Professor Department of Physical Medicine and Rehabilitation and Orthopedics Emory University Atlanta, Georgia

SriKrishna Chandran, MD

William M. Boggs, MD

President Republic Physical Therapy Republic, Missouri

Center for Clinical Trials Research University of Florida, College of Medicine Micanopy, Florida

Department of Physical Medicine and Rehabilitation Johns Hopkins Bayview Medical Center Baltimore, Maryland

Peter M. Chanliongco, PT

Martin K. Childers, DO, PhD

Professor Neurology Wake Forest Institute for Regenerative Medicine Winston-Salem, North Carolina ix

x  Contributors

Marissa H. Cohler, MD

Resident Physician Physical Medicine and Rehabilitation Rehabilitation Institute of Chicago, Northwestern University ­Feinberg School of Medicine Chicago, Illinois

William F. Craig

Physiatrist Physical Medicine and Rehabilitation Southlake Orthopaedics Birmingham, Alabama

Susan J. Dreyer, MD

Associate Professor Orthopaedic Surgery and Physical Medicine and Rehabilitation Emory University School of Medicine Emory University Hospital Atlanta, Georgia

Steve R. Geiringer, MD

Clinical Professor Physical Medicine and Rehabilitation Wayne State University Detroit, Michigan

Herman C. Gore, MD

Fellow Georgia Pain Physicians, PC Marietta, Georgia; Forest Park, Georgia; Calhoun, Georgia

Padma Gulur, MD

Instructor Anesthesia Harvard Medical School Director, Inpatient Pain Service Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts

Linda Lingzhi Hao, DOM, PhD

Vice President International Academy of Scalp Acupuncture Santa Fe, New Mexico

Danielle R. Hathcock, MS

Neuropsychological Association of Southwest Missouri, PC Springfield, Missouri

Jodi J. Hawes, MD, PT

Duke University Hospital Durham, North Carolina

Peter A. Huijbregts, PT, MSc, MHSc, DPT, OCS, FAAOMPT, FCAMT Shelbourne Physiotherapy Clinic Victoria, British Columbia, Canada

Rodney Jones, MD

Clinical Assistant Professor Anesthesiology University of Kansas School of Medicine-Wichita Active Staff Anesthesiology HCA-Wesley Via-Christi Hospitals Vice President Kansas Spine Institute, LLC Wichita, Kansas

Jatin Joshi, MD

Massachusetts General Hospital Boston, Massachusetts

Wade King, MB, BS, MMedSc, MMed (Med), DMM, FAFMM

Assistant Professor Neurology, Section of Physical Medicine and Rehabilitation Wake Forest University School of Medicine Winston-Salem, North Carolina

Research Fellow Department of Clinical Research University of Newcastle Visiting Medical Officer in Interventional Pain Medicine Royal Newcastle Centre Visiting Medical Officer in Pain Management Pendlebury Clinic Private Hospital Newcastle, New South Wales, Australia Associate Lecturer Department of Orthopaedics and Musculoskeletal Medicine University of Otago Christchurch, New Zealand

Dale A. Halfaker, PhD

Milton H. Landers, DO, PhD

Hongtao Michael Guo, MD, PhD

Neuropsychological Association of Southwest Missouri, PC Springfield, Missouri

Daniel E. Halpert, DO

Resident Physical Medicine and Rehabilitation Johns Hopkins University School of Medicine Baltimore, Maryland

Jason Jishun Hao, DOM, MTCM, MBA

President International Academy of Scalp Acupuncture Santa Fe, New Mexico

Associate Clinical Professor Department of Anesthesiology University of Kansas, School of Medicine-Wichita Medical Director Kansas Spine Institute Wichita, Kansas

Ted A. Lennard, MD

Clinical Assistant Professor Department of Physical Medicine and Rehabilitation University of Arkansas Little Rock, Arkansas Springfield Neurological and Spine Institute Cox Health Systems Springfield, Missouri

Contributors  xi

Michael S. Leong, MD

Clinical Assistant Professor Clinic Chief Anesthesia Stanford Pain Management Center Redwood City, California Stanford University Medical Center Stanford University Palo Alto, California

Karan Madan, MBBS, MPH

Instructor in Anesthesia Department of Anesthesia, Pain, and Perioperative Medicine Harvard University Associate Clinical Director Department of Anesthesia, Pain, and Peroperative Medicine Brigham and Women’s Hospital Boston, Massachusetts

Jeffrey J. Patterson, DO

Professor, Emeritis Department of Family Medicine University of Wisconsin School of Medicine and Public Health Madison, Wisconsin

Jeffrey D. Petersohn, MD

Adjunct Associate Professor Department of Anesthesiology Drexel University School of Medicine Philadelphia, Pennsylvania PainCare, PC Linwood, New Jersey

Kim Pollock, RN, MBA, CPC

Consultant Karen Zupko and Associates, Inc Chicago, Illinois

Aram Mardian, MD

Joel M. Press, MD

Curtis Mattson, MS

Elmer G. Pinzon, MD

Maricopa County Hospital Phoenix, Arizona Neuropsychological Association of Southwest Missouri, PC Springfield, Missouri

Timothy P. Maus, MD

Assistant Professor of Radiology Mayo Clinic Rochester, Minnesota

Bruce Mitchell, MM, BS, FACSP Metro Spinal Clinic Caulfield South Victoria, Australia

Alex Moroz, MD, FACP

Director of Medical Education and Residency Training Rehabilitation Medicine New York University School of Medicine Director of Integrative Musculoskeletal Medicine Program Director of Musculoskeletal Rehabilitation Unit Rusk Institute of Rehabilitation Medicine Adjunct Professor Tri-State College of Acupuncture New York, New York

Susan M. Donnelly Murphy, JD Massachusetts Bar Association Murphy and Riley, PC Boston, Massachusetts

Jordan L. Newmark, MD

Clinical Fellow in Anesthesia Department of Anesthesia Harvard Medical School Anesthesia Resident-Physician Department of Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts

Nicholas K. Olsen, DO

Clinical Instructor Physical Medicine and Rehabilitation University of Colorado at Denver and Health Sciences Center Thornton, Colorado

Center for Spine, Sports, and Occupational Rehabilitation Chicago, Illinois Fellow Georgia Pain Physicians, PC Marietta, Georgia; Forest Park, Georgia; Calhoun, Georgia

David Rabago, MD

University of Wisconsin School of Medicine and Public Health Department of Family Medicine Madison, Wisconsin

Albert C. Recio, MD, RPT, PTRP

Assistant Professor Department of Physical Medicine and Rehabilitation Johns Hopkins University, School of Medicine Medical Director of Aquatic Therapy The International Center for Spinal Cord Injury Kennedy Krieger Institute Baltimore, Maryland

Steven H. Richeimer, MD

Chief Division of Pain Medicine Associate Professor Department of Anesthesiology Keck School of Medicine, University of Southern California Los Angeles, California

Anna C. Schneider, BS

Coordinator for Faculty Research The International Center for Spinal Cord Injury Kennedy Krieger Institute Baltimore, Maryland

Robert A. Schulman, MD

Physical Medicine, Rehabilitation, Medical Acupuncture, and Electrodiagnostic Medicine New York, New York

Joel D. Sebag, DPT

Doctor of Physical Therapy, Physical Therapist, and CEO Mountaincrest Rehabilitation Services Harrison, Arkansas

xii  Contributors

Chunilal P. Shah, MD, MBBS, BS

Stevan Walkowski, DO

C. Norman Shealy, MD, PhD

Ajay D. Wasan, MD, MSc

Florida Spine Institute Clearwater, Florida

Professor Emeritus of Energy Medicine Holos University Graduate Seminary Bolivar, Missouri President Holos Institutes of Health, Inc Fair Grove, Missouri

Julie K. Silver, MD

Ohio University College of Osteopathic Medicine Athens Ohio Assistant Professor Anesthesiology and Psychiatry Harvard Medical School Brigham and Women’s Hospital Boston, Massachusetts

Robert E. Windsor, MD, FAAPMR, FAAEM, FASPM

Assistant Professor Department of Physical Medicine and Rehabilitation Harvard Medical School Boston, Massachusetts

Assistant Clinical Professor Emory University Department of Physical Medicine and Rehabilitation President, Georgia Pain Physicians, PC Marietta, Georgia; Forest Park, Georgia; Calhoun, Georgia

Aneesh K. Singla, MD, MPH

Ted L. Wunderlich, BA

Instructor Harvard Medical School Department of Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital Boston, Massachusetts

Fereshteh Sharonah Soumekh, MD

Clinical Instructor, Neurology Harvard Medical School Co-Director Pain Clinic Neurology Boston Veterans Administration Healthcare System Neurology Consultant Anesthesiology Brigham and Women’s Hospital Boston, Massachusetts

Peter Stefanovich, MD

Instructor Harvard Medical School Attending Anesthesiologist Anesthesia, Critical Care, and Pain Management Massachusetts General Hospital Boston, Massachusetts

David G. Vivian, MM, BS, FAFMM Medical Director Metro Pain Clinics Metro Spinal Clinic Clinical Intelligence Victoria, Australia

Brian J. Wainger, MD, PhD

Department of Anesthesia Critical Care and Pain Medicine Massachusetts General Hospital Boston, Massachusetts

Neuropsychological Association of Southwest Missouri, PC Springfield, Missouri

Eric Yarnell, ND

Associate Professor Botanical Medicine Bastyr University Kenmore, Washington

Ahn Young, MD

Massachusetts General Hospital Boston, Massachusetts

Jeffrey L. Young, MD

Physicians Review Network of New York New York, New York

Andrea H. Zengion, ND, MSAOM

Naturopathic Doctor and Acupuncturist San Francisco Natural Medicine San Francisco, California

Yi Zhang, MD, PhD, MSc

Instructor Anesthesia, Critical Care, and Pain Medicine Massachusetts General Hospital, Harvard Medical School Boston, Massachusetts

Li Zhang, MD, PhD

Department of Anesthesiology Columbia University Medical Center New York, New York


