Atlas of Pain Medicine Procedures PDF

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This atlas is dedicated to:
My mother Late Raniba Diwan for teaching me the meaning of life
My family Indira, Sneh, Kaushal, and Shira for their love and unconditional support
My grandchildren Jonathon and Belen for bringing joy to our lives
My friends and my mentors who supported me and guided me to the path of knowledge
My co-editor Peter Staats for his unwavering friendship and being a trusted counselor
And,
Department of Anesthesiology and Pain Medicine
Weill Cornell Medical College and New York Presbyterian Hospital of Cornell University
For being an integral part of my personal and professional success
Sudhir Diwan
To Mom and Dad. You taught me how to change the world to make it a better place,
one patient at a time, and more globally through theory and research.
To my children, Alyssa, Dylan and Rachel. I am so proud of all three of you and the
paths that you are forging. I am confident that each of you will make
the world a better place in your own way.
Most of all, to my wife Nancy, Thank you for your understanding and compassion.
Your unwavering support has made this book possible. You make me, and
everyone who knows you, a better person.
Peter S. Staats
Contents
Section Editors
Contributors
Preface
Introduction
SECTION I: Basic Applications Mark J. Lema

1. Fluoroscopy in Interventional Pain Medicine
David M. Schultz
2. Computed Tomography Guidance in Pain Management
Ronil V. Chandra, Thabele-Leslie Mazwi, Daniel Oh, Albert J. Yoo, and Joshua A. Hirsch
3. Ultrasound Guidance for Interventional Pain Management
Hariharan Shankar and Kanishka Rajput
4. Radiation Safety
Vikram B. Patel
5. Equipment Used in Pain Management
Vikram B. Patel
6. Corticosteroids: Indications, Pharmacology, and Risks in Interventional Pain Management
Carolyn Kim and Christopher Gharibo
7. Local Anesthetics
Christopher Voscopoulos and Mark J. Lema
8. Botulinum Toxins
Charles E. Argoff and Howard Smith
9. Infection: Prevention, Diagnosis, and Management
Dawood Sayed and Sudhir Diwan
10. Anticoagulation Guidelines
Nirmala R. Abraham, Cathy D. Trame, and Sudhir Diwan
11. Sedation for Interventional Pain Procedures
Nancy Staats
12. EMG and Nerve Conduction Studies
Bridget T. Carey
13. Documentation, Billing, and Coding
Laxmaiah Manchikanti
SECTION II: Head and Neck Injections Sudhir Diwan

14. Atlanto-Occipital Joint Injections
Andrea Trescot
15. Atlanto-Axial Joint Injections
Andrea Trescot
16. Cervical Nerve Root Blocks
Stanley Golovac
17. Trigeminal Ganglion and Nerve Block
Miles Day and Kenneth D. Candido
18. Sphenopalatine Ganglion Block
Samer Narouze
19. Occipital Nerve Blocks
Andrea Trescot and Lawrence Kamhi
20. Periorbital Nerve Blocks (Supraorbital, Supratrochlear, and Infraorbital Nerves)
Sanford Silverman
SECTION III: Spinal Interventions Vikram B. Patel

21. Interlaminar Epidural Steroid Injections: Cervical, Thoracic, Lumbar, and Caudal
Raj Doshi, Vikram B. Patel, and Salahadin Abdi
22. Transforaminal Epidural Steroid Injection
Vikram B. Patel
23. Facet Joint Interventions: Intra-Articular Injections, Medial Branch Blocks, and
Radiofrequency Ablations
Vikram B. Patel and Sukdeb Datta
24. Lumbar Facet Joint Cyst Drainage and Injection
Gerard P. Varlotta, Christopher Gharibo, and Z.T. Traeger
25. Dorsal Root Ganglion Blocks and Radiofrequency Procedures
Seth A. Waldman and Vladimir Kramskiy
26. Sacroiliac Joint Injections
Sheetal Kerkar Patil, Honorio T. Benzon, and Sudhir Diwan
27. Sacroiliac Joint Denervation Using Synergy System
Leonardo Kapural and Amanda Toye
28. Sacroiliac Joint Denervation by Using Simplicity III
Sudhir Diwan and Nimish Davé
29. Percutaneous Sacroplasty
Harold Cordner and Michael E. Frey
30. Percutaneous Facet Fusion
Rinoo V. Shah
31. Provocative Discogram
Vikram B. Patel and Sudhir Diwan
32. Percutaneous Disc Decompressions
Sanjay Bakshi and Gerard W. Abrahamsen
33. Hydrosurgery of Disc
Didier Demesmin and Sagar Parikh
34. Percutaneous Radiofrequency Discectomy With Disk IT
Samyadev Datta and Vikram B. Patel
35. Intradiscal Electrothermal Therapy
Jason E. Pope and Nagy Mekhail
36. Intradiscal Biacuplasty
Mark Yelle and Leonardo Kapural
37. Endoscopic Discectomy
Sudhir Diwan, Kiran Patel, Kenneth Chapman, and Vikram B. Patel
38. Minimally Invasive Lumbar Decompression (MILD procedure)
Lora L. Brown
39. Vertebral Augmentation
Ramsin Benyamin, Ricardo Vallejo, Atiq Rehman, and Allen Burton
40. Epidural Lysis of Adhesions
Rinoo V. Shah
41. Vascular Complications of Spinal Interventions
Scott E. Glaser, Rinoo V. Shah, and Peter S. Staats
SECTION IV: Sympathetic Blocks Andrea Trescot

42. Stellate Ganglion Block
Richard S. Epter
43. Thoracic (T2-3) Ganglion Block
Michael Stanton-Hicks
44. Splanchnic Nerve Blocks
Andrea Trescot
45. Celiac Plexus Block Using CT Guidance
Kenneth D. Candido and Nebojsa N. Knezevic
46. Celiac Plexus Block Using Fluoroscopic Guidance
Kenneth D. Candido, Peter S. Staats, Corey W. Hunter, and Sudhir Diwan
47. Lumbar Sympathetic Block
Joshua P. Prager
48. Superior and Inferior Hypogastric Plexus Blocks
Agnes Stogicza
49. Ganglion Impar Block
Corey W. Hunter and Sudhir Diwan
SECTION V: Musculoskeletal Injections Vijay Vad

50. Fluoroscopy and Ultrasound-Guided Joint Injections
Jennifer Solomon, Christine Roque-Dang, and James Wyss
51. Viscosupplements and Steroid Injections
Jennifer Solomon and Vijay Vad
52. Trigger Point Injections
Ricardo A. Nieves and Rinoo V. Shah
53. Neuroma Injections
Rinoo V. Shah and Ricardo A. Nieves
54. Myofascial Injections (Trigger Point, Piriformis, Iliopsoas, and Scalene Injections)
Clark C. Smith, Farooq Khan, Juan Francisco Asenjo, and Honorio T. Benzon
55. Intra-Articular Joint Injections
Michael N. Brown
56. Tendon Injections
Robert Balch III
SECTION VI: Peripheral Nerve Blocks Christopher Gharibo

57. Intercostal Nerve Block
Amitabh Gulati
58. Supraclavicular and Infraclavicular Nerve Blocks
David B. Albert, Robert Altman, and Lisa Doan
59. Ilioinguinal and Iliohypogastric Nerve Blocks
Paul J. Hubbell III
60. Genitofemoral Nerve Block
Andrea Trescot
61. Lateral Femoral Cutaneous Nerve Block
Gerard P. Varlotta and Anya Myers
62. Pudendal Nerve Block
Susanti Chowdhaury, Gail Gray, and Andrea Trescot
63. Obturator Nerve Block
Arthur Atchabahian
64. Suprascapular Nerve Block
Christopher Gharibo and Steve Aydin
SECTION VII: Intrathecal Drug Delivery Peter S. Staats

65. Commercially Available Reservoir Options for Intrathecal Drug Delivery
Corey W. Hunter and David Caraway
66. Choosing Intrathecal Medication
Philip S. Kim and Sudhir Diwan
67. Intrathecal Drug Delivery Trialing Procedures
Richard Bowman, Timothy R. Deer, and Jason E. Pope
68. Permanent Implant
Sean Li and Peter S. Staats
SECTION VIII: Neuroaugmentation Techniques Sudhir Diwan

69. Spinal Cord Stimulation: Hardware Specifications
Sudhir Diwan, Karina Gritsenko, and Neel Mehta
70. Spinal Cord Stimulation: Trialing Procedure
Richard B. North
71. Spinal Cord Stimulation: Implantation Techniques
Elias Veizi and Salim M. Hayek
72. Anterograde Versus Retrograde Lead Placement
Marshall D. Bedder
73. Dorsal Root Ganglion Stimulation: Anatomy, Physiology, and Potential for Therapeutic
Targeting in Chronic Pain
Jeffery Kramer, Christine E. Draper, Timothy R. Deer, Jason E. Pope, Robert Levy, and Eric
J. Grigsby
74. Occipital Nerve Stimulation
Erich O. Richter, Marina V. Abramova, and Kenneth M. Alo
75. Percutaneous Peripheral Nerve and Field Stimulation
Jason E. Pope, Timothy R. Deer, and Eric J. Grigsby
76. Surgical Treatment of Trigeminal Neuralgia
Michael G. Kaplitt
SECTION IX: Neurolytic Procedures Rinoo V. Shah

77. Neurolytic Blocks
Kenneth D. Candido and Nebojsa Nick Knezevic
78. Chemical Neurolysis
Michael M. Bottros and Michael A. Erdek
79. Cryoneuroablation
David Irwin and Andrea Trescot
80. Radiofrequency Neurolysis
Anand Thakur and Peter S. Staats
Section Editors
Section I: Basic Applications- Mark J. Lema, MD, PhD
Professor and Chair of Anesthesiology of Anesthesiology, Critical Care, and Pain Medicine, Roswell
Park Cancer Institute
State University of New York at Buffalo School of Medicine
Buffalo, New York
Section II: Head and Neck Injections- Sudhir Diwan MD, DABIPP, FIPP
Executive Director
Manhattan Spine and Pain Medicine
Associate Professor of Anesthesiology
SUNY Downstate Medical Center
Attending, Lenox Hill Hospital
New York, New York
Section III: Spinal Interventions- Vikram B. Patel, MD, FIPP, DABIPP

Director, Phoenix Interventional Center for Advanced Learning
Algonquin, Illinois
Section IV: Sympathetic Blocks- Andrea Trescot, MD, ABIPP, FIPP

Medical Director
Pain and Headache Center
Wasilla, Anchorage, Kenai, Alaska
Section V: Musculoskeletal Injections- Vijay Vad, MD

Assistant Professor
Rehabilitation and Sports Medicine
Weill Cornell Medical College
Hospital for Special Surgery
New York, New York
Section VI: Peripheral Nerve Blocks- Christopher Gharibo, MD

Associate Professor
Department of Anesthesiology and Orthopedics
New York University School of Medicine
New York, New York
Section VII: Intrathecal Drug Delivery- Peter S. Staats, MD, and MBA
Adjunct Associate Professor
Johns Hopkins University
Department of Anesthesiology and Critical Care Medicine
Premier Pain Centers, LLC
Shrewsbury, New Jersey
Section VIII: Neuroaugmentation Techniques- Sudhir Diwan, MD, DABIPP, FIPP

Executive Director
Manhattan Spine and Pain Medicine
Associate Professor of Clinical Anesthesiology
Pain Attending, Lenox Hill Hospital
New York, New York
Section IX: Neurolytic Procedures- Rinoo V. Shah, MD

Clinical Professor of Anesthesiology
Director, Chronic Pain
LSU Health Science Center
Shreveport, Louisiana
Contributors
Salahadin Abdi, MD, PhD (Chapter 21)
Professor and Chair
Department of Pain Medicine—Unit 409
The University of Texas MD Anderson Cancer Center
Houston, Texas
Nirmala R. Abraham, MD, FABPM (Chapter 10)

Sycamore Pain Management Center
Kettering Health Network
Miamisburg, Ohio
Gerard W. Abrahamsen, PA-C (Chapter 32)

Physician Assistant, Manhattan Spine and Pain Medicine
Physician Assistant, Lenox Hill Hospital
New York, New York
Marina V. Abramova, MD (Chapter 74)

Department of Neurosurgery
LSU Health Sciences Center
New Orleans, Louisiana
David B. Albert, MD (Chapter 58)

Department of Anesthesiology
NYU Langone Medical Center
New York, New York
Kenneth M. Alo, MD (Chapter 74)

Pain Management, The Methodist Hospital Research Institute
Houston, Texas
Robert Altman, MD (Chapter 58)

Associate Clinical Professor of Anesthesia NYU Medical School
Director of Ambulatory Anesthesia Services NYU-HJD
Director Regional Anesthesia Fellowship
New York, New York
Charles E. Argoff, MD (Chapter 8)

Professor of Neurology, Albany Medical College
Director, Comprehensive Pain Center, Albany Medical Center, Albany
New York, New York
Juan Francisco Asenjo, MD, FRCPC (Chapter 54)

Associate Professor
Department of Anesthesia and Alan Edwards McGill Pain Treatment Unit
McGill Cancer Pain Clinic
McGill University Health Center
Montréal, Quebec
Canada
Arthur Atchabahian, MD (Chapter 63)

Associate Professor
New York University School of Medicine
New York, New York
Steve M. Aydin, DO (Chapter 64)

Clinical Assistant Professor in PM&R at Hofstra North Shore-LIJ School of Medicine, Manhassett, New
York
Director of Musculoskeletal Medicine at Manhattan Spine and Pain
New York, New York
Sanjay Bakshi, MD, D.A.B.P.M (Chapter 32)

President, Manhattan Spine and Pain Medicine
President, NY Society of Interventional Pain Physicians
Attending Physician, Lenox Hill Hospital
New York, New York
Attending Physician, Beth Israel Medical Center
New York, New York
Attending Physician, Bayshore Medical Center
Holmdel, New Jersey
Member, International Spine Intervention Society
New York, New York
Robert Balch III, DO (Chapter 56)

Diplomate of the American Board of PM&R
Fellowship Trained and Board Certified in Pain Medicine
Fort Worth, Texas
Marshall D. Bedder, MD, FRCP (C) (Chapter 72)

Director Interventional Pain
Pacific Medical Centers (PacMed)
Seattle, Washington
Ramsin Benyamin, MD, DABIPP (Chapter 39)

President, American Society of Interventional Pain Physicians
President, Millennium Pain Center, Illinois
Clinical Assistant Professor of Surgery, College of Medicine, University of Illinois, Urbana-Champaign
Illinois
Honorio T. Benzon, MD (Chapters 26 and 54)

Professor of Anesthesiology
Northwestern University Feinberg School of Medicine
Chicago, Illinois
Michael M. Bottros, MD (Chapter 78)

Assistant Professor of Anesthesiology and Critical Care Medicine, Department of Anesthesiology and
Critical Care Medicine, Washington University
St. Louis School of Medicine
St. Louis, Missouri
Lora L. Brown, MD (Chapter 38)

Medical Director
TruWell, a new health
Past President, Florida Society of Interventional Pain Physicians
St. Petersburg, Florida
Michael N. Brown, MD (Chapter 55)

Private Practice
Seattle, Washington
Allen Burton, MD (Chapter 39)

Houston Pain Centers
Houston, Texas
Kenneth D. Candido, MD (Chapters 17, 45, 46 and 77)

Chairman, Department of Anesthesiology
Professor of Clinical Anesthesiology-University of Illinois, Chicago
Advocate Illinois Masonic Medical Center
Chicago, Illinois
David Caraway, MD, PhD (Chapter 65)

Medical Director
Center for Pain Relief, TriState, PLLC
Huntington, West Virginia
Bridget T. Carey, MD (Chapter 12)

Assistant Professor of Neurology
and Neuroscience,
New York, New York
Ronil V. Chandra, MBBS, FRANZCR (Chapter 2)

Neuroradiology and Neurovascular Surgery, Department of Imaging, Monash Health
Department of Surgery, Monash University
Melbourne, Australia
Kenneth Chapman, MD, FIPP (Chapter 37)

Director, Pain Management
Staten Island University Hospital
Staten Island, New York
Susanti Chowdhaury, MD (Chapter 62)

Medical Director, Advanced Pain Management Consultants
Largo, Florida
Harold Cordner, MD, FIPP (Chapter 29)

Florida Pain Management Associates
Assistant Clinical Professor, Florida State University School of Medicine
Sebastian, Florida
Sukdeb Datta, MD, MBA (Chapter 23)

President
Datta Endoscopic Back Surgery and Pain Center
Professorial Lecturer
Mount Sinai School of Medicine
New York, New York
Samyadev Datta, MD, FRCA (Chapter 34)

Center for Pain Management
Hackensack, New Jersey
Nimish Davé, MD, MPH (Chapter 28)

Kaiser Permanente Southern California
San Diego, California
Miles Day, MD, FIPP, DABIPP (Chapter 17)

Traweek-Racz Endowed Professor in Pain Research
Director—The Pain Center at Grace Clinic
Pain Management Fellowship Director
Texas Tech University HSC
Lubbock, Texas
Timothy R. Deer, MD (Chapters 67, 73 and 75)

President and CEO, The Center For Pain Relief, and Clinical Professor of Anesthesiology, West Virginia
University School of Medicine
Charleston, West Virginia
Didier Demesmin, MD (Chapter 33)

University Pain Management Center
Somerset, New Jersey
Sudhir Diwan, MD, DABIPP, FIPP (Chapters 9, 10, 26, 28, 31, 37, 46, 49, 65 and 69)
Executive Director, Manhattan Spine
and Pain Medicine
Associate Professor of Clinical Anesthesiology
Pain Attending, Lenox Hill Hospital
New York, New York
Lisa Doan, MD (Chapter 58)

New York, New York
Raj Doshi, MD (Chapter 21)

Beth Israel Deaconess Medical
Department of Anesthesia and Critical Care
Boston, Massachusetts
Christine E. Draper, PhD (Chapter 73)

Spinal Modulation
Menlo Park, California
Richard S. Epter, MD, DABAPM, DABIPP, DABPM, FIPP (Chapter 42)

Augusta Pain Center
Augusta, Georgia
Michael A. Erdek, MD (Chapter 78)

Associate Professor of Anesthesiology, Oncology, and Critical Care Medicine, Department of
Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine
Baltimore, Maryland
Michael E. Frey, MD (Chapter 29)

Advanced Pain Management and Specialist
Fort Myers, Florida
Adjunct Clinical Professor
Virginia Commonwealth University
Department of Physical Medicine and Rehabilitation
Fort Myers, Florida
Christopher Gharibo, MD (Chapters 6, 24 and 64)

Associate Professor
Department of Anesthesiology & Orthopedics
NYU School of Medicine
New York, New York
Scott E. Glaser, MD, DABIPP (Chapter 41)

President, Pain Specialists of Greater Chicago,
Board Member, American Society of Interventional Pain Physicians
Chicago, Illinois
Stanley Golovac, MD (Chapter 16)

Florida Pain
Merritt Island, Florida
Gail Gray, ARNP (Chapter 62)

Advanced Interventional Spine Consultants
Largo, Florida
Eric J. Grigsby, MD (Chapters 73 and 75)

Founding Partner, Napa Pain Institute, Napa, California; Founder and President, Neurovations
Napa, California
Karina Gritsenko, MD (Chapter 69)

Assistant Professor of Anesthesiology
Regional Anesthesia, Interventional Pain Medicine
Montefiore Medical Center
New York, New York
Amitabh Gulati, MD, FIPP (Chapter 57)

Director of Ambulatory Pain
Co-Director of the Cornell School of Medicine Pain Management Fellowship
Assistant Attending
Memorial Sloan Kettering Cancer Center
New York, New York
Salim M. Hayek MD, PhD (Chapter 71)

Professor, Department of Anesthesiology
Case Western Reserve University
Chief, Division of Pain Medicine
University Hospital Case Medical Center
Cleveland, Ohio
Joshua A. Hirsch, MD, FACR, FSIR (Chapter 2)

Director: Interventional Neuroradiology and
Endovascular Neurosurgery
Massachusetts General Hospital and
Harvard Medical School
Paul J. Hubbell, III, MD, DDS (Chapter 59)

Southern Pain and Anesthesia
Metairie, Louisiana
Corey W. Hunter, MD (Chapters 46, 49 and 65)

Ainsworth Institute of Pain Management
New York, New York
David Irwin, DO (Chapter 79)

Chief of Pain Medicine
UPMC Hamot Medical Center
Erie, Pennsylvania
Lawrence Kamhi, MD, FIPP (Chapter 19)

Spine and Interventional Pain Management
Warwick, New York
Michael G. Kaplitt, MD, PhD (Chapter 76)

Director of Stereotactic and Functional Neurosurgery and Vice-Chairman for Research
Department of Neurological Surgery
New York, New York
Leonardo Kapural, MD, PhD (Chapters 27 and 36)

Professor of Anesthesiology, Wake Forest University School of Medicine
Carolinas Pain Institute and Center for Clinical Research
Winston-Salem, North Carolina
Farooq Khan (Chapter 54)

Private Practice
Chicago, Illinois
Carolyn Kim, MD (Chapter 6)

New York, New York
Philip S. Kim, MD (Chapter 66)

Medical Director, Center for Interventional Pain Spine LLC
Newark, Delaware
Nebojsa Nick Knezevic, MD, PhD (Chapters 45 and 77)
Director of Anesthesiology Research
Clinical Assistant Professor-University of Illinois, Chicago
Advocate Illinois Masonic Medical Center
Chicago, Illinois
Jeffery Kramer, PhD (Chapter 73)

Spinal Modulation, Menlo Park, California
Department of Pharmacology and Cancer Biology University of Illinois
Peoria, Illinois
Vladimir Kramskiy, MD (Chapter 25)

Director, Ambulatory Recuperative Pain Medicine
Attending, Pain Medicine, Neurology
New York, New York
Mark J. Lema, MD, PhD (Chapter 7)

Professor and Chair of Anesthesiology, Critical Care, and Pain Medicine, Roswell Park Cancer Institute,
State University of New York at Buffalo School of Medicine
Buffalo, New York
Robert Levy MD, PhD (Chapter 73)

Professor of Neurosurgery, College of Medicine-Jacksonville, University of Florida
Jacksonville, Florida
Sean Li, MD (Chapter 68)

Laxmaiah Manchikanti, MD (Chapter 13)

Medical Director, Pain Management Centers, Paducah Kentucky
Clinical Professor of Anesthesiology and Perioperative Medicine, University of Louisville
Louisville, Kentucky
Thabele-Leslie Mazwi, MD (Chapter 2)

Departments of Interventional Neuroradiology and Endovascular Neurosurgery
Massachusetts General Hospital and Harvard Medical School
Neel Mehta, MD (Chapter 69)

Medical Director, Division of Pain Medicine
Assistant Professor of Anesthesiology
New York Presbyterian Hospital
New York, New York
Nagy Mekhail, MD, PhD (Chapter 35)

Cleveland Clinic
Pain Management Department
Cleveland, Ohio
Anya R. Myers, DO (Chapter 61)

Department of Rehabilitation Medicine
Rusk Institute of Rehabilitation Medicine
Jersey City, New Jersey
Samer Narouze, MD, PhD (Chapter 18)

Professor and Chairman
Pain Management Department
Summa Western Reserve Hospitals
Cuyahoga Falls, Ohio
Ricardo A. Nieves, MD, FAAPMR (Sub Pain, Sub Sports Med), FIPP, DABIPP (Chapters 52 and 53)
Colorado Spine, Pain and Sports Medicine, P.C.
Fort Collins, Colorado
Richard B. North, MD (Chapter 70)

Professor of Neurosurgery, Anesthesiology and Critical Care Medicine (ret.)
School of Medicine, John Hopkins University
Brooklandville, Maryland
Daniel Oh, MD (Chapter 2)

Sagar Parikh, MD (Chapter 33)

University Pain Management Center
Somerset, New Jersey
Kiran Patel, MD (Chapter 37)

Attending, Pain Management
Staten Island University Hospital
Staten Island, New York
Vikram B. Patel, MD, FIPP, DABIPP (Chapters 4, 5 21, 22, 23, 31, 34 and 37)
Director, Phoenix Interventional Center for Advanced Learning
Algonquin, Illinois
Sheetal Kerkar Patil, MD (Chapter 26)

Clinical Associate of Anesthesia and Pain Medicine
University of Chicago
Chicago, Illinois
Jason E. Pope, MD (Chapters 35, 67, 73 and 75)

Director, Intrathecal Therapeutics, The Center for Pain Relief, Charleston, West Virginia
Medical Director, Pain Relief Center
Teays Valley, West Virginia
Joshua P. Prager, MD, MS (Chapter 47)

Director, Center for the Rehabiliation of Pain Syndromes (CRPS) at UCLA Medical Plaza
Immediate Past Chair, Complex Regional Pain Syndrome Group of the International Associate for the
Study of Pain (IASP)
Senior Advisor to the Board of the North American Neuromodulation Society (NANS)
Departments of Anesthesiology and Internal Medicine David Geffen School of Medicine at UCLA
Los Angeles, California
Kanishka Rajput MD (Chapter 3)

Senior Resident, Department of Anesthesiology
Medical College of Wisconsin
Milwaukee, Wisconsin
Atiq Rehman, MD (Chapter 39)

Houston Pain Centers
Houston, Texas
Erich O. Richter, MD (Chapter 74)

Department of Neurosurgery
LSU Health Sciences Center, New Orleans
New Orleans, Louisiana
Christine Roque-Dang, DO, FAAPMR (Chapter 50)

Director of Physiatry and Attending Physiatrist
Bergen Medical Associates
Emerson, New Jersey
Dawood Sayed, MD (Chapter 9)

Assistant Professor of Anesthesiology and Pain Medicine The University of Kansas Medical Centre
Kansas City, Kansas
David M. Schultz, MD (Chapter 1)

Founder and Medical Director
Medical Advanced Pain Specialists (MAPS)
Edina, Minnesota
Rinoo V. Shah, MD (Chapters 30, 40, 41, 52 and 53)

Clinical Professor of Anesthesiology
Director, Chronic Pain
LSU Health Science Center
Shreveport, Louisiana
Hariharan Shankar, MD (Chapter 3)

Associate Professor, Department of Anesthesiology
Medical College of Wisconsin
Clement Zablocki VA Medical Center
Milwaukee, Wisconsin
Sanford Silverman, MD (Chapter 20)

Comprehensive Pain Medicine
Immediate Past President, Florida Society of Interventional Pain Physicians (FSIPP)
President-Elect Broward County Medical Association
Pompano Beach, Florida
Clark C. Smith, MD MPH (Chapter 54)

Department of Rehabilitation and Regenerative Medicine Columbia University New York Presbyterian
Hospital
Columbia University Medical School
New York, New York
Howard Smith, MD
Medical Director, Palliative medicine
Academic Director, Pain Management
Albany Medical Center
Albany, New York
Jennifer Solomon, MD (Chapters 50 and 51)

Assistant Professor
Assistant Attending
New York, New York
Nancy Staats, MD (Chapter 11)

Advanced Endoscopy and Surgery Center
Eatontown, New Jersey
Peter S. Staats, MD, MBA (Chapters 41, 46, 68 and 80)
Adjunct Associate Professor
Johns Hopkins University
Department of Anesthesiology and Critical Care Medicine
Michael Stanton-Hicks, MD (Chapter 43)

Staff Institute of Anesthesiology
Department of Pain Medicine
Institute of Neurological Restoration
Shaker Pediatric Rehabilitation Program
Cleveland Clinic
Cleveland, Ohio
Agnes Stogicza, MD (Chapter 48)

Anesthesiologist and Pain Physician
University of Washington
Harborview Medical Center
Seattle, Washington
Anand Thakur, MD (Chapter 80)

Clinical Assistant Professor
Wayne State University School of Medicine
Detroit, Michigan
Z.T. Traeger, DO (Chapter 24)

Department of Rehabilitation Medicine
NYU School of Medicine
Rusk Institute of Rehabilitation Medicine
New York, New York
Cathy D. Trame, RN, MS, CNS, BC (Chapter 10)

Sycamore Pain Management Center
Kettering Health Network
Miamisburg, Ohio
Andrea Trescot, MD, ABIPP, FIPP (Chapters 14, 15, 19, 44, 60, 62 and 79)
Medical Director
Pain and Headache Center
Wasilla, Anchorage, Kenai, Alaska
Amanda Toye, MD (Chapter 27)

Baylor University Medical Center at Dallas
Center for Pain Management
Dallas, Texas
Vijay Vad, MD (Chapter 51)

Assistant Professor
New York, New York
Gerard P. Varlotta, DO, FACSM (Chapters 24 and 61)

Associate Professor, Departments of Orthopaedic Surgery & Rehabilitation Medicine
NYU School of Medicine, Rusk Institute of Rehabilitation Medicine
New York, New York
Elias Veizi MD, PhD (Chapter 71)

Assistant Professor
Division of Pain Medicine
Case Western Reserve University
Pain Medicine & Spine Care
Cleveland Veterans Affairs Medical Center
Cleveland, Ohio
Ricardo Vellejo, MD, PhD (Chapter 39)

Director of Research, Millennium Pain Center
Medical Director, UnityPoint Methodist Comprehensive Pain Center, Peoria, Illinois
Adjunct Professor, Biology Department, Illinois State University, Normal, Illinois
Chief Editor, Techniques in Regional Anesthesia and Pain Management.
Christopher Voscopoulos, MD (Chapter 7)

Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital,
Seth A. Waldman, MD (Chapter 25)

Director, Division of Pain Management
Clinical Assistant Professor, Anesthesiology
Weil Medical College of Cornell University
New York, New York
James Wyss, MD, PT (Chapter 50)

Assistant Attending Physiatrist
Associate Fellowship Director
Physiatry Department
Assistant Professor of Clinical Rehabilitation Medicine
New York, NY
Mark Yelle, MD, PhD (Chapter 36)

Chronic Pain Medicine Center at Wake Forest University Baptist Health and Carolinas Pain Institute
Winston-Salem, North Carolina
Albert J. Yoo, MD (Chapter 2)

Department of Diagnostic Neuroradiology
Preface
The field of interventional pain management is a forever evolving field. There are new developments
occurring daily with new approaches and new equipment that make therapies safer and more effective.
This book gives clinical pearls on strategies that we use in interventional pain management. It has been
designed as an easy-to-use source for most of the interventional pain specialists needs. It is not intended
to replace a comprehensive fellowship in pain management. The pros and cons of medications, the
psychological approaches effective in pain, as well as the comprehensive use of rehabilitation and
complementary approaches are simply not covered. This book, however, does provide the physician with
relevant anatomy and should prompt a thoughtful approach to specific pain syndromes and what causes
them. Many years ago, patients with pain referred to as having “chronic pain syndrome” or sometimes
were maligned with pejorative terms. Patients were called malingerers, assumed to have major
psychiatric disorders or were assumed to be drug seeking. While all of these certainly occur, I believe
patients with legitimate medical problems were frequently misdiagnosed. This occurred because there
was not an adequate training of physicians to diagnose and treat complex pain disorders. To date, many
physicians have inadequate training in recognizing complex medical and neurologic disorders, and many
syndromes are missed.
In previous decades there were a few procedures that were commonly performed. Epidurals, Trigger
points, and major joint injections were common. Complex procedures were rarely performed.
Medications were (and still are) a mainstay of a comprehensive pain practice. While we today still use
these classes of analgesics, we are now recognizing that the medication approach is not without risks. The
use of opiates has increased dramatically over the past twenty years. With this we have seen a dramatic
rise in deaths attributed, at least in part to the use of prescription analgesics. It was estimated that in 2012
there were over 16 thousand deaths with a prescription opioid as at least a part of the problem.
Pain management is not just about giving a patient drugs. It is about making an accurate diagnosis,
developing a therapeutic plan, and devising a minimally invasive approach when possible to effectively
treat or manage the problem. The Diwan–Staats Atlas puts together what we know about various pain
states, along with the most current information in anatomy and pathophysiology. We concentrate on the
most minimally invasive techniques available, thereby enhancing safety. This book is really the “how to”
of current interventional pain management; however, it does not address the ”when to.” The “when to”
involves clinical judgment, careful evaluation, and individual case-specific issues, along with evidence-
based medicine and an assessment of the risks, benefits, and alternatives of all interventional procedures.
Summarizing all the available clinical trials would have been beyond the scope of a single volume.
There are so many leaders and influential figures that have helped the development of this field. Dr.
Bonica, Dr. Stanton Hicks, Dr. Gabor Racz, Dr. Prithvi Raj, and Dr. Lax Manchikanti are a few who have
devoted so much of their life to advancing the specialty of interventional pain. On behalf of the millions of
pain sufferers and the physicians you have taught, we thank you.
We would like to express our deep appreciation to so many individuals. First, we must thank the section
editors, Drs. Lema, Patel, Trescot, Vad, Gharibo, and Shah who have gone above and beyond, reviewing
and re-reviewing the chapters. Thank you to our numerous authors who have created such wonderful
original works. The synthesis of all of your works has made this volume special.
With all of the talk about evidence-based medicine, and the needs for multiple randomized controlled
trials to support reimbursement, and the battles in the halls of Congress, and the battles with insurers, we
sincerely hope that this book will help physicians help patients, as safely and effectively as possible.
That’s why we all do what we do.
Introduction
EVIDENCE-BASED MEDICINE
Peter S. Staats and Sudhir Diwan
“Doctors are men who give drugs of which they know little, into bodies of which they know less, for
diseases of which they know nothing at all.” Voltaire 1770s
For thousands of years, however, physicians blithely administered a variety of concoctions intended to
treat pain; a few worked, many eventually fell by the wayside; and others were reluctantly abandoned
when they failed to stand up to rigorous therapeutic analysis. Thus, although healers throughout antiquity
accurately touted the efficacy of opium, now known to contain the potent analgesic morphine, and of
willow bark, which is the source for aspirin, dusty tomes also contain scores of therapeutic
recommendations that have little merit in the management of pain.
The Skillful Physician, the mainstay of seventeenth-century medicine, unequivocally recommends
applying hot goose oil to treat sciatica.
The Concept
Evidence-based medicine, the concept that physicians should use the best available data to guide ones
practice, has become the mainstay in modern medicine. Comparative effectiveness research, comparing
two accepted strategies to determine which therapies are the most effective, is widely being considered
the standard.
The Flaws and Frustrations

While no one can argue that physicians should use the best “available data to guide the practice,” the
concept is now being misinterpreted and distorted largely by insurers and other carriers to deny
appropriate care. Years ago, the same week the media reported the CEO of a major health care insurance
company’s compensation package of over a billion dollars, one of the authors (PSS) was called to
emergently evaluate a patient (with previous back surgery in the ICU) with a lumbosacral radiculopathy
with this insurance. The request was specifically for an epidural lysis of adhesions procedure. After a
thorough evaluation it was felt to be a reasonable approach, and the procedure was performed
successfully. The next day his pain was under control for the first time in weeks, we facilitated discharge,
there was great patient and hospital satisfaction and, we succeeded in saving the insurance company
money since he was discharged from the hospital. The insurance company never paid for this procedure
and claimed that the therapy offered was experimental. This was in spite of four double-blind randomized
controlled trials demonstrating the efficacy of this therapy. The denial was appealed which was reviewed
by the insurance company’s “appeal committee” that included three physicians: a gynecologist, a
neurologist, and a general surgeon. None of whom had heard of an epidural lysis of adhesions procedure.
Not surprisingly the committee upheld the denial of the insurance carrier, indicating that there was no
“evidenced-based medicine” supporting the claim. Of course, this was patently untrue, but does highlight
several problems that can occur with evidence-based medicine if they are not judiciously applied.
Problems With Evidence-Based Medicine
• EBM is limited to clinical research only, and does not correlate well to the clinical expertise.
• It presents a “cookbook” approach to practice medicine.
• The clinical evidence should be a source of information, not a replacement of individual clinical
expertise.
• Insurance industry uses this concept as a cost-effective (cost-cutting) tool, and ignores patient’s
values and preferences.
• It promotes a state of mind that is analogous to ivory-tower, whereby the insurers define the care
path.
• Continued concern of EBM being hijacked by purchasers and insurance managers to cut costs.
Many physicians have received similar frustrating denials from insurance companies claiming the
procedures or medications being offered are experimental. We receive these denials with discography,
epidural steroids, therapeutic occipital nerve blocks, radiofrequency ablations of facet joints, spinal cord
stimulation to name a few, claiming that each of the above is “experimental.” It became clear that the
insurers are using the rationale of “no evidence-based medicine” to selectively deny high-cost
procedures, or procedures insurers have felt have been abused.
Conflicts With Common Sense

• Quantitative research from randomized controlled trials (RCTs) may not be relevant to all
treatments in all situations.
• The EBM is a slow, lengthy, and expensive process that will take years before the evidence is
produced and applied to the clinical practice.
• RCTs may restrict under-researched racial minorities and patients with comorbid diseases from
practice of EBM.
• RCTs apply to only the group of people that are included in the studies, and do not address the
individualized treatment plans based on physicians’ personal experience and knowledge.
Historical Perspective on Evidence-Based Practice

• In the 1960s, there were very few double-blind randomized controlled trials demonstrating efficacy
of any number of therapies.
• Medical decisions were largely made on the basis of clinical intuition pathophysiology and clinical
experience.
• There were few large studies, and the results of large clinical trials were rarely used to modify or
change clinical practice paradigms.
• In the 1990s, physicians began to realize that that a higher standard was required. Evidence-based
medicine and evidence-based practice were born.
What Is Evidence-Based Medicine?

