Pain Procedures in Clinical Practice E-Book
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Pain Procedures in Clinical Practice E-Book

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En savoir plus
1290 pages
English

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Description

In the 3rd Edition of Pain Procedures in Clinical Practice, Dr. Ted Lennard helps you offer the most effective care to your patients by taking you through the various approaches to pain relief used in physiatry today. In this completely updated, procedure-focused volume, you’ll find nearly a decade worth of new developments and techniques supplemented by a comprehensive online video collection of how-to procedures at www.expertconsult.com. You’ll also find extensive coverage of injection options for every joint, plus discussions of non-injection-based pain relief options such as neuromuscular ultrasound, alternative medicines, and cryotherapy.

  • Offer your patients today’s most advanced pain relief with nearly a decade worth of new developments and techniques, masterfully presented by respected physiatrist Ted Lennard, MD.
  • Make informed treatment decisions and provide effective relief with comprehensive discussions of all of the injection options for every joint.
  • Apply the latest non-injection-based treatments for pain relief including neuromuscular ultrasound, alternative medicines, and cryotherapy.
  • See how to get the best results with a comprehensive video collection of how-to procedures at www.expertconsult.com, and access the complete text and images online.

Sujets

Ebooks
Savoirs
Medecine
Médecine
Spinal stenosis
Knee pain
SAFETY
Personality disorder
Meningitis
Procedural sedation and analgesia
Scapular fracture
Hepatitis B
The Only Son
Health system
Neck pain
Radiculopathy
Dislocated shoulder
Medical procedure
Supraorbital
Spondylolysis
Ilioinguinal nerve
Meralgia paraesthetica
Pain disorder
Nerve block
Radicular pain
Family medicine
Neuralgia
Prolotherapy
Manual therapy
Endoscopic thoracic sympathectomy
Acute pancreatitis
Postherpetic neuralgia
Tennis elbow
Electroacupuncture
Demyelinating disease
Bathing
Bursitis
Transcutaneous electrical nerve stimulation
Lower extremity
Coccydynia
Anesthetic
Generalized anxiety disorder
Regional anaesthesia
Stroke
Peripheral neuropathy
Glucocorticoid
Lumbar
Osteoarthritis
Ankylosing spondylitis
Physician assistant
Daughter
Fluoroscopy
Pain management
Dysmenorrhea
Arthralgia
Device
Anesthesiologist
Lesion
Tension headache
Fibromyalgia
Trigeminal neuralgia
Shoulder problem
Tendinitis
Tetralogy of Fallot
Whiplash (medicine)
Internal medicine
Osteopathic medicine in the United States
Physical exercise
U.S. Patients' Bill of Rights
Local anesthetic
Towel
Appendectomy
Ibuprofen
Back pain
Chronic pain
Medical ultrasonography
Dietary supplement
Common cold
Posttraumatic stress disorder
Headache
Carpal tunnel syndrome
Complex regional pain syndrome
Spine
X-ray computed tomography
Multiple sclerosis
Philadelphia
Informed consent
Coding
Risk management
Rheumatoid arthritis
Physical therapy
Paraffin
Magnetic resonance imaging
Major depressive disorder
Band
Arthritis
Anxiety
Yoga
Movement
Méthamphétamine
Tenderness
Code
Pneumothorax
Lead
Acupuncture
Injection
Force
Insomnia
Gout
Traction
Lombalgie
Service
Vertigo
Massage
Thorax
Death
Son
Copyright

Informations

Publié par
Date de parution 11 juin 2011
Nombre de lectures 3
EAN13 9781437737745
Langue English
Poids de l'ouvrage 3 Mo

Informations légales : prix de location à la page 0,0364€. Cette information est donnée uniquement à titre indicatif conformément à la législation en vigueur.

Exrait

Pain Procedures in Clinical Practice
Third Edition

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
Saunders
Front Matter

Pain Procedures in Clinical Practice
3RD EDITION
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
Copyright

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: www.elsevier.com/permissions .
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
Dedication
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
Contributors

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

William M. Boggs, MD, Center for Clinical Trials Research, University of Florida, College of Medicine, Micanopy, Florida

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

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

Peter M. Chanliongco, PT, President, Republic Physical Therapy, Republic, Missouri

Martin K. Childers, DO, PhD, Professor, Neurology, Wake Forest Institute for Regenerative Medicine Winston-Salem, North Carolina

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

Hongtao Michael Guo, MD, PhD, Assistant Professor, Neurology, Section of Physical Medicine and Rehabilitation, Wake Forest University School of Medicine, Winston-Salem, North Carolina

Dale A. Halfaker, 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

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, 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

Milton H. Landers, DO, PhD, 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

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

Aram Mardian, MD, Maricopa County Hospital, Phoenix, Arizona

Curtis Mattson, MS, 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

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

Joel M. Press, MD, Center for Spine, Sports, and Occupational Rehabilitation, Chicago, Illinois

Elmer G. Pinzon, MD, 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

Chunilal P. Shah, MD, MBBS, BS, Florida Spine Institute, Clearwater, Florida

C. Norman Shealy, MD, PhD, Professor Emeritus of Energy Medicine, Holos University Graduate Seminary, Bolivar, Missouri, President, Holos Institutes of Health, Inc, Fair Grove, Missouri

Julie K. Silver, MD, Assistant Professor, Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts

Aneesh K. Singla, MD, MPH, 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

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

Ajay D. Wasan, MD, MSc, Assistant Professor, Anesthesiology and Psychiatry, Harvard Medical School, Brigham and Women’s Hospital, Boston, Massachusetts

Robert E. Windsor, MD, FAAPMR, FAAEM, FASPM, Assistant Clinical Professor, Emory University, Department of Physical Medicine and Rehabilitation, President, Georgia Pain Physicians, PC, Marietta, Georgia; Forest Park, Georgia; Calhoun, Georgia

Ted L. Wunderlich, BA, 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
Preface
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
Table of Contents
Instructions for online access
Front Matter
Copyright
Dedication
Tribute
Contributors
Preface
I: Basic Principles of Procedures
Chapter 1: Fundamentals of Procedural Care
Chapter 2: Commonly Used Medications in Procedures
Chapter 3: Psychological Aspects of Pain
Chapter 4: Conscious Sedation for Interventional Pain Procedures
Chapter 5: Radiation Safety for the Physician
Chapter 6: Complications of Common Selective Spinal Injections: Prevention and Management
Chapter 7: Procedural Documentation and Coding
Chapter 8: Medicolegal Issues
II: Soft Tissue and Joint Injections
Chapter 9: Upper Extremity Joint Injections
Chapter 10: Lower Extremity Joint Injections
Chapter 11: Bursae Injections
Chapter 12: Tendon Sheath and Insertion Injections
Chapter 13: Trigger Point Injections
Chapter 14: Botulinum Toxin Injections in Myofascial Pain Disorders
III: Complementary and Alternative Medical Procedures
Chapter 15: Prolotherapy: A CAM Therapy for Chronic Musculoskeletal Pain
Chapter 16: Percutaneous Neuromodulation Therapy
Chapter 17: Medical Acupuncture
Chapter 18: Osteopathic Manipulative Medicine: A Functional Approach to Pain
Chapter 19: The Treatment of Pain Through Chinese Scalp Acupuncture
Chapter 20: Herbal and Nutritional Supplements for Painful Conditions
Chapter 21: Body Work and Movement Therapies
Chapter 22: Mind Body Therapies and Posttraumatic Stress Disorder
IV: Peripheral Nerve Blocks
Chapter 23: Basic Principles of Neural Blockade
Chapter 24: Ultrasound-Guided Nerve Blocks
Chapter 25: Suprascapular Nerve Block
Chapter 26: Sciatic Nerve Block
Chapter 27: Lower Extremity: Saphenous Nerve Block
Chapter 28: Lower Extremity: Lateral Femoral Cutaneous Nerve Block
Chapter 29: Genitofemoral Neural Blockade
Chapter 30: Ilioinguinal and Iliohypogastric Neural Blockade
Chapter 31: Intercostal Nerve Block
Chapter 32: Supraorbital Nerve Block for Supraorbital Neuralgia
Chapter 33: Head and Facial Trigeminal Neuralgia
Chapter 34: Occipital Neuralgia
V: Spine
Chapter 35: Epidural Steroid Injections: Cervical, Thoracic, and Lumbar: Transforaminal, Interlaminar, and Caudal
Chapter 36: Zygapophysial Joint Pain: Procedures for Diagnosis and Treatment
Chapter 37: Sacroiliac Joint Pain: Procedures for Diagnosis and Treatment
Chapter 38: Discography
Chapter 39: Discogenic Pain, Internal Disc Disruption, and Radicular Pain
Chapter 40: Intradiscal and Peridiscal Therapies for Discogenic and Radicular Pain
Chapter 41: Spinal Cord Stimulation and Implanted Intrathecal Drug Infusion
Chapter 42: Sympathetic Neural Blockade
Chapter 43: Imaging for Chronic Spinal Pain
VI: Physical Modalities for Pain Management
Chapter 44: Thermal Applications
Chapter 45: Cold (Cryo) Therapy
Chapter 46: Electrical Stimulation
Chapter 47: Traction
Chapter 48: Manual Therapy
Chapter 49: Therapeutic Exercises
Index
I
Basic Principles of Procedures
1 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 well-designed 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 hair 20, 21 or applying depilatory creams 19 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 results in pain. Lidocaine 23 - 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. Small-gauge 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 G.E. Red Flags . Oakland, Calif: American Back Society Newsletter; 1991. p 23
2. Carragee E.J. Psychological and functional profiles in select subjects with low back pain. Spine J . 2001;1(3):198-204.
3 Sebben J.E. Surgical antiseptics. J Am Acad Dermatol . 1983;9:759-765.
4. Masterson B.J. Skin preparation. Clin Obstet Gynecol . 1988;31:736-743.
5. Davies J., Babb J.R., Ayliffe G.A., Wilkins M.D. Disinfection of skin of the abdomen. Br J Surg . 1979;65:855-858.
6. Lepor N.E., Madyoon H. Antiseptic skin agents for percutaneous procedures. Rev Cardiovasc Med . 2009;10(4):187-193.
7. Ritter M.A., French M.L., Eitzen H.E., 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 D.V., Gehrmann R.M., Lin S.S. Chlorhexidine provides superior skin decontamination in foot and ankle surgery: A prospective randomized study. Clin Orthop Relat Res . 2005;438:204-208.
9. Calfee D.P., Farr B.M. 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 E.J., Lilly H.A. Use of 4% chlorhexidine detergent solution (Hibiscrub) and other methods of skin disinfection. Br Med J . 1973;1:510-515.
12. Saltzman M.D., Nuber G.W., Gryzlo S.M., et al. Efficacy of surgical preparation solutions in shoulder surgery. J Bone Joint Surg Am . 2009 Aug;91(8):1949-1953.
13. Smylie H.G., Logie J.R., Smith G. From Phisohex to Hibiscrub. Br Med J . 1973;4:586-589.
14. Swenson B.R., Hedrick T.L., 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 T.G. 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 B.J., Chrisp D.B., Scrimgeour G., et al. Extensive pre-operative shaving: A costly exercise. N Z Med J . 1984;97:727-729.
18. Celik S.E., Kara A. Does shaving the incision site increase the infection rate after spinal surgery? Spine . 2007;32(15):1575-1577.
19. Seropian R., Reynolds B.M. 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 M.M., MacCallum J., McQuarrie D.G. 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 J.R. Local anesthetics: Injection techniques. Emerg Med News . 1992 March:9-16.
25. Stewart J.H., Chinn S.E., Cole G.W., et al. Neutralized lidocaine with epinephrine for local anesthesia – II. J Dermatol Surg Oncol . 1990;16:842-845.
26. Xia Y., Chen E., Tibbits D.L., 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 P.R. 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 R.W., Whish D.K. A controlled trial of pain on skin infiltration with local anaesthetics. Anaesth Intensive Care . 1984;12:113-114.
30. Varelmann D., Pancaro C., Cappiello E.C., Camann W.R. Nocebo-induced hyperalgesia during local anesthetic injection. Anesth Analg . 2010;110(3):868-870.
31. Bloom L.H., Scheie H.G., Yanoff M. The warming of local anesthetic agents to decrase discomfort. Ophthalmic Surg . 1984;15:603.
32. Mark L.C. 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.
2 Commonly Used Medications in Procedures

Susan J. Dreyer, MD, 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. Para-aminobenzoic 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 pK a s 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 CO 2 (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. CO 2 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 pK a 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 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
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 ).

Table 2-2 Comparison of Commonly Used Glucocorticoid Steroids ∗

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.
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 steroid. 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 events 29 - 31 and this must be taken into consideration. The choice corticosteroids 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 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, blood-brain 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 H 1 and H 2 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 Synvisc-One (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 (<1% to 30%) and local skin reactions (3% to 21%). A pseudoseptic reaction can occur but is uncommon (1% to 3%). 75
In summary, viscosupplementation is FDA approved for knee osteoarthritis. Randomized controlled studies have demonstrated that it is superior to placebo but the clinical effect appears to be small to modest. Some of these studies suggest that it is as efficacious as the use of NSAIDs. When other conservative measures fail or are not an option, viscosupplementation may be a viable alternative for knee osteoarthritis.

Treatment of Medication Adverse Reactions
Medication adverse reactions can be minimized by careful patient selection and vigilance during the procedure. However, it is impossible to completely eliminate the possibility of allergic or other reactions and the practitioner must be prepared to deal with these emergency situations. Immediate access to and familiarity with emergency medications and protocols is critical.
Minor medication reactions can be treated with observation to ensure symptoms do not worsen. Moderate reactions can be treated in the procedure area and do not require hospitalization. These reactions include symptomatic urticaria, bronchospasm, and vasovagal reactions. Symptomatic urticaria can be treated with 25 to 50 mg of diphenhydramine IM. Bronchospasm should be treated with supplemental oxygen by nasal cannula and O 2 saturation monitoring, intravenous access, and electrocardiogram monitoring. If needed, a beta agonist inhaler can be administered as long as bronchospasm has not worsened to laryngotracheal edema. Epinephrine 1:1000 is sometimes required in doses of 0.1 to 1 mL subcutaneously. In refractory bronchospasm and more severe reactions of laryngotracheal edema or symptomatic facial edema, intravascular epinephrine 1:10,000 is given in doses of 1 to 3 mL.
Vasovagal reactions are heralded by symptomatic bradycardia and hypotension. With early reaction these symptoms can often be aborted with simple measures of reassurance, leg elevation, and intravenous fluids. Vital signs must be monitored and supplemental oxygen should be initiated promptly if oxygen saturation begins to drop. For more severe vasovagal reactions, drops in blood pressure and pulse can be treated with atropine 0.3 to 0.5 mg IV given incrementally up to 2 mg. Vasovagal reactions with hypotension and bradycardia must be distinguished from anaphylactoid or cardiac reaction where the hypotension is associated with tachycardia.
Toxic convulsions may be treated with oxygen, airway management, and diazepam 1 to 10 mg intravenously in 1 mg increments. Hospitalization is recommended along with appropriate consultation. Cardiopulmonary arrest should be treated following standard advanced cardiac life support protocols: assess vital signs, secure airway and oxygenation, begin resuscitation, ensure intravenous access, follow appropriate treatment algorithm. After successful resuscitative attempts, the patient should be hospitalized for observation and any necessary treatment.

Conclusion
Pain physicians commonly use a core group of medications for their procedures. It is imperative the injectionist has a solid understanding of these agents to maximize benefit and minimize risk. Integration of injection procedures in appropriately selected patients increases the physician’s effectiveness.

References

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3 Psychological Aspects of Pain

Dale A. Halfaker, PhD, Steven T. Akeson, PsyD, Danielle R. Hathcock, MS, Curtis Mattson, MS, Ted L. Wunderlich, BA
The evolution of the definition of pain and the influence of the importance of various biopsychosocial factors can be observed through various theories, all of which attempt to provide a better understanding of the process of pain. One universal assumption held by each of these theories is of pain as a subjective experience, meaning that each individual may subjectively feel, experience, and interpret the meaning of their pain uniquely.

Models of Pain

Gate-Control Theory of Pain
The first major modernized medical model theory of pain, the gate-control theory, emphasized the close interaction between psychosocial and physiologic processes. The gate-control theory of pain describes how thoughts, feelings, and behavior affect pain. 1, 5 The hypothesis is that a “gate,” located within the human brain, determines the individual’s impression of pain. The gate may be opened or closed—this determines the amount of pain the individual experiences. The underlying assumption is that the pain message originates at the site of aggravation, the signal is transmitted to the brain, and the pain is then brought into the individual’s awareness.
There are many ways in which an individual may “open” or “close” the gate. Using coping strategies may close the gate (meaning that the brain will either not recognize or give credence to the pain signal), while allowing oneself to focus on thoughts of pain may open the gate (bringing the pain signal into the brain’s awareness). Negative thinking, nonconstructive, pessimistic thinking may also open the gate, as will stress, anxiety, tension, helplessness, anger, hopelessness, and despair.
The ultimate conclusion from this theory is that the process of pain can therefore be mediated by changing the way an individual cognitively processes the pain experience. This theory is often useful in clinical practice as a means of explaining pain to patients, and aids the clinician in treating pain via cognitive therapy; however, the scientific community has demanded a more comprehensive theory that accounts for the neurophysiology, neurotransmission, and opioid receptors that may all be involved in understanding and defining pain. This demand was the precursor to the neuromatrix model of pain.

Neuromatrix Model of Pain
The term neuromatrix refers to the neural network involved in the perception of pain. The neuromatrix theory integrates physiologic and psychological evidences, and assumes pain to be a multifaceted experience, with pain sensations produced by specific patterns of nerve impulses generated by a widely distributed neural network.
The neuromatrix model may be viewed as a diathesis-stress approach, meaning that predispositional factors interact with acute stressors to result in a pathologic state. The experience of pain might be thought of as such a stressor. Further explained, the theory proposes that when an organism is injured, there is an interruption of homeostatic regulation. This disruption is not only physically stressful, but it also creates psychological stress. This in turn initiates a complex response aimed at restoring homeostasis (homeostasis being the previously nonpainful state of the body). This process of homeostatic restoration can add further physical and psychological stress.
Physiologically, the body may experience deleterious effects, such as immune system suppression, hypertension, and physical discomfort such as stomach pains or heart burn. The psychological aspects of pain result in the body activating the limbic system. The limbic system plays an important role in experiencing and regulating emotions, motivation of actions, and contributes to thought patterns. In the case of pain, one’s subjective interpretation of the pain experience, fear, and anxiety all further remove the body from homeostasis. Thus, once pain is established and the body activates the necessary mechanisms to return to homeostasis, any future or additional experience of pain will be physiologically and psychologically viewed as a continual threat that creates harmful demands on the body. Thus, a cycle develops that contributes to and maintains the pain-stress process. The neuromatrix hypothesis suggests that an individual’s unique genetic makeup and his or her own subjective experience of pain are the chief components that determine the nature of the pain the organism will experience and is the basis for individual differences in the pain experience.
Both the gate-control theory and the neuromatrix model have attempted to integrate and define a great deal of psychological and physiologic scientific data, although it is thought neither of them provides a fully adequate theory to define the pain experience. They do, however, point to what is currently the most promising approach to understanding pain: the biopsychosocial approach. This approach views physical disorders, including pain, as the result of a dynamic interaction between physiologic, psychologic, and social factors that can heavily influence a subject’s clinical presentation.

Biopsychosocial Model of Pain
In an effort to explain why individual experiences of pain are unique, the biopsychosocial model examines how psychological, social, and economic factors can interact with physical pathology to modulate a patient’s report of symptoms and subsequent disability. This understanding has been the foundation for a major paradigm shift in the assessment and management of pain, moving away from a traditional biomedical reductionist approach to this more comprehensive biopsychosocial approach. In fact, this paradigm shift is so dramatic that it has resulted is a mandate from the Joint Commission on the Accreditation of Healthcare Organizations requiring physicians to consider pain as a fifth vital sign. The Pain Care Bill of Rights of the nonprofit American Pain Foundation calls for management of all types of pain, both malignant and nonmalignant.
In order to understand pain in view of the biopsychosocial model, it seems helpful to examine the distinction between disease and illness. The term disease is generally used to define “an objective biological event” that involves the disruption of specific body structures or organ systems, caused by anatomic, pathologic, or physiologic changes. Illness, in contrast, is generally defined as a subjective experience or self-attribution of disease being present. An illness will yield physical discomfort, behavioral limitations, and psychosocial distress. Therefore, illness references how a sick individual and members of his or her family live with and respond to symptoms and their resulting disabilities.
To illustrate this distinction between disease and illness is analogous to the distinction made between nociception and pain. Nociception involves the stimulation of nerves that convey information about tissue damage to the brain. Pain, however, is a more subjective perception that is the result of the transduction, transmission, and modulation of sensory input, and may be filtered through an individual’s genetic composition, prior learning history, current physiologic status, and sociocultural influences. The combination of the physiologic experience of pain and the debilitating behavior that can accompany it are the expressions of suffering and pain behavior.
Based on this notion, it is thought that pain cannot be comprehensively assessed without a full understanding of the person who is exposed to the nociception. The biopsychosocial model focuses on illness. With this perspective, diversity in pain behavior can be expected as illness experience varies from person to person. This may include severity, duration, and psychological consequences. The interrelationships among biologic changes, psychological status, and the social and cultural context all need to be taken into account in fully understanding the pain patient’s perception of and response to illness. A model or treatment approach that focuses on only one of these core set of factors will be insufficient to effectively assess and treat the patient. The biopsychosocial model has consistently demonstrated the heuristic technique in treatment. 2
When interpreting pain using the biopsychosocial model, clinicians should be aware that each of the three constructs in the model are different in their composition. Therefore, their assessment will be accomplished through different means and processes. Pain likely should be viewed longitudinally as an ongoing, multifactorial process in which there is dynamic interplay between the biologic, psychological, and social cultural factors that shape the experience and responses of patients. 2, 5
To comprehensively assess pain, it is important to account for potential interactions in the process of prescribing the best treatment regimen, individualized for a particular patient with pain. For example, a patient may present with pain resulting from an earlier accident that produced severe musculoskeletal injuries, such as bone fractures and ligament tears, that have not completely healed. In addition to these physical injuries and resultant pain, the accident may have led to the inability to return to work. The patient might also have self-esteem problems because he or she is viewed as being disabled and is stigmatized by this situation. This may have resulted in economic problems and stressors because of the sudden decrease in income. There are debts to be paid, causing family stress, turmoil, and guilt. If this patient comes from a culture in which work and activity are highly valued there may be even more psychosocial distress. Thus, there are potentially multiple levels of psychosocial stressors that all need to be assessed and considered before one can develop a comprehensive pain management program for a patient who may not be responding to conventional or conservative care as might be expected.
Another model outlined four dimensions associated with the concept of pain: (1) nociception (2) pain (3) suffering and (4) pain behavior. 3, 5 Nociception refers to the actual physical units that might affect specialized nerve fibers and signal the central nervous system that an aversive event has occurred. This may include chemical irritant, physical/mechanical, or thermal pain. Pain is the sensation arising as the result of perceived nociception. However, this definition is overly simplistic because sometimes pain is perceived in the absence of nociception. An example of this would be phantom limb pain. On the contrary nociception has been recorded to occur without being perceived, such as an individual who is in shock after experiencing a very severe injury. Nociception and pain act as signals to the central nervous system. Suffering is a reaction to these signals that can be affected by past experiences as well as anticipation of future events, and refers to the emotional association with it, such as fear, threat, or loss. 3 Because of a specific painful episode, anxiety and depression may develop as a consequence to the pain behavior. Pain behavior refers to things that individuals do when they are suffering or currently experiencing pain. For example, a person may avoid driving after experiencing an injury due to an accident. The implications for pain behavior can range from avoiding certain activities to more debilitating problems such as developing generalized anxiety surrounding any activity the person must participate in to have a functional life. As such, the interaction in the range of biopsychosocial factors can be quite broad. There are times when the nature of the patient’s response to treatment may have less to do with the objective physical condition than it does with their psychological receptivity to treatment as well as their expectations. This is the grist for the mill of the psychological evaluation and psychotherapy-related treatment process of the person with pain.

Psychological Evaluation
Because of the biopsychosocial complexity associated with pain, pain-related psychological evaluation can be helpful in cases in which symptoms are in excess of expectation or do not correlate with known physiologic processes. Psychological factors may be producing delayed recovery of function or preventing the individual from otherwise benefiting from appropriate medical treatment which, if identified, can improve the treatment process and the ultimate outcome of the case.
If psychological factors are identified as moderating or mediating the patient’s pain-related behavior, it can result in treatment recommendations that remove or ameliorate the barriers to improvement and recovery. Thus, it is thought to be helpful for treating physicians to have a basic understanding of the pain-related psychological evaluation and treatment process.
The psychological evaluation of patients with pain begins with the establishment of rapport with the individual to be assessed. In a psychology practice it is not unusual to initially encounter a patient with pain who enters the evaluation room defensively at best and offended, angry, and/or suspicious at worst. The patient with pain may interpret the pain-related psychological consultation to imply the referral source believes their problems are not real or that their complaints are psychogenic in origin. For this reason, in addition to addressing issues of informed consent and establishing rapport with the patient, there is usually a need to provide some education as to the purpose of the evaluation and how biopsychosocial variables fit into the clinical picture and subjective situation of the patient’s life.
It can be extremely helpful for the referring physician to approach the referral for a pain-related psychological evaluation in a sensitive, compassionate manner. We suggest initially explaining to patients that the dualistic view in which the mind and body are separate does not appear to hold true, and that there is a dynamic, interdependent relationship between the individual’s psyche and their physical condition. We have found it makes sense to our patients when we explain our goal to be to treat the whole person and that we want to ensure they are as psychologically and mentally fit as they can be while they are in the process of physically rehabilitating and becoming more physically fit following an injury or in treating their painful condition.
The basic purpose of the pain-related psychological evaluation is to answer the questions posed by the referral source as clearly as possible. Often, if no referral questions are forwarded with the referral, the consulting psychological examiner may need to call the referral source to clarify if there are any specific issues that need to be addressed in the evaluation. Another goal of the evaluation is to generate psychological and behavioral information that is helpful to the referral source in understanding the psychological issues in the case and promotes the care in a more efficient and effective manner. The psychological evaluation documents and preserves a record of the assessment for use in the future and may provide a baseline or outcome information regarding progress. Ultimately, appropriate diagnosis leading to specific, practical, and functional recommendations that advance the patient’s care in a meaningful way become the goal for appropriate evaluation. 4
To achieve the purposes of the evaluation, sufficient records need to be gathered and reviewed to provide an understanding of the medical issues and physiologic underpinnings of the case. A comprehensive clinical interview is necessary to elicit historical information about the onset and history of the pain, injuries, and background that may be psychologically contributing to the onset, severity, exacerbation, or maintenance of the pain. Opportunities for behavioral observation when the patient may or may not be aware he or she is being observed provide excellent data regarding the consistency of subjective complaints. Psychological testing can provide data derived from standardized samples of behavior that are quantifiable and illustrate how the individual being evaluated deviates from a normative base related to the concepts that are being assessed.
The clinical interview in these cases tends to be comprehensive in nature and covers important factors that can serve as potential barriers to recovery. Important topics for the clinical interview should likely include an understanding of the person’s cultural and ethnic background, because various cultures deal with issues of pain differently. The individual’s own personal and familial history of mental health problems should be explored to include issues of depression, anxiety, problems dealing with reality, and substance use. How the patient may have previously dealt with illness and injury may shed light on their ability to cope or the models for coping they may have witnessed in the past.
The individual’s cognitive capacity, level of intellectual functioning, ability to understand the nature of their condition, treatment options, and likely outcomes are important features to understand because they have bearing on how compliant, anxious, depressed, and motivated the individual may be in completing their treatment regimen. Contemporaneous stressors that the person may be experiencing in addition to their injury, illness, or painful condition for which they are being assessed will be important to explore to evaluate how taxed their resources are and also may provide necessary information regarding potential sources of secondary gain that may be promoting abnormal illness behavior.
The exploration and history obtained during the psychological clinical interview should likely also provide information about spousal availability or family solicitousness that may be unnecessarily reinforcing pain behaviors. Work history, prior work-related injuries, job changes or losses, and job dissatisfaction are important variables to survey as such factors may be either pressuring and propelling the person toward or repulsing them from relinquishing the disabled role and maintaining symptoms.
An awareness of issues involving litigation, finances, and availability of disability compensation can be important to understanding prolonged disability. Other significant pieces of psychosocial history that should be explored include the individual’s educational achievement, military service record, marital or relationship background, legal history, substance use patterns and habits, history of abuse, and available support systems.
The pain-related psychological evaluation must adequately cover the full range of issues that have bearing on the individual’s behavior. These will typically include affective disturbances, anxiety disorders, psychotic features, characterologic pathology, somatoform presentations, substance use factors, and magnified or feigned symptoms. Because the expanse of this evaluation casts a broad net, it is not unusual for such an evaluation to be composed of multiple psychological measures.

Screening versus Objective Personality Tests
One may also use a stepwise approach to psychologically pain-related evaluation that proceeds from global indices of emotional distress and disturbance to a more detailed evaluation of the most important interactive factors of the diagnosis that may include Axis I clinical disorders and Axis II personality disorders. 5 There are two basic types of psychological instruments that can provide useful information when working with pain patients: screening tests and objective personality tests. Some screening tests can assist persons in describing, characterizing, and quantifying pain. Other screening tests can be used to identify conditions that may complicate the course of treatment and need further treatment or evaluation. However, screening tests are typically overly sensitive, are obvious in their intent, and lack validity measures. The advantages of screening tests include: they are inexpensive, quick, and patients typically understand their purpose. Objective personality tests can provide a broader, more detailed evaluation of a patient’s functioning, but they are lengthy and require specialized training to interpret. Objective tests have greater validity and reliability than screening tests.

Pain Rating Scales
There are a number of different pain rating scales in use, many of which have been modified for a specific type of clinical setting (orthopedic, rheumatology, oncology, etc.) or specific type of problem (headache scale, neck scale, low back pain scale, etc.). The simplest and most widely used is the Numerical Pain Rating Scale (NPRS) which asks patients to rate their pain from 0 to 10 with 0 indicating no pain and 10 indicating maximum pain. 6 In some instances, clinicians will ask the patient to rate their worst pain level and best pain level in the last 30 days, as well as a range of their typical pain level. A pain level of 6 with one patient is not the same as a 6 with another patient because some are more stoic and others more catastrophizing. However, it does allow for some degree of comparison of a single patient over time. Many physicians and therapists will list the Numeric Pain Rating on each contact note to facilitate comparison over time.

Visual Analog Scale
The Visual Analog Scale (VAS) is a 10 cm line with anchor statements on the left (no pain) and on the right (extreme pain). The patient is asked to mark their current pain level on the line. They can also be asked to mark their maximum, minimum, and average pain. The examiner scores the VAS by measuring the distance in either centimeters (0 to 10) or millimeters (0 to 100) from the “no pain” anchor point. The scores tend to correlate with numerical ratings but some researchers have suggested the Visual Analog Scale is more sensitive to minor changes in pain because it can be measured in millimeters and therefore demonstrate pain changes from 47 to 53, which would both be a 5 on the Numeric Pain Rating scale. 7 However, there is no research to support that the Visual Analog Scale is any more accurate when measured in centimeters than it is when it is measured in millimeters nor is there any research on what would represent a reliable change on the VAS. This suggests that the difference in the example between a 47 and 53 is probably not significant and is appropriately viewed as equivalent pain ratings.

FACES Pain Rating Scales
The Wong-Baker FACES Pain Rating Scale and Faces Pain Scale- Revised (FPS-R) were both developed to assist children in rating pain. They both show six faces in different degrees of distress. The FACES scale starts at 0 with the statement “No Hurt” under a face with a broad smile and continues to 5 with the statement “Hurts worst” and a face with a frown and tears. The FPS-R is similar but the point totals increase in increments of 2 instead of 1 (0 to 10). The FPS-R does not include tears on the faces because they do not want to contaminate the pain rating with an emotional rating. Both scales have been used successfully and are preferred over the NPRS and VAS with children.

McGill Pain Questionnaire
The McGill Pain Questionnaire (MPQ) is a list of 78 words divided into three domains (Sensory, Affective, and Evaluative) and 6 words for current pain intensity. While the validity of the domains and the MPQ has been called into question by some researchers it continues to be one of the most extensively used pain measures in research and clinical practice. While the quantitative value of the McGill is open for debate the qualitative value is clear. Melzack identified and organized the lexicon of pain in a manner that made it accessible to patients and professionals. Within the three domains are a total to 20 subcategories each containing from 3 to 6 descriptive words. The first domain (sensory) containing subcategories 1 to 10 includes 42 descriptors; the second domain (affective) containing subcategories 11 to 15 includes 14 descriptors; the third domain (evaluative) containing subcategory 16 includes 5 descriptors; and subcategories 17 to 20 are miscellaneous items that contain 17 descriptors. Each subcategory receives a numeric score equal to the rank order of the highest descriptor chosen. For example subcategory 1 includes the following words with the numeric value in parentheses: Flickering (1), quivering (2), pulsing (3), throbbing (4), beating (5), and pounding (6). Subcategory 2 includes the following words with the numeric value in parentheses: Jumping (1), flashing (2), and shooting (3). If the patient identifies “pulsing” and “shooting” each subcategory would have a numerical value of 3 despite “pulsing” being the third of six choices and “shooting” being the third of three choices. The subjective ordinal nature and varied number of items in the subcategories decreases the psychometric soundness of the MPQ. Likewise, the sensory domain has a range of scores from 0 to 42, the affective domain has a range of scores from 0 to 14, the evaluative domain has a range of scores from 0 to 5, and the miscellaneous items can account for 0 to 17 points. As a result of the varied relative contribution of each domain they are not able to be directly compared in a quantitative manner. The domains and miscellaneous items are summed to determine the Pain Rating Index (PRI) and another set of 6 descriptors is provided to identify the Present Pain Index (PPI). Despite the statistical limitations of the MPQ the Pain Rating Index (PRI) and Present Pain Index (PPI) do appear to have high clinical and research utility. They can provide an ipsative comparison for each patient in a test-retest format and allow for a quick point of reference on each patient contact if the PPI is used alone. The descriptors provide an inclusive lexicon of pain quality which makes communication between patient and clinician more accurate and can aid with identifying pain etiology. However, the complexity of the terms can be a problem for patients of lower IQ and other measures should be used in cases of below average IQ. 8
The MPQ short-form is a modified version that provides a brief (2 to 5 minutes) alternative to the MPQ (10 to 15 minutes). 9 It consists of 15 descriptive words taken from the MPQ subcategories with a Likert scale of 0 to 3 next to each word. The 15 descriptors consist of 10 words and 1 set of combined descriptors (Hot-Burning) from the Sensory Domain and 2 words and 2 sets of combined descriptors (Tiring-Exhausting and Punishing-Cruel) from the Affective Domain. The possible range of scores is 0 to 45. The MPQ short-form also includes the Present Pain Index (PPI) and a Visual Analog Scale (VAS). The short-form has been shown to have high correlations with the original McGill Pain Scale.

Oswestry Low Back Pain Disability Questionnaire
The Oswestry Low Back Pain Disability Questionnaire (ODQ) 10 is a 60 item patient questionnaire which assesses the amount of restriction pain imposes on 10 domains (Pain Intensity, Personal Care, Lifting, Walking, Sitting, Standing, Sleeping, Sex Life, Social Life, and Traveling). 11 The Revised version of the ODQ replaced the domain Sex Life with the domain Changing Degree of Pain. While the test items have an average Flesch-Kincaid Grade Level of 5.3 the instructions are written at a Flesch-Kincaid Grade Level of 11.7. Consequently it is important to read the instructions to patients with limited reading skills and to make sure they understand the instructions. Both versions are administered and scored the same way. The patient is asked to identify which of six statements in each domain applies to them at the time of evaluation. The sentences are arranged from no impairment (0) to maximum impairment (5). The scores for each domain are added together (range from 0 to 50) and multiplied by 2 which yields a Disability Index Score percent. If not all items are completed, the score is prorated by averaging the items completed and then multiplying it by 10. A Disability Index Score of 0% to 20% equals minimal disability, 21% to 40% equals moderate disability, 41% to 60% equals severe disability, 61% to 80% equals crippled, and 81% to 100% indicates a patient that is either bed-bound or exaggerating their symptoms. Scores greater than 40% suggest a more detailed investigation is warranted.