The diagnosis and treatment of pain-related conditions have changed extensively over the last decade. These changes have included surgical advances in minimally invasive techniques, multidisciplinary approaches to complex pain problems, the development of numerous oral and injectable medications, and further advancements in pain management injection procedures. Our understanding of many of these changes has been advanced by our own specialty academies and many new societies dedicated to pain relief. These groups have been instrumental in encouraging research that has been included in much of this edition of Pain Procedures in Clinical Practice. The third edition of Pain Procedures in Clinical Practice has changed extensively since the original volume was published in 1995. The original text was directed toward practicing physiatrists and incorporated inpatient rehabilitation and outpatient pain management procedures. In 2000 the second edition was expanded as a multi-specialty textbook and intended entirely for the pain

management practitioner, regardless of medical specialty. The third edition of Pain Procedures in Clinical Practice has been further expanded to include section editors. The extensive volume of new information, research, and techniques relative to pain management necessitated this expansion. The selected section editors are well known in their respective specialities. To each of them—Dr. ­Stevan Walkowski (CAM Procedures), Dr. Aneesh Singla (Peripheral Nerve Blocks), Dr. David Vivian (Spine Procedures), and Dr. ­Steven Richiemer (Video Procedures)—I extend my gratitude for their hard work and dedication to this textbook. A huge thank-you goes out to all of the authors for contributing their expertise to this text. Numerous hours of research, writing, and review were required by each of these contributors to produce such a volume. In addition, special thanks go out to the publisher and medical artists who made this project come to fruition. Ted A. Lennard, MD Editor


Fundamentals of Procedural Care


Ted A. Lennard, MD

Pain procedures are a useful adjunct in managing pain and functional problems. The pain physician, as a diagnostician, can derive valuable information from the results of these procedures and from patient responses. This information can be invaluable in directing future treatment. Knowledge of the fundamentals of procedural care is important to novices and experienced physicians who provide such treatment to reduce complications, eliminate unnecessary procedures, and maximize patient recovery.

Procedure Planning The patient work-up should begin with a detailed history and a physical examination that focuses on the body part involved. Historical emphasis on the duration of symptoms, previous attempts at procedures, and pending litigation should be well documented. Signs of symptoms magnification and malingering should be noted.1,2 A thorough functional, social, and psychological history should be included. A comparison of historical and physical findings with available imaging studies is essential to complete the evaluation. During the evaluation period, diagnostic procedures can be useful in providing valuable insight into the patient’s pain generator, anatomic defect, threshold for pain, and psychological response to treatment. When a provisional diagnosis is made, treatment objectives should be outlined. Conservative, nonprocedural-oriented treatment should be undertaken initially if symptoms are not disabling. This treatment should include correction of underlying biomechanical disorders, activity modification in the workplace, technique changes in athletes, and flexibility and strengthening programs. Concomitant psychological disorders also should be treated. Upon deciding to proceed with a therapeutic procedure, the physician should be certain it is performed within the context of a welldesigned rehabilitation program.

General Procedure Techniques Positioning and Relaxation Positioning the patient for comfort and physician accessibility is an important step in good technique. Multiple pillows, foam plinths, and pads can be used to increase the patient’s tolerance on hard procedure tables, provide some degree of relaxation, and optimize positioning. This is especially important for the patient with cardiac or pulmonary compromise. For the physician, chairs and procedure

tables for proper height prevent fatigue during lengthy procedures and improve manual dexterity. Constant communication with the patient, including explanations of approaching procedural steps, helps reduce anxiety. Inappropriate conversation with assisting medical personnel should be avoided, thereby confirming the physician’s total attention to the patient. The patient’s gown should fit properly, enhancing relaxation and comfort. If these techniques do not lead to relaxation, oral or parenteral sedation should be provided. Skin Preparation Because skin cannot be sterilized without damage, the goal of antiseptics is to remove transient and pathogenic microorganisms while reducing resident flora to a low level.3 These agents should be safe, rapid-acting, inexpensive, and effective on a broad spectrum of organisms.3,4 Multiple agents, including iodophors (Betadine), hexachlorophene (pHisoHex), chlorhexidine (Hibiclens, Hibitane), and alcohols, are commercially available and accomplish these desired goals.3,5-7 The preferred agent remains controversial.3,8-13 Clinically, the most commonly used agents are alcohol and iodine, with the latter being superior for skin decontamination.16 Application of 70% isopropyl alcohol destroys 90% of the cutaneous bacteria in 2 minutes, whereas the usual single wipe without waiting procedure destroys, at most, 75% of cutaneous bacteria.3 Skin regions with hair should not alter one’s method of skin decontamination. Hair removal by shaving increases wound infection rate and is contraindicated.17-19 If absolutely necessary, clipping hair20,21 or applying depilatory creams19 can be safe.22 The overall risk of wound infection with most pain procedures is low and mostly depends on the technique that the practitioner employs during the procedure.

Needle Insertion and Local Anesthesia Steps should be taken to make all procedures as pain-free as possible. The liberal use of local anesthetics in adequate concentrations will promote this goal while minimizing repeat needle sticks. Small diameter needles, 28 to 30 gauge, are initially used to anesthetize the skin and subcutaneous tissue. Distracting the skin with one’s fingers while slowly advancing the needle helps to reduce pain. The tip of the needle can be placed in the subcutaneous fat and, upon injection, less pain is noted than with intradermal injections because of the distensibility of fat. Rapid infusion of medication, especially with large volumes, causes tissue distention and 3

4  Basic Principles of Procedures

results in pain. Lidocaine23-26 and bupivacaine,27 buffered with 8.4% sodium bicarbonate causes less pain than plain anesthetics and is equally efficacious. A 1:10 to 1:20 ratio of sodium bicarbonate to anesthetics can be used. Morris and colleagues found that, when injected, subcutaneous procaine and lidocaine were the least painful anesthetics.28,29 Only etidocaine was found to be more painful than bupivacaine. Varelmann and coworkers found that patients who were told “We are going to give you a local anesthetic that will numb the area and you will be comfortable during the procedure” perceived less pain than patients who were told “You are going to feel a big bee sting; this is the worst part of the procedure.”30 Other preparations used to reduce pain with initial needle injections include topical anesthetics (eutectic mixtures of local anesthetics, or EMLA), vapocoolant sprays, and preheated local anesthetics.31 If the patient is intolerant of or allergic to anesthetic agents, 0.9% intradermal saline or dilute antihistamines such as diphenhydramine (Benadryl) in 10 to 25 mg/mL injections can be used as alternatives;32 however, they are often considered painful, especially when injected intradermally. Before administering injection anesthetics, one should aspirate to prevent inadvertent injection into a vascular structure. Smallgauge needles are unreliable when aspirating for blood. Needles of 25 gauge or larger rotated in two planes are necessary for this purpose. Continual movement of the needle tip makes injection into a vessel less likely. Slow, fractionated dosing is recommended while monitoring the patient for early signs of anesthetic toxicity.

Precautions Good technique not only reduces the risk of wound infection, but also lowers the rate of viral transmission between patient and physician. Physicians who perform exposure-prone procedures should know their own human immunodeficiency virus (HIV) and hepatitis B virus (HBV) antibody status. The risk to the patient of contracting the HIV virus ranges from 1 in 42,000 to 1 in 420,000; the risk of contracting fatal HBV infection from an HBeAg positive surgeon during a procedure ranges from 1 in 76,000 to 1 in 1.4  ­million.33 Universal precautions should be understood and include the use of gloves, protective eyewear, masks, (optional), and gowns (optional). Recapping used needles should be avoided and is seldom necessary. REFERENCES   1. Becker GE. Red Flags. Oakland, Calif: American Back Society Newsletter; 1991, p 23.   2. Carragee EJ. Psychological and functional profiles in select subjects with low back pain. Spine J. 2001;1(3):198-204.   3 Sebben JE. Surgical antiseptics. J Am Acad Dermatol. 1983;9:759-765.   4. Masterson BJ. Skin preparation. Clin Obstet Gynecol. 1988;31:736-743.   5. Davies J, Babb JR, Ayliffe GA, Wilkins MD. Disinfection of skin of the abdomen. Br J Surg. 1979;65:855-858.   6. Lepor NE, Madyoon H. Antiseptic skin agents for percutaneous procedures. Rev Cardiovasc Med. 2009;10(4):187-193.   7. Ritter MA, French ML, Eitzen HE, et al. The antimicrobial effectiveness of operative-site preparative agents: a microbiological and clinical study. J Bone Joint Surg Am. 1980;62:826-828.   8. Bibbo C, Patel DV, Gehrmann RM, Lin SS. Chlorhexidine provides superior skin decontamination in foot and ankle surgery: A prospective randomized study. Clin Orthop Relat Res. 2005;438:204-208.   9. Calfee DP, Farr BM. Comparison of four antiseptic preparations for skin in the prevention of contamination of percutaneously drawn blood ­cultures: A randomized trial. J Clin Microbiol. 2002;40(5):1660-1665.