Evidence-based practice is “the conscientious, explicit and judicious use of current best evidence in
making decisions about the care of the individual patient. It means integrating individual clinical expertise
with the best available external clinical evidence from systematic research.” (Sackett D, 1996)
• Evidence-based medicine and guidelines that use evidence-based medicine are involved in
synthesizing the available published data to come up with the most effective approach to care.
• The available data is graded in a hierarchal fashion.
• Large double-blind randomized controlled trials receive the highest grade, followed by
prospective studies and retrospective reviews and even case reports and opinions of experts are
graded.
• If an approach has a large number of well-designed randomized controlled trials supporting its use,
the approach is given a high grade.
• If there are no well-designed trials, and the physician’s experience is touted as the only rationale
for proceeding with a therapy, a low grade is given.
Source and Synthesis of Evidence

• Basic science studies on and animal research: Very first step to produce evidence.
• Case reports and case series: Reports of treatment of individual cases or case series without
control groups, with a little statistical validity.
• Case-control studies: Studies with a specific condition are compared with people without the
condition. These studies are less reliable than randomized controlled trials and cohort studies.
• Cohort studies: A group of patients treated with a particular treatment and followed for an extended
period, and then compared their outcomes with a similar group that has not been treated with the
similar treatment.
• Randomized controlled trials: Carefully planned methodologies to randomize and blind the
researcher and the patient to reduce a potential bias while comparing the interventional (treated)
and control (untreated) groups. These studies provide the best evidence with high statistical
validity.
• Systemic reviews: An extensive literature search is conducted to identify studies with sound
methodology focused on a specific treatment or procedure. The studies are reviewed for quality
and results are summarized based on predetermined criteria.
• Meta-analysis: It is a large study to mathematically combine results of a number of very valid
studies that have used accepted standards of statistical methodology.
Levels of Evidence
United States Preventive Services Task Force (USPSTF) has developed systems to stratify evidence by
its quality for ranking evidence about the effectiveness of the treatment:
• Level I: Evidence obtained from at least one properly designed randomized controlled trials
• Level II-1: Evidence obtained form well-designed controlled trials without randomization
• Level II -2: Evidence obtained from well-designed multicenter cohort or case-control analysis
• Level II-3: Evidence obtained from multiple studies with or without intervention including
uncontrolled trials
• Level III: Opinions of respected authorities, based on clinical experience, descriptive studies, or
reports of expert committees
Levels of Recommendations
The risks versus benefits ratio obtained from the evidence available in literature, USPSTF uses following
levels of recommendations for clinical service or treatments.
• Level A: Good scientific evidence to suggest substantial benefits outweigh the potential risks
• Level B: Fair scientific evidence to suggest the clinical benefits outweigh the potential risks
• Level C: Fair evidence to suggest clinical benefits, but the ratio of benefits to risks is too close to
make recommendations
• Level D: Fair scientific evidence to suggest that risks of clinical service clearly outweigh the
potential benefits
• Level I: The scientific evidence is either lacking, or poor quality, or conflicting to assess the risks
of clinical service to potential benefits
Problems With Evidence-Based Medicine (EBM)

There are several problems with using evidence-based medicine to guide all care in pain management or
the development of guidelines. Frequently studies are funded by industry, either pharmaceutical or
medical device companies. Those are the companies with the money to spend on demonstrating the
efficacy of large clinical trials. These studies may have potential conflict of interest, but there is no
funding otherwise to conduct studies.
• There is a shortage of coherent and consistent scientific studies to produce evidence.
• The insurance companies obtain the evidence to their advantage from nonindexed journals with
non–peer-reviewed articles, and ignore the good evidence published in indexed journals.
• The evidence is often reviewed by the physicians who do not have hands-on experience of
particular procedures, eg, a neurologist who never performed an epidural steroid injection, writing
the guidelines for epidural steroid injections based on evidence.
• The poorly written guidelines produced by the “so-called” experts with vested produce barriers to
the practice of high-quality medicine.
Expensive Proposition
Double-blind randomized controlled trials are widely considered the gold standard for study design. The
paucity of evidence is largely due to paucity of good studies, and the cost is a big factor.
• New drug applications for the FDA require multiple studies.
• It has been estimated cost close to a billion dollars to get a new drug approved through the FDA.
• Each study costs millions to perform.
• For this reason, many well-designed studies do not come from physicians as sponsors, looking at
old drugs or new approaches to pain.
Companies with significant financial resources, that stand to make financial gain if their drug or
product is successful, are motivated to fund large-scale clinical trials to demonstrate efficacy of their
product. Older inexpensive drugs, that may be off patent, may be just as effective as a new drug but will
not be studied in large-scale clinical trials and will be given a low score in an EBM approach.
Different Standards
Limitations for Studies Regarding Interventional Procedures
• Physicians do not have the financial wherewithal to pay for the studies requested by the insurers.
• Few physicians have the time and expertise to apply for federal funding to perform these studies.
• Infrequently performed procedures may be cost effective (ie, thoracic epidurals) but have no
medical device company funding the studies. There will be a paucity of data supporting their use.
• For these reasons, many insurers are denying interventional procedures under the guise of
“evidence-based medicine.”
• Different standards: They site lack of randomized double-blind controlled trials as a rationale for
noncoverage, but allow surgical procedures that have not been subjected to the same rigor as many
of the interventional therapies discussed in this book.
Our perspective is that there has been an explosive growth in our field, associated with abuse. We as
a society and the payers, need to establish reasonable reimbursement criteria and follow those with poor
outcome, not to blanketly deny care.
Many Intricacies in Doing the Procedures

If one does not do the procedure exactly the same as another, there will be inconsistencies and results
will vary. For example, the difficulty in determining the efficacy of epidural steroids will be influenced
by the following factors.
• Blind procedures versus fluoroscopically guided procedures.
• Transforaminal versus Interlaminar.
• Cervical epidurals versus thoracic epidurals.
• The quality of pain may vary.
• The severity of the pain may be poorly controlled for.
• Coexisting diseases such as obesity or diabetes may influence the outcome.
• The doses and types of steroids may vary between practitioners.
• The technique may vary on precisely where the needle is placed.
• The use or amount of local anesthetics used may vary greatly.
Level of Skills and Experience

Inexperienced physicians may perform a procedure under fluoro guidance but may not have the same
expertise in guiding the needle to the exact position as well-experienced physician who has spent years
perfecting this approach. Thus taking one very simple examples one can see that physicians outcomes
would be expected to vary greatly. Some physicians routinely do one procedure while others do a series
of injections.
Varieties in Indications for Procedures

The indications may vary for a variety of techniques being performed for patients with:
• Herniated disc versus stenosis.
• Radiculopathy versus axial back pain.
• Epidural steroids may be used for CRPS, radiculopathy, or postherpetic neuralgia.
• Difference in rates of traditional insurance versus workman’s compensation.
Accordingly many small studies may not represent the exact patient population being studied. While it
is important for the physician to remain conversant with the literature, it is important to continually
individualize the therapy for that specific case.
Comparative Effectiveness Research

Comparative effectiveness research (CER) is the direct comparison of existing health care interventions
to determine:
• Which treatment works best for which patients
• Which treatment poses the greatest benefits and harms
• The core question of CER in which treatment works best, for whom, and under what circumstances
It is more of a pragmatic approach that attempts to compare a variety of reasonable interventions in
determining the most appropriate strategy.
Cost-Effectiveness Analysis
Cost-effectiveness analysis (CEA) is a form of economic analysis that compares the relative costs and
outcomes (effects) of two or more courses of action. CEA is distinct from cost-benefit analysis, which
assigns a monetary value to the measure of effect. CEA is often used in the field of health services, where
it may be inappropriate to monetize health effect.
Guideline Development
Guidelines on the appropriate steps in the management of various diseases have become a useful tool for
physicians.
• The guidelines synthesize the evidence-based medicine, the well-designed studies that have been
done.
• More studies on a particular therapy or drug it is more likely to receive a favorable position in the
guideline development.
• Guidelines which attempt to synthesize evidence-based medicine in to clinical paradigms, count the
number of evidence-based studies, and make recommendations based on the total number of
patients and number of studies in the literature.
• Those with better financial resources may increase the total number of studies that will lead to a
pharmaceutical or medical device approach. This type of weighted research will favor more
expensive therapies that are frequently funded by pharmaceuticals and medical device companies.
• The guideline development itself may be insidiously influenced by medical device and
pharmaceutical companies as they tend to fund those guidelines that support their development.
• Some insurers have begun funding the development of guidelines, and they tend to weigh more
heavily noninterventional therapies, in spite of a demonstrated lack of efficacy.
Conclusions
This text is an atlas of interventional pain medicine. We espouse Sackets original tenets, of using the best
available evidence, as well as those of Hippocrates to do no harm. We recognize that the practice of
medicine takes an individual approach to the management of pain. We do believe that a rationale
physician, when faced with limited data, may try therapies that make sense. The text that follows is more
of a “how to” approach. The denial of appropriate care by insurers when there is a paucity of date on a
specific approach, indicating that there is no evidence-based medicine flies in the face of what evidence-
based medicine is about. Evidenced-based medicine allows the physician to understand the literature, its
pitfalls, and extrapolate based on their clinical experience in determining the most appropriate course of
action.
Suggested Reading
Agency for health care policy and research. http://www.ahrq.gov/clinic/ptsafety/chap3.htm.
Evidence-based medicine—Wikipedia, the free encyclopedia.
Sackett D. Evidence-based medicine: what it is and what it isn’t. BMJ. 1996;312:71-72.
http://www.bmj.com/cgi/content/full/312/7023/71.
Staats PS. Introduction. In: Aronoff G, ed. The Pharmacologic Management of Pain Task Force Ratings.
http://www.ahrq.gov/clinic/3rduspstf/tating.htm.
SECTION I
BASIC APPLICATIONS
CHAPTER 1
Fluoroscopy in Interventional Pain Medicine

David M. Schultz
Since their discovery in 1895, x-rays have revolutionized the practice of medicine. By allowing doctors
to view the inside of the living body, x-rays have greatly increased our ability to diagnose and treat
disease and to precisely deliver targeted therapies. The fluoroscope was the first x-ray machine and has
evolved from its humble beginnings into a powerful and sophisticated device that has become the basis
for the new field of interventional pain management. Modern fluoroscopes enable the interventional pain
practitioner to use continuous, real-time x-ray imaging to guide interventional procedures that target the
physical generators of pain with a high degree of precision and safety. Since fluoroscopy is essential for
most invasive pain procedures, it is imperative that interventional pain physicians have a firm
understanding of the fluoroscope in order to use it safely and effectively in daily practice.
HIGHLIGHTS IN THE HISTORY OF FLUOROSCOPY

• 1895: German physicist Wilhelm Roentgen discovers x-rays and takes the first fluoroscopic image,
purportedly of his wife’s hand, winning the 1903 Nobel Prize in Physics for his efforts.
• 1896: Thomas Edison invents the first fluoroscope, which is quickly adopted for medical uses.
• 1897: Madame Curie discovers radium, which is then used to illuminate games of chance in New York
City.
• 1898: The inappropriate, nonmedical use of fluoroscopy becomes increasingly common.
• 1899: Compensation is awarded in the first medical malpractice suit involving x-ray injury.
• 1900: Radiation injuries become increasingly common, and practitioners become increasingly aware
of the dangers of x-ray exposure.
• 1910: After several years of practice, radiology pioneer Dr. Mihran Kassabian suffers severe radiation
burns to his hands and ultimately dies of radiation-induced cancer at age 34.
• 1929: The National Council on Radiation Protection and Measurement (NCRP) is created to protect
patients, healthcare workers, and the public from the harmful effects of radiation.
• 1994: Patient injuries resulting from excessive use of fluoroscopy during medical procedures prompt
the FDA to issue a Public Health Advisory.1
THE PHYSICS OF X-RAYS
X-rays are a form of ionizing radiation that can be created in the fluoroscope and harnessed for medical
imaging. X-rays are produced in the x-ray tube of the fluoroscope, which contains a cathode and metal
anode.
• When high-velocity electrons leave the cathode and collide with the metal anode, the kinetic energy
contained within the electrons is converted to electromagnetic energy and released in the form of x-
rays.
• X-rays are close to light photons on the electromagnetic spectrum but have shorter wavelength and
higher energy (Figure 1-1).
Figure 1-1. X-rays are close to light photons on the electromagnetic spectrum but have shorter
wavelength and higher energy.
The x-rays produced by the x-ray tube are directed through body tissues. When these x-rays contact
matter, they interact in one of three ways:
1. They are absorbed.
2. They are deflected and scattered.
3. They pass through matter unheeded.
Since x-rays are a form of ionizing radiation, they interact with certain media in ways that allow the
human eye to view their presence. In fluoroscopy, the x-rays cause the phosphorous in a fluorescent
screen to emit visible light. Modern fluoroscopic systems use zinc-cadmium sulfide as an effective
phosphor.
The fluoroscopic image is essentially composed of shadows created as body tissues of various
densities preferentially absorb x-rays. As the density of matter increases, x-rays are absorbed or scattered
to a greater extent, giving rise to the 5 radiologic densities commonly used to describe radiographs:
1. Air
2. Fat
3. Water (soft tissue)
4. Bone
5. Metal
Air allows most emitted x-rays to penetrate through to the underlying imaging medium. Bone and metal
are denser and absorb or deflect x-rays, allowing fewer x-rays to penetrate through to the imaging
medium. Consequently, higher-density tissues cast shadows that appear darker on the displayed image
because the x-rays contacting the phosphor create light (Figure 1-2). This is in contrast with traditional x-
ray imaging, which uses a photographic plate to capture the effects of photons (Figure 1-3). The plate
starts out as a white background that is exposed by the x-rays reaching it. The fluoroscopic image is
analogous to the photographic negative whereas the developed x-ray film is analogous to the photograph.
Figure 1-2. Fluoroscopic image with higher density structures appearing darker; note the bubbles of air
contained within the injected x-ray contrast medium.
Figure 1-3. Plain chest radiograph with denser tissues appearing lighter. (Reprinted with permission from
Fuster V, Walsh RA, Harrington RA: Hurst’s The Heart, 13th Edition: www.accessmedicine.com © The
McGraw-Hill Companies, Inc. All rights reserved.)
THE C-ARM FLUOROSCOPE

The primary function of the fluoroscope is to generate a controllable beam of x-rays that can be directed
through tissue and then captured on a viewing medium to form a visible image. Interventional pain
physicians commonly use the C-arm fluoroscope because of its maneuverability and compact design
(Figure 1-4).
Figure 1-4. Modern fluoroscope with a shielded x-ray tube contained within a movable C-arm.
The main components of a typical mobile C-arm fluoroscope include the x-ray generator, x-ray tube,
collimator, image intensifier, optical coupling chain and viewing monitor (Figure 1-5).
Figure 1-5. Modern fluoroscope with components labeled.
The x-ray generator converts alternating current to high voltage direct current, which is delivered to
the x-ray tube.
• The current determines the number of x-rays produced by the x-ray tube and therefore controls the
density and intensity of the x-ray beam.
• The voltage determines the energy of the x-rays produced and the penetrating ability of the x-ray
beam.
• The current and voltage can be automatically or manually adjusted from the base unit of the
fluoroscope (Figure 1-6).
Figure 1-6. The amount of current supplied to the x-ray tube is measured in milliamps (mA) and
determines the density and intensity of the x-ray beam.
The x-ray tube is housed in one end of the C-arm and is balanced by the image intensifier at the other
end.
• The beam that is released from the x-ray tube diverges as it moves toward the image intensifier.
• The x-ray beam is most concentrated as it exits the x-ray tube at the center point aperture.
• Severe patient injuries occur when body tissue remains in close proximity to the origin of the x-ray
beam for prolonged periods.2
Fluoroscopic images are dim and difficult to view without some mechanism to brighten the viewable
image. The image intensifier was introduced in 1934 and functions to convert x-rays into light photons,
which amplify brightness by 5000 to 20,000-fold.
Collimation allows the fluoroscope operator to reduce the size and shape of the x-ray beam to better
conform to the field of view (Figures 1-7 and 1-8). As the fluoroscope moves across areas of varying
body tissue density, the collimator automatically adjusts the x-ray beam to conform to the viewing field.
The operator can also adjust the collimation window manually to conform to a region of clinical interest
(Figure 1-9).
• By reducing the x-ray beam to include only the tissue targeted for viewing, less tissue is irradiated, and
patient exposure to radiation is reduced. In addition, there is less scattered radiation exposure to
personnel in the room.
• Unattenuated x-rays also cause glare on the image screen resulting in poor image quality. Collimation
reduces glare and improves the clarity of the image.
Figure 1-7. Without collimation, the x-ray beam is not optimized to fit the field of view, and there is a
large amount of scattered radiation from the patient and table as well as a monitor image that is relatively
degraded.
Figure 1-8. By using collimation, the x-ray beam is shaped to better fit the field of view resulting in
fewer x-rays leaving the x-ray tube, less scatter radiation, and a clearer image on the monitor.
Figure 1-9. Controls for both radial (iris) and rectangular collimation on a typical C-arm fluoroscope.
To process the images that have been brightened by the image intensifier for optimal viewing, modern
fluoroscopic systems incorporate optical coupling chains that route the image signal to a video camera.
Optical coupling enables the x-ray image to be viewed via closed-circuit television, displaying real-
time video imaging of continuous fluoroscopy.
A typical mobile C-arm fluoroscope can also display simultaneous static images on a second television
monitor for viewing of the last image in a video sequence. This “last image hold” capability allows the
interventionalist to minimize radiation exposure by performing procedures that utilize a series of static
images to follow needle placement.
Using digital image conversion technology, analogue video signals are digitized and stored in computer
memory. Using less radiation, subsequent digital enhancement of the fluoroscopic image can achieve
image clarity approaching that of x-ray film. Digital images can also be quickly and conveniently
distributed via computer networks and stored on computer workstations or archived into various digital
storage media for later retrieval.
Since materials of differing density cause x-rays to be absorbed or deflected to varying degrees,
fluoroscopy table and pad materials with high or inconsistent density can result in poor image quality.
• Denser materials in table and pad attenuate x-rays, which will result in increased patient radiation
exposure and loss of image contrast.
• Materials that are inconsistent in density tend to cast artifactual shadows on the imaging screen.
It is therefore imperative to use only x-ray tables and pads designed to optimize fluoroscopic imaging.
Newer composite materials such as carbon fiber in fluoroscopy tables provide adequate strength to
support large patients while minimizing x-ray attenuation and distortion. Likewise, thin foam pads
overlying the table have minimal effect on x-rays, but large gel supports or irregularly folded pillows may
create significant x-ray attenuation, distortion, and artifact. A diving-board table configuration allows for
easier imaging of upper body structures during interventional pain procedures.
RADIATION SAFETY
Exposure to ionizing radiation—including x-rays—can result in the formation of free radicals that cause
damage to cell structures.
• Chemical chain reactions may trigger changes in cell membrane permeability, resulting in cellular
dysfunction.
• Damage to DNA may cause somatic mutations, causing harm to subsequent generations.
• Radiation protection standards are designed to prevent unintended radiation and to maintain exposure
for therapeutic purposes “As Low As is Reasonably Achievable” (ALARA).
Dosimetry badges are solid-state radiation detection devices used to measure cumulative radiation
dose. For optimal monitoring, two badges are worn, one inside and one outside of a protective lead
apron, to determine both overall exposure and the efficacy of the lead apron protection.
• Badges are analyzed on a monthly basis and allow for monitoring of cumulative radiation exposure.
• Current occupational exposure recommendations set the upper effective dose equivalent of 50 mSv/y
(5 rem/y) and a cumulative dose not to exceed 10 mSv (1 rem) times the age of the worker. Thus,
lifetime exposure for a 50-year-old radiation worker would be 500 mSv (50 rem).
Modern x-rays are completed within milliseconds, and typical radiation exposure is a small fraction of
what it was 100 years ago; however, prolonged patient exposures to x-rays may occur as increasingly
complex procedures are performed using continuous fluoroscopy.
More than 50 reports of patient injury from prolonged exposure to x-rays during fluoroscopic
procedures occurred in 1994 alone, resulting in the health advisory issued by the Food and Drug
Administration.1
• Several reports of serious patient injuries from radiation during fluoroscopy have been recently
published.3,4
• Recognition of patient injury from fluoroscopy is often delayed, since the effects of excessive radiation
exposure are usually not immediately apparent.
• Fluoroscopy injuries documented in the past 20 years have included skin burns serious enough to
require skin grafting.
• Since reporting of fluoroscopy injury is not mandatory, the actual extent of this problem is unknown.
Occupational radiation exposure can be reduced to as low as is reasonably achievable through
adherence to 3 basic principles:
• Reduce exposure time.
• Increase the distance from the radiation source.
• Shield yourself and your patient from direct and scattered radiation.
The longer one is exposed to a radiation field, the greater the total radiation dose. Thus, limiting time of
exposure is a simple, common-sense method for reducing risk.
• With modern fluoroscopic systems, a short burst of radiation used with “last image hold” capability
allows the operator to identify needle position with minimal x-ray exposure time.
• This technique allows the interventionalist to take a fluoroscopic “snapshot” of the field, hold the static
image on the monitor, move the needle a small distance toward the target, and then obtain another brief
fluoroscopic image to determine the next needle position.
• A recent study found the average time required for needle placement during various interventional pain
procedures was 7.7 seconds, which is quite low compared to other dosimetry-measured radiation
exposure times in other medical specialties using fluoroscopy.5
Based on the inverse square law, the amount of radiation exposure is proportional to the inverse square
of the distance from the source.
• Therefore, the amount of radiation exposure declines exponentially as the operator moves away from
the source.
• With fluoroscopy, distances of 6 ft or more from the x-ray tube, and from scatter radiation coming off
the patient and table, result in minimal radiation exposure.
Lead aprons are mandatory, and thyroid shields are recommended, as standard garb within the
procedure room during fluoroscopy (Figure 1-10).
• Lead shielding can be tailored to body contours and made reasonably comfortable while providing an
effective barrier to radiation exposure especially to the thyroid and pelvis.
• A wide variety of lead glass screens can be placed between the operator and the x-ray source and/or
patient in order to reduce direct and scatter radiation exposure, respectively.
• The interventional procedure room can be configured with leaded glass screens that are attached to
ceiling mounts or used with rolling frames on the floor to fit a particular space.
• Leaded glass lenses offer an effective barrier to eye exposure and can be configured with optical
correction; however, they may be heavy and uncomfortable. Regular glass lenses also afford some
protection and other alternative materials for eye protection are becoming available (Figure 1-10).
Figure 1-10. Radiation protection with lead apron, glasses, and screen.
Some experts have advocated the use of leaded gloves in order to reduce hand exposure to x-rays
during fluoroscopic procedures.
• With lead gloves, there is less chance of hand exposure to scattered x-rays.
• However, the increased density of lead gloves placed within the x-ray field will cause the fluoroscope
to increase output as it tries to penetrate the high-density lead.
• Therefore, leaded gloves within the field of view of the monitor will cause an automatic increase in
direct and scattered radiation.
• Lead gloves are also expensive and may decrease the tactile sensation, hindering safe and accurate
needle placement.
• Keeping hands completely out of the beam is advisable with or without lead gloves.
SUMMARY
The fluoroscope has revolutionized the treatment of chronic pain. For optimal safe and effective use, the
pain specialist physician should have an in-depth understanding of fluoroscopy and the fluoroscope to
accurately diagnose and treat the physical generators of pain. Skill with the fluoroscope combined with
needle placement skills and an understanding of the anatomy and pathophysiology of chronic pain will
allow the interventional pain specialist to help patients with chronic pain more effectively than ever
before possible.
References
FDA Public Health Advisory. Avoidance of serious x-ray induced skin injuries to patients during
fluoroscopically guided procedures. Rockville, MD: Food and Drug Administration, September 9,
1994.
Wong L, Rehm J. Radiation injury from a fluoroscopic procedure. N Engl J Med. 2004;350:e23.
Sovik E, Klow NE, Hellesnes J, Lykke J. Radiation-induced skin injury after percutaneous transluminal
coronary angioplasty: case report. Acta Radiol. 1996;37:305-306.
Knautz MA, Abele DC, Reynolds TL. Radiodermatitis after transjugular intrahepatic portosystemic shunt.
South Med J. 1997;90:352-356.
Manchikanti L, Cash KA, Moss TL, Pampati V. Radiation exposure to the physician in interventional pain
management. Pain Physician. 2002;5:385-393.
CHAPTER 2
Computed Tomography Guidance in Pain

Management
Ronil V. Chandra, Thabele-Leslie Mazwi, Daniel Oh, Albert J. Yoo, and Joshua A.
Hirsch
INTRODUCTION
• Computed tomography (CT) creates an image of the body by reconstructing image slices from a series
of x-ray projections acquired as the patient is moved through the center of the CT scanner. The CT
scanner is able to measure the attenuation of the x-ray beam by the various tissues along each
projection. The spatial localization of these tissues is then determined using mathematical algorithms.
• The CT image is then displayed as a matrix of x-ray attenuation values using a reference scale
(Hounsfield units [HU]) relative to water; water is assigned a value of 0 HU on all scanners. On this
scale, air measures approximately −1000 HU and dense cortical bone approximately +1000 HU.
• A CT image can be displayed as different shades of grey by appropriately choosing the display
parameters.
• All current CT scanners offer multi-detector technology (multiple CT slices can be obtained in one
rotation of the gantry) and enable isotropic acquisition (ie, spatial resolution is equal in x, y, and z
planes) with volumetric multi-planar image reconstruction.
ADVANTAGES OF CT GUIDANCE FOR INTERVENTIONAL

PROCEDURES
Anatomical Detail
• Soft tissue structures such as nerve roots and bony constraints including severe scoliosis or large
osteophytes are accurately defined (Figure 2-1). Particularly useful for nerve root or epidural
injections in patients with advanced degenerative disease or previous surgery.
• Important neurovascular structures are visualized in real time (eg, avoidance of the vertebral artery in
cervical nerve root blocks).
• Allows precise needle localization for very small targets.
• Avoids inadvertent transgression of nontarget tissue compartments (Figure 2-2).
Figure 2-1. CT-guided facet joint injection. (A) Axial prone CT clearly identifies large facet joint
osteophytes (arrow) that would make intra-articular needle position difficult to achieve under
fluoroscopic guidance. (B) CT guidance facilitates accurate targeting of the narrowed articular space, and
intra-articular position (arrow) is achieved.
Figure 2-2. CT-guided acetabuloplasty for metastasis. (A) Axial CT clearly identifies soft tissue mass
(black arrow) in anterior column of acetabulum, with narrow needle window (dotted line) between
common femoral vessels (red arrow) and intra-abdominal compartment (star). (B) CT guidance allows
accurate needle placement without injury to neurovascular bundle nor transgression of nontarget
compartments. (C) In spite of the focal areas of cortical breach in the acetabular cortex (black arrow),
careful injection of Polymethylmethacrylate (PMMA; red arrow) under CT guidance allows delivery
without intra-articular extravasation.
Needle Placement
• Unlike fluoroscopy, which is hindered by tissue overlap, multi-planar reformats allow three
dimensional trajectory planning.
• Direct visualization allows accurate needle placement with respect to the target nervous structure
without use of contrast media.
• If required, the expected spread of injectate can be determined by injection of a small amount of
contrast media (Figure 2-3). This is useful for epidural injections where inadvertent intrathecal needle
tip position is clearly recognized by injection of contrast media.1
Figure 2-3. CT-guided celiac plexus blockade. Axial prone CT clearly identifies needle position adjacent
to the aorta during bilateral transcrural approach. Injection of a small amount of contrast reveals expected
spread of final injectate.
DISADVANTAGES OF CT GUIDANCE
• Generally more time consuming than fluoroscopic approach.
• May have greater radiation dose to patient and practitioner compared to fluoroscopy depending on
techniques used.
• Requires further expertise—an understanding of CT imaging, normal CT anatomy, and pathology.
• Less accessible modality, typically located in radiology departments.
• Requires further trained personnel—CT technologists.
PREOPERATIVE CONSIDERATIONS
• Patient positioning
For ideal needle trajectory
The simplest needle trajectory to achieve accurately is perpendicular to the floor—take
advantage of oblique prone positioning if possible (Figure 2-4).
Ideally, the entire needle trajectory should lie in one axial CT image—this can be facilitated by
angling the CT machine gantry (Figures 2-5 and 2-6).
Note that positioning in the lateral decubitus or oblique prone position alters the position of the
diaphragm, which can facilitate retroperitoneal needle access without transgressing the pleural
space.
Figure 2-4. Oblique prone positioning to facilitate easier needle placement during acetabuloplasty. (A)
Axial prone CT during planning reveals lucent mass in the posterior column of the acetabulum. With
prone positioning, an oblique needle trajectory (dotted line) is required. (B) With oblique prone imaging
a needle trajectory perpendicular to the floor (dotted line) is obtained, which is easier and less time
consuming to achieve. (C) Imaging with 11-gauge needle in place, prior to cortical entry. (D)
Postprocedure CT after PMMA injection (red arrow) and removal of needle, with no leakage into the hip
joint (black arrow).
Figure 2-5. The angled gantry approach. (A) The traditional CT gantry position is perpendicular to the
CT table. (B) Angling the CT gantry along the line of an angled needle trajectory allows the entire needle
trajectory to remain along a single CT slice.
Figure 2-6. CT-guided pelvic collection drainage using angled gantry approach. (A) Axial CT clearly
identifies pelvic collection (dotted lines) but without clear needle access. (B) Tilting the CT gantry and
repeat imaging identify a safe angled direct needle trajectory. (C) Pigtail drain tube successfully placed
into pelvic collection.
To maximize patient comfort

Maximizing patient comfort prior to commencing the procedure minimizes patient motion during
needle placement.
The prone position is well tolerated with pillows under the chest, hips, and ankles.
Further pillows, wedges, or towels may be necessary to achieve a comfortable oblique prone
position.
• Needle entry planning
Once the patient is positioned, a skin grid marker is placed over the target entry site.
An initial radiographic CT scout image is acquired to delineate the superior and inferior extent of
the planning CT scan.
An initial planning CT scan is performed to define the needle entry site, using the skin grid markers
(Figure 2-7).
The trajectory is planned, taking into account anatomical limitations.
The needle entry site is marked on the patient’s skin, the skin grid is removed, the site is prepped
with antiseptic solution, and the patient is draped appropriately.
If available, a monitor in the CT room should have the needle trajectory available as a reference
image to facilitate needle placement.
Figure 2-7. Use of skin grid to mark skin entry position. (A) Photograph of patient positioned prone
oblique on CT table, with skin grid placed (arrow), and laser light used to mark entry position. (B)
Corresponding CT image with skin grid markers (arrow) to guide needle trajectory into acetabular mass
(star).
INTRAOPERATIVE TECHNICAL STEPS

• Local anesthetic is injected at the skin entry marker site.
• It may be helpful to leave the local anesthetic needle in place along the planned needle trajectory for
subsequent confirmation by CT scanning.
• Infiltrate local anesthetic along the planned needle trajectory.
A 22G spinal needle can be used to infiltrate deeply and into the periosteum if entering a bony
target.
• As the definitive needle is placed, the needle position and trajectory should be verified with
intermittent CT imaging.
Intermittent CT imaging needs to define the entire needle course and needle tip.
The needle tip can be verified by the identification of the bevel on the needle tip or the presence of
a black shadowing artifact. Ensure adjacent CT images above and below are reviewed (Figures 2-
8 and 2-9).
If using an angled approach in the superior-inferior direction, more frequent CT imaging is
recommended.
Figure 2-8. Demonstration of needle tip. (A) Axial CT during localization of local anesthetic needle
reveals shadowing artifact arising from the tip, confirming identification of the needle tip. (B) With
placement of the larger 11-gauge needle, a larger shadowing should be expected. The identification of the
bevel of the needle tip is the most accurate method to localize the needle tip.
Figure 2-9. Demonstration of needle tip during sacroplasty. (A) Axial CT during localization reveals
minor shadowing artifact arising from near the tip, however less than expected for a 13-gauge needle. (B)
Imaging 2.5 mm cranial identifies further shadowing artifact as well as the diamond tip bevel confirming
exact needle tip position.
• Once the target location is reached, diluted contrast media can be injected to assess intended spread of
planned injectate.
• Final postprocedure CT should be performed after needle is removed.
• Use of CT fluoroscopy.
CT fluoroscopy is a technique in which the operator remains in the CT room while imaging is
acquired, displayed on a monitor, and then used to guide needle placement.
Requires additional hardware and software—a display monitor in the CT room, a foot pedal to
initiate scanning and control console to initiate table movement (Figure 2-10).
Best used when the entire needle trajectory lies in one axial slice and minimal needle manipulations
are expected. Deviation from the needle trajectory often requires multiple images to be acquired to
achieve correction.
Due to radiation exposure, the operator must wear a lead apron and thyroid shield. Lead eye
protection is recommended.
The typical radiation dose rate in CT fluoroscopy is approximately 7 times lower than the dose rate
with conventional diagnostic CT parameters, but it can be up to 60 times higher than conventional
fluoroscopy depending on dose settings.2
Figure 2-10. Photograph of patient draped and positioned in preparation for CT fluoroscopy, with in-
room monitor, controlling joystick (black arrow) and foot pedal (white arrow).
This can lead to large radiation doses to patient and operator if not used appropriately.
Furthermore, radiation dose is concentrated on a focal area of skin and can result in a large skin
radiation dose for the patient.
However, when used appropriately (low tube current and minimal exposure time), it can result
in reduced patient radiation dose and reduced procedural time compared to conventional CT
guidance.3
For selected procedures such as epidural injections and lumbar nerve root blocks, this method
can result in radiation dose levels and procedural times similar to conventional fluoroscopic
guidance.1,4
There are two modes of CT fluoroscopic imaging:
Quick check imaging
• The operator presses a pedal to acquire CT images.
• Typically 3 images are displayed on a screen, with a central image at the expected needle
location, and an image above and below.
• Lower patient and operator radiation dose than continuous imaging.2
Continuous imaging
• CT scanner can acquire continuous imaging (~10 frames per second) during needle
manipulation to reproduce live nature of imaging with conventional fluoroscopy.
• Requires nonmetallic needle holders to ensure that operator’s hands are not in gantry. This is
less tactile method for needle placement.
• Results in a high patient skin and operator radiation dose.
• If using this mode, there should be an inbuilt preset time limit for CT exposure to avoid
excessive radiation dose.
• May be of benefit in targets within particularly mobile organs such as the lung or liver.
CLINICAL PEARLS
• Prior to any case, review the mechanics of the CT gantry, and ensure that all necessary equipment is
available.
• For obese patients, ensure the patient is within the maximal CT table weight restrictions and can fit in
to the CT gantry.
• If possible, once needle trajectory is planned and local anesthetic is infiltrated, manipulate the needle
during the remainder of the procedure while the patient remains in the CT gantry—this reduces the
chance of patient motion with table movement, and reduces procedure time.
• Use the laser guiding light in the CT gantry as frequently as possible.
If the laser light bisects the needle hub, the needle trajectory will be in the plane of the CT image.
If the needle hub lies above the plane of the laser guiding light, the needle tip is pointing in the
opposite direction and can be adjusted without repeat imaging.
• If the patient needs to be moved into and out of the CT gantry, use of a pedal or sterile cover over the
CT controls can allow the operator to move the CT table immediately and independently of the CT
technician.
• If there is no safe direct access to the target in the axial plane, consider tilting the CT gantry to obtain
oblique axial imaging—this may facilitate a safe angled pathway in which the entire needle trajectory
can be visualized.
• Injection of normal saline or 5% dextrose can allow creation of a needle trajectory pathway in
between compartments, eg, facilitating access to the celiac plexus by enlarging the retroperitoneal
space or displacing adjacent tissues.
• If there is a CT contrast allergy, depending on the target location, a small amount of air can be
effectively used as a contrast medium, eg, in confirming epidural needle tip position.1
• Radiation reduction.
Any reduction in radiation to the patient also reduces radiation dose to the operator and to assisting
staff members.
Acquire images only when necessary to assess needle position and trajectory.
Step as far away from the CT gantry during image acquisition as possible. Exit the room if not using
CT fluoroscopy.
If using CT fluoroscopy.
Use the quick check method.
A lower tube current during imaging can reduce radiation dose while providing adequate
trajectory information without loss of anatomical resolution.2
Place the foot pedal further away from the gantry to reduce dose (radiation intensity is inversely
proportional to the square of the distance from the source).4
A lead drape over the patient adjacent to the scan plane can reduce scattered dose to the
operator’s hands.5
Suggested Reading
Carlson SK, Bender CE, Classic KL, et al. Benefits and safety of CT fluoroscopy in interventional
radiologic procedures. Radiology. 2001;219:515-520.
Joemai RM, Zweers D, Obermann WR, Geleijns J. Assessment of patient and occupational dose in
established and new applications of MDCT fluoroscopy. AJR Am J Roentgenol. 2009;192:881-886.
Paulson EK, Sheafor DH, Enterline DS, McAdams HP, Yoshizumi TT. CT fluoroscopy-guided
interventional procedures: techniques and radiation dose to radiologists. Radiology. 2001;220:161-
167.
Wagner AL. Selective lumbar nerve root blocks with CT fluoroscopic guidance: technique, results,
procedure time, and radiation dose. AJNR Am J Neuroradiol. 2004;25:1592-1594.
References
1. Wagner AL. CT fluoroscopy-guided epidural injections: technique and results. AJNR Am J
Neuroradiol. 2004;25: 1821-1823.
2. Paulson EK, Sheafor DH, Enterline DS, et al. CT fluoroscopy-guided interventional procedures:
techniques and radiation dose to radiologists. Radiology. 2001;220:161-167.
3. Carlson SK, Bender CE, Classic KL, et al. Benefits and safety of CT fluoroscopy in interventional
radiologic procedures. Radiology. 2001;219:515-520.
4. Wagner AL. Selective lumbar nerve root blocks with CT fluoroscopic guidance: technique, results,
procedure time, and radiation dose. AJNR Am J Neuroradiol. 2004; 25:1592-1594.
5. Nawfel RD, Judy PF, Silverman SG, Hooton S, Tuncali K, Adams DF. Patient and personnel exposure
during CT fluoroscopy-guided interventional procedures. Radiology. 2000;216:180-184.
CHAPTER 3
Ultrasound Guidance for Interventional Pain

Management
Hariharan Shankar and Kanishka Rajput
INTRODUCTION
Lazzaro Spallanzani is credited with the initial discovery of ultrasound (US) navigation by bats in 1790.
But it was Pierre Curie’s invention of the US-generating piezoelectric crystal that heralded further
development of US technology. Following its utilization in medical imaging and guidance, US imaging has
seen tremendous progress in its applications and technology in the last 5 decades. Recent years have seen
a surge in the use of US for diagnosis and therapeutic interventions in regional anesthesia. US is now
making progress in the field of pain medicine because of its utility both in the diagnosis of several nerve,
muscle, and joint pathologies and for the ability to see the target and the needle for injection of therapeutic
substances (Table 3-1).
TABLE 3-1. Advantages of Ultrasound Guidance

• Watch real time injectate spread
• Avoid structures, eg, pleura
• Decrease injectate volume
• Lack of radiation
• May avoid multiple passes
• Detect pathology in the target area
• Avoid painful muscle contractions 2° to stimulation
• Good educational tool on clinical anatomy
Following its initial use in regional anesthesia, US was quickly adopted for a variety of pain medicine
interventions (Table 3-2). Many feasibility studies have been published that attest to its safety and
convenience. Studies have also documented elimination of radiation exposure secondary to the use of US
imaging for pain medicine interventions.
TABLE 3-2. List of Common Procedures Performed in Pain Medicine Where US
Guidance is Utilized
• Musculoskeletal
Joint injections
Bursa injections
Trigger point injections
Piriformis injections
Tendon injections
Plantar fasciitis injections
• Neuraxial
Preprocedural scanning
Caudal epidural
Facet and medial branch injections
Spinal root injections
• Sympathetic blocks
Stellate ganglion block
Celiac plexus block
Hypogastric plexus block
Ganglion impar
• Peripheral nerve injections
BASIC PHYSICS OF ULTRASOUND

• Sound waves at frequencies greater than 20 kHz are called US.
• Medical US uses frequencies in the range of 2 to 20 MHz.
• When an electrical current is passed through piezoelectric crystals, they vibrate and produce
ultrasound waves.
• The US waves travel through tissues at a velocity that depends on the tissue with an average velocity of
1540 m/s assumed for all biologic tissues.
• This velocity is utilized to calculate the depth (the time from pulse generation to detection times half
the velocity).
• The distance from one crest of the waveform to the next is the wavelength.
Attenuation
• As the waves travel through tissues, there is a loss in intensity or attenuation. This is due to the wave-
induced motion of the tissues, absorption, reflection, and scattering. Attenuation is directly
proportional to the frequency and the length of the path. This is described in decibels per centimeter of
tissue traversed per megahertz, and they range from 0.3 to 0.8 dB/cm/MHz for most tissues. Attenuation
results in conversion of the mechanical energy of the waveform into thermal and nonthermal energy.
Acoustic Impedance
• Acoustic impedance between tissues, which is density times the average velocity, determines the
amount of reflection. Increasing impedance difference increases the intensity of reflection with no
echoes occurring with identical impedances. Impedance matching between the transducers and skin is
improved by applying a liberal amount of a water-soluble gel. In addition, the face of the transducer is
coated with a quarter-wave matching layer to decrease the impedance difference.
PRINCIPLES OF ULTRASOUND
• Modern US transducers have arrays of piezoelectric crystals, which are electrically excited in small
successive groups to create a sweeping effect of the beam.
• The transducers serve the dual function of generating and receiving signals reflected back from the
tissues.
• US used in medical imaging is delivered in pulses and uses a brightness mode for display.
• The image is then displayed on the screen in shades from black to white.
• When the waves are completely reflected by a tissue structure they appear white or hyperechoic, and
when none is reflected, they appear black or anechoic on the display. Bone and fascia are hyperechoic,
while blood vessels are anechoic.
• Nerves and muscles have hyperechoic structures in a bed of hypoechogenicity to anechogenicity
creating a stippled or starry sky appearance.
• Only a small percentage of the waves are returned back to the transducer, with the majority either
travelling further into the tissues or scattered because of refraction.
• The US waves move through tissues and create rarefaction and compression.
Two distinct patterns of reflection give rise to the echoes that make up an US image—specular reflection
and scattering.
1. Specular reflection. It is responsible for the bright appearance of fibrous structures such as tendons.
2. Scattering. It gives rise to the characteristic texture (echo texture) of the image seen within soft tissue
in a manner that loosely resembles the waves created by a pebble dropped into a pond.
The ultrasonic beam in modern machines scans the tissues by electronic control such that each element
is excited with a time delay, creating a sweeping motion for the image. Beam focusing is achieved by the
design of the transducer: lenses placed in the front of the transducer or with the use of phased array.
THE PORTABLE ULTRASOUND MACHINE

The modern portable US machine has made it easy to perform bedside evaluations and interventions. The
transducers, the most critical components of the US machine, contain the piezoelectric crystals and are
responsible for the transmission and receiving of the US waves. The electronic circuitry of the central
processing unit and the image display screen form the other major components. The image system has user
interfaces including a computer keyboard to enter information and buttons, knobs, and sliders to control
the various operations (Figure 3-1). Some newer machines have touch screen capabilities for adjusting
the various parameters.
Figure 3-1. (A) and (B) Key pads and other control knobs of two portable ultrasound machines.
Transducers
• Transducers are manufactured in many different shapes and sizes.
• The commonly used transducers in pain medicine are the linear array and curved array transducers
(Figure 3-2).
• The frequencies used for medical imaging are generally in the range of 1 to 18 MHz.
• Transducers have different frequency ranges to provide versatility in imaging at different depths and
are centered around their resonant frequency.
• Based on the location of the target, a suitable frequency range transducer is selected.
• The lower-frequency transducers are optimal for viewing deeper structures, and the higher frequencies
are used for more superficial structures.
• The choice of frequency is a trade-off between spatial resolution of the image and imaging depth: the
deeper the penetration, the less the resolution.
• The frequency of the selected transducer may be further adjusted using a dial.
Figure 3-2. Transducers used in pain medicine interventions. (A) Curved array transducer producing
lower ultrasound frequencies for use in imaging deeper structures. (B) Linear array transducer for use
with superficial structures. (C) Phased array transducer for use with deeper structures and abdomen. (D)
“Hockey stick” transducer for use with superficial structures and the small foot print facilitates use in
narrow areas.
IMAGE OPTIMIZATION FUNCTIONS

Some of the important adjustable functions on the key pad are depth, gain, focus, and zoom. Most portable
machines also provide color flow Doppler and power Doppler features with the ability to steer the beam.
More recently, touch screen capabilities have also been introduced. Newer machines have dynamic US
image optimization technology (Native Tissue Equalization [NTEQ]) that adjusts the gain and other
parameters while scanning, thus optimizing in real time. The computer is programmed to perform
advanced real-time motion analysis, in addition to accurately detecting and differentiating noise and
artifacts from soft tissue.
Depth
• Depth is adjusted to optimally visualize the structure of interest. It should be adjusted to approximately
1 cm greater than the target (Figure 3-3).
• Increasing the depth reduces the scale and also slows the frame rate, as each line of the image takes
slightly longer to acquire.
Figure 3-3. Setting an optimal depth. (A) The lower portion of this 3-dimensional image does not
contribute any useful information to the image and hence the depth setting should have been set as in 3B,
and (B) correct depth setting.
Gain
• Gain compensates for attenuation as sound travels deep into the body.
• The intensity of the returning signals is amplified by the receiver upon arrival so that the displayed
image is brighter.
• Gain can be adjusted for the entire field or specifically for the near or far fields.
• Excessive increase in gain adds “noise” to the image (Figure 3-4).
• Gain can also be adjusted selectively at different depths by Time Gain Compensation or TGC where up
to 10 separate depth adjustments are provided to adjust the gain at a particular depth.
Figure 3-4. Ultrasound images showing different gain settings. (A) High gain showing structures as very
bright. (B) Low gain preventing visualization of most of the tissue. (C) Optimal gain setting allowing
proper visualization.
Focus
• The pulse of US can be manipulated to be at its narrowest at a particular depth.
• This means that image quality, including lateral resolution, is maximized at that level.
• This can be manually adjusted so that a particular area can be examined with clarity.
• Selecting more than one focus level can significantly decrease the frame rate.
Zoom
• This feature magnifies a portion of the screen. This can be performed while scanning or after freezing
the image.
• For superficial structures, it is easier to obtain magnification just by reducing the depth of the image.
• During scanning, orientation becomes difficult if zoom is used.
Tissue Harmonic Imaging

• As US waves pass through tissues, they get distorted by nonlinear propagation. This creates harmonic
waves of the initial frequency.
• Out of the many harmonic frequencies, the second harmonic frequency provides better resolution and
suffers from less distortion.
• The fundamental frequency of the received beam is filtered out, and only the higher harmonics are
retained.
• Tissue harmonic imaging utilizes the second harmonic frequency of the received signals, thus avoiding
clutter and artifacts.
Doppler Functions
• US machines use the Doppler principle extensively to measure flow, range, and velocity.
• Color flow imaging provides real-time blood velocity and direction in color. It is superimposed on the
gray scale image with red, denoting flow toward the transducer, and blue, away from the transducer
(Figure 3-5).
Figure 3-5. Ultrasound image showing cross-sectional view at the level of carotid and internal jugular
vein in the neck. The use of color flow Doppler showing flow toward the transducer as red and away
from the transducer as blue.
• As the received signal is angle dependent, many machines offer steering capabilities.
• Power Doppler is more sensitive to flow, but does not provide velocity direction. Small vessels can
be adequately imaged with power Doppler, displaying the signal power over the gray scale B mode
image.
• It is prudent to use Doppler to identify vessels in the vicinity of the target during a preliminary scout
scan prior to any intervention.
Compound Spatial Imaging

• Compound imaging is a broad bandwidth technology that combines multiple coplanar images captured
from different beam angles and from multiple US frequency spectra to form a single image in real time.
• This eliminates edge-shadowing effect, reduces speckle artifacts, and improves contrast resolution.
NEEDLE APPROACHES
There are 2 methods of orienting the needle relative to the US beam: the in-plane and out-of-plane
approaches (Figure 3-6).
Figure 3-6. Commonly used techniques for needle orientation with regard to the transducer. (A) In plane
technique with the needle being advanced from one end of the transducer. (B) Corresponding ultrasound
image of in-plane technique. (C) Out-of-plane technique with the needle being introduced from the side of
the transducer. (D) The corresponding ultrasound image of the out-of-plane technique showing the needle
in cross section as a bright hyperechoic dot.
In-Plane Needle Approach

• The needle is inserted in the same plane as the US beam.
• The image captured will be a long axis view.
• Needle-beam alignment is critical to visualize the shaft of the needle in the in-plane approach.
Out-of-Plane Needle Approach

• The longitudinal axis of the needle is inserted in a plane perpendicular to that of the US beam.
• Visualizing the needle tip in this approach can be challenging, as only a cross-sectional area of the
needle is imaged; in addition, the tip and the shaft have similar appearances.
NEEDLE VISIBILITY
It is critical to the successful performance of an intervention to be able to continuously visualize the
needle shaft and tip. This is facilitated by the use of various techniques and devices. Needles used in US
guided procedures are available in different sizes and materials. Larger needles may be better visualized.
• The acoustic impedance difference between the tissues and the needle aid visualization: the greater the
difference, the better the visibility.
• Visibility of the needle tip has been shown to be better at more shallow rather than deeper needle-beam
angles.
• One of the most commonly performed techniques in difficult situations is the injection of a small
volume of 5% dextrose or saline, a technique described as hydrolocalization.
• When the needle tip is not visualized, further advancement should not be performed.
Troubleshooting if the Needle Is Not Visualized

