Pain Procedures in Clinical Practice E-Book


1290 Pages
Read an excerpt
Gain access to the library to view online
Learn more


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 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, and access the complete text and images online.


Spinal stenosis
Knee pain
Personality disorder
Procedural sedation and analgesia
Scapular fracture
Hepatitis B
The Only Son
Health system
Neck pain
Dislocated shoulder
Medical procedure
Ilioinguinal nerve
Meralgia paraesthetica
Pain disorder
Nerve block
Radicular pain
Family medicine
Manual therapy
Endoscopic thoracic sympathectomy
Acute pancreatitis
Postherpetic neuralgia
Tennis elbow
Demyelinating disease
Transcutaneous electrical nerve stimulation
Lower extremity
Generalized anxiety disorder
Regional anaesthesia
Peripheral neuropathy
Ankylosing spondylitis
Physician assistant
Pain management
Tension headache
Trigeminal neuralgia
Shoulder problem
Tetralogy of Fallot
Whiplash (medicine)
Internal medicine
Osteopathic medicine in the United States
Physical exercise
U.S. Patients' Bill of Rights
Local anesthetic
Back pain
Chronic pain
Medical ultrasonography
Dietary supplement
Common cold
Posttraumatic stress disorder
Carpal tunnel syndrome
Complex regional pain syndrome
X-ray computed tomography
Multiple sclerosis
Informed consent
Risk management
Rheumatoid arthritis
Physical therapy
Magnetic resonance imaging
Major depressive disorder


Published by
Published 11 June 2011
Reads 2
EAN13 9781437737745
Language English
Document size 3 MB

Legal information: rental price per page 0.0364€. This information is given for information only in accordance with current legislation.