Other Screening Tests
Screening tests that are helpful in dealing with patients with pain-related disorders include not only those that directly address pain but also those that screen for conditions that frequently co-occur in pain patients or can complicate the patent’s course of treatment. This can include mood disorders, anxiety disorders, personality traits, and substance-related disorders.

Beck Depression Inventory
Common screening tests of depression include the Beck Depression Inventory (BDI), Zung Self-Rating Depression Scale (SDS), and Hamilton Depression Rating Scale (HAMD). The Beck Depression Inventory has been used since 1961 and is the most common depression screening instrument. The second edition was published in 1996 (BDI-II) and represents a revision that is more consistent with current diagnostic criteria for depression. The BDI-II consists of 21 items, for example, sadness, pessimism, worthlessness. All items, except two, have four statements of increasing intensity within the domain. For example under sadness the items start with “I do not feel sad.” and end with “I am so sad or unhappy I can’t stand it.” The first item has a score of 0 while the fourth item has a score of 3. The two items evaluating changes in sleeping patterns and changes in appetite have seven total statements, one with a value of 0 indicating no change and two items each for values 1, 2, and 3 indicating mild, moderate, and severe problems (both decreased and increased sleep and decreased and increased appetite). The range of possible scores is 0 to 63. BDI-II scores are classified as minimal (0-13), mild (14-19), moderate (20-28), and severe (29-63). 11, 12 The strength of the BDI-II is the ease of use, wide age range (13 years and older), low reading level (average Flesch-Kincaid Grade Level 3.6), and substantial body of research. The weaknesses of the BDI-II are typical in screening measures: no validity scales and high face validity allows persons to easily manipulate the total score.

Zung Self-Rating Depression Scale
The Zung Self-Rating Depression Scale (SDS) consists of 20 items with a Likert type scale after each item. The scores for each item range from 1 to 4 and the SDS ranges from a raw score of 20 to a raw score of 80. Some items are reverse scored (i.e., they go from 4 down to 1). It has not been as well researched as the BDI-II but has been used in clinical trials of antidepressant medications. It was developed in 1965 and had not been updated. The reading level is even lower than the BDI-II (average Flesch-Kincaid Grade Level 2.2). SDS scores are classified as normal (<50), mild depression (50 to 59), moderate to marked major depression (60 to 69), and severe to extreme major depression (>70). The raw score can be converted to an SDS Index score by multiplying the raw score times 1.25.

Hamilton Depression Rating Scale
The Hamilton Depression Rating Scale (HAMD) is completed by the clinician as opposed to the patient. It consists of 17 items with Likert scale of either 0 to 4 or 0 to 2. Scores can range from 0 to 54. The HAMD was developed in 1957 and has been used extensively within the medical community but is not typically used by psychologists. HAMD scores correlate well with BDI-II scores and can be used in place of a self-report when a patient is unable to read. It can also be used when there are concerns about the accuracy of the patient’s self-report. HAMD scores are classified as normal (<9), mild depression (10 to 13), mild to moderate depression (14 to 17), and moderate to severe depression (>17).

Beck Anxiety Inventory
The Beck Anxiety Inventory (BAI) consists of 21 items with a Likert scale ranging from 0 to 3 and raw scores ranging from 0 to 63. It was developed in 1988 and a revised manual was published in 1993 with some changes in scoring. The BAI scores are classified as minimal anxiety (0 to 7), mild anxiety (8 to 15), moderate anxiety (16 to 25), and severe anxiety (30 to 63). The BAI correlates highly with the BDI-II indicating that although the BAI may provide useful clinical information, it is not specific and can’t be used diagnostically. The reading level is even lower than the BDI-II (average Flesch-Kincaid Grade Level 2.3. Because the instructions for the BAI are written at an 8.3 grade level, oral instructions should be given to persons with lower reading skills.

Substance Abuse Subtle Screening Inventory
Substance abuse screening tests can provide useful information when working with patients with a history of alcohol or substance abuse. The Substance Abuse Subtle Screening Inventory—Third Edition (SASSI-3) includes a set of obvious items asking about drug use and alcohol use. If the person is unwilling to openly acknowledge excessive alcohol or drug use, there are other scales that can assist in evaluating possible abuse/dependence. The SASSI-3 includes the following scales: Symptoms (SYM), Obvious Attributes (OAT), Subtle Attributes (SAT), Defensiveness (DEF), Supplemental Addiction Measure (SAM), Family versus Control Measure (FAM), Correctional (COR), and Random Answering. The defensiveness and random answering scales are rudimentary validity scales. There is a decision tree that assists with diagnostic impressions.

Objective Personality Tests
A more comprehensive evaluation can be completed by a psychologist using objective personality tests. These tests must be interpreted by a psychologist and can provide significant information useful in the diagnosis and treatment of the patient with pain. The most commonly used and thoroughly researched objective personality test is the Minnesota Multiphasic Personality Inventory which is currently in its second edition (MMPI-2). There is also a recently published somewhat shorter restructured form (MMPI-2-RF) based on the MMPI-2. The Personality Assessment Inventory (PAI), Millon Clinical Multiaxial Inventory—Third Edition (MCMI-III), and Millon Behavioral Medicine Diagnostic (MBMD) are other less frequently used objective personality measures that can provide valuable information.

Minnesota Multiphasic Personality Inventory
The MMPI-2 is the most widely used and heavily researched psychological test in the United States. Originally developed in the late 1930s and revised in 1989, it currently consists of 567 true/false questions. The MMPI-2 items make up a number of scales including 10 standard validity scales, 10 clinical scales with 28 subscales, 18 supplemental scales, and 15 content scales. The MMPI-2 can be administered to patients 18 years and older and requires a 6th grade reading level. The adolescent version (MMPI-A) is administered to persons 14 to 18 years of age and is similar to the MMPI-2, but is not nearly as well researched. The MMPI-2 is used in medical, psychological, employment, and legal settings.
The MMPI-2 is valued as much, if not more, for its validity scales than it is for the clinical information that can be derived from it. The first validity scale addresses the number of items omitted, and is the raw score of items which have not been answered as either true or false. If the patient fails to complete too many items, it may invalidate the profile. The validity scales include measures that evaluate if the patient is nonresponsive to questions. This could be due to acquiescent (yea saying) or counter-acquiescent (nay saying) response sets as measured by the True Response Inconsistency (TRIN) scale. It could also be due to inconsistency between items of similar content as measured by the Variable Response Inconsistency (VRIN) scale. Elevations on either scale could be due to reading problems, motivational problems, or haphazard response sets. In cases of marginal elevations on VRIN, the data are viewed as less reliable and interpretation of elevated scales is more cautious.
Validity scales that suggest underreporting of pathology include scales in which a person is trying to present an overly virtuous image (L), a guarded presentation (K), and a highly confident/competent self-presentation (S). When these underreporting scales are elevated, it typically reflects minimization of symptoms. While this does not typically invalidate the MMPI-2, it can lead to a suppression of symptoms to the point that there are no clinically meaningful elevations on the test.
Validity scales that suggest overreporting of pathology include a series of scales that are composed of infrequently endorsed items. These are low base rate items which are primarily vague or nonspecific symptoms. Elevations indicate the patient is endorsing an inordinate number of these low base rate symptoms. These scales include the Infrequency Scale (F), Infrequency Back (Fb), and Infrequency Psychopathology (Fp). The F and Fb are similar scales but F items occur on the first 370 items and include more chronic symptoms, whereas Fb items occur after item 280 and include more acute symptoms. Elevations on the F and/or Fb scale can be due to any or all of the following reasons: (1) random or fixed patterns of responding which would lead to elevations on VRIN and TRIN, respectively; (2) accurate descriptions of severe psychopathology; and (3) purposely overreporting symptoms. While VRIN and TRIN can help rule-out random or fixed patterns of responding, it is more difficult to differentiate between severe psychopathology and purposeful overreporting of symptoms. The Fp scale was developed to assist in this determination. The Fp scale is composed of low base rate symptoms in an inpatient psychiatric population. The Fp scale is less sensitive than F to the presence of severe psychopathology.
The Fake Bad Scale (FBS) is described as having been devised to detect a model of goal directed behavior with a focus on appearing to be honest; appearing psychologically normal, except for the influence of the alleged cause of injury; avoiding admitting to preexisting psychopathology; where preexisting complaints are known, or suspected to have been disclosed to the examining clinician, attempting to minimize those complaints; hiding preinjury behaviors that are antisocial, illegal, or minimizing it if it appears the behaviors will be discovered independently; and presenting an extent of injury or disability within a perceived limit of plausibility (Lees-Haley, English, Glenn, 1991). The FBS continues to be a controversial scale, but the publisher of the MMPI-2 has recognized the FBS as a reported scale and includes it in the standard MMPI-2 report. By using the more conservative cutoffs of raw scores (24 for males and 26 for females) the concern of a high false-positive rate has been minimized. The existent literature indicates that raw scores above 28 on the FBS are associated with a very low false-positive rate. 13 Additionally, the literature suggests that increasing confidence is placed in scores as they rise above a cutoff of 30, with a number of studies noting that no nonlitigant, nonmalingering subjects had raw scores of 30 or above. 14
There are a number of less commonly used validity scales that are used by some researchers and clinicians. One particularly interesting additional validity scale is the Meyers Validity in Chronic Pain Index (Meyers Index) that uses a chronic pain population. 15 The developers combined seven different validity scales on the MMPI-2 into a common weighted method in assessing malingering in chronic pain patients. This weighted method was able to correctly classify 100% of nonlitigants using a cutoff score of equal to or greater than 5. That study suggested chronic pain patients in litigation produce a different profile on the MMPI-2 validity scales than do nonlitigants. The Meyers Index is calculated by assigning values of 0, 1, or 2 on seven validity scales based on the level of elevation on each scale. The Meyers Index score is classified as okay (0 to 2), exaggerated (3 to 4), malingered (5 to 8), and clearly malingered (9 to 14). The Meyers Index uses the following scales (F, FBS, F-K, Fp, Ds-r, Es, and O-S).
Once an MMPI-2 profile has been determined to be valid, the Clinical Scales and Subscales can be evaluated to provide information about the patient’s psychological and emotional functioning. The MMPI-2 retained the same 10 MMPI clinical scales including the scale names and numbers. Some of the scale names are antiquated (e.g., Psychasthenia) and as such are typically referred to by number or abbreviation. For example scale 2 is Depression and is generally called scale 2 or the D scale. The Clinical Scales were initially developed using a method known as empirical criterion keying and as such are not based on any specific theory or diagnostic criteria. Each clinical scale is a combination of items that a specific group (e.g., depressed patients) answered differently than the comparison group.
The fact that the MMPI-2 is not tied to a diagnostic system such as the DSM or ICD is an advantage and disadvantage. The advantage is the MMPI-2 does not change each time the diagnostic criteria are changed. This allows for comparison of MMPI-2 profiles across time and facilities research. The disadvantage is that the MMPI-2 does not provide and lend itself well alone to making a DSM diagnosis. For example, an elevation on scale 2, the Depression scale, does not indicate the presence of major depression. It could be depressive symptoms due to dysthymic disorder, grief, or depressive symptoms due to recent emotional stressors such as a severe work-related injury to a patient’s spouse. Consequently the MMPI-2 cannot be interpreted effectively in a vacuum and “blind interpretation” of the MMPI-2 tends to lead to interpretive statements which include a substantial amount of error within the interpretive statements. This suggests great care needs to be taken in dealing with blind, computer-generated interpretive reports.
Interpretation of profiles from medical patients using a psychological or psychiatric comparison group can lead to erroneous interpretations and misdiagnosis. Consider, for example, compiled MMPI-2 norms for a chronic pain population using 209 chronic pain inpatients. 16 The chronic pain patients scored significantly higher than controls on 9 of the 10 clinical scales. Traditional interpretive methods would over-pathologize the patients with chronic pain. Clinical Scales 1, 2, and 3 are the most frequently elevated scales in a chronic pain population. The typical chronic pain profile will present a “conversion V” or somatic profile. If these scales are elevated when compared with a chronic pain reference group then a somatization or conversion disorder may be present.
In addition to the Clinical Scales there are a number of other scales on the MMPI-2. Although these are less heavily researched than the Clinical Scales, they can still provide useful information. Additional scales include the Content Scales, Supplemental Scales, and Restructured Clinical Scales. The Content Scales include the following scales: Anxiety, Fears, Obsessiveness, Depression, Health Concerns, Bizarre Mentation, Anger, Cynicism, Antisocial Practices, Type A, Low Self-Esteem, Social Discomfort, Family Problems, Work Interference, and Negative Treatment Indicators. The Supplemental Scales include the following scales: Anxiety, Repression, Overcontrol-Hostility, Dominance, Ego Strength, Social Responsibility, College Maladjustment, MacAndrew Alcoholism-Revised, Addiction Admission, Addiction Potential, Marital Distress, PTSD, Gender Role—Masculine, and Gender Role—Feminine. The Content and Supplemental Scales are labeled using more contemporary labels, which typically do not require additional explanation.

MMPI-2 Restructured Form
The Restructured Clinical Scales are relatively new scales that show promise, but have not been fully evaluated in pain patients. The Restructured Clinical Scales also form the core of a new version of the MMPI-2 which is called the MMPI-2 Restructured Form (MMPI-2-RF). The MMPI-2-RF retains many of the positive features of the MMPI-2 in a shorter format, 338 items versus the 567 items of the MMPI-2. The MMPI-2-RF includes revised versions of many of the MMPI-2 validity scales, but does not include the traditional Clinical Scales. There a several promising aspects to the new MMPI-2-RF including a new validity scale that assesses for the presence of Infrequent Somatic Responses (Fs). There are also a number of problem-specific scales that focus on Somatic/Cognitive Dysfunction.

Personality Assessment Inventory
The Personality Assessment Inventory (PAI) is another objective personality measure. It is composed of 344 items with 4 possible responses for each item (False, Slightly True, Mainly True, and Very True). It consists of 22 scales including 4 validity scales, 11 clinical scales, 5 treatment consideration scales, and 2 interpersonal scales. The reading level (average Flesch-Kincaid Grade Level 4.1) is lower than the MMPI-2. There has been some research using the PAI in chronic pain settings that should increase the utility of the test. 17 The PAI addresses psychological disorders, personality disorders, and substance abuse disorders making it a very high utility test and an acceptable alternative to the MMPI-2 in some settings. The validity scales are not as well researched as the MMPI-2, which limits its use in medicolegal settings unless used in conjunction with other symptom validity tests.

Millon Clinical Multiaxial Inventory—Third Edition
The Millon Clinical Multiaxial Inventory—Third Edition (MCMI-III) is another frequently used objective personality measure. The MCMI-III provides information about the presence of psychological disorders including personality disorders. The MCMI-III is a 175-question, true/false psychological instrument used in clinical settings with individuals 18 years and older. The reading level (average Flesch-Kincaid Grade Level 5.7) is higher than the MMPI-2.
The normative population is composed of patients seen in individual practice, clinics, mental health centers, forensic settings, residential facilities, and hospitals. The MCMI-III uses “Base Rate” scores for the purposes of reporting and interpretation. A Base Rate (BR) score of 60 [BR60] represents the median score, as opposed to T scores where 50T is the median, with BR0 being the lowest possible score and BR115 the highest. The presence of a specific personality trait is generally indicated at BR75, whereas scores of BR85 and above suggests the full presence of a personality characteristic. Base rate scores are criterion, not norm, referenced—indicating that BR scores do not indicate if a score is common or not, only whether the trait or characteristic is present.
The MCMI-III has 28 scales including 14 Personality Disorder Scales, 10 Clinical Syndrome Scales, 4 Correctional Scales. The Personality Disorder Scales include: Schizoid, Avoidant, Depressive, Dependent, Histrionic, Narcissistic, Antisocial, Sadistic (Aggressive), Compulsive, Negativistic (Passive-Aggressive), Masochistic (Self-Defeating), Schizotypal, Borderline, and Paranoid. The Clinical Syndrome Scales include: Anxiety, Somatoform, Bipolar, Manic, Dysthymia, Alcohol Dependence, Drug Dependence, Post-Traumatic Stress Disorder, Thought Disorder, Major Depression, and Delusional Disorder. The Correctional Scales include: Disclosure, Desirability, Debasement, and Validity. The Personality Disorder Scales were designed to correlate with DSM-IV Axis II disorders, whereas the Clinical Syndrome Scales correlate with the DSM-IV Axis I disorders.
Another study examined the ability of the MCMI-III to be reliably used to assess intervention in pain management at a pain management center in Paducah, Kentucky. 18 One hundred consecutive patients were evaluated for major depression or generalized anxiety disorder using a DSM-IV-TR questionnaire and physician interview; all participants also completed the MCMI-III and P-3 inventories as part of a psychological evaluation. A positive diagnosis of major depression or generalized anxiety disorder, using the DSM-IV-TR criteria, was considered the criterion standard. The diagnosis of major depression on the MCMI-III showed 100% specificity but only 54% sensitivity; for generalized anxiety disorder, the MCMI-III specificity was 89%, whereas the sensitivity was 73%.

Millon Behavioral Medicine Diagnostic
The Millon Behavioral Medicine Diagnostic (MBMD) is a revised version of the Millon Behavioral Health Inventory (MBHI) and was designed to provide helpful information on a patients’ biopsychosocial health. The test aids in recommending potential treatment strategies and may help in proactively identifying potential pitfalls to treatment. The MBMD can be used with individuals 18 years to 89 years and requires a sixth grade reading level. Consisting of 165 true/false questions, the MBMD typically takes 20 to 25 minutes to complete. The MBMD allows the clinician to select one of two normative samples—a general medical sample and a sample of prescreened bariatric surgery patients.
The MBMD consists of 29 content scales, grouped into five domains, six negative health habits, and three scales to detect response patterns. The Content Scales include the following: 5 Psychiatric Indicators (Anxiety-Tension, Depression, Cognitive Dysfunction, Emotional Liability, and Guardedness); 11 Coping Styles (Introverted, Inhibited, Dejected, Cooperative, Sociable, Confident, Non-Conforming, Forceful, Respectful, Oppositional, and Denigrated); 6 Stress Moderators (Illness Apprehension, Functional Deficits, Pain Sensitivity, Social Isolation, Future Pessimism, and Spiritual Absence), 5 Treatment Prognostics (Interventional Fragility, Medication Abuse, Information Discomfort, Utilization Excess, and Problematic Compliance), and 2 Management Guides (Adjustment Difficulties, and Psych Referral). There are 6 Negative Health Habits (Alcohol, Drugs, Eating, Caffeine, Inactivity, and Smoking). There are 3 Response Patterns (Disclosure, Desirability, and Debasement).
Despite the success of the MBMD in assessing biopsychosocial health characteristics and treatment options, practitioners have been warned to be cautious when using the MBMD because limitations in clinical use may arise in specific populations. 19

Psychotherapy
In recent decades, studies evaluating the use of psychotherapy as a treatment option in patients with pain have significantly increased. Physicians, psychologists, and patients have become increasingly aware of mind-body connections and the utility of treating the psychological conditions that may both exacerbate, and result from, chronic pain. A variety of treatment models are available to the mental health professional to help patients manage symptoms and intensity, deal with the functional limitations that chronic pain may place on their lives, gain realistic expectations and coping skills, and be able to deal with any other preexisting psychological conditions that could hamper positive therapy outcomes.
In the treatment of the individual with pain, the therapist needs to address the patient’s expectations for treatment, not only to ensure that their expectations are realistic and achievable, but to offer hope to patients who may feel marginalized and distressed. One study involving three groups of people referred to a pain management clinic found that in all three groups, the persons referred described experiencing feelings of embarrassment, frustration, and lack of self-control. 20 The patients also reported they often felt others did not believe their pain and viewed physicians as attempting to “fob them off” by prescribing pain medication. A primary goal during the initial intake process and first sessions is to normalize the experience of patients’ emotions and assist them in establishing reasonable treatment expectations. As such, no “cure” that will allow the patient to be pain-free can be guaranteed, but a treatment plan can be developed in collaboration with the patient that will address the patient’s specific concerns and help them to better manage their pain symptoms and any associated psychopathology. It is important for the therapist to understand how the experience of pain has altered or affected the patient’s activities of daily living, occupational and social functioning, affect and mood, and family relationships.
Treatment approaches can be tailored to the variety found among chronic pain patients and evidence-based practice allows for adaptation to meet the needs of the individual patient. As discussed, the importance of assessing variables that may influence or mediate the patient’s experience of pain, personality characteristics, or preexisting psychological pathology or conditions may have a significant bearing on the nature and direction of the therapeutic process. 21 - 23 The treatment models discussed in this chapter are by no means an exhaustive list; they instead highlight methods that are research-based approaches and are broad enough to be used in a variety of contexts.

Cognitive—Behavioral Therapy
The most widely acclaimed and researched approach to psychological pain management is cognitive-behavioral therapy (CBT). Both cognitive and behavioral interventions to treat chronic pain have considerable empirical support. 24 A metaanalysis of 25 randomized controlled trials of CBT for pain management revealed CBT to produce “significantly greater changes for the domains of the pain experience, cognitive coping and appraisal (positive coping measures), and reduced behavioral expression of pain when compared with alternative active treatments.” 24 CBT emphasizes changing maladaptive patterns of thinking and feeling in response to the pain, and encompasses a wide range of strategies, including relaxation training, cognitive restructuring/reframing, distraction techniques, and stress management; goal-setting is also highlighted. Additionally, this treatment model can be used in individual or group settings, relies heavily on therapist-patient collaboration, and is considered an optimistic approach to pain management because it teaches the sufferer that his or her experience of pain can be mediated by changing his or her maladaptive beliefs. 25 For example, the therapist may teach relaxation techniques, challenge irrational beliefs and cognitive errors (such as thinking of themselves as helpless or their situation as hopeless), and place behaviors within the patient’s locus of control. CBT posits behavior as voluntary and not controlled by external events, and thus may offer the patient alternative courses of action.
Patient catastrophizing (i.e., a process of exaggerated worrying, acute distress, and helplessness in response to pain) has also been found to occur with consistent regularity among patients with chronic pain. 26 Restructuring the patients’ thoughts via cognitive-type therapy helped the patients to accept their pain and mediated the catastrophizing effects of pain when applied to such variables as depression, pain-related fear, and disability. It was concluded that although helping patients accept and not catastrophize pain did not lessen pain intensity, it did help these patients improve overall functioning and emotional well-being. 26
Although CBT may be considered the ‘gold standard’ for psychotherapy, research findings have substantial variability among outcome measures and invite speculation regarding the overall efficacy of CBT. 23 It therefore behooves clinicians to be familiar with other evidence-based approaches to tailor therapy to suit the needs of individual patients. Other such approaches include Coping Skills Development (CSD), Integrated Psychosocial-Spiritual Models, and mindfulness meditation. These may be used as singular interventions or in conjunction with other types of therapy.

Coping Skills Development
The CSD program is a “biopsychosocial model with emphasis on learning general coping skills primarily and pain coping skills secondarily.” 24 The overall goal of the program was to help the patients develop an internal locus of control through teaching and helping patients integrate four basic coping skills: self-determination, self-esteem, feelings, and exercise. Although CSD differs from CBT in that it has a broader focus (for example, CSD examines the roles of self-esteem and emotions), there is a definitive cognitive component of CSD that is quite similar to CBT: CSD rests on the premise that “people who think rationally and take responsibility for what they think and do, have good self-esteem, and recognize their true feelings and express them in reasonable ways can cope well despite most trying circumstances including chronic pain” 24 This hypothesis appears to be supported: post-treatment results indicated less pain severity, less pain interference, more life control, decreased levels of depression, and more hours of activity per day. At 1-year follow-up, there remained an overall decrease in the use of prescription narcotic medication, as well as fewer health care visits, indicating that the patients were better able to manage their pain with less dependence on medication and physicians. Additionally, the percentage of persons in work or in training had increased, and those on compensation had decreased. It is noteworthy, however, that this treatment was administered in a group format; there are no outcome studies for this approach when used in individual therapy.

Integrated Psychosocial—Spiritual Model
The Integrated Psychosocial-Spiritual Model was developed to manage cancer pain, and argues that a complex, multidimensional treatment approach is necessary to effectively treat a complex, multidimensional problem such as cancer pain. 27 This model adopts a holistic approach, addressing several aspects of pain, including emotions, cognitions, social factors, behaviors, and spiritual concerns. The authors contend that each of these factors is influenced by pain, and all must be treated or addressed to create a robust therapeutic outcome.

Mindfulness Meditation
Mindfulness meditation is yet another treatment approach that can be successful for the patient with chronic pain. Mindfulness meditation promotes strategies that support emotional regulation through awareness of, and change in, dysfunctional thoughts. It also enhances positive emotions through awareness of positive states, a piece missing from traditional CBT. This model specifically targets the patient’s ability to relate differently to the thoughts and feelings associated with periods of negative affect, and to interrupt the automatic responding that often occurs in these states. Researchers who use this model have been able to highlight the necessity of assessing and considering preexisting psychological conditions that may influence therapy outcomes. For example, one study compared the efficacy of CBT and mindfulness meditation in treating patients with rheumatoid arthritis (RA). 21 The researchers assessed history of recurrent depression, formed groups based on this variable, and then assigned these groups to one of three treatment methods: mindfulness-based emotion regulation therapeutic program (aimed at promoting awareness and change of meaning given to dysfunctional thoughts), CBT, or an education group that served as the control. They measured several outcome variables, including daily pain, positive and negative affect, depressive symptoms, coping efficacy for pain, pain catastrophizing, and pain control. The patients also submitted to physician assessments of joint-tenderness and provided blood samples to measure the production of IL-6 (the proinflammatory cytokine that is associated with joint destruction in RA patients). The outcome results revealed both of the methodologies (mindfulness meditation and CBT) to be useful, but in different ways. In this case, the mindfulness meditation approach proved to be more useful for those with a history of chronic depression, whereas CBT had better outcomes for those without a history of recurrent depression. For the recurrent depression group, the mindfulness intervention made a greater difference in reducing the perception of pain and enhancing positive affect.

Influence of Personality Factors
Personality factors can be another important therapeutic consideration in the treatment of patients with pain. Correlations between personality and therapy satisfaction support the notion that treatment satisfaction may be an important predictor of outcome for medical and psychological treatments, including chronic pain. 25 In using the NEO Five Factor Inventory and brief CBT, researchers found that “the core personality dimensions of neuroticism, openness, and agreeableness were predictive of aspects of satisfaction with therapy.” 23 Specifically, neuroticism negatively affected treatment satisfaction; whereas agreeableness had a statistically significant correlation with the individual viewing the therapy sessions as running smoothly (agreeable individuals are also more likely to participate in specific therapy components, such as ‘homework assignments’). Patients scoring higher on the Openness dimension tended to evaluate the sessions as having less depth, although the researchers believed this may have been due to these patients being more willing to participate in in-depth exploration, which was not available in the brief therapy format used in this study. Perhaps longer interventions might provide the depth these patients appear to seek. This study is also helpful because it highlights the effect of variables outside of the chronic pain itself that may influence therapy outcomes. It adds to the argument that treatment selection should meet the needs of the individual patients, which includes an assessment and integration of specific characteristics, including preexisting pathology and personality.

Modes of Therapy
When considering treatment, clinicians have the option of several modes of therapy, including group, individual, long-term, or brief. Group therapy is well supported in the literature and offers many advantages that may not be available in individual therapy. 28 - 30 These include helping to disconfirm common pain myths, giving members a sense of community and universality (thus, decreasing one’s sense of alienation and isolation), promoting shared catharsis, and providing members a forum in which to offer personal skills and pain management techniques. 31 Not all patients will be suitable for group therapy, either due to personality or if the patient issues are beyond the goals of the group. 30 Clinicians should screen patients for group in order to determine suitability, as well as be willing to transfer group members to individual therapy, when appropriate.

Family Considerations
It is logical that individuals with pain do not experience their pain in a relational vacuum and it is often helpful to understand the patient within the family context because the family shapes and is shaped by the transactional patterns of the family system. 32 Families, spouses, and friends are potentially affected as they may have questions as to how to help their loved one, and have to cope with possible role changes within the relationship. The patient with pain may require financial, emotional, and personal care. Clinicians must decide in collaboration with the patient, whether, and to what extent, to include family members in treatment. In some cases, family members will need to be brought into the therapy process because they may be unwittingly reinforcing abnormal illness behavior by being overly solicitous or sometimes a lack of emotional support and encouragement may be resulting in the patient feeling alone, alienated, rejected, and/or depressed. In such cases, if appropriate family members are not part of the treatment they may maintain or perpetuate the problems of the chronic pain sufferer. 31

Conclusion
As can be seen, the psychological assessment and treatment of pain is a complex, multidimensional process. The consulting psychologist can often provide useful information to the treating physician or augment medical treatment through the use of effective psychological assessment techniques and appropriate psychotherapy. Depending on the context of the referral, the role of the psychological clinician may include helping patients delineate the psychological aspects of their pain, dealing with family and emotional issues, and providing a sense of self-efficacy that goes beyond pain reduction. Such assessment and intervention may not only lead to a lessening of pain perception, but may also provide the patient a set of tools to function more fully, enjoy a better quality of life, and reach their highest level of functioning possible despite pain.

References

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3. Loeser J.D. Concepts of pain. In: Stanton-Hicks J., Boaz R., editors. Chronic Low Back Pain . New York: Raven Press; 1982:145-148.
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6. King S. The classification and assessment of pain. International Review of Psychiatry . 2000;12:86-90.
7. Kahl C., Cleland J.A. Visual Analogue Scale, Numeric Pain Rating Scale, and the McGill Pain Questionnaire: An overview of psychometric properties. Physical Therapy Review . 2005;10:123-128.
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9. Melzack R. The short-form McGill Pain Questionnaire. Pain . 1987;30:191-197.
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12. Beck A.T., Steer R.A., Brown G.K. BDI-II Manual . San Antonio, TX: The Psychological Corporation; 1996.
13. Ben-Porath Y, Tellegan A: MMPI-2 FBS (Symptom Validity Scale). Retrieved from Pearson Assessments for Clinical and Psychological Use, 2007.
14. Larrabee G.J. Assessment of malingering. In: Larrabee G.J., editor. Forensic Neuropsychology . New York: Oxford University Press, 2005.
15. Meyers J.E., Millis S.R., Volkert K. A validity index for the MMPI-2. Arch Clin Neuropsychol . 2002;17:157-169.
16. Slesinger D., Archer R.P. Duane, W: MMPI-2 characteristics in a chronic pain population. Assessment . 2002;9:406-414.
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18. Rivera J.J., Singh V., Fellows B., et al. Reliability of psychological evaluation in chronic pain in an interventional pain management setting. Pain Physician . 2005;8:375-383.
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20. Allcock N., Elkan R., Williams J. Patients referred to a pain management clinic: Beliefs, expectations, and priorities. J Adv Nurs . 2007;60:248-256.
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4 Conscious Sedation for Interventional Pain Procedures

Michael S. Leong, MD, Steven H. Richeimer, MD
Conscious sedation and analgesia are often overlooked aspects of interventional pain procedures. Patients expect to be comfortable during their injections. Physicians tend to concentrate more on the procedure with the sedation becoming secondary. However, when the procedure is not going smoothly, oversedation and analgesia can add problems, such as interpreting paresthesias, intraneural injections, and even loss of airway reflexes—particularly problematic at outpatient surgery centers where airway specialists may not be available.
The authors of this chapter are board-certified anesthesiologists and pain medicine specialists. It may be interesting to note that the optimal sedation and analgesia seems to be the least amount possible! One of the caveats of anesthesia training is that sedation and analgesia can always be titrated to effect for the individual patient. Although anesthesiologists can induce the full spectrum of sedation including general anesthesia, most elective pain procedures require far less.
The following chapter is for safety guidelines and recommendations and not a “cookbook” on set dosages for sedation and analgesia. Appropriate preparation of the patient, procedural facility, medical support teams, and physicians with procedural techniques can make the scheduled interventions safe and relatively “pain-free” for everyone involved.

Conscious Sedation
Conscious sedation is an older term from 1985 to describe lightly sedated dental patients. 1 It is defined as the sedation depth that permits appropriate response to physical stimulation or verbal command (e.g., “open your eyes”). Many groups, including the American Association of Anesthesiology and American College of Emergency Physicians believe that the term conscious sedation is imprecise and they propose terms such as sedation/analgesia 2 or procedural sedation and analgesia (PSAA), 1 or monitored anesthesia care (MAC). 3 Indeed, in the first ASA guidelines from February 1996, a notable comment is that patients whose only response is reflex withdrawal from a painful stimulus are sedated to a greater degree than encompassed by sedation/analgesia.
A continuum of depth of sedation was described in the second ASA guidelines for sedation/analgesia. 4 From Table 4-1 , concepts ranging from minimal sedation (anxiolysis) through moderate sedation/analgesia (conscious sedation) to general anesthesia are described related to responsiveness and airway management. Of note, moderate sedation/analgesia is described as purposeful response to verbal or tactile stimulation and that no airway intervention is required. A more detailed sedation continuum ( Table 4-1 ) is proposed in a Canadian Emergency Department consensus guideline. 5 However, the transition between moderate sedation and deep sedation where airway management is required can be different with each patient.

Table 4-1 Depth of Sedation and Type of Interventional Procedure
The best approach is to establish a sedation/analgesia plan prior to starting the procedure. Optimal goals include the following 6 :
1. To provide adequate analgesia, sedation, anxiolysis, and amnesia during the performance of painful diagnostic or therapeutic procedures
2. To control unwanted motor behavior that inhibits the performance of diagnostic procedures or image-guided interventions
3. To rapidly return the patient to a state of consciousness
4. To minimize the risks of adverse events related to the provision of sedation and analgesia
In addition, the complexity and duration of the procedure involved changes the sedation/analgesia plan. Simple and short procedures may require little or no sedation with only local or topical analgesia, such as trigger point injections or piriformis muscle injections. Many procedures requiring fluoroscopic guidance can be assisted with moderate sedation including midazolam and fentanyl. Although some interventional pain experts routinely perform medial branch blocks under local analgesia only, multiple-level procedures versus single-level procedures may require more than midazolam 2 mg and fentanyl 100 mcg IV, particularly at a training institution. Cancer neurolytic blocks that can be intensely stimulating often require deeper sedation. Prolonged sedation may be required for spinal cord stimulation trials or intrathecal catheter implants due to the duration of the procedure (see Table 4-1 ). Physician preparation and experience can decrease the duration of the procedure, thereby decreasing the need for sedation and analgesia.