• Exclude gross misalignment by visually inspecting needle and transducer position.
• The transducer should then be adjusted, using three basic movements (sliding, tilting, and rotating) until
the needle shaft and tip have been brought back into view (Table 3-3).
• The transducer and needle should not be moved together, as this makes the task more difficult.
• A needle-to-beam angle of about 90° offers the best needle visibility when approaching in plane.
• When the target is deeper, a “heel-in” maneuver may be helpful. This technique involves pressing one
end (the “heel”) of the transducer more deeply into the patient than the other end (the “toe”), thus
increasing the needle-to-beam angle.
TABLE 3-3. Technique for Ultrasound Image Optimization During Scanning

Scanning PART
• Pressure—applying pressure with the transducer to see compressibility
• Alignment—sliding to trace the course lengthwise
• Rotation—aligning target to beam by turning clockwise and counterclockwise
• Tilting—optimizing the angle of incidence and maximizing the beam signal
SONOPATHOLOGY
This topic is slowly gathering interest among pain practitioners. Ultrasound may also be used to diagnose
abnormal anatomy and fluid collections without extensive training on the part of the sonographer (Figure
3-7). Its use in musculoskeletal injuries is more complex because of the possibility of artifacts based on
the angle of the US beam. Nevertheless, the use of portable US diagnostic imaging affords the ability to
narrow down the differential diagnosis and facilitates management.
Figure 3-7. Ultrasound image of an intrathecal pump seroma with the pump creating a mirror image of the
seroma beneath the pump’s surface.
LIMITATIONS OF ULTRASOUND IMAGING

• The major limitation of US imaging is the inability of US waves to penetrate through bone (Figure 3-8).
This creates an acoustic shadow preventing visualization of structures beneath it.
• Air attenuates the US wave significantly and prevents visualization, especially around the intestinal
loops or lung.
• As most commonly used, needles are not adequately visualized by US imaging, with a potential for
intravascular and intraneuronal injection.
• US contrast agents have not gained widespread acceptance for regional anesthesia and pain
interventions. Hence the reliance on techniques like “hydrolocalization” to ensure delivery to the
intended target.
Figure 3-8. Ultrasound image showing an acoustic shadow created by bone, eg, rib, and loss of
visualization through air in lungs. Structures beneath bone cannot be visualized.
COMMON ARTIFACTS
• Enhancement. Fluid, as it is less attenuating, permits US waves to pass through with little distortion.
The area beneath the fluid column will, therefore, appear brighter (Figure 3-9).
• Anisotropy. The transducer will only receive the reflected sound if the beam strikes the surface at a
right angle. Any change in the angle of insonation alters the echogenicity. This effect is called
anisotropy and is commonly used to differentiate between tendons and nerves as tendons are more
anisotropic.
• Mirror images. A large difference in acoustic impedance can reflect an image to create a mirror image
beneath the hyperechoic tissue (refer to Figure 3-7).
• Reverberation. A superficial strong reflector creates reverberation of the sound signal. This creates
evenly spaced hyperechoic lines at increasing depths (Figure 3-10).
• Comet tail. Similar to reverberation, hyperechoic lines are seen deeper to the highly reflective
structure, which gradually peters off (Figure 3-11).
Figure 3-9. Ultrasound image showing enhancement (increased brightness) beneath fluid filled structures,
eg, carotid artery and internal jugular vein.
Figure 3-10. Reverberation artifact of the needle over a hyperechoic surface during aspiration.
Figure 3-11. Comet tail artifact created by the pleural lining with the hyperechoic lines gradually
diminishing in size.
ERGONOMICS DURING ULTRASOUND IMAGING

Proper attention to body ergonomics of both the patient and the provider avoids injury. The patient should
be resting comfortably in a bed. The operator should be seated comfortably on the side of the procedure,
and the machine image display should be located on the contralateral side at an eye level to avoid neck
strain. The transducer head should be held comfortably in the palm of the nondependent hand, and contact
with the skin of the patient with the operator’s hand should be maintained at all times to avoid inadvertent
movement of the transducer. The hand should be resting comfortably without extension at the wrist. The
needle should be held in the dominant hand.
ADVANCES IN ULTRASONOGRAPHY
Capabilities for three-dimensional (3D) US images are available in most machines. Their utility in pain
interventions is yet to be realized. One of the major difficulties is the size of the transducer. Until the
recent development of the matrix array transducers, 3D technology rested on mechanically steered
transducers. The target area is scanned for a predetermined duration, usually in seconds. The computer
then collates all the images and renders the final 3D image (Figure 3-12). This can be further manipulated,
trimmed, and edited using manufacturer’s software. Four-dimensional US transducers afford real-time 3D
images by incorporating time as the fourth dimension.
Figure 3-12. Ultrasound image displayed during rendering of a 3D image by the computer program.
Mechanical and adjustable needle guides have been developed—with their own advantages and
limitations. Despite facilitating needle and transducer alignment for better visualization, they hinder finer
adjustments during target localization. Optical needle guides have a laser-sighting apparatus that
facilitates in plane needle-beam alignment. However, a portion of the needle shaft has to protrude from
the skin surface at all times to allow alignment with the laser. This may require the use of longer needles
making manipulation technically challenging. By embedding a piezoelectric crystal at the needle tip, the
needle tip may be visualized by stimulating it while using the Doppler function. In order to improve the
visibility of needles, echogenic needles have been manufactured with indentations, and polymer
encasement with a bubbling agent to facilitate needle visualization or nanoparticles (Figure 3-13). More
recently, GPS technology and electromagnetic tracking have been introduced in some machines, by adding
a sensor to the needle tip and the hub, to facilitate tracking and trajectory planning. Newer US machines
have introduced automatic needle optimization technology to enhance needle visibility (Figure 3-14).
Figure 3-13. Some echogenic needles provide optimal visualization of needle by a coating of
nanoparticles. (A) Long axis view of an echogenic needle. (B) Long axis view of an echogenic needle
with an echogenic catheter.
Figure 3-14. Needle visualization technology. (A) Image of a phantom with needle in place but not
visualized. (B) Same image with needle visualization technology showing the needle clearly.
RECOMMENDATIONS FOR ULTRASOUND IMAGING

GUIDANCE
Recommendations proposed by the American Society of Regional Anesthesia on proper technique of US
imaging may be utilized for ultrasound guidance in pain medicine interventions.
• Phantom practice
• Review relevant anatomy
• Start with simple superficial procedures
• Scan wide the area of interest
• Check with color Doppler
• Watch injectate spread
SUMMARY
US imaging, with its unique advantages of real-time imaging with clarity and facilitating needle guidance,
is proving to be a useful tool in pain medicine without any radiation exposure. A basic understanding of
the US technology improves its proper utilization. Adequate knowledge of anatomy, systematic learning of
the use of US machine, and regular practice is likely to enhance the practitioner’ skills.
Suggested Reading
Gibbs V, Cole D, Sassano A, eds. Ultrasound Physics and Technology How, Why and When. Elsevier;
2009.
Kremkau FW, ed. Sonography Principles and Instruments. 8th ed. Saunders; 2011.
Narouze SN, ed. Atlas of Ultrasound Guided Procedures in Interventional Pain Management. Springer;
2010.
CHAPTER 4
Radiation Safety
Vikram B. Patel
INDICATIONS
Fluoroscopy has been a very effective tool in interventional pain management procedures. Not only does
the x-ray image help one identify the proper target for the needle placement but also helps to determine the
proper spread of the injectate as well as identify inadvertent intravascular placement of a needle and thus
the injectate. Portable fluoroscopy units (also called the C-arm) have helped improve the effectiveness as
well as safety of interventional pain management procedures. However, at the same time, it has also
increased radiation-related injuries to physicians and their staff as well as patients. Whereas proper use
of fluoroscopy can help safe placement of the needle and the injectate, excessive and improper use of
fluoroscopy can lead to radiation-induced injuries. Physicians who performed radiography and
fluoroscopy in the first half of the 20th century had higher rates of cancer-related deaths than any other
physicians. The US Food and Drug Administration (FDA) issued an advisory in 1994 suggesting that the
key to preventing such unfortunate mishaps may be physician education, training, and credentialing in the
safe operation of fluoroscopic equipment. Proper understanding of the radiation dosage, scatter pattern of
x-rays while using the fluoroscopy machine, understanding the fluoroscopy machine and using it properly
would lead to improved patient care and minimal tissue trauma to the patient, physician, and ancillary
staff from radiation.
RELEVANT ANATOMY
Several issues need to be considered when using x-rays on a human body.
• The human body does absorb radiation.
• The human tissue can be damaged by radiation.
• Larger human beings require higher radiation exposure for proper imaging.
• Lateral mass of the human body requires more radiation than anteroposterior mass.
• Larger individuals require longer needles but provide shorter space between the body and the image
intensifier, thereby making the placement of the needle more difficult.
• Placement of the image intensifier can influence the amount of radiation scatter around the patient.
Usually the scatter is less if the image intensifier is closer to the patient (Figure 4-1).
Figure 4-1. The larger circular part of the C-arm is called the image intensifier (I-I) and the smaller part
is the actual x-ray tube. Closer placement of the image intensifier helps reduce the scatter of radiation.
BASIC CONCERNS AND CONTRAINDICATIONS

Some concerns regarding the proper use of fluoroscopy units are inadequately trained radiology
technicians, physicians who are untrained in the use of fluoroscopy, improperly maintained machines, and
inadequate space.
Use of fluoroscopy is unadvisable during pregnancy as it may lead to fetal injury from radiation,
especially during the first trimester.
Effects of radiation on different tissues are variable:
• Radiation is carcinogenic.
• Effects are permanent for the most part.
• Total dosage (absorption) is cumulative over lifetime.
• Any exposed part of the body can be vulnerable.
RELEVANT TERMINOLOGIES
A physician should be familiar with the terms used to describe radiation energy.
• Radiation is defined as “energy that is radiated or transmitted in the form of rays or waves or particles
from a central source.”
• Quantity of radiation intensity (exposure) is measured in R or coulomb—C/kg.
• Energy absorbed by a matter from radiation (depends on the matter) is measured as radiation absorbed
dose (rad) or gray “Gy”—SI unit (100 rad = 1 Gy).
• Biological effects of radiation are measured as radiation equivalent man (rem) or sievert “Sv”—SI
unit (100 rem = 1 Sy).
• For all practical purposes 1 R = 1 rad = 1 rem.
• Milliseivert (mSv) is usually used for measure of the x-ray dosimeters (Figure 4-2).
Figure 4-2. X-ray dosimeters. The circular dosimeter can be worn on the finger and the larger hexagonal
dosimeter is usually clipped over the external aspect of the thyroid shield. Some physicians also wear a
ring-dosimeter on the fingers and even an eye dosimeter on the side of the eyewear.
MAXIMUM ALLOWABLE DOSE AND EFFECTS OF RADIATION

ON HUMAN TISSUE
• The maximum total yearly dosage to a human body should be less than 50 mSv or <4 mSv per month
(4mSv ˜100 mrem).
• Maximum permissible radiation dosages (MPD).
• Typical lumbar epidural steroid injection under fluoroscopy from 1 m away—approximately 0.03
mrem (to physician).
• Chest x-ray—15 mrem.
• X-ray of the abdomen—220 mrem.
• X-ray of the L-spine—250 mrem.
• What can happen (single dose)?
Lens—200 rad = cataract
Skin—500 rad = erythema
Skin—700 rad = permanent alopecia
Whole body—200 to 700 rad = hematopoietic failure, death
Whole body—700 to 5000 rad = GI failure, death
Whole body—5000 to 10,000 = cerebral edema, death
Skin—approximately 6 Gy = rash
Skin—approximately 14 Gy = desquamation
FLUOROSCOPIC VIEWS
Various views during the fluoroscopy can influence the amount of radiation.
• An angled view requires higher amount of radiation.
• Lateral views typically require higher radiation.
• Exposure is not limited to the visible areas on the image, but it also engulfs the areas outside the
visible image on the monitors (Figure 4-3).
• Continuous exposure is unnecessary for the most part except for certain situations such as:
Figure 4-3. The radiation field extends beyond the borders of visible image on the monitor and would
expose a physician’s hands or body even if it is not visible on the monitor image. It is more spherical than
conical. The x-rays used on a patient have even a wider field due to scatter caused by the patient’s body.
Active injection of contrast during a transforaminal injection to identify vascular spread

Injection of cement during a vertebroplasty
Guiding a spinal cord stimulator lead
Using an epidural adhesiolysis catheter
Minimally invasive lumbar decompression (MILD) procedure
How to minimize the amount of radiation during interventional procedures:
• Time
Least amount of exposure time—use single shots rather than continuous exposure
• Reduce the amount of x-rays delivered from the x-ray tube (Figure 4-4)
Figure 4-4. Example of fluoroscopic images using collimation during fluoroscopy. The middle image is
without collimation. This is the best way to minimize the exposure while maintaining a superior image
quality compared to pulsed and low-dose modes. It may even enhance an image (such as in thoracic spine
with lung fields on both sides, or the cervical spine with air within the fields) by eliminating the
surrounding fields from the image.
Use of collimation (metal plates within the tube that reduce the amount of x-rays emitted by the
tube). The collimation can be linear or circular (Figures 4-5 and 4-6).
Figure 4-5. Inside view of the x-ray tube. The open circular collimation plates are visible at the top and
the linear plates are underneath. These plates prevent x-rays from being emitted from the source.
Figure 4-6. Inside view of the x-ray tube showing open and collimated circular plates. They function
similar to a camera shutter iris.
• Distance
Stay as far away from the x-ray tube as possible.
If you can touch the C-arm you are probably too close.
Radiation decays exponentially with increased distance (1 m = 0.1% of entrance skin exposure).
The x-ray tube should be as far from the patient as possible (same as the image intensifier being as
close to the patient as possible).
• Barriers and lead-based protection
Cover the patient’s body parts not subject to treatment.
Physicians should use lead aprons (preferably wrap around), thyroid shields, leaded eyewear,
leaded gloves.
Everyone including the staff in the procedure room should wear radiation protection aprons and
thyroid shields.
Equipment
Several companies make portable C-arm fluoroscopy machines. Various extras are now almost standard
in most machines such as options for data storage (built-in hard disc, CD or DVD burners, USB key
storage, network storage capabilities, etc).
• Newer fluoroscopy units use digital enhancement of the image that helps reduce radiation and also
provides better image quality.
• Flat panel monitors provide better image quality.
• Some units have low-dose exposure as well as pulsed modes (delivery of x-rays as 3-10 pulses per
second rather than continuous delivery while the button is pressed). These parameters may provide a
slightly degraded quality of the image but it is more than sufficient for identifying the osseous structures
and thus the target areas for most interventions (Figure 4-7).
• Digital subtraction angiography (DSA) is now used by many physicians to identify inadvertent
intravascular injection. This type of imaging is considered the gold standard for vascular imaging and
can help avoid intravascular injection that may lead to severe morbidity and even mortality. However,
it also requires continuous exposure while the radiologic contrast is being injected and would lead to
higher amount of radiation to the patient as well as the physicians. Fluoroscopy units equipped with
DSA capability are much costlier.
Figure 4-7. This image shows the amount of dosage reduction (as measured in mA) when a low-dose and
pulsed mode are activated (in the right image). The reduction is nearly 1/3 compared to normal exposure
without collimation.
Technique
Proper knowledge of the fluoroscopy machine is essential for an interventional pain physician. One
should try to use the least amount of time for exposure, maintain as much distance between the x-ray tube
and one self, minimize the use of continuous fluoroscopic exposure except in certain situations mentioned
above, and measure the exposure by properly wearing the dosimeters outside the lead aprons—preferably
outside the thyroid shield (Figure 4-8).
Figure 4-8. Proper protection and distance while using a fluoroscopy machine. Note the eyewear with
side protection, the radiation attenuation gloves and the thyroid shield. The wrap around apron is worn
underneath the gown. The minimal distance between the physician and the C-arm should be at least the
arm’s length (˜1 m), which would reduce the exposure to about 0.1% of the amount emitted by the x-ray
tube.
Potential complications and pitfalls include:

• Potential complications of overexposure are listed above, but any body tissue can be affected.
• Exposure to the patient cannot be ignored.
• Exposure to the procedure room staff also should be considered and proper protection should be
provided.
• It is very tempting to use the fluoroscopy with continuous exposure for easier guidance of the needle or
to identify the entry point, but should be avoided as much as possible.
• Always remember that the effects of radiation are cumulative over the life time and cannot be reversed.
Suggested Reading
Botwin KP, Thomas S, Gruber RD, Torres FM, Bouchlas CC, Rittenberg JJ, et al. Radiation exposure of
the spinal interventionalist performing fluoroscopically guided lumbar transforaminal epidural steroid
injections. Arch Phys Med Rehabil. 2002 May.
Botwin K, et al. Radiation exposure to the spinal interventionalist performing lumbar discography. Pain
Phys J. 2003 Jul.
www.epa.gov/radiation/
www.iaea.org/Publications/Booklets/Radiation/radsafe.html
www.michigan.gov/lara/0,4601,7-154-35299_63294_35791—,00.html
CHAPTER 5
Equipment Used in Pain Management

Vikram B. Patel
INTRODUCTION
Interventional pain management involves the use of image-guided procedures as well as targeted delivery
of medications to modulate pain, symptoms, and disease. To facilitate these procedures, an
interventionalist has to utilize a variety of equipment, ranging from simple needles for a trigger point
injections to the use of an MRI or a CT scanner for more complex procedures.
Without proper equipment, the procedures cannot be done in a reliable manner and are basically
described as “blind” techniques. This chapter covers various types of needles and specialized catheters
and syringes. Some major equipment such as a fluoroscopy machine is covered elsewhere in this atlas
(see Chapters 1 and 4).
RELEVANCE OF ANATOMY
Although it is necessary to consider the anatomical variations in males, females, adults, and children, the
basic need for most of the equipment remains the same. However, depending on the patient’s size and type
of a procedure, one must consider the proper type and length of needles, anticipate difficulties, and be
prepared for possible complications in case ideal equipment is not available. For example, a larger
patient would need a longer needle (and choosing a shorter needle may lead to multiple or failed attempts
as well as improper placement of the needle), a sharp needle instead of a pencil point needle may lead to
nerve damage, a spinal needle used for epidural access would lead to higher rates of dural punctures.
Without proper equipment for guidance of a needle (such as a fluoroscopy unit or an ultrasound unit), the
needle may end up in an unintended location and even cause unintentional trauma to tissue.

Based on the procedure to be performed, it is inappropriate to use certain equipment such as a long
needle for a shallow procedure which can lead to higher rate of complications.
TYPES OF EQUIPMENT
Needles (Nonepidural Placements)
Quincke (Figure 5-1)
Figure 5-1. Quincke needle—note the sharp tip of the needle which has a cutting edge. (Used with
permission from Aakash Patel.)
• Most common type of bevel seen in needles.

• It is a sharp bevel that facilitates penetration of the skin.
• Various needles that have such bevels are intended for intramuscular and intravenous access, biopsies,
subcutaneous drug delivery, etc.
• Spinal needles are mainly available with this type of bevel and are commonly used for several
interventional procedures.
Pencil point (Figure 5-2)
Figure 5-2. Pencil point needle. (Used with permission from Aakash Patel.)
• This needle has a tip that is conical in shape.

• The bevel is on the side of the needle shaft at the conical tip.
• Although considered a “blunt” type needle, it can easily penetrate delicate structures such as a vein or
even an artery if the vessel is fixed and immovable.
Bullet tip (Figure 5-3)
Figure 5-3. Bullet tip needle. (Used with permission from Aakash Patel.)
• Similar to the pencil point, but is completely blunt at the tip.

• Safer for certain procedures that are in the close proximity of nerves and blood vessels.
• Bevel is at the side of the tip.
• A sharp-tipped introducer is a must as this tip cannot penetrate the skin.
“B” bevel
• Commonly used for nerve blocks. The relatively short and noncutting tip makes it a safer choice for a
peripheral nerve block.
Chiba needle (Figure 5-4)
Figure 5-4. Chiba needle—note the angled bevel with a noncutting edge. (Used with permission from
Aakash Patel.)
• It has a very short bevel with a noncutting tip.

• Suitable for deeper procedures when a needle has to traverse delicate issues on its way to the target
such as a lumbar sympathetic block or celiac plexus block.
Day needle (Figure 5-5)
Figure 5-5. Day needle. (Used with permission from Epimed International, Inc.)
• Bullet tip Coudé needle (see below) used for various interventional procedures in the vicinity of
delicate tissues.
• The bullet tip minimizes the damage to such tissues as it has a noncutting tip.
Huber needle (Figure 5-6)
Figure 5-6. Huber needle—the tip has a noncoring edge, which is safer for the silastic injection port.
(Used with permission from Aakash Patel.)
• Used for accessing a sub-cutaneous reservoir or a port during a continuous infusion such as used in a
long term epidural infusion.
• Angled shaft helps keep the needle flat against the skin while it is placed within the port.
• The tip (similar to a Touhy needle) is also specially designed to be “noncoring” so that it does not
damage the silastic material over the entry port.
Needles (Epidural Placements)

Touhy needle (Figure 5-7)
Figure 5-7. Touhy needle—the slight curve helps guide a catheter at an angle and provides a slightly
blunter edge to prevent a dural puncture. (Used with permission from Aakash Patel.)
• A blunter tip as the opening is slightly on the side and the tip is curved.
• Helps facilitate passage of a catheter and guides it at an angle hence letting the catheter slide out of the
needle at a shallower angle and thus minimizing the risk of dural punctures.
Crawford needle—another type of an epidural needle with a short bevel that is relatively atraumatic
Hustead needle
• Epidural needle with a short bevel—slightly shorter than a Touhy needle.
• A rounded “heel”—the proximal aspect of the bevel was designed to reduce damage to the catheter if it
is withdrawn through the needle.
RX Coudé needle (Figure 5-8)
Figure 5-8. RX Coudé needle.
• Epidural access needle specially designed for placement of catheters.

• The bevel (along with the stylus) makes a flat surface that can be placed parallel to the ligamentum
flavum/dura and hence minimizes accidental dural puncture.
• Once in the epidural space, the needle is rotated towards the direction of a catheter placement.
Touhy needle with flexible introducer cannula (FIC) (Figure 5-9)
Figure 5-9. Touhy needle with flexible introducer cannula (FIC). The Racz catheter is seen within the
FIC.
• This set is used for epidural adhesiolysis using a Racz catheter.

• The soft plastic FIC minimizes damage to the Racz, or spring tip catheter while it is manipulated during
the adhesiolysis procedure.
• The FIC may have a bend at the distal end to facilitate guidance of the catheter in either direction once
inside the caudal canal.
• A regular Touhy needle may cause damage (shearing) of the outer covering of the catheter which may
then break and stay within the epidural space.
• Once the Touhy with FIC is introduced inside the caudal canal, the Touhy needle is removed leaving
the FIC in place within the caudal epidural space. The Racz catheter is then introduced through this
FIC.
Fluoroscopy Equipment
• Usually a mobile setup—also called a C-arm due to the design.
• Certain fixed fluoroscopic setups such as the ones used for interventional cardiology may also be used
for a dual exposure in procedures such as a vertebroplasty.
• Most modern machines have the capability to enhance the images using digital technology and thus
minimizing radiation exposure.
• They also have several other modes which additionally reduce the radiation (low dose, pulsed mode).
• Pulsed mode delivers the X-rays as pulses rather than a continuous radiation delivery.
• Number of pulses per second may be selectable in certain machines.
• Usual pulsed mode parameters are 3 pulses/min, 10 pulses/min, etc.
• A “low dose” setting can further reduce the radiation exposure while maintaining a good image quality
through digital enhancement.
• Newer monitors have flat panel LCD screens. Some also have touch screens to facilitate fast
interaction with the machine. Usual setup includes 2 monitors out of which 1 can be used to display a
previous image for comparison.
• Storage of images in a C-arm is important for documentation and record keeping.
• Older machines are able to store the images on a hard drive, the hard copies need to be printed on a
thermal paper.
• The newer machines have various options for image storage and transport ranging from a CD to a USB
drive using digitized images.
• Images can also be directly transmitted from the machine to an archive, using DICOM (digital imaging
and communications) technology, which can then be interfaced with electronic medical records
software.
Radiofrequency Generators
• Radiofrequency energy has been used to create tissue lesions for several decades.
• The first commercial RF generator was built in 1952.
• The RF generators are now more advanced and reliable and are manufactured by several companies.
The latest technology includes a touch screen interface and automated lesioning with predefined
parameters.
Radiofrequency parameters:
• Conventional radiofrequency—uses higher temperature parameters to create the lesion, typically a
small nerve such as the medial branches supplying a facet joint
• Pulsed radiofrequency
Application of short bursts of radio-frequency energy.
2 bursts/s, 20 ms each at 500,000 Hz.
Output at 45 V, temperature reaches ˜42°C.
Applied directly to the nervous tissue.
As the tip has the most dense electric field, it can be applied perpendicular to the nerve.
There is no nerve damage (neurolysis) at 42°C temperature and the myelinated as well as
unmyelinated nerve fibers remain normal in morphology.
Safer for use over superficial nerves (no risk of skin ulceration), cervical region (with several
sensitive structures).
• Single lesion—traditionally used for thermal neurolysis of the medial branches
• Multiple lesions—used mainly for the sacroiliac joint denervation due to its expansive nerve supply
• Bipolar lesions
Also used for the sacroiliac joint with two radiofrequency needles placed in close proximity (˜5
mm) of each other.
Multiple lesions are created along the joint border for the sacroiliac joint.
• Cooled radiofrequency
Newer technology using a water cooled cannula during the lesioning.
Rational is that the charred tissue created during a conventional radiofrequency lesioning limits the
spread of the lesion and cooling the tip of the RF cannula can help create a larger lesion.
Helpful in thoracic spine where the medial branches supplying the facet joints are not “plastered” to
the bone but rather floating more dorsally. A larger spherical lesion created by the cooled RF
generator can satisfactorily capture these medial branches.
Also effective in denervating the sacroiliac joint which similarly has “floating” nerve branches
supplying the joint.
Caution is necessary while using this technique for other areas as the lesion (which can be quite
large) may extend beyond the intended target and potentially damage an unintended nerve or other
vital structure.
Cryoablation Equipment
• The use of cryoablation has decreased in pain management during the past decade.
• The technology was used to ablate the nerves at various locations for the treatment of pain using a
freezing technique called cryoablation.
• Also used to ablate other tissues such as a tumor.
• Peripheral nerve ablations were frequently performed using this technique including lumbar medial
branches and intercostal nerves.
• As the nerve sheath remains intact after cryoablation, a neuroma formation is less likely when the nerve
regenerates.
• The equipment delivers compressed gas to the tip of the probe thus creating a freeze which ablates the
tissue due to ice crystal formation and apoptosis (with up to –75°C).
• The probes are larger, bulkier, cannot be bent and require extreme care in handling.
• Addition of a gas source also adds to the bulk of the equipment and reduces portability.
Other Specialized Equipment

Specialized Syringes
This is pressure monitoring manometric syringe with controlled rate of injection (Figure 5-10A, B).
Figure 5-10. (A) Controlled injection syringe with an external cable for manometric measurements. (B)
Controlled injection syringe with a built-in digital manometer and infrared transmitting capability for
printing the data.
Used for manometric provocation discography

• These syringes have a controlled injection rate.
• The plunger of the syringe is threaded and a very small amount of injectate (usually 0.2 mL) can be
injected with each turn of the plunger.
• Some newer syringes have a built-in manometer, which is digital and can transmit the data to a printer.
• Older syringes had an external connection cable which is then connected to an external manometric
measurement device along with a printer.
Dual needle sets for discography (Figure 5-11A, B).
Figure 5-11. (A) Discography needle set. (B) Discography needle set with a curved inner needle to
facilitate proper placement within the nucleus by helping steer the needle.
These needles are prepackaged by some companies to include a larger bore needle, which acts as an
introducer through which a thinner needle can be introduced into the nucleus of the disc.
• Advantages to these needle sets include lower risk of infection and smaller puncture into the annulus.
• A curved inner needle can help steer it for proper central placement within the nucleus with a single
pass and without multiple insertions.
Specialized Catheters
Racz catheter—used for epidural adhesiolysis (Figure 5-12)
• This is a spring-tipped steerable catheter.
• It is used for epidural adhesiolysis as well as site-specific placement of drugs.
• Various lengths are available along with varying stiffness of the catheter.
• It has a stylet that can be used to steer the catheter once slightly bent at the tip.
Figure 5-12. Racz Brevi-XL catheter with the injection port attachment. Note the slightly withdrawn
stylet that normally extends up to the tip of the catheter. The area slightly proximal to the tip is where the
injectate exits the catheter. (Used with permission from Epimed International, Inc.)
Stimulating catheter—used for continuous plexus blocks, identifying needle placement

• This type of a catheter provides a visual guidance to the catheter placement with continuing muscle
twitches while advancing the catheter along the plexus.
• The catheter is placed through a Touhy type needle which has a stimulating attachment.
• Once the needle is in place, the catheter is advanced through the needle and the stimulating connection
is shifted to the catheter from the needle.
• As the catheter advances, the resulting stimulation is visualized and a loss of stimulation provides a
visual clue as to the catheter diverting away from the nerve bundle.
DuPen® catheter— used for long-term epidural or spinal infusions either externalized or connected to
a subcutaneous injection port. This injection port can then be accessed with a Huber needle.
Although there are several other types of injection devices such as the ones used in vertebroplasty or
kyphoplasty, etc, they are usually included in the kit and hence not mentioned in this chapter.
CHAPTER 6
Corticosteroids: Indications, Pharmacology, and

Risks in Interventional Pain Management
Carolyn Kim and Christopher Gharibo
Corticosteroids have been a mainstay in the area of interventional pain management because of their
clinical effectiveness in treating numerous inflammatory subacute and chronic pain conditions. These
conditions often include significant inflammatory components as seen in certain neuraxial, intra-articular
and extra-articular disorders.
INDICATIONS FOR CORTICOSTEROIDS IN INTERVENTIONAL

PAIN MANAGEMENT
Hollander introduced the concept that injected corticosteroids can have a positive effect on inflammatory
pain conditions in 1950. Since Hollander’s study, the role of corticosteroids has expanded into treating
many other types of acute and chronic pain conditions such as degenerative and inflammatory conditions
of the peripheral joints and the spine.6
The common indications for corticosteroids in interventional pain medicine can be broadly divided into
the following categories:
• Peripheral joints
• Extra-articular tissue (eg, bursa)
• Neuraxial structures and spaces (eg, facet joints, epidural space)
Epidural steroids were introduced into the United States in the 1960s and are the most commonly
performed spinal interventions in the United States with an annual estimated Medicare spending of 175
million dollars in 2001. Studies have shown that epidural steroid can be effective in the treatment of
painful radiculopathy from:
• Disc herniations
• Spondylolysis
• Spinal stenosis
• Annular tears
• Degenerative conditions of cervical and lumbar spine
Other diseases that may benefit from corticosteroid injections include:
• Osteoarthritis of the spine and peripheral joints
• Rheumatoid arthritis and extra-articular disorders
• Tendinitis
• Bursitis
• Ligament sprain
• Tenosynovitis
• Other overuse syndromes
CONTRAINDICATIONS FOR CORTICOSTEROIDS IN

INTERVENTIONAL PAIN MANAGEMENT
The contraindications are more a function of the specific injection being performed rather than whether if
cortisone should be included in the injectate. Active infection at the needle insertion site must be
considered before all injections although this at times may prove difficult to differentiate from
noninfectious arthropathies. Bleeding disorders are especially important in neuraxial procedures as they
can lead to paralysis if the physician is not appropriately vigilant. The absolute and relative
contraindications for corticosteroid injections are listed in Table 6-1.
TABLE 6-1. Absolute and Relative Contraindications to Corticosteroid Injection
PHYSIOLOGY
• Cortisol is an endogenous glucocorticoid required for normal cellular function synthesized in the zona
fasciculata of the adrenal cortex.
• It is essential for normal metabolism, wound healing, gluconeogenesis, lipolysis, and immunologic
activity.
• It has significant anti-inflammatory actions that are beneficial in the treatment of chronic pain
conditions.
• Cortisol is under the control of the hypothalamic-pituitary-adrenal axis (HPA).
• In the presence of a stressor, the hypothalamus releases corticotropin releasing hormone (CRH).
• CRH induces the anterior pituitary gland to release adrenal corticotropic hormone (ACTH), which in
turn stimulates the adrenal cortex to release cortisol, androgen, and aldosterone.
• Normally, the human body produces 10-12 mg of cortisol per m2 of body surface area daily.
• This amount equates to a glucocorticoid secretion of 20-30 mg/day of oral hydrocortisone or 5-7
mg/day of oral prednisone.
• With stressful conditions, cortisol synthesis can increase up to 5-10 fold to 100 mg/m2/day.1
• The highest cortisol concentration is early in the morning and the lowest cortisol concentration is at
evening hours.
PHARMACOLOGY
• Cortisol is a derivative of cholesterol that exists in both bound and unbound (active) forms with 90%
being carried on cortisol-binding globulin.
• Its basic chemical structure is a 17-carbon skeleton with 6-carbon hexane rings and one 5-carbon
pentane ring.
• The different analogues that are produced and utilized in practice are created by altering the
arrangement of the steroid molecule to enhance certain anti-inflammatory properties as well as to
decrease the mineralocorticoid activity.
Cortisol has a half-life of about 90 minutes and is metabolized in the liver by its conversion to a water-
soluble compound that can be excreted by the kidney. Any change in the physical structure of the
compound, such as with the commonly used particulate preparations of steroids, will result in slower
metabolism of the product and thus a longer half-life and duration of action.
• Corticosteroids reduce inflammation by decreasing the permeability of capillaries at the affected site.
• They reduce the amount of protein and fluids that are extravasated from the vessel, thereby reducing
edema.
• Corticosteroids decrease the inflammatory component of pain by interfering with the synthesis and
release of proinflammatory substances by its inhibition of phospholipase-2 activity.
The role of corticosteroids in interrupting the inflammatory pathway is shown in Figure 6-1.
Figure 6-1. Inflammatory pathway.
Pain relief after injection of a neuroma with corticosteroids can be due to:
• Softening of the scar that enclosed the nerve fibrils
• Reducing the mechanical transmission that would produce pain
Corticosteroids act at the nerve fibers and affect the transmission of pain. A study in which the sciatic
nerves of rats were ligated and then treated with either triamcinolone hexacetonide, triamcinolone
diacetate, or dexamethasone demonstrated a statistically significant reduction in the incidence of
spontaneous discharge of the A beta fibers in a neuroma compared to the saline control. The application
of corticosteroids to the cut nerves prevented ectopic neuroma hyperexcitability and decreased the
discharge in active neuromas that had been present for 3 to 10 days postoperatively. A study by Johnasson
of corticosteroids on exposed rat nerves interestingly suggested that its application reduced the
transmission of normal unmyelinated C-fibers that carry nociceptive impulses.33
With inflammatory, neuralgic, and paresthetic pain, the initial insult results in:
• Lowered activation threshold
• Increased sensitivity to various stimuli
• Prolonged impulse discharge
• Corticosteroids can normalize the abnormally lowered activation threshold and reduce impulse
amplitude and propagation
COMPLICATIONS OF CHRONIC CORTICOSTEROID THERAPY

• Weight gain
• Hyperglycemia
• Congestive heart failure
• Adrenal insufficiency
• Cushing syndrome
Adrenal Insufficiency
Adrenal Insufficiency is a significant concern with frequent exogenous corticosteroid administration
because of the interaction with the HPA axis which functions on a feedback mechanism. Symptoms
include:
• Hypotension
• Orthostatic Hypotension
• Generalized weakness
• Weight loss
• Anorexia
• Lethargy
• Depression
• Abdominal symptoms
• Amenorrhea
The degree of adrenal suppression is affected by the dose, frequency, chronicity and intervals between
glucocorticoid administration. However, an acute suppression of ACTH after a single dose of epidural
trimacinolone and suppression of cortisol levels following an intra-articular and intramuscular injection
have also been shown. Prompt recognition and treatment are essential. The duration of adrenal
suppression with the commonly used depot corticosteroids is shown in Table 6-2. Adrenal suppression
has been reported to take up to 9 to 12 months to recover after chronic use of supraphysiologic doses of
glucocorticoids.
TABLE 6-2. Adrenal Suppression and Depot Corticosteroids16
Hyperglycemia
There are conflicting reports regarding the effect of intra-articular and epidural steroid injections on
glucose levels. Significant hyperglycemia may occur and is secondary to:
• Insulin antagonism
• Increased hepatic gluconeogenesis
• Inhibition of peripheral glucose uptake
This fact is even more relevant due to the fact that lumbar spinal stenosis is more prevalent in patients
with diabetes, thus highlighting the need for patient education and vigilance on this matter. Furthermore,
elevated glucose levels have been shown to be an important risk factor in postoperative infection after
spinal surgery and the same risk may hold for spinal injections as well.
Cushing syndrome has also been described following repeated epidural steroid administrations. This
condition manifests as:
• Truncal obesity
• Osteopenia
• Hyperglycemia
• Hypertension
Therefore, it is important to have the patient’s diabetes optimized before the injection followed by
postinjection glucose vigilance.
Some of the other complications reported with chronic administration of corticosteroid are:
• Skin depigmentation
• Skin atrophy
• Facial flushing
• Tendon rupture
• Myopathy
COMMERCIALLY AVAILABLE PREPARATIONS

Although various corticosteroids preparations are available for several different modes of administration,
the injected depot form is most commonly utilized in pain medicine due to their sustained effect in the
treated area. The most commonly used depot steroid preparations are:
• Methylprednisolone acetate
• Triamcinolone acetonide
• Triamcinolone diacetate
• Betamethasone acetate
Although data on comparative efficacy is lacking, it can be beneficial to understand the physical
properties, solubility, duration of action, particulate size, and presence of additives in individual
preparations.
Solubility is a critical component since corticosteroids with a lower solubility will theoretically result
in a longer therapeutic action with less systemic effects than that of a compound with a high solubility.
However, it should be noted that this may or may not correlate with the clinical effect. For example, when
triamcinolone hexacetonide, a compound with a lower solubility, was compared with methylprednisolone
acetate, the triamcinolone had a lesser clinical effect than methylprednisolone acetate when used in the
treatment of osteoarthritic knees.
The duration of action differs significantly among the corticosteroids. This is a highly variable value
and can range from 6 to 90 days. The following chart (Table 6-3) reviews the basic characteristics of the
different corticosteroids that are commonly used in interventional pain medicine.
TABLE 6-3. Characteristics of Corticosteroids5,20
The preservatives found in corticosteroid formulations play a role in their selection as well since there
have been case reports of adverse effects attributed to the preservatives alone. A case report of flaccid
paraparesis for 16 months following an epidural was linked to the benzyl alcohol preservative that was in
the saline solution injected through the epidural catheter. Benzyl alcohol is effective against both gram-
positive and gram-negative bacteria which can be found in epidural abscesses. Another potential culprit
is polyethylene glycol which was shown to be neurolytic and produced degeneration of rat nerves. It has
also been shown that concentrations of greater than 20% of polyethylene glycol can diminish the action
potentials of myelinated alpha, beta, and unmyelinated C-fibers. This neurotoxic risk has led to the
practice of dilution of the corticosteroid preparation in order to lessen the risk from the concentrated
preservatives as well as improve the spread of the injectate.
PARTICULATE VERSUS NONPARTICULATE