10. Kiyoyama T, Tokuda Y, Shiiki S, et al. Isopropyl alcohol compared with isopropyl alcohol plus povidone-iodine as skin preparation for prevention of blood culture contamination. J Clin Microbiol. 2009;47(1):54-58. 11. Lowbury EJ, Lilly HA. Use of 4% chlorhexidine detergent solution (Hibiscrub) and other methods of skin disinfection. Br Med J. 1973;1:510-515. 12. Saltzman MD, Nuber GW, Gryzlo SM, et al. Efficacy of surgical preparation solutions in shoulder surgery. J Bone Joint Surg Am. 2009 Aug;91(8):1949-1953. 13. Smylie HG, Logie JR, Smith G. From Phisohex to Hibiscrub. Br Med J. 1973;4:586-589. 14. Swenson BR, Hedrick TL, Metzger R, et al. Effects of preoperative skin preparation on postoperative wound infection rates: A prospective study of 3 skin preparation protocols. Infect Control Hosp Epidemiol. 2009 Oct;30(10):964-971. 15. Tunevall TG. Procedures and experiences with preoperative skin preparation in Sweden. J Hosp Infect. 1988;11 (suppl B):11-14. 16. Choudhuri M, McQueen R, Inoue S, et al. Efficiency of skin sterilization for a venipuncture with the use of commercially available alcohol or iodine pads. Am J Infect Control. 1990;18:82-85. 17. Bird BJ, Chrisp DB, Scrimgeour G. Extensive pre-operative shaving: A costly exercise. N Z Med J. 1984;97:727-729. 18. Celik SE, Kara A. Does shaving the incision site increase the infection rate after spinal surgery? Spine. 2007;32(15):1575-1577. 19. Seropian R, Reynolds BM. Wound infections after preoperative depilatory versus razor preparation. Am J Surg. 1971;121:251-254. 20. Mackenzie I. Preoperative skin preparation and surgical outcome. J Hosp Infect. 1988;11:27-32. 21. Olson MM, MacCallum J, McQuarrie DG. Preoperative hair removal with clippers does not increase infection rate in clean surgical wounds. Surg Gynecol Obstet. 1986;162:181-182. 22. Tanner J, Moncaster K, Woodings D. Preoperative hair removal: A systematic review. J Perioper Pract. 2007;17(3):118-121, 124-132. 23. McKay W, Morris R, Mushlin P. Sodium bicarbonate attenuates pain on skin infiltration with lidocaine, with or without epinephrine. Anesth Analg. 1987;66:572-574. 24. Roberts JR. Local anesthetics: Injection techniques. Emerg Med News. 1992 March;9-16. 25. Stewart JH, Chinn SE, Cole GW, et al. Neutralized lidocaine with ­epinephrine for local anesthesia – II. J Dermatol Surg Oncol. 1990;16: 842-845. 26. Xia Y, Chen E, Tibbits DL, et al. Comparison of effects of lidocaine hydrochloride, buffered lidocaine, diphenhydramine, and normal saline after intradermal injection. J Clin Anesth. 2002;14(5):339-343. 27. Cheney PR. Molzen G, Tandberg D: The effect of pH buffering on reducing the pain associated with subcutaneous infiltration of bupivicaine. Am J Emerg Med. 1991;9:147-148. 28. Morris R, McKay W, Mushlin P. Comparison of pain associated with intradermal and subcutaneous infiltration with various local anesthetic solutions. Anesth Analg. 1987;66:1180-1182. 29. Morris RW, Whish DK. A controlled trial of pain on skin infiltration with local anaesthetics. Anaesth Intensive Care. 1984;12:113-114. 30. Varelmann D, Pancaro C, Cappiello EC, Camann WR. Noceboinduced hyperalgesia during local anesthetic injection. Anesth Analg. 2010;110(3):868-870. 31. Bloom LH, Scheie HG, Yanoff M. The warming of local anesthetic agents to decrase discomfort. Ophthalmic Surg. 1984;15:603. 32. Mark LC. Avoiding the pain of venipuncture (letter to the editor). N Engl J Med. 1976;294:614. 33. Lo B, Steinbrook R. Health care workers infected with the human immunodeficiency virus. The next steps. JAMA. 1992;267:1100-1105.

Commonly Used Medications in Procedures


Susan J. Dreyer, MD, and William Jeremy Beckworth, MD

Local anesthetics, corticosteroids, contrast agents, neurolytic agents, and viscosupplementation are used commonly in pain management procedures. At times, medications to treat adverse reactions are required. As emphasized throughout this text, every interventional physician must be knowledgeable of the pharmacology, pharmacokinetics, and potential adverse reactions of the drugs he or she administers. Furthermore, the physician needs to be familiar with medications used to treat potential procedure complications. This chapter examines medications commonly employed during pain management procedures.

Local Anesthetics Local anesthetics are widely used and are generally safe when administered properly. Local anesthetics are therapeutically employed in most injections to provide local anesthesia or analgesia of a painful structure. The ability of local anesthetics to relieve pain can also be used diagnostically to help confirm a pain generator. Common applications include skin and soft tissue anesthesia for other procedures; intraarticular injections; injection for bursitis, tenosynovitis, entrapment neuropathies, painful ganglia; spinal injections; and nerve blocks. Local anesthetics are subdivided into esters and amides, referring to the bond that links the hydrophilic and lipophilic rings. The amide class is less allergenic and more commonly employed in local, intraarticular, and spinal injections. The most widely used agents in pain management practice are lidocaine (Xylocaine) and bupivacaine (Marcaine), both amide local anesthetics. Amide local anesthetics are hydrolyzed by the liver microsomal enzymes to inactive products. Thus, patients with hepatic failure or reduced hepatic flow are more sensitive to those agents. For this reason, patients taking beta blockers or who have congestive heart failure, have a lower maximum dosage because of their reduced hepatic flow and decreased elimination rates of the amide local anesthetics. In contrast, the ester anesthetics are rapidly hydrolyzed by plasma cholinesterase into para-aminobenzoic acid (PABA) and other metabolites that are excreted unchanged in the urine. Paraaminobenzoic acid is a known allergen in certain individuals. However, the rapid metabolism of ester local anesthetics lowers their potential for toxicity. Procaine is an amino ester commonly, but not exclusively, employed in differential spinal blocks. 2-­Cholorprocaine can be used for infiltration, epidural or peripheral nerve block, and is also an ester.

Mechanism of Action Local anesthetics exert their effect by reversibly inhibiting neural impulse transmission. The local anesthetic molecules diffuse across neural membranes to block sodium channels and inhibit the influx of sodium ions; therefore, proximity of the local anesthetic to the nerve to be blocked is required. Only a short segment of the nerve (5 to 10 mm) needs to be affected to cease neural firing. Epidural analgesia from local anesthetic is believed by some to occur because of uptake across the dura, a back door approach to spinal block. The ability of a local anesthetic to diffuse through tissues and then block sodium channels relies on the ability of these molecules to dissociate at physiologic pH of 7.4. The pKas for local anesthetics are greater than the pH found in tissue. As a result, local anesthetics in vivo exist primarily as cations, the form of the molecule that blocks the sodium channel. The base form of the local anesthetic allows it to penetrate the hydrophobic tissues and arrive at the axoplasm. In addition to host factors, neural blockade by local anesthetics is affected by the volume and concentration of local anesthetic injected, the absence or presence of vasoconstrictor additives, the site of injection, the addition of bicarbonate, and temperature of the local anesthetic.1 Increasing the total milligrams of a local anesthetic dose shortens the onset and increases the duration of the local anesthetic. Epinephrine, norepinephrine, and phenylephrine are sometimes added to local anesthetics to reverse the intrinsic vasodilation effects of many of the local anesthetics and thereby reduce their systemic absorption. This increases the amount of local anesthetic available to block the nerve. More anesthetic means a quicker onset and longer duration. Application of the local anesthetic close to the nerve improves its ability to diffuse across the axon and block sodium channels. Highly vascular sites such as the intercostal nerve and caudal epidural space tend to result in slightly shorter duration of action. The addition of bicarbonate or CO2 (700 mm Hg) to local anesthetics hasten their onset. Bicarbonate raises the pH and the amount of uncharged local anesthetic for diffusion through the nerve membrane. CO2 will diffuse across the axonal membrane and lower the intracellular pH making more of the charged form of the local anesthetic available intracellularly to block the sodium channels. Temperature elevations decrease the pKa of the local anesthetic and hasten the onset of action.

Individual Agents Local anesthetics are administered in the intradermal, subcutaneous, intraarticular, intramuscular, perineural, and epidural spaces during pain management procedures. Injections into vascular 5

6  Basic Principles of Procedures

regions such as the oral mucosa and epidural space may result in rapid absorption and higher systemic concentrations. Local anesthetics administered into or near the epidural space should be preservative free. Methylparaben is a common preservative in multidose vials and is also a common allergen.2 Lidocaine Lidocaine is the most versatile and widely used of the local anesthetics. It has a short onset of action, 0.5 to 15 minutes, and short duration of action, typically 0.5 to 3 hours. The difference between the effective dose and the toxic does is wide, resulting in a high therapeutic index compared to other common local anesthetics. Maximum doses are variably reported in the range of 400 to 500 mg of lidocaine. Typical concentrations are 0.5% to 2%. Final concentration is often diluted by the addition of a corticosteroid.1 Concentration percentages are easily converted to milligrams. For example, a 1% solution of lidocaine has 1 g of lidocaine in 100 mL of fluid. This is equivalent to 1000 mg/100 mL or 10 mg/mL. Volume of lidocaine injected varies widely with location and practitioner. Using the aforementioned guidelines, total injection of 1% lidocaine should remain below 40 mL (40 mL × 10 mg/mL = 400 mg).

Bupivicaine Bupivacaine (Marcaine) is another widely used local anesthetic. Bupivacaine’s duration of action (2 to 5 hr) is longer than lidocaine’s as is its onset of action (5 to 20 min). Bupivacaine is commonly used in concentrations of 0.125% to 0.75%. Final concentrations are often diluted by 30% to 50% by the addition of a corticosteroid. The higher concentrations generally have a faster onset of action. Bupivacaine has more cardiotoxicity than lidocaine, especially if an injection is given intravenously inadvertently. The toxic dose of bupivacaine is only 80 mg (16 mL of a 0.5% solution) when given intravascularly, but may be up to 225 mg with an extravascular injection.1

Toxicity Action of local anesthetics is affected by numerous factors reviewed above. Location of injection plays a primary role in determining the onset, duration, and toxic dose of these agents (Table 2-1). Vasoconstrictors such as epinephrine reduce local bleeding and thereby prolong the onset and duration, but are generally not employed in a pain management practice.