Patient Preparation
One of the main ways of decreasing sedation and analgesia requirements is to prepare patients for what happens during the procedure and hence reducing their anxiety of the unknown. It is easiest for those patients who are returning for a series of the same procedure. Short procedural materials or websites describing the procedure can help patients with questions in the office or preoperative area. Although the literature is insufficient in supporting preprocedural preparation, the ASA consultants agree that “appropriate preprocedure counseling of patients regarding risks, benefits, and alternatives to sedation and analgesia increases patient satisfaction.” 4
Table 4-2 ASA Classification Class Systemic Disturbance Mortality 1 Healthy patient with no disease outside of the surgical process <0.03% 2 Mild-to-moderate systemic disease caused by the surgical condition or by other pathologic processes 0.2% 3 Severe disease process that limits activity but is not incapacitating 1.2% 4 Severe incapacitating disease process that is a constant threat to life 8% 5 Moribund patient not expected to survive 24 hours with or without an operation 34% E Suffix to indicate an emergency surgery for any class Increased
ASA, American Society of Anesthesiologists.
From Cohen MM, Duncan PG, Tate RB: Does anesthesia contribute to operative mortality? JAMA 1988;260:2859-2863.
ASA preoperative classification can help stratify a patient’s risk for a medical event during procedural sedation/analgesia. At one author’s institution, only ASA 1 and 2 (healthy, low health risk) patients are offered procedures at the outpatient surgery center. ASA 3 and higher patients have their procedures at the main hospital with a higher medical acuity support staff.
Because interventional pain procedures are almost always elective, particularly for chronic pain patients, ASA fasting guidelines should be observed as per Table 4-3 . Of note, patients can have a small amount of clear liquids up to 2 hours prior to procedure. Otherwise, many surgery centers will allow the procedure to be performed only under local or topical analgesia. 4
Table 4-3 Summary of ASA Preprocedure Fasting Guidelines ∗ Ingested Material Minimum Fasting Period † Clear liquids ‡ 2 hr Breast milk 4 hr Infant formula 6 hr Nonhuman milk § 6 hr (Light meal) 6 hr
ASA, American Society of Anesthesiologists.
(A light meal typically consists of toast and clear liquids. Meals that include fried or fatty foods or meat may prolong gastric emptying time. Both the amount and type of foods ingested must be considered when determining an appropriate fasting period.)
∗ These recommendations apply to healthy patients who are undergoing elective procedures. They are not intended for women in labor. Following the Guidelines does not guarantee a complete gastric emptying has occurred.
† The fasting periods apply to all ages.
‡ Examples of clear liquids include water, fruit juices without pulp, carbonated beverages, clear tea, and black coffee.
§ Since nonhuman milk is similar to solids in gastric emptying time, the amount ingested must be considered when determining an appropriate fasting period.
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.
Medical morbid conditions, particularly cardiopulmonary disease, can be problematic for a nonanesthesiologist providing sedation. A history of sleep apnea and difficult airway physical habitus as specified by Table 4-4 may suggest less sedation or having a monitoring anesthesiologist for the procedure would be appropriate.
Table 4-4 Airway Assessment for Sedation and Analgesia
Positive pressure ventilation, with or without tracheal intubation, may be necessary if respiratory compromise develops during sedation-analgesia. This may be more difficult in patients with atypical airway anatomy. In addition, some airway abnormalities may increase the likelihood of airway obstruction during spontaneous ventilation. Some factors that may be associated with difficulty in airway management are:
History
Previous problems with anesthesia or sedation
Stridor, snoring, or sleep apnea
Advanced rheumatoid arthritis
Chromosomal abnormality (e.g., trisomy 21)
Physical Examination
Habitus
Significant obesity (especially involving the neck and facial structures)
Head and Neck
Short neck, limited neck extension, decreased hyoid-mental distance (< 3 cm in an adult), neck mass, cervical spine disease or trauma, tracheal deviation, dysmorphic facial features (e.g., Pierre-Robin syndrome)
Mouth
Small opening (< 3 cm in an adult); edentulous; protruding incisors; loose or capped teeth; dental appliances; high arched palate; macroglossia; tonsillar hypertrophy; nonvisible uvula
Jaw
Micrognathia, retrognathia, trismus, significant malocclusion
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.

Allergies
The main allergies that most interventional pain management specialists encounter are allergies to latex, iodine/contrast, or to local anesthetics.
Latex and iodine allergies can be easily prevented with advanced notice. Most interventional pain procedures can document correct placement fluoroscopically without contrast patterns and by anatomical landmarks. Surface preparation solutions, such as chlorhexidine can be used instead. Indeed, the authors routinely use chlorhexidine because some literature suggests that it may be the best antiseptic for regional and interventional pain procedures. 8
Most local anesthetic allergies are caused by amide local anesthetic compounds, such as lidocaine or bupivacaine. Some patients also describe an allergy from a combination of these agents mixed with epinephrine. Often the epinephrine in a prior event was absorbed intravascularly causing an increase in heart rate. An alternative to using amide local anesthetics are esters: chloroprocaine or procaine. The main question to ask is whether the patient had a “true” allergic reaction with skin rash, throat tightness, difficulty breathing or swallowing. If the patient has a rash caused by benzocaine, a common ester local anesthetic in suntan lotions, the patient may be allergic to esters. Typically, patients are allergic to one chemical structure of local anesthetic: amides or esters; so the other class may be dosed during procedures. Dosing recommendations will follow later in this chapter.

Monitoring and Room Set-Up
In general, a procedure room must be able to accommodate pulse oximetry, blood pressure, oxygen, intravenous access, and other monitors, a space for a designated health care provider to record the patient’s vital signs and provide medications, and enough room to place the patient on a gurney for transport.
According to Medicare guidelines:
• Moderate Sedation should be provided by a qualified physician. Physician must be continuously present to monitor the patient and personally provide care.
• During Moderate Sedation, the patient’s oxygenation, ventilation, circulation, and temperature should be evaluated by whatever method is deemed most suitable by the attending physician.
• The following Centers for Medicare & Medicaid Services (CMS) requirements for Moderate Sedation should be the same as for MAC and general anesthesia with regard to the performance of presedation examination and evaluation, prescription of the sedation, care required for the completion of a record, the administration of necessary oral or parenteral medications, and the provision of indicated postoperative care. Appropriate documentation must be available to reflect pre- and postsedation evaluations and intraoperative monitoring.
• The Moderate Sedation service rendered must be appropriate and medically reasonable and necessary.
The provider who monitors the patient should have training and understanding of the agents that are administered and they should be readily available. Emergency equipment should be available as listed on example III from ASA guidelines. 4 Most outpatient surgery centers require on-site staff with ACLS certification and/or physicians trained in anesthesiology or emergency medicine who can manage airway emergencies ( Table 4-5 ).
Table 4-5 Emergency Equipment for Sedation and Analgesia Appropriate emergency equipment should be available whenever sedative or analgesic drugs capable of causing cardiorespiratory depression are administered. The lists below should be used as a guide, which should be modified depending on the individual practice circumstances. Items in brackets are recommended when infants or children are sedated.
Intravenous equipment
Gloves
Tourniquets
Alcohol wipes
Sterile gauze pads
Intravenous catheters [24-22 gauge]
Intravenous tubing [pediatric “micro drip” 60 drops/mL]
Intravenous fluid
Assorted needles for drug aspiration, intramuscular injection (intraosseous bone marrow needle)
Appropriately sized syringes [1-mL syringes]
Tape
Basic airway management equipment
Source of compressed oxygen (tank with regulator or pipeline supply with flowmeter)
Source of suction
Suction catheters [pediatric suction catheters]
Yankauer-type suction
Face masks [infant/child]
Self-inflating breathing bag-valve set [pediatric]
Oral and nasal airways [infant/child-sized]
Lubricant
Advanced airway management equipment (for practitioners with intubation skills)
Laryngeal mask airways [pediatric]
Laryngoscope handles (tested)
Laryngoscope blades [pediatric]
Endotracheal tubes
Cuffed 6.0, 7.0, 8.0 mm ID
(Uncuffed 2.5, 3.0, 3.5, 4.0, 4.5, 5.0, 5.5, 6.0 mm ID)
Stylet (appropriately sized for endotracheal tubes)
Pharmacologic Antagonists
Naloxone
Flumazenil
Emergency medications
Epinephrine
Ephedrine
Vasopressin
Atropine
Nitroglycerin (tablets or spray)
Amiodarone
Lidocaine
Glucose, 50% [10 or 25%]
Diphenhydramine
Hydrocortisone, methylprednisolone, or dexamethasone
Diazepam or midazolam
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.
At the authors’ institutions, the World Health Organization (WHO) surgical guidelines are used. Just before starting a procedure, a surgical stop is initiated and documented by nursing staff. That one last check has empirically prevented allergens from being given and other procedural complications.

Nonpharmacologic Management of Procedural Pain
Two main nonpharmacologic techniques have been used to reduce procedural pain: acupuncture and cognitive behavioral strategies. A recent metaanalysis review on acupuncture suggests that there is a small analgesic effect across multiple pain studies, including headache, low back pain, and postoperative pain, and it is difficult to separate whether the pain relief is independent of the psychological impact of the ritual treatment. 9 The cognitive strategies of distraction and hypnosis in the treatment of procedural pain in children are clearly effective. 10 It seems likely that distraction and other cognitive techniques can help with adult procedural pain as well.

Common Side-Effects and Complaints

Adjuvants: Particularly Antiemetics
Patient satisfaction is clearly an important aspect of any pain procedure. One study by Dr. Macario and others sought to survey what clinical anesthesia outcomes are important to avoid from a patient’s perspective. 11 Of the patients, 24% ranked vomiting as their least desirable outcome with avoiding nausea also having high importance. The main way of avoiding nausea for interventional pain procedures is to limit the amount of opioids, such as fentanyl, for analgesia.
An expert consensus was published by Dr. Gan and colleagues in 2003 12 for the management of postoperative nausea and vomiting. If a patient has received no prophylaxis, 5-HT3 receptor therapy is recommended, which includes ondansetron 1.0 mg, dolasetron 12.5 mg, granisetron 0.1mg, and tropisetron 0.5 mg. The panel agreed that there is no evidence of any difference in the efficacy and safety profiles of the serotonin receptor antagonists. Other alternative therapies for rescue include: droperidol 0.625 mg IV, dexamethasone 2 to 4 mg IV, and promethazine 12.5 mg IV. Of note, droperidol has a black box warning for QT prolongation and torsades de pointes as well as neuroleptic effects ( Table 4-6 ).
Table 4-6 Antiemetic Treatment for Postoperative Nausea Initial Therapy Failed Prophylaxis No prophylaxis or dexamethasone 5-HT 3 antagonist ∗ plus second agent † Triple therapy with 5-HT 3 antagonist ∗ plus two other agents † when PONV occurs <6 hr after surgery (V) Triple therapy with 5-HT 3 antagonist ∗ plus two other agents † when PONV occurs >6 hr after surgery (V) Administer small-dose 5-HT 3 antagonist ∗ (IIA) Use drug from different class (V) Do not repeat initial therapy (IIIA) Use drug from different class (V) or propofol, 20 mg as needed in postanesthesia care unit (adults) (IIIB) Repeat 5-HT 3 antagonist ∗ and droperidol (not dexamethasone or transdermal scopolamine) Use drug from different class (V)
5-HT 3 = serotonin.
∗ Small-dose 5-HT antagonist dosing: ondansetron 1.0 mg, dolasetron 12.5 mg, granisetron 0.1 mg, and tropisetron 0.5 mg.
† Alternative therapies for rescue: droperidol 0.625 mg IV, dexamethasone 2-4 mg IV, and promethazine 12.5 mg IV.
From Gan TJ, Meyer T, Apfel CC, et al: Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg 2003;97:62-71.
If a patient is known to have high risk for postoperative nausea and vomiting, dexamethasone 4 mg IV preoperatively can be highly effective both from an efficacy and cost perspective. 13 One question is whether a single dose of dexamethasone IV can affect the interpretation of whether the interventional procedure has changed the patient’s pain scores. Even doses of up to 8 mg of dexamethasone preoperatively has no effect on pain and mobilization scores after colorectal surgery. 14 Dexamethasone 8 mg can elevate postprocedural glucose concentrations in patients with impaired glucose tolerance and may not be the best first-line choice for nausea prophylaxis, especially if the patient is receiving steroids for the interventional block as well.

Medications

Sedatives and Amnestics
The main goal of intravenous sedation is to provide a short duration anxiolytic and amnestic that is controlled so that airway compromise is avoided. In general, benzodiazepines are used as first line agents. Benzodiazepines induce sedation and anxiolysis by modulating GABA transmission in the CNS. GABA is one of the most common inhibitory neurotransmitters in the brain and benzodiazepines bind to GABA A receptors, increase chloride ion channel influx, and subsequently decrease neuronal excitation. 15 Midazolam (Versed) is usually the most preferred benzodiazepine administered compared to lorazepam (Ativan) or diazepam (Valium) because of the shorter elimination half-life (approximately 2 hours for midazolam compared to 12 hours for lorazepam, and 20 to 50 hours for diazepam). 16 Typical intermittent dosages of midazolam range from 0.5 mg to 1 mg repeated, lorazepam 0.25 mg repeated, and diazepam 1 to 2 mg repeated. Habitual alcohol usage increases the clearance of midazolam so higher dosages may be required for sedation. Lorazepam is less affected by enzyme induction and other factors that alter cytochrome P450 metabolism. Age and smoking decrease the metabolism of diazepam and can prolong sedative effects. Diazepam may be used if the patient is already taking that agent as an antispasmotic or muscle relaxant or if it is used as an anxiolytic orally many hours prior to the procedure. Midazolam is probably the preferred choice for short interventional procedures, especially if the patient is not taking chronic benzodiazepines as anxiolytics.
Flumazenil is a benzodiazepine antagonist that is similar to midazolam in structure. It reverses benzodiazepine overdosage or oversedation in a dose-dependent manner. Although it is the primary benzodiazepine reversal agent available, compared with benzodiazepine antagonists (midazolam, lorazepam, diazepam), it has the highest clearance and shortest elimination half-life—approximately 1 hour. 16 Hence, flumazenil will provide rapid onset of reversal but will require continued monitoring for resedation and even a continuous intravenous infusion to outlast the original benzodiazepine agonist. Flumazenil may be dosed at 0.1 to 0.2 mg every 1 to 2 minutes to a maximum of 1.0 mg. Practitioners should note that flumazenil will reverse any lowering of seizure threshold that the initial benzodiazepine dosage may have induced.

Deeper Sedation
Other agents, namely etomidate, propofol, and ketamine have been utilized for procedural sedation. Etomidate and propofol can be used as induction agents for general anesthesia, so airway resuscitative measures should always be available including training by the medical provider administering the drug.
Etomidate is an anesthetic induction drug that has a similar affect to benzodiazepines by increasing the number of GABA receptors and, thereby increasing GABA inhibition. 15 The duration of a single dosage lasts approximately 5 minutes at standard induction dosages (0.3 mg/kg or about 20 to 40 mg) and is rapidly metabolized in the liver. 17 In anesthesia, the main advantage of etomidate is that it does not produce cardiac hypotension when compared with other induction agents such as propofol. A single dose of etomidate can cause adrenocortical suppression 18 as well as myoclonic activity. A single dosage of etomidate at 10 mg is used for cardioversion procedures in adults.
Propofol has revolutionalized outpatient surgical procedures with its rapid onset, short duration of action, and quick recovery for patients. 19 It has a chemical structure that is unrelated to other sedative hypnotic compounds 18 but does affect GABA-mediated transmission. It has amnestic properties but they are not as marked as the benzodiazepines. Of note, propofol is a cardiovascular depressant and can be associated with respiratory depression at anesthetic induction doses (2 to 2.5 mg/kg or approximately 140 to 175 mg). Propofol is also extensively metabolized and excreted in the urine (>88%).
There is an additive and synergistic hypnotic effect with propofol and other amnestics. So even when titrating propofol at 2.5 to 5 mg increments every few minutes after a base of midazolam and fentanyl, oversedation and respiratory compromise can occur. In addition, cognitive impairment can occur even after short procedures such as outpatient colonoscopy. 20 Administration of >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 tract 22 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 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, 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.
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.
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 S.M., Krauss B. Procedural sedation terminology: Moving beyond “conscious sedation”. Ann Emerg Med . 2002;39:433-435.
2. Gross J.B., Bailey P.L., Caplan R.A., 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 Non-Anesthesiologists. 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 M.L., Lennox P.H. Sedation and analgesia in the interventional radiology department. J Vasc Interv Radiol . 2003;14:1119-1128.
7. Cohen M.M., Duncan P.G., Tate R.B. Does anesthesia contribute to operative mortality? JAMA . 1988;260:2859-2863.
8. Dailey P.A. Chlorhexidine or Povidone-Iodine. CSA Bulletin, 58. 2009:45-47. http://www.csahq.org/pdf/bulletin/chlorhex_58_3.pdf . Accessed Nov 22, 2009
9. Madsen M.V., Gotzsche P.C., 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 T.J., Meyer T., Apfel C.C., et al. Consensus guidelines for managing postoperative nausea and vomiting. Anesth Analg . 2003;97:62-71.
13. Apfel C.C., 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 P.G. 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 P.F. Propofol: Its role in changing the practice of anesthesia. Anesthesiology . 2008;109:1132-1136.
20. Padmanabhan U., Leslie K., Eer A.S., 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 R.M., Morgan B.W., Murphy M. Ketamine in the ED: Medical politics versus patient care. Am J Emerg Med . 1999;17:722-725.
22. White P.F., Way W.L., Trevor A.J. Ketamine: Its pharmacology and therapeutic uses. Anesthesiology . 1982;56:119-136.
23. Hocking G., Cousins M.J. Ketamine in chronic pain management: An evidence-based review. Anesth Analg . 2003;97:1730-1739.
24. Raeder J.C., Stenseth L.B. Ketamine: A new look at an old drug. Curr Opin Anaesthesiol . 2000;13:463-468.
25. Laulin J.P., Maurette P., Corcuff J.B., et al. The role of ketamine in preventing fentanyl-induced hyperalgesia and subsequent acute morphine tolerance. Anesth Analg . 2002;94:1263-1269.
26. Ng K.C., Ang S.Y. Sedation with ketamine for paediatric procedures in the emergency department—A review of 500 cases. Singapore Med J . 2002;43:300-304.
27. Raj P.P. Practical Management of Pain , 3rd ed. St. Louis: Mosby; 2000. 462
28. Guignard B., Bossard A.E., Coste C., et al. Acute opioid tolerance—Intraoperative remifentanil increases postoperative pain and morphine requirement. Anesthesiology . 2000;93:409-417.
5 Radiation Safety for the Physician

Kenneth P. Botwin, MD, Philip Ceraulo, DO, 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

Table 5-1 Radiation Quantities and Units

Terminology
Like matter, energy can be transformed from one form to another. When ice (solid) melts and turns to H 2 O (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.

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.)

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 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.

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

Factors Affecting Radiation Exposure
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 (a s l ow a s r easonably a chievable) 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 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.

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.)
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, hold-and-store image capability, and beam collimation—all of which can minimize exposure time. A high kilovolt-low milliamperage approach to imaging will minimize the absorption of x-ray by the patient and improve the contrast of the visualized image ( Fig. 5-4 ). Freeze-frame capabilities minimize repeated exposures and should be used to review the last image in preparation for needle adjustments during the procedure.

Figure 5-4 The use of higher kilovoltage (kVp) and lower milliamperage (mAs) reduces patient dose. A, The use of high kVp and low mAs results in a high-energy, penetrating x-ray beam and a small patient (absorbed) dose. B, The use of low kVp and high mAs results in a low-energy x-ray beam, most of which is easily absorbed by the patient.
(From Statkiewicz MA, Ritenour ER: Radiation Protection for Student Radiographers. St. Louis, Mosby, 1983, with permission.)

Radiation Risks to the Patient During Fluoroscopic Procedures
Ionizing radiation occurs naturally in the environment: the general population usually is exposed to an individual effective dose equivalent of 360 millirem (mrem) of radioactivity per year. This exposure comes from numerous sources, the most significant of which is naturally occurring radon ( Table 5-2 ). 4, 8

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

Assessment of Risk
Risk assessment for patients subject to diagnostic and therapeutic radiographs is an inexact science, and the body of knowledge is constantly evolving. Current estimation of risk from radiographic exposure to a specific body part is based on the biologic effects of whole-body exposure (e.g., a survivor of an atomic bomb attack) converted by weight factors specific for individual organs and tissues. This concept was adopted by the International Commission on Radiological Protection in 1977 and was modified in 1991. 9 Termed the effective dose equivalent , the calculation has been adopted by most authoritative bodies that determine radiation risk and recommend protective measures.

Extent of Exposure
Radiation exposure to the patient during fluoroscopic procedures can exceed those associated with routine radiographs. The amount of radiation absorbed by an individual patient depends on a number of unalterable factors relating to his or her habitus, including the type, density, and location of tissue involved. For example, bone absorbs more ionizing radiation than soft tissues. An obese person will absorb more radiation than a slender one. Because of the frequency of exposure, skin at the entry site is the area most susceptible to radiation-induced injury. Different tissues have varying degrees of sensitivity to ionizing radiation ( Table 5-3 ). 4 , 6 , 9
Table 5-3 Specific Organ Cancer Risks of Radiation (Per 10,000 per Sv or Per 1,000,000 per Rem) Organ or Cancer Probability of Radiation-Induced Cancer Breast 50-200 Thyroid 50-150 Lung 50 Leukemia 15-25 Stomach 10-20 Brain 5-20 Colon 10-15 Liver 10-15 Lymphoma 4-12 Uterus 7-10 Salivary glands 5-10 Ovary 8 Bladder 4-7 Bone 2-5 Esophagus 2-5 Pancreas 2-5 Paranasal sinuses 2-5
From International Commission on Radiological Protection: Recommendations of the International Commission on Radiation Protection 26. Ann Int Commission Radiat Prot 1:1-53, 1977, with permission.
For instance, transient skin erythema can result from as little as 200 rad, and at 300 rad temporary hair loss may occur. The threshold for permanent injury is 700 rad, and doses >1800 rad can cause dermal necrosis. The skin dose is typically used to interpret a patient’s radiation exposure to diagnostic x-rays. In the absence of a dosimeter, the skin dose may be calculated using a variety of complicated techniques. In fluoroscopy, the patient’s exposure is more difficult to estimate because of the movement and variation in size of the radiation field. In the absence of absolute measurements, it usually is sufficient to estimate the fluoroscopic skin dose at 2 rad/mA/min. In order to determine the approximate exposure, first it is necessary to know the exposure time and milliamperage. For example, if a fluoroscopically guided transforaminal epidural corticosteroid injection requires 30 seconds to perform and the average milliamperage is 8 mA, exposure is estimated as follows: (2 rad/mA/min)(8 mA)(0.5 min) = 8 rad.
The primary controllable factor contributing to patient exposure is the length of the procedure. Depending on the complexity of the procedure, exposure times can last a few moments to an hour or more. Fluoroscopes usually produce between 1 and 5 R/min of ionizing radiation. The typical rem exposure to patients during common diagnostic and treatment procedures is shown in Table 5-4 .
Table 5-4 Radiation Exposure Comparison Procedure/Activity Exposure Body Part Natural background 100-200 mrem/yr Total body Lumbar epidural with fluoroscopy—patient 2.5 rem/30 sec Lumbar region Lumbar epidural with fluoroscopy—physician 2.5 mrem ∗ /30 sec Total body Swallowing videofluoroscopy (patient) 3 mrem/min † Face/neck Posteroanterior chest x-ray 10-30 mrem Chest CT scan of head 3-5 rem Head
∗ Exposure estimated without shielded protection and at a distance of approximately 1 meter.
† Data collected by Charles Beasley, Radiation Safety Officer, St. John’s Regional Hospital, Springfield, MO, based on operation at 85 kVp/0.2 mA.
Calculating the health risks from radiation is a relatively inexact science, but the risk from low-level exposure appears small. However, this low-level exposure has a significant effect on the developing fetus. 10

Radiation Risks to the Physician and Assisting Personnel
The maximum safe allowable exposure limits have been established by the National Council on Radiation Protection and Measurement as a maximum permissible dose (MPD). 11 The general radiation whole-body exposure guidelines allow no more than 5 rem/year ( Table 5-5 ).
Table 5-5 National Council on Radiation Protection and Measurements Recommendations for Occupational Radiation Exposure 1. Effective dose limits Annual 50 mSv (5 rem) Cumulative 10 mSv (1 rem) × age 2. Annual dose limits for tissues and organs Lens of the eye 150 mSv (15 rem) Skin, hands, and feet 500 mSv (50 rem) 3. Embryo/fetus Total dose equivalent 5 mSv (0.5 rem) Monthly dose equivalent 0.5 mSv (0.05 rem)
mSv, millisievert.
Adapted from National Council on Radiation Protection and Measurements (NCRP): Ionizing Radiation Exposures of the Population of the United States. Report No. 116. Washington, DC, NCRP, 1993, with permission.

Guidelines for Exposure
Several studies have evaluated radiation exposure to clinicians during fluoroscopically assisted orthopedic procedures. One study demonstrated that unprotected individuals working ≤24 inches from a fluoroscopic beam received significant amounts of radiation, whereas those working ≥36 inches from the beam received an extremely low amount of radiation. 12 Risk of radiation exposure to orthopedic surgeons also has been studied. One prospective study showed that radiation doses over a 6-month period were well below the maximum dose limits for ionizing radiation as recommended by the European Economic Communities (EURATOM) directives. 13 Using a phantom patient, this experiment revealed that exposure to ionizing radiation during the insertion of a dynamic hip screw was minimal. Caution during fluoroscopy was recommended nevertheless. The cutaneous effects of long-term skin exposure in a physician are clearly visible ( Fig. 5-5 ).

Figure 5-5 Fingers of an 83-year-old general practitioner who set fractures under fluoroscopy for 35 years. Note the changes in the nails. A basal cell carcinoma was earlier resected from a proximal phalanx.
(From Lennard TA: Fundamentals of procedural care. In: Lennard TA, ed: Physiatric Procedures in Clinical Practice. Philadelphia, Hanley & Belfus, 1995, pp 1-13, with permission.)

Protective Measures
In order to monitor the amount of radiation the technologist and physicians are exposed to, a film dosimetry system should be used to provide accurate personal dosimetry and comprehensive diagnostic evaluation. The Gardray film consists of a slim, light, clip-on badge that can easily be worn on either the torso (body badge) or extremities (finger/ring badge). The film is placed in a holder that incorporates six absorbers to optimize the determination of the type and level of exposure. Metal absorbers are U-shaped to permit the film to be filtered for radiation exposure not only from the front but also from the bottom and behind. The finger/ring badge should be worn with the film facing the inside part of the hand nearest the radiation source. The body badge is worn in the same position closest to the radiation source each day. A badge also may be placed on protective eyewear to determine exposure to the lenses of the eye. The badges and rings are sent in monthly for processing to monitor the type and amount of radiation exposure (as measured in mrem) received by each participant. Results are reported as monthly and 12-month accumulated dosages. Exposure is divided into three dose-equivalent columns for shallow, deep, and eye lens exposures. The shallow dose equivalent applies to the external exposure of the skin or extremity and is taken as the dose equivalent at a tissue depth of 0.007 cm averaged over an area of 1 cm squared 14 ; the deep dose equivalent applies to external whole-body exposure and is the dose equivalent at a tissue depth of 1 cm; and the eye dose equivalent applies to the external exposure of the lens of the eye and is taken as the dose equivalent at a tissue depth of 0.3 cm. Cataract development may occur with cumulative eye lens exposure of ≥400 rad. 15

Clinical Application of Radiation Safety
There have been several published studies that help the interventionalist to approximate their potential radiation exposure. 16 - 21 These studies were able to predict the exact exposure based on a specific procedure. The interventionalist can therefore, based on the type of procedure, at least approximate their amount of radiation exposure.

Conclusion
Through compliance with an occupational dosimetry program, the application of cautious work habits, and attention to the three essentials of radiation safety—distance, time, and shielding—the physician can minimize exposure and maximize long-term safety in the fluoroscopy suite. By using the proper safety standards, the interventionalist can thereby reduce exposure times.

Acknowledgment
The authors would like to acknowledge Carol Barragen for secretarial assistance.

References

1. Wycoff H.O. The international system of units (SI). Radiology . 1978;128:833-835.
2. Boone J.M., Levin D.C. Radiation exposure to angiographers under different fluoroscopic imaging conditions. Radiology . 1991;180:861-865.
3. Marx MV: Interventional procedures: Risks to patients and personnel. In: American College of Radiology Commission on Physics and Radiation Safety: Radiation Risks: A Primer . Reston, Va. American College of Radiology; 1996: 22-25.
4. Larimore E (Radiation Consultants): [Personal communication to TA Lennard], 1994. Reported in Lennard TA: Fundamentals of procedural care. In: Lennard TA ed: Physiatric Procedures in Clinical Practice . Philadelphia, Hanley & Belfus; 1995: 1–13.
5. ProTech Radiation Apparel and Accessories, Palm Beach Gardens, FL.
6. Vehmas T. Finger doses during interventional radiology: The value of flexible protective gloves. Rofo . 1991;154:555-559.
7. ProTech Leaded Eyewear, Palm Beach Gardens, FL.
8. National Council on Radiation Protection and Measurements (NCRP). Ionizing Radiation Exposures of the Population of the United States. Report No. 93 . Washington, DC: NCRP; 1987.
9. International Commission on Radiological Protection. Recommendation of the International Commission on Radiation Protection 26. Ann Int Commission Radiat Prot . 1977;1:1-53.
10. Gray JE. Safety risk of diagnosis radiology exposures. In: American College of Radiology Commission on Physics and Radiation Safety ed: Radiation Risks: A Primer. Reston, Va, American College of Radiology; 1996: 15–18.
11. National Council on Radiation Protection and Measurements (NCRP): Ionizing Radiation Exposures of the Population of the United States. Report No. 116. Washington, DC, NCRP, 1993.
12. Barendsen G.W. Parameters of linear-quadratic radiation dose-effect relationships: Dependence on LET and mechanisms of reproductive cell death. Int J Radiat Biol . 1997;71:649-655.
13. O’Rourke P.J., Crerand S., Harrington P., et al. Risks of radiation exposure to orthopedic surgeons. J R Coll Surg Edinb . 1996;1:40-43.
14. Landauer, Inc., 2 Science Road, Glenwood, IL 60425-1586.
15. Marx M.V., Niklason L., Mauger E.A. Occupational radiation exposure to interventional radiologists: A prospective study. J Vasc Interv Radiol . 1992;3:597-606.
16. Harstall R., Heini P.F. Mini, Orler R: Radiation exposure to the surgeon during fluoroscopically assisted percutaneous vertebroplasty: A prospective study. Spine . 2005;30(16):1893-1898.
17. Manchikanti L., Cash K., Moss T., Pampati V. Effectiveness of protective measures in reducing risk of radiation exposure in interventional pain management: a prospective evaluation. Pain Physician . 2003;6:301-305.
18. Manchikanti L., Cash K., Moss T., et al. Risk of whole body radiation exposure and protective measures in fluoroscopically guided interventional techniques: A prospective evaluation. BMC Anesthesiol . 2003;3(1):2.
19. Botwin K.P., Fuoco G.S., Torres F.M., et al. Radiation exposure to the spinal interventionalist performing lumbar discography. Pain Physician . 2003;6:295-300.
20. Botwin K.P., Freeman E.D., Gruber R.D., et al. Radiation exposure to the physician performing fluoroscopically guided caudal epidural steroid injections. Pain Physician . 2001;4:343-348.
21. Botwin K.P., Thomas S., Gruber R.D., et al. Radiation exposure of the spinal interventionalist performing fluoroscopically guided lumbar transforaminal epidural steroid injections. Arch Phys Med Rehabil . 2002;83:697-701.
6 Complications of Common Selective Spinal Injections
Prevention and Management

Robert E. Windsor, MD, FAAPMR, FAAEM, FASPM, Elmer G. Pinzon, MD, Herman C. Gore, MD
Selective spinal injections are being performed with increasing frequency in the management of acute and chronic pain syndromes. 1 - 3 Because these procedures require placing a needle in or around the spine, a risk of complications is always present. Therefore, knowledge about prevention of complications, and early recognition and management when they do occur, are paramount to appropriate patient care. This requires adequate physician training and appropriate patient preparation and monitoring. This chapter will discuss physician training, patient preparation and monitoring, and specific complications and their treatment ( Appendix II ).

Physician Training
The level of physician training required to safely perform selective spinal injections is a topic of debate. This debate is fueled by differing standards from one region of the country to another, and from one specialty to another. Some people are concerned, for example, that certain physicians are performing selective spinal injections without appropriate training, thereby placing their patients at undue risk.
Although it is true that uncomplicated lumbar procedures (in an otherwise healthy population) do not require the degree of training and expertise that high-risk procedures performed in a medically unstable population do, certain standards must still be met. Currently, the American Academy of Physical Medicine and Rehabilitation (AAPM&R) has adopted guidelines that recommend a minimum level of documented didactic and clinical training in complication prevention, recognition and management, spinal injection technique, and patient selection, such as that provided in an appropriate fellowship or residency program. 4 This program must provide specific training in spinal injections and the recognition, prevention and treatment of related complications; and advanced cardiac life support (ACLS) certification.
In addition, the residency chairman or fellowship director must be confident in the abilities of the physician in question, prior to recommending his or her approval for spinal interventions. Specifically, selective spinal injection courses alone, although valuable, do not provide enough training (or depth of training) for the novice injectionist to safely perform spinal injections in practice.

Patient Preparation
Patient preparation issues include patient education, 5, 6 informed consent statement, NPO ( nil per os ; “nothing by mouth”) status, IV access, certainty that no procedural contraindications exist, patient positioning, sterile preparation and draping, supplemental intravenous (IV) fluids and oxygen, and plans for appropriate recovery following the procedure. Depending on the procedure and patient status, prophylactic antibiotics may also be included.
Patient education should include a thorough description of the procedure, including potential risks, benefits, alternatives, and likely outcomes. 6 An informed consent statement, confirming the conversation, should be executed. The statement should include signatures of the patient, the doctor, and a witness.
Prior to the procedure, the patient should be NPO for 12 hours for solid foods and for 8 hours for fluids, preoperatively, to ensure that all gastric contents are distal to the ligament of Treitz. 7
A large-bore IV (ideally 20 guage or larger) should be started in a large proximal upper-extremity or neck vein. This is to allow immediate IV access in an emergent setting. Small-gauge or peripherally-placed IV catheters do not allow adequate access to the central venous supply for resuscitative purposes when peripheral vasoconstriction occurs.
Procedural contraindications or relative contraindications that may not have been present or recognized during the last physician office visit should be evaluated, such as chest pain, shortness of breath, fever, systemic infection, uncontrolled hypertension or other medical problems.
If the procedure involves placement of a needle or other instrument into a disc, or implantation of a device, then preprocedure laboratory work should be performed. In addition, if the patient is recovering from a known systemic infection (e.g., pneumonia or urinary tract infection), then preprocedure laboratory work should also be performed.
If the patient has coexisting medical problems (e.g., has chronic obstructive pulmonary disease [COPD], heart disease, etc.), clearance from the patient’s primary care or specialty doctor should be obtained. Depending on the patient’s problem, preprocedure laboratory work may include a complete blood count with differential diagnosis, liver function tests, urinalysis, chest radiograph, ECG, blood culture and sensitivity, urine culture and sensitivity, and erythrocyte sedimentation rate.
The patient should be positioned on the procedure table in a comfortable manner that will allow the treating physician unencumbered access to the region of the patient’s body under treatment. The patient’s position should be comfortable enough for him or her to lie still for the duration of the procedure.
Care must be taken to ensure there is no region of neural compression or stretch, particularly if sedating medication will be used. Areas that are particularly vulnerable to neural compression or stretch include the ulnar nerve at the elbow and the brachial plexus. 8 If necessary, use an arm board, tape, strapping or padding to make the patient more comfortable, enable him or her to hold the appropriate position, and prevent the patient’s hands from inadvertently compromising the sterile field.
Sterile preparation should minimally include scrubbing the region of the body to be treated and surrounding areas with a povidone-iodine preparation and allowing it to dry. If the patient has an iodine allergy, chlorhexidine gluconate and/or isopropyl alcohol should be used. For discography or any type of implant, use a triple scrub, including isopropyl alcohol, chlorhexidine gluconate, and povidone-iodine, lasting for at least 5 minutes. Allow the povidone-iodine to dry. For these procedures, use pre- and postprocedure antibiotics, as well.
The degree of sterile draping required depends on the procedure. If a lumbar epidural is being performed, draping the immediate area around the penetration with sterile towels is adequate. If a spinal implant, percutaneous discectomy, or other more invasive spinal procedure is being performed, full-body draping with a fenestrated drape, iodine-impregnated adhesive biodrapes, sterile towels, and half-sheets should be used as needed to ensure a sterile field.
Supplemental fluids are important during most procedures, not just high-risk procedures. When a patient has been NPO for 3 hours (especially during morning procedures when he or she has been NPO since the night before), they are somewhat volume-depleted and more prone to vasovagal reactions. Supplemental fluids before, during, and after procedures help prevent such reactions.
In addition, having fluids already flowing, in the event the patient becomes hypotensive, is advantageous; this can also help flush medication(s) through the line. Supplemental fluids should be used cautiously if the patient is volume-sensitive, such as with congestive heart failure or renal pathology.
Supplemental oxygen should be dictated by the situation. If IV sedation is administered, supplemental oxygen should be used as needed to help maintain the patient’s oxygen saturation above 92%. If the patient has COPD or other pulmonary pathology, supplemental oxygen should be used sparingly because too much oxygen may further suppress respiratory drive.
In addition, if the patient has chronic pulmonary disease, the treating physician must confirm that they can tolerate the position required by the procedure. If necessary, obtain clearance from the patient’s pulmonologist or internist.