Report a problem

Pain Procedures in Clinical
Third Edition
Ted A. Lennard, MD
Clinical Assistant Professor, Department of Physical Medicine
and Rehabilitation, University of Arkansas, Little Rock,
Springfield Neurological and Spine Institute, Cox Health
Systems, Springfield, Missouri
Stevan Walkowski, DO
Ohio University College of Osteopathic Medicine, Athens,
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
S a u n d e r s)
Front Matter
Pain Procedures in Clinical Practice
Ted A. Lennard, MD
Clinical Assistant Professor, Department of Physical Medicine and
Rehabilitation, University of Arkansas, Little Rock, Arkansas, Spring eld
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,
David G. Vivian, MM, BS, FAFMM
Medical Director, Metro Pain Clinics, Metro Spinal Clinic, Clinical
Intelligence, Victoria, AustraliaCopyright
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899 ISBN: 978-1-4160-3779-8
Copyright © 2011, 2000 by Elsevier Inc. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or
by any means, electronic or mechanical, including photocopying, recording, or
any information storage and retrieval system, without permission in writing from
the publisher. Details on how to seek permission, further information about the
Publisher’s permissions policies and our arrangements with organizations such as
the Copyright Clearance Center and the Copyright Licensing Agency, can be found
at our website:
This book and the individual contributions contained in it are protected under
copyright by the Publisher (other than as may be noted herein).
Knowledge and best practice in this ; eld 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 identi; ed, 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 1Dedication
To my wife, Suzanne, and our four daughters, Selby, Claire, Julia, and Maura.
Ted A. LennardTribute
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, MDContributors
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 andMusculoskeletal 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,
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
WinstonSalem, 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,
Susan J. Dreyer, MD, Associate Professor, OrthopaedicSurgery 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,
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,
MissouriJodi 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,
HCAWesley, 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 UniversityMedical Center, Stanford University, Palo Alto,
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,
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,
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, PhysicalMedicine 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,
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, MarylandRobert 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,
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, AustraliaBrian 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,
Li Zhang, MD, PhD, Department of Anesthesiology,
Columbia University Medical Center, New York, New
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, EditorTable of Contents
Instructions for online access
Front Matter
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 ProceduresChapter 15: Prolotherapy: A CAM Therapy for Chronic Musculoskeletal
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
Chapter 37: Sacroiliac Joint Pain: Procedures for Diagnosis and
Chapter 38: Discography
Chapter 39: Discogenic Pain, Internal Disc Disruption, and RadicularPain
Chapter 40: Intradiscal and Peridiscal Therapies for Discogenic and
Radicular Pain
Chapter 41: Spinal Cord Stimulation and Implanted Intrathecal Drug
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
Basic Principles of
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 magni cation and malingering
1,2should be noted.
A thorough functional, social, and psychological history should be included. A
comparison of historical and physical ndings 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
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 modi cation in the workplace, technique changes
in athletes, and , exibility 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
Constant communication with the patient, including explanations of approaching
procedural steps, helps reduce anxiety. Inappropriate conversation with assisting
medical personnel should be avoided, thereby con rming the physician’s total
attention to the patient. The patient’s gown should t 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 , ora to a
3low level. These agents should be safe, rapid-acting, inexpensive, and e3ective on
3,4a broad spectrum of organisms. Multiple agents, including iodophors (Betadine),
hexachlorophene (pHisoHex), chlorhexidine (Hibiclens, Hibitane), and alcohols,
3,5-7are commercially available and accomplish these desired goals.
3,8-13The preferred agent remains controversial. Clinically, the most commonly
used agents are alcohol and iodine, with the latter being superior for skin
16decontamination. Application of 70% isopropyl alcohol destroys 90% of the
cutaneous bacteria in 2 minutes, whereas the usual single wipe without waiting
3procedure destroys, at most, 75% of cutaneous bacteria.
Skin regions with hair should not alter one’s method of skin decontamination.
Hair removal by shaving increases wound infection rate and is
17-19 20,21contraindicated. If absolutely necessary, clipping hair or applying
19 22depilatory creams can be safe. 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 ngers 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
23-26 27results in pain. Lidocaine and bupivacaine, bu3ered with 8.4% sodium
bicarbonate causes less pain than plain anesthetics and is equally e cacious. 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
28,29the least painful anesthetics. 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
Other preparations used to reduce pain with initial needle injections include
topical anesthetics (eutectic mixtures of local anesthetics, or EMLA), vapocoolant
31sprays, and preheated local anesthetics. 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
32alternatives; however, they are often considered painful, especially when injected
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.
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 immunode ciency 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
33procedure ranges from 1 in 76,000 to 1 in 1.4 million. 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.
References1. 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.
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.
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.
24. Roberts J.R. Local anesthetics: Injection techniques. Emerg Med News. 1992
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.
28. Morris R., McKay W., Mushlin P. Comparison of pain associated with intradermal
and subcutaneous infiltration with various local anesthetic solutions. Anesth Analg.
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.
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
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 con" rm 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 ) ow 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 di/ erential
spinal blocks. 2-Cholorprocaine can be used for in" ltration, epidural or peripheral nerve block, and is also
an ester.
Mechanism of Action
Local anesthetics exert their e/ ect by reversibly inhibiting neural impulse transmission. The local anesthetic
molecules di/ use across neural membranes to block sodium channels and inhibit the in) ux 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 a/ ected to cease neural " ring. 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 di/ use through tissues and then block sodium channels relies on the
ability of these molecules to dissociate at physiologic pH of 7.4. The pK s for local anesthetics are greatera
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 a/ ected by the volume andconcentration of local anesthetic injected, the absence or presence of vasoconstrictor additives, the site of
1injection, the addition of bicarbonate, and temperature of the local anesthetic. 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 e/ ects 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
di/ use 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 (700 mm Hg) to local anesthetics hasten their onset. Bicarbonate raises the pH and the amount of2
uncharged local anesthetic for di/ usion through the nerve membrane. CO will di/ use across the axonal2
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 of the local anesthetica
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
2a common preservative in multidose vials and is also a common allergen.
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 di/ erence between the e/ ective 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
1concentrations are 0.5% to 2%. Final concentration is often diluted by the addition of a corticosteroid.
Concentration percentages are easily converted to milligrams. For example, a 1% solution of lidocaine has
1 g of lidocaine in 100 mL of ) uid. 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).
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
1mg with an extravascular injection.
Action of local anesthetics is a/ ected 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 AnestheticsExcess amounts of local anesthetics may cause CNS e/ ects 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,
3depression or drowsiness. Injections into the head and neck area require the utmost care. Even small doses
of local anesthetic may produce adverse reactions similar to systemic toxicity seen with unintentional
4intravascular injections of larger doses. Deaths have been reported.
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 e/ ect and should be treated with intravenous ) uids 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 are administered in a pain practice for their potent antiin) ammatory properties. These
injections to relieve pain and in) ammation work well temporarily, but questions remain regarding their role
in the management of many chronic musculoskeletal conditions. Corticosteroids may result in signi" cantside e/ ects. The potential for these adverse e/ ects, ranging from a relatively innocuous facial ) ushing e/ ect
to joint destroying avascular necrosis, must be weighed against potential bene" ts. 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).
Comparison of Commonly Used Glucocorticoid SteroidsTable 2-2
Mechanism of Action
All corticosteroids have both glucocorticoid, antiin) ammatory, and mineralocorticoid activity. Agents with
signi" cant 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 antiin) ammatory and immunosuppressive e/ ects in humans. The primary
5mechanism of action may be their ability to inhibit the release of cytokines by immune cells. The e/ ects of
6corticosteroids are species speci" c. Lymphocytes in humans are much less sensitive to the e/ ects of
corticosteroids than lymphocytes in common laboratory animals including the mouse, rat, and rabbit. In
humans, corticosteroids reduce the accumulation of lymphocytes at in) ammatory sites by a migratory
7effect. In contrast to this lymphopenia, is the neutrophilia seen by demargination of neutrocytes from the
8endothelium and an accelerated rate of release from the bone marrow. 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 antiin) ammatory e/ ects of corticosteroid also occur at the microvascular level. They block the
passage of immune complexes across the basement membrane, suppress superoxide radicals, and reduce
9 10capillary permeability and blood ) ow. Corticosteroids inhibit prostaglandin synthesis, decrease
collagenase formation, and inhibit granulation tissue formation.
The immunosuppressant e/ ects of corticosteroids are generally via e/ ects on T cells. These e/ ects are not
the desired e/ ect of corticosteroid used in pain management procedures and are not observed following
11 11-14epidural injections. A review of these immunosuppressant effects can be found in other texts.
Individual Agents
Commonly used corticosteroid preparations include betamethasone, methylprednisolone, triamcinolone,
dexamethasone, prednisolone, and hydrocortisone. Of these, betamethasone and dexamethasone have the
strongest glucocorticoid or antiin) ammatory e/ ects. Corticosteroid e/ ects can be highly variable between
individuals and it is not possible to de" nitively state a safe dosage of corticosteroid. The following shouldserve only as a guide and must be tailored to each individual.
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
15osteoarthritis, tenosynovitis, gouty arthritis, bursitis, epicondylitis, and rheumatoid arthritis. 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 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 bisul" te 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
15tissue in" ltration 2 to 6 mg. Sul" tes are common in the preparations of this salt also. Dexamethasone is
approved for the treatment of osteoarthritis, bursitis, tendonitis, rheumatoid arthritis ) ares, epicondylitis,
15tenosynovitis, and gouty arthritis. Because it is considered to be a nonparticulate steroid it is also used o/ -
label for epidural steroid injections as discussed subsequently.
Methylprednisolone acetate (Depo-Medrol) has 1/5 to 1/6 the glucocorticoid potency of betamethasone but
similar antiin) ammatory e/ ects 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
15osteoarthritis, bursitis, tenosynovitis, gouty arthritis, epicondylitis, and rheumatoid arthritis. 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
16cause arachnoiditis with (inadvertent) intrathecal injections. Animal studies have not demonstrated any
17adverse e/ ects on neural tissues from the application of glucocorticoid. 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
15peritendon 4 to 30 mg.
Triamcinolone is available as three di/ erent 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
15fat atrophy and hypopigmentation.
Spinal Injections
Unique considerations are taken into account when considering corticosteroids for spinal injections. In
particular, cervical transforaminal injections have lead to rare but signi" cant neurologic complications such18-22as spinal cord injury, stroke, and even death.
The postulated cause of the majority of these complications is undetected vascular injections in the
22,23vertebral or spinal radicular arteries with particulate steroids causing embolic infarctions.
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
24injections into radicular arteries or the reinforcing radicular artery known as the artery of Adamkiewicz.
This artery typically arises at thoracic levels but it can occur as low as L2 or L3 in about 1% of patients and
25more rarely at lower levels.
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
26,27arteries. 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
27sodium phosphate, which is a nonparticulate steroid. 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 e/ ects. The
28MRIs and subsequent histologic analysis were also normal in this group of animals.
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
29-31may also lead to embolic events 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 ) uoroscopy 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 e/ ective but studies suggest that particulate
32,33steroids may be slightly more eJ cacious than nonparticulate steroids. 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
15,34history of steroid psychosis, or a history of severe or multiple allergies. Intraarticular injections have
been associated with osteonecrosis, infection, tendon rupture, postinjection ) are, hypersensitivities, and
15systemic reactions. Intraspinal injections have been associated with adhesive arachnoiditis, meningitis,
16and conus medullaris syndrome.
Adverse reactions to injected corticosteroids include a transient ) are 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
insuJ ciency 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
35are used, the allergic response may not occur until a week after the injection. Even with local injections of
corticosteroids, some systemic response may occur.Generally less serious side e/ ects of corticosteroids include facial ) ushing, injection site
hypopigmentation, subcutaneous fat atrophy, increased appetite, peripheral edema or ) uid retention,
15dyspepsia, malaise, and insomnia. 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 e/ ect of the corticosteroid. Macrolide antibiotics (e.g., erythromycin, azithromycin) may
greatly increase the e/ ect of methylprednisolone by decreasing its clearance. In contrast, the hydantoins
(e.g., phenytoin), rifampin, phenobarbital, and carbamazepine may increase corticosteroid clearance and
decrease the antiin) ammatory therapeutic e/ ect. Theophylline and oral anticoagulants can interact