Table 2-1  Classification and Uses of Local Anesthetics Clinical Uses

Usual ­Concentration (%)

Usual Onset

Usual Duration (hours)

Maximum* Single Dose (mg)

Unique Characteristics


Infiltration PNB Epidural

1 2 2-3

Fast Fast Fast

0.5-1.0 0.5-1.0 0.5-1.5

1000 + EPI 1000 + EPI 1000 + EPI

Lowest systemic toxicity Intrathecal route may be neurotoxic


Infiltration PNB Spinal

1 1-2 10

Fast Slow Moderate

0.5-1.0 0.5-1.0 0.5-1.0

1000 1000 200

Used for differential spinal


Topical Spinal

2 0.5

Slow Fast

0.5-1.0 2-4

80 20

Topical Infiltration IV regional PNB Epidural Spinal

4 0.5-1.0 0.25-0.5 1.0-1.5 1-2 5

Fast Fast

0.5-1.0 1-2 1-3

Fast Fast Fast


500 + EPI 500 + EPI 500 500 + EPI 500 + EPI 100


IV regional PNB Epidural

4 1.5-2.0 1-3



600 600 600

Least toxic amide Methemoglobinemia possible when >600 mg


PNB Epidural

1.0-1.5 1-2

Fast Fast

2-3 1.0-2.5

500 + EPI 500 + EPI

Duration of plain solutions longer than lidocaine with EPI, useful when EPI contraindicated


PNB Epidural Spinal

0.25-0.5 0.25-0.75 0.5-0.75

Slow Moderate Fast

4-12 2-4 2-4

200 + EPI 200 + EPI 20

Exaggerated cardiotoxicity with accidental IV injection Low doses produce sensory > motor blockade


PNB Epidural

0.5-1.0 1.0-1.5

Fast Fast

3-12 2-4

300 + EPI 300 + EPI

Motor > sensory blockade


Aminoamides Lidocaine

EPI, epinephrine; IV, intravenous; PNB, peripheral nerve block. *Maximum single dosage is affected by many factors, this is only a guide. Modified from Barash PG, Cullen BF, Stoelting RK: Handbook of Clinical Anesthesia, 2nd ed. Philadelphia, J.B. Lippincott, 1993, pp 206-207.

Commonly Used Medications in Procedures  7

Excess amounts of local anesthetics may cause CNS effects including confusion, convulsions, respiratory arrest, seizures, and even death. The risk for complications increases if the local anesthetics are given intravascularly. Other potential adverse reactions to local anesthetics include cardiodepression, anaphylaxis, and malignant hyperthermia. Patients with decreased renal function, hepatic function or plasma esterases eliminate local anesthetics more slowly and, therefore, have an increased risk of toxicity. Toxic blood levels of lidocaine are approximately 5 to 10 μg/mL, but adverse effects can be seen at lower blood levels. Patients should be monitored for signs of toxicity including restlessness, anxiety, incoherent speech, lightheadedness, numbness, and tingling of the mouth and lips, blurred vision, tremors, twitching, depression or drowsiness. Injections into the head and neck area require the utmost care.3 Even small doses of local anesthetic may produce adverse reactions similar to systemic toxicity seen with unintentional intravascular injections of larger doses. Deaths have been reported.4 Resuscitative equipment and drugs should be immediately available when local anesthetics are used. Management of local anesthetic overdose begins with prevention by monitoring total dose administered, frequently aspirating for vascular uptake, and use of contrast to avoid vascular uptake when appropriate. Recognition of symptoms of toxicity and support of oxygenation with supplemental oxygen are keys to the initial management. Airway must be maintained and respiratory support should be provided as needed. Hypotension is the most common circulatory effect and should be treated with intravenous fluids and a vasopressor such as ephedrine in appropriate candidates. Convulsions persisting despite respiratory support are often treated with a benzodiazepine such as diazepam. If cardiac arrest occurs, standard cardiopulmonary resuscitative measures should be instituted.

Corticosteroids Corticosteroids are administered in a pain practice for their potent antiinflammatory properties. These injections to relieve pain and inflammation work well temporarily, but questions remain regarding their role in the management of many chronic musculoskeletal conditions. Corticosteroids may result in significant side effects.

The potential for these adverse effects, ranging from a relatively innocuous facial flushing effect to joint destroying avascular necrosis, must be weighed against potential benefits. Some locally injected corticosteroids are absorbed systemically and can produce transient systemic effects. Corticosteroids can be helpful in a variety of conditions including rheumatoid arthritis, bursitis, tenosynovitis, entrapment neuropathies, crystal-induced arthropathies in patients who cannot tolerate systemic treatment well, radiculopathies, and at times, osteoarthritis (OA). Corticosteroids should never be injected directly into a tendon or nerve, subcutaneous fat, or an infected joint, bursa, or tendon (Table 2-2).

Mechanism of Action All corticosteroids have both glucocorticoid, antiinflammatory, and mineralocorticoid activity. Agents with significant glucocorticoid and minimal mineralocorticoid activity include betamethasone (Celestone), dexamethasone (Decadron), methylprednisolone acetate (Depo-Medrol) and triamcinolone hexacetonide (Aristospan). Corticosteroids can be mixed in the same syringe with local anesthetics. Corticosteroids produce both antiinflammatory and immunosuppressive effects in humans. The primary mechanism of action may be their ability to inhibit the release of cytokines by immune cells.5 The effects of corticosteroids are species specific.6 Lymphocytes in humans are much less sensitive to the effects of corticosteroids than lymphocytes in common laboratory animals including the mouse, rat, and rabbit. In humans, corticosteroids reduce the accumulation of lymphocytes at inflammatory sites by a migratory effect.7 In contrast to this lymphopenia, is the neutrophilia seen by demargination of neutrocytes from the endothelium and an accelerated rate of release from the bone marrow.8 A temporary rise in white blood cell count is commonly observed for this reason after a corticosteroid dose and in isolation does not mark a post injection infection. The antiinflammatory effects of corticosteroid also occur at the microvascular level. They block the passage of immune complexes across the basement membrane, suppress superoxide radicals, and reduce capillary permeability and blood flow.9 Corticosteroids inhibit prostaglandin synthesis,10 decrease collagenase formation, and inhibit granulation tissue formation.

Table 2-2  Comparison of Commonly Used Glucocorticoid Steroids* Agent

Antiinflammatory Potency*

Salt Retention Property

Plasma Half-life (min)


Equivalent Oral Dose (mg)

Hydrocortisone (cortisol)
























Methylprednisolone (Medrol, Depo-Medrol)






Triamcinolone (Aristocort, Kenalog)






Betamethasone (Celestone)






Dexamethasone (Decadron)







to hydrocortisone. short; I,= intermediate; L, long. From Lennard TA: Fundamentals of Procedural Care. In Lennard TA (ed): Physiatric Procedures in Clinical Practice. Philadelphia, Saunders, 1995. †S,


8  Basic Principles of Procedures

The immunosuppressant effects of corticosteroids are generally via effects on T cells. These effects are not the desired effect of corticosteroid used in pain management procedures and are not observed following epidural injections.11 A review of these immunosuppressant effects can be found in other texts.11-14

Individual Agents Commonly used corticosteroid preparations include betamethasone, methylprednisolone, triamcinolone, dexamethasone, prednisolone, and hydrocortisone. Of these, betamethasone and dexamethasone have the strongest glucocorticoid or antiinflammatory effects. Corticosteroid effects can be highly variable between individuals and it is not possible to definitively state a safe dosage of corticosteroid. The following should serve only as a guide and must be tailored to each individual. Betamethasone An equal mixture of two betamethasone salts, Celestone Soluspan, allows for both immediate and delayed corticosteroid responses. Betamethasone sodium phosphate acts within hours, whereas betamethasone acetate is a suspension that is slowly absorbed over approximately 2 weeks. Betamethasone (Celestone Soluspan) is approved for intraarticular or soft tissue injection to provide short-term adjuvant therapy in osteoarthritis, tenosynovitis, gouty arthritis, bursitis, epicondylitis, and rheumatoid arthritis.15 It is also commonly employed in epidural injections. Typical intraarticular doses vary with the size of the joint and range from 0.25 to 2 mL (1.5 mg to 12 mg). Typically epidural injections range from 1 to 3 mL (6 to 18 mg). Betamethasone should not be mixed with local anesthetics that contain preservatives such as methylparaben as these may cause flocculation of the steroid. Dexamethasone Dexamethasone acetate (Decadron-LA) has a rapid onset and long duration of action. It is usually given in doses of 8 to 16 mg intramuscularly or 4 to 16 mg for intraarticular or soft tissue injections. The most common preparations have 8 mg of dexamethasone acetate per milliliter, therefore 0.5 to 2 mL quantities are the most common. Most preparations contain sodium bisulfite that can trigger allergic reactions in susceptible individuals. It contains long-acting particulates and it is not used for intravenous administration. Dexamethasone sodium phosphate (Decadron Phosphate) is a rapid onset, short duration formulation of dexamethasone. It is available in a variety of strengths ranging from 4 mg/mL to 24 mg/mL. Large joints are often injected with 2 to 4 mg, small joints 0.8 to 1 mg, bursae 2 to 3mg, tendon sheaths 0.4 to 1mg, soft tissue infiltration 2 to 6 mg.15 Sulfites are common in the preparations of this salt also. Dexamethasone is approved for the treatment of osteoarthritis, bursitis, tendonitis, rheumatoid arthritis flares, epicondylitis, tenosynovitis, and gouty arthritis.15 Because it is considered to be a nonparticulate steroid it is also used off-label for epidural steroid injections as discussed subsequently. Methylprednisolone Methylprednisolone acetate (Depo-Medrol) has 1/5 to 1/6 the glucocorticoid potency of betamethasone but similar antiinflammatory effects to prednisolone. It has an intermediate duration of action. It, like the other corticosteroids, is approved for intraarticular and soft tissue injections for short-term adjuvant therapy of osteoarthritis, bursitis, tenosynovitis, gouty arthritis, epicondylitis, and

rheumatoid arthritis.15 Depo-Medrol has been used for epidural administration also. Preparations of methylprednisolone acetate include polyethylene glycol as a suspending agent. Concerns developed as to whether the polyethylene glycol can cause arachnoiditis with (inadvertent) intrathecal injections.16 Animal studies have not demonstrated any adverse effects on neural tissues from the application of glucocorticoid.17 Methylprednisolone is now available without polyethylene glycol, PEG free. Typical doses range from 4 to 80 mg. Small joints are typically injected with 4 to 10 mg, medium joints 10 to 40mg, large joints 20 to 80 mg, bursae and peritendon 4 to 30 mg.15 Triamcinolone Triamcinolone is available as three different salts: triamcinolone diacetate (Aristocort Forte), triamcinolone hexacetonide (Aristospan), and triamcinolone acetonide (Kenalog). Duration of action is shortest with the diacetate and longest with the acetonide formulations. Triamcinolone has similar glucocorticoid activity to methylprednisolone with a long half-life. The approved uses are the same as for the agents listed earlier and it, too, is used in epidural injections. Unfortunately, it has a higher incidence of adverse reactions including fat atrophy and hypopigmentation.15