CORTICOSTEROIDS
Particle size in corticosteroids has posed an important debate in the treatment of chronic pain. Solutions
with larger particles would seem to be preferred given their longer duration of action. The risk of
embolization has been brought up as a hypothetical concern with particulate solutions. Although all
synthetic corticosteroids have long biological half lives (36-72 hours), this duration can be further
prolonged by a particulate formulation that can slowly release into the localized area. However, multiple
case reports of paraplegia, conus infarction, quadriparesis, cerebellar infarction, and death have been
cited, primarily after cervical transforaminal injections.
The exact mechanism of neural injury is uncertain in many of these cases. The cause of injury may be
due to one or more of the following factors:
• Sustained compressive effect of the injectate that exceeds the local arterial pressure or neural
perfusion pressure in the area injected producing local or distant neural ischemia.
• Mechanical needle injury to the vasculature that disrupts the neural blood supply.
• An advancing needle provoking vasospasm of inflamed vasculature
• Intra-arterial injection and distal embolization of a particulate steroid
• Previous spine surgery appears to be an independent risk factor for spinal cord infarction possibly due
to altered anatomy, vascular relocation, and neovascularization
Almost all the cases of lumbar transforaminal epidural steroids resulting in spinal cord infarction were
patients who had prior lumbar spine surgery. Although less likely, an intraosseous injection (due to
osteopenia) with a particulate steroid has been demonstrated to travel to the inferior vena cava. It is
questionable whether such communication can occur with the arterial circulation leading to
cerebrovascular or spinal embolization or whether venous embolism of steroid particles would be of
sufficient caliber to result in neural damage.
The pathogenesis of the final injury may be due to any one of the above factors alone or a combination
of them. There has been much discussion of types of steroids injected in the epidural space and specific
focus on particulate steroid size in relation to the inner blood vessel diameter in the region. However,
when the particulate steroid embolization is put into perspective, it is only one of many potential
explanations for neural injury.
The highly variable vascular anatomy of the spinal cord presents a certain amount of inherent risk
during any spinal injection. The steroid particles have been analyzed and measured under a high-power
microscope to characterize their physical properties more accurately. Both methylprednisolone and
triamcinolone could aggregate to greater than 100 micrometers which could contribute to occlusion. The
different particle characteristics are shown in Figure 6-2.
Figure 6-2. Microscopic appearance of corticosteroids.5 (Reproduced with permission from The Spine
Journal 2004; 4: 468-474.
Derby et al in a corollary experiment used the size of a red blood cell (7.5 × 7.8 μm in diameter) as the
reference point for a blood vessel and compared it to the sizes of the particulate matter of the
corticosteroid preparations.30 Derby’s observations are shown in Table 6-4.
TABLE 6-4. Size of Steroid Particles Compared to RBC (7.5-7. μm)
There is no conclusive evidence that compares the efficacy of particulate versus nonparticulate
steroids. Most studies with positive results for epidural steroids injections have been performed with
particulate steroids suggesting that the use of nonparticulate steroids based on a theoretical risk may not
be comparably efficacious.
Suggested Reading
Hollander J et al. Hydrocortisone and cortisone injected into arthritic joints. JAMA. 1951;147:1629-
1635.
Kushnerik V, Altman G, Gozenput P. Pharmacology of steroids used during epidural steroid injections.
Tech Regl Anesth Pain Manag. 2009;13:212-216.
Manchikanti L. Role of neuroaxial steroids in interventional pain management. Pain Physician
2002;5:182-199.
References
1. Kushnerik V, Altman G, Gozenput P. Pharmacology of steroids used during epidural steroid injections.
Tech Regl Anesth Pain Manag. 2009;13:212-216.
2. Devor V, Govrin-Lippmann R, Raber P. Corticosteroids suppress ectopic neural discharge originating
in experimental neuromas. Pain. 1985;22:127-137.
3. Craig D, Habib G. Flaccid paraparesis following obstetrical epidural anesthesia: possible role of
benzyl alcohol. Anesth Analgesia. 1977;2:219-221.
4. Zaloga G, Marik P. Hypothalamic-pituitary-adrenal insufficiency. Crit Care Clin. 2001;17:25-41.
5. Tiso R, Cutler T, Catania JA, Whalen K. Adverse central nervous system sequelae after selective
transforaminal block: the role of corticosteroids. Spine J. 2004;4:468-474.
6. Hollander J, Brown EM, Jessar RA, Brown CY. Hydrocortisone and cortisone injected into arthritic
joints. JAMA. 1951;147:1629-1635.
7. Benzon H. Epidural steroid injection for low back pain and lumbosacral radiculopathy. Pain.
1986;24:277-295.
8. Kumar N, Newman R. Complications of intra- and peri-articular steroid injections. Br J Gen Pract.
1999;49: 465-466.
9. Dieppe P, Sathapatayavongs B, Jones HE, Bacon PA, Ring EF. Intra-articular steroid in osteoarthritis.
Rheumatol Rehabilitation. 1980;19:212-217.
10. Raynauld JP, Buckland-Wright C, Ward R, et al. Safety and efficacy of long term intraarticular steroid
injections in osteoarthritis of the knee. Arthritis Rheum. 2003;48:370-377.
11. Caldwell J. Intra-articular corticosteroids. Drugs 1996; 4:507-514.
12. Lazarevic M, Skosey JL, Djordjevic-Denic G, Swedler WI, Zgradic I, Myones BL. Reduction of
cortisol levels after single intra-articular and intramuscular steroid injection. Am J Med 1995;99:370-
373.
13. Reid DM, Patel S, Reid IW, Eastmond CJ, Rennie, JAN. Hypothalamic-pituitary-adrenal axis function
in patients receiving long term intra-articular corticosteroids. Clin Rheumatol. 1983;2:159-161.
14. Rull M, Clayburne G, Sieck M, Shumacher HR. Intraarticular corticosteroid preparations: different
characteristics and their effect during inflammation induced by monosodium urate crystals in the rat
subcutaneous air pouch. Rheumatology. 2003;42:1093-1100.
15. Smith J, Gomez N. Local injection therapy of neuromata of the hand with triamcinolone acetonide: a
preliminary study of twenty two patients. J Bone Joint Surg. 1970; 1:71-83.
16. Manchikanti L. Role of neuroaxial steroids in interventional pain management. Pain Physician.
2002;5:182-199.
17. Kay J, Findling JW, Raff H. Epidural triamcinolone suppresses the pituitary-adrenal axis in human
subjects. Anesthesia Analgesia. 1994;79:501-505.
18. Abdi S, Datta S, Trescot AM, Epidural steroids in the management of chronic spinal pain: a
systematic review; Pain Physician. 2007;10:185-212.
19. Noerdlinger M, Fadale P. The role of injectable corticosteroids in orthopedics. Orthopedics.
2001;24:400-405.
20. Cole B, Schumacher R. Injectable corticosteroids in modern practice. J Am Acad Orthop Surg.
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21. Benzon H, Chew TL, McCarthy RJ, Benzon HA, Walega DR. Comparison of the particle sizes of
different steroids and the effect of dilution. Anesthesiology. 2007;106:331-338.
22. Ackerman W, Ahmad M. The efficacy of lumbar epidural steroid injections in patients with lumbar
disc herniations. Anesthesia Analgesia. 2007;104:1217-1222.
23. Swartz S, Dluhy R. Corticosteroids: clinical pharmacology and therapeutic use. Drugs. 1978;15:238-
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24. Gharibo C, Koo C, Chung J, Moroz A. Epidural steroid injections: an update on mechanisms of injury
and safety. Tech Regl Anesth Pain Manag. 2009;13:266-271.
25. Altman R. Practical considerations for the pharmacological management of osteoarthritis. Am J
Managed Care. 2009;15:236S-244S.
26. Deer T, Ranson M, Kapural L, Diwan S. Guidelines for the proper use of epidural steroid injections
for the chronic pain patient. Tech Regl Anesth Pain Manag. 2009;13:288-295.
27. Derendorf H, Möllmann H, Grüner A, Haack D, Gyselby G. Pharmacokinetics and pharmacodynamics
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28. Knight Cl, Burnell JC. Systemic side-effects of extradural steroids. Anesthesia. 1980;35:593-594.
29. Nelson DA, Landau WM. Intraspinal steroids: history, efficacy, accidentality, and controversy with
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injections. Pain Med. 2008;9:227-234.
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particulate and nonparticulate corticosteroid preparations for cervical radicular pain. Pain Med.
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32. Elven J, Crosby C, Song, Mcgirt M, Devin C. Effects of epidural steroid injections on blood glucose
levels in patients with diabetes mellitus. Spine.
33. Johansson A, Hao J, Sjolund B. Local corticosteroid application blocks transmission in normal
nociceptive C-fibers. Aeta Anaesthesiol Scand. 1990;34:335-338.
34. Olmarker K, Byröd G, Cornefjord M, Nordborg C, Rydevik B. Effects of methylprednisolone on
nucleus pulposus-induced nerve root injury. Spine. 1994; 19:1803-1808.
35. Carette S, Marcoux S, Truchon R et al. A controlled trial of corticosteroid injections into facet joints
for chronic low back pain. N Engl J Med. 1991;14:1003-1007.
36. McGrath J, Schaefer M, Malkamaki D. Incidence and characteristics of complications from epidural
steroid injections. Pain Med. 2011;12:726-731.
37. Habib G, Abu-Ahmad R. Lack of effect of corticosteroid injection at the shoulder join on blood
glucose levels in diabetic patients. Clin Rheumatol. 2007;26:566-568.
38. Tuel S, Meythaler J, Cross L. Cushing’s syndrome from epidural methylprednisolone. Pain.
1990;40:81-84.
39. Barash P, Cullen B, Stoelting R, Cahalan M, Stock C. Handbook of Clinical Anesthesia. Philadelphia,
PA: Wolters Kluer Health; 2009.
CHAPTER 7
Local Anesthetics
Christopher Voscopoulos and Mark J. Lema
INTRODUCTION
Local anesthetics (LAs) are used in many clinical scenarios that require the pain practitioner to be
intimately familiar with their pharmacokinetic and pharmacodynamic properties. They are used in the
prevention of acute, inflammatory, nociceptive, cancer-related, neuropathic, and chronic pain, for
diagnostic and prognostic purposes, and in the possible prevention of chronic pain.1
Operating primarily by their interaction with sodium voltage dependent channels (NaVs) to block
sodium (Na+) entry into the neuron, LAs interrupt nerve impulse conduction and propagation. However, in
recent years, other actions, such as LA interaction with other non-Na+ ion channels and G-protein
receptors, which may be important in their ability to prevent and treat pain, have been described.2 These
interactions take place in both the central and peripheral nervous system. In a concentration dependent
fashion, LAs interrupt autonomic, sensory, and motor impulses, giving rise to autonomic system blockage,
sensory analgesia, and muscle paralysis. With a deeper understanding of both the pharmacokinetics and
pharmacodynamics of LAs, a higher rate of treatment success can be achieved, with a reduction in side
effects. This chapter aims to focus on the newest information regarding LA mechanisms,
pharmacodynamics, and toxicity.
PREPARATIONS
LAs, being poorly soluble in water, are mixed with hydrochloride salts. If epinephrine is added to the
solution, sodium bisulfate is often added to further lower the pH to about 4 to prevent its oxidative
decomposition.
LAs such as lidocaine, tetracaine, and bupivacaine are also manufactured in liposomal vesicles. Such a
formulation provides for a prolongation of action and a decrease in toxicity.3 Such a formulation allows
for the slow continuous subcutaneous infiltration of the drug providing analgesia for up to 96 hours to
decrease toxicity.4
Since the pKa of most LAs is approximately 8, within the acidic carrier medium they are dissolved in,
pH 3.9 to 6.5, only approximately 3% of the drug exists in the lipid-soluble form. Because the lipid-
soluble form is felt important for LA mechanism of action, alkalinization, via addition of sodium
bicarbonate, is used by some practitioners. This process shifts the pH of the medium to become closer to
the pKa of the drug, allowing for more of the drug to exist in the lipid-soluble form. The result is a
hastening of the onset of LAs in peripheral nerve and neuraxial blocks by 3 to 5 minutes, a deepening of
the depth of sensory and motor block, and an increase in the epidural spread of the drug.5 However,
prolonged or excessive alkalinization can cause LA molecules to precipitate from suspension.
Additionally, the value of adding sodium bicarbonate to solutions to enhance speed of onset also depends
on the injection site and the specific physiochemical properties of the individual LA used.6
STRUCTURE
LAs consist of 4 portions:
1. Aromatic ring
2. Ester or amide linkage
3. Hydrocarbon chain
4. Tertiary amine group (Figure 7-1)
Figure 7-1. The four parts of a local anesthetic molecule. Local anesthetics consist of four portions: (1)
aromatic ring, (2) ester or amide linkage, (3) hydrocarbon chain, and (4) tertiary amine group.
By analyzing the type of bond that conjoins the hydrocarbon chain to the lipophilic aromatic ring, two
types of LA classes are discerned; the amino ester–linked local anesthetics and the amino amide–linked
local anesthetics (Figure 7-2).
Figure 7-2. Prototypic amino amide, lidocaine, and amino ester, procaine, local anesthetics. Note the
amide bond conjoining the hydrocarbon chain of the lidocaine molecule to the aromatic ring, and the ester
bond conjoining the hydrocarbon chain of the procaine molecule to the aromatic ring. These different
types of bonds are what distinguish the two classes of local anesthetics.
Four LAs are characterized as pipecoloxylidides:

1. Mepivacaine
2. Bupivacaine
3. Levobupivacaine
4. Ropivacaine
Because the pipecoloxylidides have an asymmetric carbon atom, they are chiral drugs, which means
they can have a left (S) or right (R) handed configuration. These configurations are mirror images of each
other and are known as enantiomers or stereoisomers (Figure 7-3).
Figure 7-3. Chemical structure of ester and amide local anesthetics. Esters and amides share many
features, including a substituted benzene ring at one end of the molecule, and a tertiary amine nitrogen at
the other end. Note that prilocaine is an exception in that it has a secondary amine on its hydrophilic end.
Mepivacaine, bupivacaine, and ropivacaine are chiral drugs because the molecules possess an
asymmetric carbon. The red underscore line highlights the common benzene ring, the blue arrow
highlights the common tertiary amine nitrogen, the green underscore highlights the chiral carbon, and the
green box highlights the chiral drugs.
Aside from ropivacaine and levobupivacaine, all other LAs are either racemic mixtures, or have no
asymmetric (chiral) carbons.
It is easy to appreciate that these two forms of chiral LAs, the S and R forms, have their own
pharmacodynamic, pharmacokinetic, and toxicity profiles.7 Generally speaking in reference to LAs, the S
form is less toxic, more potent, and longer acting than the R form or the racemic mixture.6
Because of these observations, ropivacaine and levobupivacaine were developed as pure S
enantiomers, which offer less neurotoxicity and cardiotoxicity.8
A complete comparative pharmacology of LAs can be found in Table 7-1.
TABLE 7-1. Comparative Pharmacology of Local Anesthetics

As evident in Figure 7-4, since the creation of chloroprocaine in 1955, emphasis has shifted toward the
development of amide LAs.
Figure 7-4. Chronology of the development of local anesthetics.
This is due to the allergenic potential of esters, as well as their instability. As the evolution of amide
LAs progressed, the testing of various modifications to the template structures of procaine and lidocaine
revealed that increasing the molecular weight of the molecules, by adding carbon atoms to either end of
the structure or to the amide link, generally increases the lipid solubility, protein binding, duration of
action and toxicity, and influences biotransformation and metabolism of the molecule.6
MECHANISM OF ACTION
Voltage-gated sodium channels, NaV1.1–NaV1.9, are essential for voltage sensing, generation, and ion
conduction of electrical impulses in excitable cells.9 Na+ ions are naturally permeable through these ion-
selective channels. Simplistically speaking, by inhibiting the passage of Na+ ions through these ion-
selective sodium channels, by preventing them from “opening,” LAs prevent threshold potential, and,
hence, action potential propagation10 (Figure 7-5).
Figure 7-5. How local anesthetics interact with sodium channels to prevent threshold activation Local
anesthetics slow the rate of depolarization of the nerve action potential such that the threshold potential is
not reached. As a result, an action potential cannot be propagated in the presence of local anesthetic, and
conduction blockade results.
NaV channels are divided into those that are tetrodotoxin sensitive (TTX-S Na+) and tetrodotoxin
resistant (TTX-R Na+) channels.
• Sensory neurons tend to express tetrodotoxin sensitive NaV channels.
• In contrast, many nociceptive A-delta and C-fibers expressed in dorsal root ganglion cells express
tetrodotoxin-resistant NaV channels. There is evidence that channels from both groups are involved in
pain states.
If used in lower concentrations, LAs can produce sensory block with little or no motor block.
A number of factors contribute to sensory versus motor differential block:
• Including anatomic factors, the relative binding affinity of different local anesthetics to the variety of
NaV channels
• As well as possible contribution from other ion channels such as potassium (K) channels6
The administration of systemically administered intravenous lidocaine produces analgesia in several

acute and chronic conditions.9,11–18 The antinociceptive effect of bupivacaine may be due to direct
modulation of NMDA receptors in the superficial dorsal horn.19 Cited most commonly is LA binding to
normal or altered NaV channels located throughout the pain processing pathways of the body as the main
site of action for pain sensation modulation. It has been shown that lidocaine infusions (most commonly 5
mg/kg IV) or mexiletine are as effective as morphine, gabapentin, amitriptyline, and amantadine in the
treatment of neuropathic pain.20
Many chronic pain conditions, including complex regional pain syndromes I and II, are exacerbated by
sympathetic fibers that sprout into the dorsal root ganglia (DRG) after peripheral nerve injury, forming
abnormal connections with sensory neurons.21 Systemic lidocaine administered at the time of surgery via
an implanted osmotic pump remarkably reduces sympathetic sprouting two- to threefold.18 These effects
of systemic lidocaine lasted more than 7 days after the termination of administration.18 Nerve growth
factor (NGF) also contributes to the sympathetic sprouting. Lidocaine, bupivacaine, and procaine have
been shown to decrease NGF signaling by suppression of NGF-stimulated neurite outgrowth in PC12
cells, which is a cellular model of sympathetic sprouting.22
VOLTAGE-GATED NA (NaV) CHANNELS

NaV channels exist in 3 states:
• Resting-closed
• Activated-open
• Inactivated-closed
These correspond to the nerve membrane cycle of polarized, depolarized, and repolarized during action
potential evolution (Figure 7-6).
Figure 7-6. Functional states of voltage-gated sodium channels. Voltage-gated sodium channels exist in
three states, resting-closed, activated-open, and inactivated-closed, corresponding to the nerve membrane
cycle of polarized, depolarized, and repolarized during action potential evolution.
The resting-closed NaV channel represents the resting polarized state of the nerve fiber, the activated-
open state allows Na+ ions to flow into the cell.
• While the inactivated-closed state is impermeable to Na+ ions; hence Na+ flux ceases during this
phase, which represents the refractory period, and is an important element for the propagation of action
potentials down an axon.10
The affinity of LAs binding to NaV channels is ordered according to the conformational state of the
NaV channel, with the arrangement being activated-open > inactivated-closed > resting-closed.6 In
addition to the conformational state, stereospecificity, of both the LA and NaV channel is also important.
LAs bind primarily to the activated-open state, stabilizing this conformation and preventing the eventual
change of the channel to the resting-closed state in response to action potential propagation.
Upon closer examination, channels in the inactivated state are believed to be blocked by LAs on their
intracellular side at a specific site, a so called inner gate, activation gate, or H gate. This notion is also
consistent with LA potency being related to its lipid-soluble state allowing passage into the cell. This gate
is then removed in response to stimulation that opens the channel.
Once inside the cell, the low pH causes a greater fraction of the LA to assume an ionized state, and it is
this ionized state that binds to receptor.10 Upon LA binding to the intracellular portion of the receptor, it is
thought that a tethered plug is formed to produce an inactivation gate.
LAs also appear able to bind to the external opening of the NaV channel in the inactivated-closed state.
Because of their different chemical structures, LAs bind to differing sites on NaV channels along a
continuum, and binding is weak secondary to a poor fit. This poor binding helps to explain why the
inclusion of epinephrine to most LA helps prolong the binding opportunities of the LA to the receptor. By
decreasing blood flow to the receptor, epinephrine can help decrease the concentration gradient, between
the NaV channel and the regional blood vessels, across which the LA can diffuse.
Though the detailed description of the NaV channel above centered around LAs, it is important to note
that many compounds can inhibit these channels other than LAs, including general anesthetics, α2-agonists,
tricyclic antidepressants, alcohols, and toxins.10,23–28
SODIUM VOLTAGE DEPENDENT CHANNELS IN PAIN STATES

The responses of nociceptors to stimuli are encoded by action potentials, whose genesis and propagation
are dependent on NaVs, and it is thus not surprising that aberrant expression patterns of channels and
inherited sodium channelopathies have been linked to neuropathic and inflammatory pain.9
• Humans have a total of 9 functional genes that code for NaV channels.
• Seven of these genes code for neuronal NaV channels, and 2 codes for skeletal or cardiac NaV
channels.16
• Neuron specific NaV channels, such as NaV1.3, NaV1.6, NaV1.7, NaV1.8, and NaV1.9, are found on
unmyelinated axons, nodes of Ranvier, and small dorsal root ganglion nociceptors (DGRs), and are
pivotal for signal transmission along the pain axis.9
• Nav1.3, Nav1.7, Nav1.8, and Nav1.9 are preferentially expressed in peripheral sensory neurons and
Nav1.3 is upregulated along pain-signaling pathways after nervous system injuries9 (Table 7-2).
• Nonneuronal NaV channels include NaV1.4, found in skeletal muscle, and NaV1.5, found in cardiac
muscle. Further variation amidst individual NaV channels is seen by alternative splicing of genes.
TABLE 7-2. Sodium Channels Preferentially Expressed in Peripheral Neurons Add

Reference and Acquire Permission
An example of this is the NaV1.7 channel, in which 4 alternative splice variants are expressed in
human DRG neurons.
Furthermore, it has been found that this alternative splicing of the human NaV1.7 can specifically
modulate the biophysical properties and cAMP-mediated regulation of this channel possibly
influencing neuronal excitability and pain sensation.11,29
Individual isoforms are known to be particularly important in the pathophysiology of chronic pain
syndromes9 (Table 7-3).
TABLE 7-3. Results of Knock-Down and Knock-Out Studies on Sodium Channels
FREQUENCY-DEPENDENT AND STATE DEPENDENT BLOCK

Because LAs bind preferentially to the NaV receptor in the activated-open state, an action potential must
first be propagated to allow the receptor to assume this configuration.
The larger the activation potential and the more rapid the degree of firing, the greater the assumption of
the activated-open state, and, hence the more rapid the block.
• This phenomenon is termed frequency-dependent block.
• It is also sometimes called “use-dependent,” when reference is made concerning the degree and
rapidity of firing, and “state-dependent” block when reference is made concerning the activated-open
state of the NaV channel having the greatest affinity for LAs.
• Of note, LAs do not just passively bind to one of the preexisting channel conformations, but may
actively deform the channel, as described by the induced fit model.30,31
OTHER SITES OF ACTION

Since LAs have low potency, and are relatively nonselective for the NaV channel, they also bind and
inhibit a variety of other channels, with nearly the same low affinity as for Na channels, and arguments
have been put forward to include each of these receptors in the possible mechanism of action of
LAs.10,32–38
To begin to appreciate whether or not these other channels play a role in the mechanism of action of
local anesthetics in producing nerve conduction blockade, lidocaine 1 mM will reliably inhibit most Na
channels, but will also inhibit (to a greater or lesser extent) nearly every other enzyme or ion channel.39
These additional binding sites could possibly contribute to LAs mechanism of action.32,39
Perhaps the main area of importance of receptors other than the NaV channels lies in their potential
identification of binding sites and mechanisms that could contribute to local anesthetic production of
neuraxial anesthesia, side effects, and clinical differences among the local anesthetics that cannot be
explained by their relative affinities for Na channels.
MINIMUM CONCENTRATION
During the application of LAs for use in regional anesthesia, only a small fraction of these drugs will be
bound to NaV channels.40
• In order for the intended anesthesia to ensure, a “critical length” of the nerve must be blocked.
• This length, though it varies based on nerve fiber type, generally exceeds 2 cm.
• For conceptual purposes, two or three consecutive nodes of Ranvier are approximately 1 cm.
• Note is made here that this length of greater than 2 cm for blockade is considerably larger than the
commonly described 3 nodes of Ranvier. This length description is accurate except at very high LA
concentrations.41
Cm is the term used to describe the minimum concentration of local anesthetic needed for conduction
blockade. Several factors are known to influence Cm.
• A larger nerve fiber size requires a higher concentration of LA, whereas higher tissue pH and
frequency of nerve stimulation decreases Cm.
• Each LA has its own individual Cm, however, as a generality motor fibers require twice the Cm as
sensory fibers to be blocked.
• This observation contributes to the ability of LAs to provide sensory anesthesia without muscle
paralysis.
Though animal studies have shown that lower volumes of more concentrated lidocaine produce shorter
latencies and longer duration, it is the mass of drug delivered that determines the success of block.42
Accordingly, to achieve this mass effect, improvement in anesthesia is seen by both increasing volume or
concentration.43,44
In comparing the relativity of ease of nerve impulse blockade, the most easily blocked nerve fiber types
are preganglionic B fibers, which contributes to the sympathectomy seen with epidural anesthesia.
This concept describes differential conduction blockade, in which differing concentrations of LAs will
block differing fibers.
• Following progressively higher concentrations, C fibers and small to medium A fibers are blocked;
higher concentrations of LAs are generally required to block C fibers as compared to Aδ or Aβ
fibers.45,46
• Blockade of these fibers at this concentration will block pain and temperature, however, touch,
proprioception, and motor function will still be intact.
• For clinical applications, it is observed that the fastest onset and shortest duration of anesthesia occur
with intrathecal or subcutaneous injections. This is compared to a slower onset and longer duration
obtained with plexus blocks.
Changes in sensitivity to LAs can be seen in pregnancy in which more rapid onset of conduction
blockade is seen with reduced doses.47 This is felt to be caused by protein binding characteristic changes
in alpha-1-acid glycoprotein, the main binding protein of amide LAs, in which both total protein binding
and protein concentration are reduced, caused by a nonprogesterone effect.48–50 It is also important to note
that the spread of neuraxial anesthesia also increases during pregnancy, possibly related to an
engorgement of epidural veins and the subsequent decreasing of the epidural fat space.10,51,52
PHARMACOKINETICS
LAs are weak bases with pKa ranging from 7.6 to 8.9 (see Table 7-1). This said, at physiologic pH
(range from 7.35 to 7.45), less than half of LAs will exist in a nonionized, and, hence, a non-nerve
penetrable form.
• As an example, procaine, with the highest pKa of LAs at 8.9, less than 5% of the molecule will exist in
the nonionized form at physiologic pH.
• Conversely, LAs with pKas closest to physiologic pH, such as mepivacaine, pKa of 7.6, have the most
rapid onset of action, having a more favorable ratio of nonionized molecules. It is the nonionized form
of an LA that gains entrance into the cell though diffusion through the cell membrane.
• The onset of anesthesia generally slows with increasing LA lipid solubility.
ABSORPTION AND DISTRIBUTION

Several factors will influence the ultimate absorption into the systemic circulation of LAs.
These include:
• The site of injection, as LAs will have differing absorption rates at differing sites (Figure 7-7)
• Dosage
• Use of epinephrine
• Characteristics of the drug
• Mode of administration
Figure 7-7. Peak plasma concentrations of local anesthetics are influenced by the site of injection for
accomplishment of regional anesthesia.
Plasma concentration will be determined by

• Rate of tissue distribution and/or redistribution.
• Rate of clearance of the drug.53–55
Cardiac output is also a factor in tissue distribution and intercompartment clearance.56 Lipid solubility
is important in redistribution, and is a primary determinant of intrinsic LA potency.
• LAs are ultimately cleared from the plasma via metabolism and excretion.
• Age and hepatic function will influence the absorption and plasma concentrations of LAs.
• Protein binding of LAs influence their distribution and excretion.
• Protein binding for LAs is in direct proportion to their lipid solubility, and inversely proportional to
the plasma clearance of the drug.57–59
• Because of their slower metabolism (see below), amide LAs are more widely distributed in tissues
compared with ester LAs.
It is well established that systemic absorption of local anesthetics correlates positively with the
vascularity of the injection site, with ordering as follows:
intravenous > tracheal > intracostal > paracervical > epidural > brachial plexus > sciatic >
subcutaneous6
In addition to site, duration of LA administration is also a factor.
PLACENTAL TRANSFER
Several factors influence the amount and degree of LA transfer between the maternal umbilical artery and
the umbilical vein of the fetus:
• Protein binding of the LA
• Metabolism of the LA
• pH status of the fetus
In terms of protein binding, bupivacaine is approximately 95% protein bound, lidocaine is
approximately 70% protein bound, and prilocaine is approximately 55% protein bound, and this order is
in congruence with the lipid solubility of these compounds. When local anesthetics bind to proteins, they
are unable to cross membranes via diffusion, as their free soluble fraction is not available. In reference to
a drug’s ability to cross the placenta, only the free fraction in plasma is able to do so, and the amount that
crosses the plasma through the placenta and into the fetal circulation is expressed as a maternal umbilical
artery to fetal umbilical vein ratio (MUA/FUV).
As it follows, bupivacaine has an MUA/FUV of only 0.32, lidocaine 0.73, and prilocaine 0.85.60 Since
ester LAs are rapidly hydrolyzed within seconds after they enter the systemic circulation, they are not
available to transfer across the placenta in significant amounts. Additionally, once ester local anesthetics
cross the placenta, they are rapidly degraded in the fetal circulation as well, further limiting their fetal
toxicity.
Only the nonionized form of LAs can cross cell membranes. However, since LAs are weak bases, any
acidic medium they encounter can cause ionization of the LA and prevent it from being able to diffuse
passively across cell membranes. Such a scenario is possible in the fetus. When a fetus is stressed,
secondary to a myriad causes normally related to hypoperfusion, the fetal pH can become acidotic. As
such, any LAs that had diffused across the placenta in a nonionized form can become ionized in the fetus
and, subsequently, trapped in the fetal circulation. This phenomenon has been described and termed the
“ion trapping” of LAs. Clinically, given the widespread use of lidocaine in obstetric anesthesia, and
lidocaine’s pharmacokinetic profile as described above, the risk of ion trapping is likely greatest with
this LA.
CLEARANCE
Amide LAs are primarily metabolized in the liver. Their renal excretion in an unchanged form is minimal.
Ester LAs are rapidly metabolized via intravascular hydrolysis by pseudocholinesterase, and, if able to
reach the liver, hydrolysis within the liver as well. Because this degradation is so rapid, pharmacokinetic
studies are limited.
TOXICITY
True IgE mediated type I, or immediate, hypersensitivity allergies to LAs are associated with esters, not
amides.
In comparison to the type I hypersensitivity reactions encountered with ester LAs, amide LAs can cause
a type IV, or cell mediated hypersensitivity reaction. Accordingly, the intradermal injection patch test is
the screening method used to determine if a specific substance causes allergic inflammation of the skin
indicative of type IV hypersensitivity.
Because effects are more closely tied to the specific properties of local anesthetics, as a generalization,
initial symptoms of local anesthetic toxicity
• Are lightheadedness and dizziness
• Followed shortly thereafter by perioral numbness
• Tinnitus
• Metallic taste in the mouth
• Progressive excitatory CNS effects can ensue and
Include visual and auditory abnormalities
Shivering
Muscular twitching
In its highest level of CNS excitation, generalize tonic-clonic seizures
• Furthermore, CNS depression can lead to respiratory depression or arrest.
In addition to allergic reactions, myotoxicity and neurotoxicity can be caused by all LAs if high enough
concentrations are used. Transient neurologic symptoms (TNS) and cauda equina syndrome have been
reported with the use of 2% and 5% lidocaine administered intrathecally.
In a study to determine the relative risk for developing TNS after spinal anesthesia with LAs, lidocaine
was found to produce a greater incidence of TNS as compared to bupivacaine, prilocaine, procaine, and
mepivacaine.61 Furthermore, in reference to TNS incidence, the lithotomy position appears to be a
predisposing factor.
In an analysis of the myotoxic effects of LAs on muscle tissue, 1% procaine, 0.2% tetracaine, 0.5%
lidocaine, and 0.75% bupivacaine, produced effects that were confined principally to the muscle fiber,
whereas 2% chloroprocaine, 0.25% dibucaine, 0.5% lidocaine with 1:200,000 epinephrine and 2%
piperocaine produced toxic effects on other tissue components of the muscles in addition to affecting
muscle fibers.62
These effects were restored by regeneration and 30-day muscles showed relatively few long-term
effects of the damage. However, it was concluded that procaine produces the least and bupivacaine the
most severe muscle injury.62
In another study with ropivacaine, bupivacaine causes tissue damage of a significantly larger extent,
and, additionally, induces apoptosis in skeletal muscle cells.63
When the iron within the hemoglobin molecule becomes oxidized, it changes from the ferrous (Fe2++) to
the ferric state (Fe3+++), and methemoglobin results. Several LAs can produce methemoglobinemia, with
prilocaine, usually administered via ELMA cream, and benzocaine, being the most recognized.
It is because of benzocaine’s association with methemoglobinemia, usually in the form of hurricane
spray, that many hospital pharmacy systems in the US have stopped carrying this LA. However, it is
important to note that both lidocaine and bupivacaine are also capable of forming methemoglobin as well.
Studies have revealed that the doses of bupivacaine required to produce convulsive activity and
cardiac collapse are lower than that required of other LAs. In human studies, bupivacaine also causes
CNS and cardiovascular toxicity at doses lower than that of either ropivacaine or levobupivacaine, which
cause toxicity at approximately equipotent doses.64–67
Seizures induced by local anesthetics are usually self-limiting, and require maintenance of respiratory
gas exchange and control of muscle contractions (eg, intubation, oxygenation, short-acting muscle
paralysis).6
Drugs such as propofol, thiopental, midazolam, and diazepam are effective against these seizures.6,68–80
This also means that patients premedicated with midazolam or diazepam could manifest LA toxicity as
cardiac collapse without seizures, especially with the use of bupivacaine.70
To state the apparent, should signs or symptoms of toxicity develop, one should cease the
administration of LA.
As with all procedures, vital signs should be monitored in an effort to detect signs or symptoms of LAs
as early as possible. Since it is not so much the total dosing of LA, but the rate of rise of LAs that most
closely reflects risk for toxicity, care should be taken to avoid intravascular injections, especially intra-
arterial injections that may expose the CNS to LA without a first pass metabolism through the liver or
lungs. Additionally, injecting total doses of LA over multiple injections will also reduce the total plasma
rate of rise of LA, and should be considered when feasible for interventional pain management
procedures. Although the use of ultrasound, and other methods of direct visualization, for the placement of
regional anesthesia and/or pain procedure blocks have allowed practitioners the ability to use lower
volumes of LA, accidental intravenous or intra-arterial injection remains a risk.
In addition to the Advanced Cardiac Life Support recommendations for treatment of cardiac related
symptoms secondary to the use of LA, there is evidence for the use of lipid emulsion in the treatment of
bupivacaine cardiac toxicity.81 Until recently, it was unclear whether or not this treatment cross applies to
other LAs is not known.82–85 However, a recent case report of a patient successfully resuscitated with
lipid emulsion therapy after prolonged and intractable lidocaine toxicity perhaps demonstrates the need to
consider lipid emulsion therapy in the advanced cardiac life support algorithm for lidocaine toxicity, as
well as other lipid-soluble drug intoxications.86
METABOLISM AND UNIQUE PROPERTIES OF AMIDE LOCAL

ANESTHETICS
Amide LAs are metabolized primarily in the liver via cytochrome P450 microsomal enzymes.
Metabolites retaining LA activity and toxicity potential usually do so with lower potency than the parent
compound, depending on the LA involved. Accordingly, of the amide LAs, prilocaine is metabolized the
fastest, followed by lidocaine and mepivacaine, and, then followed by etidocaine, bupivacaine, and
ropivacaine.
Since the metabolism of amide LAs are slower, compared with that of ester LAs, accumulation, and
sustained plasma concentrations, are possible. As compared to ester LAs, this leads to a higher risk of
systemic toxicity with the amide LAs.
Lidocaine. Lidocaine undergoes oxidative dealkylation in the liver to monoethylglycinexylidide, which
is then hydrolyzed to xylidide.
Monoethylglycinexylidide is an active metabolite with a long elimination half-time. It has about 80% of
the activity of lidocaine in protecting against cardiac dysrhythmias.
Etidocaine. Less than 1% of etidocaine is secreted in the urine unchanged. Etidocaine causes a motor
block before blocking sensory nerves. Additionally, the motor block can out last the sensory block, giving
rise to a very unpleasant experience of a patient being in pain, however, lacking motor ability.87,88
Because of this, it is rarely used in current clinical practice.
Prilocaine. Prilocaine can be metabolized to an oxidizing metabolite, orthotoluidine. Orthotoluidine
can oxidize the iron molecule in hemoglobin to form methemoglobin. When methemoglobin levels reach 3
to 5 mg/dL, oxygen carrying capacity can be reduced such as a patient may appear cyanotic. Typically,
prilocaine doses >600 mg can cause this. Methemoglobinemia can be reversed with the use of methylene
blue.
Mepivacaine. Mepivacaine also lacks vasodilator activity, and, as such, is an alternative when desiring
to use an LA without epinephrine in a given clinical scenario. If used in neonates, the clearance of
mepivacaine can be prolonged.
Given mepivacaine’s fast onset, mepivacaine has been mixed with bupivacaine in an attempt to
decrease the speed of onset of the block. However, data is lacking as to the onset, duration, or quality of
the ensuing block. This said, toxicity seems added, as the seizure dosages and arterial plasma levels for
drug mixtures have been investigated and found as such.89
Bupivacaine. Bupivacaine is metabolized effectively in humans, as less than 1% of bupivacaine is
excreted unchanged in the urine.90 Four metabolic processes have been proposed: (1) aromatic
hydroxylation, (2) N-dealkylation, (3) amide hydrolysis, and (4) conjugation.91,92 Ring 4′-hydroxylation
and N-dealkylation, and subsequent conjugation, are minor metabolic pathways in humans, whereas
preliminary results indicate that bupivacaine may be resistant to amide hydrolysis.90,92,93
Its toxicity includes seizures and refractory cardiac arrhythmias.94 The plasma threshold in which these
toxic effects occur varies between 2 and 5 ug/L. The reason why such a wide range is given, is because
the toxic effects of bupivacaine rely more on the rate of rise of the serum concentration, then on the
absolute amount of the drug administered.
Levobupivacaine. Levobupivacaine is the S-enantiomer of bupivacaine. In relation to bupivacaine, its
duration of action is longer, it possesses less vasodilation compared with bupivacaine, and it is
approximately 13% less potent than racemic bupivacaine.
Ropivacaine. Ropivacaine is largely excreted in the urine (86%), however, unchanged ropivacaine is
excreted by the kidney only approximately 1%. It is mainly metabolized by the liver cytochrome p450
system into 2, 6-pipecoloxylidide and 3-hydroxyroropivacaine, both significantly less potent than the
parent compound.
METABOLISM AND UNIQUE PROPERTIES OF ESTER LOCAL

ANESTHETICS
As a whole, ester type local anesthetics are hydrolyzed rapidly in the blood by cholinesterase enzymes,
particularly pseudocholinesterase, and by a smaller amount of these enzymes in the liver. In general, the
rate of hydrolysis varies among the ester type local anesthetics, with the order, from the quickest to the
longest, being Chloroprocaine, procaine, and tetracaine. The longer the drug is available to exert its effect
on the body, the longer it is able to produce toxic effects as well. Accordingly, toxicity is inversely
related to the rate of hydrolysis. Procaine and benzocaine are metabolized to p-aminobenzoic acid
(PABA).
2-Choloroprocaine
Choloroprocaine is perhaps the only ester type local anesthetic still used commonly in current clinical
settings. Choloroprocaine undergoes oxidative decomposition, and, as such, numerous formulations have
been tried to decrease this event. Currently, it is manufactured in colored vials to reduce the entry of light
that can catalyze this event.
In the pregnant state, in vitro plasma half-life is 21 seconds in maternal blood and 43 seconds in fetal
blood, hence making fetal effects virtually nonsignificant. Even in cases of atypical cholinesterase were
individuals are homozygous for the atypical pseudocholinesterase, the half-life is only prolonged to about
2 minutes.
Aside from ester, local anesthetics not being used in IV regional blocks because they are broken down
rapidly in the blood, there has also been noted the incidence of thrombophlebitis with the use of
choloroprocaine.
Procaine
Less than 50% of procaine is excreted in the urine, whereas the rest is metabolized to both
paraaminobenzoic acid and diethylaminoethanol. Paraaminobenzoic acid is excreted unchanged in the
urine, whereas diethylaminoethanol is further metabolized. Allergy to procaine is usually due to
paraaminobenzoic acid, and not procaine itself. PABA is not associated with symptoms of systemic
toxicity.
Procaine, having vasodilator properties, it is often used in conjunction with epinephrine.
Benzocaine
Benzocaine is the ethyl ester of PABA, and, as such, PABA is formed as a metabolite in its metabolism.
Considering its nonionized form, it is ideally suited for topical uses as it can more easily penetrate
epithelial surfaces with a rapid onset and duration of 30 to 60 minutes. As such, a common use is for
awake tracheal intubation, in which single sprays of formulations of 20% benzocaine delivers the
recommended dose of 200 to 300 mg. Benzocaine has the potential to form methemoglobinemia should
doses exceed the recommended dose. Another popular formulation is cetacaine, which is a combination
of 14% benzocaine, 2% tetracaine, and 2% butamben.
Tetracaine
Like all esters, tetracaine is metabolized by hydrolysis by cholinesterases, primarily in the plasma and to
a lesser extent by the liver. Its metabolites include a PABA containing metabolite diethylaminoethanol.
In current medical practice it is occasionally used in spinal anesthesia.
Cocaine
Cocaine is metabolized by plasma and liver cholinesterases into water-soluble metabolites that are
excreted in the urine. About 1% of the drug is excreted unchanged in the urine. With the primary metabolic
event being hydrolytic ester cleavage, the main metabolite is benzoylecgonine (BE), with lesser
metabolites being ecgonine methyl ester (EME) and ecgonine, and additional minor metabolites including
norcocaine, p-hydroxycocaine, m-hydrococaine, p-hydroxybenzoylecgonine (pOHBE), and m-
hydroxybenzoylecgonine.95 These metabolites are used for assays to detect cocaine use in suspected
patients. In general, contingent on hepatic and renal function, benzoylecgonine can be detected as soon as
4 hours within the urine, and could be detectable for up to 8 days.
Accordingly, any disease or physiological states, such as pseudocholinesterase deficiency or pregnancy
can prolong the elimination life of cocaine. Cocaine in addition to being a local anesthetic, is a serotonin-
norepinephrine-dopamine reuptake inhibitor, with affects on the mesolimbic reward pathway that renders
it addictive.96
Given cocaine’s strong inherent ability to produce intense vasoconstriction, in modern medical
practice, it is predominantly used for nasal and lacrimal duct surgery and as an adjunct in nasal fiberoptic
intubation.
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CHAPTER 8
Botulinum Toxins
Charles E. Argoff and Howard Smith
BACKGROUND
Botulinum toxins are neurotoxins produced by the gram-positive, spore-forming, anaerobic bacteria,
Clostridium botulinum, as well as C butyricum, C baratii, and C argentinense.1,2 These toxins are the
most deadly human neurotoxins known. Clinically, botulism can occur following ingestion of
contaminated food or from a wound infection. The clinical signs of botulism include limb paralysis, facial
weakness, ophthalmoplegia, dysarthria, dysphagia, dyspnea progressing to respiratory arrest, constipation
progressing to ileus, and urinary retention.3 C botulinum produces 7 antigenically (immunologically)
distinct neurotoxins: A, B, C1, D, E, F, and G.
• Varied mechanisms of action of botulinum neurotoxin (BoNT) subtype are believed to be due to its
ability to inhibit multiple neurotransmitters from presynaptic vesicles. Specific proteins involved in
this process are affected by different toxins and thus different strains of toxin do not necessarily work
via the same mechanism.
• Only types A and B toxin are currently routinely used in clinical practice.
• Currently, there are 3 types of botulinum toxin type A commercially available in the United States
including onabotulinum toxin A (Botox), abobotulinum toxin A (Dysport), and incobotulinum toxin A
(Xeomin).
• Rimabotulinum toxin B (Myobloc) is the only botulinum toxin type B currently available in the United
States.
• Each toxin has been developed with different dosing units and they are not interchangeable—this
is clinically important to remember. Synaptosomal-associated protein (SNAP 25) is inactivated by
botulinum toxin type A and vesicle associated membrane protein (VAMP) is inactivated by botulinum
toxin type B.
• Its effect on motor function through inhibition of release of acetylcholine has been well documented.
Cleavage of either one of these proteins results in inhibition of acetylcholine release, disruption of
neuromuscular transmission, and paralysis of the muscle.
• Most important recent scientific discovery is of SNAP 25 on motor and sensory neurons.
• Several animal studies demonstrating the toxin’s inhibition of substance P, calcitonin-gene related
peptide (CGRP), glutamate, bradykinin, ATP, and purinergic receptors.
• Additional animal studies have suggested a clinically relevant central analgesic effect of type A toxin
as well.
The only FDA-approved specific pain indication for any current commercially available botulinum
toxin is chronic migraine for onabotulinum toxin A (Botox).4 The “off-label” use of botulinum toxin for
the treatment of other chronic painful conditions has been reported for cervical dystonia–associated neck
pain, chronic low back pain, and chronic lateral epicondylitis. Jabbari and Machado have recently
published a review of the use of botulinum toxin for refractory pain based on the evidence according to
the AAN evidence rating approach. The reader can review these references for additional information
regarding the use of botulinum toxins for chronic pain.
BOTULINUM TOXIN FOR THE TREATMENT OF CHRONIC