15variably with corticosteroids.
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
36,37radiofrequency lesioning. Neurolytic agents are nonspeci" c in destroying all nerve " ber 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 is the most widely instilled agent to treat severe spasticity. Phenol can be injected around a motor
38,39nerve to selectively reduce hypertonicity. 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
40,41sympathetic fibers.
Mechanism of Action
Phenol (carbolic acid) denatures protein and thereby causes denervation. Histologic sections show
42-44nonselective nerve destruction, muscle atrophy, and necrosis at the site of phenol injections. Higher
concentrations of phenol are associated with greater tissue destruction. Optimal concentration has not been
44determined and long-term di/ erence between injection of 2% and 3% solution have not been noted.
45Denervation potentials are seen as early as 3 weeks following phenol blocks. Clinical response of
43,44decreased pain or spasticity last between 2 months and 2 years irrespective of underlying disorder.
Endoneural " brosis is seen following phenol injections and is believed to impede reinnervation of the muscle
by slow wallerian regeneration.
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 e/ ects 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
42inflammation. This discomfort can be relieved with ice packs and analgesics and typically resolves within
24 hours. If the needle is withdrawn without ) ushing it with saline, phenol may come in contact with theskin 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.
38,46-55Paresthesias/dysesthesias occur in up to 25% of nerve blocks and resolve within 3 months. Repeat
blocks often alleviate these symptoms indicating the dysesthesias may stem more from an incomplete block
than from phenol-induced dysesthesias.
56-59Systemic reactions to phenol are usually the result of inadvertent intravascular or central blockade.
58Adverse systemic reactions most commonly affect the cardiovascular and central nervous systems. Cardiac
dysrhythmias, hypotension, venous thrombosis, spinal cord infarcts, cortical infarcts, meningitis, and
58,60,61arachnoiditis have been reported.
Contrast Agents
Contrast agents are administered to help visualize the location of the needle tip, con" rm the ) ow 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 ) uoroscopic guidance helps minimize these toxicities.
Contrast agents are all iodinated compounds that allow opaci" cation 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
62,63as nausea and urticaria, they have not been shown to decrease the incidence of more severe reactions.
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, signi" cant 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
64,65) uoroscopy and contrast enhancement. 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 " rst 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 suJ cient for the experienced injectionist to con" rm location
and spread of the contrast. These agents are 90% eliminated through the kidneys within 24 hours. Side
66effects are uncommon but include nausea, headaches, and CNS disturbances.
Ionic contrast agents such as diatrizoate (Renogra" n) 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
54,66-68sensitivities. If premedication with diphenhydramine and methylprednisolone is given, the risk of
66anaphylactoid reactions is reduced to approximately 3.1%. The current recommended prophylactic69protocol is methylprednisolone 32 mg by mouth 12 and 2 hours prior to contrast use. Concurrent use of
70,71specific H and H blockers is also recommended.1 2
Viscosupplemenation with hyaluronic acid (HA) injections is FDA approved for knee osteoarthritis although
it is sometimes used o/ -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 ) uid. It is a viscous component of synovial ) uid and acts as a lubricant and
cushion for joints. In osteoarthritis, the synovial ) uid 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
72but the clinical eJ cacy is likely modest. A 2003 meta-analysis in JAMA looking at 22 trials concluded
that HA was superior to placebo injections but had a relatively small e/ ect. The e/ ect was probably similar
to NSAIDs. It also raised concern about a possible publication bias with 17 of 22 trials being industry
73sponsored, which may overestimate effects of viscosupplementation.
Another meta-analysis in 2004 looked at 13 randomized controlled trials and found that it is an e/ ective
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
74longer. A more recent review of viscosupplementation suggested that clinical improvement attributable to
75viscosupplementation is likely small.
Adverse reactions with HA injections are generally mild but reports vary regarding frequency. Mild side
e/ ects include pain at injection site (1% to 33%), local joint pain and swelling (<_125_ to="" _3025_29_=""
and="" local="" skin="" reactions="" _28_325_="" _2125_29_.="" a="" pseudoseptic="" reaction=""
75can="" occur="" but="" is="" uncommon="" _28_125_="">
In summary, viscosupplementation is FDA approved for knee osteoarthritis. Randomized controlled
studies have demonstrated that it is superior to placebo but the clinical e/ ect appears to be small to modest.
Some of these studies suggest that it is as eJ cacious 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 saturation monitoring, intravenous access, and electrocardiogram monitoring. If needed, a2
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 ) uids.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.
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 bene" t and minimize risk. Integration of
injection procedures in appropriately selected patients increases the physician’s effectiveness.
1. Williams M.J. Pharmacology for regional anesthetic techniques. In: Hahn M.B., McQuillan P.M., Sheplock
G.J., editors. Regional anesthesia: An atlas of anatomy and techniques. St. Louis: Mosby-Year Book; 1996:3-17.
2. SchorrParaben Allergy W.F. Jama. 1968;204:107-110.
3. Covino B.G. Clinical pharmacology of local anesthetic agents. In: Cousins M.J., Bridenbaugh P.O., editors.
Neural blockade in clinical anesthesia and pain management. Philadelphia: J.B.Lippincott; 1996:111-144.
4. Olin B.R. Miscellaneous products: Local anesthetics, injectable. B.R. Olin. St. Louis: Wolters Kluwer.
5. Crabtree G.R., Gillis S., Smith K.A., Munck A. Glucocorticoids and immune responses.[Review]. Arthritis
Rheum. 1979;22(11):1246-1256.
6. Claman H.N. Corticosteroids and lymphoid cells. N Engl J Med. 1972;287(8):388-397.
7. Peters W.P., Holland J.F., Senn H., et al. Corticosteroid administration and localized leukocyte mobilization
in man. N Engl J Med. 1972;286(7):342-345.
8. Fauci A.S., Dale D.C., Balow J.E. Glucocorticosteroid Therapy: Mechanism of action and clinical
considerations. Ann Intern Med. 1976;84(3):304-315.
9. Schayer R.S. Synthesis of histamine, microcircularoty regulation and the mechanisms of action of the adrenal
glucocorticoid hormones. Prog Allergy. 1963;7:187.
10. Robinson D.R. Prostaglandins and the mechanism of action of anti-inflammatory drugs.[Review]. Am J Med.
11. Robinson J.P., Brown P.B. Medications in low back pain. Phys Med Rehabil Clin North Am. 1991;2:97-126.
12. Brown P.B. The use of steroidal agents in the oral route. In: Wilkens R.F., Dali S.L., editors. Therapeutic
Controversies in the Rheumatic Diseases. Orlando: Grune and Stratton, 1987. p 71
13. Cupps R.R., Fauci A.S. Corticosteroid-mediated immunoregulation in man.[Review]. Immunol Rev.
14. Fauci A.S., Dale D.C., Balow J.E. Glucocorticosteroid therapy: mechanism of action and clinical
considerations. Ann Intern Med. 1976;84(3):304-315.
15. Olin B.R., editor. Facts and Comparisons. St Louis: Wolters Kluwer. 1993:458-486.
16. Nelson D.A. Intraspinal therapy using methylprednisolone acetate. Spine. 1993;18:278-286.
17. Delaney T., Rowlingson R.C., Carron H. Epidural steroid effects on nerve and meninges. Anesth Analg.
18. McMillan M.R., Crumpton C. Cortical blindness and neurologic injury complicating cervical transforaminal
injection for cervical radiculopathy. Anesthesiology. 2003;99:509-511.19. Rozin L., Rozin R., Koehler S.A., et al. Death during a transforaminal epidural steroid nerve root block(C7)
due to perforation of the left vertebral artery. Am J Forensic Med Path. 2003;24:351-355.
20. Tiso R.L., Cutler T., Catania J.A., Whalen K. Adverse central nervous system sequelae after selective
transforaminal block: The role of corticosteroids. Spine J. 2004;4:468-474.
21. Brouwers P.J.A.M., Kottnik E.J.B.L., Simon M.A.M., Prevo R.L. A cervical anterior spinal artery syndrome
after diagnostic blockade of the right C6-nerve root. Pain. 2001;91:397-399.
22. Baker R., Dreyfuss P., Mercer S., Bogduk N. Cervical transforaminal injection of corticosteroids into a
radicular artery: A possible mechanism for spinal cord injury. Pain. 2003;103:211-215.
23. Rathmell J.R., Aprill C., Bogduk N. Cervical transforaminal injection of steroids. Anesthesiology.
24. Bogduk N., Dreyfuss P., Baker R., et al. Complications of spinal diagnostic and treatment procedures. Pain
Med. 2008;9:S11-S34.
25. Lo D., Vallee J.N., Spell L., et al. Unusual origin of the artery of Adamkiewicz from the fourth lumbar artery.
Neuroradiology. 44, 2002. 153–17
26. Tiso R.L., Cutler T., Catania J.A., Whalen K. Adverse central nervous system sequelae after selective
transforaminal block: The role of corticosteroids. Spine J. 2004;4:468-474.
27. Derby R., Date E., Lee C.H., et al. Size and aggregation of corticosteroids used for epidural injections.
Interventional Spine. ISIS Newsletter. 2005;5(4):30-37.
28. Okubadejo G.O., Talcott M.R., Schmidt R.E., et al. Perils of intravascular methylprednisolone injection into
the vertebral artery. An animal study. J Bone Joint Surg Am. 2008;90:1932-1938.
29. Somyaji H.S., Saifuddin A., Casey A.T.H., Briggs T.W.R. Spinal cord infarction following therapeutic
CTguided left L2 nerve root injection. Spine. 2005;30:E106-E108.
30. Houten J.K., Errico T.J. Paraplegia after lumbosacral nerve root block: Report of three cases. Spine J.
31. Quintero N., Laffont I., Bouhmidi L., et al. Transforaminal epidural steroid injection and paraplegia: Case
report and bibliographic review. Ann Readapt Med Phys. 2006;49:242-247.
32. Dreyfuss P., Baker R., Bogduk N. Comparative effectiveness of cervical transforaminal injections with
particulate and nonparticulate corticosteroid preparations for cervical radicular pain. Pain Med.
33. O’Donnell C., Cano W., Eramo G. Comparison of triamcinolone to dexamethasone in the treatment of low
back pain and leg pain via lumbar transforaminal epidural steroid injection. Spine J. 2008;8:S65.
34. Goebert H.W., Jallo S.J., Gardner W.J., Wasmuth C.E. Painful radiculopathy treated with epidural injections
of procaine and hydrocortisone acetate: Results in 113 patients. Anesth Analg. 1961;140:130-134.
35. Preuss L. Allergic reactions to systemic glucocorticoids: A review. Ann Allergy. 1985;55:772-775.
36. Dreyfuss P., Halbrook B., Pauza K., et al. Lumbar percutaneous RF medial branch neurotomy for chronic
zygapophysial joint pain—a pilot study. Denver: International Spinal Injection Society; 1997.
37. Lord S.M., Barnsley L., Wallis B.J., et al. Percutaneous radio-frequency neurotomy for chronic cervical
zygapophyseal-joint pain. New Engl J Med. 1996;335(23):1721-1726.
38. Khalili A.A., Harmel M.H., Forster S., et al. Management of spasticity by selective peripheral nerve block
with dilute phenol solutions in clinical rehabilitation. Arch Phys Med Rehabil. 1964;45:513-519.
39. Wood K.M. The use of phenol as a neurolytic agent: A review. Pain. 1978;5:205-229.
40. Hughes-Davies D.I., Redman L.R. Chemical lumbar sympathectomy. Anesthesia. 1976;31:1068-1075.
41. Reid W., Watt J.K., Gray T.G. Phenol injections of the sympathetic chain. Br J Surg. 1970;57:45-50.
42. Garland D.E., Lucie R.S., Waters R.I. Current uses of open phenol nerve block for adult acquired spasticity.
Clin Orthop Rel Res. 1982;165:217-222.
43. Halpern D. Histologic studies in animals after intramuscular neurolysis with phenol. Arch Phys Med Rehabil.
44. Mooney V., Frykman G., McLamb J. Current status of intraneural phenol injections. Clin Orthop Relat Res.
1969;63:122-131.45. Brattstrom M., Moritz U., Svantesson G. Electromyographic studies of peripheral nerve block with phenol.
Scand J Rehabil Med. 1970;2:17-22.
46. Copp E.P., Harris R., Keenan J. Peripheral nerve block and motor point block with phenol in the
management of spasticity. Proc R Soc Med. 1970;63:937-938.
47. Copp E.P., Keenan J. Phenol nerve and motor point block in spasticity. Rheum Phys Med. 1972;11:287-292.
48. Katz J.K., Knott L.W., Feldman D.J. Peripheral nerve injections with phenol in the management of spastic
patients. Arch Phys Med Rehabil. 1967;48:97-99.
49. Khalili A.A. Physiatric management of spasticity by phenol nerve and motor point block. In: Ruskin A.P.,
editor. Current Therapy in Physiatry. Philadelphia: Saunders, 1984. 464-474
50. Khalili A.A., Betts H.B. Peripheral nerve block with phenol in the management of spasticity. Indications and
complications. JAMA. 1967;200:1155-1157.
51. Petrillo C., Chu D., Davis S. Phenol block of the tibial nerve in the hemiplegic patient. Orthopedics.
52. Petrillo C., Knoploch S. Phenol block of the tibial nerve for spasticity: A long-term follow-up study. Int
Disabil Stud. 1988;10:97-100.
53. Reeves K.D., Baker A. A mixed somatic peripheral phenol nerve block for painful or intractable spasticity: A
review of 30 years of use. Am J Pain Manage. 1992;2:205-210.
54. Shehadi W.H. Contrast media adverse reactions: Occurrence, recurrence and distribution patterns. Radiology.
55. Spira R. Management of spasticity in cerebral palsied children by peripheral nerve block with phenol. Dev
Med Child Neurol. 1971;13:164-173.
56. Benzon H.T. Convulsions secondary to intravascular pheno: A hazard of celiac plexus block. Anesth Analg.
57. Holland A.J.C., Yousseff M. A complicaton of subarachnoid phenol blockade. Anesthesia. 1979;34:260-262.
58. Swerdlow M. Complications of neurolytic neural blockade. In: Cousins M.J., Bridenbaugh P.O., editors.
Neural blockade in clinical anesthesia and management of pain. New York: J.B. Lippincott; 1988:719-735.
59. Totoki T., Kato T., Nomoto Y., et al. Anterior spinal artery syndrome: A complication of cervical intrathecal
phenol injections. Pain. 1979;6:99-104.
60. Macek C. Venous thrombosis results from some phenol injections. JAMA. 1983;249:1807.
61. Morrison J.E.Jr., Matthews D., Washington R., et al. Phenol motor point blocks in children: Plasma
concentrations and cardiac dysrhythmias. Anesthesiology. 1991;75:359-362.
62. Lawrence V., Matthai W., Hartmaier S. Comparative safety of high-osmolality and low-osmolality
radiographic contrast agents. Report of a multidisciplinary working group. Invest Radiol. 1992;27:2-28.
63. Steinberg E.P., Moore R.D., Powe N.R., et al. Safety and cost effectiveness of high-osmolality as compared
with low-osmolality contrast material in patients undergoing cardiac angiography. N Engl J Med.
64. Renfrew D.L. Correct placement of epidural steroid injections: Fluoroscopic guidance and contrast
administration. Am J Neuroradiol. 1991;12:1003-1007.
65. White A.H., Derby R., Wynne G. Epidural injections for diagnosis and treatment of low-back pain. Spine.
66. Olin B.R. Miscellaneous products: Radiopaque agents. In: Olin B.R., editor. Facts and Comparisions. St. Louis:
Wolters Kluwer.; 1993:2824-2831.
67. Caro J.J., Trindade E., McGregor M. The risks of death and of severe nonfatal reactions with high- vs.
lowosmolality contrast media: A meta-analysis. Am J Roentgenol. 1991;156:825-832.
68. Katayama H., Yamaguchi K., Kozuka T., et al. Adverse reactions to ionic and nonionic contrast media: A
report from the Japanese Committee on the Safety of Contrast Media. Radiology. 1990;175:621-628.
69. Lasser E.C., Berry C.C., Talner L.B., et al. Pretreatment with corticosteroids to alleviate reactions to
intravenous contrast material. N Engl J Med. 1987;317(14):845-849.
70. Cusmano J. Premedication regimen eases contrast reaction. Diagn Imaging. 1992. 181-182, 185-18671. Greenberger P.A., Patterson R. The prevention of immediate generalized reactions to radiocontrast media in
high-risk patients. J Allergy Clin Immunol. 1991;87:867-872.
72. Roberts W.N., Furst D.E., Romain P.L. Intraarticular and soft tissue injections: What agent(s) to inject and
how frequently? 2009;17:1.
73. Lo G.H., LaValley M., McAlindon T., Felson D.T. Intra-articular hyaluronic acid in treatment of knee
osteoarthritis: A meta-analysis. JAMA. 2003;290:3115.
74. Aggarwal A., Sempowski I.P. Hyaluronic acid injections for knee osteoarthritis. Systematic review of the
literature. Can Fam Physician. 2004;50:249-256.
75. Woods S., Davis E., Schechtel M., et al. Three treatments for osteoarthritis of the knee: Evidence shows lack
of benefit. Agency for Healthcare Research and Quality. U.S. Department of Health and Human Services.