Patient Monitoring
Patient monitoring should minimally include blood-pressure and heart-rate monitoring. If the patient is infirm, a high-risk procedure is being performed, or IV sedation is being used, cardiac monitoring and pulse oximetry should also be employed. Baseline vital signs should be obtained before the procedure (for purposes of comparison during and after the procedure).
Preprocedure hypertension should be approached with caution. A patient with cerebrovascular disease may require a higher-than-normal blood pressure to maintain cerebral perfusion; thus, adjusting his or her blood pressure could incite a stroke. If lowering the patient’s blood pressure is medically safe and appropriate, gentle IV sedation is generally all that is required. Sublingual calcium channel blockers should be avoided. In addition, if IV sedation for the procedure is planned, blood pressure reduction with other medications should be avoided prior to sedation, as this combination of drugs could lower the blood pressure to dangerous levels.
Cardiac monitoring should be employed for any patient with a significant cardiovascular history—or when known risks of the planned procedure might place the patient at risk for cardiovascular complication. In general, cardiac monitoring should be performed for any patient with a known history of myocardial infarction or angina; for any significantly invasive procedure (e.g., spinal implant); for any intraspinal cervical or thoracic procedure; for any procedure that may place a significant volume of local anesthetic or narcotic in the spinal canal or systemic circulation; or for anyprocedure that will require a significant amount of IV sedation. A rhythm strip should be run before, during, and after the procedure and included on the patient’s chart.

Patient Recovery
The recovery of the patient following the procedure is critically important and is often ignored. The postprocedural period is when most procedure-related complications occur. Complications that can occur during the immediate postprocedure period include hypotension, vasovagal reactions, sensorimotor blockade, excessive somnolence, respiratory suppression, and cardiovascular complications arising from one or more of the aforementioned complications.
For these reasons, a medically-reasonable recovery protocol (ultimately allowing the patient to recover in a monitored situation until he or she is alert, oriented, and able to tolerate fluids and ambulate as well as expected) is important. The following abbreviated version of the protocol for routine spinal-injection procedures, with minimal or no sedation, is recommended.
The patient is allowed to remain in the procedure room in the recumbent position for 5 to 10 minutes under the observation of the nurse, while two additional sets of vital signs are taken. If the patient is in satisfactory condition, he or she is slowly moved to a sitting position and transferred to a wheel chair, or assisted with ambulation to the recovery area. The patient is observed there with intermittent vital-sign monitoring for at least 20 minutes, or until they have met the above criteria. Another person must drive the patient home if IV sedation was given during the procedure.
If the specific intervention was more significant than a simple spinal injection (e.g., spinal implant, percutaneous discectomy), the recovery period may last up to 8 hours. It may be necessary to hold the patient overnight if the previously listed criteria are not met. When they have met discharge criteria, they are discharged with appropriate safety and follow-up instructions.

General Complications of Spinal Injections

Infectious Complications
Infections, ranging from minor to severe conditions such as meningitis, 9, 10 epidural abscess, 11 - 13 and osteomyelitis ( Figs. 6-1 and 6-2 ) , 14, 15 occur in 1% to 2% of spinal injections. Severe infections are rare and occur in from 1 in 1000 to 1 in 10,000 spinal injections. Severe infections may have far-reaching sequelae, such as sepsis, spinal-cord injury, or spreading to other sites in the body via Batson plexus or direct contiguous spreading. Poor sterile technique is the most common cause of infection. Staphylococcus aureus is the most common offending organism causing infection from skin structures.

Figure 6-1 Lumbar epidural abscess (MRI view). T2-weighted image demonstrating an epidural abscess ( white arrows) severely compressing the thecal sac at C-6 and C-7 levels.

Figure 6-2 Vertebral osteomyelitis and paraspinal abscess (CT scan view). A, Note the paraspinal soft tissue mass in front of the destructive process of the L-5 vertebra. B, Soft tissue windows following intravenous contrast enhancement showing the large multilocular abscess in the soft tissues enhanced ( black arrows) .
Infection from gram-negative aerobes and anaerobes may occur from inadvertent intestinal penetration. Usually, discitis from lumbar discography involves a gram-negative aerobe, is self-limited, and resolves with early recognition and administration of appropriate antibiotics. Cervical discitis, however, is often life threatening, due to the aggressive gram-negative anaerobes that colonize the esophagus.
If the infection is a mild cutaneous infection and the patient is immunocompetent, it will probably resolve with local disinfection. The physician should make specific hygiene recommendations and monitor this infection expectantly. If it appears to pursue a more aggressive course but does not involve spinal structures, appropriate oral antibiotics on an outpatient basis and frequent follow-up may be all that is required.
If the infection appears to progress to spinal structures or spaces, or if the patient is infirm or otherwise predisposed to infection, in-patient evaluation and care with appropriate IV antibiotics is usually required. If epidural abscess occurs, emergent surgical drainage must be considered to avoid neural damage or other complications. 16 Early detection and treatment of epidural or intrathecal infection is necessary to avoid morbidity and mortality. It usually manifests with severe back or neck pain, fever, and chills, with a leukocytosis developing on the third day following the injection. 13
Patients with diabetes or other immunocompromised conditions are more susceptible to infection and should be followed very closely following spinal injections. With these patients, if infection is suspected or confirmed, they must be evaluated and treated aggressively.
Preexisting systemic infection is a relative contraindication to spinal injection. If the spinal injection is critical to the overall care of the patient with preexisting systemic infection, the risks and benefits must be carefully weighed before performing the injection. In addition, administering prophylactic antibiotics for 72 hours before the injection should be considered. Knowing the local standards of care for preventing or treating spinal injection-related infections and routinely reviewing current microorganism susceptibilities are important.

Cardiovascular Complications
Bleeding is a risk inherent to all injection and surgical procedures. The potential for bleeding during spinal injection is increased by liver disease, the consumption of warfarin or other anticoagulants, 5, 17, 18 certain inherited anemias (such as G6PD deficiency or sickle-cell anemia), coagulopathy from any cause, and venous puncture.
The epidural vasculature is injured in 0.5% to 1% of spinal injections on average, and is more common with placement of the needle in the lateral portion of the spinal canal than the midline. 19 Significant epidural bleeding may cause the development of an epidural hematoma. Clinically-significant epidural hematomas are rare, with a reported incidence of less than 1 in 4000 to 1 in 10,000 lumbar epidural cortisone injections; and may lead to irreversible neurologic compromise if not surgically decompressed within 24 hours. 19 - 25 Retroperitoneal hematomas may occur following spinal injection if the large vessels are inadvertently penetrated. These hematomas are usually self-limited but may be a cause of acute hypovolemia or anemia. In addition to bleeding, a variety of dysrhythmias may occur. When a dysrhythmia occurs, treatment should be initiated immediately. The entire team of primary care physicians (PCPs) must be able to function synergistically when treating a dysrhythmia.
ACLS code scenarios should be run in the procedure facility no less than quarterly; all PCPs should know how to alert other staff and extended PCPs immediately; and everyone should know their specific roles in such situations. In addition, all PCPs should know where emergency care equipment is located and how to use it within the limits of their roles. Treatment of individual dysrhythmias is beyond the scope of this chapter; however, the reader is directed to the Emergency Cardiac Care Algorithms included in Appendix I and other sources for more detailed information. 26, 27

Neurologic Complications
Neurologic complications are rare. The most common causes of neural injury during spinal injection are: direct trauma to the spinal cord or nerve roots from a needle; compression from an epidural hematoma; or involvement by infectious exudate. Other causes include stroke from injection-, sedation- or cardiac-induced hypotension; dislodgement of plaque from intraarterial injection; or anoxia from respiratory arrest or laryngeal obstruction.
The proximity of the vertebral artery during cervical transforaminal or facet joint injections requires particular knowledge of the three-dimensional anatomy of the cervical spine, as well as specific training and expertise in cervical spinal-injection procedures, to consistently protect these structures. Injection into this vessel may cause a posterior circulation stroke, hematoma formation and occlusion of the vessel, or injection of air. Seizure may also occur if local anesthetic is injected into the vessel.
Studies demonstrate that fluoroscopically-guided spinal injections are less apt to cause inadvertent neural injury or injection into a vascular structure. 28 A pertinent neurologic review of symptoms and a physical examination should be performed immediately if a neurologic complication is suspected.

Respiratory Complications
Respiratory arrest occurs when a patient becomes apneic for greater than 1 minute, due to lack of central respiratory drive or paralysis of the muscles of respiration. 29 Respiratory arrest may occur from a variety of causes, including oversedation, central nervous system trauma, and intrathecal or epidural injection of a sufficient amount of local anesthetic to cause spinal anesthesia.
Treatment requires immediate recognition of the condition and emergent support of vital signs. If the cause is self-limited, treatment may require the support of respiration and other vital signs as needed until spontaneous and adequate respiration resumes. If the cause can be easily reversed, it should be (as when too much narcotic or sedative has been given). In this particular situation, it is important to remember the half-life of the reversing agent, compared to the half-life of the narcotic or sedative being reversed. If the narcotic or sedative’s half-life is longer than that of the reversing agent, respiratory compromise may resume when the reversing agent has been metabolized.
The true incidence of respiratory depression due to spinal opioid administration is unknown. Factors that may cause respiratory depression include the use of sedatives, parenteral or spinal opioids, and local anesthetics. One of the main advantages of spinal versus parenteral opioid administration is the lack of respiratory depression with the former. 30 It should be emphasized that respiratory rate alone is inadequate to establish the presence or lack of respiratory depression. The measurement of blood gases remains the preferred option. 29
Other respiratory complications due to spinal injections include pneumothorax and injury to the recurrent laryngeal nerve. A pneumothorax may occur during a lower cervical procedure such as a discogram, selective nerve root block, or thoracic procedure (such as an intercostal nerve block). As a general rule, a pneumothorax may not occur if a needle penetrates the pleural cavity or lung parenchyma, unless it is placed through a bleb, the needle is 18-gauge or larger, or a solution has been injected.
When a pneumothorax does occur, it is usually self-limited and causes only minor collapse(s) of the lung (10%). 31 Treatment includes close observation with supportive care, usually in a hospital, and serial chest radiographs. A chest tube should be placed if the pneumothorax advances significantly over 25% or the patient develops shortness of breath or other signs of respiratory distress.
Injury to the recurrent laryngeal nerve may cause unilateral vocal-cord paralysis, reduced ability to protect the airway, and hoarseness. This injury is usually self-limited and resolves on its own; but it may be clinically significant while the patient is recovering from sedation, or when there is preexisting underlying pathology that causes marginal airway protection (e.g., stroke or laryngeal cancer).

Urological Complications
The application of local anesthetics and/or opioids to the lumbar and sacral nerve roots results in higher incidence of urinary retention. 32 This side-effect of lumbar epidural nerve block is seen more commonly in elderly males, multiparous females, and patients who have undergone inguinal and perineal surgery. Overflow incontinence may occur if such a patient is unable to void or bladder catheterization is not utilized. All patients undergoing lumbar epidural nerve block should demonstrate the ability to void the bladder prior to discharge from the pain center.

Dural Puncture
In the hands of the experienced interventional spine specialist, inadvertent dural puncture during lumbar epidural injections should occur in <0.5% of cases (or 1 in 200 epidural injections). 33 This occurs when the dura mater is violated by the epidural needle, and a sufficient amount of cerebrospinal fluid leaks out from the thecal sac, causing a positional headache. 34 - 37 The rare occurrence of postdural puncture (spinal-tap) headache is an annoying side effect, but is generally benign for the most part and will pass without permanent harm or morbidity to the patient.
Rarely, with dehydration and severe nausea and vomiting, uncal herniation may occur, with associated brainstem involvement and potentially death. 38 If a needle is placed subdurally and epidural doses of local anesthetics are administered, the signs and symptoms are similar to subarachnoid injection. 39 The subdural or subarachnoid injection of large doses of local anesthetics may cause total spinal anesthesia, loss of consciousness, hypotension, cardiovascular arrest, apnea, and even death. This condition requires immediate resuscitative measures and support of all vital signs until the condition resolves. Intubation is usually required to adequately control the airway and ventilate the patient.

Fluoroscopic Exposure
Epidural injections performed without fluoroscopy are not always placed into the epidural space, at the desired vertebral interspace; or the medication does not get to the desired target organ due to anatomic abnormality, as noted in various sources. 40 - 48 For this reason, most spine-management specialists recommend fluoroscopic direction and the use of nonionic or low ionic contrast agents for epidural injections. This helps confirm accurate needle placement and the delivery of the injected solution to the appropriate target organ. 48
The risk of fluoroscopic exposure to the patient is minimal, for one procedure or several isolated ones because each procedure should require minimal (<20 seconds) fluoroscopic exposure time. Related exposure to the physician, attending nurse, x-ray technician, and anyone else consistently in the procedure room should be viewed as cumulative.
To limit exposure to these patient care providers (PCPs), it is important to note that radiation dissipates at the inverse of the square of the distance from the tube. As a result, if PCPs are able to stand six feet or more away from the fluoroscopic tube, their risk of excessive exposure is minimal. The fluoroscopy anode should also be kept under the procedure table because this anode is the source of the radiation. With these precautions, the patient absorbs the bulk of the directed radiation. The vast majority of the relatively small amount of other radiation spilled into the room is known as “scatter radiation”, which has much less ability to penetrate tissues than directed radiation.
In addition, the PCPs should wear appropriate protective garments. The physician should wear a lead apron, thyroid shield, radiation-attenuating gloves, and perhaps lead-lined glasses. The nurse and x-ray technician should wear wrap-around lead aprons because their backs are frequently turned toward the radiation source, and thyroid shields. All PCPs should wear radiation badges on their thyroid shields and aprons; and the physician should consider wearing a ring badge, if his or her hand is routinely in the radiation field during active fluoroscopy.
Finally, the fluoroscopy unit must be routinely maintained and inspected to confirm its proper function and safety. Proper fluoroscopy use (including safe radiation practices) can direct and confirm accurate needle placement, maximizing benefits while limiting potential risks for patients and PCPs.

Medication Reactions
Adverse drug reactions are rarely seen with medications used during spinal injections. The treating physician should be aware of drug toxicity, side effects, allergic reactions, and concentration and dosing of all medicines used.
Lidocaine and bupivacaine are the most common local anesthetics used during spinal injections. Awareness of their potential central nervous system (CNS) effects, cardiovascular toxicity, and side effects is very important. Strict cardiovascular and neurologic monitoring is required before, during, and after the procedure. Although most anaphylactic reactions typically occur within 2 hours after the epidural injection, they have been known to occur up to 6 hours later. 49
Local anesthetics primarily function by reversibly blocking sodium channels in nerve and muscle membranes, having a direct effect on sympathetic nerves when injected into the subarachnoid space and the cardiac tissue (when injected intravascularly). If the sympathetic system is sufficiently blocked, hypotension may result; and if cardiac muscle is sufficiently blocked, decreased contractility may result.
When injected intravenously, lidocaine is “fast-in and fast-out,” reaching steady state in one to two heart beats. Bupivacaine is “fast-in and slow-out,” and its blocking action increases as the heart works harder. These are the main direct effects that can cause cardiac arrest. Cervical and thoracic level blocks have an increased risk for complications because of the regional neural supply to the heart and respiratory control.
Central nervous-system toxicity by 1% lidocaine has an onset at plasma concentrations of 5-10 mcg/mL, which is slightly more than 400 mg (or 40 mL) of total intravenous bolus. Bupivacaine is about four times more toxic than lidocaine, with a toxic bolus of 100 mg (or 10 mL). 50
A person with CNS toxicity usually presents with complaints of circumoral numbness, disorientation, lightheadedness, nystagmus, tinnitus, and/or muscle twitching in the face or distal extremities. Peak plasma concentrations occur 10 to 20 minutes after injection. For that reason, patient monitoring for at least 30 minutes following an epidural injection with a significant bolus of lidocaine or bupivacaine is mandatory.
Methylprednisolone, triamcinolone, and betamethasone are the most commonly used corticosteroid preparations. Side effects are uncommon but could include headache, dizziness, insomnia, facial erythema, rash and pruritus, low-grade “fever” (<100° F), hyperglycemia, transient hypotension and hypertension, increased back or limb pain, fluid retention, mood swing, euphoria, menstrual irregularity, and gastritis. 17 Other rare side effects include elevation of cerebrospinal-fluid protein levels, septic or aseptic meningitis, worsening of multiple sclerosis symptoms, sclerosing spinal pachymeningitis, exacerbation of latent infection, near-fatal septic meningitis (intrathecal injection), hypercorticism, and congestive heart failure.

Anaphylactic and Allergy Reactions
Anaphylactoid (without histologic immune response) and anaphylaxis (with a histologic immune response) occur most often within 2 hours after the epidural injection, and have been known to develop up to 6 hours later. 49 These usually cause fatalities by respiratory-related complications involving mechanical airway obstruction. Therefore, monitoring patients closely for approximately 30 minutes after the procedure is recommended. Informing the patient about possible risks and side effects can also expedite early identification of complications.

Bleeding Complications
Epidural hematoma formation following injection is extremely rare. Bleeding usually occurs because of damage to the veins in the highly vascular epidural space. Medications that interfere with the clotting mechanism include heparin, warfarin, aspirin, and most nonsteroidal anti-inflammatory drugs (NSAIDs). 5, 17, 18
Patients usually present with severe neck or back pain, associated with any significant neurologic complaint, right after the procedure. 17 An immediate physical examination, followed by a computer tomography (CT) scan or MRI (magnetic resonance imaging) scan, is essential for patients thought to have an epidural hematoma because early surgical intervention can limit or even prevent permanent neurologic damage ( Fig. 6-3 ).

Figure 6-3 Acute epidural hematoma and subarachnoid hemorrhage (CT scan view). Thoracic spine view showing a lenticular, high-density epidural hematoma ( open arrow) causing spinal cord compression. Acute hemorrhage is noted in the subarachnoid space.

Specific Complications of Selective Spinal Injections

Lumbar Epidural Injections
The lumbar epidural space is highly vascular. Inadvertent intravenous placement of the epidural needle occurs in approximately 0.5% to 1% of patients undergoing lumbar epidural anesthesia. 33 This rare complication is mostly seen with distended epidural veins, such as those present in pregnant patients and patients with large abdominal tumor masses.
If the misplacement is unrecognized, injection of a large volume of local anesthetic directly into an epidural vein may result in significant local anesthetic toxicity. 51 Careful four-quadrant aspiration (aspiration in all four quadrants by rotating the needle), prior to injection of drugs into the epidural space, is mandatory in identifying the vascular placement of the needle when performing a “blind” (nonfluoroscopically-guided) epidural injection.
Neurologic complications of lumbar nerve block are uncommon if proper technique is used. Usually, these complications are associated with a preexisting neurologic lesion or with surgical or obstetric trauma, rather than with the lumbar block itself. 32
Direct trauma to the spinal cord or nerve roots is usually accompanied by pain. Any significant pain that occurs during placement of the epidural needle or catheter, or during injection, should warn the injectionist to pause and confirm needle placement before proceeding. 33 The use of deep intravenous sedation or general anesthesia prior to initiation of epidural nerve block may reduce the patient’s ability to provide accurate verbal feedback if needle misplacement occurs. Therefore, conscious sedation or general anesthesia prior to epidural nerve block should be employed with caution. 52
When the patient’s lower-extremity neurologic status deteriorates rapidly or when a cauda equina syndrome is suspected within 24 to 48 hours following an epidural procedure, an expanding epidural hematoma should be considered. 53 If the injectionist suspects that diagnosis, an immediate and complete clinical evaluation is mandatory. If the diagnosis is still suspected following the clinical evaluation, a lumbar CT scan or MRI scan should be obtained ( Figs. 6-4 through 6-6 ). If the diagnosis is confirmed, an emergent surgical consult to consider decompression should be arranged.

Figure 6-4 Herniated nucleus pulposus (MRI view). A, T1-weighted sagittal image showing impingement of the thecal sac by the herniated nuclear material ( white arrow). B, Axial sagittal gradient echo image showing the herniation shifted to the left ( black arrow).

Figure 6-5 Posterolateral disc herniation (CT scan view). Left-sided focal protrusion of the disc ( black arrow), leading to posterior displacement of the left S1 nerve root ( open arrow) and effacement of the anterior epidural fat. This is in contrast to the epidural fat on the right and normal location of the right S1 nerve root ( white arrow).

Figure 6-6 Posterolateral disc herniation (lumbar myelogram view). Oblique view performed with water-soluble contrast revealing the abrupt termination and widening of the S1 nerve root sleeve ( white arrow ).

Caudal Epidural Injections
Incorrect needle placement during caudal epidural injection occurs 25% to 40% of the time. 54, 55 The needle may be placed outside the sacral canal, resulting in injection of air or fluid into the subcutaneous tissues, periosteum, sacrococcygeal ligament, sacral marrow cavity, and/or pelvic cavity, possibly entering both the rectum and/or vaginal vault.
The application of local anesthetic and opioids to the sacral nerve roots results in increased incidence of urinary retention, especially in elderly males and multiparous females, and after inguinal and perineal surgery. The use of smaller doses of local anesthetic will help avoid these burdensome complications, without adversely affecting the efficacy of caudal epidural steroid injections when treating painful conditions. 56
Because of the proximity of the sacral hiatus to the perineum, there is increased incidence of epidural abscess and meningitis compared to the interlaminar or transforaminal injection route. When placing the epidural needle, remembering that the thecal sac usually ends at the S2 bony level, but may end as low as S4, is important. Therefore, the needle should be placed no higher than absolutely necessary to assure epidural injection.
If the needle penetrates the thecal sac, results may include a positional headache and/or lowering of the body’s protection against meningitis because the thecal sac will have been violated. In addition, if this needle malposition is not detected prior to injection, an intrathecal injection may occur—potentially causing a spinal block and its associated sequelae.

Cervical Epidural Injections
Because of the potential for hematogenous spread via Batson plexus, local infection and sepsis represent absolute contraindications to the cervical approach to the epidural space. Anticoagulation and coagulopathy also represent absolute contraindications to cervical epidural nerve block because of the risk of epidural hematoma. 5, 6, 17, 18
Because the spinal cord lies within the spinal canal, there is increased risk for spinal cord injury with the injection technique, as compared to lower- or midlumbar injections. Central canal stenosis, either from bony eburnation, central disc herniation, or congenital shortening of the pedicles, represents an absolute contraindication to performing an interlaminar epidural injection at that level ( Figs. 6-7 and 6-8 ). 57, 58

Figure 6-7 Degenerative central spinal stenosis (schematic view). Lumbar vertebra at the disc level is noted in the axial view. It is noted that the osteophytes derived from the articular processes can lead to thecal sac compression.

Figure 6-8 Central spinal stenosis (CT scan view). Marked hypertrophy of the ligamentum flavum ( open arrows) is noted to directly cause thecal sac compression; also seen is mild annular bulging and facet joint arthropathy.

Thoracic Epidural Injections
Thoracic epidural techniques are similar to lumbar techniques; but the presence of the narrow epidural space, and proximity to the spinal cord in the thoracic vertebral canal, makes spinal cord trauma more likely. The incidence of spinal cord damage is unknown, although the incidence of infection is increased in the thoracic spine when compared to the lumbar spine. 59
The presence of the lungs on either side of the spine makes a pneumothorax a potential complication not usually considered with either a cervical or lumbar injection. The injection of local anesthetic in the mid-thoracic epidural space may cause inhibition of the cardiac accelerator zone, causing hypotension and bradycardia and its potential sequelae. In addition, a thoracic motor block from either the epidural or intrathecal injection of local anesthetic can cause up to 50% reduction in tidal volume, making adequate ventilation of a patient with pulmonary disease difficult.

Selective Nerve Root Blocks
Selective nerve root blockade has been used interchangeably as a spinal nerve block, selective epidural, or an anterior ramus block. 48 In this brief discussion we will deal with each separately.
A spinal nerve block occurs when the needle tip is placed within the neural foramen; and local anesthetic affects only the spinal nerve and does not migrate inside the spinal canal. The main risk of this injection technique is trauma to the spinal nerve or dorsal root ganglion. If the needle penetrates the dural sleeve, an intrathecal injection may occur with associated risks and complications.
A selective epidural occurs when fluid is injected into the epidural space via a neural foramen. To accomplish this, the needle is also placed within the neural foramen; thus, trauma to the spinal nerve or dorsal root ganglion is possible. Injection into the dural sleeve is also possible—with all its associated risks and complications.
An anterior ramus block is an extraspinal injection of the anterior ramus. This occurs 1 to 2 cm outside of the neural foramen and local anesthetic does not reach the spinal canal or spinal nerve. The main complication of this blockade is direct trauma to the anterior ramus from the needle or the disruption of the neural vasculature, causing an intraparenchymal hematoma or neural infarct.

Discography
The most common severe complication after discography is infection of the disc, commonly referred to as discitis. This should occur no more frequently than in 1 in 500 to 1 in 750 discs injected. 60, 61 The most common organisms infecting the lumbar disc are S. aureus and Staphylococcus epidermidis. 60, 62
Occasionally, a colonic organism involves the lumbar discs, resulting from penetration of the colon with the discography needle. Because of the limited blood supply of the disc, such infections may prove difficult to eradicate.
Discitis usually manifests as an increase in spine pain 5 to 14 days following discography. Acutely, there should be no change in the patient’s neurologic status. An elevated sedimentation rate will be seen within the first week to 10 days. 63 - 65 The preferred option in the detection of discitis is now considered to be magnetic resonance imaging (MRI), which was found to be superior to bone scanning with a 92% sensitivity, 97% specificity, and 95% overall accuracy ( Fig. 6-9 ). 66 - 68

Figure 6-9 Lumbar disc space infection (MRI view). T1-weighted image showing areas of low signal of the L-4 and L-5, with the anterior paraspinal mass noted ( white arrow).
The incidence of thoracic discitis following a thoracic discogram is unknown, but the organisms infecting those discs following discography should be similar to those involving the lumbar discs. Similarly, the incidence of pneumothorax and large-vessel damage following thoracic discography is also unknown. In one series of 230 outpatient thoracic discograms, Schellhas reported a zero incidence of pneumothorax. 69 Although this is encouraging, the complication does still occur; thus, the procedure should not be attempted without substantial experience and training.
Cervical discitis is generally profound and life threatening. The esophagus has gram-negative and anaerobic bacteria as components of its normal flora. Therefore, placing the discography needle through it and into the disc may seed the disc with bacteria that may initiate a profound infection.
In the mid- and lower-cervical spine, the esophagus lies on the left side of the larynx. The carotid sheath lies on the anterolateral surface of the cervical spinal column. As a result, a cervical discogram should be performed using a right-sided paralaryngeal approach. In performing this approach, the esophagus should be pushed to the left and the carotid sheath to the right, thereby minimizing the risk of trauma to these structures. If the needle does penetrate the carotid sheath, direct injury to the vagus nerve or carotid artery could occur with associated risks and complications.
In addition to infectious complications, pneumothorax may occur after cervical and thoracic discography. This complication should rarely occur if appropriate techniques are used. Most pneumothoraces following cervical or thoracic discography are small (10% to 15% of lung volume) and can often be treated conservatively. However, all pneumothoraces must be taken seriously and observed overnight, with serial chest radiographs and close monitoring of vital signs and blood gases. If the pneumothorax progresses, a chest tube must be placed.
Direct trauma to the nerve roots and the spinal cord can occur if the needle is allowed to traverse the entire disc or is placed too laterally. These complications should rarely occur if appropriate techniques and precautions are used. Such needle-induced trauma to the cervical spinal cord can result in syrinx formation with attendant progressive neurologic deficit, including quadriplegia.

Intercostal Nerve Blocks
Given the proximity of the pleural space, pneumothorax after intercostal nerve blocks is a distinct possibility. The incidence of the complication is less than 1% (0.082%), 70 but it occurs with greater frequency in patients with chronic obstructive pulmonary disease. Because of the proximity to the intercostal nerve and artery, when analgesia is produced from the intercostal block, the compensatory vasoconstriction eases, and the patient may become hypotensive. In a similar manner, intercostal blocks can lead to respiratory failure when pain relief from the block unmasks the ventilatory depression of previously administered, but ineffective, parenteral narcotics. 71

Facet Joint Nerve Blocks
The problem cited most often with these procedures is a transient exacerbation in pain (about 2% incidence), lasting as long as 6 weeks to 8 months in some cases. 17, 72, 73 Spinal anesthesia may occur after facet joint injection if the needle is positioned within the thecal sac, or if there is an abnormal communication between the facet joint capsule and the thecal sac. Chemical meningitis after lumbar facet block has been reported. 73 - 75 These complications are thought to have occurred after inadvertent dural puncture. Facet-capsule rupture also occurs, especially if more than 2.0 mL of injectate is used for intraarticular injections. 48
During performance of cervical facet blockade, there is potential risk of entry into the intervertebral foramen, spinal canal, and vertebral artery. These complications occur more frequently using a lateral intraarticular technique than with blockade of the medial branches innervating the cervical facets because the former technique requires deeper penetration of the needle into the joint and toward the spinal structures. Local anesthetic may leak out of the joint into these areas, causing motor and sensory blockade with attendant risks and complications.
Third occipital nerve blocks can cause transient ataxia and unsteadiness due to partial blockade of the upper cervical proprioceptive afferents and the righting response. 76, 77 In one study of cervical facet joint radiofrequency denervation, 13% of patients complained of postprocedure pain that resolved in 2 to 6 weeks. Four percent of patients complained of occipital hypesthesia, probably due to a lesion of the third occipital nerve, which resolved in 3 months. 77 No persistent motor or sensory deficits occurred.

Sympathetic Nerve Blocks
In the cervicothoracic (stellate ganglion) block, acute, potentially life-threatening complications may occur, including seizure, spinal block, hypotension, or pneumothorax. 78 - 82 Additional complications could include block or injury to the recurrent laryngeal nerve, phrenic nerve, sympathetic trunk, apex of the lung, or brachial plexus.
In the lumbar sympathetic block, potential complications include intravascular injections, intradural injections with spinal anesthesia or postural headaches, hypotension, lumbar-plexus block, renal puncture, or genitofemoral neuralgia. 79, 83, 84 Other risks include injury to the spleen, intestines, and/or liver, and injection of large volumes of local anesthetic into the aorta or inferior vena cava.

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Appendix I
American Heart Association, Advanced Cardiac Life Support (ACLS) Protocols, 2005

Appendix II Treatment of Acute Reactions

Urticaria

• Discontinue injection
• Diphenhydramine (Benadryl) or hydroxyzine (Vistaril), PO/IM/IV, 25-50 mg
• Cimetidine PO/IV, 300 mg or ranitidine PO/IV, 50 mg
• If severely disseminated, give epinephrine SC (1:1000), 0.1-0.3 mL

Facial and laryngeal edema

• Epinephrine SC (1:1000), 0.1-0.2 mL; or if hypotensive, give 1:10,000, slowly, IV, 0.1 mL
• Oxygen via mask/endotracheal tube, 6-10 L/min ∗
• If resuscitation needed, initiate ACLS protocol and call EMS

Bronchospasm

• Oxygen via mask, 6-10 L/min ∗
• Monitor vital signs (BP, pulse oximetry, and ECG)
• Beta-agonist inhalers (e.g., albuterol)
• Epinephrine SC (1:1000), 0.1-0.2 mL; or if hypotensive, give 1:10,000, slowly, IV, 0.1 mL
• If oxygen saturations persist <88%, initiate ACLS protocol and call EMS

Hypotension with tachycardia

• Reverse Trendelenburg position
• Monitor vital signs (BP, pulse oximetry, and ECG)
• Oxygen via mask, 6-10 L/min ∗
• Rapid administration of large volumes, IV, isotonic Ringer lactate or normal saline solution
• If poorly responsive, epinephrine SC (1:10,000), 1.0 mL, slowly, IV

Hypotension with bradycardia—vagal reaction

• Reverse Trendelenburg position
• Monitor vital signs (BP, pulse oximetry, and ECG)
• Oxygen via mask, 6-10 L/min ∗
• Secure IV access and initiate rapid administration of large volumes, IV, of isotonic Ringer lactate or normal saline solution
• If poorly responsive, atropine, 0.6-1.0 mg, slowly, IV
• Repeat atropine to a total dose of 0.04 mg/kg (2-3 mg) in adult patient

Hypertension (severe)

• Monitor vital signs (BP, pulse oximetry, and ECG)
• Nitroglycerin, 0.4 mg, SL or Nitropaste topical ointment, 1-2 inch
• If persistent, transfer for further evaluation to ER or ICU setting
• For pheochromocytoma, give phentolamine, 5 mg (adults), 1 mg (children)

Seizures—convulsions

• Monitor vital signs (BP, pulse oximetry, and ECG)
• Oxygen via mask, 6-10 L/min ∗
• Maintain IV access
• Protect patient from physical injury during seizure
• Insert bite block
• If seizure is longer than 2 minutes, secure airway and oxygenate
• Obtain neurologic consult
• Give diazepam (Valium), 5 mg, IV, or midazolam (Versed) 2.5 mg, IV
• If longer effect needed, consider phenytoin (Dilantin) infusion, 15-18 mg/kg, at rate of 50 mg/min
• Consider ACLS protocol, if intubation is needed

Pulmonary edema

• Elevate torso; rotating tourniquets (venous compression)
• Oxygen via mask, 6-10 L/min ∗
• Diuretics—furosemide (Lasix), 40 mg, IV, slow push
• Consider morphine
• Transfer to ICU or ER setting, for further management

Prophylaxis for adverse intravascular iodinated contrast media reactions

• Avoid unnecessary exposure to contrast medium
• Substitute nonionic for ionic contrast medium
• In adults, give prednisone, 50 mg, PO, 12 hrs, then 2 hrs prior to procedure
• Give diphenhydramine (Benadryl), 50 mg, PO, 1 hr prior to procedure
• For pheochromocytoma; give phenoxybenzamine, 10-20 mg, 3-4 times/day, PO, for 7-10 days; or 24 hours prior to procedure, give phenoxybenzamine, 0.5 mg/kg in 250 mL of D5W, slowly, IV, over 2 hrs

Dysrhythmias

• Refer to ACLS protocol

∗ Always administer supplemental oxygen with caution in a patient with chronic pulmonary disease.
7 Procedural Documentation and Coding

Kim Pollock, RN, MBA, CPC
Successful pain management practices have implemented processes and procedures that focus on customer service, physician and staff efficiency, and risk reduction which result in optimizing the revenue cycle. The goal is to ensure that all revenue cycle tasks are performed by the right number of people at the right time with the right tools to collect timely and optimal revenue. The revenue cycle, or the process of getting paid, begins with the patient entering a pain management practice and ends with collection of all collectable dollars associated with the services provided to that patient. Every employee and provider in the practice, from the person who answers phones to the pain management professional, has an important role to play in the revenue cycle.
Revenue cycle processes can be divided into two types as shown in Table 7-1 —the processes performed on the front-end and the processes performed on the back-end. Front-end processes are those that typically are performed with patient involvement, whereas back-end processes are performed without the patient’s involvement or presence. The accuracy of patient information and timely completion of front-end processes drives the success of the back-end processes to ultimately achieve revenue optimization.
Table 7-1 The Front-End and Back-End Revenue Cycle Processes Front-End Processes Back-End Processes Appointment scheduling and pre-registration Claim/statement production Insurance verification and referral management Payment processing and analysis Check-in Denials management Patient encounter Accounts receivable follow-up Test/procedure coordination   Check-out  

Front-End Processes
Front-end processes in the revenue cycle include appointment scheduling and preregistration, insurance verification and referral management, check-in, the patient encounter (where coding and documentation occur), test/procedure coordination, and check-out.