Spinal Injections Unique considerations are taken into account when considering corticosteroids for spinal injections. In particular, cervical transforaminal injections have lead to rare but significant neurologic complications such as spinal cord injury, stroke, and even death.18-22 The postulated cause of the majority of these complications is undetected vascular injections in the vertebral or spinal radicular arteries with particulate steroids causing embolic infarctions.22,23 Thoracic and lumbar transforaminal injections have similarly been implicated in neurologic complications with particulate steroids. Major complications are thought to arise from embolic events associated with injections into radicular arteries or the reinforcing radicular artery known as the artery of Adamkiewicz.24 This artery typically arises at thoracic levels but it can occur as low as L2 or L3 in about 1% of patients and more rarely at lower levels.25 Anatomic studies show that the size of particles in commonly used steroid preparations such as triamcinolone, methylprednisolone, and betamethasone equals or exceeds the caliber of many radicular arteries.26,27 These particulate steroids either are larger in diameter than a red blood cell or tend to aggregate and/or pack together to be larger than a red blood cell. This is not the case with dexamethasone sodium phosphate, which is a nonparticulate ster­ oid.27 Thus, dexamethasone sodium phosphate should reduce the risk of embolic infarcts following intravascular injections. Consistent with this, a study looked at vertebral artery injection of particulate and nonparticulate steroids in pigs while under general anesthesia. The animals that were injected with particulate steroids never regained consciousness. Subsequent magnetic resonance images (MRIs) revealed upper cervical cord and brain stem edema and histologic analysis showed ischemic changes. The animals injected with nonparticulate steroids did not have ischemic events and recovered without apparent adverse effects. The MRIs and subsequent histologic analysis were also normal in this group of animals.28 The risk with particulate steroids in cervical and thoracic transforaminal injections has led to the common use of dexamethasone sodium phosphate in these procedures. Thoracic and lumbar transforaminal injections may also lead to embolic events29-31 and this must be taken into consideration. The choice corticosteroids

Commonly Used Medications in Procedures  9

in lumbosacral transforaminal injections is debatable, especially if appropriate safety measures are used, such as contrast administration under live fluoroscopy and use of digital subtraction angiography. If vascular uptake is noted, the needle should be repositioned or the procedure aborted. Other spinal procedures such as interlaminar epidural injections or intraarticular injections have not been associated with embolic events with particulate steroids. Both particulate and nonparticulate steroids appear to be effective but studies suggest that particulate steroids may be slightly more efficacious than nonparticulate steroids.32,33 Further studies are needed to clarify this.

Adverse Reactions Corticosteroid use should be carefully considered and avoided if possible in patients at increased risk for adverse reactions, including patients with active ulcer disease, ulcerative colitis with impending perforation or abscess, poorly controlled hypertension, congestive heart failure, renal disease, psychiatric illness or history of steroid psychosis, or a history of severe or multiple allergies.15,34 Intraarticular injections have been associated with osteonecrosis, infection, tendon rupture, postinjection flare, hypersensitivities, and systemic reactions.15 Intraspinal injections have been associated with adhesive arachnoiditis, meningitis, and conus medullaris syndrome.16 Adverse reactions to injected corticosteroids include a transient flare of pain for 24 to 48 hours in up to 10% of patients. Diabetics and those individuals with a predisposition to diabetes may become hyperglycemic and appropriate monitoring and corrective measures should be instituted. Adrenal cortical insufficiency is generally not seen associated with intermittent injections of corticosteroids, but remains a serious adverse reaction that could be precipitated by indiscriminate, frequent high-dose corticosteroid injections. Allergic reactions to systemic glucocorticoids have been reported and if slow release formulations are used, the allergic response may not occur until a week after the injection.35 Even with local injections of corticosteroids, some systemic response may occur. Generally less serious side effects of corticosteroids include facial flushing, injection site hypopigmentation, subcutaneous fat atrophy, increased appetite, peripheral edema or fluid retention, dyspepsia, malaise, and insomnia.15 Prolonged or repeated doses can result in cushingoid changes.

Drug Interactions A number of drug-drug interactions for corticosteroids have been reported. Some of the more common ones encountered in a pain management practice are mentioned here. Estrogens and oral contraceptives may potentiate the effect of the corticosteroid. Macrolide antibiotics (e.g., erythromycin, azithromycin) may greatly increase the effect of methylprednisolone by decreasing its clearance. In contrast, the hydantoins (e.g., phenytoin), rifampin, phenobarbital, and carbamazepine may increase corticosteroid clearance and decrease the antiinflammatory therapeutic effect. Theophylline and oral anticoagulants can interact variably with corticosteroids.15

Neurolytic Agents Neurolytic drugs such as phenol are employed in pain management practice primarily to treat spasticity. Neurolytic agents also have been used for treating chronic pain including intractable cancer

pain and facet denervation procedures. The use of neurolytic agents for facet joint neurotomies is being replaced by radiofrequency lesioning.36,37 Neurolytic agents are nonspecific in destroying all nerve fiber types. Phenol, ethyl alcohol, propylene glycol, chlorocresol, glycerol, cold saline, and hypertonic and hypotonic solutions have been employed as neurolytics. Of these, phenol is the most studied and widely used neurolytic.

Phenol Phenol is the most widely instilled agent to treat severe spasticity. Phenol can be injected around a motor nerve to selectively reduce hypertonicity.38,39 Intrathecal injections of phenol have been used to treat spasticity of spinal cord origin and intractable pain disorders. Sympathectomies for peripheral vascular disease have also been accomplished by injection of phenol along the paravertebral and perivascular sympathetic fibers.40,41

Mechanism of Action Phenol (carbolic acid) denatures protein and thereby causes denervation. Histologic sections show nonselective nerve destruction, muscle atrophy, and necrosis at the site of phenol injections.42-44 Higher concentrations of phenol are associated with greater tissue destruction. Optimal concentration has not been determined and long-term difference between injection of 2% and 3% solution have not been noted.44 Denervation potentials are seen as early as 3 weeks following phenol blocks.45 Clinical response of decreased pain or spasticity last between 2 months and 2 years irrespective of underlying disorder.43,44 Endoneural fibrosis is seen following phenol injections and is believed to impede reinnervation of the muscle by slow wallerian regeneration.

Dosage Phenol is placed in an aqueous solution, glycerin or lipids for administration. Commercially available phenol is an 89% solution and must be diluted to the desired concentration, typically 2 to 3%. Commonly it is mixed with equal part glycerin and then diluted with normal saline to 2% to 5%. The maximum daily injectable dose is 1 g. Toxic effects are uncommon in doses ≤100 mg. Phenol is eliminated through the liver; use in patients with significant liver disease should be avoided.

Adverse Reactions Local reactions to phenol injection include delayed soreness from the associated necrosis and inflammation.42 This discomfort can be relieved with ice packs and analgesics and typically resolves within 24 hours. If the needle is withdrawn without flushing it with saline, phenol may come in contact with the skin and cause erythema, sloughing, and skin necrosis. Protective eyewear can minimize the chance of eye irritation—conjunctivitis from any phenol splashing into the patient’s or physician’s eyes. Paresthesias or dysesthesias from mixed somatic nerve blocks are probably due to an incomplete block. Paresthesias/dysesthesias occur in up to 25% of nerve blocks and resolve within 3 months.38,46-55 Repeat blocks often alleviate these symptoms indicating the dysesthesias may stem more from an incomplete block than from phenol-induced dysesthesias. Systemic reactions to phenol are usually the result of inadvertent intravascular or central blockade.56-59 Adverse systemic


10  Basic Principles of Procedures

reactions most commonly affect the cardiovascular and central nervous systems.58 Cardiac dysrhythmias, hypotension, venous thrombosis, spinal cord infarcts, cortical infarcts, meningitis, and arachnoiditis have been reported.58,60,61

Contrast Agents Contrast agents are administered to help visualize the location of the needle tip, confirm the flow of injectant or visualize the involved structure (e.g., joint, bladder, bursa). Inadvertent vascular uptake despite negative aspiration is not uncommon. The toxicity of local anesthetics and corticosteroids increases with intravascular injection and contrast-enhanced fluoroscopic guidance helps minimize these toxicities. Contrast agents are all iodinated compounds that allow opacification of structures for visualization. Contrast media is divided into ionic and nonionic agents. The nonionic contrast agents are low osmolality and may decrease the potential for adverse reactions. Although these nonionic agents decrease minor reactions such as nausea and urticaria, they have not been shown to decrease the incidence of more severe reactions.62,63 They do not eliminate the possibility of severe or fatal anaphylactic reactions. Potential for adverse reaction can be minimized by limiting the quantity of the contrast media injected and adequately screening patients. Patients with a history of contrast reaction, significant allergies, impaired cardiac function/limited cardiac reserve, bloodbrain barrier breakdown, and severe anxiety are at increased risk for generalized reactions including urticaria, nausea, vomiting, and anaphylaxis. Patients with impaired renal function and paraproteinemias are at increased risk for renal failure with the administration of contrast agents. Renal complications can be minimized by limiting the volume of contrast agent, ensuring adequate hydration before, during, and after the procedure and using the low osmolality agents for patients more than 70 years with Cr ≥ 2 mg/dL. Spinal procedures including epidural steroid injections, facet joint injections, sympathetic blocks, discography, spinal nerve blocks, and sacroiliac joint injections are all ideally performed with the aid of fluoroscopy and contrast enhancement.64,65 The nonionic contrast agents are used for these injections because the potential for subarachnoid spread exists with any of these procedures. The two most common nonionic agents are iopamidol (Isovue) and iohexol (Omnipaque). Both agents are nonionic, readily available as an injectable liquid, water soluble and quickly cleared. The first of the nonionic contrast agents, metrizamide (Amipaque), is a powder which must be reconstituted. Metrizamide also is associated with a higher incidence of seizures than either iohexol or iopamidol and is rarely used now for procedures. Generally, 0.2 to 2 mL of nonionic contrast is sufficient for the experienced injectionist to confirm location and spread of the contrast. These agents are 90% eliminated through the kidneys within 24 hours. Side effects are uncommon but include nausea, headaches, and CNS disturbances.66 Ionic contrast agents such as diatrizoate (Renografin) and iothalamate (Conray) can be used for other contrast enhanced injections including arthrograms, cystometrograms, and bursa injections. These agents are well tolerated in these situations when total volume of contrast is limited to 15mL or less.