Psychological Aspects of Pain
Dale A. Halfaker, PhD, Steven T. Akeson, PsyD, Danielle
R. Hathcock, MS, Curtis Mattson, MS, Ted L. Wunderlich,
The evolution of the de nition of pain and the in uence 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 rst 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
1,5a" ect pain. 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
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
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 scienti c community has demanded a more comprehensive theory

that accounts for the neurophysiology, neurotransmission, and opioid receptors that
may all be involved in understanding and de ning 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 speci c patterns of nerve impulses generated by a widely distributed neural
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 e" ects, 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 de ne a great deal of psychological and physiologic scienti c data,
although it is thought neither of them provides a fully adequate theory to de ne
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 e" ort 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 fth vital sign.
The Pain Care Bill of Rights of the nonpro t 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 de ne “an objective biological event” that involves the disruption
of speci c body structures or organ systems, caused by anatomic, pathologic, or
physiologic changes. Illness, in contrast, is generally de ned 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 ltered through an
individual’s genetic composition, prior learning history, current physiologic status,
and sociocultural in uences. 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 insu: cient to e" ectively
assess and treat the patient. The biopsychosocial model has consistently
2demonstrated the heuristic technique in treatment.
When interpreting pain using the biopsychosocial model, clinicians should be
aware that each of the three constructs in the model are di" erent in their
composition. Therefore, their assessment will be accomplished through di" erent
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
2,5of patients.
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
Another model outlined four dimensions associated with the concept of pain: (1)
3,5nociception (2) pain (3) su" ering and (4) pain behavior. Nociception refers to
the actual physical units that might a" ect specialized nerve bers 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 de nition 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. Su" ering is a reaction to these signals that can be
a" ected by past experiences as well as anticipation of future events, and refers to
3the emotional association with it, such as fear, threat, or loss. Because of a speci c