MIGRAINE
The most evidence for treatment with botulinum toxin is for the specific condition, chronic migraine. The
importance of defining this group has become vital for proper patient selection. The FDA has approved
the use of onabotulinum toxin A (Botox) for the treatment of chronic migraine only, and not tension type or
episodic migraine.
Chronic migraine has been defined as:
• A headache syndrome for more than 3 months
• At least 15 or more headache days per month
• The headache experienced for at least 4 hours
• The headache experienced for at least 8 months
A randomized placebo controlled study examined the use of 100 units of onabotulinum toxin in fixed
injection sites including the glabella, frontalis, temporalis, trapezius, and suboccipital regions in 41
patients with chronic migraine. Onabotulinum toxin A resulted in fewer migraine episodes 4 weeks after
injection with both reduced headache days and a reduced headache index (composite measure of both
headache frequency and intensity) at 16 weeks. Two much larger studies, PREEMPT 1 and PREEMPT 2
each evaluating approximately 700 patients consisted of a 24-week blinded period followed by an
extended open label arm. In contrast to the smaller study, which excluded chronic headache associated
with medication overuse, the PREEMPT trials included these patients. The primary outcome measure for
PREEMPT 1, the number of headache episodes, was not met but in PREEMPT 2, the primary outcome
measure, the number of headache days, was met. The change in headache days for treated patients in
PREEMPT 2 was 9 days vs. 6.7 days for placebo treated patients (p<0.001). PREEMPT 1 did meet its
secondary outcomes including number of migraine days. The FDA approved onabotulinum toxin A for the
treatment of chronic migraine in October, 2010, noting that it felt that a reduction in headache days was
more meaningful than a reduction in absolute number of headaches. The injection paradigm used in the
PREEMPT trials is seen in Table 8-1. Many consider the availability of this treatment to be a great
advance in the ability to treat chronic migraine. Published studies and our own experience would suggest
that other headache syndromes, for example, episodic migraine, or tension-type headache are not clearly
responsive to onabotulinum toxin A (Botox) injections.
TABLE 8-1. Onabotulinumtoxin A Dosing for Chronic Migraine by Muscle Using the
PREEMPT Injection Paradigm
Preprocedure Considerations
• Informed consent and appropriate explanation of the procedure including the potential benefits as well
as risks.
• We have performed with procedure safely in individuals on antiplatelet or anticoagulant therapy only
after checking with the physician prescribing such treatment.
• The patient can be seated during the procedure.
• This procedure is contraindicated with a known allergy or hypersensitivity to onabotulinum toxin A
(Botox).
• Fluoroscopy is not required nor recommended for this procedure.
Equipment
• Onabotulinum toxin A (Botox) is supplied in single-use 100 units or 200 units per vial.
• Four 1 cc syringes
• Two 3 cc syringes
• 20 gauge 1.5 in needle for reconstitution
• 30 gauge ½ -1 needle for injection
Botox must be reconstituted before using as toxin in the vial is vacuum dried.
The manufacturer of Botox recommends reconstituting the toxin with sterile, preservative free 0.9%
sodium chloride USP; however, some injectors have described successfully reconstitution with 1%
preservative free lidocaine. The dilution instructions for Botox vials are seen in Table 8-2. After drawing
up the appropriate amount of diluent into the correct size syringe, it should be slowly injected into the vial
and then gently mixed by gentle rotation of the vial. The Botox should be administered within 24 hours
after constitution and it can be stored after reconstitution in a refrigerator during this 24-hour period
(2°-8°C).
TABLE 8-2. General Considerations for Treatment

1. Currently, none of the available botulinum toxins is FDA-approved for a specific painful
state except for onabotulinum toxin A (Botox) for chronic migraine; therefore, use
otherwise for chronic pain is in an off-labeled manner. Patients should be informed of
this prior to treatment.
2. Significant side effects are uncommon. Pain, muscle weakness, and flu-like symptoms
have been reported. Spread of toxin has been noted with weakness, sometimes involving
muscles that were not directly injected. Autonomic side effects appear to be more
commonly seen with type B toxin.
3. Contraindications to treatment with botulinum toxin include pregnancy (category C), the
concurrent use of aminoglycoside antibiotics, myasthenia gravis, Eaton-Lambert
syndrome, or known sensitivity to the toxins.
4. Treating more frequently than the recommended interval of 12 wk may lead to the
development of antibodies to the toxin, which may also be associated with the
development of clinical resistance.
5. There is no valid way to reliably and consistently convert doses of different type A toxin
to other type A toxins nor to doses of type B toxin at present.
6. The use of botulinum toxin for pain management is part of a comprehensive treatment
program that has been developed based on an accurate diagnosis.
7. Be aware of current storage and handling recommendations for each of the toxins.
8. Whenever possible, use an injection technique, including needle size, that is the least
likely to cause additional pain.
9. Guidance techniques such as EMG, CT, or fluoroscopy should be used at the discretion
of the injector.
10. Prolonged observation following the injections is generally not warranted.
11. Follow-up should be arranged for 4-6 wk following injections.
12. More than 1 series of injections may be required to achieve maximal analgesic response.
Technical Considerations
• For chronic migraine, the recommended dilution is 50 U/mL (final concentration of 5 units/0.1 mL).
• The FDA approved dose for treating chronic migraine is 155 units administered intramuscularly.
• Each site is injected with 5 units via a sterile 30 gauge 0.5 in needle.
• For some people a 1-in needle may be needed in the cervical region.
• Only the procerus is injected unilaterally. All other injections are bilateral and symmetrical.
• The recommended interval between injection sessions is 12 weeks.
• Care must be taken to avoid over injection so that clinically significant muscle weakness will not
occur.
Postprocedure Follow-Up
• We recommend initial follow-up at 6 weeks after the first injection.
• Thereafter, every 12 weeks follow-up at the time of injection sessions unless otherwise requested by
the patient.
• It is important to remind the patient that it may take up to 3 to 5 sessions to maximize outcome.
• Local bruising or soreness at the injection sites is common and patients should be advised to apply
cold packs if it occurs.
Potential Complications and Pitfalls

• Muscle weakness.
• Spread of toxin and the development of swallowing difficulties.
• Infection is uncommon if the procedure is done aseptically.
• Excessive bleeding is uncommon.
CLINICAL PEARLS
• Be patient—the best results may not occur until after the third treatment. Many patients have described
“failing” Botox injection treatment of their chronic migraine because they were incorrectly told by their
“injector” that if they did not benefit sufficiently after the first treatment, then there was no reason to
continue. This has serious implications because the treatment can be very helpful even for those who
have failed to respond adequately to other approaches.
• Success will be measured in reduced number of headache days as well as reduced intensity of
headaches.
• There are no clear guidelines regarding when to stop treatment even when successful.
• Openly discuss this subject with your patients and generally those who are in a vulnerable age group
for chronic migraine who are successfully treated with Botox would prefer to continue with treatment
since this becomes their prophylactic regimen and they do not want to risk a severe, potentially
disabling exacerbation.
• Certainly, as a patient’s susceptibility to migraine may change with time, this can be considered with
respect to ongoing treatment with Botox.
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2005;87:503-507.
21. Aurora SK, Dodick DW, Turkel CC, et al. PREEMPT 1 Chronic Migraine Study Group.
Onabotulinumtoxin A for treatment of chronic migraine: results from the double-blind, randomized,
placebo-controlled phase of the PREEMPT I trial. Cephalagia. 2010;30:793-803.
22. Diener HC, Dodick DW, Aurora SK, et al. PREEMPT 2 Chronic Migraine Study Group.
Onabotulinumtoxin A for treatment of chronic migraine: results from the double-blind, randomized,
placebo-controlled phase of the PREEMPT 2 trial. Cephalagia. 2010;30:804-814.
CHAPTER 9
Infection: Prevention, Diagnosis, and

Management
Dawood Sayed and Sudhir Diwan
INTRODUCTION
Prevention of infection in patients undergoing interventional procedures remains a top priority of the
interventional pain physician. Proper techniques and standard precautions must be strictly adhered to
prevent infectious complications in patients receiving interventional procedures ranging from peripheral
joint injections to the implantation of devices such as spinal cord stimulators and intrathecal medication
delivery systems. Infectious complications include, but are not limited to, epidural, spinal, or subdural
abscess; paravertebral, paraspinous, or psoas abscess; meningitis; encephalitis; sepsis; bacteremia;
viremia; fungemia; osteomyelitis; local subcutaneous infection; hardware infections causing removal of
expensive equipment; or discitis. The risk of infection may be reduced by identifying patients who are at
increased risk for infection, adhering to the standard of care for reducing the risks, and considering
prompt interventions to improve outcomes after infectious complications.
HISTORY AND PHYSICAL EXAMINATION

A focused history and physical examination of the patient receiving an interventional procedure or
implantable device can be helpful in identifying patients at risk for developing infectious complications.
• Coexisting medical conditions can impair the immune system and increase the risks of infections such
as cancer, chemotherapy, radiation, AIDS, and diabetes.
• Preexisting infection, pancreatitis, drug, or alcohol abuse may be associated with a higher incidence of
infectious complications.
• Bacteremia and septicemia are contraindications; however, distal localized infection without any
indication of systemic disease are not contraindications.
• Close postoperative follow-up and a high index of suspicion for infection in the high-risk patients.
• Review of current lab values such as CBC to assess for leukocytosis can be helpful, although routine
preprocedure measurement is not recommended.
IMPACT OF SURGICAL SITE INFECTIONS
The procedures that involve implantable devices are done in the operating rooms and follow the strict
intraoperative discipline to prevent the infection to reduce the financial burden.
• In United States, more than 40 million inpatient surgical procedures each year; 2% to 5% complicated
by surgical site infections (SSIs).
• The infection rate varies from 3% to 6%.
• SSIs are second most common nosocomial infection (24% of all nosocomial infections).
• Infection is responsible for prolonged hospital stay by 7.4 days.
• It costs $400 to $2600 per infection depending on the surgical site and type of device.
• The cost of treatment of infection from neurosurgic implants to vascular shunts can be as high as 50,000
per case.
INFECTION WITH IMPLANTABLE DEVICES

• It varies from 2.5% (clean cases) to 9% (immunocompromised patients).
Most Common Organisms

• Staphylococcus aureus: coagulase positive
• Staphylococcus epidermidis: coagulase negative
• Methicillin-resistant S aureus (MRSA)
• Vancomycin-resistant enterococci (VRE)
• Vancomycin-resistant S aureus (VRSA)
• Multidrug-resistant organisms (MDRO)
MRSA Infection
• Usually staphylococci are sensitive to β-lactam antibiotics (ampicillin, methicillin, and
cephalosporin).
• Two strains exist: Less-resistant community-acquired MRSA (CA-MRSA) and highly resistant
hospital-acquired MRSA (HA-MRSA).
• It carries high risk of toxic shock syndrome due to exotoxins.
• Usually treated with vancomycin, linezolid, or teicoplanin.
Patients at High Risks for Contracting MRSA Infection
• Frequent hospitalization
• Inappropriate use of antibiotics
• Patients with type I or type II diabetes
What is a Coagulase Test?

It is a test to identify coagulase enzyme that is produced by pathogenic strains of staphylococci. It causes
fibrin clots of blood plasma and eventually fibrin clot makes organism resistant to:
• Phagocytosis
• Host’s immune response
• Penetration of antimicrobial agents
Pathophysiology of Implant Infection

The process of infection creates a “biofilm” around the implant composed of fibrinogen, fibronectin, and
collagen. This biofilm:
• Enhances bacterial adherence
• Promotes multiplication of pathogens
• Enhances toxin liberation
• Decreases penetration of antibiotics
Surgical site infection is defined according to the site and depth of infection to help understand the
seriousness of the issue and formulate a treatment plan.
• Superficial infection: Infection of skin and subcutaneous tissue, suture, or incisional infection
• Deep infection: Involves deeper soft tissue or pocket infection
• Organ/space infection: Infection spreads deeper layers to involve specific structures, for example,
meninges
Sources of Infection
Exogenous:
• Contamination by patient
• Surgical personnel
• Operating room environment
• Instruments
• Materials
Endogenous
• Blood borne
• Seeding from distant site
• Implant provides nidus for the infection
Patient-Related Risk Factors

Following risk factors should be taken into account while doing any interventional spinal procedures,
especially important while performing surgical procedures for implantable devices.
• Obesity
• Infection at remote site
• Systemic steroid use
• Nicotine use
• Immunocompromised patient
• Diabetes
• Malnutrition
• Prolonged hospitalization
As placement of implantable devices like spinal cord stimulators and intrathecal drug delivery
reservoirs has become common practice by interventional pain physicians, it is of paramount importance
to understand the intraoperative discipline to maintain sterility. Many implanters may not have formal
surgical training, and need to be scrupulous and attentive to details required to maintain sterile condition.
As our interventions are directly connected to spinal cord and central nervous system, an infection in this
setting can lead to significant complications. The surgical risk factors include:
• Inappropriate use and/or lack of antimicrobial prophylaxis
• Lack of aseptic techniques
• Poor surgical technique
• Longer duration of surgery
Prevention of Infection
The practice of aseptic techniques should be closely monitored and strictly adhered to without looking for
any shortcuts when performing interventional procedures or surgery. Three target areas should be closely
monitored. They are:
1. Preoperative or preprocedural considerations 1.
2. Intraoperative discipline 2.
3. Postoperative or postprocedural course 3.
Preprocedural or preoperative considerations:
• Routine interventions generally do not require antibiotic prophylaxis.
• Strict sugar control is recommended for diabetic patients.
• Wear appropriate surgical attire including scrub suits, masks, and caps; remove jewelry.
• For surgical procedures of implantable devices, the aseptic technique should include complete surgical
scrub and gowning.
• Every steps of proper prepping and draping should be followed.
• Use either chlorhexadine with alcohol or an alcohol combined with povidone-iodine solution for hand
scrubbing and skin antisepsis prior to performing procedures and injections.
Avagard Pump (Figure 9-1)
• The active ingredients of Avagard are 1% chlorhexidine gluconate in 61% ethyl alcohol.
• It is waterless, scrub-less, and brush-free hand antiseptic.
• It provides rapid antisepsis against broad spectrum of organisms without disrupting natural barrier of
skin.
Figure 9-1. Avagard pump.
Prophylactic Antibiotics
Antimicrobial prophylaxis has been one of the most important advancements in reducing SSIs. Most SSIs
are associated with skin microorganisms, especially the patient’s own bacteria. The decision to
administer prophylactic antibiotics depends largely on the nature of the procedure being performed. In
general, antibiotic prophylaxis is not indicated for neuraxial techniques such as epidurals, facet blocks,
and medial branch blocks; radiofrequency ablation; peripheral joint injections; and nerve blocks and
sympathetic blocks.
Provocative Discography
Discitis is a known and feared complication of provocative discography. It is recommended that some
form of antibiotic be given prior to discography. A standard practice is to administer 1 g of an intravenous
cephalosporin prior to the procedure. Staphylococcus epidermidis is the pathogen most likely to be
responsible for discitis.1 To overcome this incomplete intradiscal penetrance, some believe to administer
intradiscally in addition to intravenous antibiotics. In the case of cephalosporin allergy, clindamycin can
be substituted.
Vertebral Augmentation
Infection involving the implanted polymethyl methacrylate (PMMA) in the spine is a disastrous
complication. Common antibiotic prophylaxis practice measures include antibiotics to the PMMA
mixture, giving preoperative IV antibiotics, both, or neither. The role of antibiotic prophylaxis in
vertebral augmentation is not uniformly agreed upon. If the patient is debilitated or immunocompromised,
antibiotic prophylaxis is recommended.
Implantable Devices
Infection remains the number one cause of nonequipment-related complication in SCS and reservoir
implantation. Antimicrobial prophylaxis has been one of the most important advances in the reduction of
SSIs.
• Routine antibiotic prophylaxis are warranted in all patients with implantable devices. (Evidence level
I-a, Recommended grade A.)
• Antibiotic prophylaxis is associated with a 5-fold decrease in SSI rates.
• It decreases the bacterial infection--related mortality if used in neutropenic patients.
• Timing of antibiotics should be less than 2 hours, preferably within 30 minutes of incision.
• Cefazoline 1-2 g IV 30 minutes before incision.
• Clindamycin 600 mg IV in patients with β-lactam allergy.
• Vancomycin 1 g IV over 60 minutes for patients who are carriers of MRSA.
Though the use of antibiotics has drastically reduced postoperative infection rate, it is also of
paramount importance to understand that improper use of antibiotics is not without potential risks.
• Hypersensitivity reaction: Ranging from skin rashes to anaphylactic shock
• Superinfection: Alteration of normal bacterial flora and overgrowth of opportunistic organisms, for
example, fungi
• Emergence of resistant strain due to intermittent colonization as a result of overuse of antibiotics
Pseudomembranous colitis is a serious medical emergency condition that can occur secondary to
overuse of antibiotics, mainly clindamycin.
• It promotes overgrowth of organism C defficile.
• It can occur with ampicillin, amoxicillin, ciprofloxacin, bactrim, and cephalosporins.
• It is a medical emergency and should be promptly treated as following:
1. Stop antibiotics.
2. Correct dehydration
and electrolyte imbalance.
3. Give flagyl and vancomycin orally for 10 days.
Prepping and Draping for Implant Placement (Figures 9-2 to 9-7):

Figure 9-2. Isolate the surgical area with plastic drapes.
Figure 9-3. Prep the area with betidine gel or chloropre. Prepare surgical site by antiseptic solution in
“concentric” manner from incision site to periphery.
Figure 9-4. Isolate the prepped area with blue sticky sterile towels.
Figure 9-5. Full surgical drape placed.
Figure 9-6. Place antimicrobial surgical drapes with an iodophor impregnated adhesive, which is
designed to provide a sterile surface all the way to the wound edge and continuous antimicrobial activity
throughout the procedure.
Figure 9-7. Don’t forget to drape the fluoroscope!
Intraoperative Considerations for Implantable Devices

Use double gloves, larger size in and smaller out. Select device or model suitable for patient’s size and
habitus. Consider surgical scars, ostomies, waistline, and clothing in selection of pocket site for the
device. Avoid placing device directly under suture line and consider subfascial placement in underweight
patients.
• Remove devitalized tissue from the surgical wounds.
• Maintain adequate hemostasis.
• Consider gentle handling tissues to minimize surgical trauma.
• Eradicate dead space to reduce fluid collection and subsequent infection.
• Irrigate the wound with antibiotic solution to remove debris, foreign materials, and blood clots and to
decrease contamination and infection.
• Close the incision in anatomical layers.
• Apply bio-occlusive, antiseptic wound dressing.
Postoperative Course
It is of paramount importance to closely monitor the wound for postoperative complications like bleeding
and infection.
• Keep dressing dry and clean.
• Monitor for localized redness and tenderness.
• Monitor WBC, fever, and neurologic deficit.
• The dressing change must be with aseptic technique.
• No need to continue antibiotic unless warranted.
• Treat threatened incision aggressively.
Intrathecal Versus Epidural Infection

Due to direct connection of SCS leads and intrathecal catheter to the neuraxial structures, the disastrous
complications with unfavorable outcome is a strong possibility.
• Epidural infection usually produces “space”-occupying lesion and creates pressure over dorsal surface
of spinal cord eventually causing kink of anterior spinal artery and subsequent ischemia of two-thirds
of spinal cord and motor deficit. Symptoms vary from sensory deficit to motor paralysis.
• Depending on the extent of injury and the time spent after first indication of infection, the outcome is
usually unfavorable. Epidural infection may be treated with IV antibiotics, but abscess will need
emergency surgical decompression. Neurologic functions usually recover completely if surgery is
performed within 24 hours of first neurologic deficit. Partial recovery if decompression is done within
24 to 36 hours and “no” recovery after 36 hours.
• Intrathecal infection produces signs and symptoms of meningeal irritation, for example, stiff neck,
photophobia, and headache. Patient may also show cerebral signs due to bacterial encephalitis, for
example, irritability, lethargy, and mental status changes.
• Both conditions usually present with fever, increased WBC, increased ESR, and increased C-reactive
protein (CRP) in CSF.
• Diagnosis is confirmed by imaging studies and positive CSF culture.
Diagnosis and Treatment of Infection

Proper screening, history and physical examination, sterile technique, and proper use of prophylactic
antibiotics do not ensure 100% prevention of infectious complications. Close monitoring, high degree of
suspicion, and early diagnosis are extremely important to prevent infectious complications and potential
devastating sequela. Each patient is at risk for each procedure, and every patient should be closely
monitored post procedurally for signs and symptoms of infection. Lack of external localized tenderness
and erythema does not ensure neuraxial infection. Early indications to increase index of suspicion of
infection include:
• Spiking temperature
• Increasing backache
• Headache
• Localized erythema and tenderness at the insertion site
• Changes in sensory and motor function should increase the index of suspicion for infection
More ominous signs include:
• Stiff neck
• Photophobia
• Changing mental status and confusion
• Increasing radiating pain
• Increasing motor deficit; in addition, specific attention should be focused on the neurologic
examination
Laboratory Tests and Imaging

If signs and symptoms lead to suspicion of infection, laboratory and imaging studies can be used to
confirm the diagnosis. Laboratory studies such as:
• Leukocyte count
• Erythrocyte sedimentation rate (ESR)
• C-reactive protein (CRP)
It should be noted that these studies are nonspecific and can be elevated in patients without infection. If
the suspicion of infection is high and associated with neurologic signs, CT scan or MRI, with and without
contrast should be obtained promptly to confirm the diagnosis.
Management of Infection
When the diagnosis of infection is suspected and confirmed, prompt treatment must be initiated. Proper
treatment usually involves initiating appropriate antibiotic therapy, consultation with a physician
specializing in the diagnosis, and treatment of infectious diseases should be considered.
Superficial infection is a salvageable condition and if the treatment started promptly.
• Individualize the treatment plan depending on the extent of infection.
• Involve Infectious Disease MD to appropriately manage infection.
• Obvious fluid/pus collection should be drained.
• Obtain culture and sensitivity (C&S) status of the wound discharge.
• Oral and/or parenteral antibiotics should be administered as per the C&S.
• Closely monitor WBC, fever, and neurologic examination.
In case of deep and neuraxial infection, it is critical to take appropriate and adequate steps to avoid
disastrous outcome. If there is any evidence of deep organ infection, for example, meningitis, erythema,
induration, or tenderness along the course of catheter
• Plan to explants the device as soon as possible.
• Hold antibiotics until specimen for culture and sensitivity is obtained from the wound.
• Remove the entire implant system including anchors.
• Postoperatively, leave the implant wound open or provide drain if you close.
• Provide proper postoperative wound care and aseptic dressing change.
• Place peripherally inserted central catheter (PICC) line and antibiotics as per infectious disease
recommendations (4 weeks).
• Obtain negative surveillance cultures of blood and CSF before 2nd stage reimplantation surgery is
planned.
Additionally, if epidural abscess is suspected, surgical evaluation should be obtained on whether to
perform percutaneous drainage or laminectomy. It should be noted that treating a surgical site infection
without removing the device poses high risk of deeper migration as SCS leads and intrathecal catheter
form a conduit to the epidural or intrathecal space and can lead to epidural abscess or meningitis.
Wound Seroma
It is a small collection of aseptic fluid at the suture line or around the implant and is not an infrequent
occurrence.
• It is a collection of sterile serosanguinous fluid in the pocket.
• Small amount usually spontaneously resolves.
• Abdominal binder may help reduce the primary collection and recollection after aspiration.
• Avoid repeated aspiration as it is a potential cause for infection.
• If aspiration is indicated for larger collections, culture the aspirate to rule out infection.
• Bacterial growth is confirmation of infection of the wound.
Postprocedural discitis is a rare complication after-intradiscal procedures. It is imperative for the
treating physician to maintain a high index of suspicion. Appropriate laboratory and imaging studies are
invaluable in establishing a timely diagnosis. In the majority of patients, antibiotic treatment along with
spinal immobilization has been shown to produce good long-term outcomes. Operative intervention is
rarely necessary in patients failing conservative treatment.
CONCLUSION
Interventional pain management specialists perform a variety of techniques ranging from neuraxial
injections, neuroablative procedures, diagnostic and therapeutic intradiscal procedures, and the
implantation of spinal cord stimulators and intrathecal pumps. Core knowledge of the risks of infections
for each technique in every patient and systematic approach to prevention, diagnosis, and management of
these complications is extremely vital.
• Appropriate prophylactic antibiotics as and where indicated.
• Strict sugar control in diabetic patients.
• Strict intraoperative discipline.
• Employ proper surgical techniques and provide adequate hemostasis.
• Intraoperative antibiotic irrigation is important to clean devitalized tissue before closure.
• Provide close postprocedural and postoperative monitoring of surgical site.
• Keep high index of suspicion and provide individualized treatment plan for infections.
• Ask for help from infectious disease (ID) experts sooner than later.
• Understand the resistant microorganism.
• Avoid improper and overuse of antibiotics.
Develop a surgical conscience that allows for no compromise in the principles of aseptic techniques,
since anything less could increase the potential risk of infection, resulting in harm to the patient. As a
physician proving care to our patients, we have greater responsibility of monitoring and maintaining
aseptic environment during periprocedural and perioperative period, thus preventing harm to our patients.
Suggested Reading
Cameron T. Safety and efficacy of Spinal Cord Stimulation for the treatment of chronic pain: a 20-year
literature review. J Neurosurg: Spine. 2004;100(3),245-267.
Darouiche RO. Treatment of infection associated with surgical implants. N Engl J Med. 2004;350:1422-
1429.
Follett KA, Boortz-Marx RL, Drake JM, et al. Prevention and management of intrathecal drug delivery
and spinal cord stimulation infections. Anesthesiology. 2004;100:1582-1594.
Fraser RD, Osti OL, Vernon-Roberts B. Iatrogenic discitis: the role of intravenous antibiotics in
prevention and treatment. Spine. 1989;14:1025-1032.
Kinirons B, Mimoz O, Lafendi L, et al. Chlorhexidine versus povidone iodine in preventing colonization
of continuous epidural catheters in children: a randomized, controlled trial. Anesthesiology.
2001;94:239-244.
Mahendru V, Bacon DR, Lema MJ. Multiple epidural abscesses and spinal anesthesia in a diabetic
patient. Reg Anesth. 1994;19:66-68.
Practice Advisory for the Prevention, Diagnosis, and Management of Infectious Complications
Associated with Neuraxial Techniques. A Report by the American Society of Anesthesiologists Task
Force on Infectious Complications Associated with Neuraxial Techniques. Anesthesiology. 2010;112.
Rathmell JP, Lake T, Ramundo MB. Infectious risks of chronic pain treatments: injection therapy, surgical
implants, and intradiscal techniques. Reg Anesth Pain Med. 2006;31(4):346-352.
Sellors J, Cyna A, Simmons S. Aseptic precautions for inserting an epidural catheter. Anesthesia.
2002;57:593-605.
Shibata S, Shibata I, Tsudy A, et al. Comparative effects of disinfectants on the epidural needle/catheter
contamination with indigenous skin bacterial flora. Anesthesiology 2004;101:A1363.
Siegel JD, Rhinehart E, Jackson M, et al. Healthcare Infection Control Practices Advisory Committee.
Management of multi-drug resistant organisms in healthcare settings. Am J Infect Control.
2007;35(10):165S-193S.
Silber JS, Anderson DG, Vacarro AR, et al. Management of post procedural discitis. Spine J. 2002 Jul-
Aug;2(4):279-287.
Sillevis SP, Tsafka A, Teng-van de Zande F, et al. Outcome and complications of epidural analgesia in
patients with chronic cancer pain. Cancer. 1998;83:2015-2022.
Reference
1. Lang R, Saba K, Folmon Y, et al. Penetration of ceftriaxone into the intervertebral disc. J Bone Joint
Surg Am. 1994; 76:689-691.
CHAPTER 10
Anticoagulation Guidelines
Nirmala R. Abraham, Cathy D. Trame, and Sudhir Diwan
INTRODUCTION
Patients seeking interventional treatment for chronic pain can have a variety of medical problems. The
aging population in particular can present with complex medical conditions that require anticoagulation
therapy.
In 2010, the American Society of Regional Anesthesia and Pain Medicine published a practice
advisory regarding the use of regional anesthesia in patients receiving anticoagulation to enhance safety as
well as quality patient care. The third edition of guidelines reports a consensus statement utilizing the
collective experience of experts in neuraxial anesthesia and anticoagulation. The guidelines presented are
comprehensive and based on case reports, clinical series, pharmacology, hematology and risk factors for
surgical bleeding. This is a very complex issue for which there is no simple template to follow. Each case
must be reviewed on an individual basis. There should be communication with the patient’s health care
providers such as the cardiologist, regarding safest treatment options. This collaboration is essential in
diminishing life-threatening bleeding complications associated with neuraxial anesthesia.
Typical scenarios interventional pain physicians encounter with patients on chronic anticoagulation
therapy include:
• Patients on venous thromboembolic treatment
• Patients with vascular stents in place
• Epidural/spinal injections for patients having joint replacement surgery
• Extended period of DVT prophylaxis in orthopedic patients
The problems in patients who are on chronic anticoagulation therapy are:
• Therapy-associated mortality (5%-12%)
• Spontaneous bleeding requiring discontinuation of therapy (15%-20%)
• Heparin-induced immune-mediated thrombocytopenia (HIT) (3.5%-7%)
• 25% patients with HIT develop new venous and/or arterial thrombotic event
• Warfarin crosses placenta and cannot be given in pregnancy
• Dose adjustment of fondaparinux in patients with compromised renal function
This creates a challenge when preparing patients for invasive procedures. Patients undergoing
interventional treatment for chronic pain, particularly neuraxial anesthesia, are at increased risk for
complications associated with bleeding.
The risk of clinically significant bleeding is exacerbated by the following:
• Increased age
• Spinal cord or vertebral column abnormalities
• Coagulopathies
• Needle placement difficulties
• Continued anticoagulation with neuraxial catheter in place.1
It is important to weigh the risk-benefit ratio when determining when to stop anticoagulant or
antiplatelet therapy along with determining exactly when to restart treatment postintervention.
• The incidence of hemorrhagic complications and resulting neurologic deficit after neuraxial
intervention is unknown.
• The incidence of bleeding is less than 1 in 150,000 epidurals and 1 in 220,000 spinal anesthetics.
• More recent surveys are revealing an incidence as high as 1 in 3000 in high-risk patient populations.
• High index of suspicion, prompt diagnosis, and treatment of bleeding is critical to decreasing the
incidence of permanent neurological deficit.
A review of the literature from 1906 to 1994 by Vandermeulen et al4 reported:
• 61 cases of spinal hematoma reported to be associated with epidural or spinal anesthesia
• 60% of these cases occurred in the last 10 years of the study period
• 68% of the patients (n = 42) had hemostatic abnormality when the spinal hematoma occurred
• 68% of patients had neurologic compromise as a progression of sensory/motor blockade
• 8% of patients had reported bowel/bladder dysfunction
• Severe radicular back pain was not a presenting sign in many cases
• 38% of patients had partial or good neurologic recovery
• Spinal cord ischemia was reversible in patients that received a decompressive laminectomy within 8
hours of onset of neurologic dysfunction
These findings clearly emphasize the need for close monitoring, evaluation, and treatment of neurologic
dysfunction. Because of the possibility of neurologic dysfunction, it is of critical importance to evaluate
each patient for the risk versus benefit when determining whether a patient taking chronic anticoagulation
therapy is an appropriate candidate for interventional pain management procedures.
This chapter discusses the most commonly utilized anticoagulant and antiplatelet agents and their
relevant pharmacologic factors, including mechanism of action, indications, and when to stop and restart
pre- and postprocedure to promote patient safety to prevent poor outcomes.
Our concerns are:
• When to stop ongoing anticoagulation therapy, and risks of thrombosis by stopping
• When to restart the therapy after the procedure, and risks of bleeding by restarting
• What laboratory test to order to normalize the coagulation profile
• Optimize the risks versus benefits ratio
Predisposing factors for deep vein thrombosis (DVT) and thromboembolic events:
• Patients with multiple trauma
• Conditions that promote venous stasis
• Lack of ambulation (postoperation, fractures)
• Pregnancy
• Low CO (CHF, MI)
• Morbid obesity
• Advanced age
• Race: higher in African Americans
• Sex: M > F
• Cancer and cancer therapy
Patients who require anticoagulation due to hypercoagulable states:
• Hypercoagulable syndromes: Recurrent thromboses, family Hx of thrombosis, Hx of spontaneous
abortions, multiple exposures to heparin
• Activated protein-C resistance (venous)
• Antiphospholipid syndrome (Dx: anticardiolipin antibodies)
• Congenital deficiency of antithrombin III
• Protein C and S deficiency: vitamin K dependent
• Hyperhomocysteinemia: homocysteine is coagulant
WARFARIN (COUMADIN)
Warfarin is used in a variety of medical conditions as an anticoagulant in the prevention of ischemic
stroke, myocardial infarction as well as peripheral vascular disease as well for patients with stents to
prevent deep thrombus formation and or pulmonary emboli.
• Direct thrombin inhibitor.
• Inhibits synthesis of vitamin K–dependent coagulation factors II, VII, IX, and X.
• Anticoagulation effects start after 12 to 16 hours of administration.
• Warfarin does not affect already synthesized coagulation factors.
• Peak effect is at approximately 40 hours.
• The half-life of warfarin is from 20 to 60 hours; with a mean of 40 minutes.
• The length of effect is 2 to 5 days.
• Vitamin K can be administered to reverse the effects of warfarin, although the replacement of vitamin
K is slow and may take 24 to 30 hours.
• For emergency surgery/intervention use fresh frozen plasma.
For high risk thromboembolic patients a consultation with primary care physician to understand the
risks of stopping the anticoagulation therapy and for possible bridging anticoagulation therapy to minimize
the risks may need to be considered.
• Warfarin should be stopped 5 days before the planned procedure.
• PT/INR should be rechecked immediately prior to the procedure; must be normalized.
• Concurrent medications (NSAIDs, heparin, etc) can increase the risks and may not reflect on PT/INR.
• If warfarin is started postoperation, catheter can be removed when INR is <1.5.
THROMBIN INHIBITORS
Dabigatran (Pradaxa)
Dabigatran (Pradaxa), approved by the Federal Drug Administration (FDA) in October 2010, is the first
oral anticoagulant approved in 50 years since coumadin. The FDA approved dabigatran primarily based
on the outcomes of the RELY (randomized evaluation of long-term anticoagulation therapy) noninferiority
study with 18,113 participants.5 It is utilized primarily to prevent the formation of clots and reduce the
risk of stroke in patients with nonvalvular atrial fibrillation.
• Direct thrombin inhibitor.
• Dosed as 150 mg daily for patients with creatinine clearance of greater than 30 mL/min; for a
creatinine clearance of 15 to 30 mL/min the dosage is reduced to 75 mg daily.
• No dietary restrictions, blood monitoring requirements, or dosage adjustments needed.
• Discontinued prior to invasive procedures based on the patient’s creatinine clearance values:
1 to 2 days prior to an invasive procedure if the creatinine clearance is equal to or greater than 50
mL/min.
3 to 5 days prior to an invasive procedure if creatinine clearance is of less than 50 mL/min.
• The half-life of dabigatran is 12 to 17 hours.5
• No reversal agent for this drug.
• ASRA does not support neuraxial techniques in patients on thrombin inhibitors. Being reevaluated by
the FDA based on postmarketing reports of critical bleeding events. The FDA still believes dabigatran
offers valuable health benefit when used as recommended.10
Other thrombin inhibitors: desirudin (Revax), lepirudin (Refludan), bivalirudin (Angiomax), and
argatroban (Acova)
• Inhibit clot-bound thrombin.
• Indicated to treat heparin-induced thrombocytopenia to prevent thrombosis, and as an adjuvant to
angioplasty; desirudin is FDA approved for prevention of DVT and PE after hip replacement.
• Monitor aPTT, present 1 to 3 hours after IV administration.
• Neuraxial techniques are not recommended until further studies have been completed due to long half-
life and difficulty with reversal; no antidote known.
Heparin (Unfractionated)
Heparin (unfractionated or UFH), an anticoagulant whose activity is dose related, as well as molecular
size dependent, although its effects are not incremental and increase unequally with elevated doses.1
• Binds to antithrombin III and inhibits conversion of prothrombin to thrombin, prolonging clotting time;
results in an increase in partial thromboplastin time (PTT).
• Prevents fibrin formation and limits expansion of thrombi; however, it is ineffective on platelet
aggregation.11
• Prior to invasive interventions check PTT, hemoglobin and hematocrit levels.
• Subcutaneous heparin injection results in 1 to 2 hours activation time.
• Heparin given intravenously has an immediate anticoagulation effect and a short half-life of
approximately 60 to 90 minutes.
• Hemostasis restoration for intravenous heparin is 3 to 4 hours after discontinuing the therapeutic
dose.12
• Subcutaneous heparin duration of action is 8 to 12 hours.13
• Rapid reversal agent for heparin is protamine sulfate 1 mg for every 100 units of IV heparin; a
protamine infusion may be necessary due to continued absorption.1
• Fresh frozen plasma should not be used to reverse the effects of unfractionated heparin as it provides
additional antithrombin which may increase the bleeding effects of the medication.7
LOW MOLECULAR WEIGHT HEPARIN

Enoxaparin (Lovenox), dalteparin (Fragmin), tinzaparin (Innohep).
Low molecular weight heparins (LMWH) have some very different properties from UFH, the primary
ones being that LMWH are not able to be measured regarding their anticoagulant effect; they have a
prolonged half-life and they are not reversible with protamine.1 Each medication has specific indications
including prevention of deep venous thrombosis, pulmonary embolism, and ischemic complications
related to unstable angina and non–ST-segment-elevation myocardial infarction.
• Causes selective inhibition of Xa and mild anti-IIa preventing thrombus formation.
• PTT is not prolonged, so monitoring this parameter is not necessary.
• Use extreme caution when caring for patients taking low molecular weight heparins when considering
spinal/epidural anesthesia,13 including interventional therapies for chronic pain.
If LMWH is being utilized as a bridging agent for high-risk patients requiring chronic
anticoagulation, close monitoring is imperative to minimize the increased risk of bleeding.
Horlocker et al,1 purports age and gender (elderly women) are considerable patient risk factors
along with concomitant use of multiple hemostasis-altering medications due to possible synergistic
effects.
• Half-life of LMWH is approximately 4 hours.7
• Hemostatic restoration after discontinuing the therapeutic dose of the drug is 12 to 24 hours.12
• Invasive interventional guidelines include needle placement 24 hours after last dose of LMWH.
• May be restarted 24 hours after surgery and 2 hours after a block.
• Should not be restarted prior to the removal of epidural catheters.
• With a traumatic needle placement during an interventional procedure there is no need to cancel
surgery; may still start 24 hours after surgery.
• The risk of hematoma increases with concomitant anticoagulant usage.11
• To monitor for side effects obtain: complete blood cell (CBC) counts, platelet level, and stool for
occult blood during therapy.
• Patients who are obese or with renal dysfunction
Consideration can be given to monitoring LMWH with anti-Xa assay5,13 as the half-life is prolonged
in the plasma.1
Horlocker et al1 do not recommend using anti-Xa level routinely as it is not predictive of bleeding
risk.
• Protamine can be used as a reversal agent for some of the anticoagulant effects of LMWH,7 although
protamine binds poorly to LMWH fractions.1
PENTASACCHARIDE AGENTS (FONDAPARINUX [ARIXTRA])

Indicated for the prophylaxis of deep vein thrombosis, which may lead to pulmonary embolism.8
• Antithrombin III mediated selective inhibitor of factor Xa that does not inhibit thrombin.7
• Anti-Xa assay can be used to monitor the effects of pentasaccharide agents.
• Half-life is approximately 21 hours or longer with renal insufficiency.
• Neuraxial techniques validated in clinical trials include single pass needle techniques and atraumatic
needle placement. Indwelling neuraxial catheters should be avoided.
• Stop 24 to 30 hours prior to a procedure.
• No specific emergent antidote has been identified, although rFVlla can be used as a reversal agent.7
• After discontinuing fondaparinux (Arixtra) hemostatic restoration is reestablished in 24 to 30 hours.7
ANTIPLATELET AGENTS
Antiplatelet agents include NSAIDs, thienopyridine derivatives (ticlopidine and clopidogrel), and
platelet GP IIb/IIIa receptor antagonists (abciximab, eptifibatide, and tirofiban).
Aspirin
Aspirin is utilized to decrease the occurrence of transient ischemic attacks, unstable angina, coronary
artery thrombosis with myocardial infarction, and prevents thrombus formation after coronary artery
bypass surgery. It can also be used for mild to moderate pain.
• Antiplatelet agent, “inhibits the synthesis of thromboxane (TXA) by irreversible acetylation of the
enzyme cyclooxygenase.”6
• Irreversibly binds to cyclooxygenase-1 enzyme (COX-1) and inhibits TXA2 production in all platelets
exposed to aspirin.7
• Low dose half-life is 2 to 3 hours; high dose half-life is 15 to 30 hours.
• Antiplatelet effect of aspirin lasts for 5 to 10 days or the life of a platelet6; therefore, 10 days is needed
to restore hemostasis after discontinuing the therapeutic dose (the amount of time to produce
platelets).12
• No specific antidote for aspirin, although 1 unit of platelet transfusion is the current mode of reversal.
• Aspirin is easily detected by the PFA-100 test.7
Clopidogrel (Plavix)
Clopidogrel is used in wide variety of cardiovascular and cerebrovascular diseases7 to ultimately
decrease myocardial infarction, stroke, and vascular death.12
• Antiplatelet agent inhibiting an adenosine diphosphate (ADP)–dependent pathway for platelet
activation. Also interferes with platelet-fibrinogen binding which affects platelet–platelet interactions.7
• Platelet dysfunction is greater with clopidogrel than with aspirin.7
• Platelet aggregometry test can be used to monitor platelet function.7
• Platelet function returns to normal 5 to 7 days after discontinuing the medication.
• Discontinue 7 to 10 days prior to surgery or procedure (low risk for cardiac event).
• If patient is high risk for cardiac event without anticoagulant, discontinue 5 days prior to
procedure/surgery, ideally 10 days prior.
• Restart 24 hours postprocedure.
• Similar to aspirin, there is no antidote, although 2 units platelet concentrate can be used as a reversal
agent.
Ticlopidine (Ticlid)
Ticlopidine may also be used for cardiovascular and cerebrovascular diseases but is not preferred over
clopidogrel due to delayed and prolonged effect.
• Antiplatelet that interferes with platelet-fibrinogen binding and ADP pathway for platelet activation.
• Steady state achieved in 14 to 21 days; may be accomplished sooner with higher doses.
• Discontinue 14 days prior to surgery or procedure; document platelet function just prior to procedure;
normal platelet function may return in as little as 10 days, but conservatively should wait 14 days.
• Restart 24 hours postprocedure.
Platelet GP IIb/IIIa Receptor Antagonists

Abciximab (Reopro), eptifibatide (Integrilin), and tirofiban (Aggrastat)
Platelet GP IIb/IIIa receptor antagonists are most often used to treat acute coronary syndromes with or
without a percutaneous coronary procedure.
• Interferes with platelet-fibrinogen binding and platelet-von Willebrand factor binding.
• Blocks the final pathway to platelet aggregation by inhibiting the GPIIb/IIIa receptors.
• Commonly coadministered with aspirin and heparin.
• Contraindicated if the patient has had surgery within the last 4 to 6 weeks.
• Time to normal platelet aggregation is 24 to 48 hours for abciximab; 4 to 8 hours for eptifibatide and
tirofiban.
• During therapy, epidural procedures and puncture of non-compressible sites should be avoided per
manufacturer’s recommendations. No further studies available to substantiate safety during neuraxial
blockade. Additionally, combination with other anticoagulants being coadministered, greatly increase
bleeding risks.
CONCLUSION
Those patient populations requiring anticoagulant and/or antiplatelet agents for various therapeutic
purposes can present challenges for interventional pain procedures. Specifically, patients undergoing
neuraxial anesthesia and nerve blocks (with or without catheters) are at increased risk for epidural and
spinal hematomas. An understanding of mechanisms of action, half-life and dosing can assist in
developing a treatment plan for patients requiring anticoagulation therapy. It is also helpful to coordinate
with the other health care providers involved in monitoring a patient’s anticoagulation treatment and
status, to develop a risk-benefit stratification approach to the treatment plan. Exactly when to stop and
restart these medications, or if a substitution anticoagulant needs to be instituted, should be determined in
collaboration with the patient’s other health care providers.
References
1. Horlocker TT, Wedel DJ, Rowlingson JC, et al. Regional Anesthesia in the Patient Receiving
Antithrombotic or Thrombolytic Therapy (American Society of Regional Anesthesia and Pain
Medicine Evidence-Based Guidelines, 3rd edition). Reg Anesth Pain Med. 2010;35:64-101.
2. Horlocker TT, Wedel DJ. Neuraxial block and low-molecular-weight heparin: Balancing
perioperative analgesia and thromboprophylaxis. Reg Anes Pain Med. 1998; 23:164-177.
3. Horlocker TT, Wedel DJ. Anticoagulation and neuraxial block: historical perspective, aesthetic
implications and risk management. Reg Anes Pain Med. 1998;23:129-134.
4. Vandermeulun EP, Van Aken H, Vermulen J. Anticoagulants and spinal epidural anesthesia. Anesth
Analg. 1994;79: 1165-1177.
5. Connolly SJ, Ezekowitz MD, Yusuf S, et al. RE-LY Steering Committee and Investigators. Dabigatran
versus Warfarin in patients with atrial fibrillation. NEJM. 2009;361:1139-1151.
6. Katzung BG. Basic & Clinical Pharmacology. London, McGraw Hill; 2007.
7. Beshay JE, Morgan H, et al. Emergency reversal of anticoagulation and antiplatelet therapies in
neurosurgical patients. J Neurosurg. 2010;112:302-312.
8. DrugLib.com
9. Baker RI, Coughlin PB, Gallus AS, Harper PL, Salem HH, Wood EM. Warfarin reversal: consensus
guidelines, on behalf of the Australasian Society of Thrombosis and Haemostasis. Med J Australia.
2004;181:492-497.
10. Federal Drug Administration (www.fda.gov/Drugs/DrugSafety/ucm282724.htm).
11. Diwan S and Rubin E. Coagulation Challenges During the Perioperative Period. Current reviews in
Clinical Anesthesia, 29, 191-198,2009.
12. Levi M. Emergency reversal of antithrombotic treatment. Int Emerg Med. 2009;4:137-145.
13. Osinbowale O, Ali L, Chi Y. Venous thromboembolism: a clinical review. Postgraduate Medicine.
2010;122:54-65.
CHAPTER 11
Sedation for Interventional Pain Procedures