Premedication for Allergic Reactions The risk of anaphylactoid reactions is 1% to 2% when radiopaque agents are used. This risk increases to 17% to 35% when repeat exposure to radiopaque agents occurs in individuals with known

sensitivities.54,66-68 If premedication with diphenhydramine and methylprednisolone is given, the risk of anaphylactoid reactions is reduced to approximately 3.1%.66 The current recommended prophylactic protocol is methylprednisolone 32 mg by mouth 12 and 2 hours prior to contrast use.69 Concurrent use of specific H1 and H2 blockers is also recommended.70,71

Viscosupplementation Viscosupplemenation with hyaluronic acid (HA) injections is FDA approved for knee osteoarthritis although it is sometimes used off-label for osteoarthritis of other joints.Hyaluronic acid is a large macromolecule, a glycosaminoglycan composed of repeating disaccharides of glucuronic acid and N-acetylglucosamine, that is naturally occurring in synovial fluid. It is a viscous component of synovial fluid and acts as a lubricant and cushion for joints. In osteoarthritis, the synovial fluid breaks down into smaller units, thereby decreasing its lubricating and shock-absorbing abilities. HA injections are believed to improve the elastoviscosity of the arthritic joint by increasing the HA concentration. Commonly available agents are Hyalgan (hyaluronate sodium), Orthovisc (hyaluron), Supartz (hyaluronan), Synvisc and SynviscOne (hylan GF-20). These are given once a week over 3 to 5 weeks depending on the agent used. The one exception is Synvisc-One, which is injected once. Several randomized controlled trials have demonstrated that viscosupplementation is superior to placebo but the clinical efficacy is likely modest.72 A 2003 meta-analysis in JAMA looking at 22 trials concluded that HA was superior to placebo injections but had a relatively small effect. The effect was probably similar to NSAIDs. It also raised concern about a possible publication bias with 17 of 22 trials being industry sponsored, which may overestimate effects of viscosupplementation.73 Another meta-analysis in 2004 looked at 13 randomized controlled trials and found that it is an effective treatment for patients with knee OA who have ongoing pain or are unable to tolerate conservative treatment or joint replacement. HA appears to have a slower onset than intraarticular steroid injections and may last longer.74 A more recent review of viscosupplementation suggested that clinical improvement attributable to viscosupplementation is likely small.75 Adverse reactions with HA injections are generally mild but reports vary regarding frequency. Mild side effects include pain at injection site (1% to 33%), local joint pain and swelling (2 mg of midazolam was a predictor of impaired cognitive function at discharge. Typically, propofol seems to be used with interventional pain procedures that have become extended or problematic, often when moderate dosages of midazolam and/or fentanyl have been given. Ketamine is one of the oldest anesthetics (>30 years) that provides moderate sedation and analgesia in one compound. It does not suppress pharyngeal and laryngeal reflexes and can be administered in nonoperating room conditions by nonanesthesiologists.21 Ketamine produces a “dissociative” anesthetic state, which is characterized as a state of catalepsy in which the eyes remain open with a slow nystagmic gaze while corneal and light reflexes remain intact.22 The chemical structure is similar to phencyclidine (PCP) so one of the main side-effects is psychotomimetic experiences or “weird trips.”23 Ketamine’s mechanism of action is at NMDA receptors as well as cholinergic receptors of the muscarinic type and brain acetylcholinesterase. Potentiation of GABA inhibition has also been reported with high doses.24 Because of activity at NMDA receptors, ketamine could theoretically be more effective in treating neuropathic pain states or patients who are opioid tolerant.25 Current evidence

does not support routine use of ketamine for treatment of chronic pain.23 As an adjunct to outpatient interventional pain procedures, a dosage of 0.5 to 2 mg/kg (approximately 30 to 140 mg) can be administered as an induction bolus. One of the author’s recommendations would be to dose 20 to 30 mg IV bolus at one time and observe the effect, particularly if the patient has already received other sedative and analgesic agents. Ketamine undergoes extensive hepatic metabolism by the cytochrome P-450 system. It may produce hyperreactive airway reflexes, especially in the presence of inflammation of the upper respiratory tract22 and can give rise to myoclonic jerks or involuntary movements.26

Opioid Analgesics Opioid analgesic agents are the first-line medications for the relief of acute pain.27 Although morphine, the gold standard, and meperidine have been available for many years, their slower onset >10 minutes and prolonged duration of 1 to 2 hours have steered most interventional pain physicians to use the short-acting fentanyl family of synthetic opioids for procedural analgesia. All opioids act at mu receptors at the spinal cord and supraspinal levels causing a decrease in nociceptive input at the spinal lamina and activation of descending inhibitory control centers of the periaqueductal grey. Fentanyl, alfentanil, sufentanil, and remifentanil are highly lipophilic opioid analgesics compared to morphine. Fentanyl has a rapid onset of action, high clearance, and short duration of action making it ideal for procedural analgesia. Dosages of 25 to 50 mcg every 5 minutes to a total dosage of 200 mcg for healthy noncompromised patients is not uncommon for a duration of effect of 30 minutes. Fentanyl is metabolized by cytochrome P450 enzymes. The high lipid solubility leads to a slow removal in fat pools with a half-life longer than morphine; thus, the respiratory depressant effects can outlast analgesia and so postprocedural monitoring is required. Alfentanil is less lipid soluble than fentanyl and has a shorter duration of action. This agent was used to provide analgesia for the placement of peribulbar blocks in one of the author’s institutions prior to eye surgery and provided significant intraoperative analgesia but little to no postoperative analgesia. In addition, the half-life of alfentanil is shorter in children and longer in the elderly and obese, making the opioid a bit less predictable than fentanyl for standard analgesic usage. Sufentanil is approximately 10 times more potent than fentanyl and has a much higher lipophilicity. It also has a rapid onset, high clearance, and shorter duration of action than fentanyl. Dosages of 2.5 to 5 mcg every 5 minutes for a total dose of 15 mcg for a duration of effect of 15 minutes. Because of the extreme potency of this opioid, it has been often used for cardiac anesthesia or for treating extremely opioid-tolerant patients that are resistant to fentanyl. Opioid naïve patients should not be dosed with this drug without the practitioner being able to perform airway resuscitation. Remifentanil is the most lipid-soluble opioid in the fentanyl family and can provide analgesia only by continuous infusion due to ultrahigh clearance by esterases in the blood and tissues. This agent probably does not have a use in standard interventional pain procedures particularly because of the possibility of increasing postoperative pain.28 Morphine and meperidine may be used sparingly in the postoperative setting. Titrating morphine at 2 to 4 mg intravenously every 10 minutes can provide additional pain relief for


28  Basic Principles of Procedures

opioid-tolerant patients for a duration of 2 to 4 hours or the duration of most patient’s travel home. Nausea and urinary retention rates are higher with morphine than with fentanyl. Meperidine is a weak opioid agonist that has been used for treatment of postoperative shivers at 25 mg IV. Because higher doses (700 mg) can produce seizures from normeperidine accumulation making interpretation of local anesthetic toxicity difficult, the authors recommend not using more than 25 to 50 mg IV for perioperative shivering. The main reversal agent for all opioids is naloxone. Naloxone will reverse respiratory depression but also any opioid analgesia as well. Dosages of 40 mcg increments every 2 to 5 minutes with respiratory support can allow the patient to recover spontaneous ventilation. The duration of effect of naloxone is less than 90 minutes, which may be less than the duration of the last opioid given, usually morphine. Further naloxone dosing with continuous monitoring and respiratory support may be required.

A Brief Word on Local Anesthetics One of the main ways to decrease the dosage of drugs used for sedation and analgesia is to use an appropriate amount of local anesthetic. All local anesthetics have similar structures with an aromatic benzene ring and an amino group connected by a linkage. This linkage is either an amide or an ester. All amide local anesthetics have an “i” in their generic name before “caine”: lidocaine, bupivacaine, ropivacaine. The other local anesthetics are esters: procaine, chloroprocaine. Local anesthetics block sodium channels and stop nerve conduction of impulses. Lidocaine is typically administered in 0.5% to 2% concentrations or 5% as a topical gel. The onset of action is approximately 5 minutes with a duration of 1 to 2 hours without epinephrine. The maximal safe dose is 3 mg/kg or about 250 mg without epinephrine.

With epinephrine the safe dosage increases to 7 mg/kg or about 500 mg. Bicarbonating 0.5% lidocaine will decrease initial pain of injection site pain. Bupivacaine has a slower onset of action of 5 to 10 minutes but longer duration of action (3 to 6 hours). Typical concentrations used are 0.25% to 0.75% without epinephrine. A maximum safe dose is 150 mg without epinephrine. Bupivacaine is highly cardiotoxic so ropivacaine, a chiral version of bupivacaine is sometimes used in its place particularly for higher volume injections. Ropivacaine has concentrations from 0.2% to 1% and a maximal safe dose is 300 mg, which is less cardiotoxic than bupivacaine. One of the authors has received many calls from other physicians about patients with “lidocaine” allergies. Other than skin testing, the best option is to avoid amide local anesthetics and use an ester: chloroprocaine. 2-chloroprocaine is a rapid onset local anesthetic similar to lidocaine. It works within 5 minutes and has a duration of 30 to 60 minutes. It is the most rapidly metabolized local anesthetic in use. Prior concerns existed over reports of spinal toxicity when administered into the epidural space. New formulations have had the prior ethylenediaminetetraacetic acid (EDTA) removed, which may have caused paraspinal spasms in the past.27 Chloroprocaine may not be used if the patient reports an allergy to suntan lotion that contains benzocaine, a topical ester local anesthetic.