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 su" ering
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 bene ting from appropriate medical treatment which, if identi ed,
can improve the treatment process and the ultimate outcome of the case.
If psychological factors are identi ed 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 o" ended, 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 t as they can be while they are in the process of
physically rehabilitating and becoming more physically t 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 speci c 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 e: cient and e" ective 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 speci c, practical, and functional recommendations that
advance the patient’s care in a meaningful way become the goal for appropriate
To achieve the purposes of the evaluation, su: cient 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
quanti able 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 di" erently. 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, nances, and availability of disability
compensation can be important to understanding prolonged disability. Other
signi cant 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 a" ective disturbances, anxiety disorders, psychotic features,
characterologic pathology, somatoform presentations, substance use factors, and
magni ed 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
5may include Axis I clinical disorders and Axis II personality disorders. 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 di" erent pain rating scales in use, many of which have been
modi ed for a speci c type of clinical setting (orthopedic, rheumatology, oncology,
etc.) or speci c 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
6pain and 10 indicating maximum pain. 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
7Pain Rating scale. 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 di" erence in the example
between a 47 and 53 is probably not signi cant 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
di" erent 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, A" ective, 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 identi ed 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 rst domain (sensory) containing
subcategories 1 to 10 includes 42 descriptors; the second domain (a" ective)
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), ashing (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 a" ective 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
8measures should be used in cases of below average IQ.
The MPQ short-form is a modi ed version that provides a brief (2 to 5 minutes)
9alternative to the MPQ (10 to 15 minutes). 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
(HotBurning) from the Sensory Domain and 2 words and 2 sets of combined descriptors
(Tiring-Exhausting and Punishing-Cruel) from the A" ective 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
10The Oswestry Low Back Pain Disability Questionnaire (ODQ) 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
11Life, Social Life, and Traveling). 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
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 rst 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 classi ed as minimal (0-13), mild (14-19),
11,12moderate (20-28), and severe (29-63). 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 classi ed as normal
(<_5029_2c_ mild="" depression="" _28_50="" to="" _5929_2c_="" moderate=""
marked="" major="" _28_60="" _6929_2c_="" and="" severe="" extreme=""
_28_="">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
classi ed as normal (<_929_2c_ mild="" depression="" _28_10="" to=""
_1329_2c_="" moderate="" _28_14="" _1729_2c_="" and="" severe=""
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 classi ed 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 speci c 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 signi cant 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
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 rst 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 pro le. 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 con dent/competent self-presentation (S). When these underreporting
scales are elevated, it typically re ects 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 nonspeci c 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 rst
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 xed 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 xed patterns of
responding, it is more di: cult to di" erentiate 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
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 in uence 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 cuto" s 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
13raw scores above 28 on the FBS are associated with a very low false-positive rate.
Additionally, the literature suggests that increasing confidence is placed in scores as
they rise above a cuto" of 30, with a number of studies noting that no nonlitigant,
14nonmalingering subjects had raw scores of 30 or above.
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
15population. The developers combined seven di" erent 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 cuto" score of equal to or greater than 5. That study suggested chronic
pain patients in litigation produce a di" erent pro le 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 classi ed 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 pro le 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 speci c theory or
diagnostic criteria. Each clinical scale is a combination of items that a speci c
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 pro les 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 e" ectively 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 pro les 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
16population using 209 chronic pain inpatients. The chronic pain patients scored
signi cantly 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 pro le will present a “conversion V” or
somatic pro le. 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
MMPI2. 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
17pain settings that should increase the utility of the test. 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
FleschKincaid 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 speci c 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,
18Kentucky. 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
MCMIIII showed 100% speci city 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 ve 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, Con dent,
NonConforming, Forceful, Respectful, Oppositional, and Denigrated); 6 Stress
Moderators (Illness Apprehension, Functional De cits, 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
Di: culties, and Psych Referral). There are 6 Negative Health Habits (Alcohol,
Drugs, Eating, Ca" eine, 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
19specific populations.
In recent decades, studies evaluating the use of psychotherapy as a treatment
option in patients with pain have signi cantly 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 o" er 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
20experiencing feelings of embarrassment, frustration, and lack of self-control. The
patients also reported they often felt others did not believe their pain and viewed
physicians as attempting to “fob them o" ” by prescribing pain medication. A
primary goal during the initial intake process and rst 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
painfree can be guaranteed, but a treatment plan can be developed in collaboration
with the patient that will address the patient’s speci c 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
a" ected 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
in uence or mediate the patient’s experience of pain, personality characteristics, or
preexisting psychological pathology or conditions may have a signi cant bearing
21-23on the nature and direction of the therapeutic process. 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
24interventions to treat chronic pain have considerable empirical support. A
metaanalysis of 25 randomized controlled trials of CBT for pain management
revealed CBT to produce “signi cantly 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
24treatments.” 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 su" erer that his or her experience of pain can
25be mediated by changing his or her maladaptive beliefs. 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
26regularity among patients with chronic pain. Restructuring the patients’ thoughts
via cognitive-type therapy helped the patients to accept their pain and mediated
the catastrophizing e" ects 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
26patients improve overall functioning and emotional well-being.
Although CBT may be considered the ‘gold standard’ for psychotherapy, research
ndings have substantial variability among outcome measures and invite
23speculation regarding the overall efficacy of CBT. 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
24coping skills primarily and pain coping skills secondarily.” 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 di" ers from CBT in that it has a
broader focus (for example, CSD examines the roles of self-esteem and emotions),
there is a de nitive 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
24circumstances including chronic pain” 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
1year 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
27e" ectively treat a complex, multidimensional problem such as cancer pain. 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 in uenced 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 speci cally targets the patient’s
ability to relate di" erently to the thoughts and feelings associated with periods of
negative a" ect, 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 in uence therapy outcomes. For example, one study compared the e: cacy of
CBT and mindfulness meditation in treating patients with rheumatoid arthritis
21(RA). 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 a" ect, depressive
symptoms, coping e: cacy 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 proin ammatory 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 di" erent 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 di" erence
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
25pain. In using the NEO Five Factor Inventory and brief CBT, researchers found
that “the core personality dimensions of neuroticism, openness, and agreeableness
23were predictive of aspects of satisfaction with therapy.” Speci cally, neuroticism
negatively a" ected treatment satisfaction; whereas agreeableness had a statistically