Nancy Staats
INTRODUCTION
• Many patients with acute and chronic pain may require sedation for interventional pain procedures.
• Patients may have extreme anxiety about the pending procedure or be in so much pain that even
positioning them without some analgesia and/or sedation becomes impractical.
• There is great variability in type of sedation required to perform minimally invasive procedures, and
depends on the procedure, the surgeon, and the patient.
• Some physicians perform most procedures without any sedation, while other physicians may want
deeper level of sedation for some or many of their procedures.
• The personnel may differ depending on the locations of the procedures performed. Sometimes, a
sedation nurse (RN or other) trained in OR sedation administers the medication, and other times the
sedation is administered by an anesthesiologist.
• The choice of anesthesia may differ depending on locations: (1) office-based procedures, (2)
surgicenters, and (3) hospital.
• While both scenarios occur, it should be noted that current FDA recommendations state that propofol
should only be administered by an individual trained in airway management (ie, anesthesiologist or
CRNA).
• Currently, there is no consensus on the appropriate overall strategy.
There are a wide range of procedures being performed—from epidural steroid injections to implantation
of spinal cord stimulators. Different procedures may require different levels of and different sedation
techniques in order to optimize the outcome and the experience for the patient. Some proponents of using
an anesthesiologist for sedation point to an appropriate analgesic experience for the patient, lack of
movement, and safety in the operating room. Others are less inclined to utilize an anesthesiologist, citing
risk of overuse of sedative medications, sometimes even resulting in spinal cord injury with deep
sedation, along with an increased cost of care. When appropriately used, sedation can make the
experience safer, more effective, efficient, and more comfortable without jeopardizing patient safety.
Clearly if sedation is utilized, it is important to follow safe guidelines. There remain some principles that
should be followed in providing sedation when performing interventional procedures.
TYPES OF ANESTHESIA
• General anesthesia: rarely used for pain management procedures and will not be covered in this
chapter.
• Monitored anesthesia care or moderate sedation: used most often.
• Conscious sedation or light anesthesia: appropriate for some procedures where patient’s feedback is
important, eg, cervical blocks.
• Local anesthesia: can be used for many of the minor procedures, such as trigger points and some
epidural steroid injections. The payment for anesthesia for some of the more minor procedures can be
dictated by particular insurers/providers in the region; this will also not be covered in this chapter.
• Regional anesthesia: rarely used and will not be covered in this chapter.
PREOPERATIVE ASSESSMENT
As with any patient undergoing anesthesia of any kind, patients need an appropriate preoperative
assessment, including risk level. While many of the procedures performed by the interventional pain
physician may be considered minor, it is important to consider preoperative risk factors. Sicker patients
have increased risk, even for a minor procedure. Complete preoperative assessment guidelines are
readily available elsewhere they include but are not limited to:
• Airway assessment
• Adverse reaction to drugs/substances
Contrast (possible co-reaction with allergy to shellfish)
Antibiotics
Allergies to anesthetics, egg whites, sulfites
Latex
• NPO status
• Medications, including anticoagulants
• Cardiopulmonary function and vital signs
• Obesity/BMI and associated issues
• Mental status
• Counseling regarding procedure and expectations of the patient
RELEVANT FACTORS SPECIFIC TO THE CHRONIC PAIN

PATIENT
• High level of anxiety
• Use of opioids and anxiolytics
• Previous painful experience with pain procedures
• Location of the block and prone position making difficult to mask
• Chronic use of opiates—this can delay gastric emptying and increase nausea
• Hypertension is not unusual in patients undergoing a procedure, particularly those having pain
PREOPERATIVE ANTICOAGULANTS
Chronic or acute use of medications that interfere with coagulation—though controversy exists, in general
the patient taking NSAIDs or other classes of anti-inflammatory agents, including aspirin, are at low risk.
For certain larger procedures, however, a PFA (platelet function assay) may be warranted. Warfarin
should be stopped 4 to 5 days before the spinal procedures, and check INR and/or PT/PTT on the day of
procedure. For more details, refer to anticoagulation chapter in this book. Weigh risks of stopping the
anticoagulants to risks of epidural and/or spinal hematoma. The important factor is communication
between the patient, surgeon and the anesthesiologist to decide the appropriate preoperative tests in order
to minimize late cancellations.
MULTIPLE ALLERGIES
Multiple allergies (it’s important to inquire about “true” allergies). True allergy to local anesthetics, and
particularly the amide local anesthetics, is extremely
• Allergy to egg products, and particularly egg whites, has been considered a relative contraindication to
propofol use; however, clinically significant allergic reactions to propofol are fortunately quite rare.
There seems to be a higher risk when patients have multiple allergies, in particular multiple food
allergies, and history of anaphylaxis.
• Allergy to sulfites can occur, although not as common as allergy to sulfa. Use the sulfite-free
preparation of Propofol.
• Allergy to antibiotics is often real (ask for specifics, to determine whether it is in fact a true allergy or
merely a vasovagal reaction from a shot, GI symptoms, etc) and care needs to be taken, avoiding the
offending class of antibiotic.
• Allergy to contrast solutions or iodine is also common, and there can be crossover with reactions to
shellfish; consider pretreatment with diphenhydramine, H2 blocker, and steroid. Consider using
gadolinium-based contrast gadopentetate dimeglumine (Magnevist).
Follow the NPO guidelines appropriately and optimally. Our policy is NPO for 8 hours for solids and 4
hours for clear liquids; sips of water or other clear liquid up to 2 hours before is permitted. However, it
is anesthesiologist’s responsibility to individualize the anesthetic plan for safety and efficiency.
REALISTIC EXPECTATIONS
Sometimes, the patient states “just put me out, I don’t want to feel a thing!” One must take the time to
educate the patient regarding the reasons for the procedure and why their input may be critical to its safety
and success. Furthermore, having realistic expectations makes it easier for everyone, and the vast
majority of patients will understand when it is explained to them. The patient provides valuable feedback,
whether negative (intraneural or intravascular placement) or positive (stimulator in the correct place).
Many patients are comforted knowing that they will have someone with them for the entire time, making
sure they are safe, stable, and as comfortable as possible.
DIAGNOSTIC BLOCKS
When performing diagnostic procedures, it is best to avoid opioid analgesics as they can alter the
response to the diagnostic test. Diagnostic medial branch facet injections, discography, and diagnostic
sympathetic blocks are common examples of such diagnostic procedures. After each block, the
interventional pain physician will want to understand the response to the block. For example, if a patient
has excellent relief with a medial branch block under most circumstances that may lead to performance of
a radio frequency (RF) ablation. For example, if a patient received fentanyl prior to the injection or
during the injection, the response is unreliable and may lead to ineffective RF ablation.
INTRAOPERATIVE CARE
Similar to any patient undergoing sedation, the pain patient undergoing an interventional procedure
requires continuous monitoring of oxygen saturation, blood pressure, electrocardiogram, and respiratory
rate throughout (see Table 11-1). We often give an anxiolytic agent like midazolam immediately upon
entering the OR, prior to final positioning. We then explain everything and sedate with propofol to
achieve an appropriate level of sedation for the procedure. Opioids may be needed in patients in
significant pain prior to the procedure, although they need to be avoided during any diagnostic blocks. It
is very important not to over-sedate patients undergoing a cervical block near the spinal cord.
TABLE 11-1. Table of Typical Agents Used for Sedation

POST ANESTHETIC CARE
As with any patient after receiving sedation, patients require appropriate postoperative care. Our policy
is the patient cannot drive, use alcohol or sedatives for approximately 24 hours (or at least until the next
day, whichever is less) after anesthesia. When light sedation is used prior to diagnostic neural blockade,
patients should be monitored after the procedure. Patient should not be discharged without an escort.
Suggested Reading
Manchikanti. Pain Physician. 2011 Jul-Aug;14(4):317-329.
Horlocker TT, Neal JM, Rathmell JP, Reg Anesth Pain Med. 2011 Jan-Feb;36(1):1-3.
Baluga JC. Allergol Immunol. 2002 Jan-Feb;30(1):14-19.
Fuzier R. Pharmacoepidemiolog Drug Saf. 2009 Jul;18(7): 595-601.
Murphy A. Anesth Analg. 2011 Jul;113(1):140-144.
Dewachter P. Curr Opin Anesthesiol. 2011 Jun;24(3):320-325.
CHAPTER 12
EMG and Nerve Conduction Studies

Bridget T. Carey
OVERVIEW
In the practice of pain medicine, nerve conduction studies and electromyography provide useful
information through the diagnosis of peripheral neurologic injury. By precisely identifying and localizing
spinal root and peripheral nerve injury, these studies provide an important role in confirming the
anatomical site active in pain generation. This knowledge increases the success of focal procedural and
other interventions. It should be noted that these tools should be used to optimize patient care or help
guide surgical and interventional practice.
DEFINITIONS
Electromyography (EMG) and nerve conduction studies (NCS) are electrodiagnostic tests performed to
evaluate the function of the peripheral nervous system. These tests are usually but not invariably
performed together and interpreted in conjunction. Often the single term “EMG” is used to mean an
examination comprising both NCS and EMG studies, though this is technically an imprecise usage. Both
examinations evaluate and measure aspects of the electrophysiological properties inherent in peripheral
nerve and muscle tissue. Through assessment of these neurophysiological parameters, these studies
provide accurate diagnostic information to the clinician regarding the integrity and function of the spinal
nerve roots, nerve plexi, peripheral nerves, neuromuscular junction, and muscle.
INDICATIONS
EMG/NCS are performed in patients for the following reasons:
• To evaluate if a symptom is due to injury within the peripheral nervous system (PNS)
• To localize the site of nerve injury within the PNS (ie, to spinal root, nerve plexus, peripheral nerve,
neuromuscular junction, and/or muscle)
• To assess the nature of the injury, including severity, chronicity, and at times pathophysiology
Symptoms consistent with possible peripheral nerve injury, either in isolation or combination, include
the following:
• Pain in limb
• Neck pain
• Back pain
• Numbness in feet
• Numbness or tingling of limbs
• Weakness of arms or legs
• Clumsiness in hands
• Gait impairment
CONTRAINDICATIONS
NCS and EMG are relatively safe tests, with few potential associated complications or side effects.
Some patients find the study uncomfortable; however, when performed correctly, both NCS and needle
EMG examination are well tolerated by most patients.
There are no absolute contraindications to NCS/EMG; however, the following relative
contraindications are considered:
• Needle electromyography is performed with caution in patients on anticoagulation and/or on
antiplatelet therapy.
The examination is generally modified to exclude muscles at noncompressible sites to eliminate the
risk of hematoma.
Although not absolutely contraindicated, examination of the paraspinal musculature is generally
avoided in patients on anticoagulation due to potential adverse effects of possible hematoma
formation adjacent to spinal structures.
• Needle electromyography is not performed in muscles where overlying skin infection or other tissue
pathology is seen or suspected.
• Needle electromyography is avoided in affected limbs of patients with lymphedema.
• Nerve conduction studies requiring proximal stimulation at Erb point or the neck are not performed in
patients with permanent pacemakers, internal defibrillators, or other implanted electrical devices.
RELEVANT ANATOMY
• Spinal nerve roots from C1-C4 form the cervical plexus, and supply sensory function to the back of the
head and neck, and motor innervation to cervical musculature.
• Roots from C5-T1 supply neurologic function to the upper extremities. The nerve roots from these
levels combine fibers and ramify in the anterior neck forming the brachial plexus, off of which branch
the peripheral nerves supplying sensory and motor function to the shoulders, arms, and hands.
• Roots from the thoracic vertebrae innervate the dermatomes and myotomes of the anterior and posterior
trunk.
• Roots from L1-S2 supply neurologic function to the lower extremities, via the lumbosacral plexus,
from which arise the peripheral nerves subserving sensory and motor function of the legs and feet.
(Figures 12-1 to 12-3).
Figure 12-1. Dermatome map.
Figure 12-2. UE nerve schematic drawing.
Figure 12-3. LE nerve schematic drawing.
TECHNICAL ASPECTS AND CONSIDERATIONS

NCS/EMGs are most frequently performed in the outpatient office setting. NCS may be performed by a
trained technician or physician; however, the EMG portion is always performed by a physician. Both
examinations are performed in “real time,” with findings elicited during the examination influencing the
extent and specific subsequent course of the study. Study design and the interpretation of all information
derived from these tests must be performed by a physician with training in electrodiagnostic medicine and
a solid understanding of clinical neurophysiology (Figure 12-4).
Figure 12-4. EMG/NCS machine. A typical EMG/NCS system which has settings for both nerve
conduction studies and electromyography.
NERVE CONDUCTION STUDIES

Nerve conduction studies (NCS) involve the delivery of an electrical stimulus externally over the skin
along the course of a peripheral nerve. This stimulus activates the selected underlying nerve; that is, it
depolarizes the nerve causing an action potential. The response evoked by stimulation of the nerve is then
measured at a site distant to the stimulation by a recording electrode placed on the surface of the skin.
Motor nerves, sensory nerves, and reflex pathways involving both can be studied in this method, with
slight variations in technique (Figures 12-5 and 12-6).
Figure 12-5. NCS stimulator. The bipolar prongs are held against the skin overlying the nerve to provide
an electrical potential that induces depolarization over the stimulated nerve segment.
Figure 12-6. Surface and needle electrodes. Recording and ground electrodes for NCS, and single-use
disposable needle electrodes for EMG.
Motor NCS are performed by stimulating over the selected nerve, and recording the compound muscle
action potential (CMAP) with a surface electrode placed over a muscle that the selected nerve is known
to innervate. Standard procedures have been established for the commonly (and less commonly) studied
nerves that identify specific sites for stimulation and recording.
In general for all motor NCS:
• Stimulation is performed at least 2 sites, a distal site and a proximal site/sites.
• A single recording site is used to measure the responses from all stimulation sites.
For example, a recording electrode for the median nerve is placed over the abductor pollicis brevis
(APB) muscle over the thenar eminence, and the nerve is first stimulated at the wrist (distal site) and then
at the antecubital fossa (proximal site) (Figures 12-7 and 12-8).
Figure 12-7. Median nerve conduction studies, distal stimulation. Recording electrodes are placed over
the abductor pollicis brevis muscle, and the nerve is stimulated at the wrist (distal stimulation site).
Figure 12-8. Median motor nerve conduction studies, proximal stimulation. Recording electrodes are
placed over the abductor pollicis brevis muscle, and the nerve is stimulated at the antecubital fossa
(proximal stimulation site).
For the peroneal nerve, a recording electrode is placed over the extensor digitorum brevis (EDB)
muscle in the foot. The nerve is first stimulated at the ankle (distal site), then below the neck of the fibula,
then again above the neck of the fibula (Figure 12-9).
Figure 12-9. Peroneal motor nerve conduction studies, distal stimulation. Recording electrodes are
placed over the extensor digitorum brevis muscle, and the nerve is stimulated at the anterior ankle (distal
stimulation site).
Several electrophysiological parameters are recorded, measured, and analyzed, including:

• Distal motor latency
• Compound muscle action potential (CMAP) amplitude
• Motor nerve conduction velocity
Results are then analyzed in comparison with normative data for the specific nerve and
electrophysiological parameter studied (Figure 12-10 and Table 12-1).
Figure 12-10. Median motor tracing. Motor nerve conduction study of the median nerve. The top line
displays the compound muscle action potential (CMAP) obtained by distal stimulation, and the bottom
line displays the CMAP obtained by proximal stimulation. Numerical data pertaining to the CMAP
responses is displayed on the right of the screen.
TABLE 12-1. Motor Nerve Conduction Studies: Electrophysiological Parameters and

Normal Values of Frequently Evaluated Nerves
Sensory NCS are performed by stimulating the sensory nerve endings in a specific nerve distribution,
and measuring the sensory nerve action potential (SNAP) this produces.
• A recording electrode is placed superficially over the selected nerve.
• The nerve is stimulated at a single site.
As with motor NCS, standard procedures have been established for the commonly (and less commonly)
studied nerves that identify specific sites for stimulation and recording.
For example, for a median sensory study, we stimulate the skin of the (palmar) index finger, and record
over the median nerve at the wrist (Figure 12-11).
Figure 12-11. Median sensory nerve conduction study. Recording electrodes are placed over the course
of the median nerve at the wrist, and ring electrodes are used to stimulate the median sensory nerves in the
index finger.
The electrophysiological parameters recorded, measured, and analyzed for sensory NCS are:
• Sensory nerve action potential (SNAP) amplitude (Figure 12-12)
Figure 12-12. Median sensory tracing. Sensory nerve conduction study of the median nerve. The median
sensory nerve action potential (SNAP) is displayed on the top 2 lines, and in this case the bottom 2 lines
display the ulnar SNAP. Numerical data pertaining to the SNAP responses is displayed on the right.
• Sensory nerve conduction velocity (Table 12-2)
TABLE 12-2. Sensory Nerve Conduction Studies: Electrophysiological Parameters and

Normal Values of Frequently Evaluated Nerves
ELECTROMYOGRAPHY
A needle electrode is placed percutaneously into a specific target muscle. The needle electrode then
records the physiologic electrical activity of the muscle, which is amplified and displayed on an
oscilloscope screen. The electrical signal from the muscle is seen visually as a waveform, and is also
translated into sound, which is heard on a speaker in “real time.”
• The needle is inserted into the desired target muscle.
• The electrical activity of the muscle is evaluated at physiologic rest; that is, with the patient relaxing
the instrumented muscle to the extent possible.
• The patient is subsequently requested to move the muscle being recorded, at which time the muscle
fibers are observed in activation.
• The needle electrode is then removed from the muscle.
• Additional muscles are examined in sequence.
• The total number and specific selection of muscles examined is determined on a neuroanatomical
basis, by the findings observed in previously examined muscles (Figures 12-13 and 12-14).
Figure 12-13. Needle EMG of tibialis anterior muscle. A recording needle electrode is introduced
percutaneously into the tibialis anterior muscle. A surface ground electrode is applied over the skin.
Figure 12-14. Needle EMG extensor carpi radialis muscle. A recording needle electrode is introduced
percutaneously into the extensor carpi radialis muscle. A surface ground electrode is applied over the
skin.
Muscle fibers conform to identifiable electrophysiologic patterns in health and in disease. When the
nerve supply to a muscle is impaired, the muscle will respond to the injury in characteristic ways, which
can be recognized and measured (Figure 12-15 and Table 12-3).
Figure 12-15. EMG. Motor unit potentials are recorded by the needle and displayed on the screen for
analysis.
TABLE 12-3. Needle Electromyography: Electrophysiological Parameters and Normal

Values of Frequently Evaluated Upper Extremity Muscles
In the design of an electromyography (EMG) study, muscles are selected for study based on their
peripheral innervation, from spinal root through terminal peripheral nerve branch. In this way, the
location of a nerve injury can be “mapped” by determining which muscles reflect denervation injury and
which muscles are spared (Tables 12-4 and 12-5).
TABLE 12-4. Example: Lower Extremity Emg Study
TABLE 12-5. Example: Upper Extremity Emg Study
Additional muscles may then be selected as indicated, based on the above “screening” of roots and
peripheral nerves.
For example, if electrophysiological evidence of denervation is observed solely in the first dorsal
interosseous muscle, on the basis of this finding alone, nerve injury could localize to either of 2 sites:
• T1 root
• Ulnar nerve
To determine which of these 2 possibilities is correct, subsequent examination could then be performed
of
• Abductor pollicis brevis muscle: C8, T1; median nerve, that is, a T1 muscle not innervated by the
ulnar nerve
• Flexor digitorum profundus (3,4) muscle: C7, C8; ulnar nerve, that is, an ulnar muscle not innervated
by T1
CLINICAL BENEFITS
NCS/EMG are studies of “function” as opposed to “structure” and therefore complement imaging studies,
which evaluate structure only. For example, an MRI can show that a nerve is compressed, but cannot
provide information about the functional integrity of the compressed nerve, whereas NCS/EMG can.
Case Example
Patient with symptoms of neck pain radiating into the medial aspect of right arm, with episodic
paresthesias affecting right fourth and fifth fingers. Cervical spine MRI reveals multilevel degenerative
disease with resulting various degrees of impingement of C6, C7, and C8 exiting nerve roots.
Scenario #1
• NCS are normal.
• EMG demonstrates evidence of active C8 radiculopathy, but no evidence of C6, C7, or other root
injury.
This patient has active right C8 radiculopathy, which likely accounts for both pain and paresthesias.
There is a high likelihood that this patient would benefit from a focal procedural intervention targeted at
the right C8 root.
Scenario #2
• NCS reveal evidence of mild right ulnar compression across the elbow.
• EMG demonstrates evidence of chronic right C6 radiculopathy, but no evidence of C7, C8, or other
root injury.
This patient likely has neck pain from C6 radiculopathy and/or mechanical causes, and hand
paresthesias from ulnar neuropathy. A focal procedural intervention targeted at the right C8 root is far less
likely to result in satisfactory outcome for this patient.
Neurologists consider electrodiagnostic studies, including NCS and EMG, to be an extension of the
neurologic examination. On the basis of peripheral neuroanatomy, the localization of a nerve injury to a
specific spinal root, plexus, or peripheral nerve can at times be determined clinically through careful
neurologic examination alone. Some injuries may involve a clear dermatomal/myotomal pattern, as
opposed to a peripheral nerve distribution, or vice versa. Frequently, however, clear localizing signs
and/or symptoms are either not identifiable, or may be confounded by additional factors. In some cases,
dermatomal/myotomal patterns closely approximate the territory subserved by a peripheral nerve. In other
cases, more than one diagnosis may be present. In these cases, NCS/EMG plays an essential role in the
diagnosis and localization of neuropathic injury. It is important to recognize that in small percentage of
patients, in an appropriately performed test, subtle lesions may not be identified on the EMG/NCV and in
these settings the physicians’ clinical acumen should prevail.
Suggested Reading
Donofrio PD, Albers JW. Polyneuropathy: classification by nerve conduction studies and
electromyography. Muscle Nerve. 1990;(13):889-903.
Gruis KL, Little AA, Zebarah VA, Albers JW. Survey of electrodiagnostic laboratories regarding
hemorrhagic complications from needle electromyography. Muscle Nerve. 2006;(34):356-358.
Guarantors of Brain. Aids to the Examination of the Peripheral Nervous System. Saunders Elsevier
Limited; 2000.
Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice. 3rd ed. Oxford
University Press; 2001.
Lynch SL, Boon AJ, Smith J, et al. Complications of needle electromyography: hematoma risk and
correlation with anticoagulation and antiplatelet therapy. Muscle Nerve. 2008;(38):1225-1230.
Oh SJ. Clinical Electromyography Nerve Conduction Studies. 2nd ed. William & Wilkins; 1993.
Preston DC, Shapiro BE. Electromyography and Neuromuscular Disorders, Clinical-
Electrophysiologic Correlations. Boston, MA: Butterworth-Heinemann; 1998.
Wilbourn AJ, Aminoff MJ. The electrodiagnostic examination in patients with radiculopathies. Muscle
Nerve. 1998;(21):1612-1631.
CHAPTER 13
Documentation, Billing, and Coding

Laxmaiah Manchikanti
Multiple issues related to documentation, billing, and coding are facts of life for physicians practicing
interventional pain management. Emphasis continues on the description and definition of what the
physician does for and to the patient. Various issues related to billing and coding in interventional pain
management requires understanding of procedural coding systems, diagnostic coding systems, and
appropriate documentation for interventional techniques and other services provided by physicians.
Consequently, documentation of medical services is necessary to provide information, which is medically
necessary and indicated, to assist health care professionals in providing services to patients. Furthermore,
appropriate documentation, billing, and coding also reflect the competence and character of the physician
while assisting in the financial survival.
DIAGNOSTIC CODING SYSTEMS

The medical necessity for any physician or provider encounter requires appropriate diagnosis and coding
by the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) to
justify services rendered and to indicate the severity of a patient’s condition.1,2 Coding should be
completed to the highest degree of certainty for each encounter. Coding also should correlate with
multiple components of a patient’s medical record, including initial evaluation or follow-up visits and the
billing statement.
The ICD-9-CM is a coding system used to report patient illnesses, injuries, complaints, or symptoms,
termed diagnoses.2 The ICD-9-CM communicates to third-party payers—the need for medical services or
why a physician performed a service. The ICD-9-CM system consists of code numbers and narrative
descriptions similar to those found in the Current Procedural Terminology (CPT), even though the two
systems are distinctly separate and different.
In addition to the ICD-9-CM diagnostic coding systems, other diagnostic coding systems are also
available. The Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV), for
psychiatric and mental health services is one such system.3 The International Association for the Study of
Pain (IASP) also has published a diagnostic classification of pain disorders, a coding system entirely
different from the ICD-9-CM and the DSM-IV.4
Subsequent to ICD-9, ICD-10, the 10th revision has been introduced for coding of diseases, signs and
symptoms, abnormal findings, complaints, social circumstances, and external causes of injury or diseases,
as classified by the World Health Organization (WHO).5 While the United States is considering its
application, approximately 25 countries already use ICD-10 for reimbursement and resource allocation in
their health systems. The United States will begin official use of ICD-10 on October 1, 2013, using
clinical modification of ICD-10-CM for diagnosis coding and procedure coding and ICD-10-PCS for
inpatient hospital procedure coding.5
PROCEDURAL CODING SYSTEMS

Procedural coding systems communicate the procedures and services provided to patients and the reasons
they were provided. It is required for physicians to understand procedural coding systems not only for
proper reimbursement and for appropriate record keeping, but also to avoid fraud and abuse implications.
The advent of the Medicare resource–based relative value scale (RVS) replacing the long existing usual,
reasonable, customary charge; impact of fraud and abuse regulations on medical practices; and, the
economic impact of improper coding and the positive results of accurate documentation and coding have
made it mandatory for providers to understand procedural coding systems, along with diagnostic coding
systems.6 Procedural coding systems consist of CPT, ICD-9, and Healthcare Common Procedure Coding
System (HCPCS).1,2,6-10
• CPT, developed and updated by the American Medical Association (AMA), is the most commonly
used coding system not only in the United States, but also in other countries.
• The second popular coding system is the Centers for Medicare and Medicaid Services (CMS) common
procedure coding system known as HCPCS.10
MEDICAL NECESSITY
Medical necessity requires appropriate diagnosis and coding by the ICD-9-CM to justify services
rendered and indicates the severity of a patient’s condition.11 The Balanced Budget Act (BBA) (HR 2015,
Section 4317) requires all physicians to provide diagnostic information for all Medicare/Medicaid
patients starting from January 1, 1998.12,13 Physicians are required to code by listing the ICD-9-CM
diagnostic codes shown in the medical record to be chiefly responsible or the services provided. Coding
should be to the highest degree of certainty for each encounter. Medical necessity is defined in numerous
ways:
• Black’s Dictionary of Law14 defined medical necessity as “an absolute physical necessity, an
inevitability, or convenient, useful, appropriate, suitable, proper or conducive to the end sought.”
• The Centers for Medicare and Medicaid Services (CMS)15 defined medical necessity in these
terms: “no payment may be made under Part A or Part B for any expense incurred for items or services
which … are not reasonable and necessary for the diagnosis or treatment of illness or injury or to
improve the functioning of a participant.”
• The American Medical Association (AMA)16 defined medical necessity as, “health care services or
procedures that a prudent physician would provide to a patient for the purpose of preventing,
diagnosing or treating an illness, injury, disease or its symptoms in a manner that is:
In accordance with generally accepted standards of medical practice.
Clinically appropriate in terms of type, frequency, extent, site, and duration.
Not primarily for the convenience of the patient, physician, or other healthcare provider.”
WIDE ARENA OF DOCUMENTATION
Federal, state, third party payor, and managed care plans rely heavily on provider documentation when
assessing the claims for various parameters. These include the following:
• Was the billed service actually rendered or provided to the patient?
• Was the level of service or extent of the service accurately reported?
• Was the service or procedure medically necessary?
• Was the claim sent to the correct primary insurer for the service or procedure performed?
Medical Record
A medical record is a document with confidential information that functions as a clinical record and a
business record. The medical record (Table 13-1) facilitates various functions:9,16-19
• The ability of a physician and other health care professionals to evaluate and plan patients’ treatment
and to monitor their health care over a period of time.
• Communication and continuity of care among physicians and other health care professionals involved
in patients’ care.
• Accurate and timely claims review and payment.
• Appropriate utilization review and quality of care evaluations.
• Collection of data that may be useful for research and education.
TABLE 13-1. Functions and Requirements of Patient’s Medical Record

The typical information for an interventional pain management medical chart (electronic and/or hard
copy) is as follows:
• Patient demographic data
Medical insurance card copy
Patient’s driver license copy
Patient guarantee and authorization forms
Advanced beneficiary note
• Summary sheet with problems and medication history
• Patient questionnaires
• Initial evaluation
• Progress notes
• Laboratory test results
Radiographic evaluation results
Results of various medical tests
• Medical records from other providers
Facility notes
Consultation reports
Correspondence
Documentation Process
A multitude of personnel associated with a practice or a facility are responsible for documentation. They
include physician assistants, nurse practitioners, clinical nurse specialists, physical therapists,
psychologists, nurses, and medical assistants who obtain patient histories and vital signs, administer
injections, and otherwise provide certain restricted services.
To meet the entire documentation criteria, the following checklist must be utilized:
• Authorization for making entries and policies should be defended.
Support the medical necessity of the service performed.
Provide a clear description of the procedure or service including technique and end results.
Make it clear that the procedure was performed by the reporting or billing physician.
Document appropriate and specific diagnostic code as ICD-9-CM diagnostic code.
Provide documentation of indications and medical necessity, which may be reviewed by payors at
any time.
Follow correct coding initiatives (CCIs) and Local Coverage Determinations (LCDs) with the
limitations, which become part of documentation.
Electronic Documentation
The evolution of medical records from paper to electronic changes the work processes for seeing a
patient for storing information, for accessing information, and the look of the output when the note is
printed. However, using electronic health records or electronic medical records does not change the duty
to comply with the basic medical record guidelines. Some of the issues such as legibility, storage in one
place, locking the records in the office at night, and off-site access become nonissues.
Types of Documentation
Documentation includes evaluation and management services and interventional techniques.
Documentation for interventional techniques may vary based on whether the procedure was performed in
a facility setting such as hospital outpatient department or ambulatory surgery center (ASC) versus in a
physician’s office.
DOCUMENTATION OF INTERVENTIONAL PROCEDURES

All interventional techniques are considered surgical procedures. Documentation requirements are as
follows:
• History and physical
• Indications and medical necessity
• Intraoperative procedural description
• Postoperative monitoring and ambulation
• Discharge/disposition
Multiple developments in evolution of interventional pain management include changes in CPT 2000 to
20117,8,11,12; the final rules for 2011 on physician payment policies; the Medicare program prospective
payment system for hospital outpatient services and ASCs; and ongoing development of CCIs, affecting
almost all interventional techniques.
Issues of correct coding and medical necessity and guidelines with regards to effectiveness and
frequency and number of interventions, combination of blocks/interventions, and number of interventions
per setting continue to remain contentious.20-24 Further, enactment of the Affordable Care Act (ACA)25
also is responsible for significant changes in not only billing, coding, etc, but the entire practice of
medicine.
CORRECT CODING POLICIES

A multitude of codes reflect the wide spectrum of services provided by various medical providers, and
many medical services can be rendered by different methods and combinations of various procedures.
Hence, multiple codes describing similar services are frequently necessary to accurately reflect the
particular service a physician performs. However, when multiple procedures are performed at the same
session, the procedure and postprocedure work do not have to be repeated for each procedure; and,
therefore, a comprehensive code describing the multiple services commonly performed together can be
used. Many activities which are integral to a procedure are considered as generic activities and are
assumed to be included as acceptable medical/surgical practice and, while they could be performed
separately, they should not be considered as such when a code narrative is defined. Hence, all services
integral to accomplishing a procedure will be considered to be included in that procedure and, therefore,
will be considered a component and part of the comprehensive code.
Standards of Medical/Surgical Practice

Many of the provider activities during a procedure are integral to a procedure and termed as generic
activities, which are assumed to be included as acceptable medical/surgical practice, considered to be
included in that procedure and therefore considered a component of the procedure. Some generic services
integral to standard medical/surgical services include many of the components as illustrated in Table 13-
2.
TABLE 13-2. Multiple Generic Services Integral to Standard Medical/Surgical Services.

Cleansing, shaving, and prepping of the skin
Draping of the patient
Positioning of the patient
Insertion of intravenous access
Administration of sedation
Local, topical, or regional anesthetic administration
Identification of the surgical approach
Surgical cultures
Wound irrigation
Insertion and removal of drains, suction devices, dressings,
and pumps. Application, management, and removal of
postoperative dressings, including transcutaneous electrical
nerve stimulation units and institution of patient-controlled
analgesia
Preoperative, intraoperative, and postoperative
documentation
Surgical supplies, unless accepted by existing CMS policy
Further, intravenous access, cardiopulmonary monitoring, and anesthesia by a physician, and conscious
sedation are considered as included in the medical/surgical package. A majority of invasive procedures
require the availability of vascular and/or airway access, cardiopulmonary monitoring, anesthesia by
physician, and conscious sedation. Thus, these are already included in the value of the comprehensive
procedure as a part of medical/surgical package.
In addition, evaluation and management services with a procedure are considered as an integral part of
a comprehensive procedure.
Add-On Codes
The CPT coding system identifies certain codes that are submitted with other codes. These codes are
identified generally with a statement such as, “List separately in addition to code for primary procedure”
in parentheses. The supplemental code is to be used only with certain primary codes that are identified in
parentheses. The purpose of these CPT codes is to enable providers to separately identify a service that is
performed in certain situations as an additional service.
Add-on codes relevant to interventional pain management are subsequent transforaminal epidural
injections (CPT codes 64480 and 64484), facet joint blocks (CPT codes 64491, 64492, 64494, and
64495), and facet joint neurolysis (CPT codes 64623 and 64627).
Modifiers
In order to expand the information provided by the five-digit CPT codes, a number of modifiers have
been created by the AMA, CMS, and local Medicare carriers. These modifiers, in the form of two digits,
either numbers, letters, or a combination of each, are intended to convey specific information regarding
the procedure or service to which they are appended. Modifiers are attached to the end of a code to
indicate that a service or procedure described in the code definition has been modified by some
circumstance. However, explicit understanding of the purpose of each modifier is required prior to its
usage.
• The –22 modifier is used to describe unusual procedural services, extensive, or a procedure performed
under unusual circumstances.
• The –25 modifier is used to identify a significant, separately identifiable evaluation and management
service by the same physician on the same day of the procedure or other service.
• Modifier 59 is used to describe a distinct procedural service under certain circumstances indicating
that a procedure or service was distinct or independent from other services performed on the same day.
• Modifier 50 is used to report bilateral procedures.
• Modifier 51 is used to report additional procedure(s).
Family of Codes
The CPT manual describes certain codes that include two or more component codes that should not be
reported separately, as these are considered members of a code family and included in the more
comprehensive code. As such, comprehensive codes include certain services that are separately
identified by other component codes. Although, component codes as members of the comprehensive code
family represent parts of the procedure, they should not be listed separately when the complete procedure
is performed; the component codes are considered individually only if the procedures they describe are
performed independently of the complete procedure. If this is not the case, all services listed in the
comprehensive codes are considered to make up the total service.
Unlisted Services or Procedures

Multiple sections in the CPT manual list certain codes that end in “99” or “9,” in a few cases used to
report a service that is not described in any code listed elsewhere in the CPT manual.
Mutually exclusive codes are codes for procedures that cannot reasonably be performed in the same
session.
• Modifier indicator and definitions are as follows:
• 0 (not allowed). There are no modifiers associated with NCCI that are allowed to be used with this
code pair; there are no circumstances in which both procedures of the code pair should be paid for the
same beneficiary on the same day by the same provider.
• 1 (allowed). The modifiers associated with NCCI are allowed with this code pair when appropriate.
• 9 (not applicable). This indicator means that an NCCI edit does not apply to this code pair. The edit for
this code pair was deleted retroactively.
Medically Unlikely Edits

CMS implemented Medically Unlikely Edits (MUE) January 1, 2007, as another means to reduce
improper payments due to reporting errors on claims. CMS gives this definition of an MUE: “An MUE for
an HCPCS/CPT code is the maximum units of service that a provider would report under most
circumstances for a single beneficiary on a single date of service.” Not every code has an MUE and CMS
does not publish every MUE.
Incorrect Coding
Incorrect coding is defined as the intentional or unintentional billing of multiple procedure codes for a
group of procedures that are covered by a single comprehensive code. Incorrect coding includes both
unbundling and upcoding. Various types of incorrect coding examples include:
• Fragmenting one service into component parts and coding each component as if it were a separate
service
• Reporting separate codes for related services when the comprehensive code includes all related
services
• Breaking out bilateral procedures when one code is appropriate
• Downcoding a service in order to use an additional code when one higher-level, more comprehensive
code is appropriate
• Separating a surgical approach from a major surgical service
References
1. Manchikanti L, Singh V, Fellows B. Diagnostic coding systems. In: Manchikanti L, Christo PJ, Trescot
AM, Falco FJE, eds. Foundations of Pain Medicine and Interventional Pain Management: A
Comprehensive Review. Paducah, KY: ASIPP Publishing; 2011;433-440.
2. 2011 ICD-9-CM: International Classification of Diseases, 9th Revision — Clinical Modification,
professional edition. St Louis, MO: Saunders/Elsevier; 2011.
3. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Text Revision (DSM-IV-TR).
Washington, DC: American Psychiatric Association; 2000.
4. Merskey H, Bogduk N. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes
and Definition of Pain Terms. 2nd ed. Task Force on Taxonomy of the International Association for
the Study of Pain. Seattle, WA: IASP Press; 1994.
5. Manchikanti L, Falco FJE, Hirsch JA. Necessity and implications of ICD-10: facts and fallacies. Pain
Physician 2011; in press.
6. Manchikanti L, Singh V. Procedural coding systems. In: Manchikanti L, Christo PJ, Trescot AM, Falco
FJE, eds. Foundations of Pain Medicine and Interventional Pain Management: A Comprehensive
Review. Paducah, KY: ASIPP Publishing; 2011;441-454.
7. Manchikanti L, Singh V, Caraway DL, et al. Medicare physician payment systems: impact of 2011
schedule on interventional pain management. Pain Physician. 2011; 14(1):E5-E33.
8. Manchikanti L, Parr AT, Singh V, Fellows B. Ambulatory surgery centers and interventional
techniques: a look at long-term survival. Pain Physician. 2011;14(2):E177-E215.
9. Current Procedural Terminology. CPT 2011. Chicago, IL: American Medical Association; 2010.
10. Healthcare Common Procedure Coding System (HCPCS) Level II Coding Procedures, Revised June
15, 2010. www.cms.gov/MedHCPCSGenInfo/Downloads/LevelIICodingProcedures.pdf
11. Manchikanti L, Singh V, Hirsch JA. Documentation for interventional techniques. In: Manchikanti L,
Christo PJ, Trescot AM, Falco FJE, eds. Foundations of Pain Medicine and Interventional Pain
Management: A Comprehensive Review. ASIPP Publishing, Paducah, KY; 2011;471-486.
12. Manchikanti L, Singh V, Pampati V, et al. Description of documentation in the management of chronic
spinal pain. Pain Physician. 2009;12(4):E199-E224.
13. H.R. 2015. Balanced Budget Act of 1997. P.L. 105-33, August 5, 1997.
14. Garner BA, ed. Black’s Law Dictionary. 8th ed. St Paul, MN: Thomson West; 2004.
15. Centers for Medicare and Medicaid Services (CMS) Billing Guide. Medicare Part B. NHIC Corp.,
March 2009.
16. American Medical Association. Model Managed Care Contract. 2nd ed. 2000. www.ama-
assn.org/ama/upload/mm/395/modelmgdcare.pdf
17. 1995 Documentation Guidelines for Evaluation and Management Services. Centers for Medicare &
Medicaid Services. www.cms.hhs.gov/MLNProducts/Downloads/1995dg.pdf
18. 1997 Documentation Guidelines for Evaluation and Management Services. Centers for Medicare &
Medicaid Services. www.cms.hhs.gov/MLNProducts/Downloads/MASTER1.pdf
19. Evaluation & Management Services Guide. Centers for Medicare & Medicaid Services. July 2009.
www.cms.hhs.gov/MLNProducts/Downloads/eval_mgmt_serv_guide.pdf
20. Manchikanti L, Boswell MV, Singh V, et al. Comprehensive evidence-based guidelines for
interventional techniques in the management of chronic spinal pain. Pain Physician. 2009;12(4):699-
802.
21. Manchikanti L, Helm S, Singh V, et al. An algorithmic approach for clinical management of chronic
spinal pain. Pain Physician. 2009;12(4):E225-E264.
22. Manchikanti L, Datta S, Derby R, et al. A critical review of the American Pain Society clinical
practice guidelines for interventional techniques: Part 1. Diagnostic interventions. Pain Physician.
2010;13(3):E141-E174.
23. Manchikanti L, Datta S, Gupta S, et al. A critical review of the American Pain Society clinical
practice guidelines for interventional techniques: Part 2. Therapeutic interventions. Pain Physician.
2010;13(4):E215-E264.
24. Chou R, Huffman L. Guideline for the Evaluation and Management of Low Back Pain: Evidence
Review. American Pain Society, Glenview, IL, 2009. www.ampainsoc.org/pub/pdf/LBPEvidRev.pdf
25. Manchikanti L, Caraway DL, Parr AT, Fellows B, Hirsch JA. Patient Protection and Affordable Care
Act of 2010: Reforming health care reform for the new decade. Pain Physician. 2011;14(1):E35-E67.
SECTION II
HEAD AND NECK INJECTIONS