Appointment Scheduling
Appointment scheduling is typically the practice’s first encounter with the patient and is one of the most critical steps in the revenue cycle. Future third-party billings and collections efforts depend on the quality of the data obtained at this time. Therefore, it is imperative that accurate and complete patient demographic and insurance information be obtained. The appointment scheduling process includes, but may not be limited to, the following tasks:
• Obtain all patient demographic and referring provider information and enter into the practice management information system (PMIS); this is called preregistration
• Re-register all established patients (e.g., verify or update previously obtained demographic and insurance information)
• Make the appointment, hopefully within patient’s desired time frame
• Inform the patient of practice’s financial policies including collection of co-payment at the point of service (POS),
• Refer the patient to the practice’s website (if one is available) to download a map, health history form, other patient education materials
• Coordinate or make a reminder phone call to the patient about the appointment and financial policies
Successful practices obtain patient demographic information directly from the patient, rather than from the referring physician’s office, to ensure accuracy. Practices that are business savvy offer on their website the ability to make an appointment and provide preregistration demographic and insurance information.

Insurance Verification
Insurance verification and referral management can be a separate process, depending on the size of the pain management practice, or it can be performed at the time of appointment scheduling. Practices obtain required managed care referrals and verify the patient’s insurance eligibility and benefits prior to all new patient appointments to ensure appropriate collections on the back-end. Successful practices will re-verify insurance benefits on all established patients not in a postoperative global period. All too often a practice finds that a patient, new or established, does not have the insurance coverage he or she claims to have and the practice ultimately is not paid for rendered services.
Validation of insurance eligibility and benefits as well as obtainment of referrals for pain management services may be done electronically through on-line capabilities with many payors. It is not always necessary to have this task performed via telephone call requiring staff time. The on-line capabilities come in various formats, such as accessing information directly from a payor’s on-line database or through the PMIS vendor who might perform “batch” (for a group of patients) or “on demand” (for an individual patient) eligibility and benefits verification for the practice.
In summary, the goal of the first two steps in the revenue cycle is to gather and verify patient demographic and insurance information prior to the appointment to provide an optimal opportunity to assess the financial risk, verify insurance eligibility, and obtain proper referrals to ensure appropriate revenue collection when the service is provided.

Check-In
The receptionist plays an important role in the revenue cycle process by validating the patient’s identity and the previously obtained insurance information, as well as collecting any mandatory copayment. Tasks required at the check-in phase of the revenue cycle include, but are not limited to:
• Marking the patient as “arrived” in the PMIS so the system “looks for,” or reconciles, a corresponding charge for the service provided
• Scanning the patient’s insurance card into the PMIS (or photocopying for the paper chart)
• Validating the patient’s identity by comparing the name on the insurance card to the name on a government-issued photo identification card to the patient’s actual identity
• Obtaining required signatures on practice forms or electronic documents (e.g., consent to treat, information release) and communicating the projected patient financial responsibility for the service
• Collecting any insurance company mandated co-payment, entering this action in the PMIS, and providing a system-generated receipt to the patient
It is imperative that co-payments be collected at the point-of-service because this is the point at which the patient’s motivation to pay is greatest and the cost of collections is lowest.

Patient Encounter
The pain management provider renders a service in the office (e.g., evaluation and management code, radiology code) or a procedural service (e.g., injection code, surgery code) and is responsible for documenting and coding the service so accurate billing can occur. Coding for, and documentation of, services performed is best performed by the rendering provider because these are critical components of the revenue cycle. Coding is typically performed on a paper charge ticket, also called an encounter form, or may be done electronically through the PMIS.

CPT Codes
Current procedural terminology (CPT) is a set of codes, descriptions, and guidelines intended to describe procedures and services performed by physicians and other health care providers. Each procedure or service is identified with a five-digit code. The CPT manual is updated annually by the American Medical Association (AMA) and the pain management professional specialty societies contribute to CPT code development and maintenance. There are extensive service and procedure coding requirements published in the CPT manual. Providers are responsible for knowing how to accurately report, and document, CPT codes for the services rendered.
There are three categories of CPT codes. Category I CPT codes describe a procedure or service identified with a five-digit numeric CPT code and descriptor nomenclature; these are considered the “usual” CPT codes and are widely accepted by third party payors.
Category II codes, five-digit codes with four numbers and ending with the letter “F”, are intended to facilitate data collection on positive health outcomes and quality patient care. Category III codes, five-digit codes with four numbers but ending with the letter “T”, facilitate data collection on and assessment of, new services and procedures and are used to report procedures that do not have a Category I code. Payors require a valid Category I and/or Category III code(s) for payment consideration. The various types of CPT codes are listed in Table 7-2 with a notation of the application to the pain management specialty.
Table 7-2 Types of CPT Codes ∗ and Application to Pain Management Category I CPT Codes CPT Code Number Type of CPT Code Application for Pain Management 00100-01999, 99100-99140 Anesthesiology Codes describe administration of anesthesia during procedures (generally surgery CPT codes) performed by another provider/physician 10021-69990 Surgery Includes codes for injections, placement of pain pumps, and other pain management diagnostic and therapeutic services 70010-79999 Radiology (including nuclear medicine and diagnostic ultrasound) Includes fluoroscopic guidance and localization of needle or catheter tip for pain management procedures as well as diagnostic radiologic procedures 80047-89356 Pathology and laboratory These codes are generally not used by pain management providers 90281-99199, 99500-99607 Medicine (except anesthesiology) Includes nerve conduction and electromyography diagnostic testing codes 99201-99499 Evaluation and management Includes codes for office visits, consultations, and hospital visits used by pain management providers Category II CPT Codes 0001F-7025F These codes are supplemental tracking codes that can be used for performance management. They are intended to facilitate data collection about quality of care rendered; the use of these codes is optional. Includes codes for oncologic pain management as well as assessment and examination of back pain Category III CPT Codes 0016T-0196T These codes are used to report temporary codes for emerging technology, services, and procedures and are used instead of an unlisted Category I CPT code (e.g., 64999). Includes code for percutaneous intradiscal annuloplasty
∗ As per CPT 2009.

ICD-9-CM Codes
ICD-9-CM codes classify diseases and a wide variety of signs, symptoms, abnormal findings, complaints, social circumstances, and external causes of injury or disease. These three, four, and five digit diagnosis codes are used to support, or justify, the CPT codes reported by providers. ICD-9-CM codes are published by the World Health Organization (WHO), whereas the annual coordination and maintenance process is jointly controlled by two branches of the United States government—the National Center for Health Statistics (NCHS) and the Centers for Medicare and Medicaid Services (CMS).
Audits comparing code(s) selected by pain management providers to the documentation should be performed on a regular basis to ensure compliance with third party payor and AMA guidelines. Regular audits and coding education are important components to a practice’s revenue and compliance success.

Test/Procedure Coordination
Many pain management practice patients will require further diagnostic testing and/or diagnostic or therapeutic procedures after seeing a pain management professional. Third party payors often require precertification for testing, such as radiologic procedures, including plain films, magnetic resonance imaging (MRI), and CAT (computerized axial tomography) scans. Successful practices will incorporate this precertification need into the revenue cycle process, particularly if the practice has the capabilities of performing the imaging service. Imaging services performed, and billed, by a pain management professional require the production of a radiologic interpretation report which must be separate from the office visit documentation.
Procedural services, such as injections and surgical procedures, also may require precertification prior to performance of the procedure. The procedure coordinator’s duties include, but are not limited to:
• Reverification of insurance eligibility if significant time has passed since the previous insurance eligibility verification
• Precertification and specific third party benefits information for the service (some payors allow this to be performed on-line)
• Scheduling necessary preprocedure or preadmission testing
• Scheduling the procedure in the designated facility (e.g., ambulatory surgery center, hospital)
• Presurgical financial counseling and collection of a procedure deposit to include the projected patient financial responsibility calculated after obtaining third party benefits information
• Procedure/surgery charge entry (or this may be done on the back-end)
• Reconciling the procedure scheduling log to ensure all charges are received from the rendering pain management professional

Check-Out
After the office encounter is complete, successful practices have incorporated at the point-of-service the task of collecting from the patient any estimated co-insurance, unmet deductible, as well as any previously unpaid balance. Alternatively, previously unpaid balances may be collected during the check-in process. Like collection of co-payments at check-in, collecting patient-responsible portions of the service charge will result in optimal collections and a reduction in expense for patient statement production.
Additional duties performed at check-out include, but are not limited to:
• Scheduling follow-up appointment to avoid delayed follow-up or accessibility problems
• Checking for unanswered questions and additional service opportunities
• Checking service to ensure the patient’s experience was good
• Posting charges for the service(s) rendered as well as any payments and generating a receipt from the PMIS
• Reconciling “arrived” patients to provider completed charge tickets/encounter forms received to ensure a charge is received for each patient seen that session
The best time to collect from a patient is at the point-of-service on the front-end where there is direct patient contact.

Back-End Processes
Back-end processes in the revenue cycle include claim/statement production, payment processing and analysis, claim denials management, and accounts receivable follow-up.

Claim and Statement Production
Professional claims to third party payors can be sent electronically or on paper (also known as hard copy) using a CMS 1500 health insurance claim form. Successful practices submit accurate electronic claims on a daily basis to as many payors as possible; some payors, such as many worker’s compensation plans, require paper claims. Payors tend to process electronic claims in a more timely manner, which helps pain management practices improve cash flow and keep the accounts receivable low.
Table 7-3 includes seven very important tips for successful claim submission. The goal is to submit only once a “clean” claim, meaning one without errors or omissions, and be paid in a timely manner.
Table 7-3 Tips for Successful Claim Submission
• Enter the patient’s name as it appears on the insurance benefits card. Watch for patients using their middle name as a first name and be sure to enter initials.
• Enter patient or payor identification numbers with proper prefixes and/or suffixes.
• Correlate CPT code(s), in box 24D, to the corporate ICD-9-CM code(s) listed in box 21 on the claim form.
• Report CPT codes in descending value order—the highest listed first.
• Enter bilateral procedures, using modifier 50, either on one line (called the “bundled” format) or on two lines (“line-item” format) as noted below. Check with payors for format preference of bilateral procedures to ensure appropriate reimbursement.
• Bundled format Line-item format
• 64475-50 1 unit Double fee 64475 1 unit Single fee
• 64475-50 1 unit Single fee
• List the name and national provider identification number (NPI) of the provider requesting the consultation in boxes 17, 17A, and 17B of the CMS 1500 health insurance claim form.
• Generally box 23 is used for referral, authorization, or precertification numbers, although some plans may use box 19 instead. Check with individual payors for preference.
Practices typically send third party payor claims to a clearinghouse for review, or “scrubbing”, to ensure the demographic, insurance, and code information is appropriate prior to the claim being sent to the insurance company. The edit report, or list of errors noted on the submitted claim, received by the practice must be rectified on a daily basis.
Patients are sent statements on a periodic basis, usually monthly, showing the balance owed to the provider. The first statement should be sent, if a patient balance exists, immediately on the practice’s receipt of a third party payment. Patient statements may be generated by the PMIS or outsourced to a third party for processing and mailing. Again, it is important to collect as much from patients at the time of service (office or procedure) to avoid the expense of sending a statement after the service is rendered.

Payment Processing and Analysis
Payments from third party payors and patients come to the practice in various ways including:
• Mailed directly to the practice
• Mailed to a bank lockbox
• Electronically paid using the practice’s website capabilities
• Electronically paid to the practice’s bank account (also known as electronic funds transfer, or EFT).
Third party payor payments are usually accompanied by an explanation of benefit (EOB) form that describes the payor’s payment or nonpayment of services submitted. Specific EOB information necessary for analysis includes, but is not limited to:
• Payment amount
• Contractual allowances
• Co-payment, deductible, and co-insurance amounts (e.g., patient financial responsibility)
• Rejection or denial codes
The practice should expect to receive an EOB for every service submitted to a third party payor. EOBs may be received on paper or electronically, called electronic remittance advice (ERA). Many payors will show their payment by “line item,” or by each CPT code billed. Yet, others lump services as medical services or surgical services. When the latter happens, the practice’s staff must contact the payor to determine how to allocate in the PMIS all payments for each service and determine that the payment is correct.
Efficient practices receive as many electronic payments, and EOBs, as possible to decrease human resource expense for posting payments and EOB information into the PMIS. Payment posting into the PMIS and analysis of the payment and EOB must occur to:
• Ensure the practice was paid according to the third party contract terms
• Focus on trends where services are denied for the following reasons: inappropriate bundling, medical necessity, low-pay appeals, incorrect coding, and inappropriate reporting of services during the global period
• Track the following rejections to identify front-end process-related problems:
• demographic errors
• eligibility-related denials
• wrong primary/secondary insurance company
• no referral authorization
• no coverage at time of service
Appropriate analysis of each EOB is critical because the data elements on the EOB drive the next steps in the revenue cycle—whether to bill a secondary third party payor for any balance or send a statement to the patient for payment of the balance. Another important aspect of EOB analysis is to determine any primary third party claim follow-up course of action such as a denial appeal or internal practice process change to avoid future denials. The pain management professional should be involved in denial appeals for medical necessity and coding denials.

Accounts Receivable Follow-Up
Some third party payors reimburse pain management professionals in a timely manner. For example, Medicare reimburses a provider within 14 days of a clean electronic claim, whereas other payors may take weeks to months to reimburse. Unpaid charges or claims, called accounts receivable (A/R), should be monitored in 30-day increments. For example, “current” A/R is 0 to 30 days from the date of service, whereas older charges are measured in 31 to 60, 61 to 90, and greater than 90-day increments.
Older charges, whether the responsibility of a third party payor or a patient, are generally more difficult to collect. The best opportunity for a pain management practice to collect from the patient is while the patient is in the office or facility. It is essential that pain management practices have an organized methodology implemented for monitoring and follow-up on unpaid balances.
Occasionally, a pain management practice may need to send an unpaid balance to a collection agency or take legal action for payment. It is imperative that the rendering pain management professional, rather than billing staff or the office manager, be responsible for making the decision to pursue a formal outside collections process.

Conclusion
A successful revenue cycle involves efficient, cost-effective, compliant, and accurate processes on the front-end as well as back-end of a pain management practice’s operations to achieve optimal collections for rendered services.
8 Medicolegal Issues

Julie K. Silver, MD, Susan M. Donnelly Murphy, JD
Physicians who routinely perform pain procedures need to understand certain elements of informed consent to minimize their risk of medicolegal entanglements. Often physicians have little or no training in obtaining informed consent. Even when they do obtain training, the instruction may be incomplete or incorrect. Understanding and documenting the consent process before the procedure is as important as the procedure itself.

Understanding Informed Consent
The law implicitly recognizes that a person has a strong interest in being free from nonconsensual invasion of bodily integrity. 1 In short, the law recognizes the individual’s interest in preserving the “inviolability of the person,” 1 an interest protected within the context of medical malpractice with the doctrine of informed consent. It has long been accepted that a patient must agree to any procedures or treatment. However, earlier it was accepted that the physician could steer the patient in the direction that he or she wanted. This has changed: it is now recognized that “[I]t is the prerogative of the patient, not the physician, to determine the direction in which his … interests lie.” 1 Consequently, a body of law that dictates the manner in which the patient’s consent or refusal needs to be obtained has developed. Some consider the right to informed consent to be the most important aspect of patients’ rights. 2
If patients are to intelligently exercise control of their bodies and attendant medical care, they must be provided with appropriate and complete medical information on which to base their decision. The dilemma facing medical practitioners is the determination of when such informed consent needs to be obtained and the manner in which to obtain it. This requires knowledge of the type and extent of information to be given to an individual patient and the manner in which it is to be presented.
Although the vast majority of claims of medical malpractice focus on errors in diagnosis and improper treatment and performance of procedures, a recent analysis found that allegations of failure to inform and breach of warranty were present in 6% of cases. 3

The Legal Framework for Informed Consent
Complete informed consent should be obtained for all therapeutic and diagnostic procedures. Any course of treatment that carries with it the risk of permanent injury requires a full disclosure before consent. Full informed consent should precede medical treatment even for procedures with a risk of temporary injury alone. Only under emergency conditions or in situations in which there are no therapeutic options should informed consent be omitted. There is no excuse to fail to obtain informed consent for an elective procedure.
The physician performing the procedure is the appropriate person to meet with the patient. Of course, other health care providers are of great assistance to reaffirm the consent, answer additional questions a patient may have, and continue a dialogue. To enable a patient to make an informed decision, “the physician owes to his patient the duty to disclose in a reasonable manner all significant medical information that the physician possesses or reasonably should possess that is material to an intelligent decision by the patient whether to undergo a proposed procedure.” 1 The specific law varies somewhat from jurisdiction to jurisdiction. Use of this language facilitates discussion of the two perspectives involved in the decision-making process: the physician and the patient.

Role of the Physician
The major role of the physician in the process of obtaining informed consent is that of an expert. Through education and experience, the physician is able to recognize the risks and benefits of the proposed treatment. Because the patient has limited knowledge of the medical and technical aspects of the procedure, the physician should begin the discussion with a reasonable explanation of the medical diagnosis—an obvious but often overlooked point. Thereafter, significant information includes the nature and probability of risks involved in the procedure, expected benefits, the irreversibility of the procedure, the available alternatives to the proposed procedure, and the likely result of no treatment. 1 Whether a physician has provided appropriate information to a patient generally will be measured by what is customarily done or by the standard of what the average physician should tell a patient about a given procedure. It often is essentially the same information that the physician has imparted to countless previous patients. In general, the duty to disclose does not require the physician to disclose all possible and/or remote risks, nor does it require the physician to discuss with a patient the information that he believes the patient already has, such as the risk of infection or other inherent risks of a procedure. 1
Recent studies have focused on the manner in which informed consent is obtained. For example, in a prospective, randomized, controlled study conducted by Bennet and colleagues, 99 out of 109 patients undergoing imaging-guided spinal injections agreed to particpate and were assigned to one of three groups. 4 The control group was given informed consent in the customary manner at the investigators’ institution with 12 key points of consent discussed conversationally. The “teach-the-teacher” group had to repeat the 12 key points back to the investigator before informed consent could be completed. The third group viewed a set of diagrams illustrating the 12 key points before signing the informed consent. Following the procedure, all participants completed a survey to test knowledge recall, anxiety, and pain during the procedure. Statistically significant results included a lower survey score for the control group. Not surprisingly, it took significantly longer to obtain informed consent in the “teach the teacher” group than in the control group or in the diagram group. Overall, the diagram method was optimal and required less time and had improved patient-physician communication.
The manner in which information is given and how much information is offered, are both important considerations. Too much information may actually increase anxiety just prior to a procedure. 5 A recent review on informed consent in Pain Practices found that although “disclosure has improved, but is still uneven, comprehension is often poor, for both patients and research subjects.” 6 An important factor is not only the improvement of consent forms, but also improving the consent process. A group of Swiss researchers studied the effect of combined written and oral information versus just oral information when obtaining informed consent. In this study, participants who were given the written information as well as the oral instructions rated the quality of information they received as higher than the oral-only group. 7

Role of the Patient
Although explanations to patients may be nearly identical for a given procedure, the law often also requires that the conversation be tailored to the particular patient. It is incumbent on the physician to have an appreciation of what information is important to a particular patient. The patient has the right to know all information that he or she considers material to his or her decision. Materiality is defined as the significance a specific patient attaches to the disclosed risks in deciding whether to undergo the proposed procedure. 8 Materiality of information about a side effect or consequence is a function not only of the severity of that consequence, but also of the likelihood that it will occur. 8 Remote risks whose likelihood of occurrence is not more than negligible need not warrant discussion. In summary, provide the patient with a realistic appreciation of his or her medical condition and an appropriate explanation of the treatments available. Never forget that however unwise his or her sense of values may be in the eyes of the medical profession, every patient has the right to forgo treatment or even cure if it entails personally intolerable consequences or risks. 8

Avoiding Legal Entanglements
Lack of informed consent may develop into a lawsuit only when a physician fails to disclose a risk that subsequently becomes an injury. Otherwise, as one court stated, “an omission (of material information), however unpardonable, is legally without consequence.” 9 Practically, the patient must demonstrate that, had the proper information been disclosed, he or she would not have consented to the course of therapy. To control the subjectivity of this application, some jurisdictions require the patient to prove that if the risk had been disclosed neither this patient, nor a reasonable person in this patient’s situation, would have consented. 1

Requirements of Documentation
A signed form entitled “consent to treatment” is required for all procedures; note, however, that the form only proves consent, not that it was informed. 10 The exchange of information that precedes the signed consent is crucial to the process. Good chart documentation (including signed consent forms, which are often and appropriately recommended by attorneys and risk managers) does not insulate a physician from a lawsuit but does make the defense of one considerably less difficult. Malpractice claims often are made years after the treatment was rendered, by which time any specific discussion with the patient in question has long since faded from memory. A standard consent form does nothing to jog the memory of the physician or the patient about the discussion; thus, it is highly important to tailor the discussion (and the subsequent documentation) for each patient, regardless of the procedure. Gone are the days when the phrase “reviewed the risks and benefits and the patient consents” was sufficient. On the standard consent form there usually is an area in which additional information may be added—savvy doctors will make pertinent notes in this body before every procedure ( Fig. 8-1 ). For example, if trigger-point injections are to be given in the piriformis muscle, note that injury to the sciatic nerve is possible. If the injections are to be done in the region of the middle trapezius, noting that potential complications include a pneumothorax is more appropriate. Any notations on the consent form may be bolstered by further documentation in the medical record regarding the details of the discussion. In certain circumstances, it may be advisable to provide the patient with a written summary of the discussion to take home and review before the procedure.

Figure 8-1 Sample consent form.
It is also advisable to document concerns that the patient expressed and how these concerns were addressed. Finally, note all persons present for the discussion, including other health care providers or individuals who accompanied the patient. If possible, have one of the additional medical persons present for the discussion also sign the consent form. This person can subsequently be available to the patient for further information, and, should there be an adverse outcome, this person can attest to the completeness of the consent discussion.

The Role of the Doctor-Patient Relationship
In studies that have explored the relationship between physicians’ claims experience and the quality of care they provide, a common theme is that the differences between sued and never-sued physicians are not necessarily explained by their quality of care or their chart documentation. “[I]f quality of care, medical negligence, and chart documentation are not the critical factors leading to litigation, what factors are critical? Patient dissatisfaction is critical.” 11 Although the law dictates what needs to be said to a patient, experience dictates that the manner in which it is said and the amount of time it takes to say it are equally important in providing good quality care and in avoiding a malpractice allegation. Effective communication between the patient and the physician not only enhances treatment outcomes but also enhances patient satisfaction. This combination tips the balance away from litigation, even in the face of unfavorable procedure outcomes.
One study found that routine visits with physicians with no malpractice claims were longer than routine visits with physicians who had experienced malpractice claims. 11 This same study found that the malpractice claims were more strongly correlated with the process and tone of a discussion than the content of that discussion.

When Medical Negligence Is an Issue
Full and complete informed consent is never a substitute for competent medical care. Claims arising exclusively under the doctrine of informed consent assume that the treatment was rendered appropriately and that a known and accepted risk occurred in the absence of negligence. When the procedure was not performed appropriately, there is a basis for the additional (and more common) claim for medical negligence.
By virtue of the doctor-patient relationship, a physician must exercise the degree of knowledge and skill of the average qualified physician practicing the specialty. 12 Any breach of this standard that results in injury to a patient may be actionable as a medical malpractice claim. Proof of compliance with the standard of practice usually will come through a review by an expert witness, who will offer opinions based on his or her education, training, and experience in the specialty, and, in particular, in the procedure at issue. In addition, an expert opinion must be based on the facts of the case.
The medical records best demonstrate facts. It is essential to accurately and completely describe every procedure. The procedure note should contain the indications for the procedure, the details of its performance, and the patient’s reaction or initial outcome. For example, the diagnosis for a trigger-point injection may be fibromyalgia, and the indications may be to alleviate pain and muscle spasm. Symptoms and their duration and prior treatment intervention also should be documented. The following sample documentation may be useful: “Under sterile conditions using a 1-inch, 27-gauge sterile disposable needle and a solution of 2 mL 1% lidocaine (Xylocaine) and 10 mL 0.25% bupivacaine (Sensorcaine), a total of 6 trigger-point injections were done in the bilateral upper trapezii. A 2 mL aliquot of the mixture was used at each site. Patient tolerated the procedure well and reported immediate relief of pain in the cervical region.” Finally, follow-up plans should be clearly documented. Once again, providing the patient with a copy of the plan may be appropriate.
After analysis of the records, an expert may evaluate the physician’s proficiency with the procedure. “When a new procedure is instituted into clinical practice, proctorship and supervision by a more experienced colleague or other specialist with appropriate documentation may help establish a basis for indicating that the physician has attained the requisite degree of knowledge and skill for the procedure.” 13
In conclusion, informed consent involves explaining the diagnosis to the patient in language that he or she understands, possible treatment options, and the risks and benefits of the proposed treatment (procedure). Thoroughly documenting informed consent in an individualized manner is imperative. Improving the process by using written and oral instructions, as well as diagrams, may be helpful.

References

1. Harnish v Children’s Hospital Medical Center, 387 Mass. 152, 439 N.E.2d, 240 (1982).
2. Annas G.J. A national bill of patients’ rights. N Engl J Med . 1998;338:695-699.
3. Physician Insurers Association of America: Cumulative Data Sharing Reports, 1997.
4. Bennett D.L., Dharia C.V., Ferguson K.J., Okon A.E. Patient-physician communication: informed consent for imaging-guided spinal injections. J Am Coll Radiol . 2009;6:38-44.
5. Yucel A., Gecici O., Emul M., et al. Effect of informed consent for intravascular contrast material on the level of anxiety: How much information should be given? Acta Radiol . 2005;46:701-707.
6. Cahana A., Hurst S.A. Voluntary informed consent in research and clinical care: An update. Pain Pract . 2008;8:446-451.
7. Felley C., Perneger T.V., Goulet I., et al. Combined written and oral information prior to gastrointestinal endoscopy compared with oral information alone: A randomized trial. BMC Gastroenterol . 2008;8:22.
8. Precourt v Frederick, 395 Mass. 689, 481 N.E.2d 1144 (1985).
9. Cobbs v Grant, 8 Cal. 3d 229, 104 Cal. Rptr. 505, 502 P. 2d 1 (1972).
10. Urbanski P.K. Getting the “go ahead”: Helping patients understand informed consent. AWHONN Lifelines . 1997; 1(3):45-48.
11. Levinson W., Roter D.L., Mullooly J.P., et al. Physician-patient communication: The relationship with malpractice claims among primary care physicians and surgeons. JAMA . 1997;277:553-559.
12. Brune v Belinkoff, 354 Mass. 102, 235 N.E.2d 793 (1968).
13. Brenner R.J. Interventional procedures of the breast: Medicolegal considerations. Radiology . 1995;195:611-615.
II
Soft Tissue and Joint Injections
9 Upper Extremity Joint Injections

Ted A. Lennard, MD
Intraarticular injections with corticosteroids and anesthetic can be a useful treatment option for patients with disabling peripheral joint pain. The anesthetic injected can provide useful diagnostic information and help determine a patient’s pain generator. These forms of injections are performed in conjunction with a comprehensive treatment program. This chapter will review common indications for intraarticular corticosteroid injections, dosing of medications injected, and discuss the technique for upper extremity intraarticular joint injections.

Indications for Intraarticular Steroids
The most common use of corticosteroids in the peripheral joints is in patients with rheumatoid arthritis. 1 These drugs are used specifically to reduce inflammation and provide relief from pain attributable to synovitis and conditions associated with rheumatoid arthritis. Other indications for the use of corticosteroids into joints include painful osteoarthritis and adhesive capsulitis. Aspiration of synovial fluid for pain relief and laboratory evaluation of the synovial fluid and arthrography for the evaluation of joints are common diagnostic tools that facilitate the rehabilitation of painful joints.

Drugs: Action, Selection, Dosage
Corticosteroids produce significant antiinflammatory effects. Numerous long-acting corticosteroid ester preparations are available. The most widely used corticosteroids include triamcinolone acetonide (Kenalog), triamcinolone hexacetonide (Aristospan), betamethasone sodium phosphate (Celestone) and betamethasone acetate (Soluspan), and methylprednisolone acetate (Depo-Medrol). 2 These compounds were developed to reduce undesirable hormonal side effects with less rapid dissipation from the joint. None of these corticosteroid derivatives appears to have any superiority over another; however, triamcinolone hexacetonide is the least water-soluble preparation and thus provides the longest duration of effectiveness within the peripheral joint space. 3 Systemic absorption after peripheral joint injection occurs within 2 to 3 weeks. Improvement of inflammatory processes remote from the injection site demonstrates that intraarticular corticosteroids exert a systemic effect. The pharmacology of corticosteroids and anesthetics is discussed in Chapter 2 .
Estimated dosages for the peripheral joints vary widely and usually depend on the size of the joint. The larger joints, such as the knee and shoulder, respond well to a 40-mg dose of methylprednisolone acetate or the equivalent of another agent. The smaller joints, such as the elbow and ankle, respond to a 20- to 30-mg dose of methylprednisolone acetate or the equivalent. Even smaller joints, such as the acromioclavicular and sternoclavicular joints, respond to a 10- to 20-mg dose of methylprednisolone acetate or the equivalent.
The number of injections per joint is also widely variable. Commonly, joints that are injected for the purpose of reducing inflammation in rheumatoid arthritis will be injected many times over the course of the disease process. These multiple injections have been shown to cause interference with normal cartilage protein synthesis. 2 However, it has also been demonstrated that patients with long-standing rheumatoid arthritis who do not receive intraarticular corticosteroid injections have joint disuse and decreased function much sooner than those who receive the injections. 4 For the purposes of pain reduction in osteoarthritis as well as an adjunct in the mobilization of the treatment of adhesive capsulitis, injections at the rate of one per 4 to 6 weeks for a maximum of three injections is the most commonly accepted regimen. This regimen, of course, is subject to the patient’s response to his or her overall treatment plan, of which the intraarticular corticosteroid injection is but one part.
It is usual practice to combine the corticosteroid medications with an anesthetic substance, such as procaine (Novocain) or lidocaine (Xylocaine) or the equivalent. The combined use of corticosteroids and anesthetic agents provides a larger volume of injectable material with which to bathe the joint more adequately. The added effect of analgesia is also desirable for patient comfort and for a more immediate response to treatment. Thus, the patient may obtain immediate pain relief and provide valuable feedback with which to help determine the overall rehabilitation plan. The usual anesthetic injected is lidocaine, 1% without epinephrine, with which the practitioner can provide a preliminary skin wheal and a control test before proceeding with the deeper injection. Bupivacaine (Marcaine, Sensorcaine), 0.25% or 0.5%, is also useful in providing a longer-acting analgesic effect for the patient. The dosages of lidocaine and bupivacaine also vary widely with the size of the joint. Usually, the smaller joints such as the acromioclavicular, sternoclavicular, and elbow joints would take 1 to 2 mL of 1% lidocaine combined with the corticosteroid. The glenohumeral, knee, and hip joints would take 2-4 mL of anesthetic agent. Bupivacaine is often preferable for non–weight-bearing joints such as the shoulder, elbow, acromioclavicular, and sternoclavicular joints, so long as these joints can be somewhat immobilized for several hours. Likewise, lidocaine is the drug of choice for injections in the weight-bearing joints, such as the knee, because its duration is much shorter and, thus, the joint is subject to less postinjection trauma by the seemingly compliant patient.

Contraindications and Complications
The clinician must be acutely sensitive to contraindications and complications of intraarticular corticosteroid therapy. 1, 4, 5, 7, 22, 26 Some of the most obvious contraindications include infection of the joint or of the skin overlying the joint. A patient with generalized infection also should be considered an unsuitable candidate for corticosteroid injection. Injection of corticosteroids may render a joint susceptible to hematogenous seeding from more distant skin lesions. Thus, the overall health of the patient must be assessed before considering the use of intraarticular corticosteroids. 6 Other obvious contraindications include hypersensitivity to any of the anesthetic preparations or the corticosteroids themselves. Patients receiving intraarticular injections in the presence of anticoagulants would be susceptible to bleeding. Determination of prothrombin time is suggested before injection therapy in these patients.
Patients with a recent injury to the joint such as a ligamentous destruction or bony destruction of the underlying joint should not be subjected to corticosteroid therapy. Instead, aspiration of the joint may be indicated if there is a relatively large inflammatory effusion. 7 Soft tissue or bony tumors at or near the underlying joint would also be a major contraindication to corticosteroid injections.
Even small doses of corticosteroids with intraarticular injections may trigger episodes of hyperglycemia, glycosuria, and even electrolyte imbalance in patients with diabetes; caution must be exercised in such situations. 8
Although rare, infections can be a serious complication. 9, 10 Usually, infections can be avoided by using an aseptic technique. 11 Infections may be quite subtle in patients with long-standing rheumatoid arthritis and in those receiving immunosuppressive agents. The most common organism is Staphylococcus aureus . 12, 13 One must also use caution in geriatric patients and in those with debilitating diseases.
Hypercorticism from systemic corticosteroid therapy may be a complication if the patient receives multiple intraarticular injections in succession or if the patient is receiving concomitant oral cortisone therapy. Corticosteroid arthropathy with avascular necrosis also has been reported 14 but is rare and has not been noted to occur after single corticosteroid injections. Joint capsule calcification is also a potential complication of multiple intraarticular corticosteroid injections. 15
Depigmentation and subcutaneous fat necrosis occasionally occur. The depigmentation is cosmetically unacceptable, especially in individuals with darker skin in whom it can be quite noticeable. Fat necrosis usually is not a complication in superficial joints that have minimal amounts of overlying fat tissue. Using a small amount of lidocaine to flush the needle to avoid leaving a needle track of corticosteroid suspension will help to minimize this complication.
A common complication in patients with rheumatoid arthritis who are receiving corticosteroid injections in the joints is “postinjection flare” (the joint appears inflamed or even infected), which tends to subside spontaneously in 24 to 72 hours. 16 Other less common complications include Tachon syndrome (intense dorsal spine pain immediately following an injection that quickly subsides) 17 and chorioretinopathy. 18

Alternatives to Corticosteroids
Alternatives to intraarticular corticosteroids include viscosupplementation and plasma-rich platelet (PRP) injections. Viscosupplementation injections use gel-like substances such as hyaluronates to supplement the viscous properties of synovial fluid and have been approved for use in the knee joint. Other joints including the shoulder have been treated with this form of injections with good results. 19, 20
Plasma rich platelet injections use concentrated platelets from autologous blood to stimulate a healing response in damaged tissue. Blood is drawn from the patient and placed in a centrifuge. The concentrated platelets are removed and reinjected directly into the patient’s abnormal joint, usually under ultrasound guidance. These concentrated platelets produce growth factors that include platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and transforming growth factor-beta (TGF-β). These compounds are instrumental in attracting cells that promote healing by stimulating neovascularization and cellular reproduction. 16, 21 - 23 The efficacy of PRP injections and appropriate clinical indications (when and where it should be used) are currently being researched and yet to be definitively determined. Initial results of clinical studies appear promising. 24 - 26

Techniques for Intraarticular Injections
When the clinician has established that a peripheral joint needs to be injected or aspirated, the specific preparation for the injection is essentially the same for all joints. Thorough understanding of the underlying anatomy is important to accomplish a painless injection. The optimal site for injection of the joint usually is the extensor surface at a point where the synovium is closest to the skin. Approaching the joint from the extensor surfaces allows the injection to be as remote as possible from any major arteries, veins, and nerves. 27 When the site of injection has been determined, it can be marked with the needle hub or a retracted ballpoint pen by pressing the skin to produce a temporary indentation to mark the point of entry. The skin is then prepared by cleansing a generous area with a detergent or cleaner such as an iodine-based surgical scrub. This area is then painted with an antiseptic solution and allowed to dry. Aseptic technique is always advised, including the wearing of sterile gloves so that the area to be injected may be continually palpated and the anatomy appreciated throughout the procedure. A small skin wheal may then be raised using 1% lidocaine with no epinephrine (or an equivalent anesthetic agent). A 27-gauge skin needle approximately 0.75 to 1.0 inch long is used with approximately 1 mL of anesthetic agent. For joints distended with fluid or those that are particularly close to the surface of the skin, such as the acromioclavicular and sternoclavicular joints, the raising of a skin wheal or preanesthesia is usually not necessary. If a patient is particularly apprehensive about the injection procedure, one of the vapo-coolant sprays such as dichlorotetrafluoroethane or ethyl chloride may provide adequate anesthesia.
After the skin wheal is raised, a 25- or 22-gauge needle approximately 1.5 inches long may be used to introduce the injectant. The needle is then slid gently into the joint, with the clinician avoiding a strong thrusting motion. Just before beginning the actual injection, the practitioner should aspirate to ensure there is no return of blood. After ascertaining the needle’s positioned in the joint space, the injectable material should be introduced using slow, steady pressure on the plunger.
If the joint is to be aspirated before introduction of a corticosteroid, the same technique is used in preparation; however, a larger needle may be introduced, such as a 20- or even an 18-gauge needle. Again, slow, steady pressure is used when the needle is introduced into the joint. The aspirate is then withdrawn with the practitioner gently pulling the plunger on the syringe with the dominant hand, holding the syringe barrel steady with the nondominant hand. If it is suspected that not all of the aspirate has been obtained from the joint, the needle tip may be moved around within the joint, and the joint itself may be “milked,” using steady pressure with the opposite hand on the joint itself by kneading the skin toward the site of aspiration. After all of the available fluid is aspirated, the needle may be left in place with the syringe removed. A separate syringe may then be attached to the aspirating needle, and the injectant may then be introduced into the joint itself. Again, a slow, gentle introduction of the injectable material is desired.
If resistance is met during the time of the injection, the needle should be readjusted so that there is no resistance. Any time the needle is readjusted, the plunger on the syringe should be withdrawn to ensure that the needle tip does not pierce a blood vessel.
After the drug or drugs have been injected, the needle is withdrawn and mild pressure is applied with a sterile gauze pad to prevent bleeding. Whenever the injected material includes corticosteroids, a slight amount of lidocaine may be used to clear the needle before withdrawal. As mentioned earlier, this technique prevents leaving a steroid track through the adipose tissue and skin, which may cause depigmentation or subcutaneous necrosis.
Psychological care of the patient is important to the success of these injections. Throughout the procedure, the patient must be coaxed to achieve muscle relaxation and reassured of the importance of the procedure. It is likewise important that the patient be reminded of the practitioner’s skill with and knowledge of the procedure. After the procedure, the patient should be assessed carefully to be sure that he or she is not exhibiting a vasovagal response and that appropriate measures are taken to prevent any secondary harm, such as falling as a result of transient hypotension.