signi cant correlation with the individual viewing the therapy sessions as running
smoothly (agreeable individuals are also more likely to participate in speci c
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 e" ect of variables outside of the chronic pain itself that may
in uence 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 speci c characteristics, including preexisting pathology and
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 o" ers many advantages that may not be available
28-30in individual therapy. These include helping to discon rm 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 o" er personal skills and pain management
31techniques. Not all patients will be suitable for group therapy, either due to
30personality or if the patient issues are beyond the goals of the group. 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
32system. Families, spouses, and friends are potentially a" ected 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 nancial,
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. Insuch cases, if appropriate family members are not part of the treatment they may
31maintain or perpetuate the problems of the chronic pain sufferer.
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 e" ective 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-e: cacy 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.
1. Melzack R., Wall P.D. Pain mechanisms: A new theory. Science. 1965;50:971-979.
2. Turk D.C., Monarch E.S. Biopsychosocial Perspective on Chronic Pain. In: Turk D.C.,
Gatchel R.J., editors. Psychological Approaches to Pain Management: A Practitioner’s
Handbook. 2nd ed. New York: Guilford Press; 2002:1-29.
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.
4. Ownby R.L. Psychological Reports: A Guide to Report Writing in Professional Psychology,
3rd ed. New York: John Wiley and Sons; 1997.
5. Gatchel R.J. Clinical Essentials of Pain Management. Washington, DC: American
Psychological Association; 2005.
6. King S. The classification and assessment of pain. International Review of Psychiatry.
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.
8. Melzack R. The McGill Pain Questionnaire. In: Plake B.S., Impara J.C., editors. The
Fourteenth Mental Measurements Yearbook. Lincoln University, University of
Nebraska Press, 2001.
9. Melzack R. The short-form McGill Pain Questionnaire. Pain. 1987;30:191-197.
10. Fairbank J.C., Couper J., Davies J.B., O’Brien J.P. The Oswestry low back pain
disability questionnaire. Physiotherapy. 1980;66:271-273.
11. Gonzales V.A., Martelli M.F., Baker J.M. Psychological assessment of persons withchronic pain. NeuroRehabilitation. 2000;14:69-83.
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.
17. Karlin B.E., Creech S.K., Grimes J.S., et al. The Personality Assessment Inventory
with chronic pain patients: Psychometric properties and clinical utility. J Clin
Psychol. 2005;61:1571-1585.
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.
19. Walfish S., Wise E.A., Streiner D.L. Limitations of the Millon Behavioral Medicine
Diagnostic (MBMD) with bariatric surgical candidates. Obes Surg.
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.
21. Zautra A.J., Davis M.C., Reich J.W., et al. Comparison of cognitive behavioral and
mindfulness meditation interventions on adaptation to rheumatoid arthritis for
patients with and without history of recurrent depression. J Consult Clin Psychol.
22. Cole J.D. Psychotherapy with the chronic pain client using coping skills
development: Outcome study. J Occup Health Psychol. 1998;3:217-226.
23. Green S.M., Hadjistavropoulos T., Sharpe D. Client personality characteristics
predict satisfaction with cognitive behavior therapy. J Clin Psychol. 2008;64:40-51.
24. Otis J.D. Managing chronic pain: A cognitive-behavioral therapy approach. New York:
Oxford University Press; 2007.
25. Holzman A.D., Turk D.C., Kerns R.D. The cognitive-behavioral approach to the
management of chronic pain. In: Holzman A.D., Turk D.C., editors. Pain
management. Elmsford, New York: Pergamon Press; 1986:31-50.
26. Vowles K.E., McCracken L.M., Eccleston C. Patient functioning and
catastrophizing in chronic pain: The mediating effects of acceptance. Health
Psychol. 2008;27(suppl 2):S136-S143.
27. Otis-Green S., Sherman R., Perez M., Baird R.P. An integrated psychosocial-spiritual model for cancer pain management. Cancer Pract. 2002;10(suppl
28. Mannerkorpi K., Gard G. Physiotherapy group treatment for patients with
fibromyalgia—an embodied learning process. Disabil Rehabil. 2003;25:1372-1380.
29. Bogart R.K., McDaniel R.J., Dunn W.J., et al. Efficacy of group cognitive behavior
therapy for the treatment of masticatory myosascial pain. Military Medicine.
30. Yalom I. The theory and practice of group psychotherapy, 3rd ed. New York: Basic
Books; 1985. 1-16
31. Gentry W.D., Owens D. Pain groups. In: Holzman A.D., Turk D.C., editors. Pain
management. Elmsford, New York: Pergamon Press, 1986.
32. Roy R. A problem-centered family systems approach in treating chronic pain. In:
Holzman A.D., Turck D.C., editors. Pain management. Elmsford, New York:
Pergamon Press; 1986:113-130.
33. Lewandowski W., Morris R., Draucker C.B., Risko J. Chronic pain and the family:
Theory-driven treatment approaches. Issues Ment Health Nurs. 2007;28:1019-1044.4
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-certi" ed 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 e&ect 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
1Conscious sedation is an older term from 1985 to describe lightly sedated dental patients. It is de" ned 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
2 1 3propose terms such as sedation/analgesia or procedural sedation and analgesia (PSAA), or monitored anesthesia care (MAC). Indeed, in
the " rst ASA guidelines from February 1996, a notable comment is that patients whose only response is re8ex withdrawal from a painful
stimulus are sedated to a greater degree than encompassed by sedation/analgesia.
4A continuum of depth of sedation was described in the second ASA guidelines for sedation/analgesia. 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
5Emergency Department consensus guideline. 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
6The best approach is to establish a sedation/analgesia plan prior to starting the procedure. Optimal goals include the following :
1. To provide adequate analgesia, sedation, anxiolysis, and amnesia during the performance of painful diagnostic or therapeutic
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 8uoroscopic 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 o ce or preoperative area. Although the
literature is insu cient in supporting preprocedural preparation, the ASA consultants agree that “appropriate preprocedure counseling of
4patients regarding risks, benefits, and alternatives to sedation and analgesia increases patient satisfaction.”
Table 4-2 ASA Classification
Class Systemic Disturbance Mortality
1 Healthy patient with no disease outside of the surgical process
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 classi" cation 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 o&ered 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
4surgery centers will allow the procedure to be performed only under local or topical analgesia.
Summary of ASA Preprocedure Fasting GuidelinesTable 4-3
†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 di cult airway physical habitus as speci" ed 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
sedationanalgesia. 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:
Previous problems with anesthesia or sedation
Stridor, snoring, or sleep apnea
Advanced rheumatoid arthritis
Chromosomal abnormality (e.g., trisomy 21)
Physical Examination
Significant obesity (especially involving the neck and facial structures)
Head and Neck
Short neck, limited neck extension, decreased hyoid-mental distance (
Small opening (
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.
The main allergies that most interventional pain management specialists encounter are allergies to latex, iodine/contrast, or to local
Latex and iodine allergies can be easily prevented with advanced notice. Most interventional pain procedures can document correct
placement 8uoroscopically 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
8regional and interventional pain procedures.
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, di culty 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
4readily available. Emergency equipment should be available as listed on example III from ASA guidelines. Most outpatient surgery centers
require on-site sta& with ACLS certi" cation 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
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]
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]
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
Emergency medications
Nitroglycerin (tablets or spray)
Glucose, 50% [10 or 25%]
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 sta&. 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 e&ect across multiple pain studies, including headache,
low back pain, and postoperative pain, and it is di cult to separate whether the pain relief is independent of the psychological impact of
9the ritual treatment. The cognitive strategies of distraction and hypnosis in the treatment of procedural pain in children are clearly
10effective. 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
11clinical anesthesia outcomes are important to avoid from a patient’s perspective. 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.
12An expert consensus was published by Dr. Gan and colleagues in 2003 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 di&erence in the e cacy and safety pro" les
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 Administer small-dose 5-HT antagonist (IIA)3
5-HT antagonist plus second agent†3 Use drug from different class (V)
Triple therapy with 5-HT antagonist plus two other agents† when Do not repeat initial therapy (IIIA)3
Use drug from different class (V) or propofol, 20 mg as neededPONV occurs <6 hr="" after="" surgery="">
in postanesthesia care unit (adults) (IIIB)Triple therapy with 5-HT antagonist plus two other agents† when3
Repeat 5-HT antagonist and droperidol (not dexamethasone3PONV occurs >6 hr after surgery (V)
or transdermal scopolamine)
Use drug from different class (V)
5-HT = serotonin.3
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
13e&ective both from an e cacy and cost perspective. One question is whether a single dose of dexamethasone IV can a&ect the
interpretation of whether the interventional procedure has changed the patient’s pain scores. Even doses of up to 8 mg of dexamethasone
14preoperatively has no e&ect on pain and mobilization scores after colorectal surgery. Dexamethasone 8 mg can elevate postprocedural
glucose concentrations in patients with impaired glucose tolerance and may not be the best " rst-line choice for nausea prophylaxis,
especially if the patient is receiving steroids for the interventional block as well.
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 " rst 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 GABAA
15receptors, increase chloride ion channel in8ux, and subsequently decrease neuronal excitation. Midazolam (Versed) is usually the most
preferred benzodiazepine administered compared to lorazepam (Ativan) or diazepam (Valium) because of the shorter elimination half-life
16(approximately 2 hours for midazolam compared to 12 hours for lorazepam, and 20 to 50 hours for diazepam). 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 a&ected by enzyme
induction and other factors that alter cytochrome P450 metabolism. Age and smoking decrease the metabolism of diazepam and can
prolong sedative e&ects. 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—
16approximately 1 hour. Hence, 8umazenil 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 8umazenil 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 a&ect to benzodiazepines by increasing the number of GABA receptors and,
15thereby increasing GABA inhibition. 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 suppression18 as well as myoclonic activity. A single dosage of etomidate at 10 mg is used for cardioversion procedures in
Propofol has revolutionalized outpatient surgical procedures with its rapid onset, short duration of action, and quick recovery for
19 18patients. It has a chemical structure that is unrelated to other sedative hypnotic compounds but does a&ect 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 e&ect 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,
20cognitive impairment can occur even after short procedures such as outpatient colonoscopy. 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
21suppress pharyngeal and laryngeal re8exes and can be administered in nonoperating room conditions by nonanesthesiologists. Ketamine
produces a “dissociative” anesthetic state, which is characterized as a state of catalepsy in which the eyes remain open with a slow
22nystagmic gaze while corneal and light re8exes remain intact. The chemical structure is similar to phencyclidine (PCP) so one of the
23main side-effects is psychotomimetic experiences or “weird trips.”
Ketamine’s mechanism of action is at NMDA receptors as well as cholinergic receptors of the muscarinic type and brain
24acetylcholinesterase. Potentiation of GABA inhibition has also been reported with high doses. Because of activity at NMDA receptors,
25ketamine could theoretically be more e&ective in treating neuropathic pain states or patients who are opioid tolerant. Current evidence
23does not support routine use of ketamine for treatment of chronic pain.
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 e&ect, 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 re8exes, especially in the presence of in8ammation of
22 26the upper respiratory tract and can give rise to myoclonic jerks or involuntary movements.
Opioid Analgesics
27Opioid analgesic agents are the " rst-line medications for the relief of acute pain. 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 e&ect 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 signi" cant 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 e&ect 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
28procedures particularly because of the possibility of increasing postoperative pain.
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 di cult, the authors recommend not using more than 25 to 50 mg IV forperioperative 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 e&ect 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
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
27spasms in the past. 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 sta& 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
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 sta& 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.
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. 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.
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.
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.
Radiation Safety for the Physician
Kenneth P. Botwin, MD, Philip Ceraulo, DO, Chunilal P. Shah,
Currently, uoroscopic 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 de%ned in 1960 by the General Conference of Weights and
Measurements is primarily used in Europe. Each system has its unique terms (Table
Table 5-1 Radiation Quantities and Units
TerminologyLike matter, energy can be transformed from one form to another. When ice (solid) melts
and turns to H O (liquid) and then evaporates (gas), a transformation of matter has2
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 e9ects; the only di9erence 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 su cient dose of electrical current, measured in milliamperes (mA), are
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 de%nition describes the electrical charge per unit mass of air
-4(1 R = 2.58 × 10 coulombs/kg of air). The output of x-ray machines usually is
speci%ed 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 de%nition, 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 e9ects 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 %lm
Radiologic Procedures
In general, there are two types of x-ray procedures: radiography and uoroscopy.
Conventional uoroscopic procedures, such as myelography, barium enemas, upper
gastrointestinal series, and swallowing studies, usually are conducted on a uoroscopic
table. The conventional uoroscope consists of an x-ray tube located above a %xed
examining table. The physician is provided with dynamic images that are portrayed on a
uoroscopic 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 uoroscopy 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 uoroscopes with image intensi%cation 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
intensi%cation is achieved through the addition of an image-intensi%er tube located
opposite the x-ray tube. The intensi%er 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
imageintensi%ed uoroscopy, the x-ray tube delivers currents between 1 and 8 mA. Federal
regulations limit the maximum output for C-arm uoroscopes 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 uoroscopic
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 re ected 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 uoroscopic suite. In addition, the concept of ALARA (as lo w as
reasonably achievable) should be applied in all situations of radiation exposure.
Distance is the most e9ective 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 uoroscopic 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
2distance from the fluoroscope at all times. 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
Shielding factors include %ltration, 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
3uoroscopic equipment. In %ltration, metal %lters (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 sta9. 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
3to reduce exposure to the physician and technologist. Such shielding decreases radiation
4exposure by 90% to critical body areas. Lead-impregnated leather or vinyl aprons and
gloves may be ordered in di9erent thicknesses ranging from 0.55 mm Pb protection,
5which protects at 80 kVp, to 0.58 mm Pb, which protects at 120 kVp. The use of a
leaded thyroid shield also is recommended because of the super%cial location and
sensitivity of the thyroid gland and to protect a limited amount of cervical bone marrow.