Postprocedural Care and Monitoring The ASA has provided thorough recommendations for recovery and discharge criteria after sedation and analgesia (Table 4-7). In general, recovery room providers must be able to assess and manage procedural complications, such as respiratory distress, seizure,

Table 4-7  Recovery and Discharge Criteria after Sedation and Analgesia Each patient-care facility in which sedation-analgesia is administered should develop recovery and discharge criteria that are suitable for its specific patients and procedures. Some of the basic principles that might be incorporated in these criteria are enumerated below. General principles 1. Medical supervision of recovery and discharge after moderate or deep sedation is the responsibility of the operating practitioner or a licensed physician. 2. The recovery area should be equipped with, or have direct access to, appropriate monitoring and resuscitation equipment. 3. Patients receiving moderate or deep sedation should be monitored until appropriate discharge criteria are satisfied. The duration and frequency of ­monitoring should be individualized depending on the level of sedation achieved, the overall condition of the patient, and the nature of the intervention for which sedation/analgesia was administered. Oxygenation should be monitored until patients are no longer at risk for respiratory depression. 4. Level of consciousness, vital signs, and oxygenation (when indicated) should be recorded at regular intervals. 5. A nurse or other individual trained to monitor patients and recognize complications should be in attendance until discharge criteria are fulfilled. 6. An individual capable of managing complications (e.g., establishing a patient airway and providing positive pressure ventilation) should be immediately available until discharge criteria are fulfilled. Guidelines for discharge 1. Patients should be alert and oriented; infants and patients whose mental status was initially abnormal should have returned to their baseline status. Practitioners and parents must be aware that pediatric patients are at risk for airway obstruction should the head fall forward while the child is secured in a car seat. 2. Vital signs should be stable and within acceptable limits. 3. Use of scoring systems may assist in documentation of fitness for discharge. 4. Sufficient time (up to 2 hr) should have elapsed after the last administration of reversal agents (naloxone, flumazenil) to ensure that patients do not become resedated after reversal effects have worn off. 5. Outpatients should be discharged in the presence of a responsible adult who will accompany them home and be able to report any postprocedure ­complications. 6. Outpatients and their escorts should be provided with written instructions regarding postprocedure diet, medications, activities, and a phone number to be called in case of emergency. From American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by  non-­anesthesiologists. Anesthesiology. 2002;96:1004-1017.

Conscious Sedation for Interventional Pain Procedures  29

neurologic events, and cognitive changes. In particular, many outpatient surgery centers are requiring physicians and other staff to have ACLS credentialing particularly if anesthesiologists or emergency medicine specialists with airway management training are not available on site. Overall, sedation and analgesia is generally a safe and rewarding experience for most patients. Preparation of the patient, physician performing the procedure, and supporting medical staff is the most important key to that success. The authors hope the information given in this chapter will help surgical or procedural centers run safely and smoothly. REFERENCES   1. Green SM, Krauss B. Procedural sedation terminology: Moving beyond “conscious sedation”. Ann Emerg Med. 2002;39:433-435.   2. Gross JB, Bailey PL, Caplan RA, et al. Practice Guidelines for sedation and analgesia by non-anesthesiologists: A report by the American Society of Anesthesiologists Task Force on Sedation and Analgesia by NonAnesthesiologists. Anesthesiology. 1996;84:459-471.   3. Smith I, Taylor E. Monitored Anesthesia Care. Int Anesthesiol Clin. 1994;32:99-112.   4. American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology. 2002;96:1004-1017.   5. Innes G, Murphy M, Nijssen-Jordan C, et al. Procedural sedation and analgesia in the emergency department. Canadian Consensus Guidelines. J Emerg Med. 1999;17:145-156.   6. Martin ML, Lennox PH. Sedation and analgesia in the interventional radiology department. J Vasc Interv Radiol. 2003;14:1119-1128.   7. Cohen MM, Duncan PG, Tate RB. Does anesthesia contribute to operative mortality? JAMA. 1988;260:2859-2863.   8. Dailey PA. Chlorhexidine or Povidone-Iodine. CSA Bulletin. 2009;58:45-47. Accessed Nov 22, 2009.   9. Madsen MV, Gotzsche PC, Hrobjartsson A. Acupuncture treatment for pain: systematic review of randomised clinical trials with acupuncture, placebo acupuncture, and no acupuncture groups. BMJ. 2009;338:a3115. 10. Stinson J, Yamada J, Dickson A, et al. Review of systematic reviews on acute procedural pain in children in the hospital setting. Pain Res Manag. 2008;13:51-57. 11. Macario A, Weinger M, Carney S, Kim A. Which clinical anesthesia outcomes are important to avoid? The perspective of patients. Anesth Analg. 1999;89:652-658.

12. Gan TJ, Meyer T, Apfel CC, et al. Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg. 2003;97:62-71. 13. Apfel CC, Korttila K, Abdalla M, et al. A factorial trial of six interventions for the prevention of postoperative nausea and vomiting. N Engl J Med. 2004;350:2441-2451. 14. Kirdak T, Yilmazlar A, Cavun S, et al. Does single, low-dose preoperative dexamethasone improve outcomes after colorectal surgery based on an enhanced recovery protocol? Double-blind, randomized clinical trial. Am Surg. 2008;74(2):160-167. 15. Barash PG. Clinical Anesthesia. Philadelphia: Lippincott; 1993, p 388. 16. Miller’s Anesthesia. 1994:249-258. 17. Absalom A, Pledger D, Kong A. Etomidate USP Dispensing Information. Micromedex. 2001;1:1459-1461. 18. Absalom A, Pledger D, Kong A. Adrenocortical function in critically ill patients 24h after a single dose of etomidate. Anaesthesia. 1999;54(9):861-867. 19. White PF. Propofol: Its role in changing the practice of anesthesia. Anesthesiology. 2008;109:1132-1136. 20. Padmanabhan U, Leslie K, Eer AS, et al. Early cognitive impairment after sedation for colonoscopy: The effect of adding midazolam and/or fentanyl to propofol. Anesth Analg. 2009;109:1448-1455. 21. Sobel RM, Morgan BW, Murphy M. Ketamine in the ED: Medical politics versus patient care. Am J Emerg Med. 1999;17:722-725. 22. White PF, Way WL, Trevor AJ. Ketamine: Its pharmacology and therapeutic uses. Anesthesiology. 1982;56:119-136. 23. Hocking G, Cousins MJ. Ketamine in chronic pain management: An evidence-based review. Anesth Analg. 2003;97:1730-1739. 24. Raeder JC, Stenseth LB. Ketamine: A new look at an old drug. Curr Opin Anaesthesiol. 2000;13:463-468. 25. Laulin JP, Maurette P, Corcuff JB, et al. The role of ketamine in preventing fentanyl-induced hyperalgesia and subsequent acute morphine tolerance. Anesth Analg. 2002;94:1263-1269. 26. Ng KC, Ang SY. Sedation with ketamine for paediatric procedures in the emergency department—A review of 500 cases. Singapore Med J. 2002;43:300-304. 27. Raj PP. Practical Management of Pain. 3rd ed. St. Louis: Mosby; 2000: 462. 28. Guignard B, Bossard AE, Coste C, et al. Acute opioid tolerance—­ Intraoperative remifentanil increases postoperative pain and morphine requirement. Anesthesiology. 2000;93:409-417.



Radiation Safety for the ­Physician Kenneth P. Botwin, MD, Philip Ceraulo, DO, and Chunilal P. Shah, MD, MBBS, BS Currently, fluoroscopic guidance is used routinely for many interventional pain management procedures to obtain more precise localization of anatomic target areas. Fluoroscopy is used in many procedures, including swallowing studies, urologic evaluations, peripheral joint injections, and, perhaps most commonly, interventional spine procedures. The ability to perform many spinal injections, including transforaminal epidurals, facet joint injections, medial branch blocks, sympathetic blocks, discograms, and sacroiliac joint injections, is entirely dependent on fluoroscopic imaging. This chapter reviews the basic concepts of radiation safety and their practical application in the fluoroscopy suite to minimize exposure risks for the patient and spinal interventionalist.

Radiation Concepts Radiologic nomenclature describes the quantity of radiation in terms of exposure, dose, dose equivalent, and activity. Conventional terms are used in the United States, and an international system of units defined in 1960 by the General Conference of Weights and Measurements is primarily used in Europe. Each system has its unique terms (Table 5-1).1

Terminology Like matter, energy can be transformed from one form to another. When ice (solid) melts and turns to H2O (liquid) and then evaporates (gas), a transformation of matter has occurred. Similarly, x-rays transform electrical energy (electricity) into electromagnetic energy (x-rays), which then transforms into chemical energy (radiographic image). Electromagnetic energy emitted into and transferred through matter is called radiation. The spectrum of electromagnetic radiation extends more than 25 orders of magnitude and includes not only x-rays, but also the wavelengths responsible for visible light, magnetic resonance imaging (MRI), microwaves, radio, television, and cellular phone transmission (Fig. 5-1).10 Irradiation occurs when matter is exposed to radiation and absorbs all or part of it. Ionizing Radiation The two basic types of electromagnetic radiation are ionizing and nonionizing. A unique characteristic of ionizing radiation is the ability to alter the molecular structure of materials by removing bound orbital electrons from its atom to create an electrically charged positive ion. The ejected electron and the resulting positively charged atom

are called an ion pair. Ionizing radiation gradually uses its energy as it collides with the atoms of the material through which it travels. This transfer of energy and the resulting electrically charged ions can induce molecular changes and potentially lead to somatic and genetic damage. X-Rays and Gamma Rays Ionizing radiation includes x-rays and gamma rays, which are emitted from x-ray machines, nuclear reactors, and radioactive materials. Gamma rays and x-rays are identical in their physical properties and biologic effects; the only difference is that gamma rays are natural products of radioactive atoms, whereas x-rays are produced in machines. In the production of x-rays, a high dose of voltage, measured in kilovolts (kVp), and a sufficient dose of electrical current, measured in milliamperes (mA), are required. X-ray is a form of electromagnetic energy of very short wavelength (0.5 to 0.06 ångstrom), which allows it to readily penetrate matter. When an object or body is exposed to ionizing radiation, the total amount of exposure is a unit of measurement called the roentgen (R). The definition describes the electrical charge per unit mass of air (1 R = 2.58 × 10-4 coulombs/kg of air). The output of x-ray machines usually is specified in roentgen (R) or milliroentgens (mR). Ionizing radiation exposed to a body interacts with the atoms of the material it comes in contact with in the form of transfer of energy. This dose of transferred energy is called absorption, and the quantity of absorbed energy in humans is referred to as the radiation absorbed dose (rad). By definition, 1 rad = 100 ergs/g where the erg (joule) is a unit of energy and the gram is a unit of mass. The gray (Gy) is a commonly used international unit of measurement to describe absorbed dosages and can be calculated by multiplying the rad by 0.01. Biologic effects usually are related to the rad, which is the unit most often used to describe the quantity of radiation received by a patient. The rad equivalent man (rem) is the unit of occupational radiation exposure and is used to monitor personnel exposure devices such as film badges.