Upper Extremity Joints

Glenohumeral Joint
The glenohumeral joint is subject to multiple traumatic and pathologic problems more frequently than any other joint except the knee. The anatomy of the shoulder must be well understood for a relatively painless injection to be achieved. 40 In entering the subacromial space in the shoulder, there is little anterior space for placement of the needle. A lateral or posterior approach may be more desirable. 28
When injecting the shoulder for problems such as bicipital tendinitis, the anterior approach is necessary ( Fig. 9-1 ). The patient is placed in a sitting position, the anterior portion of the shoulder is prepared aseptically, and, if desired, a cutaneous wheal is raised medial to the head of the humerus and just inferior to the tip of the coracoid process. It is useful to have obese patients lie supine with the forearm across the abdomen. In this position, the shoulder may be passively rotated internally and externally to identify the head of the humerus. The coracoid process is then easily palpated. The needle is directed in the anteroposterior plane just lateral to the coracoid process. The needle is advanced into the groove between the medial aspect of the humeral head and the glenoid. No resistance should be felt as the needle is advanced.

Figure 9-1 Diagram depicting needle placement for an anterior and lateral glenohumeral joint injection. ( A ) Surface landmarks for lateral ( B ) and anterior ( C ) entry points for injection.
The lateral approach to injection of the shoulder is sometimes useful when treating supraspinatus tendinitis (see Fig. 9-1 ). 28 The patient is placed in a sitting position with the arm relaxed in the lap, which increases the subacromial space. The lateral-most point of the shoulder is palpated and the needle is prepared for insertion below the acromion. After aseptic preparation, the needle is directed almost perpendicularly to the skin surface, with a slight upward angle. The space is then easily entered, and no resistance should be felt as the needle is advanced.
The posterior approach to the shoulder is popular for conditions such as adhesive capsulitis as well as synovitis or chronic osteoarthritis ( Fig. 9-2 ). 29 The posterior approach also allows the practitioner to be out of the patient’s vision, thereby reducing any apprehension. The patient is placed in the sitting position with his or her arm in the lap, which allows internal rotation of the shoulder and adduction of the arm. The skin is prepared aseptically, and the site of injection is palpated. The site of injection is just under the posteroinferior border of the posterolateral angle of the acromion. It is useful for the practitioner to palpate the patient’s coracoid process in the anterior portion of the shoulder with the index finger. This is the point at which the needle is “aimed.” The needle is then inserted approximately 1 inch below the posterolateral acromion process and directed from the posterolateral portion of the shoulder to the anteromedial portion of the shoulder toward the coracoid process. If resistance is encountered, the needle may be withdrawn slightly and angled upward. The needle will then be in the upper recess of the shoulder joint away from the head of the humerus.

Figure 9-2 Diagram depicting needle placement for a posterior glenohumeral injection ( A ). Surface landmarks for posterior injection ( B ).

Acromioclavicular Joint
The acromioclavicular joint is small and superficial ( Figs. 9-3 and 9-4 ). It is occasionally swollen and usually tender during palpation when inflamed. This joint can be injected easily using a 25-gauge needle with the patient sitting or supine and the shoulder propped on a pillow. Usually, injections into this joint are for chronic pain, such as occurs in shoulder separations that have not responded to noninvasive treatment.

Figure 9-3 Acromioclavicular (AC) joint injection ( A ) with surface landmarks ( B ).

Figure 9-4 Oblique ultrasound image of the acromioclavicular joint. A, Acromion; C, Clavicle; Arrows, AC joint space; Arrowhead, Fibrocartilaginous disk.
(From Jacobson J: Fundamentals of Musculoskeletal Ultrasound. Philadelphia, Saunders, 2007, p 45.)
Many times, the joint is injected for diagnostic purposes to delineate the source of pain in the shoulder, and therefore corticosteroids are not used. However, with chronic pain that does not subside after a trial of anesthetics (such as lidocaine), corticosteroids may be used.
The joint is prepared aseptically, as described earlier. The joint is easily palpated by locating the tip of the distal clavicle and injecting from either a superior angle or an anterosuperior angle into the joint space. In a degenerative joint, many times the needle will not pass easily into the joint, which then needs to be probed gently so that the needle can be advanced just to the proximal margin of the joint’s surface. It is usually not necessary to penetrate the joint any deeper.

Sternoclavicular Joint
The sternoclavicular joint is easily located just lateral to the notch of the sternum ( Fig. 9-5 ). Many times the sternoclavicular joint is slightly dislocated, providing a source of pain and making it easily palpable because the proximal clavicle may be slightly elevated in relationship to the sternum. This joint is small and may be difficult to inject unless a 25- or 27-gauge needle is used. Great care should be taken that these injections into the sternoclavicular area are done superficially because immediately posterior to the sternoclavicular joint are the brachiocephalic veins.

Figure 9-5 Sternoclavicular joint injection technique ( A ) and surface landmarks ( B ).

Elbow
The elbow region is usually subject to periarticular problems, including lateral epicondylitis and medial epicondylitis; however, in this chapter, attention is directed to the joint space itself. Aspiration for problems such as synovitis in patients with rheumatoid arthritis and arthrography of the joint for delineation of multiple pathologic processes, including loose bodies, are the initial approaches to treatment. 30 When it is determined that an intraarticular injection is needed, the practitioner must remember that the extensor surfaces of the joint are the safest places to avoid vessels and nerves. Thus, the injection should be directed to the posterolateral portion of the elbow or to the posterior portion of the elbow ( Figs. 9-6 and 9-7 ). These approaches will allow the practitioner to enter the humeroulnar joint, the true elbow joint.

Figure 9-6 Drawing depicting elbow joint injections ( A ) and surface anatomy ( B ) lateral, and ( C ) posterior.

Figure 9-7 Sagittal ultrasound view of the elbow joint. C, Capitellum; R,  Radial head; F , Fat pad; Arrowheads , Articular cartilage.
(From Jacobson, J, Fundamentals of Musculoskeletal Ultrasound, Philadelphia, Saunders, 2007, p 110.)
The patient is placed with the elbow positioned between 50 and 90 degrees of flexion. The posterior and/or lateral skin surfaces are prepared aseptically. For the posterolateral approach, the lateral epicondyle area and the posterior olecranon area are palpated. The groove between the olecranon below and the lateral epicondyle of the humerus is located. The needle is then directed proximally toward the head of the radius and medially into the elbow joint. Again, no resistance should be felt when the needle enters the joint. Aspiration or injection of the joint may then be undertaken. The posterior approach to the elbow is relatively simple. The posterior olecranon is palpated with the lateral olecranon groove located just posterior to the lateral epicondyle. The needle is then inserted above the superior aspect of and lateral to the olecranon. It is advanced into the joint, and, again, no resistance should be felt.

Wrist
Many of the small joints of the wrist have interconnecting synovial spaces, making it possible to provide relief to the entire joint complex with one injection. The wrist may be infiltrated by several methods. 31 - 33 The route of entry may be influenced by the site of inflammation or desired anatomic area. The preferred method is the dorsal approach, which may be facilitated with slight flexion of the hand. This can be easily accomplished by flexing the hand over a rolled towel. The point of entry ( Fig. 9-8 ) is just medial to the extensor pollicis longus tendon in the distal aspect of the midpoint of the radius and ulna. This can be easily palpated as a depression between the radius and the scaphoid and lunate bones. The needle is placed perpendicular to the skin and inserted 1 to 2 cm lateral to the extensor pollicis longus tendon. 32 Optional approaches to the wrist include the ulnar or the dorsal snuffbox approach. With the ulnar approach, the injection is made just distal to the lateral ulnar margin in a palpable gap between the border of the distal ulna and the carpal bones. A third approach is the dorsal aspect just medial to the anatomic snuffbox between the radius and carpal bones ( Fig. 9-9 ). Anesthetic and corticosteroid preparations may diffuse throughout the joint and are facilitated by range-of-motion exercises following injection. 7, 34 The approach used should be based on the area of maximal point tenderness or site of inflammation and specific anatomic structures underlying the region to be infiltrated, such as the scapholunate ligaments or the triangular fibrocartilaginous complex. Caution should be taken to arrive at an accurate diagnosis when treating a chronic condition. An underlying wrist injury with unremarkable initial radiographs may cause scapholunate dissociation, carpal instability, or avascular necrosis. These disorders should be considered in the differential diagnosis during conservative management.

Figure 9-8 Wrist joint injection—dorsal approach. The needle is inserted medial to the extensor pollicis longus tendon.

Figure 9-9 Needle placement adjacent to the anatomic snuffbox between the radius and carpal bones.

Intercarpal Joints
Injection into the intercarpal joints such as the triquetrolunate space can be accomplished by palpating the borders of the carpal bone. Palpation is easier to perform when the joint is swollen and fluctuant. 33 Ultrasound or fluoroscopic guidance may be necessary for precise location.

Carpometacarpal Joint
The first carpometacarpal joint or trapeziometacarpal joint is a frequent source of pain in osteoarthritis and from occupations or sports that subject the patient to undue stress. The joint may be infiltrated or aspirated from the dorsal aspect of the radial side of the carpometacarpal joint ( Fig. 9-10 ) by holding the thumb in slight flexion and palpating for the point of maximal tenderness. 14, 31, 35 When injecting the carpometacarpal joint, care should be taken to avoid the radial artery and the extensor pollicis tendon. 36 To avoid the radial artery, the needle should be placed toward the dorsal side of the extensor pollicis brevis tendon.

Figure 9-10 Needle placement into the carpometacarpal joint.

Interphalangeal Joints
The proximal and distal interphalangeal joints are affected most frequently by arthritic processes. The proximal interphalangeal joint is frequently affected in rheumatoid arthritis. 12, 33 These smaller joints require a small-gauge needle (25- or 27-gauge) to facilitate entry. A vapo-coolant spray may be used for superficial skin anesthesia with or without a superficial skin wheal to diminish the pain on initial infiltration; infiltration of these smaller joints is painful. 31 Because the joint space is very small, the tip of the needle must be advanced gently into the intraarticular capsule. The joint will accommodate only a small amount of fluid, usually less than 2 mL, and overdistention should be avoided. Pericapsular and subcutaneous injections have been known to provide some beneficial effect when direct joint infiltration could not be obtained, presumably by transport of the corticosteroids to inflamed capsule and synovium. 36 The proximal and distal interphalangeal joints are infiltrated by palpating the borders of the joint and advancing a fine needle, preferably with a small syringe (2 mL) to facilitate fine motor control. Splinting the affected joint may allow resolution of an inflammatory response. 37 - 39

Conclusion
The upper extremity peripheral joints are not difficult to inject. With practice, the clinician can become adept at entering these joints with ease, providing an effective addition to the management of peripheral joint problems. After the joints are injected, they should not be subjected to intensive exercise or motion for several days. This period of relative rest helps to promote the retention of the corticosteroid in the joint, allowing longer contact with the joint surface and delaying absorption of the drug systemically. 7

Acknowledgment
The editor would like to extend a special thanks to John P. Obermiller, MD and Dennis M. Lox, MD for their original work on this chapter.

References

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10 Lower Extremity Joint Injections

Ted A. Lennard, MD
Lower extremity intraarticular injections with corticosteroids and anesthetics are useful treatment options for patients with hip, knee, ankle, or foot pain. 4 Injections are given to treat acutely painful joints refractory to rest and oral medications. The indications, patient selection, complications, 1, 2, 6, 7, 9, 14, 16, 19 and general technique of joint injections 10, 25 were covered in the previous chapter. This chapter will focus on the technique of specific lower extremity intraarticular joint injections. Knowledge of multiple techniques is helpful. 26

Hip Joint
The hip joint is often difficult to infiltrate or aspirate because of its depth and the surrounding tissue. Fluoroscopic guidance with injection of contrast material or ultrasound guidance is often necessary to confirm proper needle placement. This joint may be infiltrated by an anterior or lateral approach ( Figs. 10-1 , 10-2 , 10-3 ). The anterior approach is preferred. 18, 23, 24 With the anterior approach, the patient is in the supine position with the lower extremity externally rotated. The length of the needle will depend on the patient’s size. The anatomic landmarks for the anterior approach are 2 cm distal to the anterior superior iliac spine and 3 cm lateral to the palpated femoral artery at a level corresponding to the superior margins of the greater trochanter. After superficial anesthesia is administered, the needle is advanced at an angle 60 degrees posteromedially through the tough capsular ligaments, advanced to bone, and slightly withdrawn. This technique places the tip of the needle directly into the joint, and aspiration or injection may be performed. This approach is much simpler using image guidance to direct the needle posteromedially into the joint. When the capsular ligaments have been penetrated, 2 to 4 mL of anesthetic and corticosteroid suspension may be introduced.

Figure 10-1 Intraarticular injection of the hip joint, lateral approach.

Figure 10-2 Intraarticular injection of the hip joint, anterior approach.

Figure 10-3 A, Sagittal ultrasound view of the proximal hip joint. B, Transverse ultrasound view of the proximal hip joint. A, Acetabulum; H , Femoral head; I, Iliopsoas muscle; N , Femoral neck. Arrowhead denotes the collapsed anterior joint recess. Arrow denotes the labrum.
(From Jacobson J: Fundamentals of Musculoskeletal Ultrasound, WB Saunders, 2007, p 182.)
The lateral approach is performed by palpating the greater trochanter of the femur, which may be facilitated by externally rotating the lower extremity. Superficial anesthesia may be used and, again, depending on the size of the patient, the appropriate-length needle is selected. A 3- to 4-inch needle is usually sufficient; however, in larger patients, longer needles may be necessary. Just anterior to the greater trochanter, the needle is advanced and walked medially along the neck of the femur until the joint is reached. Aspiration may be obtained but is more difficult with the lateral approach. The amount of fluid that may be introduced may be limited, depending on the integrity of the joint.

Knee
The knee is the most commonly aspirated and injected joint in the body. It contains the largest synovial space and demonstrates the most visible and palpable effusion (when present). A patient is usually most comfortable lying supine with sufficient pillows. The knee is prepared using an aseptic technique. If a large effusion is present, whether medially or laterally, the site of entry should be over the maximal expansion of the effusion in order to cause the least discomfort during the procedure. For injections in which a large effusion is not present, the lateral, medial, suprapatellar, or anterior approach may be used ( Fig. 10-4 ). Before injecting or aspirating the knee, the patella should be grasped between the examiner’s thumb and forefinger and rocked gently from side to side to ensure that the patient’s muscles are relaxed.

Figure 10-4 A, Drawing of medial and lateral injection approaches to the knee. Surface location of a lateral ( B ) and medial ( C ) injection.
The medial approach to the knee is simple. First, the practitioner puts a small amount of lateral pressure on the patella, pushing it slightly medially and displacing it somewhat to increase the gap between the patella and the femur medially. The needle is then introduced about midway between the superior and inferior pole of the patella, medial to the patella and midway between the medial border of the patella and the femur. A preinjection skin wheal may be raised with an anesthetic agent, or the skin itself may be anesthetized with a vapo-coolant spray for patient comfort. As the needle is introduced into the joint space, the needle should be aspirated progressively. If no aspirate is obtained, the corticosteroid can be injected. Before withdrawal of the needle, the needle tract again should be flushed with a small amount of anesthetic.
The lateral approach to the knee is also simple. With the patient supine, the knee is fully extended or placed in slight flexion. The patella is slightly displaced laterally to increase the gap between the patella and femur laterally. The skin may then be anesthetized with 1% lidocaine. The needle is introduced halfway between the superior pole of the patella and the midline of the patella lateral and inferior to the patella. As the needle is introduced, aspiration is performed until the needle is inside the joint. The joint can then be aspirated or injected.
If a large effusion is present, the suprapatellar approach may be used. This does not have any specific advantage over the lateral approach unless the effusion is expanding the suprapatellar bursa. The needle is introduced at the point of maximal expansion of the effusion, and the joint is then aspirated. This approach is usually not as good as the lateral approach if the knee is to be injected only and not aspirated. It is much easier to enter the joint space with the medial or lateral approach.
On occasion, an anterior approach to the knee may be desired if a patient cannot fully extend the knee. In these cases, the patient may be sitting or supine with the knee flexed to 90 degrees. The needle is inserted just inferior to the inferior patellar pole from either the lateral or medial side of the patellar tendon. The needle is then advanced parallel to the tibial plateau until the joint space is entered. It is more difficult to aspirate a knee effusion when using this approach. 23 Moreover, the risk of puncturing the articular cartilage is much higher, as is the risk to the infrapatellar fat pad. Occasionally, the knee is approached anteriorly by inserting the needle directly through the patellar tendon. This approach has no merit because it increases discomfort to the patient and may cause bleeding in the patellar ligament.

Ankle Mortise
The ankle joint is not commonly injected; however, it may be subject to osteoarthritis, rheumatoid arthritis, or chronic pain resulting from instability. 8, 12, 13, 27, 28 An anterior medial or anterior lateral approach may be used, depending on the location of pain or pathologic process ( Figs. 10-5 and 10-6 ). For the medial approach, a slight depression is felt between the extensor hallucis longus tendon laterally and tibialis anterior tendon medially on the inferior border of the tibia superiorly and the talus inferiorly. The needle is then directed slightly laterally and perpendicular to the tibial joint surface. The talus has a superior curve, and the needle may need to be angled slightly superiorly to avoid contact with the talar joint surface.

Figure 10-5 A, Drawing of the different approaches to an ankle injection. Surface location of a medial ( B ), lateral ( C ), and posterior ( D ) sites for injections.

Figure 10-6 Ultrasound image of the ankle joint. Sagittal imaging reveals the anterior fad pad ( F ), between the tibia ( Tib ) and talus ( Tal ). Arrowheads depict the hyaline articular cartilage.
(From Jacobson J: Fundamentals of Musculoskeletal Ultrasound, WB Saunders, 2007, p 272.)
The lateral approach is useful in situations in which pathologic processes in the ankle appear to be most prominent either at the talofibular joint or the tibiotalar joint. Here, the foot is placed in moderate plantar flexion. The area enclosed by the tibia superiorly, the talus inferiorly, and the fibular head laterally is palpated. The extensor tendons of the toes should be medial to the injection site. The needle is then inserted from an anterolateral position and is directed toward the posterior edge of the medial malleolus. If the joint surface is encountered, the physician should direct the needle slightly upward, remembering that the talar dome arches superiorly.

Subtalar Joint
Occasionally, the subtalar joint is the site of a pathologic process. 3 The easiest approach to this joint is to have the patient lie prone with his or her feet extending over the end of the examination table. This allows the ankle to be in the neutral position. The posterior and lateral portions of the ankle are then prepared aseptically. The site of entry for the injection is along a line drawn from the most prominent portion of the distal fibula posterior to the Achilles tendon. This line should be parallel to the plantar aspect of the foot with the foot in neutral position; halfway between the prominent aspect of the lateral malleolus and the Achilles tendon, the needle is inserted and directed toward a point inferior and medial to the medial malleolus. Fluoroscopic or ultrasound guidance can be very helpful during subtalar joint injections. 5 . 11 ,15 ,17

Intertarsal Joints
Injection of the tarsal joints may be accomplished similarly to injection of the carpal joints. Palpation of the bony landmarks is carried out, the needle is inserted between the tarsal bones to the desired depth, and aspiration is accomplished if necessary. Fluoroscopic needle guidance simplifies this procedure and ascertains precise needle placement.

Metatarsophalangeal Joints
The metatarsophalangeal joints are most frequently infiltrated with a dorsal approach ( Fig. 10-7 ). This approach is carried out by palpating the metatarsophalangeal margins with plantar flexion of the toe to facilitate insertion of the needle. The needle is then advanced into the joint. The first metatarsophalangeal joint is frequently affected by arthritic conditions and gout. When a swollen joint is encountered, infiltration and aspiration may be easier with a swollen capsule.

Figure 10-7 Dorsal approach to the first metatarsophalangeal joint.

Conclusion
The lower extremity peripheral joints are not difficult to inject. With the use of ultrasound or fluoroscopic guidance, the clinician can become adept at entering these joints with ease, providing an effective addition to the management of peripheral joint problems.

Acknowledgment
The editor would like to extend a special thanks to John P. Obermiller, MD and Dennis M. Lox, MD for their original work on this chapter.

References

1. Bliddal H., Qvistgaard E., Terslev L., et al. A randomized, controlled study of a single intra-articular injection of etanercept or glucocorticosteroids in patients with rheumatoid arthritis. Scand J Rheumatol . 2006;35(5):341-345.
2. Hajjioui A., Nys A., Poiraudeau S., Revel M. An unusual complication of intra-articular injections of corticosteroids: Tachon syndrome. Two case reports. Ann Readapt Med Phys . 2007;50(9):721-723.
3. Shortt C.P., Morrison W.B., Roberts C.C., et al. Shoulder, hip, and knee arthrography needle placement using fluoroscopic guidance: Practice patterns of musculoskeletal radiologists in North America. Skeletal Radiol . 2009;38(4):377-385.
4. Pfenninger J.L. Infections of joints and soft tissue: Part I. General guidelines. Am Fam Physician . 1991;44:1196-1202.
5. Beukelman T., Arabshahi B., Cahill A.M., et al. Benefit of intraarticular corticosteroid injection under fluoroscopic guidance for subtalar arthritis in juvenile idiopathic arthritis. J Rheumatol . 2006;33(11):2330-2336.
6. Cahill A.M., Cho S.S., Baskin K.M., et al. Benefit of fluoroscopically guided intraarticular, long-acting corticosteroid injection for subtalar arthritis in juvenile idiopathic arthritis. Pediatr Radiol . 2007;37(6):544-548.
7. Henning T., Finnoff J.T., Smith J. Sonographically guided posterior subtalar joint injections; Anatomic study and validation of 3 approaches. PM R . 2009;1(10):925-931.
8. Khosla S., Thiele R., Baumhauer J.F. Ultrasound guidance for intra-articular injections of the foot and ankle. Foot Ankle Int . 2009;30(9):886-890.
9. Kirk K.L., Campbell J.T., Guyton G.P., Schon L.C. Accuracy of posterior subtalar joint injection without fluoroscopy. Clin Orthop Relat Res . 2008;466(11):2856-2860.
10. Hasegawa M., Nakoshi Y., Tsujii M., et al. Changes in biochemical markers and prediction of effectiveness of intra-articular hyaluronan in patients with knee osteoarthritis. Osteoarthritis Cartilage . 2008;16(4):526-529.
11. Gray R.G., Gottlieb N.L. Rheumatic disorders associated with diabetes mellitus: Literature review. Semin Arthritis Rheum . 1976;6:19-34.
12. Hollander J.L. Intrasynovial corticosteroid therapy in arthritis. Md State Med J . 1970;19:62-66.
13. Hollander J.L. Joint problems in the elderly: How to help patients cope. Postgrad Med . 1988;84:209-211. 215216
14. Jalava S. Periarticular calcification after intra-articular triamcinolone hexacetonide. Scand J Rheumatol . 1980;9:190-192.
15. Gray R.G., Tenenbaum J., Gottlieb N.L. Local corticosteroid injection treatment in rheumatic disorders. Semin Arthritis Rheum . 1981;10:231-245.
16. Kothari T., Reyes M.P., Brooks N., et al. Pseudomonas cepacia septic arthritis due to intra-articular injections of methylprednisolone. Can Med Assoc J . 1977;116:1230-1235.
17. Balch H.W., Gibson J.M., El-Ghobarey A.F., et al. Repeated corticosteroid injections into knee joints. Rheumatol Rehabil . 1977;16:137-140.
18. Leversee J.H. Aspiration of joint and soft tissue injections. Prim Care . 1986;13:579-599.
19. McCarty D.J., McCarthy G., Carrera G. Intra-articular corticosteroids possibly leading to local osteonecrosis and marrow fat-induced synovitis. J Rheumatol . 1991;18:1091-1094.
20. Owen D.F. Intra-articular and soft tissue aspiration injection. Clin Rheumatol Pract (Mar-May) . 1986:52-63.
21. Peterson C., Hodler J. Evidence-based radiology (Part 2): Is there sufficient research to support the use of therapeutic injections into the peripheral joints? Skeletal Radiol . 2010;39(1):11-18.
22. Perrot S., Laroche F., Poncet C., et al. Are joint and soft tissue injections painful? Results of a national French cross-sectional study of procedural pain in rheumatological practice. BMC Musculoskelet Disord . 2010;11(1):16.
23. Adleberg J.S., Smith G.H. Corticosteroid-induced avascular necrosis of the talus. J Foot Surg . 1991;30:66-69.
24. Pfenninger J.L. Injections of joints and soft tissues: Part II. Guidelines for specific joints. Am Fam Physician . 1991;44:1690-1701.
25. Shimizu M., Higuchi H., Takagishi K., et al. Clinical and biochemical characteristics after intra-articular injection for the treatment of osteoarthritis of the knee: Prospective randomized study of sodium hyaluronate and corticosteroid. J Orthop Sci . 2010;15(1):51-56.
26. Gordon G.V., Schumacher H.R. Electron microscopic study for depot corticosteroid crystals with clinical studies after intra-articular injection. J Rheumatol . 1979;6:7-14.
27. Stefanich R.J. Intra-articular corticosteroids in treatment of osteoarthritis. Orthop Rev . 1986;15:65-71.
28. Wilke W.S., Tuggle C.J. Optimal techniques for intra-articular and peri-articular joint injections. Mod Med . 1988;56:58-72.
11 Bursae Injections

Nicholas K. Olsen, DO, Joel M. Press, MD, Jeffrey L. Young, MD
Bursitis is commonly diagnosed and treated in clinical practices that focus on musculoskeletal medicine. Inflamed bursae often respond to conservative treatments including rest, cryotherapy, compression, physical/occupational therapy and nonsteroidal antiinflammatory drugs (NSAIDs). 1a In patients who fail to respond to conservative rehabilitation, a corticosteroid injection into the bursa can serve as a useful diagnostic and therapeutic adjunct to a comprehensive course of rehabilitation.
Bursae are purse-like sacs containing fluid and function to reduce friction at a joint. They are positioned between two muscles or between a muscle and its tendon or bone. Inflammation may occur during repetitive activities involving poor body mechanics or following direct trauma. An accurate diagnosis includes a thorough history, and an investigation of the occupational and recreational factors predisposing a patient to repetitive overload or joint stress. Correction of improper biomechanics is essential to reduce joint tension early in the course of treatment to avoid chronic bursitis.
Physical examination will reveal focal tenderness, swelling, and pain during direct palpation. If the injury is due to acute trauma, a fracture or ligamentous instability of the joint should be considered. In cases of chronic bursitis, calcifications may be identified on plain radiographs. However, the most common etiology combines repetitive motion with improper biomechanics. The physical examination should include a survey of peripheral joints to rule out a systemic process such as an underlying rheumatic disease. Skin overlying the area of tenderness should be examined for evidence of warmth, redness, swelling, or penetrating trauma. Rarely an infected bursa is diagnosed, and skin warmth appreciated on palpation may be the most sensitive physical indicator. 1 The treatment of bursitis requires that an infection be considered prior to initiating treatment protocols. Aspiration of a septic bursa and identification of a bacterial pathogen are necessary to initiate appropriate antibiotic treatment. Laboratory studies of the serum should include an erythrocyte sedimentation rate, complete blood cell count, and microscopic examination to screen for leukocytosis, bacteria on Gram stain, or crystals. Operative incision and drainage of a septic bursa may be required for effective treatment. 2, 3 Contraindications to bursal injection with corticosteroids include cellulitis, generalized infection, and coagulation disorders.
Bursal injections serve a diagnostic and a therapeutic role. An initial bursal injection with local anesthetic alone can provide important information that will confirm the diagnosis. Bursitis from a noninfectious etiology may be considered for an injection of corticosteroid and anesthetic reducing bursal pain and inflammation, thereby allowing the patient to engage in a comprehensive rehabilitation program. Following the injection, the patient should be given instructions to ice and observe relative rest prior to resumption of a therapeutic exercise program. The clinician should direct the patient in a home exercise program and a physical therapist may be consulted for soft tissue mobilization and instruction in a stretching and strengthening program. Ice may be a useful adjunct during the initial phases of treatment, and NSAIDs may provide additional relief. Each of these options should be individualized for the clinical situation, and none of these, especially bursal injections, is to be used as the primary form of therapy. Re-examination should be scheduled within the first few weeks, and the rehabilitative program should be tailored to the patient as symptoms subside.
This chapter describes the basic approach to injection of many of the bursae encountered in clinical practice. Although the rehabilitation program for each bursa has not been detailed to allow for closer attention to procedural techniques, it is essential to employ a comprehensive rehabilitation to maximize the success of injections.

Subacromial (Subdeltoid) Bursitis
The subacromial bursa rests on the supraspinatus and is covered by the acromion, the coracoacromial ligament, and the deltoid. This is the most common site of bursitis of the shoulder, with inflammation usually occurring secondary to rotator cuff tendinitis or shoulder impingement syndrome. In a pure subacromial bursitis, the impingement signs may be absent, and the inflamed bursa may limit full passive abduction due to compression at the near end range of shoulder motion. 4 More commonly, subacromial bursitis coexists with impingement syndrome or rotator cuff syndrome. Determining the etiology of shoulder pain may be difficult, and a diagnostic injection into the bursa can narrow the field of possibilities. A diagnostic injection may help distinguish weakness and loss of range of motion secondary to a painful bursitis from a full-thickness rotator cuff tear. The patient should be thoroughly examined prior to the administration of local anesthetic and then reexamined 5 to 10 minutes after injection. Postinjection, the patient may be less guarded and more cooperative during the physical examination, yielding further diagnostic information.
Although an anterior, posterior, or lateral approach may be used, the posterolateral approach is preferred. Following sterile technique, the skin is cleansed with povidone-iodine, and the patient is directed to retract the shoulder to a neutral posture. The posterolateral angle of the acromion is identified by palpation, and the needle is advanced in an anteromedial and slightly inferior direction ( Figs. 11-1 and 11-2 ). 5 If the soft tissues resist needle insertion, a small volume can be injected to expand the bursa so that the needle can be advanced further, resulting in optimal needle position. A mixture of 2 to 4 mL of 1% or 2% lidocaine hydrochloride and 2 to 4 mL of 0.5% bupivacaine hydrochloride is injected into the bursa after a 25-gauge, 1.5-inch needle is introduced approximately 1 inch. 6 In the authors’ experience, an inflamed subacromial bursa accepts 4 to 6 mL of total volume. Following the injection, a reduction of pain with improved strength supports the diagnoses of shoulder impingement, supraspinatus tendinitis, and subdeltoid bursitis. Patients who respond with greater than 50% relief are good candidates for an immediate follow-up injection with 1 mL of betamethasone sodium phosphate. 6 Alternatively, the anesthetics can be mixed with the corticosteroids and administered in a single injection when the clinical examination is clear. Subacromial bursography is helpful when the initial blind anesthetic injection is unsuccessful or in a patient whose diagnosis is unclear. A normal bursogram casts doubt on a diagnosis of subacromial impingement. 7

Figure 11-1 The subacromial bursa is approached from posterolateral attitude.

Figure 11-2 Schematic of subacromial bursa injection.
(Modified from Vander Slam TJ: Atlas of Bedside Procedures. Boston, Little, Brown, 1988.)
The strengthening component of a rehabilitative program should not progress too rapidly after corticosteroid injection, to avoid aggravation of inflammation and to avoid the rare risk for tendon rupture.

Olecranon Bursitis (Draftsmen’s Elbow)
The olecranon bursa is subcutaneous, protecting the proximal ulna frequently subjected to trauma. Inflammation of this bursa is commonly associated with rheumatologic disorders. Aspiration of the bursa should always precede injection and may be helpful to ensure proper location of the needle because the wall of the bursa is often thickened and fibrotic from chronic irritation. Gout may be seen at the olecranon, and any bursal fluid aspirated should undergo microscopic examination for crystals. Aspiration of the bursa is more successful using a larger bore needle (18 gauge), because the fluid may be gelatinous. The needle enters the skin perpendicular to the central swelling while the clinician withdraws on the syringe ( Fig. 11-3 ). 5 The procedure is followed with the application of a compressive dressing, and the patient is instructed to protect the elbow from further trauma. Persistent cases may benefit from a low-dose corticosteroid injection. Rarely, surgical excision or an arthroscopic bursectomy is warranted after failure of conservative measures. 2

Figure 11-3 Approach for olecranon aspiration and injection.
(Modified from Vander Slam TJ: Atlas of Bedside Procedures. Boston, Little, Brown, 1988.)