Protective, exible lead-lined gloves also may reduce exposure without sacri%cing
dexterity; however, their use is no substitute for vigilant avoidance of direct x-ray beam
6exposure. Leaded glasses or goggles will e9ectively 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%
7attenuation up to 120 kVp. Clear, leaded glass x-ray protective barriers are available in
several styles and shapes. They may be height-adjustable or full-height, oor-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
xray 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
highand low-dose modes, pulsed uoroscopy, 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
xray 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 e9ective dose equivalent of 360 millirem (mrem) of
radioactivity per year. This exposure comes from numerous sources, the most signi%cant
4,8of which is naturally occurring radon (Table 5-2).
Table 5-2 Average Annual E9ective Dose Equivalent of Ionizing Radiations to a Member
of the United States Population0

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 speci%c body part is based on the biologic e9ects of
whole-body exposure (e.g., a survivor of an atomic bomb attack) converted by weight
factors speci%c for individual organs and tissues. This concept was adopted by the
9International Commission on Radiological Protection in 1977 and was modified in 1991.
Termed the e ective 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 uoroscopic 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. Di9erent tissues have varying degrees of
sensitivity to ionizing radiation (Table 5-3).4,6,9

Table 5-3 Speci%c 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
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 uoroscopy, the
patient’s exposure is more di cult to estimate because of the movement and variation in
size of the radiation %eld. In the absence of absolute measurements, it usually is su cient
to estimate the uoroscopic skin dose at 2 rad/mA/min. In order to determine the
approximate exposure, %rst it is necessary to know the exposure time and milliamperage.
For example, if a uoroscopically 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
† Data collected by Charles Beasley, Radiation Safety O cer, 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 signi%cant
10effect on the developing fetus.
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
11(MPD). 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 uoroscopically
assisted orthopedic procedures. One study demonstrated that unprotected individuals
working ≤24 inches from a uoroscopic beam received signi%cant amounts of radiation,
whereas those working ≥36 inches from the beam received an extremely low amount of
12radiation. 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
13Communities (EURATOM) directives. Using a phantom patient, this experiment
revealed that exposure to ionizing radiation during the insertion of a dynamic hip screw
was minimal. Caution during uoroscopy 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
uoroscopy 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 %lm dosimetry system should be used to provide accurate personal dosimetry and
comprehensive diagnostic evaluation. The Gardray %lm consists of a slim, light, clip-on
badge that can easily be worn on either the torso (body badge) or extremities (%nger/ring
badge). The %lm 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 %lm to be %ltered for radiation exposure not only from the front but also from the
bottom and behind. The %nger/ring badge should be worn with the %lm 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
14depth of 0.007 cm averaged over an area of 1 cm squared ; 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
15may occur with cumulative eye lens exposure of ≥400 rad.
Clinical Application of Radiation Safety
There have been several published studies that help the interventionalist to approximate
16-21their potential radiation exposure. These studies were able to predict the exact
exposure based on a speci%c procedure. The interventionalist can therefore, based on the
type of procedure, at least approximate their amount of radiation exposure.
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 uoroscopy suite. By using the proper safety standards, the interventionalist
can thereby reduce exposure times.
The authors would like to acknowledge Carol Barragen for secretarial assistance.
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 fluoroscopicimaging 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;
9. International Commission on Radiological Protection. Recommendation of the
International Commission on Radiation Protection 26. Ann Int Commission Radiat Prot.
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.
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.
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.
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
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
1-3management of acute and chronic pain syndromes. 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 speci" c 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 di( ering 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
Although it is true that uncomplicated lumbar procedures (in an otherwise
healthy population) do not require the degree of training and expertise that
highrisk 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,
4such as that provided in an appropriate fellowship or residency program. This
program must provide speci" c 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 con" dent in
the abilities of the physician in question, prior to recommending his or her
approval for spinal interventions. Speci" cally, 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
5,6Patient preparation issues include patient education, 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) 8uids 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,
6including potential risks, bene" ts, alternatives, and likely outcomes. An informed
consent statement, con" rming 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 8uids, preoperatively, to ensure that all gastric contents are
7distal to the ligament of Treitz.
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 o? ce 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
di( erential diagnosis, liver function tests, urinalysis, chest radiograph, ECG, bloodculture and sensitivity, urine culture and sensitivity, and erythrocyte sedimentation
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
8and the brachial plexus. 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
povidoneiodine, 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
halfsheets should be used as needed to ensure a sterile field.
Supplemental 8uids 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 8uids already 8owing, in the event the patient becomes
hypotensive, is advantageous; this can also help 8ush medication(s) through the
line. Supplemental 8uids should be used cautiously if the patient is
volumesensitive, 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 toomuch oxygen may further suppress respiratory drive.
In addition, if the patient has chronic pulmonary disease, the treating physician
must con" rm 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 in" rm, 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
Cardiac monitoring should be employed for any patient with a signi" cant
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 signi" cantly invasive procedure (e.g., spinal implant); for any
intraspinal cervical or thoracic procedure; for any procedure that may place a
signi" cant volume of local anesthetic or narcotic in the spinal canal or systemic
circulation; or for anyprocedure that will require a signi" cant 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 allowingthe patient to recover in a monitored situation until he or she is alert, oriented, and
able to tolerate 8uids 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 speci" c intervention was more signi" cant 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
9,10Infections, ranging from minor to severe conditions such as meningitis,
11-13 14,15epidural abscess, and osteomyelitis (Figs. 6-1 and 6-2), 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 o( ending 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
gramnegative aerobe, is self-limited, and resolves with early recognition andadministration of appropriate antibiotics. Cervical discitis, however, is often life
threatening, due to the aggressive gram-negative anaerobes that colonize the
If the infection is a mild cutaneous infection and the patient is
immunocompetent, it will probably resolve with local disinfection. The physician
should make speci" c 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 in" rm 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
16complications. 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
13following the injection.
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 con" rmed, 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 bene" ts 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
5,17,18warfarin or other anticoagulants, certain inherited anemias (such as G6PD
de" ciency or sickle-cell anemia), coagulopathy from any cause, and venous
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
19the spinal canal than the midline. Signi" cant epidural bleeding may cause the
development of an epidural hematoma. Clinically-signi" cant epidural hematomasare 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
19-25not surgically decompressed within 24 hours. 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 sta( and extended PCPs
immediately; and everyone should know their speci" c 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
26,27more detailed information.
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 speci" c 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 8uoroscopically-guided spinal injections are less apt to
28cause inadvertent neural injury or injection into a vascular structure. 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,
29due to lack of central respiratory drive or paralysis of the muscles of respiration.Respiratory arrest may occur from a variety of causes, including oversedation,
central nervous system trauma, and intrathecal or epidural injection of a su? cient
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
halflife 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
30respiratory depression with the former. It should be emphasized that respiratory
rate alone is inadequate to establish the presence or lack of respiratory depression.
29The measurement of blood gases remains the preferred option.
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
31minor collapse(s) of the lung (10%). 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 signi" cantly 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
selflimited and resolves on its own; but it may be clinically signi" cant 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 nerve32roots results in higher incidence of urinary retention. This side-e( ect of lumbar
epidural nerve block is seen more commonly in elderly males, multiparous females,
and patients who have undergone inguinal and perineal surgery. Over8ow
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
Dural Puncture
In the hands of the experienced interventional spine specialist, inadvertent dural
puncture during lumbar epidural injections should occur in <_0.525_ of=""
33cases="" _28_or="" 1="" in="" 200="" epidural=""> This occurs when the
dura mater is violated by the epidural needle, and a su? cient amount of
cerebrospinal 8uid leaks out from the thecal sac, causing a positional
34-37headache. The rare occurrence of postdural puncture (spinal-tap) headache is
an annoying side e( ect, 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
38occur, with associated brainstem involvement and potentially death. If a needle
is placed subdurally and epidural doses of local anesthetics are administered, the
39signs and symptoms are similar to subarachnoid injection. 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 8uoroscopy 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
40-48sources. For this reason, most spine-management specialists recommend
8uoroscopic direction and the use of nonionic or low ionic contrast agents for
epidural injections. This helps con" rm accurate needle placement and the delivery
48of the injected solution to the appropriate target organ.
The risk of 8uoroscopic exposure to the patient is minimal, for one procedure or
several isolated ones because each procedure should require minimal (<20
_seconds29_="" 8uoroscopic="" exposure="" time.="" related="" to="" the=""
_physician2c_="" attending="" _nurse2c_="" x-ray="" _technician2c_="" and=""anyone="" else="" consistently="" in="" procedure="" room="" should="" be=""
viewed="" as="">
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 8uoroscopic
tube, their risk of excessive exposure is minimal. The 8uoroscopy 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
wraparound 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 8uoroscopy unit must be routinely maintained and inspected to
con" rm its proper function and safety. Proper 8uoroscopy use (including safe
radiation practices) can direct and con" rm 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 e( ects,
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) e( ects,
cardiovascular toxicity, and side e( ects 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
49injection, they have been known to occur up to 6 hours later.
Local anesthetics primarily function by reversibly blocking sodium channels in
nerve and muscle membranes, having a direct e( ect on sympathetic nerves when
injected into the subarachnoid space and the cardiac tissue (when injected
intravascularly). If the sympathetic system is su? ciently blocked, hypotension may
result; and if cardiac muscle is su? ciently 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
e( ects 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,
50with a toxic bolus of 100 mg (or 10 mL).
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 signi" cant bolus of lidocaine or
bupivacaine is mandatory.
Methylprednisolone, triamcinolone, and betamethasone are the most commonly
used corticosteroid preparations. Side e( ects are uncommon but could include
headache, dizziness, insomnia, facial erythema, rash and pruritus, low-grade
“fever” (<_100c2b0_ _f29_2c_="" _hyperglycemia2c_="" transient=""
hypotension="" and="" _hypertension2c_="" increased="" back="" or=""
limb="" _pain2c_="" 8uid="" _retention2c_="" mood="" _swing2c_=""
17_euphoria2c_="" menstrual="" _irregularity2c_=""> Other rare side e( ects
include elevation of cerebrospinal-8uid 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
49injection, and have been known to develop up to 6 hours later. 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 epiduralspace. Medications that interfere with the clotting mechanism include heparin,
5,17,18warfarin, aspirin, and most nonsteroidal anti-inflammatory drugs (NSAIDs).
Patients usually present with severe neck or back pain, associated with any
17signi" cant neurologic complaint, right after the procedure. 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
33lumbar epidural anesthesia. 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 signi" cant local anesthetic
51toxicity. 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
32block itself.
Direct trauma to the spinal cord or nerve roots is usually accompanied by pain.
Any signi" cant pain that occurs during placement of the epidural needle or
catheter, or during injection, should warn the injectionist to pause and con" rm
33needle placement before proceeding. 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
52should be employed with caution.
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
53epidural procedure, an expanding epidural hematoma should be considered. 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
66). If the diagnosis is con" rmed, 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 theleft (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 e( acement 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
54,55the time. The needle may be placed outside the sacral canal, resulting in
injection of air or 8uid 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 a( ecting the e? cacy of caudal epidural steroid injections when treating
56painful conditions.
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
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
57,58(Figs. 6-7 and 6-8).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 8avum (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
59spine when compared to the lumbar spine.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
48block, selective epidural, or an anterior ramus block. 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 a( ects 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 8uid 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
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.
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
60,61500 to 1 in 750 discs injected. The most common organisms infecting the
60,62lumbar disc are S. aureus and Staphylococcus epidermidis.
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.63-65An elevated sedimentation rate will be seen within the " rst week to 10 days.
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
66-6892% sensitivity, 97% specificity, and 95% overall accuracy (Fig. 6-9).
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
largevessel damage following thoracic discography is also unknown. In one series of 230
outpatient thoracic discograms, Schellhas reported a zero incidence of
69pneumothorax. Although this is encouraging, the complication does still occur;
thus, the procedure should not be attempted without substantial experience and
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%
70(0.082%), 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
71ineffective, parenteral narcotics.
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
17,72,73cases. 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
73-75block has been reported. These complications are thought to have occurred
after inadvertent dural puncture. Facet-capsule rupture also occurs, especially if
48more than 2.0 mL of injectate is used for intraarticular injections.
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 a( erents and the righting
76,77response. 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
77the third occipital nerve, which resolved in 3 months. 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
78-82pneumothorax. 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
79,83,84neuralgia. 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
1. Falco F.J. Lumbar spine injection procedures in the management of low back pain.
Occup Med. 1998;13(1):121-149.
2. Moskovich R. Epidural injections for the treatment of low back pain. Bull Hosp Jt
Dis. 1996;55(4):178-184.
3. Kinard R.E. Diagnostic spinal injection procedures. Neurosurg Clin N Am.
4. PASSOR: PASSOR Fellowship Guidelines. Endorsed by the AAPM&R Board of
Governors; 1998.
5. PASSOR: PASSOR Educational Guidelines for Interventional Spinal Procedures.
Accepted by the PASSOR Board of Governors and AAPM&R Board of Governors;
June, 2001; Update, 2004.
6. North American Spine Society. Epidural Steroid Injections. General Information.
7. Demling R. Preoperative Care. In: Way L.W., editor. Current Surgical Diagnosis and
Treatment. Conn. Appleton & Lange: Norwalk, 1991. p.9.8
8. Sunderland S. Nerves and Nerve Injuries, 2nd ed. Edinburgh: Churchill Livingstone;
1978.9. Dougherty J.H.Jr, Fraser R.A. Complications following intraspinal injections of
steroids: Reports of two cases. J Neurosurg. 1978;48:1023-1025.
10. Gutknecht D.R. Chemical meningitis following injections of epidural steroids. Am J
Med. 1987;82(3):570. [Letter]
11. Shealy C.N. Dangers of spinal injections without proper diagnosis. JAMA.
12. Goucke C.R., Graziotti P. Extradural abscess following local anesthetic and steroid
injection for chronic low back pain. Br J Anaesth. 1990;65(3):427-429.
13. Chan S.T., Leung S. Spinal epidural abscess following steroid injection for sciatica.
Case report. Spine. 1984;14(1):106-108.
14. Tham E.J., Stoodley M.A., Macintyre P.E., Jones N.R. Back pain following
postoperative epidural analgesia: An indicator of possible infection. Anaesth
Intensive Care. 1997;25(3):297-301.
15. Cooper A.B., Sharpe M.D., et al. Bacterial meningitis and cauda equina syndrome
after epidural steroid injections. Can J Anaesth. 1996;43(5 Part 1):471-474.
16. Baker A.S., Ojemann R.G., Swartz M.N., Richardson E.P.Jr. Spinal epidural
abscess. N Engl J Med. 1975;293:463-468.
17. University of Rochester Spine Center; Department of Orthopaedic Surgery;
Department of Physical Medicine & Rehabilitation; University of Rochester School
of Medicine; Strong Memorial Health System: What Are Possible Side Effects and
Complications of Spine Procedures? 2007.
18. Derby R., Baker R.M., Lee C.H., Anderson P.A. Evidence-informed management of
chronic low back pain with intradiscal electrothermal therapy. Spine J.
19. Bonica J.J. Diagnostic and therapeutic blocks. A reappraisal based on 15 years’
experience. Anesth Analg. 1958;37:58-68.
20. Odoom J.A., Sih I.L. Epidural analgesia and anticoagulant therapy: Experience
with one thousand cases of continuous epidurals. Anesthesia. 1983;38:254-259.
21. Rao T.L., El-Etr A.A. Anticoagulation following placement of epidural and
subarachnoid catheters: an evaluation of neurologic sequelae. Anesthesiology.
22. Delaney T.J., Rowlingson J.C., Carron H., et al. Epidural steroid effects on nerves
and meninges. Anesth Analg. 1980;59:610-614.
23. Knight C.L., Burnell J.C. Systemic side-effects of extradural steroids. Anaesthesia.
24. Goebert H.W.Jr., Jallo S.J., Gardner W.J., Wasmuth C.E. Painful radiculopathy
treated with epidural injections of procaine and hydrocortisone acetate: results in
113 patients. Anesth Analg. 1961;40:130-134.
25. Knutsen O., Ygge H. Prolonged extradural anesthesia with bupivicaine at lumbagoand sciatica. Acta Orthop Scand. 1971;42:338-352.
26. American Heart Association. Textbook of Advanced Cardiac Life Support. 3rd ed.
27. American Heart Association. Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiac Care. JAMA. 1992;268(16):2171-2302.
28. Racz G. Personal communication. Lubbock, Texas.
29. Rawal N., Wattwil M. Respiratory depression following epidural morphine: An
experimental and clinical study. Anesth Analg. 1984;63:8-14.
30. Rawal N., Arntr S., Gustafsson L.L., Allvin R. Present state of epidural and
intrathecal opiate analgesia in Sweden. A nationwide follow-up survey. Br J
Anaesth. 1987;59:791-799.
31. Bridenbaugh P.O., DuPen S.L., Moore D.C., et al. Post-operative intercostal nerve
block analgesia versus narcotic analgesia. Anesth Analg. 1973;52:81-85.
32. Armitage E.N. Lumbar and thoracic epidural. In: Wildsmith J.A.W., Armitage E.N.,
editors. Principles and Practice of Regional Anesthesia. New York: Churchill
Livingstone; 1987:109.
33. Bromage P.R. Complications and contraindications. In: Bromage P.R., editor.
Epidural Analgesia. Philadelphia: WB Saunders; 1978:654-711.
34. Benzon H. Epidural steroid injections for low back pain and lumbosacral
radiculopathy. Pain. 1986;24:277-295.
35. Swerdlow M., Sayle-Creer W. A study of extradural medication in the relief of the
lumbosciatic syndrome. Anaesthesia. 1970;25:341-345.
36. Warr A., Wilkinson J.A., Burn J.M., et al. Chronic lumbosciatic syndrome treated
by epidural injection and manipulation. Practitioner. 1972;209:53-59.
37. Kepes E.R., Duncalf D. Treatment of backache with spinal injections of local
anesthetics, spinal and systemic steroids: A review. Pain. 1985;22(1):33-47.
38. Deisenhammer E. Clinical and experimental studies on headaches after
myelography. Neuroradiology. 1975;9:99-102.
39. Waldman S.D. Subdural injection as a cause of unexplained neurological
symptoms. Reg Anesth. 1992;17:55.
40. El-Khoury Ehara S, Weinstein J.N., et al. Epidural injections: A procedure ideally
performed with fluoroscopic control. Radiology. 1988;168:554-557.
41. Mehta M., Salmon N. Extradural block. Confirmation of the injection site by x-ray
monitoring. Anaesthesia. 1985;40:1009-1012.
42. Dreyfuss P. Epidural steroid injections: A procedure ideally performed with
fluoroscopic control and contrast media. ISIS Newsletter. 1(5), 1993.
43. Stewart H.D., Quinnell R.C., Dann N. Epidurography in the management of
sciatica. Br J Rheumatol. 1987;26:424-429.
44. Forrest J.B. The response to epidural steroid injections in chronic dorsal root pain.Can Anaesth Soc J. 1980;27:40-46.
45. White A.H., Derby R., Wynne G. Injection techniques for the diagnosis and
treatment of low back pain. Spine. 1980;5:78-86.
46. Renfrew D.L., Moore T.E., Kathol M.H., et al. Correct placement of epidural
steroid injections: Fluoroscopic guidance and contrast administration. AJNR.
47. White A.H. Injection techniques for the diagnosis and treatment of low back pain.
Orthop Clin North Am. 1983;14:553-567.
48. Hildebrandt J. Relevance of nerve blocks in treating and diagnosing low back pain—is
the quality decisive? Schmerz. (article in German). 2001;15(6):474-483.
49. Simon D.L., Kunz R.D., German J.D., et al. Allergic or pseudoallergic reaction
following epidural steroid deposition and skin testing. Reg Anesth.
50. Covino BG. Clinical pharmacology of local anesthetic agents. In: Cousins MJ, et al,
editors. Neural Blockade in Clinical Anesthesia and Management of Pain.
Philadelphia: Lippincott; 1988:111-114.
51. Braid D.P., Scott D.B. The systemic absorption of local analgesic drugs. Br J
Anaesth. 1965;37:394-404.
52. Cousins M.J., et al. Epidural neural blockade. In: Cousins M.J., Bridenbaugh M.J.,
Phillip O., editors. Neural Blockade. Philadelphia: Lippincott; 1988:340-341.
53. Cousins M.J. Hematoma following epidural block. Anesthesiology. 1972;37:263.
54. Waldman S.D., Winnie A.D. Caudal epidural nerve block. In: Waldman S.D.,
editor. Interventional Pain Management. Philadelphia: WB Saunders; 1996:381-382.
55. Derby R., Bogduk N., Kine G. Precision percutaneous blocking procedures for
localizing spinal pain. Part 2. The lumbar neuroaxial compartment. Pain Digest.
56. Dincer U., Kiralp M.Z., Cakar E., et al. Caudal epidural injection versus
nonsteroidal anti-inflammatory drugs in the treatment of low back pain accompanied
with radicular pain. Joint Bone Spine. 2007;74(5):467-471.
57. Lerner SM, Gutterman P, Jenkins F, et al. Epidural hematoma and paraplegia after
numerous lumbar punctures. Anesthesiology. 1973;39:550-551.
58. Waldman S.D. Complications of cervical epidural nerve blocks with steroids: a
prospective study of 790 consecutive blocks. Reg Anesth. 1989;11:149-151.
59. Redekop G.J., Del Maestro R.F. Diagnosis and management of spinal epidural
abscess. Can J Neurol Sci. 1992;19:180-187.
60. Fraser R.D., Osti O.L., Vernon-Roberts B. Discitis after discography. J Bone Joint
Surgery. 1987;69:26-35.
61. Crock H. Practice of Spinal Surgery. New York: Springer-Verlag; 1983.
62. Guyer R.D., Collier R., Stith W.J., et al. Discitis after discography. Spine.1988;13:1352-1354.
63. Fernand R., Lee C.K. Post-laminectomy disc space infection. A review of the
literature and a report of three cases. Clin Orthop Relat Res. 1986;209:215-218.
64. Lindholm T.S., Pylkkanen P. Discitis following removal intervertebral disc. Spine.
65. Thibodeau A.A. Closed space infection following the removal of lumbar
intervertebral disc. J Bone Joint Surg Am. 1968;50:400-410.
66. Arrington J.A., Murtagh F.R., Silbiger M.L., et al. Magnetic resonance imaging of
postdiscogram discitis and osteomyelitis in the lumbar spine: case report. J Fla
Med Assoc. 1986;73:192-194.
67. Modic M.T., Feiglin D.H., Piraino D.W., et al. Vertebral osteomyelitis: Assessment
using MR. Radiology. 1985;157:157-166.
68. Szypryt E.P., Hardy J.G., Hinton C.E., et al. A comparison between magnetic
resonance imaging and scintigraphic bone imaging in the diagnosis of disc space
infection in an animal model. Spine. 1988;13:1042-1048.
69. Schellhas KP, Pollei K. Thoracic disc degeneration: Correlation of MR imaging and
discography. Presented at the 8th Annual Assembly of the North American Spine
Society. San Diego, CA; oct 14-16.
70. Moore D.C., Bridenbaugh L.D. Oxygen: the antidote for systemic toxic reactions
from local anesthetic drugs. JAMA. 1960;174:842-847.
71. Cory P.C., Mulroy M.F. Post-operative respiratory failure following intercostal
block. Anethesiology. 1981;54:418-419.
72. Falco F.J., Irwin L., Zhu J. Lumbar spine injection and interventional procedures
in the management of low back pain. Clin Occup Environ Med. 2006;5(3):655-702.
73. Bous R.A. Facet joint injections. In: Stanton-Hicks M., Bous R., editors. Chronic Low
Back Pain. New York: Raven Press; 1982:199-211.
74. Thomson S.J., Lomax D.M., Collett B.J., et al. Chemical meningism after lumbar
facet joint nerve block with local anesthetic and steroids. Anaesthesia.
75. Berrigan T. Chemical meningism after lumbar facet joint block. Anaesthesia.
76. Pawl R.P. Headache, cervical spondylosis, and anterior cervical fusion. Surg Annu.
77. Bogduk N., Marsland A. The cervical zygapophysial joints as a source of neck pain.
Spine. 1988;13:610-617.
78. Carron H., Litwiller R. Stellate ganglion block. Anesth Analg. 1975;54:567-570.
79. Lofstrom J., Cousins M.J. Sympathetic neural blockade of upper and lower
extremity. In: Cousins M., editor. Neural Blockade in Clinical Management of Pain.Philadelphia: Lippincott; 1988:461.
80. Malmqvist E., Bengtsson M., Sorensen J., et al. Efficacy of stellate ganglion block:
A clinical study with bupivacaine. Reg Anesth. 1992;17:340-347.
81. Sachs B.L., Zindrick M.R., Beasley R.D. Reflex sympathetic dystrophy after
operative procedures on the lumbar spine. J Bone Joint Surg Am. 1993;75:721-725.
82. Wallace M.S., Milholland A.V. Contralateral spread of local anesthetic with stellate
ganglion block. Reg Anesth. 1993;18:55-59.
83. Schmidt S.D., Gibbons J.J. Postdural puncture headache after
fluoroscopicallyguided lumbar paravertebral sympathetic block. Anesthesiology. 1993;78:198-200.
84. Sprague R.S., Ramamurthy S. Identification of the anterior psoas sheath as a
landmark for lumbar sympathetic block. Reg Anesth. 1990;15:253-255.
85. Waldman S.D., Winnie A.P. Interventional Pain Management. W B Saunders; 1996.
86. Kricun R., Kricun M.E. Computed Tomography of the Spine: Diagnostic Exercises.
Aspen Publications. 1987.
87. Daffner R.H. Clinical Radiology: The Essentials. Williams & Wilkins; 1993.
Appendix I
American Heart Association, Advanced Cardiac Life Support (ACLS) Protocols,
Appendix II Treatment of Acute Reactions
• 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 <_8825_2c_ initiate="" acls="" protocol="" and=""
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)
• 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
• 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
• Refer to ACLS protocol
Always administer supplemental oxygen with caution in a patient with chronic
pulmonary disease.