Radiologic Procedures Fluoroscopy In general, there are two types of x-ray procedures: radiography and fluoroscopy. Conventional fluoroscopic procedures, such as myelography, barium enemas, upper gastrointestinal series, and swallowing studies, usually are conducted on a fluoroscopic table. The conventional fluoroscope consists of an x-ray tube located 31

32  Basic Principles of Procedures

above a fixed examining table. The physician is provided with dynamic images that are portrayed on a fluoroscopic screen and the ability to hold and store (“freeze frame”) an image in memory for review or to print as a radiograph (“spot view”) for future reference. Conventional fluoroscopy is considered suboptimal for spinal interventional procedures because of the inability to manipulate the x-ray tube around the patient, and it has been virtually replaced by C-arm fluoroscopes with image intensification for use in spinal injection procedures. The C-arm permits the physician to rotate and angle the x-ray tube around the patient while the patient rests

on a radiolucent support table (Fig. 5-2). Image intensification is achieved through the addition of an image-intensifier tube located opposite the x-ray tube. The intensifier receives remnant x-ray beams that have passed through the patient and converts them into light energy, thereby increasing the brightness of the displayed image and making it easier to interpret. In the current image-intensified fluoroscopy, the x-ray tube delivers currents between 1 and 8  mA. Federal regulations limit the maximum output for C-arm fluoroscopes to 10 R/min at 12 inches from the image intensifier.

Factors Affecting Radiation Exposure Table 5-1  Radiation Quantities and Units Quantity

Conventional Unit


SI Unit


Roentgen (R)

Coulomb/kg of air (C/kg)

1 C/kg = 3876 R 1 R = 258 μC/kg 1 R = 2.58 × 10-4 C/kg


Rad (100 ergs/g)

Gray (Gy) (joule/kg)

1 Gy = 100 rad 0.01 Gy = 1 cGy = 1 rad 0.001 Gy = 1 mGy = 100 mrad

Dose equivalent

Rem (rad × Q)

Sievert (Sv) (Gy × Q)

1 Sv = 100 rem 0.01 Sv = 1 cSv = 1 rem 0.001 Sv = 1 mSv = 100 mrem


Curie (Ci)

Becquerel (Bq)

1 mCi = 37 MBq

Adapted from Wycoff HO: The international system of units. Radiology ­128:833-835, 1978.

Energy (eV)

X-ray imaging

Visual imaging

MR imaging

1010 109 108 107 1 MeV 106 105 104 1 nanometer 103 1 keV 102 101 100 1 micron 10−1 10−2 10−3 1 centimeter 10−4 10−5 10−6 10−7 1 megahertz 10−8 1 kilometer 10−9 10−10 10−11 1 kilohertz 10−12

Frequency (Hz) 1024 1023 1022 1021 1020 1019 1018 1017 1016 1015 1014 1013 1012 1011 1010 109 108 107 106 105 104 103 102

Exposure to ionizing radiation is an unavoidable event while performing fluoroscopic procedures. If one cannot avoid the radiation, then one must minimize its absorption by biologic tissues. The primary source of radiation to the physician during such procedures is from scatter reflected back from the patient. Of lesser concern is the small amount of radiation leakage from the equipment housing. The cardinal principles of radiation protection are: (1) maximize distance from the radiation source; (2) use shielding materials; and (3) minimize exposure time. These principles are derived from protective measures that were adopted by individuals who worked on the atomic bomb in the Manhattan Project; such measures also may be instituted in the fluoroscopic suite. In addition, the concept of ALARA (as low as reasonably achievable) should be applied in all situations of radiation exposure. Distance Distance is the most effective means of minimizing exposure to a given source of ionizing radiation. According to the inverse square law, the intensity of the radiation is inversely proportional to the square of Wavelength (m) 10−16 10−15 10−14 10−13 10−12 10−11 10−10 10−9 10−8 10−7 10−6 10−5 10−4 10−3 10−2 10−1 100 101 102 103 104 105 106

Gamma rays X-rays

Ultraviolet Visible light Infrared

Megavoltage therapy Supervoltage therapy Superficial therapy Diagnostic Contact therapy Grenz rays Violet Blue Green Yellow Red



UHF VHF Shortwave Standard broadcast Longwave

Figure 5-1  The electromagnetic spectrum extends over more than 25 orders of magnitude. This chart shows the values of energy, frequency, and wavelength and identifies some common values and regions of the spectrum. (From Bushong S: Radiologic Science for Technologists: Physics, Biology, and Protection, 4th ed. St. Louis, Mosby, 1988, with permission.)

Radiation Safety for the Physician  33

the distance. That is, when a given amount of radiation travels twice the distance, the covered area becomes four times as large and the intensity of exposure reduces to 1⁄4 (Fig. 5-3). Therefore, at four times the distance from the source, exposure is reduced to 1⁄16 the intensity. A rough estimate of the physician’s exposure at a distance of 1 meter from the x-ray tube is 1/1000th of the patient’s exposure.6 It is therefore recommended that the technician and physician remain as far away from the examining table as practical during fluoroscopic procedures. The position of the physician’s body, especially the hands, should be closely monitored and his or her position should be kept at a maximum distance from the fluoroscope at all times.2 For example, it is advisable that the physician deliberately step away from the patient before acquiring each image and also use extension tubing during contrast injection to maximize the physician’s distance from the beam. Shielding Shielding factors include filtration, beam collimation, intensifying screens, protective apparel (e.g., leaded aprons, eyewear, and gloves), and protective barriers (e.g., leaded glass panels or drapes). Appropriate shielding of critical tissues (i.e., gonads, thyroid, lungs, breast, eyes, and bone marrow) from ionizing radiation is critical to the safe use of fluoroscopic equipment.3 In filtration, metal filters (usually aluminum) are inserted into the x-ray tube housing so that low energy x-rays emitted by the tube are absorbed before they reach the patient or medical staff. Beam collimation constricts the useful x-ray beam to the part of the body under examination, thereby sparing adjacent tissue from unnecessary exposure. It also serves to reduce scatter radiation and thus enhances imaging contrast. Protective apparel, such as a leaded apron ≥0.5 mm Pb, is mandatory to reduce exposure to the physician and technologist.3 Such shielding decreases radiation exposure by 90% to critical body areas.4 Lead-impregnated leather or vinyl aprons and gloves may be ordered in different thicknesses ranging from 0.55 mm Pb protection, which protects at 80 kVp, to 0.58 mm Pb, which protects at 120 kVp.5 The use of a leaded thyroid shield also is recommended because of the superficial location and sensitivity of the thyroid gland and to protect a limited amount of cervical bone marrow. Protective, flexible lead-lined gloves also may reduce exposure without sacrificing dexterity; however, their use is no substitute for vigilant avoidance of direct x-ray beam exposure.6 Leaded glasses or goggles will effectively eliminate approximately 90% of scatter radiation from frontal and side eye exposure. The leaded acrylic shields are made of clear lead equivalent to 0.3 mm Pb at 7-mm thickness. The lenses are leaded glass with a minimum thickness of 2.5 mm,



which creates a lead shielding with more than 97% attenuation up to 120 kVp.7 Clear, leaded glass x-ray protective barriers are available in several styles and shapes. They may be height-adjustable or full-height, floor-rolling radiation barriers or suspendable on an overhead track. They weigh between 100 and 400 lbs with lead thicknesses of 0.5 to 1.0 mm. When it is necessary to remain near the x-ray beam during a procedure, additional shielding should be used. Exposure Time To minimize exposure time to ionizing radiation, the clinician and radiologic technician need to work as a team. The technologist assists by optimally orienting the C-arm around the patient before beginning any kind of interventional procedure. The technologist also should ensure that the orientation of the C-arm is such that the x-ray tube is positioned directly under the patient to minimize scatter to that which is attenuated through the patient. The operator should minimize exposure time through the judicious use of the “beam on” controls (i.e., a foot or hand switch). If the technologist is responsible for the controls, then communication with the physician is critical to avoid unintended exposure. Training and experience of all personnel in the intricacies of complex procedures help to reduce unnecessary exposure. Fluoroscopic equipment may have features such as high- and low-dose modes, pulsed fluoroscopy,

2x Point source of X-rays

x d d



At d (1 meter), area = x2

At 2d (2 meters), area = 4x2

Figure 5-3  When the distance from a point source of radiation is doubled, the radiation covers an area four times larger than the original area. ­However, the intensity at the new distance is only one fourth of the original ­intensity. (From Statkiewicz MA, Ritenour ER: Radiation Protection for ­Student ­Radiographers. St. Louis, Mosby, 1983, with permission.)


Figure 5-2  The C-arm rotated to the anteroposterior projection (A), oblique projection (B), and lateral projection (C).


34  Basic Principles of Procedures Low kVp, high mAs

High kVp, low mAs X-ray tube

Table 5-2  Average Annual Effective Dose Equivalent of Ionizing Radiations to a Member of the United States Population Dose Equivalenta Source

High energy, penetrating X-ray beam

Low energy X-ray beam



Effective Dose Equivalent mSv


Natural Radonb




















Total natural



X-ray diagnosis





Nuclear medicine





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