CHAPTER 14
Atlanto-Occipital Joint Injections

Andrea Trescot
INTRODUCTION
The atlanto-occipital (AO) and atlanto-axial (AA) joints are unique joints in the spine, connecting the
cervical region to the base of the skull. The AA and AO joints are an often under-appreciated cause of
pain, and should be part of the differential diagnosis of cervical spine pain and occipital headaches.
INDICATIONS
AO joint injections are indicated for:
• The diagnosis and treatment of AO joint pathology, which presents as deep pain in the suboccipital
region, often unilateral
Especially after flexion/extension injuries
Particularly when movement in flexion and extension causes pain
• Cervicogenic headaches that are impairing functional life indices (restorative sleep capacity,
endurance, and quality of life)
• Persistent upper cervical pain that is leading to escalating opioids to control symptoms
• Persistent occipital neuralgia poorly responsive to occipital nerve blocks
The AO joint primarily refers to the ipsilateral suboccipital and retromastoid region, although pain may
also refer to the paracervical, suprascapular, and levator scapular regions.1 The normal AO joint is
ellipsoid, and permits passive flexion and extension of about 10 degrees as well as 10 degrees rotation
and side bending of about 10 degrees.2 There may be decreased range of motion, crepitance, and
abnormal head position. When there is pain with side bending during protraction or retraction, the most
likely joint affected is the AO joint. Pain or decreased range of motion when nodding from a full rotation
is usually related to the AO joint. Unfortunately, the radiologic diagnosis of AO joint pathology has a high
false-negative result, since onset of pain precedes any observable structural abnormalities. Characteristic
referred pain patterns from AA and AO joint pathology overlap those patterns from the greater and lesser
occipital nerves as well as the pain from the C2/3 facet joint,1 making clinical diagnosis difficult. See
Figure 14-1.
Figure 14-1. Patterns of occipital pain. (Used with permission from Andrea Trescot, MD.)
CONTRAINDICATIONS
• Infection at the injection site
• Coagulopathy
• Cervical spine instability
• Previous cervical fusion at that level
RELEVANT ANATOMY
The first two bones of the cervical spine are unique in their shape and function (Figure 14-2). The C1, or
atlas, vertebra is unique in that it does not have a ventral vertebral body, but rather functions as a relay
between the occiput and C2. The AO joint is the articulation of the superior articular facet of C1 (the
atlas) and the occiput. The AO joint articulates the atlas (C1) with the occiput (C0) and constitutes the
C0-1 joint. The AO joint straddles the spinal cord with the foramen magnum on either side and is V-
shaped, slanting caudally and medially (Figure 14-3); it holds a volume of 1.0 cc.3
Figure 14-2. Lateral view of AA and AO joints.
Figure 14-3. AP drawing of AA and AO joints.
The posterior arch of C2 is very deep to the skin and difficult to palpate. The transverse processes are
long and perforated by a foramen, which protects the vertebral artery, and the anterior and posterior
arches form a triangular conduit for the brainstem. There are grooves in the C1 posterior surface that
accommodate the vertebral arteries. The vertebral artery transverses a variable pattern through the wide
opening within the transverse process of C2 and travels across the body of C1, running on the lateral one-
third of the AA joint dorsally, to enter the foramen magnum medial to the AO joint (Figure 14-4).
Figure 14-4. Vertebral artery and relationship to AA and AO injection sites. (Used with permission from
Andrea Trescot, MD.)
The AO joint shares similar innervation with the AA joint, and is responsible for paracervical
myofascial pain, bony joint pain, and intra-articular pain in a variably represented referred pain pattern.
A torturous and unpredictable anatomical variance between the vertebral artery and the bony structures
(Figure 14-5) suggests that no reliable placement of needle may be expected to be completely safe, and
trans-arterial or intra-arterial injections are always a potential disastrous complication; therefore, IV
access is mandated. If the patient is anticoagulated, these medications should be stopped. The risk/reward
ratio should be in the patient’s favor when assessing when anticoagulation therapy should cease. This
requires communication with the patient’s primary care practitioner to further define the risk of bleeding
versus the risk of cardiovascular event.
Figure 14-5. Tortuous vertebral artery. (Used with permission from Andrea Trescot, MD.)
FLUOROSCOPIC VIEWS
The fluoroscope is positioned in order to visualize the AO joint as a crisp line. An “open mouth” view
may be necessary to adequately visualize the joint (Figure 14-6). An alternative lateral approach places
the patient in the lateral position with the symptomatic side up and the head flexed and rotated 45 degrees
toward the table. The C2 and C3 segments are aligned and the fluoroscopic beam then angled cephalad or
caudad to view the greatest joint opening. From this position, both the AA and the AO joints can be
accessed.
Figure 14-6. Open-mouth view of AO and AA joints. (Used with permission from Andrea Trescot, MD.)
POSITIONING OF PATIENT
The patient is placed in the prone position with the neck slightly flexed and the chest on a pillow, or in the
lateral position with the head flexed and rotated 45 degrees for the lateral approach.
SELECTION OF NEEDLES, MEDICATIONS, AND EQUIPMENT

• Needles
22-gauge 3.5-in Quinke needle or blunt tipped needle with introducer
Extension tubing
3cc syringes (Luer locked)
• Medications
Nonionic contrast
Non-particulate steroid
Local anesthetic (lidocaine, bupivicaine)
• Equipment
C-arm

• After a sterile prep and drape, subcutaneous local anesthetic is injected.
• 22g subarachnoid needle (thinner needles are too flexible) is advanced under fluoroscopic control
using a “gun barrel” technique to guide the needle to the inferior lateral aspect of the AO joint.
• Once needle contact is made on the inferior edge of the joint line, the needle slides (not losing contact
with the periosteum) just off the edge of bone into the joint capsule (Figure 14-7).
• The C-arm is then rotated into a lateral view for confirmation that the needle has entered the joint
space (Figure 14-8).
• 0.25 to 0.5 cc of nonionic contrast is then injected, utilizing extension tubing to decrease needle
movement. Contrast should spread throughout the joint capsule.
• Venous runoff of the contrast almost always means that the needle is outside the joint, which has a rich
vascular plexus (primarily venous).
Figure 14-7. Needle placement (AP) in AO joint. (Used with permission from Andrea Trescot, MD.)
Figure 14-8. Needle placement (lateral) in AO joint. (Used with permission from Andrea Trescot, MD.)
If there is runoff, or spread the contrast into the epidural space, the injection should be terminated.
• After confirmation of location and negative aspiration, a total of 1 cc of local anesthetic and steroid is
injected.
Because of the proximity to vascular structures, concerns regarding intravascular injections of
particulate steroid, prudence may suggest the use of a nonparticulate steroid.
• The use of a new curve blunt tip “stealth” needle (Epimed) allows for an approach to the suboccipital
region from a cephalad approach (Figure 14-9).
Figure 14-9. Stealth needle placement. (Used with permission from Andrea Trescot, MD.)
POSTPROCEDURE CONSIDERATIONS
• Because there may be a loss of proprioception at the base of the skull with this injection, dizziness and
ataxia as well as a sensation of upper neck “weakness” are not unexpected.
MONITORING OF POTENTIAL COMPLICATIONS

• The most dreaded complication of the AO joint injection is an intravascular injection into the adjacent
venous plexus, vertebral artery, or carotid artery, with the resultant risk of seizures.
• It is therefore recommended that only a small amount of local anesthetic be injected to decrease the
potential for cardiovascular or central nervous system toxicity.
• Anatomically, these joints may share a connection to the epidural space, and careful evaluation of
epidural extravasation is necessary prior to injection of local anesthetic to avoid a high epidural or
spinal anesthesia.
• Other complications include infections, postdural puncture headache, spinal cord injury, and ataxia.
CLINICAL PEARLS AND PITFALLS

• The AO joint is a more difficult target than the AA joint.
• The AO and AA joints are often evaluated and treated together.
• Although a 25g needle has been described, it is a matter of concern that it is too flexible and would
more likely deflect in an undesirable direction.
• Although differential local anesthetic blocks are often recommended in other areas of the cervical,
thoracic, and lumbar spine, because of the difficulty in performing the AA and AO injections, it
probably is not necessary or appropriate to use “double local anesthetic” techniques.
Suggested Reading
Racz GB, Sanel H, Diede JH. Atlanto-occipital and atlantoaxial injections in the treatment of headache
and neck pain. In: Waldman S, Winnie A, eds. Interventional Pain Management. Philadelphia, PA:
WB Saunders; 1996:220-222.
Aprill C, Axinn MJ, Bogduk N. Occipital headaches stemming from the lateral atlanto-axial (C1-) joint.
Cephalgia. 2002;22:15-22.
Ogoke BA. The management of the atlanto-occipital and atlanto-axial joint pain. Pain Physician. 2000
Jul;3(3):289-293.
Trescot AM, Hansen HC. Atlanto-occipital and atlanto-axial interventions. In: Manchikanti L, Singh V,
eds. Interventional Pain Techniques in Chronic Spinal Pain. Amer Soc Interventional Pain
Physicians Publishing, Paducah, KY; 2007: chap 21, pp 321-330.
References
1. Dreyfuss P, Michaelsen M, Fletcher D. Atlanto-occipital and lateral atlanto-axial joint pain patterns.
Spine. 1994 May 15; 19(10):1125-1131.
2. Jofe M, White AG, Panjabi M. Clinically relevant kinematics of the cervical spine. In: Sherk H, Dunn
E, Eismon TF, et al, eds. The Cervical Spine. Philadelphia, PA: JB Lippincott; 1989:57-69.
3. Dreyfuss P, Rogers J, Dreyer S, Fletcher D. Atlanto-occipital joint pain. A report of three cases and
description of an intraarticular joint block technique. Reg Anesth. 1994 Sep-Oct;19(5):344-351.
CHAPTER 15
Atlanto-Axial Joint Injections

Andrea Trescot
INTRODUCTION
The atlanto-occipital (AO) and atlanto-axial (AA) joints are unique joints in the spine, connecting the
cervical region to the base of the skull. The AA and AO joints are an often under-appreciated cause of
pain and should be part of the differential diagnosis of cervical spine pain and occipital headaches.
INDICATIONS
AA joint injections are indicated for:
• The diagnosis and treatment of AA joint pathology, which presents as deep pain in the suboccipital
region, often unilateral.
Especially after flexion/extension injuries
Particularly when movement in rotation causes pain
• Cervicogenic headaches that are impairing functional life indices (poor restorative sleep capacity,
endurance, and quality of life).
• Persistent upper cervical pain that is leading to escalating opioids to control symptoms.
• Persistent occipital neuralgia poorly responsive to occipital nerve blocks.
The lateral AA joint is a common cause of cervicogenic headache and may account for up to 16% of
patients with occipital headache.1 The AA joint primarily refers to the occipito-cervical region, radiating
to the posterior auricular region.2 There may be decreased range of motion, crepitance, and abnormal
head position. When pain is increased at far cervical rotation, either during protraction or retraction, the
AA joint is likely to be responsible. Unfortunately, the radiologic diagnosis of AA joint pathology has a
high false-negative result, since onset of pain precedes any observable structural abnormalities.
Characteristic referred pain patterns from AA and AO joint pathology overlap those patterns from the
greater and lesser occipital nerves as well as the pain from the C2/C3 facet joint,2 making clinical
diagnosis difficult.
CONTRAINDICATIONS
• Infection at the injection site
• Coagulopathy
• Cervical spine instability
• Previous cervical fusion at that level
RELEVANT ANATOMY
• The first two bones of the cervical spine are unique in their shape and function. The C1, or atlas,
vertebra is unique in that it does not have a ventral vertebral body, but rather functions as a relay
between the occiput and C2 (Figure 15-1).
• The AA joint articulates the atlas (C1) with the axis (C2) and constitutes the C1-C2 joint.
• The AA joint slopes caudally and laterally (Figures 15-2 and 15-3).
• Unlike the lower cervical segments, the AO and AA joints lack intervertebral discs and uncinate
processes.
• The C1 and C2 nerves, which are primarily sensory, travel through the suboccipital muscles to the
occipital area as the greater occipital nerve and the lesser occipital nerve (Figure 15-4).
• The dorsal root ganglion of C2 lies at the medial portion of the AA joint.
• The posterior arch of C2 is very deep to the skin and difficult to palpate.
• The transverse processes are long and perforated by a foramen, which protects the vertebral artery, and
the anterior and posterior arches form a triangular conduit for the brainstem.
• There are grooves in the C1 posterior surface that accommodate the vertebral arteries. The vertebral
artery transverses a variable pattern through the wide opening within the transverse process of C2 and
travels across the body of C1, runs on the lateral one-third of the AA joint dorsally, to enter the
foramen magnum medial to the AO joint (Figure 15-5).
Figure 15-1. Lateral view of AA and AO joints.

Figure 15-2. AP drawing of AA and AO joints.
Figure 15-3. CT reconstruction image of AA joints.

Figure 15-4. Greater, lesser, and third occipital nerve path.
Figure 15-5. Vertebral artery and relationship to AA and AO injection sites.
The AA joint shares similar innervation with the AO joint, and is responsible for paracervical
myofascial pain, bony joint pain, and intraarticular pain in a variably represented referred pain pattern.
The AA joint holds 0.7 cc.3
A torturous and unpredictable anatomical variance between the vertebral artery and the bony structures
(Figure 15-6) suggests that no reliable placement of needle may be expected to be completely safe, and
trans-arterial or intra-arterial injections are always a potential disastrous complication; therefore, IV
access is mandated. If the patient is anticoagulated, these medications should be stopped. The risk-reward
ratio should be in the patient’s favor whenever assessing when anticoagulation therapy should cease. This
requires communication with the patient’s primary care practitioner to further define the risk of bleeding
versus the risk of cardiovascular event.
Figure 15-6. Tortuous vertebral artery.
Fluoroscopic Views
The fluoroscope is positioned in order to visualize the AA joint as a crisp line. An “open mouth” view
may be necessary to adequately visualize the joint (Figure 15-7).
Figure 15-7. Open mouth view of AA joint.
Positioning of Patient
The patient is placed in the prone position with the neck slightly flexed and the chest on a pillow, or in the
lateral position with the head flexed and rotated 45 degree for the lateral approach.
Selection of Needles, Medications, and Equipment

Needles
22-gauge 3.5″ Quinke needle or blunt tipped needle with introducer
Extension tubing
3-cc syringes (Luer locked)
Medications
Nonionic contrast
Nonparticulate steroid
Local anesthetic (lidocaine, bupivicaine)
Equipment
C-arm

• After a sterile prep and drape, subcutaneous local anesthetic is injected. A 22-gauge subarachnoid
needle (thinner needles are too flexible) is advanced under fluoroscopic control using a “gun barrel”
technique to guide the needle to the inferior medial aspect of the AA joint (Figure 15-8).
• Once needle contact is made on the inferior edge of the joint line, the needle slides (not losing contact
with the periosteum) just off the edge of bone into the joint capsule (Figure 15-9).
• A distinctive “pop” is often felt as the AA joint is entered.
• The C-arm is then rotated into a lateral view for confirmation that the needle has entered the joint
space (Figure 15-10).
• About ¼ to ½ cc of nonionic contrast is then injected, utilizing extension tubing to decrease needle
movement. Contrast should spread throughout the joint capsule (Figures 15-11 to 15-13).
• Venous runoff of the contrast almost always means that the needle is outside the joint, which has a rich
vascular plexus (primarily venous).
Figure 15-8. Placement of needle on inferior AA joint.
Figure 15-9. Advancement of needle into AA joint.
Figure 15-10. Lateral view of AA joint needle placement.
Figure 15-11. Lateral view of AA joint injection of contrast.
Figure 15-12. AP view of AA joint injection of contrast.
Figure 15-13. CT 3D reconstruction of AA joint injection.
If there is runoff, or spread the contrast into the epidural space, the injection should be terminated.
• After confirmation of location and negative aspiration, a total of 0.5 cc of local anesthetic and steroid
is injected.
Because of the proximity to vascular structures, concerns regarding intravascular injections of
particulate steroid, prudence may suggest the use of a non-particulate steroid.
Because there may be a loss of proprioception at the base of the skull with this injection, dizziness and
ataxia as well as a sensation of upper neck “weakness” are not unexpected.
Monitoring of Potential Complications

• The most dreaded complication of the AA joint injection is an intravascular injection into the adjacent
venous plexus, vertebral artery, or carotid artery, with the resultant risk of seizures.
• It is therefore recommended that only a small amount of local anesthetic be injected to decrease the
potential for cardiovascular or central nervous system toxicity. Anatomically, these joints may share a
connection to the epidural space, and careful evaluation of epidural extravasation is necessary prior to
injection of local anesthetic to avoid a high epidural or spinal anesthesia.
• Other complications include infections, post dural puncture headache, spinal cord injury, and ataxia.
Clinical Pearls and Pitfalls

• Although a 25-gauge needle has been described, I am concerned that it is too flexible, and would more
likely deflect in an undesirable direction.
• The AO and AA joints are often evaluated and treated together.
• Although differential local anesthetic blocks are often recommended in other areas of the cervical,
thoracic, and lumbar spine because of the difficulty in performing the AA and AO injections, it
probably is not necessary or appropriate to use “double local anesthetic” techniques.
Suggested Reading
Aprill C, Axinn MJ, Bogduk N. Occipital headaches stemming from the lateral atlanto-axial (C1-) joint.
Cephalgia. 2002;22: 15-22.
Ogoke BA. The management of the atlanto-occipital and atlanto-axial joint pain. Pain Physician. 2000
Jul;3(3):289-293.
Racz GB, Sanel H, Diede JH. Atlanto-occipital and atlanto-axial injections in the treatment of headache
and neck pain. In: Waldman S, Winnie A, ed. Interventional Pain Management. Philadelphia, PA: WB
Saunders; 1996:220-222.
Trescot AM, Hansen HC. Atlanto-occipital an atlanto-axial interventions. In: Manchikanti L, Singh V, eds.
Interventional Pain Techniques in Chronic Spinal Pain. Paducah, KY: Amer Soc Interventional Pain
Physicians Publishing: 2007:321-330. (Chapter 21)
References
1. Aprill C, Axinn MJ, Bogduk N. Occipital headaches stemming from the lateral atlanto-axial (C1-2)
joint. Cephalalgia. 2002 Feb;22(1):15-22.
2. Dreyfuss P, Michaelsen M, Fletcher D. Atlanto-occipital and lateral atlanto-axial joint pain patterns.
Spine. 1994 May 15; 19(10):1125-1131.
3. Dreyfuss P, Rogers J, Dreyer S, Fletcher D. Atlanto-occipital joint pain. A report of three cases and
description of an intraarticular joint block technique. Reg Anesth. 1994 Sep-Oct;19(5):344-351.
CHAPTER 16
Cervical Nerve Root Blocks

Stanley Golovac
INTRODUCTION
The use of cervical root blocks can be used both diagnostically and/or therapeutically. In certain
conditions, a nerve root block can help determine whether the nerve root in question is either contributing
or the cause of the pain. Because the technique lends itself to both diagnostic and therapeutic uses,
cervical nerve root blocks are an essential part of an interventional practice. Each of the levels, other than
C1 and C2, can be accessed for a selective injection. A selective nerve root block is intended to
determine whether the suspected nerve root is involved in the pathology and pain from the nerve root
compression or irritation.
Cervical radiculitis affects approximately 83 per 100,000 people per year.1 The most common causes
of cervical radiculitis in this study were herniated disk in 21.9% and spondylosis in 68.4%. Anderberg
and colleagues2 described the method of a cervical diagnostic SNRB technique and assessed its ability to
correlate clinical symptoms with MRI findings in patients with cervical radicular pain and a single level
degenerative disease.
• The majority of those affected did not undergo surgery.
• Outcomes were favorable in both surgically and nonsurgically treated groups without reproducible
significant outcome differences of one treatment over the other.1-3
• The favorable outcome from cervical radiculitis from herniated disk may be due in part to the natural
regression of disk herniation over time.4,5
• However, well-designed randomized trials of surgical and nonsurgical outcomes for specific
diagnostic entities have not been performed.
• Current treatment strategies typically involve a gradual progression in the aggressiveness of
intervention, progressing from less to more invasive interventions only in refractory cases.
ANATOMY
The cervical spine consists of seven vertebrae, eight nerves, and two vertebral arteries that supply the
posterior aspect of the brain contributing to the circle of Willis (Figure 16-1).
Figure 16-1. Cervical spine anatomy.
Understanding cervical spine anatomy is imperative to the interventionalist performing cervical spine
procedures.
• The epidural space is triangular extending from the foramen magnum to the sacral hiatus. The inner
border is the thecal sac-dura mater.
• The outer border is the bony spinal canal and the covering periosteum.
• The anterior border is the posterior longitudinal ligament. The posterior border is the lamina and
ligamentum flavum.
• The lateral border is the pedicle and intervertebral foramen.
• The epidural space contains loose areolar tissue, venous plexus, spinal nerve roots, radicular arteries,
superficial and deep cervical arteries, arachnoid granules, and lymphatics.
• The ligamentum flavum is fused in the midline in approximately half of individuals and the interspinous
ligament is absent.
• Rootlets arise from the cord to form ventral and dorsal nerve roots that exit with the thecal sac covered
with the dura root sleeve.
• The dura ends at the proximal margin of the dorsal root ganglion.
CERVICAL FORAMEN
• The ventral and dorsal roots coalesce to form the spinal nerve that exits from the foramen.
• The dura extends as the epiradicular sheath covering the dorsal root ganglion and spinal nerve.
• The spinal nerve is located in the inferior aspect of the foramen.
• The foramen is formed by the superior and inferior pedicle.
• The superior articular process of the zygapophyseal joint forms the posterior wall.
• The anterior wall is superior vertebral endplate and disk.
• The spinal nerve is posterior to the vertebral artery.
VASCULAR ANATOMY
• The vertebral artery arises from the subclavian and enters the costotransverse foramen at C6 and exits
at C1 but can enter at C5 (Figure 16-2).
• The vertebral artery crosses posterior to C1 arch before entering the skull through the foramen
magnum.
• Branches from the vertebral artery descend forming the anterior spinal artery.
• The anterior spinal artery is divided into cervical, thoracic, and lumbar segments (Figure 16-3).
• Spinal arteries arising from the vertebral, subclavian, and ascending cervical and deep cervical
arteries enter through the foramen and divide into the anterior and posterior cervical radicular arteries.
• Most radicular arteries supply the nerve root.
• A variable number of anterior radicular arteries supply the anterior spinal artery.
• These radiculomedullary arteries are larger and may ascend and descend within the thecal sac
supplying the anterior spinal artery (see Figure 16-3).
• In the cervical region a variable number of radiculomedullary arteries are present and may enter
anywhere from C3 to C8.
• The radicular and radiculomedullary arteries may be located posterior to the spinal nerve in the
posterior-inferior aspect of the foramen, close to the target zone of transforaminal injections (Figure
16-4).
• Because the vertebrobasilar artery is the posterior contributor of the circle of Willis, it is important to
understand that any injection performed may have serious consequences (Figure 16-5).
Figure 16-2. Tortuous course of vertebral artery. Extraforaminal in front of transverse process of C7,
passes through vertebral foramen C2-C6, lateral to atlanto-axial and medial to atlanto-occipital joint.
Figure 16-3. Vascular neuroforamina of cervical spine with ascending cervical, deep cervical and
segmental branches, and anterior and posterior radiculomedullary branches.
Figure 16-4. Semidiagram of the spinal, or central, end of a segmental nerve, after removal of the
meninges, showing relationship to vertebral artery.
Figure 16-5. Circle of Willis providing branches to form one anterior spinal artery that supplies anterior
2/3rd of spinal cord, and two posterior-inferior cerebellar arteries to form two posterior spinal arteries
supplying only posterior 1/3rd of spinal cord, hence increased area of ischemia of spinal cord in case of
injury or embolism of anterior spinal artery.
• It is each one of these arteries and veins that is a concern when a transforaminal injection is performed.
• Baker et al7 has shown that without subdigital angiography an injection into an artery can occur with
potential devastating effects.
Recent case reports and literature reviews have questioned the safety of performing cervical
transforaminal epidural steroid injections.6,7 Various theories have been postulated to account for more
severe complications occurring after cervical transforaminal epidural steroid injections, which have been
reported to include cerebellar herniation, and anterior spinal syndrome resulting in paralysis, stroke, and
death.8
Proposed mechanism accounting for anterior spinal artery includes:
• Vasospasm
• Embolism from particulate containing steroids
• Direct needle trauma to a radicular artery that supplies the anterior spinal artery or the posterior spinal
artery.9
Huntoon performed an elegant anatomical study of 10 cadavers that demonstrated the presence of
ascending and deep cervical artery branches in the posterior intervertebral foramen that would be in the
path of the classic approach to cervical transforaminal epidural injections.10
Indications for a selective nerve root block:
• Diagnosis of a specific level of pain from a nerve root suspicious of pathology
• Treatment of pain from a compressed nerve root
• Radiculitis
• Neuropathic pain
• CRPS
• Compartment syndrome
• Lateral cervicalgia
• Occipital neuralgia
• Headaches
• Auricular temporal pain
• Cervical stenosis
• Cervical brachial syndrome
It is of primary importance to perform a detailed history and physical on the patient presenting for a
selective cervical nerve root block. Understanding the correct dermatome of the pain pathway is
important to understand the contributing nerve roots in presenting pain pattern.
• The physical examination should focus on the neurologic aspect of the pain pathway.
• Evaluate for motor strength, sensory deficits, and whether the symptoms correlate with the pain pattern.
• In patients with neurological deficits, must review MRI study before considering the procedure.
• For those who can not have MRI, a CT or CT myelogram would be an alternative examination to
review.
• Reviews of plain x-ray films are helpful in evaluating joint disease, degenerative disc disease,
spondylolisthesis, spondylosis, stenosis, bony lesions, and spine orientation.
• Bone scans are helpful when there is a suspicion of bone disease, cancer, infection, unrecognized
fracture, or benign tumors.
After reviewing the objective data such as an MRI or a CT scan of the anatomical location, create a
differential diagnosis of the suspected pathology. In order to affirm the suspicion, a selective nerve root
block of the level in question can be initiated.
Basic concerns for injection are:
• Immunocompromised patients are potentially at high risk for infection, which is of particular relevance
in patients with malignancy. In this instance, the physician may direct the care to a specialist for further
work up and a treatment plan.
• Patients may have thrombocytopenia secondary to chemotherapy, coagulation disorders, and using
anticoagulants for precautionary conditions such as: stroke prevention, arrhythmia disorders, and
peripheral vascular disease.
• Patients with allodynia who could benefit from this injection may also have pain in the very area of the
injection that could complicate the ability of one to tolerate the procedure.
According to the Washington State Department of Labor and Industries’ review criteria for cervical
surgery for entrapment of a single nerve root (2004), a positive response to SNRB that correlates with
imaging abnormality is needed if there are complaints of radicular pain with no motor, sensory, reflex, or
electromyographic changes. An SNRB may be considered “positive” if it initially produces pain in the
distribution of the nerve root being blocked and produces at least 75% reduction in pain for a duration
consistent with the type of local anesthetic used for the block.13
Contraindications:
• Infection, systemic or localized
• Coagulopathy that cannot be treated or temporarily halted for the injection
• Distorted or complicated anatomy
• Patient refusal
Technique
Either a supine or lateral approach is used for what one would describe as the “classic” approach albeit
there is no “real” classic approach to accessing the epidural space from either a lateral to medial access
versus medial to lateral technique with a catheter. Sedation is a matter of choice from a comfort and safety
point of view.
Transforaminal approach:
• With the neck turned approximately 25 to 30 degrees to the opposite side, the area is prepped with
betadine and alcohol.
• The fluoroscopy is used to identify the bony landmarks in AP view, and check in AP, lateral and
oblique views as needed.
• 2 to 3 cc of 0.5% to 1% lidocaine infiltrated subcutaneously in the area of target nerve root.
• A 25g, 2 inch needle advanced with a trajectory to the posterior aspect of the foramen.
• With direct visualization, one should contact the lamina and carefully enter the foramen and stop.
• The needle position should be checked in an AP view on the fluoroscope to determine that the needle
has not entered beyond the mid line of the pedicle.
• Should a paraesthesia occur, one should retract the needle and inject a nonionic contrast such as
Omnipaque 240 or IsoVue 200M.
Posterior interlaminar approach:
• If the posterior approach is chosen via the interlaminar, then the access route is performed with a
Coude needle from EpiMed (Farmers Branch, TX).
• Enter the epidural space by either a hanging drop technique or a loss of resistance.
• Next step is to place a feather-light catheter into the epidural space and guide the tip to the foramen of
the designated target.
• Once at the level in question is approached, slowly inject the contrast agent of choice and visualize the
enhancement of the nerve root.
• If the injection is of diagnostic value, inject the nerve with 1 cc of the local anesthetic of choice and
observe for distal spread.
• If not sedated, the patient should describe warmth and a feeling of pain alleviation at the dermatome.
• On the other hand, if this is a therapeutic treatment, then the placement of a steroid compound would be
appropriate at this time.
• Again observance of the least amount of medication possible due to the fact that the foramen is
compromised already (Figures 16-6 to 16-8).
Figure 16-6. The anterior approach: both of these utilize entering from a lateral entrance to the medial
aspect of the targeted nerve root.
Figure 16-7. The last approach uses a guided catheter to enter the interlaminar space a thread a guided
catheter to the nerve root targeted.
Figure 16-8. Each of these meets the same objective of accurately placing medications at the targeted
area but safety becomes the issue. As noted earlier with the Dreyfuss picture, a lurking artery may
challenge the operator when injecting a substance such as a local anesthetic or steroid.
The common injectate solutions are:

• Local anesthetics that block the sodium channel, completely halting the electrical impulse conduction in
peripheral nerves, spinal roots, and autonomic ganglia. Lidocaine is the agent of choice with several
concentrations to utilize—0.5%, 1%, 1.5%, and 2%.
• For diagnostic purposes, using a basic concentration of 1% will give a sensory blockade without the
motor impairing effects.
• Ropivacaine may offer similar but longer lasting sensory effects.
• As for corticosteroids, a controversy exists and is yet to be answered—whether one should use a
particulate solution such as Aristocort Triamcinolone or DepoMedrol Methylprednisolone, or a
nonparticulate solution such as decadron dexamethasone.
• For diagnostic purposes only a local anesthetic should be used to confirm pain alleviation of the
affecting nerve root (Table 16-1).
TABLE 16-1. Local Anesthetic Should Be Used to Confirm Pain Alleviation of the
Affecting Nerve Root
CLINICAL PEARLS
• Be aware of false loss of resistance between interspinous ligament and ligamentum flavum.
• Ligamentum flavum is thinnest in cervical region and thickest in lumbar region.
• Use appropriate accessories for proper patient positioning for patient comfort and safety of the
procedure.
• Be careful in elderly patients with osteoarthritis and who has history of atlanto-axial subluxation with
spinal instability.
• Use only nonionic, hydrophilic monomer with low osmolality contrast like iohexol (Omnipaque) and
iopamidol (Isovue).
• Digital subtraction provides electronically enhanced image and requires reduced amount of contrast
and detects intra-arterial contrast spread.
• While advancing the needle with trajectory to posterior aspect of foramen, it is important to impinge
the needle on bone to avoid the disastrous complication of spinal cord injury.
CONCLUSION
Transforaminal selective nerve root blocks have been purported to be more efficacious than the
interlaminar approach.6 The vast majority of literature supporting transforaminal steroid injections is
confined to the lumbar spine due to reports of catastrophic complications occurring in the cervical spine.
Scanlon and colleagues recently reported a survey in which 78 complications were reported with the
transforaminal approach to the cervical epidural steroid injection.7 The most serious complications
included 16 vertebrobasilar brain infarcts, 12 cervical spinal cord infarcts, and two combined
brain/spinal cord infarcts.
Epidural steroid injections are efficacious and safe when performed by physicians who have been
properly trained in the use of fluoroscopy in neuraxial interventions in select patient populations. Studies
that suggest that epidural steroids are not efficacious in patients with cervical radiculopathy and
postlaminectomy syndrome have been primarily based on studies performed by inexperienced physicians,
that did not employ fluoroscopy, and were not double blind. There are no well-designed quality studies to
support abandoning epidural steroid injections in patients with axial cervical pain. Epidural selective
nerve root injections offer clinical relevance when performed at the targeted nerve root and when
diagnostic information is needed and desired to understand where the etiology of the patient’s pain is
derived from. No matter which approach is actually utilized, the term of adherence remains the same
—“vigilance” is of utmost importance.
References
1. Radhakrishnan K, Litchy WJ, O’Fallon WM, Kurland LT. Epidemiology of cervical radiculopathy: a
population-based study of Rochester, Minnesota, 1976-1990. Brain. 1994;117:325-335. doi:
10.1093/brain/117.2.325.
2. Anderberg L, Annertz M, Brandt L, Saveland H. Selective diagnostic cervical nerve root block—
correlation with clinical symptoms and MRI-pathology. Acta Neurochir (Wien). 2004;146(6):559-
565; discussion 565.
3. Sampath P, Bendebba M, Davis JD, Ducker T. Outcome in patients with cervical radiculopathy.
Prospective, multicenter study with independent clinical review. Spine. 1999;24(6):591-597.
4. Heckmann JG, Lang CJG, Zobelein I, et al. Herniated cervical intervertebral discs with radiculopathy:
an outcome study of conservatively or surgically treated patients. J Spinal Disord. 1999;12:396-401.
doi: 10.1097/00002517-199912050-00008.
5. Maigne JY, Deligne L. Computed tomographic follow-up study of 21 cases of nonoperatively treated
cervical intervertebral soft disc herniation. Spine. 1994;19:189-191.
6. Bush K, Chaudhuri R, Hillier S, Penny J. The pathomorphologic changes that accompany the
resolution of cervical radiculopathy: a prospective study with repeat magnetic resonance imaging.
Spine. 1997;22:183-186.
7. Baker R et al injection of radicular artery at C 5-6 during an attempted transforaminal epidural
steroid.
8. Scanlon GC, Moeller-Bertram T, Romanowsky SM, Wallace MS. Think? Spine. 2007;32:1249-1256.
9. Rathmell JP, April C, Bogduk N. Cervical transforaminal injections of steroids. Anesthesiology.
2004;100:1595-1600.
10. Baker R, Dreyfuss P, Mercer S, Bogduk N. Cervical transforaminal injection of a corticosteroids into
a radicular artery: possible mechanism for a spinal cord injury. Pain. 2003;103:211-215.
11. Huntoon MA. Anatomy of the cervical intervertebral foramina: vulnerable arteries and ischemic
neurologic injuries after transforaminal epidural steroid injections. Pain. 2005;117:104-111.
12. Washington State Department of Labor and Industries. Review criteria for cervical surgery for
entrapment of a single nerve root. Olympia, WA: Washington State Department of Labor and
Industries; June 2004. Available at:
http://www.lni.wa.gov/ClaimsIns/Providers/Billing/ProvBulletins/default.asp. Accessed January 31,
2006.
CHAPTER 17
Trigeminal Ganglion and Nerve Block

Miles Day and Kenneth D. Candido
INTRODUCTION
Blockade of the trigeminal ganglion and/or its peripheral branches is a useful technique that can benefit
patients who have refractory facial pain and certain types of headaches that have not responded to
conservative measures. The trigeminal ganglion was first described by the anatomist Johann Gasser and
blockade of the ganglion was first described by Hartel in 1912.
INDICATIONS
Indications for blockade of the ganglion and/or its peripheral branches include:
• Tic douloureux (trigeminal neuralgia)
• Atypical trigeminal neuralgia
• Chronic, intractable cluster headaches1-5
• Persistent idiopathic facial pain
• Herpes zoster
• Palliation of cancer-related pain
RELEVANT ANATOMY
The trigeminal ganglion resides in the middle cranial fossa.6-8 The ganglion is formed by the fusion of a
series of cell bodies that originate at the mid-pontine level of the brainstem. It is situated in a fold of dura
mater that forms an invagination around the posterior two-thirds of the ganglion. This region is referred to
as the Meckel cavity and contains cerebrospinal fluid.
• The ganglion is bound medially by the cavernous sinus and optic and trochlear nerves; superiorly by
the inferior surface of the temporal lobe of the brain; and posteriorly by the brain stem. Access to the
ganglion requires passage of the block needle through foramen ovale.
• The ganglion is situated in the posterior part of the sphenoid bone, posterolateral to foramen rotundum.
• Within foramen ovale lies the mandibular nerve, accessory meningeal artery and the lesser petrosal
nerve.
• The ganglion has three major divisions: ophthalmic (V1), maxillary (V2), and mandibular (V3). The
ophthalmic division is located dorsally, the maxillary branch intermediate, and the mandibular branch
ventrally. This arrangement is important when a thermal rhizotomy is being considered.
• The ophthalmic division leaves the ganglion and passes into the orbit through the superior orbital
fissure. It further divides into the supraorbital, supratrochlear, and nasociliary nerves which innervate
the forehead and the nose.8
• The maxillary division exits the middle cranial fossa via foramen rotundum, crosses the
pterygopalatine fossa, and enters the orbit through the inferior orbital fissure. Branches include the
infraorbital, superior alveolar, palatine, and zygomatic nerves which carry sensory information from
the maxilla and overlying skin, the nasal cavity, palate, nasopharynx and meninges of the anterior and
middle cranial fossa.8
• The mandibular division exits through foramen ovale and divides into the buccal, lingual, inferior
alveolar, and auriculotemporal nerves. These nerves carry sensory input from the buccal region, the
side of the head and scalp, and the lower jaw including teeth, gums, anterior two-thirds of the tongue,
chin, and lower lip.8
• The motor component of V3 innervates the masseter, temporalis, and medial and lateral pterygoids.
• The ganglion interferes with the autonomic nervous system via the ciliary, sphenopalatine, otic, and
submaxillary ganglia. It also communicates with the oculomotor, facial, and glossopharyngeal nerves.
The key to successively block the trigeminal ganglion is to identify the following structures
radiographically:
• Ramus of the mandible
• Foramen ovale
• Sella turcica
• Clivus
• Mastoid air cells
External landmarks that are important include:
• Ipsilateral pupil
• Ipsilateral tragus
Given that blockade of the trigeminal ganglion can be a painful procedure, conscious sedation may be
required. With this in mind, the patient’s overall health status must be maximized prior to the procedure.
• All prescribed medications should be continued unless there is a contraindication.
• The vascular nature of the region necessitates a review of the concomitant use of anticoagulants.
• While guidelines exist for the use of anticoagulants and regional anesthesia,10 there are no guidelines
per se when it comes to pain management procedures.
• While up for debate, our institution holds nonsteroidal anti-inflammatory drugs for 4 days, aspirin
(baby and full dose) for 5 days, Coumadin for 5 days (with a preprocedure INR), clopidogrel (Plavix)
for 7 to 10 days, and ticlopidine (Ticlid) for 10 to 14 days prior to the procedure.
• There is very little information regarding newer anticoagulant drugs such as dabigatran etexilate
(Pradaxa) and rivaroxaban (Xarelto) in relation to pain management procedures.
The benefits and risks of discontinuing an anticoagulant must be entertained and discussed with the
patient prior to the procedure. Permission from the prescribing physician to discontinue the medication
should also be sought and documented. One also needs to question the patient about homeopathic
remedies, especially anything that begins with the letter “G,” eg, ginko, garlic, ginseng, and fish oil, as
these can also affect bleeding status.
CONTRAINDICATIONS
Contraindications are broken down into absolute and relative. While absolute contraindications are
straight forward, relative contraindications require a benefit-risk discussion with the patient. Absolute
contraindications for a trigeminal ganglion block are:
• Increased intracranial pressure
• Patient refusal
• Infection in the region where the block is to be performed
• Inability to stop anticoagulant medication
• Untreated psychopathologies
Relative contraindications include anticoagulant use.
FLUOROSCOPIC VIEWS
• The initial anterior-posterior fluoroscopic image should be with the head in the neutral position with
the nasal septum squared (Figure 17-1). The nasal septum unless deviated should appear as a solid
black line.
• Submental view. The image intensifier should be angled approximately 25 to 30 degrees in the caudal
direction (Figure 17-2). This allows the physician to look up into the base of the skull.
• Oblique view. The image intensifier should be rotated approximately 20 to 30 degrees toward the
intended side to bring the foramen ovale into view (Figure 17-3). The foramen should be close to the
medial side of the mandible at the level of the second molar.
• Lateral view. Sella turcica should be identified just cephalad and posterior to the shadow of the
pterygomaxillary fissure (Figure 17-4).
Figure 17-1. AP of the face. The septum of the nose is squared.
Figure 17-2. A 30-degree submental view.
Figure 17-3. A 20-degree oblique view. The arrow indicates foramen ovale.
Figure 17-4. Lateral view. The white arrow denotes the angle formed by the clivus and the petrous
portion of the temporal bone.
Equipment
• 25-gauge, 1.5-in needle for skin infiltration
• 22-gauge, 3.5-in spinal needle or 22-gauge, 10-cm blunt tipped block needle
• 22-gauge radiofrequency needle with a 2 to 3-mm active tip (for thermal rhizotomy)
• 18-gauge angiocatheter (if using a blunt needle)
• 5-cc syringe for local anesthetic
• 3-cc syringe for contrast
• 3-cc syringe for local anesthetic/steroid mixture
• Extension connector tubing
Medications
• 1% lidocaine (skin infiltration)
• 0.25% bupivacaine or 0.2% ropivacaine (block local anesthetic)
• Omnipaque 240 (nonionic, water-soluble contrast)
• Corticosteroid (for radiofrequency lesioning)
TECHNIQUE
As previously stated, blockade of the trigeminal ganglion can be a painful procedure and conscious
sedation may be necessary. Therefore, monitoring to include heart rate, ECG, blood pressure, and pulse
oximetry is required. Supplemental oxygen should also be provided through a nasal cannula positioned
out of the way of the sterile field.
• Place the patient on the bed supine with the head in a neutral position. A radiolucent head cradle can
also be used to keep the head in a stable position.
• Prep and drape the block side sterilely, keeping the ipsilateral eye exposed.
• Obtain a PA view and adjust the C-arm to square the nasal septum.
• Tilt the image intensifier approximately 25 to 30 degrees in the caudal direction.
• Oblique the image intensifier 20 to 30 degrees ipsilaterally.
• Make subtle adjustments to identify foramen ovale which should be just medial to the ramus of the
mandible (Figure 17-5).
• Mark the skin entry site which is approximately 2 cm lateral to the corner of the mouth.
• Anesthetize the skin and insert the block needle. Advance in a coaxial fashion using intermittent
fluoroscopic images (Figure 17-6). If utilizing external landmarks, aim toward the midline, ipsilateral
pupil and just anterior to the tragus of the ear. If using the blunt needle, the angiocatheter should be
inserted first.
• Once the needle is engaged in the soft tissue of the cheek, obtain a lateral image to check the depth and
direction of the needle. Aim toward the angle produced by the clivus and the petrous portion of the
temporal bone (Figure 17-4).
• Check an oblique image to ensure the needle is advancing toward foramen ovale.
• Return to the lateral view and advance the needle through foramen ovale (Figure 17-7). With a blunt
needle, slight force may be required to advance the tip through foramen ovale. Be careful not to
advance the needle tip past the clivus as the tip could enter brain matter. If using a sharp needle,
cerebrospinal fluid (CSF) may be encountered if the tip of the needle passes through the dura covering
the ganglion. In the first author’s experience, this has not occurred with the use of a blunt-tipped
needle.
• Remove the stylet and aspirate. If blood is aspirated, reposition the needle tip and repeat the
aspiration. If blood is encountered again, reposition the needle tip. If blood is once again encountered,
abort the procedure. Aspiration of CSF also requires repositioning of the needle tip. CSF will not
interfere with a thermal rhizotomy, but it could lead to side effects and complications if a chemical
rhizotomy is planned. If cerebrospinal fluid is obtained, the needle tip can be withdrawn until fluid is
no longer appreciated. If an abundant cerebrospinal fluid leak is present, the remainder of the
procedure should be halted. With a significant leak, a high spinal block can be caused with even low
volumes of local anesthetic. A small leak of cerebrospinal fluid may or may not cause a high spinal and
if present, the pain practitioner should proceed with caution.
• After negative aspiration for blood and CSF, slowly inject a small amount (no more than 0.5-1.0 cc) of
nonionic, water-soluble contrast to confirm position and filling of the Meckel cavity. Any vascular
runoff requires repositioning of the needle.
• Slowly inject local anesthetic in volumes of 0.25-0.5 cc at a time, up to 1-2 cc, and observe for effect.
Remove the needle.
Figure 17-5. Submental oblique. Foramen ovale is just cephalad to the black arrow.
Figure 17-6. A 22-gauge curved, blunt block needle slightly posterior to foramen ovale.
Figure 17-7. Final position of the needle on the lateral view. The white arrow indicates the tip of the
needle.
THERMAL RHIZOTOMY
Needle placement is the same as with a local anesthetic block with a few differences. In place of the
block needle, a radiofrequency needle of the same caliber with a 2- to 3-mm active tip is used. Sensory
and motor stimulations are required to properly position the needle tip. This requires the patient to be
able to respond to questions, so the level of sedation needs to be monitored closely.
• After the needle has entered foramen ovale, perform motor stimulation at 2 Hz, up to 2 V. Mandible
contraction should be observed secondary to stimulation of the mandibular division. Next, perform
sensory stimulation at 50 Hz, up to 1 V. The goal is to position the needle tip on the portion of the
ganglion that will elicit a paresthesia in the desired division.
• Once the needle tip is positioned, and after negative aspiration of blood and CSF, inject local
anesthetic and wait approximately 1 minute. The first author also mixes a small amount of
corticosteroid (2 mg dexamethasone) with the local anesthetic.
• Commence lesioning at 70°C for 1 minute. Repeat stimulation and observe if the paresthesia in the
intended division has diminished. Based on the repeat stimulation, a second lesion may be necessary.
• If lesioning of more than one division is required, the needle tip will have to be repositioned to create
a larger lesion. Begin with lesioning of the portion of the ganglion of the more distal division, and
withdraw the needle tip to the more proximal portion, eg, lesion the portion of the ganglion
corresponding to the maxillary division before the mandibular division.
• Lesioning of the ophthalmic division requires special consideration as this division innervates the
cornea. Perform lesioning at 60°C. Check the corneal reflex intermittently during lesioning. If the reflex
diminishes, stop the lesioning.
CHEMICAL RHIZOTOMY
Glycerol and phenol in glycerin can also be used to achieve long-term analgesia.
• Once through the foramen ovale, advance the needle until cerebrospinal fluid is observed returning
through the needle.
• Place the patient in a semisitting position with the neck flexed. Inject water-soluble, nonionic contrast
solution in 0.1 mL aliquots (up to 0.5 mL) into the trigeminal cistern.11 Failure of visualization or
diffusion of the contrast requires repositioning the needle.
• Once the cistern is visualized, draw back the contrast material by free flow. The flow of contrast is
slower than cerebrospinal fluid.
• Inject the same amount of glycerol into the cistern.
• Flush the needle with 0.5 mL of saline prior to removal.
• Keep the patient in a semisitting position for 2 hours. During the procedure, patients often report pain,
burning, or paresthesia in the affected division(s).16
PULSED RADIOFREQUENCY
The use of nonthermal radiofrequency, ie, pulsed radiofrequency, can also be performed.
• After proper positioning of the needle tip, perform 2 to 3 pulsed radiofrequency cycles for 120 seconds
each at 45 V. The temperature of the needle tip rarely exceeds 42°C, thus local anesthetic is not
required.
• If significant masseter contraction is noted during pulsing, inject 1 to 2 mL of local anesthetic to
diminish this, or hold the patient’s mouth closed with your hand while the cycles are completed.
POSTPROCEDURE
Monitor the patient for at least 1 hour. In the case of a chemical rhizotomy, observe for 2 hours. Vitals
signs including blood pressure, heart rate, and oxygen saturation should be recorded. An ice pack over the
injection site can be helpful to decrease swelling and pain. Once awake, assess the patient’s pain level
and degree of hypoesthesia in the trigeminal division blocked or lesioned.
COMPLICATIONS
The location of the trigeminal ganglion and adjacent structures is important in understanding the potential
complications of this procedure. Also, prior to rhizotomy the difference between a side effect and a
complication must be thoroughly explained to the patient. Sensory loss in the division lesioned is
expected and is not considered a complication. It can be as high as 98% with thermal rhizotomy compared
to 60% seen with chemical rhizotomy.12 Thermal rhizotomy (TR) had a higher rate of complications at
29.2% compared to chemical rhizotomy (CR) at 24.8%.13 Potential complications include, but are not
limited to:
• Bleeding
• Retrobulbar hematoma
• Local infection
• Meningitis
• High spinal
• Adjacent cranial nerve palsies (usually transient)
• Corneal anesthesia (TR > CR),14 keratitis, ulceration, and hypesthesia
• Masseter weakness (TR >>> CR)14 when lesioning the mandibular division
• Anesthesia dolorosa up to 4% (TR > CR)14
TRIGEMINAL NERVE DIVISION BLOCKS