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 sta e ciency, 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
backend. 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 Payment processing and
management analysis
Check-in Denials management
Patient encounter Accounts receivable follow-up
Test/procedure coordination
Front-End Processes

Front-end processes in the revenue cycle include appointment scheduling and
preregistration, insurance veri. cation 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 . rst encounter with the patient
and is one of the most critical steps in the revenue cycle. Future third-party billings
and collections e orts 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
copayment 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 o ce, to ensure accuracy.
Practices that are business savvy o er on their website the ability to make an
appointment and provide preregistration demographic and insurance information.
Insurance Verification
Insurance veri. cation 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 bene. ts prior to all new
patient appointments to ensure appropriate collections on the back-end. Successful
practices will re-verify insurance bene. ts on all established patients not in a
postoperative global period. All too often a practice . nds 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 bene. ts 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 sta 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 bene. ts
verification for the practice.
In summary, the goal of the . rst 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 . nancial risk, verify insurance
eligibility, and obtain proper referrals to ensure appropriate revenue collection
when the service is provided.
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
• 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 o ce (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 identi. ed with a . ve-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 identi. ed with a . ve-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, . ve-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, . ve-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.
Types of CPT Codes and Application to Pain ManagementTable 7-2
Category I CPT Codes
CPT Application for Pain
Code Type of CPT Code Management
00100- Anesthesiology Codes describe
01999, administration of anesthesia
99100- during procedures99140 (generally surgery CPT
codes) performed by
another provider/physician
10021- Surgery Includes codes for injections,
69990 placement of pain pumps,
and other pain management
diagnostic and therapeutic
70010- Radiology (including nuclear medicine Includes fluoroscopic
79999 and diagnostic ultrasound) guidance and localization of
needle or catheter tip for
pain management
procedures as well as
diagnostic radiologic
80047- Pathology and laboratory These codes are generally
89356 not used by pain
management providers
90281- Medicine (except anesthesiology) Includes nerve conduction
99199, and electromyography
99500- diagnostic testing codes
99201- Evaluation and management Includes codes for office
99499 visits, consultations, and
hospital visits used by pain
management providers
Category II CPT Codes
0001F- These codes are supplemental tracking Includes codes for oncologic
7025F codes that can be used for performance pain management as well as
management. They are intended to assessment and examination
facilitate data collection about quality of back pain
of care rendered; the use of these codes
is optional.
Category III CPT Codes
0016T- These codes are used to report Includes code for
0196T temporary codes for emerging percutaneous intradiscaltechnology, services, and procedures annuloplasty
and are used instead of an unlisted
Category I CPT code (e.g., 64999).
As per CPT 2009.
ICD-9-CM Codes
ICD-9-CM codes classify diseases and a wide variety of signs, symptoms, abnormal
. ndings, complaints, social circumstances, and external causes of injury or disease.
These three, four, and . ve 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 precerti. cation for testing, such as
radiologic procedures, including plain . lms, magnetic resonance imaging (MRI),
and CAT (computerized axial tomography) scans. Successful practices will
incorporate this precerti. cation 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
precerti. cation 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
After the o ce 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
• 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 ProductionProfessional 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 I ow 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
• 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
• 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

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 . rst 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 (o ce 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
bene. t (EOB) form that describes the payor’s payment or nonpayment of services
submitted. Speci. c 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
• 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 sta must contact the
payor to determine how to allocate in the PMIS all payments for each service and

determine that the payment is correct.
E cient 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 di cult to collect. The best opportunity for a pain management
practice to collect from the patient is while the patient is in the o ce 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 sta or the o ce
manager, be responsible for making the decision to pursue a formal outside
collections process.
A successful revenue cycle involves e cient, cost-e ective, 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
1nonconsensual invasion of bodily integrity. In short, the law recognizes the
1individual’s interest in preserving the “inviolability of the person,” 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
1determine the direction in which his … interests lie.” 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
2most important aspect of patients’ rights.
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
36% of cases.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
rea5 rm 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 signi6cant 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
1procedure.” 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 bene6ts 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, signi6cant information
includes the nature and probability of risks involved in the procedure, expected
bene6ts, the irreversibility of the procedure, the available alternatives to the
1proposed procedure, and the likely result of no treatment. 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
1risks of a procedure.
Recent studies have focused on the manner in which informed consent is
obtained. For example, in a prospective, randomized, controlled study conductedby Bennet and colleagues, 99 out of 109 patients undergoing imaging-guided
4spinal injections agreed to particpate and were assigned to one of three groups.
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 signi6cant results
included a lower survey score for the control group. Not surprisingly, it took
signi6cantly 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
The manner in which information is given and how much information is oAered,
are both important considerations. Too much information may actually increase
5anxiety just prior to a procedure. A recent review on informed consent in Pain
Practices found that although “disclosure has improved, but is still uneven,
6comprehension is often poor, for both patients and research subjects.” An
important factor is not only the improvement of consent forms, but also improving
the consent process. A group of Swiss researchers studied the eAect 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
7than the oral-only group.
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
de6ned as the signi6cance a speci6c patient attaches to the disclosed risks in
8deciding whether to undergo the proposed procedure. Materiality of information
about a side eAect or consequence is a function not only of the severity of that
8consequence, but also of the likelihood that it will occur. 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