Trochanteric Bursitis
Several bursae may be implicated in trochanteric bursitis. The subgluteus maximus bursa lies lateral to the greater trochanter and the insertion of the gluteus medius and minimus. The subgluteus medius bursa is situated superior and posterior to the trochanter. The gluteus minimus bursa lies anterior to the trochanter. All three bursae may be part of a greater trochanteric pain syndrome.
Trochanteric bursitis is commonly seen in an elderly population and manifests as pain in the lateral thigh during ambulation. 5a Patients may describe a pseudoradicular pattern with the pain extending down the lateral aspect of the lower extremity and into the buttock. The symptoms can be elicited by placing the lower extremity in external rotation and abduction. Direct palpation or deep pressure applied posterior and superior to the trochanter will reproduce the pain. 8 The patient should be examined for limitations in flexibility involving the gluteus maximus, medius, and minimus and the tensor fasciae latae. Trendelenburg gait as a result of hip abduction weakness may contribute to increased friction and irritation of the bursa. If the history and physical examination are consistent with bursitis, a corticosteroid combined with anesthetic agent is delivered via a 3.5-inch, 22-gauge needle directed at the point of maximal tenderness overlying the greater trochanter ( Fig. 11-4 ). 5, 9 Persistent hip pain despite injection therapy and comprehensive rehabilitation should alert the physician to alternate sources of pain including the lumbar spine, hip joint, and distal lower extremity joints. 10, 11

Figure 11-4 Greater trochanteric bursal injection.
(Modified from Vander Slam TJ: Atlas of Bedside Procedures. Boston, Little, Brown, 1988.)

Iliopectineal Bursa
The iliopectineal (iliopsoas) bursa, the largest bursa near the hip joint, is located anterior to the hip capsule and is covered by the iliopsoas. Inflammation of the bursa is not particularly common and may be functionally limiting in that it causes the patient to avoid extension of the lower extremity during the gait cycle. Patients hold the lower extremity in external rotation with the hip in flexion to relieve pressure on the inflamed bursa. Referral pain following the femoral nerve distribution may be seen in cases of iliopectineal bursitis. The examiner may elicit symptoms by passively extending the hip in either a supine or prone position. Injection under fluoroscopic guidance is recommended because the bursa may communicate with the hip capsule and correct needle placement is essential. 8, 12 Once placement is confirmed by a bursogram, a mixture of anesthetic and corticosteroid is injected through the 3.5-inch spinal needle.

Ischial Bursitis
The ischial bursa lies between the ischial tuberosity and the gluteus maximus. The examiner’s index of suspicion must be high because ischial bursitis—so-called “tailor’s or weaver’s bottom”—is not common. Classically, ischial bursitis occurs from friction and the trauma of prolonged sitting on a hard surface. It may occur in adolescent runners, often in conjunction with ischial apophysitis. Pain is most commonly aggravated during uphill running. 13 The pain is distributed down the posterior aspect of the thigh and occurs with activation of the hamstring muscles. Initial treatment approaches should address modification of the patient’s activity, including a decrease in the duration and frequency of running. If an alternative to running includes cycling, the patient should be advised to avoid the use of toe clips, which increase activation of the hamstrings. When the etiology is due to prolonged sitting, the patient’s work station should be modified to allow activities to be conducted in a standing position, and a cushion should be used during sitting. Ice and NSAIDs are helpful in controlling symptoms. Adolescent athletes may require a radiologic series to screen for callus formation secondary to ischial apophysitis if the pain does not resolve with conservative measures. Persistent pain may benefit from injection as an adjunct to rest, ice, and NSAIDs. To perform this, the patient lies on his or her side with the knees fully flexed to relax the hamstrings. A 3-inch, 22-gauge needle is held in a horizontal position and directed toward the point of maximal tenderness overlying the ischial tuberosity. The injection of contrast dye into the bursa under fluoroscopy may be necessary to verify needle placement.

Anserine Bursitis
The anserine bursa separates the three conjoined tendons of the pes anserinus, or goose’s foot (semitendinosus, sartorius, and gracilis muscles), from the medial collateral ligament and the tibia. It is one of the most commonly inflamed bursae in the lower extremity. Anserine bursitis is commonly seen in women with heavy thighs and osteoarthritis of the knees. The bursa may also become inflamed as the result of direct trauma in athletes, especially soccer players. 4, 13 Patients report pain inferior to the anteromedial surface of the knee with ascension of stairs. Moving the patient’s knee in flexion and extension while internally rotating the leg will reproduce the symptoms. The palpatory examination will localize the pain to the anserine bursa. The injection is straightforward and effective in reducing inflammatory symptoms. After sterile preparation, the knee is fully extended and a 1.0- to 1.5-inch, 22-gauge needle is directed at the point of maximal tenderness ( Fig. 11-5 ) 5 to deliver a 1- to 3-mL combination of anesthetic and corticosteroid. The patient should enter a rehabilitation program emphasizing flexibility, and the athlete at risk for repetitive trauma may benefit from padded knee protection.

Figure 11-5 Anserine bursal injection.
(Modified from Vander Slam TJ: Atlas of Bedside Procedures. Boston, Little, Brown, 1988.)

Tibial Collateral Ligament Bursitis
The tibial collateral ligament (TCL) bursa, referred to as the “no name, no fame” bursa, 14 is located between the deep and superficial aspects of the tibial collateral ligament. 14a The bursa does not adhere to the medial meniscus, and it appears to reduce friction between the superficial layer of the TCL and the medial meniscus. TCL bursitis should be considered in any patient with medial joint line tenderness. During a 3-year study, Kerlan found that 5% of orthopedic patients presenting with medial knee pain suffered from TCL bursitis. 15 Physical examination will not show evidence of new ligamentous or capsular instability. Treatment consists of a local injection of lidocaine (2 to 4 mL) and 1 mL of triamcinolone (40 mg/mL) 15 directed perpendicular to the medial joint line at the point of maximal tenderness ( Fig. 11-6 ).

Figure 11-6 Approach for tibial collateral bursa.

Prepatellar Bursitis
Prepatellar bursitis, often called “housemaid’s knee,” is the result of frequent kneeling that produces swelling and effusion of the subcutaneous bursa at the anterior surface of the patella. The patient infrequently complains of pain unless direct pressure is applied to the bursa. The area is easily entered with a needle at the middle to superior pole of the patella. Repeat injections may be required because the bursa is often multiloculated. Occupational adjustments should include patient education, avoidance of kneeling, and the use of knee pads when pressure must be applied to the patella. A Cryo/cuff can be used to control the inflammatory response in a bursitis that approximates a peripheral joint.

Infrapatellar Bursitis
Infrapatellar bursitis, or clergyman’s knee, occurs with pressure from direct kneeling. The bursa rest on the superior anterior pole of the tibia and is covered by the infrapatellar tendon. Rest and avoidance of direct pressure, cryotherapy with compression and improved flexibility in the quadriceps mechanism are advised. The rehabilitation effort should be maximized prior to consideration of injection therapy because the tendon is at risk for ruptures with administration of corticosteroids.

Retrocalcaneal (Subtendinous) Bursitis
The retrocalcaneal bursa lies between the posterior surface of the calcaneus and the tendon of the triceps surae. Inflammation of the bursa may occur from overtraining, such as too early assumption of increased mileage in a runner, or an ill-fitting shoe resulting in pressure from a restricting heel counter. A positive indicator is discomfort when the examiner places the thumb and index finger on the anterior edges of the Achilles tendon and applies pressure. Modification of the footwear is an important first step to alleviating pain, and symptoms should be controlled with ice and NSAIDs. As the pain is controlled, the patient should stretch the triceps surae complex daily to avoid recurrence. Injections into the bursa are considered only after the aforementioned measures have been pursued. A 20- to 22-gauge needle should be inserted where the bursa demonstrates the greatest distention, often on the lateral aspect of the heel. The needle is advanced with an anterior angle of 15 to 20 degrees to avoid instilling corticosteroid into the Achilles tendon, which weakens the structure and increases the risk of tendon rupture.

Subcutaneous Bursitis
Subcutaneous bursitis, also known as Achilles bursitis or achillobursitis , affects the bursa that lies subcutaneous to the posterior surface of the tendon. Midline swelling develops where the upper edge of the heel counter comes in contact with the heel cord. Subcutaneous bursitis is common in patients who wear high-heeled shoes that apply direct pressure on the bursa. The mainstay of treatment is to have the patient change the shoes. Ice and antiinflammatory medications help provide symptomatic relief. Injection of the bursa is usually not necessary, but if the symptoms persist, an injection may be considered. Care should be given to avoid the Achilles tendon because it is susceptible to rupture.

Calcaneal Bursitis
Calcaneal bursitis often develops in elderly patients from a calcified spur that subjects the bursa to trauma after prolonged walking or running. Evaluation of the footwear may reveal poor shock-absorbing capacity. Injection into the point of maximum tenderness may have diagnostic and therapeutic value. Selection of an appropriate walking or running shoe and the use of a heel cup are beneficial. Athletes should be encouraged to change running shoes every 200 to 300 miles because midsole breakdown occurs after this amount of wear. 16

Pharmacologic Agents for Bursal Injection
A number of local anesthetics are available for bursal injections, and clinicians should be familiar with their pharmacologic properties. Concentrations of 0.5% to 1.0% lidocaine or 0.25% to 0.5% bupivacaine are appropriate for bursal injection. The onset and duration of the anesthetic effect is related to the volume and concentration injected. Lidocaine has an onset of action within 5 to 15 minutes and may last 3 to 4 hours, whereas bupivacaine begins to work in 10 to 20 minutes, but the anesthetic effect can last 4 to 6 hours. 17 Bach describes the benefits of using a combination of lidocaine hydrochloride and bupivacaine hydrochloride in subacromial space injections to obtain an early onset of action with prolonged anesthesia. 6
Corticosteroids are widely available and very effective in alleviating bursal inflammation. Corticosteroids of intermediate or long duration are suitable for treatment of bursitis. Triamcinolone acetonide (10 mg/mL and 40 mg/mL) is a commonly used intermediate-acting agent with a half-life of 24 to 36 hours. Betamethasone is a longer acting corticosteroid with a half-life of 36 to 72 hours and a relative antiinflammatory potency five times greater than triamcinolone. 17 The dosage is adjusted to the size of the bursa, and the lowest effective dose should be delivered to the bursa. Clinicians may want to avoid corticosteroid injection acutely (the first 7 days after an initial injury) because corticosteroids theoretically inhibit the healing process. 18 About 14 to 21 days after injury, glucocorticoids can control the inflammation and edema of the proliferative phase. The Achilles, patellar, and rotator cuff tendons should be avoided because direct injection into the tendon can place the patient at risk for rupture. 18
The clinician must be careful to select a combination of medications within the recommended volumes to avoid further injury to the bursae. Table 11-1 may be used as a guideline for selecting the type and volume of corticosteroid and anesthetic to be administered.

Table 11-1 Guidelines for Bursal Injections

Conclusion
Bursal injections provide a useful diagnostic and therapeutic approach within a comprehensive rehabilitation program. The clinician should have a strong foundation in anatomy and must be familiar with the pharmacologic agents. Diagnosing bursitis can be difficult with only a physical examination, and injection therapy is a useful diagnostic tool. Strong palpatory skills can aid in the injection process, verifying placement of medication into a superficial bursa such as the pes anserine. Fluoroscopic or ultrasound guidance can further ensure accurate delivery of medications to deep-lying bursae, avoiding unnecessary repeat injections due to an inaccurately placed needle. Injection therapy is neither a beginning nor an end point of a comprehensive rehabilitation program. Underlying biomechanical deficits of muscle weakness and tightness must be aggressively sought and corrected for an optimal result.

References

1. Smith D.L., McAfee J.H., Lucas L.M., et al. Septic and non-septic olecranon bursitis: Utility of the surface temperature probe in the early differentiation of septic and nonseptic cases. Arch Intern Med . 1989;149:1581-1585.
1a. Kelley W.N., Harris E.D., Ruddy S., Sledge C.B. Textbook of Rheumatology . Philadelphia: WB Saunders; 1993. 545-560
2. Kerr D.R. Prepatellar and olecranon arthroscopic bursectomy. Clin Sports Med . 1993;12:137-142.
3. Waters P., Kasser J. Infection of the infrapatellar bursa. A report of two cases. J Bone Joint Surg Am . 1990;72A:1095-1096.
4. Magee D.J. Orthopedic Physical Assessment . Philadelphia: WB Saunders; 2008. p 706
5. Vander Slam T.J. Atlas of Bedside Procedures . Boston: Little Brown; 1988. 455, 459, 461
5a. Swezey R.L. Pseudo-radiculopathy in subacute trochanteric bursitis of the subgluteus maximus bursa. Arch Phys Med Rehabil . 1976;57:387-390.
6. Bach B.R., Bush-Joseph C. Subacromial space injections: A tool for evaluating shoulder pain. Physician Sportsmed . 1992;2:93-98.
7. Nicholas J.A., Hershman E.B. The Upper Extremity in Sports Medicine . St. Louis: Mosby; 1995. 124-125
8. Klippel J.H., editor. Primer on the Rheumatic Diseases. Atlanta: Arthritis Foundation. 2008:143-146.
9. Ege Rasmussen K.J., Fanø N. Trochanteric bursitis: Treatment by corticosteroid injection. Scand J Rheumatol . 1985;14:417-420.
10. Collée G., Dijkmans B.A., Vandenbroucke J.P., Cats A. Greater trochanteric pain syndrome (trochanteric bursitis) in low back pain. Scand J Rheumatol . 1991;20:262-266.
11. Traycoff R.B. “Pseudotrochanteric Bursitis”: The differential diagnosis of lateral hip pain. J Rheumatol . 1991;18:1810-1812.
12. Shbeeb M.I., Matteson E.L. Trochanteric bursitis (greater trochanter pain syndrome). Mayo Clin Proc . 1996;71:565-569.
13. Reid D.C. Sports Injury Assessment and Rehabilitation . New York: Churchill Livingstone; 1992. 631, 1564, 1625–1626, 1636
13a. Hemler D.E., Ward W.K., Karstetter K.W., Bryant P.M. Saphenous nerve entrapment caused by pes anserine bursitis mimicking stress fracture of the tibia. Arch Phys Med Rehabil . 1991;72:336-337.
14. Stuttle F.L. The no-name, no-fame bursa. Clin Orthop . 1959;15:197-199.
14a. Lee J.K., Yao L. Tibial collateral ligament bursa: MR imaging. Radiology . 1991;178:855-857.
15. Kerlan R.K., Glousman R.E. Tibial collateral ligament bursitis. Am J Sports Med . 1988;16:344-346.
16. Young J.L., Press J.M. Rehabilitation of running injuries. In: Buschbacher R.H., Braddom R.L., editors. Sports Medicine and Rehabilitation: A Sport-Specific Approach . Philadelphia: Hanley & Belfus; 1994:123-134.
17. Covino B.G., Scott D.B. Handbook of Epidural Anesthesia and Analgesia . Orlando: Grune & Stratton; 1985. 58-74
18. Saal J.A. General principles and guidelines for rehabilitation of the injured athlete. Phys Med Rehabil State Art Rev . 1987;1:523-536.
12 Tendon Sheath and Insertion Injections

Steve R. Geiringer, MD, Ted A. Lennard, MD
Tendons are impressively strong structures that link muscles to bone. They function to transmit the force of muscular contraction to a bone, thereby moving a joint or helping to immobilize a body part. Their microscopic organization is thoroughly described elsewhere. 1 - 3
The organizational unit in a tendon is the collagen fibril, which collectively forms fascicles, which as a group compose the tendon itself. 4 Some tendons, especially long ones, are guided and lubricated along their paths by sheaths ( Fig. 12-1 ) (e.g., biceps brachii, ( Fig. 12-2 ) extensor pollicis brevis, and abductor pollicis longus).

Figure 12-1 Drawing demonstrating a flexor tendon ( A ) within its sheath. The paratendinous septum is reflected ( B ).

Figure 12-2 Biceps brachii long head tendon ultrasound evaluation. A, Transverse imaging view over the biceps groove. Note transverse humeral ligament ( arrowheads ) and tendon. ( arrows ) B, Longitudinal imaging view of the biceps tendon in the anterior arm ( arrows ).
(From Jacobson J: Fundamentals of Musculoskeletal Ultrasound, Saunders, 2007, p 42.)
A prototypical muscle consists of the muscle belly centrally, two musculotendinous junctions, and tendinous insertions into bone at the points of anatomic origin and insertion. 5 Some muscles, such as the extensor carpi radialis longus and brevis at the elbow, attach directly into bone ( Figs. 12-3 ), an arrangement that may be more susceptible to injury. 6

Figure 12-3 Common forearm extensor tendon at the lateral epicondyle—ultrasound evaluation. A, Longitudinal imaging of the common extensor tendon ( arrows ) and radial head (R). B, Longitudinal imaging of the common extensor tendon ( arrowheads ) demonstrating tendinosis ( arrows ) as hypoechoic swelling. L , Lateral epicondyle; R, radius.
(From Jacobson J: Fundamentals of Musculoskeletal Ultrasound, Saunders, 2007, pp 110, 124.)
Much is known about a tendon’s response to laceration and operative repair, 2 although this clinical situation is not frequently encountered. Less is understood about the more common and clinically relevant overuse tendinitis. A tendon and its sheath (if present) will undergo a typical inflammatory response to acute or chronic overuse injury, followed by a regenerative repair process. 2, 7, 8 The distinction between an overload type of acute injury and a chronic overuse mechanism will aid in successful rehabilitation of tendinitis. 9

Corticosteroid Injections
Cortisone and its derivatives are known to reduce or prevent inflammation. Numerous corticosteroid preparations are available for local injection 10 (see Chapter 2 on medications). The injectable corticosteroids are suspensions of insoluble particles, and therefore, the antiinflammatory effect is profound only where the material is deposited. 11 The ability of corticosteroids to control inflammation makes them a valuable adjunct in treating tendon injuries because they do not alter the underlying process that leads to inflammation. 10

Efficacy
As with many other physical medicine treatment modalities, well-designed scientific studies regarding the usefulness of corticosteroid injections are rare. These injections should be considered when, in the practitioner’s judgment, the recognized antiinflammatory effect of local corticosteroid placement may be beneficial for the conditions of tendinitis, enthesitis, or tenosynovitis, and no harm will likely result.
McWhorter and colleagues injected hydrocortisone acetate into rat Achilles peritenons that had been previously injured. 3 There were no deleterious effects of one, three, or even five injections, measured biomechanically (tension to failure) or histologically (light microscopy), compared to controls. This finding should reassure physicians that they are not doing harm with properly placed steroid injections. A 30-year literature review identified eight prospective, placebo-controlled studies of steroid injection treatment for sports-related tendinitis. 12 Three of the studies showed beneficial effects of injections at clinical follow-up. A meta-analysis of properly designed investigations of steroid injection for Achilles tendinitis found no beneficial effects, 13 although very few studies qualified as rigorous. Adverse side effects occurred with a 1% incidence. No “proof” of the usefulness or uselessness of this treatment modality exists.

Contraindications, Complications, and Side Effects
The lack of a specific diagnosis is the single largest contraindication to a local corticosteroid injection. If the diagnosis is clear and the antiinflammatory effect of a corticosteroid may facilitate the rehabilitation process, injection can be considered. 10
Repeated injections to the same area must be avoided, particularly into joints. Alterations in articular cartilage have been documented with repeated administration, 14 possibly resulting in joint damage and weakened ligaments. 15 A widely recognized complication of steroid injection is tendon rupture, a negative outcome that appears to be decreasing in frequency because it is now well understood. Achilles and other tendon ruptures have been reported, 16 - 26 and deposition of injected material directly into any tendon substance is contraindicated. One report links the effect of repeated steroid injections to rupture of the plantar fascia. 27
Some experimental findings have suggested that corticosteroid administration led to smaller, weaker tendons as a side effect. 28 A more common side effect is subcutaneous atrophy, especially at the knee and lateral elbow and more frequently with the use of triamcinolone. 10 Theoretically, atrophy of the specialized fat pads of the heel following steroid injection for plantar fasciitis may lead to a significant disability in an athlete, due to the loss of cushioning effect.

Alternatives to Corticosteroids
In recent years alternatives to corticosteroids have emerged for the treatment of chronic localized musculotendinous pain. These treatments include percutaneous tenotomies and platelet rich plasma (PRP) injections.
Percutaneous tenotomies have been described for treatment of chronic lateral epicondylitis and plantar fasciitis. 18, 29 These injections are performed with large bore needles (18 or 20 gauge) under ultrasound guidance. The needle tip is used to repeatedly fenestrate the affected tissue under local anesthetic. The bony surface (i.e., epicondyle) can be abraded and calcifications may be fragmented. This technique is thought to be a safe and effective alternative to corticosteroid injections. 18, 29
Platelet rich plasma injections use concentrated platelets from autologous blood to stimulate a healing response in damaged tissue. Blood is drawn from the patient and placed in a centrifuge. The concentrated platelets are removed and reinjected directly into the patient’s abnormal musculotendinous tissue or ligament usually under ultrasound guidance. These concentrated platelets produce growth factors that include platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and transforming growth factor-beta (TGF-β). These compounds are instrumental in attracting cells that promote healing by stimulating neovascularization and cellular reproduction. 4, 5, 7, 30 The efficacy of PRP injections and appropriate clinical indications (when and where it should be used) are currently being researched and yet to be definitively determined. Initial results of clinical studies appear promising. 13, 31, 32

Methods of Injection
Tendon and tendon sheath injections are office procedures, typically performed under clean or sterile conditions. The corticosteroid of choice is often combined with a local anesthetic, the latter helping to confirm the proper location of the deposited material. Diagnostic ultrasound has been advocated to guide injections near the heel when guidance by palpation alone fails. 33
Immobilization of the treated structure usually is not needed following injection, although vigorous use of weight-bearing tendons (Achilles, patellar) should be avoided for 48 hours. Ice application may help when the local anesthesia fades, along with other physical medicine modalities as indicated by the particular condition present, usually starting after 48 hours.
If an initial corticosteroid injection proves useful, one or two repeat injections separated by a few weeks or more may be considered. Numerous injections over time should not be considered the sole or primary treatment.

Indications

Diagnosis
Corticosteroid or local anesthetic injections should not be used routinely to arrive at diagnoses pertinent to the musculoskeletal system. The range of physical examination techniques used by the physician is described elsewhere 34 and, in most cases, will suffice at pinpointing the specific cause of pain. The distinction between the conditions of subacromial bursitis and rotator cuff tendinitis can be clarified with injection, 10 but even in this case the physical examination and subsequent rehabilitation program deservedly receive most of the attention.

Treatment
In most instances, the literature supports an adjunctive, not primary, role for injections in the treatment of tendon and tendon sheath injuries. 10, 20 When the doctor and patient decide to proceed with injection, the control of inflammation that is obtained should be used to facilitate the prescribed rehabilitation program, rather than being the only treatment. The area of exception to this generalization is the wrist and hand (to be discussed in detail later).

Upper Extremity Injections
The literature supports the use of corticosteroid injections as a primary treatment for stenosing flexor tenosynovitis in the hand, known as trigger thumb or trigger digit. 30, 35 - 41 In this setting, injection has been shown to be as effective as operative release of the tendon sheath and to have fewer complications. 42 Injection has been employed successfully into the hands of patients with diabetes mellitus and trigger digit, but the success rate may be reduced. 43, 44 Instillation of the material directly into the tendon sheath has no apparent benefit over subcutaneous placement. 45 Multiple pulley rupture 17 and flexor digitorum profundus and superficialis tendon rupture 16 has been reported as a complication from this injection. As with other soft tissue injections, a physician treating trigger finger with instillation of corticosteroid needs to maintain expertise by performing this procedure at least several times yearly.
Stenosing tenosynovitis of the first dorsal wrist compartment also is known as de Quervain syndrome. This compartment typically transmits the tendons of both the abductor pollicis longus (APL) and extensor pollicis brevis (EPB). However, anatomic studies have demonstrated that multiple APL slips are common, as are two subcompartments. 39 Interestingly, although one or more injections are usually successful in treating de Quervain syndrome nonoperatively, 22, 46 patients requiring subsequent operative release have been found to have two subcompartments in greater than expected frequency. 22, 46 Trigger digit and de Quervain syndrome, therefore, are usually treated successfully nonoperatively, and corticosteroid injection is the primary component of the management ( Fig. 12-4 ).

Figure 12-4 Injection technique for first dorsal compartment stenosing tenosynovitis (de Quervain syndrome). The needle is parallel to the tendon.
The use of corticosteroid injection for lateral epicondylitis (tennis elbow) appears widespread ( Fig. 12-5 ), although carefully controlled studies to confirm its efficacy are absent from the literature. 47 One prospective investigation found that corticosteroid injection was more effective in controlling symptoms 8 weeks after injury than anesthetic alone, but the benefit disappeared by 24 weeks. 29 This may be explained by the finding that the histology of tennis elbow is noninflammatory. 48 A prospective chart review found that injection alone was effective in 91% of patients within 1 week, but was associated with a 51% recurrence after 3 months. Initially, a standard physical therapy regimen led to improvement in only 74%, but the recurrence rate dropped to 5%. 49 In the typical clinical setting, of course, injection(s) and physical therapy are often combined with careful consideration of the intrinsic and extrinsic biomechanical factors that may be contributors. 9, 50

Figure 12-5 Injection technique for lateral epicondylitis. The needle tip is placed into the point of maximum tenderness at the edge of the bone.
No recent studies have examined the use of corticosteroid injections in the treatment of biceps brachii tendinitis. In this area, care should be taken to deposit the suspension to bathe the tendon sheath rather than into the body of the tendon itself ( Fig. 12-6 ). Additionally, heavy lifting or vigorous exercise of the arm should be restricted for 48 to 72 hours following injection.

Figure 12-6 Injection technique for long head of biceps brachii. The needle is directed parallel to the tendon.
Corticosteroid injection has been found to be effective for rotator cuff tendinitis—at least for the first several weeks. In one study, injection was superior to placebo and to oral antiinflammatory medication over the course of 4 weeks. 51 No more than three injections are recommended. 10 The technique itself is detailed elsewhere. 11 After corticosteroid injection for treatment of rotator cuff tendinitis, heavy lifting and excessive overhead work are to be avoided for at least 2 days.

Lower Extremity Injections
The literature contains relatively few references to corticosteroid injections of the lower limb for tendon or tendon sheath injuries. In this arena, as in much of musculoskeletal medicine, the practitioner must rely on anecdotal evidence, clinical experience and judgment, and trial and error when choosing a course of treatment.
Although it is not a true tendinitis, plantar fasciitis is commonly treated with steroid injection(s) ( Fig. 12-7 ). If used, they must be considered complementary to a complete rehabilitation program that includes flexibility training and correction of any contributing intrinsic or extrinsic biomechanical factors. 10 If lipoatrophy occurs in the fat pad of the heel secondary to corticosteroid deposition, true disability in the active individual may result. Cosmesis is less of a problem because of the location.

Figure 12-7 Injection technique for plantar fasciitis. The needle tip is advanced to the insertion of the plantar fascia adjacent to the bone.
Most physicians are aware of possible tendon rupture if corticosteroid is injected directly into the Achilles tendon. 34, 52, 53 On the other hand, the Achilles sheath can be injected, 11 often with a good therapeutic result. One double-blind, randomized, controlled study found no advantage of Achilles tendon sheath injections when compared with standard physical therapy measures. 54
Iliotibial band tendinitis, refractory to other measures, sometimes responds to corticosteroid injection. The material is placed around the insertion of the iliotibial band at the proximal, lateral tibia, or, depending on the site of symptoms, where it passes over the prominence of the lateral femoral condyle. 10 Iliopsoas tendinitis has been similarly treated, 55 with up to 2 years of symptomatic relief. The quadriceps (infrapatellar) tendon can be injected for cases of tendinitis, 11 but because this is a weight-bearing structure, many practitioners avoid this procedure for fear of rupture.

Conclusion
In most cases of tendinitis or tenosynovitis of the upper or lower limb, corticosteroid injection for control of inflammation should be considered as a supplement to an individualized, well-designed, rehabilitation program. Notable exceptions are trigger digit or thumb, in which corticosteroid therapy is a successful primary intervention, and, to a lesser extent, de Quervain syndrome. The physician using corticosteroid injections must perform them often enough to maintain technical expertise. Three injections for any given injured area is considered a conservative maximum. Subcutaneous atrophy is a common side effect, and the known complication of tendon rupture strongly recommends against injections of corticosteroid directly into the substance of tendons.

References

1. Cooper R.R., Misol S. Tendon and ligament insertion. J Bone Joint Surg Am . 1970;52:1-20.
2. Kennedy J.C., Willis R.B. The effects of local steroid injections on tendons: A biomechanical and microscopic correlative study. Am J Sports Med . 1976;4:11-21.
3. McWhorter J.W., Francis R.S., Heckmann R.A. Influence of local steroid injections on traumatized tendon properties. A biomechanical and histological study. Am J Sports Med . 1991;19:435-439.
4. Menetrey J., Kasemkijwattana C., Day C.S., et al. Growth factors improve muscle healing in vivo. J Bone Joint Surg Br . 2000;82:131-137.
5. Yasuda K., Tomita F., Yamazaki S., et al. The effect of growth factors on biomechancical properties of the bone-patellar tendon-bone graft after anterior cruciate ligament reconstruction: a canine model study. Am J Sports Med . 2004;32:870-880.
6. Brophy D.P., Cunnane G., Fitzgerald O., Gibney R.G. Technical report: Ultrasound guidance for injection of soft tissue lesions around the heel in chronic inflammatory arthritis. Clin Radiol . 1995;50:120-122.
7. Anitua E., Andia I., Sanchez M., et al. Autologous preparations rich in growth factors promote proliferation and induce VEGF and HGF production by human tendon cells in culture. J Orthop Res . 2005;23:281-286.
8. Badalamente M.A., Sampson S.P., Dowd A. The cellular pathobiology of cumulative trauma disorders/entrapment syndromes: Trigger finger, de Quervain’s disease and carpal tunnel syndrome. Trans Orthop Res Soc . 1992;17:677.
9. Fauno P., Anderson H.J., Simonsen O. A long-term follow-up of the effect of repeated corticosteroid injections for stenosing tenovaginitis. J Hand Surg Br . 1989;14:242-243.
10. Halpern A.A., Horowitz B.G., Nagel D.A. Tendon ruptures associated with corticosteroid therapy. West J Med . 1977;127:378-382.
11. Curwin S., Stanish W.D., Tendinitis. Its Etiology and Treatment. In Lexington . Collamore Press; 1984.
12. Almekinders L.C., Temple J.D. Etiology, diagnosis, and treatment of tendonitis: An analysis of the literature. Med Sci Sports Exerc . 1998;30:1183-1190.
13. Mishra A., Pavelko T. Treatment of chronic elbow tendinosis with buffered platelet-rich plasma. Am J Sports Med . 2006;34(11):1774-1778.
14. Kerlan R.K., Glousman R.E. Injections and techniques in athletic medicine. Clin Sports Med . 1989;8:541-560.
15. Mankin H.J., Conger K.A. The acute effects of intra-articular hydrocortisone on articular cartilage in rabbits. J Bone Joint Surg Am . 1966;48:1383-1388.
16. Fitzgerald B.T., Hofmeister E.P., Fan R.A., et al. Delayed flexor digitorum superficialis and profundus ruptures in a trigger finger after a steroid injection: A case report. J Hand Surg Am . 2005;30(3):479-482.
17. Gyuricza C., Umoh E., Wolfe S.W. Multiple pulley rupture following corticosteroid injection for trigger digit: A case report. J Hand Surg Am . 2009;34(8):1444-1448.
18. Housner J.A., Jacobson J.A., Misko R. Sonographically guided pecutaneous needle tenotomy for the treatment of chronic tendinosis. J Ultrasound Med . 2009;28:1187-1192.
19. Leach R., Jones R., Silva T. Rupture of the plantar fascia in athletes. J Bone Joint Surg Am . 1978;60:537-539.
20. Minamikawa Y., Peimer C.A., Cox W.L., et al. De Quervain’s syndrome: Surgical and anatomical studies of the fibroosseous canal. Orthopedics . 1991;14:545-549.
21. Noyes F., Grood E., Nussbaum N. Effect of intra-articular corticosteroids on ligament properties: a biomechanical and histological study in rhesus knees. Clin Orthop Relat Res . 1977;123:197-209.
22. Peters-Veluthamaningal C., Winters J.C., Groenier K.H., et al. Randomised controlled trial of local corticosteroid injections for de Quervain’s tenosynovitis in general practice. BMC Musculoskelet Disord . 2009 Oct 27;10:131.
23. Reid D.C. Connective tissue healing and classification of ligament and tendon pathology. In: Reid D.C., editor. Sports Injury Assessment and Rehabilitation . New York: Churchill Livingstone; 1992:65-83.
24. Sweetnam R. Corticosteroid arthropathy and tendon rupture. J Bone Joint Surg Br . 1969;51:397-398.
25. Tonkin M.A., Stern H.S. Spontaneous rupture of the flexor carpi radialis tendon. J Hand Surg Br . 1991;16:72-74.
26. Velan G.J., Hendel D. Degenerative tear of the tibialis anterior tendon after corticosteroid injection-augmentation with the extensor hallucis longus tendon, case report. Acta Orthop Scand . 1997;68:308-309.
27. Kapetanos G. The effect of the local corticosteroids on the healing and biomechanical properties of the partially injured tendon. Clin Orthop Relat Res . 1982;163:170-179.
28. Geiringer S.R., Bowyer B.L., Press J.M. Sports medicine. 1. The physiatric approach. Arch Phys Med Rehabil . 1993;74:S428-S432.
29. McShane J.M., Nazarian L.N., Harwood M.I. Sonographically guided percutaneous needle tenotomy for treatment of common extensor tendinosis in the elbow. J Ultrasound Med . 2006;25:1281-1289.
30. de Mos M., van der Windt A.E., Jahr H., et al. Can platelet-rich plasma enhance tendon repair? A cell culture study. Am J Sports Med . 2008;36(6):1171-1178.
31. Sanchez M., Azofra J., Anitua E., et al. Plasma rich in growth factors to treat articular cartilage avulsion: A case report. Med Sci Sports Exerc . 2003;35:1648-1652.
32. Sanchez M., Anitua E., Azofra J., et al. Comparison of surgically repaired Achilles tendon tears using platelet-rich fibrin matrices. Am J Sports Med . 2007;35:245-251.
33. Becker C., Heidersdorf S., Drewlo S., et al. Efficacy of epidural perineural injections with autologous conditioned serum for lumbar radicular compression: an investigator-initiated, prospective, double-blind, reference-controlled study. Spine . 2007;32(17):1803-1808.
34. Dijs H., Mortier G., Driessens M., et al. A retrospective study of the conservative treatment of tennis elbow. Acta Belg Med Phys . 1990;13:73-77.
35. Anderson B., Kaye S. Treatment of flexor tenosynovitis of the hand (“trigger finger”) with corticosteroids: A prospective study of the response to local injection. Arch Intern Med . 1991;151:153-156.
36. Kalaci A., Cakici H., Hapa O., et al. Treatment of plantar fasciitis using four different local injection modalities: A randomized prospective clinical trial. J Am Podiatr Med Assoc . 2009;99(2):108-113.
37. Kerrigan C.L., Stanwix M.G. Using evidence to minimize the cost of trigger finger care. J Hand Surg Am . 2009;34(6):997-1005.
38. Kleinman M., Gross A. Achilles tendon rupture following steroid injection. Report of three cases. J Bone Joint Surg Am . 1983;65:1345-1347.
39. Lambert M.A., Morton R.J., Sloan J.P. Controlled study of the use of local steroid injection in the treatment of trigger finger and thumb. J Hand Surg Br . 1992;17:69-70.
40. Marks M.R., Gunther S.F. Efficacy of cortisone injection in treatment of trigger fingers and thumbs. J Hand Surg Am . 1989;14:722-727.
41. Taras J.S., Raphael J.S., Pan W.T., et al. Corticosteroid injections for trigger digits: Is intrasheath injection necessary? J Hand Surg Am . 1998;23:717-722.
42. Jeyapalan K., Choudhary S. Ultrasound-guided injection of triamcinolone and bupivacaine in the management of DeQuervain’s disease. Skeletal Radiol . 2009;38(11):1099-1103.
43. Nimigan AS, Ross DC, Gan BS. Steroid injections in the management of trigger fingers. Am J Phys Med Rehabil. 206;85(1):36-43.
44. Sibbitt W.L., Eaton R.P. Corticosteroid responsive tenosynovitis is a common pathway for limited joint mobility in the diabetic hand. J Rheumatol . 1997;24:931-936.
45. O’Brien M. Functional anatomy and physiology of tendons. Clin Sports Med . 1992;11:505-520.
46. Sawaizumi T., Nanno M., Ito H. DeQuervain’s disease: Efficacy of intrasheath triamcinolone injection. Int Orthop . 2007;31(2):265-268.
47. Price R., Sinclair H., Heinrich I., et al. Local injection treatment of tennis elbow-hydrocortisone, triamcinolone and lignocaine compared. Br J Rheumatol . 1991;30:39-44.
48. Leadbetter W.B. Cell-matrix response in tendon injury. Clin Sports Med . 1992;11:533-578.
49. DaCruz D.J., Geeson M., Allen M.J., Phair I. Achilles paratendonitis: An evaluation of steroid injection. Br J Sports Med . 1988;22:64-65.
50. Rineer C.A., Ruch D.S. Elbow tendinopathy and tendon ruptures: epicondylitis, biceps and triceps ruptures. J Hand Surg Am . 2009;34(3):566-576.
51. Adebajo A.O., Nash P., Hazleman B.L. A prospective double blind dummy placebo controlled study comparing triamcinolone hexacetonide injection with oral diclofenac 50 mg TDS in patients with rotator cuff tendinitis. J Rheumatol . 1990;17:1207-1210.
52. Galloway M.T., Jokl P., Dayton O.W. Achilles tendon overuse injuries. Clin Sports Med . 1992;11:771-782.
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55. Vaccaro J.P., Sauser D.D., Beals R.K. Iliopsoas bursa imaging: Efficacy in depicting abnormal iliopsoas tendon motion in patients with internal snapping hip syndrome. Radiology . 1995;197:853-856.
56. Warwick R., Williams P.L. Gray’s Anatomy , 36th ed. Edinburgh: Churchill Livingstone; 1980.
13 Trigger Point Injections

Ted A. Lennard, MD
Trigger point injections (TIs) are helpful treatment options in patients with acute and chronic muscle pain often associated with underlying bone or nerve pathology. This chapter will discuss the differences in trigger points (TrPs) and tender spots (TSs), describe the three common types of trigger point injections, and discuss the specific techniques of these types of injections.

Trigger Points versus Tender Spots
Trigger points (TrPs) are small, exquisitely tender areas in various soft tissues, including muscles, ligaments, periosteum, tendons, and pericapsular areas. 1 - 1d These points may radiate pain into a specific distant area called a “reference pain zone.” 1d - 9 The referred pain may be present at rest. The pain may occur only on activation of the trigger point by local pressure, piercing by an injection needle, or activity of the involved muscle (particularly its overuse). TrPs located in muscles are called myofascial because they also may involve the fascia. In addition to the focal tenderness, they are characterized by the presence of a taut band 6, 8, 9 that is sensitive to pressure, which indicates sensitization of the nerve endings within. The hard resistance to palpation and needle penetration is interpreted as evidence that a group of the affected muscle fibers is constantly contracted. Later, approximately 6 to 8 weeks after an injury, the resistance to the needle usually becomes very hard. This is characteristic of fibrotic (scar) tissues that fail to respond to conservative therapy. Because there are no definitive histologic studies of TrPs at different stages, it may be assumed that the damaged tissue has healed by a scar.
Trigger point injections represent specific techniques used for alleviation of pain caused by the trigger area. Optimally, TIs are aimed at mechanically breaking up the entire abnormal tissue that causes pain. The most frequent findings related to pain are tender spots, a term reserved for point tenderness without radiating pain. TSs are frequently located within taut bands that have identical characteristics as TrPs. TIs have the same effect, indications, and limitations in both TSs and TrPs. Therefore, the rest of this chapter uses the expression “TrPs” for both tender spots and TrPs, because the technique of injection in both cases is identical: directed at the point of maximum tenderness and taut bands.
Commonly, tender spots and some TrPs represent local tissue damage that causes inflammation and irritation that can be diagnosed by increased sensitivity to pressure. Figures 13-1 and 13-2 illustrate a possible concept of pathologic changes following local tissue damage. This hypothesis may explain clinical findings in acute and chronic injury and the effect of needling. Conceptually, the TSs or TrP at the chronic stage can be thought of as a pocket of fibrotic tissue that contains sensitizing agents that are the products of tissue damage. These substances cause sensitization of the entrapped nerve fibers. This sensitization increases the nerve’s reactivity so that a lower pressure produces pain.

Figure 13-1 Conceptual illustration of pathologic changes in acute tissue injury ( A ) that causes focal tenderness with pain.
Conceptual illustration of pathologic changes in chronic tissue injury ( B ) that causes focal tenderness with pain.
The effect of needling that breaks up the abnormal tissue is also shown ( C ).

Figure 13-2 Physical findings over a trigger point and taut band before, during, and after trigger point injection with needling.
Even without infiltration by anesthetic, the needling instantaneously abolishes the pain, tenderness, and fibrotic type of resistance. Such effect of dry needling can be best explained by breaking up a fibrotic pocket that has entrapped the nerve endings along with sensitizing substances. This allows the entering blood flow to wash away the sensitizing substances. This concept may explain the effect of TIs but has not been substantiated by histologic studies. Needling also may interrupt neuromuscular mechanisms involved in TrP activity.
Figure 13-2 and Table 13-1 illustrate physical findings over TrPs and taut bands before, during, and after injection combined with needling. TrPs and TSs are the immediate cause of pain in a variety of conditions. These include sports or work-related injuries, sprains, strains, or muscle tension related to nonphysiologic posture or stress. Headaches also are frequently caused by TrPs. Certain hormonal disorders such as thyroid or estrogen deficiencies are frequent causes and perpetuators of widespread TrPs.
Table 13-1 Physical Findings Before, During, and After Trigger Point Injections Before Injection During Injection After Injection Normal Muscle Tissue Elastic soft resistance; nontender Minimal resistance to needle progression; no pain Normal tissue findings Taut Band Hard and tender. Local twitch response can be elicited on snapping. Penetration of the needle causes pain and encounters hard resistance as in fibrotic tissue (particularly in chronic TrP). Local twitch response occurs when the needle enters the hyperirritable fibers. The hard and tender areas on palpation become nontender. Pressure pain sensitivity becomes normal immediately. Soreness from injection resolves in 3-5 days. Local twitch response can no longer be elicited. Hyperirritability resolves. Trigger Point Maximum tender point within the taut band. Maximum pain on needle penetration with hard resistance as in the taut band. Trigger point sensitivity to pressure disappears. Hard consistency becomes normal, similar to improvement in taut bands.
TrP , Trigger point.

Trigger Point Injections
Needling represents the most effective treatment of trigger points and TSs. 9a - 9f Injecting a local anesthetic (usually lidocaine) is combined with a special needling technique to break up the abnormal tissue that causes the pain. The critical factor in TIs is not the injected substance but rather the mechanical disruption of the abnormal tissue and interruption of the TrP mechanism if one has developed. 2, 10, 11 Intensive stimulation also may contribute to the prolonged relief of pain by TrP injections. 12 The fact that the symptoms originated in the treated TrP is confirmed by observing whether the pain is reproduced by pressure on the trigger area and relieved after the TrP injection. 13 The injections are followed by a specific program of stretching and exercises. After fibrotic tissue (scar) has formed in the damaged tissue, the most effective way to break it up is through needling: the repetitive insertion and withdrawal of the injection needle in the affected area.
Local anesthetics, such as 1% lidocaine or 0.5% procaine, provide temporary relief, lasting about 45 minutes. Long-term relief from pain is achieved by the needling, which mechanically breaks up the abnormal tissue. 13a The number of injections needed depends on the number of TrPs present.
One or two areas are usually injected during each treatment visit. Injections may be given 2 or 3 times a week for acute pain; once per week or once every 2 weeks is usually adequate as pain relief is being achieved. Each trigger point requires at least one injection. However, in large TrPs, injection may be limited to one segment per visit, depending on the patient’s tolerance. Sufficient tissue must be left around the needled areas for proper healing. Without proper treatment, TrPs tend to spread to additional muscles, causing flare-up of pain.
The injection technique used for TrPs (combination of needling with infiltration) is effective in alleviating pain and restoring function in focal tenderness. The procedure is effective regardless of the underlying pathology and whether or not the pain is referred or limited to the tender area. Sprains and strains of muscles, ligaments, soft tissue injuries, inflammation, injuries of pericapsular tissues, and bursitis are the most common conditions that improve dramatically after needling combined with injection of local anesthetic. TrPs caused by endocrine dysfunction (especially thyroid or estrogen deficiency), fibromyalgia, psychological tension, or ischemia caused by muscle spasm also may be treated effectively by TIs. Often psychological tension and muscle spasm may not be alleviated without eliminating TrPs, which prevent relaxation of the muscle. Inability to relax tight muscles produces more TrPs, and a vicious cycle ensues.
The main contraindications for TIs include bleeding disorders, local infection, anticoagulant therapy, certain psychiatric conditions (anxiety, paranoia, schizophrenia), and inability to rest the injured body part following the procedure. Unless the conditions that caused the TrPs and perpetuating factors are diagnosed and treated, the TrPs will recur.

Common Trigger Point Injection Techniques
Three commonly employed trigger point techniques include needling combined with infiltration of the entire taut band, technique of Travell and Simons, and injection of corticosteroids. There are some clinicians who have proposed ultrasound guidance in the cervicothoracic regions to prevent complications. 13
1. Needling combined with infiltration of the entire taut band appears to be the most effective technique of TIs. Infiltration with a local anesthetic such as 1% lidocaine or 0.5% procaine is combined with needling. After withdrawal of the needle to the subcutaneous level, repetitive insertion and redirection of the needle is required to cover the entire abnormal (painful) area with as few skin penetrations as possible. The needling and infiltration is extended over the entire taut band, which harbors the TrP/TSs, including its attachment to the bones (enthesopathy).
2. Technique of J. Travell and D.G. Simons . 14 - 17 A small amount of 0.5% procaine is injected into the TrP to desensitize the most tender spot. This approach limits the needling and injection of 0.5% procaine to the most tender focus. The goal is to inactivate the neuromuscular TrP mechanism. The needling progresses in millimeters rather than centimeters, as described later.
3. Steroid injection . A 1.5-inch needle, usually 25-gauge, is used. Corticosteroids are combined with a small amount (1 to 3 mL) of local anesthetic, usually lidocaine. Corticosteroids are not necessary for myofascial TrP treatment. Precise needling, which breaks up the abnormal tissue, is more effective. In fact, corticosteroids may induce local myopathy. However, corticosteroids may be useful in the treatment of conditions involving passive tissues such as bursitis, tendinitis, epicondylitis, or ligament sprain. The disadvantages of corticosteroid injections into ligaments and tendons include loosening and incomplete healing. This may make the injected structures more susceptible to reinjury. Also, the number of corticosteroid injections is limited to 3 to 5, leaving numerous TrPs untreated.

Trigger Point Injection Techniques
The purpose of the injection is to mechanically break up the abnormal and sensitized, tender tissue by needling. Injection of any fluid adds to the mechanical effect of the procedure. Usually 1% lidocaine is optimal. However, in case of allergy to the “-caine” group, saline is satisfactory. The anesthetic also blocks pain and the irritation resulting from tissue damaged by the needle.
The needle should be sufficiently long to be able to reach deeper than the trigger point. The diameter of the needle should be large enough to facilitate mechanical disruption of the abnormal tissue areas. 18 A 22- to 25-gauge needle is usually sufficient. The total amount of 1% lidocaine injected ranges from 1 to 12 mL. Commonly, an extensive area must be infiltrated that ranges from 3 to 25 cm in length and 2 to 10 cm in width. The size of the infiltration depends on the extent of the trigger point and on the length of the affected muscle fibers. At each stop of the needle’s penetration, no more than 0.1 or 0.2 mL should be injected. Larger volumes can damage the muscle, negating any benefit.

Injection Procedure

1. Ask the patient to point out with one finger the area of most intense pain. If this pain is diffuse and corresponds to a trigger point’s reference zone(s), locate the TrP causing the symptoms. 2, 6, 8, 9 Palpate the muscle or ligament 2 that has a corresponding reference zone. Position the patient so that you have proper access to the painful area.
2. Palpate the point of maximum tenderness. Mark it by impression of a fingernail. Palpate around to find the entire taut and tender band, which may reach from the origin to the insertion of the muscle, and mark it by fingernail impressions.
3. Explain the procedure to the patient.
4. Clean the skin with povidone-iodine or alcohol. Use surgical gloves.
5. Spray with ethyl chloride to frost. If patient does not like the vapo-coolant, pinch the skin in the area of injection and immediately insert the needle. Because the pinching distracts and occupies the sensory pathways, the patient does not feel the needle.
6. Needle the entire area where an increased fibrotic type of resistance is present, including the entire taut band. Explore with the needle beyond the border of the trigger point and the taut band. Inject only a small amount (0.1 to 0.3 mL) each time you stop the needle penetration. It is of great importance to always aspirate at each needle stop before the injection, especially when the neck or upper body is treated. Terminate the injection if blood is aspirated.
7. Proceed with the needle insertions through the taut band. Stop in 1 to 2 cm increments and again deposit only a small amount of anesthetic (0.1 to 0.2 mL) at each stop. When you reach the normal muscle below the taut band, the pain and hard resistance to the needle cease. Inject a smaller amount in the normal tissue and then withdraw the needle to the subcutaneous level. Make sure that the needle is out of the muscle when you change the direction of the needle; otherwise, you will cut the tissue. Redirect the needle tip within the subcutaneous tissue along the plane of the taut band. Enter the band in distances 1 to 3 cm from the previous infiltration. The distance to the next insertion depends on the size of the muscle and the taut band. Proceed similarly until you needle and infiltrate the entire taut band. Depending on the patient’s tolerance, about 10 local infiltrations can be performed in one session, covering one large TrP and its taut band. If the patient becomes annoyed or the planned amount of anesthetic has been reached, the injection is terminated. If necessary, the remaining parts of the taut band can be injected in the following session, usually 1 week later.
Immediately following an effective injection, the tenderness of the TrP and taut band, as well as the associated harder consistency of the surrounding tissue, disappears or diminishes substantially.
Special attention should be directed to injecting the myotendon junction as well as the origin and the insertion of the involved muscle(s). Injection is usually particularly painful at these sites. Technique of injection to specific muscles has been described, 4, 8, 9 and it is highly recommended that these textbooks are consulted before a novice starts TIs.
8. Compress the injected site for about 2 minutes to prevent bleeding. Cover area with an adhesive bandage.

Postinjection Care
Postinjection care includes the following steps:
1. Promote hemostasis by pressure.
2. Encourage active slow movement of the injected muscle to its full range; repeat three times.
3. Apply heat locally.
4. Use physiotherapy consisting of hot packs and electric stimulation using sinusoid surging current (adjust volume to induce strong contractions that are not too painful). Use vapo-coolant spray to inactivate remaining painful areas. This is followed by limbering and stretching exercises.
5. If soreness is excessive, give acetaminophen or an NSAID.
6. Limbering exercises and/or passive stretching should be performed by the patient every 2 hours. Limbering exercises have been proven effective in preventing the recurrence of low back pain. 19 Experience shows that this applies to all types of muscle pain.
7. Advise the patient to avoid heavy use of the injected muscle such as walking or driving long distances after lower body injections and to avoid sports after upper body injections.

Other Injections
Currently, trigger point injections may be combined with other injection techniques such as preinjection blocks and paraspinous blocks.
1. Paraspinous block , which desensitizes the irritated spinal segment, is the first in sequence if spinal segmental sensitization is present. This is usually part of a cycle consisting of discopathy, radiculopathy, and paraspinal muscle spasm. 10 The paraspinous block consists of two steps: (1) the spreading of the anesthetic (1% lidocaine) along the sprained (tender) supra/interspinous ligaments to achieve long-term healing and relief of spinal segmental sensitization; and (2) needling and infiltration of the sprained supra/interspinous ligaments. 13
2. Preinjection block spreads anesthetic to prevent nociceptive impulses from the tender area to be injected. 3, 5, 7 Preinjection block is administered before the injection of the tender area. The purpose is to block the pain sensation from the sensitive structure about to be injected. Preinjection block prevents central sensitization caused by injecting the irritative focus (a tender area) and also relaxes the neurogenic component of the taut band associated with the trigger point or tender spot. 5 This makes the trigger point injection easier to perform and renders needling and infiltration more effective. 5, 7

References

1. Fischer A.A. Pressure threshold measurement for diagnosis of myofascial pain and evaluation of treatment results. Clin J Pain . 1987;2:207-214.
1a. Fischer A.A. Documentation of myofascial trigger points. Arch Phys Med Rehabil . 1988;69:286-291.
1b. Kraus H. Diagnosis and Treatment of Muscle Pain . Chicago: Quintessence; 1988.
1c. Kraus H., Fischer A.A. Diagnosis and treatment of myofascial pain. Mt Sinai J Med . 1991;58:235-239.
1d. Affaitati G., Fabrizio A., Savini A., et al. A randomized, controlled study comparing a lidocaine patch, a placebo patch, and anesthetic injection for treatment of trigger points in patients with myofascial pain syndrome: Evaluation of pain and somatic pain thresholds. Clin Ther . 2009;31(4):705-720.
2. Fischer A.A. Quantitative and objective compliance recording. In: Nordhoff L.S., editor. Motor Vehicle Collision Injuries . Gaithersburg, Md: Aspen; 1996:142-148.
3. Fischer A.A. New approaches in treatment of myofascial pain. Phys Med Rehabil Clin North Am . 1997;8:153-169.
4. Fischer A.A. New developments in diagnosis of myofascial pain and fibromyalgia. Phys Med Rehabil Clin North Am . 1997;8:1-21.
5. Fischer A.A. Algometry in diagnosis of musculoskeletal pain and evaluation of treatment outcome: An update. In: Fischer A.A., editor. Muscle Pain Syndromes and Fibromyalgia . New York: Haworth Medical Press; 1998:5-32.
6. Fischer A.A. Treatment of myofascial pain. J Musculoskeletal Pain . 1999;7:131-142.
7. Fischer A.A., Imamura S.T., Imamura M. Myofascial trigger points are most frequently a manifestation of segmental spinal sensitization. J Musculoskeletal Pain . 1998;6(Suppl 2):20.
8. Fischer A.A., Imamura S.T., Kaziyama H.S., Imamura M. Trigger point injections and “paraspinous blocks” which relieve segmental spinal sensitization are effective treatment for chronic pain. J Musculoskeletal Pain . 1998;6(Suppl 2):52.
9. Frost F.A., Jessen B., Siggaard-Andersen J. A control, double-blind comparison of mepivacaine injection versus saline injection for myofascial pain. Lancet . 1980;1:499-500.
9a. Deyo R.A. Conservative therapy for low back pain. Distinguishing useful from useless therapy. JAMA . 1983;250:1057-1062.
9b. Fischer A.A. Diagnosis and management of chronic pain in physical medicine and rehabilitation. In: Ruskin A.P., editor. Current Therapy in Physiatry . Philadelphia: WB Saunders, 1984.
9c. Garvey T.A., Marks M.R., Wiesel S.W. A prospective, randomized, double-blind evaluation of trigger-point injection therapy for low-back pain. Spine . 1989;14:962-964.
9d. Melzack R. Prolonged relief of pain by brief, intense transcutaneous somatic stimulation. Pain . 1975;1:357-373.
9e. Hackett G.S. Ligament and Tendon Relaxation Treated by Prolotherapy , 3rd ed. Springfield, Ill: Charles C Thomas; 1958.
9f. Scott N.A., Guo B., Barton P.M., Gerwin R.D. Trigger point injections for chronic non-malignant musculoskeletal pain: A systematic review. Pain Med . 2009;10(1):54-69.
10. Fischer A.A. Local injections in pain management. Trigger point needling with infiltration and somatic blocks. Phys Med Rehabil Clin North Am . 1995;6:851-870.
11. Fischer A.A. Injection techniques in the management of local pain. J Back Musculoskeletal Rehabil . 1996;7:107-117.
12. Fischer A.A. Myofascial pain. In: Windsor R.E., Lox D.M., editors. Soft Tissue Injuries: Diagnosis and Treatment . Philadelphia: Hanley & Belfus; 1998:85-100.
13. Bonica J.J. Management of myofascial pain syndromes in general practice. J Am Med Assoc . 1957;164:732-738.
13a. Venancio Rde A., Alencar F.G.Jr. Zamperini C. Botulinum toxin, lidocaine, and dry-needling injections in patients with myofascial pain and headaches. Cranio . 2009;27(1):46-53.
14. Simons D.G. Myofascial pain syndromes due to trigger points. In: Goodgold J., editor. Rehabilitation Medicine . St. Louis: Mosby, 1988.
15. Simons D.G. Muscular pain syndromes. In: Fricton J.R., Awad E.A., editors. Advances in Pain Research and Therapy . New York: Raven Press, 1990.
16. Travell J.G., Simons D.G. Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol. I. Baltimore: Williams & Wilkins. 1983.
17. Tavell J.G., Simons D.G. Myofascial Pain and Dysfunction: The Trigger Point Manual. The Lower Extremities, Vol. II. Baltimore: Williams & Wilkins. 1992.
18. Yoon SH, Rah UW, Sheen SS, Cho KH. Comparison of 3 needle sizes for trigger point injection in myofascial pain syndrome of upper and middle trapezius muscle: A randomized controlled trial. Arch Phys Med Rehabil. 2009; 90(8):1332-1339.
19. Botwin K.P., Sharma K., Saliba R., Patel B.C. Ultrasound-guided trigger point injections in the cervicothoracic musculature: A new and unreported technique. Pain Physician . 2008;11(6):885-889.
14 Botulinum Toxin Injections in Myofascial Pain Disorders

Hongtao Michael Guo, MD, PhD, Jodi J. Hawes, MD, PT, Martin K. Childers, DO, PhD
This chapter will discuss the uses of botulinum toxin for pain management in three of the myofascial pain disorders: cervical dystonia, myofascial pain syndrome and the piriformis syndrome. Although the uses for botulinum toxin that are licensed by the Food and Drug Administration (FDA) do not include pain management, it has been used by a range of medical specialists to address pain control of various etiologies. The purpose of this chapter is to provide clinical insights for clinicians regarding the use of botulinum toxin in three disorders that involve myofascial pain, based on the authors’ experience and literature review. As with all medications and procedures, clinicians must obtain the necessary training and knowledge to achieve the most effective and safe outcome. Accordingly, one should know essential features about this toxin before treating patients for pain. These vital elements include: mechanism of action 1, 2 ; concept of median lethal dose (LD 50 ); dosing and administration 3 ; basic neuromuscular anatomy and physiology; conjunctive therapy with botulinum toxin for optimal treatments; 4, 5 and contraindications, of using this toxin. Because it is beyond the scope of this chapter to address all of the topics just listed, the authors urge the reader to visit other informational sources listed at the end of this chapter.

Botulinum Toxin and Its Clinical Use
Justinus Kerner, a German physician and poet, provided the first accurate and complete description of the clinical symptoms of food-borne botulism. He described 230 patients in the 1820s who suffered all the muscular and autonomic symptoms including gastrointestinal disturbances, dry eyes, dry skin, and weakness associated with the ingestion of contaminated meats. 6 Kerner termed this condition “sausage poison” and “fatty poison”. He went on to perform animal experiments and experiments on himself. He administered botulinum toxin extracted from contaminated sausages to birds, cats, rabbits, frogs, flies, locusts, and snails. 7 Kerner developed hypotheses from his experiments on the pathophysiology of the toxin. In his monograph he stated: “The nerve conduction is brought by the toxin into a condition in which its influence on the chemical process of life is interrupted. The capacity of nerve conduction is interrupted by the toxin in the same way as in an electrical conductor by rust.” Later in the monograph, he conceives of the idea of using the toxin for therapeutic uses. 7
The term botulism was derived from the Latin term, “botulus”, which means sausage. Edward Schantz first isolated the toxin and he and Alan Scott began work on a standardized botulinum toxin preparation in the late 1960s. 6 Scott first used botulinum toxin type A in monkey experiments in 1973 and he first used botulinum toxin type A in humans to treat strabismus in 1980. 6 Botulinum toxin type A was approved by the Food and Drug Administration (FDA) in 1989 for the treatment of strabismus, blepharospasm, and hemifacial spasm in patients more than 12 years of age. Botulinum toxin type B received FDA approval for treatment of cervical dystonia in 2000, and botulinum toxin type A was approved by the FDA to treat severe primary axillary hyperhydrosis and moderate-to-severe glabellar frown lines in 2002.
In addition to the approved uses in the United States, there are other published uses of botulinum toxin, 8 which include painful or potentially painful conditions such as: achalasia; anismus (painful); bladder detrusor hyperactivity; essential tremor; myofascial pain syndrome (painful); focal dystonias (sometimes painful); muscle spasm (often painful); piriformis syndrome (painful); spasmodic dysphonia; spasticity (sometimes painful); whiplash (painful); chronic focal painful neuropathies; migraines and other headache disorders; temporomandibular joint pain disorders; gastrointestinal dysmotility disorders; chronic low back pain.
Aside from publications, noteworthy medical organizations have commented on the effectiveness and safety of botulinum toxin. The National Institutes of Health (NIH) Consensus Development Conference published a statement in 1990 that summarized the indications and contraindications of botulinum toxin usage for the treatment of a variety of conditions. 9 The NIH conference endorsed the use of the neurotoxin as safe and effective for the symptomatic treatment of adductor spasmodic dysphonia, blepharospasm, cervical dystonia, hemifacial spasm, jaw-closing oromandibular dystonia, and strabismus. The same year, the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology further endorsed the use of botulinum toxin for the symptomatic treatment of these conditions. 10
Botulinum toxin is held to be one of the deadliest poisons known to mankind, yet by harnessing this activity, it has resulted in great advances in the treatment of numerous conditions. 2 The understanding of the mechanism of action of botulinum toxin had its beginnings in 1949 when Burgen’s group discovered that botulinum toxin blocks neuromuscular transmission. 11 In the 1950s, researchers discovered that injecting overactive muscles with small quantities of botulinum toxin type A resulted in decreased muscle activity by blocking the release of acetylcholine (Ach) at the neuromuscular junction. 11 The understanding of this mechanism of action led to the application of botulinum toxin in most clinical settings. Since then, significant advances have occurred in the understanding of the mechanisms of action of botulinum toxin other than muscle paralysis—and this is leading to additional applications.
There are seven serotypes (A, B, C1, D, E, F and G) of botulinum toxin that act by inhibiting the exocytosis of Ach from presynaptic boutons of cholinergic neurons. Botulinum toxin is synthesized as a single-chain polypeptide (~150 kDa) that is activated by proteolytic cleavage into a 100-kDa heavy chain and 50-kDa light chain linked by a disulfide bond. The heavy chain domain is involved in cellular uptake into the presynaptic terminal by binding to extracellular receptors and in the transport of the neurotoxin through the lipid bilayer. The toxin is now intracellular but is sequestered in a membranous organelle without access to its targets, which reside in the cytoplasm. It is one of the functional domains (amino) of the heavy chain of the toxin that undergoes a conformational change facilitating translocation of the light chain through the lipid bilayer into the cytoplasm. Finally, the disulfide bond between the heavy and light chain is cleaved, allowing the light chain access to the cytoplasm. The light chain is a zinc-dependent endoprotease and the targets of the protease are presynaptic proteins required for intracellular trafficking of acetylcholine vesicles into the synaptic cleft. The presynaptic proteins targeted by the protease are called SNARE proteins (soluble N -ethylmaleimide-sensitive fusion protein attachment receptor) and are critical for the exocytosis of synaptic vesicles. It is this step, the proteolytic cleavage of the SNARE proteins, that is best understood in the intoxication by botulinum neurotoxin. 12
The release of Ach into the synaptic cleft requires docking of the Ach-containing vesicle to the presynaptic membrane. 12 The docking of the vesicle requires various proteins that are located in the wall of the vesicle, in the presynaptic membrane or in the cytoplasm. This family of proteins (SNAREs) includes vesicle-associated membrane protein (VAMP)/synaptobrevin, syntaxin, and SNAP-25. These proteins form a complex that allows the vesicle to fuse with the motor nerve terminus membrane and release the acetylcholine into the synaptic cleft. The site of action of botulinum toxin type A is SNAP-25 (synaptosome-associated protein with a molecular weight of 25 kDa), which is a presynaptic membrane protein. Botulinum toxin type B targets VAMP (vesicle-associated membrane protein), which is located in the wall of the vesicle. Cleavage of the proteins prevents the assembly of the fusion complex and thereby blocks the docking of the vesicle and the release of the Ach leading to relaxation of the muscle cell and a state of chemical denervation. 12
Of significant clinical importance is the duration of action of the toxin effect. In general terms, the clinical effects of botulinum toxin injections are delayed a day or two with the maximal effects of functional muscular weakness peaking at about 2 weeks. 1, 5 The therapeutic effect of botulinum toxin-induced neuromuscular blockade usually lasts 3 to 4 months and ranges 2 to 6 months following an injection. 13 Several factors likely contribute to the duration of action of the toxin. The best understood factor and most often quoted is the synaptic remodeling; however, other factors such as the duration of protease activity in the nerve terminal, the rate of replacement of the cleaved SNARE proteins, and the activity of the cleavage products may also influence the rate of function recovery. 6
The development of neutralizing antibodies to botulinum toxin can be a therapeutic problem for patients and physicians. 14 Patients who initially respond well to treatment with botulinum toxin can become nonresponders. 15 The incidence rates of neutralizing antibody development and the exact cause in individual patients remains unknown. 14 More frequent injections, more “booster injections,” and higher doses are possible risk factors, thus extending the time between injections, minimizing the dose, and avoiding booster injections may decrease the development of neutralizing antibodies. 15
Some authors have noted that the pain relief preceded muscle decontraction and exceeded the degree and duration expected as a consequence of its neuromuscular actions. 13 These observations suggest that botulinum toxin may have antinociceptive properties independent of the muscle relaxation. These observations and the expanding body of literature examining botulinum toxin for primary headache disorders and muscle conditions including a pain component led to further investigation into botulinum toxin in pain. 16
A number of in vitro experiments have provided evidence that botulinum toxin inhibits neurogenic inflammation by attenuation of the release of neurotransmitters. 17 Botulinum toxin was found to inhibit substance P release from cultured embryonic dorsal root ganglion neurons and to reduce stimulated release of calcitonin gene-related peptide from cultured trigeminal ganglia neurons. 18
Additional support has come from animal experiments demonstrating reduction in nociceptive behaviors in animal models of inflammatory and traumatic neuropathic pain following peripheral injections of botulinum toxin. 17 In rats with induced trigeminal neuropathy, intradermal injection of botulinum toxin in the area of the infraorbital branch of the trigeminal nerve alleviated the mechanical allodynia and reduced the exaggerated neurotransmitter release. 19 In another experiment by Cui and colleagues, a rat formalin model of inflammatory pain was inhibited by subcutaneous administration of botulinum toxin injection and this inhibition was associated with a reduction in neurotransmitter release from the peripheral terminals of nociceptive sensory neurons. 20 It was Cui’s study in 2002 that provided the first evidence that botulinum toxin had an effect on nociceptive sensory nerves in vivo. 20 In studies by Aoki, botulinum toxin inhibited several of the neurophysiologic and neurochemical effects of formalin in the rat formalin-pain model including glutamate release, Fos-LI in the dorsal horn, and evoked-activity of WDR neurons in the spinal cord. 16
The efficacy of botulinum toxin in neuropathic pain initially was suggested in small anecdotal case studies and small open-label trials. 21 An open study of botulinum toxin in 13 volunteers with trigeminal neuralgia found a reduction in visual analog scale scores and surface area of pain. 22 Tsai and coworkers conducted an open label, prospective pilot study using botulinum toxin injected intracarpally in five patients with primary carpal tunnel syndrome. 23 Their data suggested a long-acting antinociceptive effect of botulinum toxin.
More recently, two well designed clinical trials evaluated the efficacy of botulinum toxin for chronic neuropathic pain and diabetic neuropathic pain. 17, 24 Ranoux and colleagues published a randomized, double-blind, placebo-controlled, parallel group study providing evidence in support of the efficacy of botulinum toxin for the pain associated with focal neuropathies such as postherpetic neuralgia and posttraumatic or postoperative neuropathy. 17 The study included 29 patients with focal painful neuropathies and mechanical allodynia, and treatment consisted of a one-time intradermal administration of botulinum toxin into the painful area. Outcome measures included average spontaneous pain intensity, quantified testing of thermal and mechanical perception of pain, allodynia to brush and decreased pain threshold to cold; the measures were evaluated at baseline, 4, 12, and 24 weeks. The results indicated that botulinum toxin treatment, relative to placebo, was associated with persistent effects on spontaneous pain intensity from 2 weeks after the injection to 14 weeks. 12 A recent study by Yuan and associates report the results of a double-blind, placebo-controlled, crossover trial of intradermal botulinum toxin for diabetic neuropathic pain in 18 patients. 24 The authors found a significant reduction in visual analog scale of pain at 1, 4, 8, and 12 weeks after botulinum toxin injection when compared to the placebo group. Specifically, within the botulinum toxin group, 44.4% of the participants experienced a reduction of the visual analog scale greater than or equal to 3 within 3 months after the injection, in contrast to the placebo group that reported no similar response. In addition, the authors evaluated sleep quality using the Chinese version of the Pittsburgh Sleep Quality Index and found a difference in the improvement in sleep quality between the botulinum toxin treatment group and the placebo group. The difference between the groups reached significance ( P < .05) only 4 weeks after the initial injection, but did not support sleep improvement with botulinum toxin at week 12, which was the endpoint of the study design. 24
Both reports (Yuan and colleagues 24 and Ranoux and associates 17 ) are small studies but each support a trend of reduced pain perception beginning at 1 week postinjection and extending to 12 weeks in the Yuan and colleagues’ study and 14 weeks in the Ranoux and associates’ study. 17, 24 Both studies report essentially no adverse events and this is supported by the general botulinum toxin literature. Although this suggests a promising approach to the treatment of neuropathy, additional larger, well designed, multicenter clinical trials with longer periods of follow-up are necessary.

Cervical Dystonia
Cervical dystonia (CD), also known as spasmodic torticollis and torsion dystonia, is a common form of focal dystonia manifesting as involuntary contraction and twisting of the neck muscles. 25, 26 These features lead to abnormal postures and movements of the head. The deviation of the head can be multidirectional and is described as torticollis (the most common form of CD with patient’s head turned to one side); laterocollis (lateral flexion of the neck), anterocollis (flexion of the neck) and retrocollis (extension of the neck). It is possible that one can have a combination of these forms. The prevalence of CD was reported to be 8.9/1,000,000 27 and it is recently estimated by the Dystonia Medical Research Foundation that 250,000 people suffer from CD in the United States. It is believed that 66% to 75% of the patients with CD are disabled from the pain associated with CD. 27 - 30 CD is mostly idiopathic and about 12% of those affected have a family history. 31 Idiopathic CD is the most common form of adult-onset focal dystonia slowly developed over several years in patients 30 to 50 years old. 32 Cervical dystonia can be caused by any injury or inflammation of the cervical muscles or cranial nerves from various disease processes, including head, neck, and shoulder trauma 33 or from taking dopaminergic block agents. 34 There is evidence indicating that CD arises from basal ganglia circuit abnormalities leading to dopaminergic dysfunction, which in turn causes disinhibited thalamocortical output and dystonic postures. 31, 35 - 37
Patients with CD can have a wide spectrum of symptoms involving the head, neck, upper extremity, and other body parts with sustained painful muscle contraction, pulling, and/or stiffness. 28, 31, 37 The severity of the pain is usually relative to the intensity of the dystonia and muscle spasms.

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