Ophthalmic Nerve Blocks
The ophthalmic division can only be blocked at 2 of its peripheral branches which are the supraorbital
and supratrochlear nerves. The usual indications are trigeminal neuralgia and post-herpetic neuralgia
although it has been used for intractable frontal headaches. Preoperative considerations and
contraindications are essentially the same as for the trigeminal ganglion block. Sedation is not typically
required. Complications include bleeding, hematoma, infection, and nerve injury.
For the supraorbital nerve:
• Palpate the supraorbital notch/foramen which is located on the mid superior orbital ridge.
• After sterile prep, insert a short 25- or 22-gauge needle perpendicular to the skin and advance until
bone is touched. Avoid advancing the needle into the foramen.
• Withdraw the needle slightly and after negative aspiration for blood, inject 1 to 2 cc of local
anesthetic.
For the supratrochlear nerve:
• Palpate the supratrochlear notch/foramen which is located on the medial aspect of the superior orbital
ridge in line with the medial canthus.
anesthetic.
Maxillary Nerve Block

Blockade of the maxillary nerve can be accomplished by blocking it in the pterygopalatine fossa or by
blocking one of its peripheral branches, the infraorbital nerve. Preoperative considerations and
contraindications are essentially the same as for the trigeminal ganglion block. Indications are trigeminal
neuralgia of the maxillary division, and idiopathic or secondary maxillary neuralgia. Complications are
the same as for the trigeminal ganglion block except for the ophthalmic complications and high spinal. An
infraorbital nerve block does not usually require sedation, but for the maxillary nerve block in the
pterygopalatine fossa, follow the trigeminal ganglion block protocol.
Infraorbital nerve block:
• Palpate the infraorbital notch/foramen which is located on the mid inferior orbital ridge.
anesthetic.
Maxillary nerve block:
• Place the patient in the supine position with the head in a neutral position.
• Obtain a lateral fluoroscopic image to identify the coronoid notch. It can also be identified by asking
the patient to open and close their mouths, and with palpation anterior and inferior to the external
auditory meatus.
• Once the landmarks are identified, anesthetize the skin and advance a 22-gauge, 3.5-in spinal needle or
blunt tipped block needle (will first require insertion of an 18-gauge angiocatheter) perpendicular to
the skin of the side of the face, just below the zygomatic arch directly in the center of the coronoid arch.
• Once the lateral pterygoid plate is contacted (at about 4-5 cm from the skin), redirect the needle
cephalad, anterior and medial toward the cephalad portion of the pterygopalatine fossa. Intermittent,
lateral fluoroscopic images will facilitate proper placement of the needle.
• Obtain an AP fluoroscopic image to check the depth of the needle. The tip should be cephalad to the
middle turbinate and adjacent to the palatine bone. Sometimes a paresthesia is elicited and should be
felt in the upper teeth.
• After negative aspiration for blood, inject 3 cc of local anesthetic. For a neurolytic block, 1 to 1.5 cc
of 6% phenol in iohexol can be injected.
• A thermal rhizotomy is not recommended, but pulsed radiofrequency can be performed. Once a 10-cm
radiofrequency needle with a 5-mm active tip is in position, perform sensory stimulation at 50 Hz, up
to 1 V. Stimulation at less than 0.5 V is desirable. The patient should experience a paresthesia in the
upper teeth. Inject 1 cc of local anesthetic and perform 2 to 3 pulsed radiofrequency cycles for 120
seconds each at 45 V.
Mandibular Nerve Block

Blockade of the mandibular nerve can be accomplished by following the coronoid approach to the
maxillary nerve protocol, but redirecting the needle posteriorly when the lateral pterygoid plate is
touched. Preoperative considerations and contraindications are essentially the same as for the trigeminal
ganglion block. Indications are trigeminal neuralgia of the mandibular division, and idiopathic or
secondary mandibular neuralgia. Complications are the same as for the trigeminal ganglion block except
for the ophthalmic complications and high spinal. Weakness of the muscle of mastication can occur after a
neurolytic procedure and this should be thoroughly discussed. Follow the trigeminal ganglion block
protocol with regards to sedation.
• Place the patient in the supine position with the head in a neutral position.
• Obtain a lateral fluoroscopic image to identify the coronoid notch.
• Once the landmarks are identified, anesthetize the skin and advance a 22-gauge, 3.5-in spinal needle or
blunt-tipped block needle (will first require insertion of an 18-gauge angiocatheter) perpendicular to
the skin of the side of the face, just below the zygomatic arch directly in the center of the coronoid arch.
• Once the lateral pterygoid plate is contacted (at about 4-5 cm from the skin), obtain an AP fluoroscopic
image to confirm location.
• Redirect the needle posteriorly and inferiorly no more than 1 cm. A paresthesia is usually elicited in
the lower jaw and lip, ear, and ipsilateral tongue.
• After negative aspiration for blood, inject 3 cc of local anesthetic. For a neurolytic block, 1 to 1.5 cc
of 6% phenol in iohexol can be injected.
• A thermal rhizotomy is not recommended, but pulsed radiofrequency can be performed. Once a 10-cm
radiofrequency needle with a 5-mm active tip is in position, perform sensory stimulation at 50 Hz, up
to 1 V. Stimulation at less than 0.5 V is desirable and should be felt in the lower jaw and lip, ear, and
ipsilateral tongue. Inject 1 cc of local anesthetic and perform 2 to 3 pulsed radiofrequency cycles for
120 seconds each at 45 V.
CLINICAL PEARLS
• Detailed knowledge of the anatomy of the head and neck is imperative. This will increase the success
of the block while theoretically decreasing the potential for complications.
• Always perform a diagnostic block first before proceeding to a rhizotomy. On occasion, a diagnostic
block can have therapeutic benefit.
• Thoroughly explain the difference between an expected side effect and a complication before
performing a rhizotomy.
References
1. Ekbom K, Lindgren L, Nilsson B, Hardebo J, Waldenlind E. Retro-gasserian glycerol injection in the
treatment of chronic cluster headache. Cephalgia. 1987;21-27.
2. Mathew N, Hurt W. Percutaneous trigeminal gangliorhizolysis in intractable cluster headaches.
Headache. 1988;328-331.
3. Hassenbusch S, Kunkel R, Kosmorsky G, Covington E, Pillay P. Trigeminal cistern injection of
glycerol for treatment of chronic intractable cluster headaches. Neurosurgery. 1991;504-508.
4. Taha J, Tew J. Long-term results of radiofrequency rhizotomy in the treatment of cluster headache.
Headache. 1995;193-196.
5. Pieper D, Dickerson J, Hassenbusch S. Percutaneous retrogasserian glycerol rhizolysis for treatment
of chronic intractable cluster headaches: long-term results. Neurosurgery. 2000;363-368.
6. Murphy T. Somatic blockade of the head and neck. In: Cousins P, Bridenbaugh P, eds. Clinical
Anesthesia and Management of Pain. Philadelphia, PA: Lippencott-Raven; 2000:489-514.
7. Romanoff M. Somatic nerve blocks of the head and neck. In: Raj P, ed. Practical Management of
Pain. St. Louis, MO: Mosby; 1996:177-184.
8. Wilson-Pauwels L, Akesson E, Stewart P. Cranial Nerves. 1st ed. Philadelphia, PA: BC Decker Inc;
1988.
9. Ruiz-Lopez R, Erdine S. Treatment of cranio-facial pain with radiofrequency procedures. Pain
Practice. 2002;206-213.
10. Horlocker T, Wedel D, Benzon H, et al. Regional anesthesia in the anticoagulated patient: defining the
risks. Reg Anesth Pain Med. 2004;29:1-11.
11. Raj P, Erdine S. Pain Relieving Procedures: The Illustrated Guide. 1st ed. West Sussex, UK: Wiley-
Blackwell; 2012.
12. Taha J, Tew J Jr. Comparison of surgical treatments for trigeminal neuralgia: reevaluation of
radiofrequency rhizotomy. Neurosurg. 1996;865-871.
13. Lopez BC, Hamlyn PJ, Zakrzewska JM, et al. Systematic review of ablative neurosurgical techniques
for the treatment of trigeminal neuralgia. Neurosurg. 2004;973-983.
14. Raj P, Lou L, Erdine S, Staats P, Waldman S. Radiographical Imaging for Regional Anesthesia and
Pain Management. 1st ed. Philadelphia, PA: Churchill-Livingston; 2003.
CHAPTER 18
Sphenopalatine Ganglion Block

Samer Narouze
INDICATIONS
The sphenopalatine ganglion (SPG) is a large extracranial structure that has rich sympathetic and
parasympathetic autonomic innervations, which explains the autonomic features associated with cluster
headache. Cluster headache involves activation of the parasympathetic outflow from the superior salivary
nucleus of the facial nerve, predominantly through the SPG.1
• SPG block and radiofrequency ablation (RFA) are indicated in the management of intractable
medically resistant cluster headaches, migraine, and other trigeminal autonomic cephalalgias.
• Intractable orofacial pain syndromes (eg, persistent idiopathic facial pain, “atypical facial pain”).
SPHENOPALATINE GANGLION NEUROANATOMY

The SPG has rich parasympathetic (preganglionic axons and postganglionic cell bodies and axons) and
sympathetic (postganglionic axons) components. The parasympathetic preganglionic cell bodies
projecting to the SPG originate in the superior salivatory nucleus (SSN) of the facial nerve in the pons.
The efferent fibers of the SSN travel in the nervus intermedius and divide at the geniculate ganglion to
become the greater petrosal nerve and chorda tympani nerve. The first-order parasympathetic neurons in
the greater petrosal nerve are joined by the postganglionic sympathetic fibers from the deep petrosal
nerve, forming the nerve to the pterygoid canal (vidian nerve). The preganglionic parasympathetic
neurons then synapse with the second-order parasympathetic neuronal cell bodies located in the SPG.
The postganglionic parasympathetic fibers then run with branches of the maxillary nerve (V2) to reach
their targets. Therefore, the only cell bodies located within the SPG are those of the second-order
postganglionic parasympathetic neurons, which may explain the clinical observation that patients after
radiofrequency ablation (RFA) of the SPG usually notice improvement of the autonomic parasympathetic
symptoms either earlier or even without improvement of the headache pain.
The sympathetic cell bodies projecting to the SPG originate in the upper thoracic spinal cord (T1-T2).
The preganglionic sympathetic neurons then synapse in the cervical sympathetic ganglia, mainly the
superior cervical ganglion. The postganglionic second-order sympathetic neurons form the carotid
sympathetic plexus and reach the pterygoid canal through the deep petrosal nerve where it joins the first-
order parasympathetic neurons in the greater petrosal nerve, forming the nerve to the pterygoid canal
(vidian nerve). Postganglionic sympathetic fibers pass through the SPG without synapsing and innervate
mainly the blood vessels.
SPHENOPALATINE GANGLION ANATOMY
The SPG is located in the pterygopalatine fossa (PPF), which is a small, upside-down pyramidal space 2
cm high and 1 cm wide.
• The pterygopalatine fossa is located behind the posterior wall of the maxillary sinus and is bordered
posteriorly by the medial plate of the pterygoid process, superiorly by the sphenoid sinus, medially by
the perpendicular plate of the palatine bone, and laterally it communicates with the infratemporal fossa.
• Superolaterally lies the foramen rotundum with the exiting maxillary nerve, and inferomedially there is
the vidian nerve (greater petrosal and deep petrosal nerves) within the pterygoid canal (Table 18-1).
• The pterygopalatine fossa contains the internal maxillary artery and its branches, the maxillary nerve,
and the SPG and its afferent and efferent branches.
• The SPG is located posterior to the middle turbinate and is few millimeters deep to the lateral nasal
mucosa.
• It is suspended from the maxillary nerve by the pterygopalatine nerves, inferiorly it is connected to the
greater and lesser palatine nerves, and posteriorly it is connected to the vidian nerve.
• Efferent branches of the SPG form the posterior lateral nasal and pharyngeal nerves.2,3
TABLE 18-1. The Pterygopalatine Fossa Foramina and Connections

The key to successfully locating the pterygopalatine fossa lies in identifying its boundaries:
• Anterior. Superomedial part of the infratemporal surface of maxilla.
• Posterior. Root of the pterygoid process and adjoining anterior surface of the greater wing of sphenoid
bone.
• Medial. Perpendicular plate of the palatine bone and its orbital sphenoidal processes.
• Lateral. Pterygomaxillary fissure.
• Superior. Sphenoid sinus.
• Inferior. Part of the floor is formed by the pyramidal process of the palatine bone.
The key to successfully locating the pterygopalatine fossa by lateral x-ray view lies in identifying the
following structures:
• Maxilla anteriorly
• Lateral pterygoid plate posteriorly
• Coronoid notch of the mandible (for the transcoronoid needle approach)

As with any intervention, one must weigh the potential benefits to the potential risks. Given the relatively
invasive nature of the procedure, sphenopalatine ganglion blockade/neurolysis should be considered only
in intractable, medically resistant cluster/migraine headache and neuropathic face pain disorders.
• Immunocompromised patients are potentially at high risk for infection; this is of particular relevance in
patient with facial malignancy.
• Infection, systemic or localized.
• Coagulopathy and thrombocytopenia.
• Distorted or complicated anatomy.
• Patient refusal.
• Informed consent and proper explanation of all potential complications.
• Anticoagulation. It is essential to review the patient’s medications and obtain international normalized
ratio/prothrombin time and platelet counts when appropriate as there is a possibility of injury to the
maxillary artery or branches.
• Physical examination of the area for infection.
• Intravenous access for IV fluid and medications for sedation or to manage complications should any
arise.
• Evaluation for contrast allergy. This is important as the utilization of contrast will allow for precise
needle placement in the PPF and to role out intravascular injections.
Fluoroscopic Views
• Lateral view. This is most important view in identifying the PPF. This view should be the starting view
to identify the maxilla, lateral pterygoid plate and the coronoid notch. A slight tilt will allow for proper
overlapping of the pterygoid plates for proper visualization of the fossa (Figures 18-1 and 18-2).
• Anterior-posterior (AP) view. Once the needle is placed in the proper direction with the lateral
fluoroscopy, the physician should immediately shift to the AP view as it allows to control the depth of
the needle tip as it advances toward the lateral nasal wall (Figure 18-3).
Figure 18-1. Lateral x-ray showing SPG block with the anterior approach. Please note that the x-ray
cursor is overlying the coronoid notch. (Reproduced with permission from Ohio Pain and Headache
Institute.)
Figure 18-2. Lateral x-ray showing SPG block with the coronoid approach. (Reproduced with
permission from Ohio Pain and Headache Institute.)
Figure 18-3. AP x-ray view showing the needle tip just lateral to the nasal wall. The contrast agent is
delineating the PPF. (Reproduced with permission from Ohio Pain and Headache Institute.)
Equipment
• Pointer and skin marker
• 25-gauge 1.5-in needle (local needle)
• 22-gauge 3.5-in blunt Tuohy needle (block needle)
• 3- or 5-cc syringe for local anaesthetic
• 1- or 3-cc syringe for contrast
• 3- or 5-cc syringe for medications
• Exrension tubing
Medications
• 5-mL 1% lidocaine
• 3-mL 0.25% or 0.5% bupivacaine
• 1-mL Iohexol 180 (nonionic water-soluble contrast)
• Triamcinolone (preferred as it is nonparticulate) or methylprednisolone
APPROACHES TO THE SPHENOPALATINE GANGLION
Transnasal Approach
As the SPG is located couple of millimeters deep to the lateral nasal mucosa, topical application of local
anesthetic solution to the posterior wall of the nasopharynx in the region of the middle turbinate can
diffuse across the nasal mucosa to block the SPG.
Transnasal blockade of the SPG was first reported using topical cocaine4; currently lidocaine 4% is
usually used.
• The patient is placed in the supine position with the neck extended into a sniffing position.
• 10-cm cotton tipped applicator soaked with 4% lidocaine is slowly advanced along the superior
border of the middle turbinate until it reaches the posterior wall of the nasopharynx.
• The applicator is usually left in place for approximately 20 to 30 minutes to allow the local anesthetic
to diffuse across the mucosa and reach the SPG.
Transnasal Endoscopic Approach
This endoscopic technique for transnasal injection and blockade of the SPG was first described by
Prasanna in 1993.5 This technique allows a needle to be inserted transnasally under vision through the
sphenopalatine foramen into the PPF.
Transoral Approach
The pteygopalatine fossa can also be accessed transorally by placing a 27-gauge needle inside the greater
palatine foramen. This approach is usually utilized by dentists to block the palatine nerves.6
Infrazygomatic Approach
Neuroablation techniques are only feasible with this infrazygomatic approach. Needle placement is
usually guided by fluoroscopy; however, CT guidance is reported as well.7
The infrazygomatic approach could be either anterior to the mandible or through the coronoid notch of
the mandible.
Anterior approach. The needle entry is inferior to the zygomatic arch, just anterior to the mandible,
between the mandibular ramus and the posterior border of the zygomatic bone. We prefer this approach
as the needle can be advanced in a target view toward the PPF without the need to walk the needle off
the lateral pteygoid plate (which is usually very painful) (Figure 18-1). Also it is much easier to steer
the needle (cephalad-caudad or anterior-posterior) within the fossa to selectively target different
structures within the fossa. However, this approach is not feasible in all patients as there might not be
enough room between the mandible and the zygoma to insert the needle.8
Coronoid approach. The needle entry is through the coronoid notch of the mandible. The needle is
usually advanced to target the lateral pterygoid plate first and then walked off the bone interiorly to
enter the PPF. By that time, the needle usually acquired certain direction and it is hard to manipulate the
needle once it is inside the fossa (Figure 18-2).
Technique of SPG Block (Infrazygomatic Approach)
• With the patient in the supine position and the head inside the C-arm, a lateral view is obtained and
either the C-arm or the head of the patient is rotated until both pterygoid plates are superimposed on
each other to better visualize the pterygopalatine fossa.
• The skin entry site overlying the fossa is marked just inferior to the zygomatic arch either anterior to the
mandible (anterior approach, my preferred approach) or through the coronoid notch (transcoronoid
approach).
• A 22-gauge, 3.5-in blunt needle with a slight bend at the tip is used.
• The needle is first introduced in the lateral view and advanced medially and superiorly toward the
pterygopalatine fossa using real-time fluoroscopy.
• Once in a proper direction, an anteroposterior view is obtained, and the tip of the needle is advanced
to be just lateral to the nasal wall (Figure 18-3).
• If the lateral pterygoid plate is encountered, the needle should be walked off the bone anteriorly and
cephalad to slip into the fossa (the curved tip will help to guide the needle).
• 0.1 to 0.2 mL of contrast agent is injected under real-time fluoroscopy to rule out intravascular spread
as the PPF contains the maxillary artery and its branches (mainly the sphenopalatine artery).
• After negative aspiration of blood or air (the needle tip is too advanced into the nasal cavity or the
maxillary sinus), 1 to 2 L of 0.5% bupivacaine with or without steroids is injected slowly.
POSTPROCEDURE FOLLOW-UPS
The patient should be monitored in the recovery room for 40 to 60 minutes for any signs of bleeding or
unexpected neurologic symptoms/signs. Patient should be advised to call pain service for any procedure-
related complications and/or any unexpected neurologic deficit. Patient should be monitored closely for
the following:
• Bleeding, epistaxis
• Facial numbness or weakness
• Double vision
• Fever
• Exacerbation of symptoms
• Headache side shifts
Radiofrequency Ablation Technique
• With the patient in the supine position and the head inside the C-arm, a lateral view is obtained and
either the C-arm or the head of the patient is rotated until both pterygoid plates are superimposed on
each other to better visualize the pterygopalatine fossa.
• The skin entry site overlying the fossa is marked just inferior to the zygomatic arch either anterior to the
mandible or through the coronoid notch.
• A 22-gauge, 10-cm, blunt RFA needle with a 2-mm or 5-mm active tip with a slight bend at the tip is
used (Figure 18-4). The needle is first introduced in the lateral view and advanced medially and
superiorly toward the pterygopalatine fossa using real-time fluoroscopy.
• Once in a proper direction, an anteroposterior view is obtained, and the tip of the needle is advanced
to be just lateral to the nasal wall.
• If the lateral pterygoid plate is encountered, the needle should be walked off the bone anteriorly and
cephalad to slip into the fossa (the curved tip will help to guide the needle).
• Sensory stimulation is obtained with 50 Hz to look for deep paresthesias behind the root of the nose at
>0.5 V (Table 18-2).
• Once proper stimulation is achieved and prior to lesioning, 0.1 to 0.2 mL of contrast agent is injected
under real-time fluoroscopy to rule out intravascular spread.
• Then, 0.5 mL of lidocaine 2% is injected and two radiofrequency lesions are carried out at 80°C for 60
seconds each.
• After lesioning, 0.5 mL of bupivacaine 0.5% and 5 mg of triamcinolone are injected with the aim to
prevent postprocedure neuritis.9
Figure 18-4. Lateral x-ray view showing the RFA needle inside the PPF. Note that the tip is curved
downward to avoid lesioning of the naxillary nerve which runs at the roof of the PPF. (Reproduced with
TABLE 18-2. Possible Scenarios of Stimulation before Attempting Radiofrequency

Thermocoagulation of the Sphenopalatine Ganglion
A thorough understanding of the anatomy allows the clinician to predict correct needle placement
during RFA according to the result of the stimulation and hence can reduce the incidence of complications
(Table 18-2).10
Efficacy of Sphenopalatine Ganglion Radiofrequency Ablation
In a retrospective analysis of patients with refractory cluster headache treated by radiofrequency lesion of
the sphenopalatine ganglion, 56 patients with episodic cluster headache and 10 patients with chronic
cluster headache were followed over a period of 12 to 70 months.2 In the episodic cluster headache
group, 60.7% experienced complete pain relief, whereas only 3 of 10 patients with chronic cluster
headache had the same result. The above report showed that RFA of the PPG may improve episodic
cluster headache but not chronic cluster headache. Recently, however, Narouze and colleagues9 reported
favorable outcome after intractable chronic cluster headache as well. They reported significant
improvement in both mean attack intensity and mean attack frequency for up to 18 months in 15 patients.
Of these patients, 20% (3 out of 15 patients) reported no change or increase in the headache intensity
and/or frequency during the first few postprocedure weeks before noticing improvements in their
headache pattern. However, 46.7% of the patients (7 out of 15 patients) reported change in the headache
pattern with return to the episodic form of cluster headache at a mean follow-up period of 18 months.
Three patients remained headache-free and off medications for the duration of the follow-up (18-24
months).
Two patients reported complete relief of their usual unilateral headache symptoms, and instead they
developed episodic cluster headache on the contralateral side.9
COMPLICATIONS OF SPG BLOCK AND NEUROLYSIS

• Epistaxis is more common after intranasal topical application of local anesthetic; however, it can occur
with the infrazygomatic approach if the needle is advanced too far medially through the lateral nasal
wall.10
• Intravascular injection and hematoma formation can occur after maxillary artery or branches injury,
which are located within the pterygopalatine fossa (Figure 18-5). Cheek hematoma is the most common
complication.
• Infection is always a possibility especially if the oral or nasal mucosa was accidentally penetrated.10
• Reflex bradycardia was reported during radiofrequency lesioning, which could be explained by the
rich parasympathetic connections to the SPG.11
• Radiofrequency lesioning of the SPG can result in permanent or, more commonly, temporary
hypoesthesia or dysesthesia in the palate, maxilla, or posterior pharynx.2,3,9 Pulsed radiofrequency
would seem to be safer; however, there is limited data for its efficacy.12
• Dryness of the eye as a result of interruption of the parasympathetic supply is also common; however, it
is usually only temporary.
• Temporary diplopia, which is more common after local anesthetic injections rather than RFA, can be
explained by the spread of the injectate from the pterygopalatine fossa to the inferior orbital fissure
containing the abducent nerve.13 This is the reason why we limit the injectate volume to only 1 to 2 mL
(Figure 18-6).
Figure 18-5. SPG block with the anterior approach showing intravascular spread. (Reproduced with
Figure 18-6. SPG block with the coronoid approach. The contrast is spreading into the inferior orbital
fissure (arrow). (Reproduced with permission from Ohio Pain and Headache Institute.)
References
1. Goadsby P. Pathophysiology of cluster headache: a trigeminal autonomic cephalgia. Lancet Neurol.
2002;1:251-257.
2. Salar G, Ori C, Iob I, Fiore D. Percutaneous thermocoagulation for sphenopalatine ganglion neuralgia.
Acta Neurochir (Wien). 1987;84:24-28.
3. Sanders M, Zuurmond W. Efficacy of sphenopalatine ganglion blockade in 66 patients suffering from
cluster headaches: a 12- to 17-month follow-up evaluation. J Neurosurg. 1997;87:876-880.
4. Sluder G. The role of the sphenopalatine ganglion in nasal headache. NY State J Med. 1908;27:8-13.
5. Prasanna A, Murthy PS. Sphenopalatine ganglion block under vision using rigid nasal sinuscope. Reg
Anesth. 1993;18:139-140.
6. Ruskin SL. Techniques of sphenopalatine therapy. Eye Ear Nose Throat Mon. 1951;30:28-31.
7. Vallejo R, Benyamin R, Yousuf N, Kramer J. Computed tomography-enhanced sphenopalatine
ganglion blockade. Pain Pract. 2007;7(1):44-46.
8. Narouze S. Head and neck blocks. In: Huntoon M, Benzon H, Narouze S, eds. Spinal Injections and
Peripheral Nerve Blocks. In: Deer T (series editor). Interventional and Neuromodulatory
Techniques for Pain Management. 1st ed. Elsevier; 2011.
9. Narouze S, Kapural L, Casanova J, Mekhail N. Sphenopalatine ganglion radiofrequency ablation for
the management of chronic cluster headache. Headache. 2009;49:571-577.
10. Narouze S. Complications of head and neck procedures. Tech Reg Anesth Pain Manag. 2007;11:171-
177.
11. Konen A. Unexpected effects due to radiofrequency thermocoagulation of the sphenopalatine ganglion:
two case reports. Pain Digest. 2000;10:30-33.
12. Bayer E, Racz GB, Miles D, Heavner J. Sphenopalatine ganglion pulsed radiofrequency treatment in
30 patients suffering from chronic face and head pain. Pain Pract. 2005;5:223-227.
13. Narouze SN. Role of sphenopalatine ganglion neuroablation in the management of cluster headache.
Curr Pain Headache Rep. 2010;14:160-163.
CHAPTER 19
Occipital Nerve Blocks

Andrea Trescot and Lawrence Kamhi
INTRODUCTION
Beruto and Ramus first described occipital neuralgia in 1821.1 In the beginning of the 1900’s, Luff2 as
well as Osler and McRae3 emphasized occipital neuralgia as a cause of occipital pain and headaches.
Most patients with primary headache syndromes who have frequent attacks of pain have tenderness in the
suboccipital region.4 Neural blockade of the greater, lesser, and third occipital nerves are interventions
employed in the diagnosis and treatment of upper neck pain and headache believed to be caused by
pathology in the superior cervical spine. In the clinical setting, neck pain and headache are common
complaints, so, when evaluating such patients, the clinician will be well served by eliciting as precise a
history as possible and seeking any past cervical spine or head trauma.
INDICATIONS
The medical terms occipital neuralgia and cervicogenic headache describe a syndrome of neck and
head pain primarily referred to the occiput, as well as in the temporal area, forehead and retrobulbar
areas, that may arise some distance away, in the upper cervical spine. This occurs because the first three
cervical spinal nerve segments (C1-C3) that make up the occipital nerves share a relay-station in the
brainstem that continues into the upper cervical spinal cord with the trigeminal cell bodies (the cervico-
trigeminal nucleus), and the pain of occipital neuralgia and cervicogenic headaches is referred to
structures innervated by the branches of the trigeminal nerve, namely, the forehead, temples, and eyes
(Figure 19-1). Neuralgia of C2 (occipital neuralgia) is typically described as a deep or dull pain that
usually radiates from the occipital to parietal, temporal, frontal, and periorbital regions. A paroxysmal
sharp or shock-like pain is often superimposed over the constant pain. Ipsilateral eye lacrimation and
conjunctival injection are common associated signs.5
Figure 19-1. Cervico-trigeminal nucleus. (Used with permission from Dr. David Schultz.)
Indications for occipital nerve blocks therefore include:

• Neck pain felt in the upper back of the neck, potentially referring to the occiput, temporal, forehead and
retrobulbar regions of the head.
• A history of whiplash injury or similar trauma.
• The presence of a migraine-like headache syndrome not responding to pharmacologic treatment alone.
CONTRAINDICATIONS
• Infection of the scalp.
• Coagulopathy.
• Cervical instability or acute fracture.
• Arnold-Chiari syndrome.
• Inability to lie in the prone or sitting position.
• Inability to provide informed consent.
RELEVANT ANATOMY
The suboccipital nerve (the dorsal ramus of C1) innervates the atlanto-occipital (AO) joint (C0-1), and
thus can refer pain to the back of the head, mistakenly attributed to the occipital nerve. The C2 dorsal root
ganglion and nerve root innervate the capsule of the atlanto-axial (AA) joint (C1-2) as well as the C2-3
facet, so that trauma to these joints will also refer to the occiput.
• The greater occipital nerve (GON) receives fibers from the dorsal primary rami of the second and
third cervical nerve roots.
• The lesser occipital nerve (LON), however, receives fibers from the posterior rami of the second and
third cervical nerves.
• The third occipital nerve (the superficial medial branch of the dorsal ramus of C3) crosses the lateral
and posterior aspects of the C2-3 facet, and innervates the C2-3 zygapophyseal joint.
• The C23 joint and thus the third occipital nerve appear vulnerable to trauma from acceleration-
deceleration injuries of the neck6 (Figure 19-2).
Figure 19-2. Occipital nerves.
There are usually two greater occipital nerves, two lesser occipital nerves, and two third occipital nerves
in each patient, though this may be variable. For instance, in one report, bilateral triplication of the lesser
occipital nerve was described.7
THE GREATER OCCIPITAL NERVE (GON)

• It exits the C2 foramen laterally, crosses over the atlanto-axial joint on top of the inferior oblique, and
then ascends in the posterior neck medially, pierces the semispinalis muscle and then pierces the
lateral edge of the conjoined tendon (Figure 19-3A and B).
• It then becomes superficial immediately inferior to the superior nuchal ridge, where it is joined more
cephalad by the occipital artery.
• This nerve could therefore be considered to have 3 parts (part 1, part 2, and part 3) as well as two
bends (bend 1 and bend 2)8 (Figure 19-4).
• The GON supplies the main sensory innervation to the posterior scalp and climbs in a cephalad fashion
laterally to the vertex and temporal areas,9 where it borders with the area innervated by the
supraorbital and auriculotemporal nerve.
• The actual location of the occipital nerve can be very variable; in 10 embalmed cadavers, the GON
was located anywhere from 5 to 28 mm from the midline.10 In a dissection of 20 cadavers with no
known headache history, the trapezius muscle was penetrated by the GON in 45% of cases, the
semispinal muscle was penetrated in 90% of cases, and the inferior oblique was penetrated in 7.5% of
cases.11
• When the occipital artery is palpable, the nerve will be medial to the artery.
Figure 19-3. (A, B) Occipital nerve and artery.
Figure 19-4. Occipital pathway. IO, internal oblique; P1, part 1; P2, part 2; P3, part 3; B1, bend 1; B2,
bend 2.8
THE LESSER OCCIPITAL NERVE

• It usually arises from the posterior ramus of C23, and travels along the posterior border of the
sternocleidomastoid muscle as part of the superficial cervical plexus, becoming most superficial and
accessible at about the level of the mastoid process, 32 to 90 mm from the midline10 (Figure 19-5).
• Accordingly, the lesser occipital nerves supply sensory innervation to the lateral portion of the
posterior scalp as well as the posterosuperior surface of the pinna of the ear12 (Figure 19-6).
• The LON has been reported to arise anomalously from the trunk of the suprascapular nerve.7
Figure 19-5. Occipital nerve dissection: A, greater occipital; B, lesser occipital.
Figure 19-6. Greater occipital versus lesser occipital pattern. (Used with permission from Nicole Gear.)
The Third Occipital Nerve

• It arises from the medial sensory branch of the posterior division of C3, passes through the trapezius
and splenius muscles slightly medial to the greater occipital nerve.
• It is sensory to the skin of the midline occipital region.
• It also supplies the proprioceptive fibers to the semispinalis muscles.
• The C2-3 joint and the third occipital nerve appear vulnerable to trauma from acceleration-
deceleration injuries of the neck.6
Cadaver studies have shown a great variability in nerve anatomy, both interindividually and
intraindividually. For example, in one study,10 the greater occipital nerve was found between 5 and 28
mm from the midline along the intermastoid line, while the lesser occipital nerve was found between 32
and 90 mm from the midline along the same landmark. In most cases, both the greater occipital nerve and
the lesser occipital nerve pierced the occipital aponeurosis after branching. There can also be
connections between the two (Figure 19-7).
Figure 19-7. Connection between greater and lesser occipital nerves.
Although originally associated only tension-type headaches and occipital pain, entrapment of the occipital
nerve has recently been recognized as one of the causes of unilateral, throbbing headaches, associated
with photophobia, phonophobia, and nausea, which meet the International Headache Society criteria for
migraine. Anatomic recognition of multiple occipital nerves (the greater occipital, the lesser occipital,
and the third occipital nerve), each with different patterns of pain, neurologic origin, and treatment
modalities, has been facilitated by the use of precision diagnostic injections and the search for more
aggressive treatment of intractable headaches and upper cervical neck pain. Decisions need to be made
preoperatively as to blind versus fluoroscopic versus ultrasound guidance, as well as distal versus
proximal injections. In general, the more distal the injection, the lesser the need for image guidance, but
the more likely one is to miss the entrapment.
According to a prospective study by Afridi et al,4 there was no significant association between
presence of anesthesia in the distribution of the GON after an injection and the response to occipital nerve
blocks, but there was a significant relationship between tenderness in the occipital region, and response.
Unfortunately, there is no standardized approach to occipital nerve injections, with volumes of injectate
ranging from 0.5 to 10 cc,13 local anesthetic with or without steroids13 or botulinum toxin,14,15 with or
without epinephrine, single injections or up to 10 injections,13 followed for 1 week16 up to 6 months,
which has made comparing efficacy difficult.
DOCUMENTATION FOR OFF-LABEL INDICATIONS

Because of the plethora of techniques available and the large volumes usually used, as well as the lack of
a “gold standard,” there has been a great deal of confusion and a lack of convincing evidence regarding
the efficacy and effectiveness of occipital nerve block. As a result, many insurance companies have
deemed this procedure “experimental.” In addition, the AMA CPT code 64405 is specific for greater
occipital nerve blocks, and there is not currently a specific code for lesser or third occipital nerves. Nor
is there a specific code for fluoroscopic or ultrasound guidance, or for the occipital decompression
technique (see below). Patients need to be made aware of these “off label” uses.
FLUOROSCOPIC VIEWS
Although often performed as a blind technique (see below), fluoroscopy is utilized for the more proximal
injections at the C2 and C3 facet level (Figure 19-8) and the occipital decompression approach (see
below).
Figure 19-8. Fluoroscopic location of occipital nerves.
For the blind procedure, the patient is positioned seated, neck flexed, with their head supported on their
hands. This position may also be desirable for ultrasound imaging as well. For fluoroscopic imaging, the
patient is usually positioned prone.

• Equipment for a blind diagnostic or therapeutic occipital nerve block includes:
A 3-cc syringe for each site
An 18-gauge needle to draw up the desired local anesthetic and corticosteroid solution
A 27-gauge needle for injection
A pair of sterile procedure gloves
Alcohol swabs
Local anesthetic, either 1% to 2% lidocaine or 0.5% bupivacaine
Corticosteroid
Although a deposteroid is most desired for longer-term effect, there is concern that the proximity
of the vertebral occipital arteries could lead to an unexpected vascular injection. Dr Gabor Racz
(personal communication), therefore, recommends that a particulate-free steroid be used.
• Additional equipment for a fluoroscopic diagnostic or therapeutic occipital nerve block includes:
Fluoroscopic imaging equipment and table
Because of potential vascular injections, consider equipment with digital subtraction angiography
(DSA) capability
A 30-gauge needle for skin infiltration
A 22-gauge 3.5-in Quincke-type needle vs a 20-gauge blunt tip needle with introducer
Nonionic contrast
• Additional equipment for an ultrasound diagnostic or therapeutic occipital nerve block includes:
Ultrasound imaging equipment
Consider ultrasound-enhanced needles
• Additional equipment for an occipital adhesiolysis includes:
Fluoroscopic imaging equipment and table
A Stealth needle (Epimed®, Johnstown, NY)
A 18-gauge needle to break the skin
Nonionic contrast
Preservative-free saline

• Blind technique
The greater, lesser, and third occipital nerves may be blocked with the patient either sitting with the
head flexed forward and the head resting on the hands or lying prone on an examination table. If
prone, a pillow placed underneath the chest permits easier flexion of head and neck. The clinician
stands behind the patient if sitting and on the left side of the patient (if right handed) when the
patient is prone. Routine monitors such as a blood pressure cuff and pulse oximeter may be used,
but an IV and sedation are generally not required.
The classic approach involves identifying the nuchal ridge, feeling for the occipital artery, and
injecting a large volume (up to 10 cc) medial to the artery or as a strip (Figure 19-9). This was
initially described as a technique for surgical anesthesia, attempting to anesthetize all three nerves
at the same time.
For the Trescot approach,17 3 landmarks are appreciated with the clinician’s left hand: the foramen
magnum, the conjoined tendon, and the occipital nerve groove of the skull just lateral to the tendon
(Figure 19-10A, B, and C).
The scalp can be cleaned over the planned injection sites with an alcohol pad.
Complete sterilization of the scalp is not necessary and the hair should not be shaved.
Figure 19-9. Occipital nerve injection sites and landmarks: A, traditional anesthesia injection technique;
B, Trescot occipital injection site; C, lesser occipital entrapment site; D, conjoined tendon.
Figure 19-10. (A) Examiner’s middle finger in the foramen magnum. (B) Examiner’s index finger on the
conjoined tendon. (C) Examiner’s thumb on the occipital nerve.
The small-gauged needle (27 gauge 1.5 inch) is aimed superiorly and medially and advanced until
contact is made with the bony skull (Figure 19-11). After aspiration, injection may then be made of
no more than 2 cc of the therapeutic solution (local anesthetic and steroid). Note that this injection
site is inferior to the nuchal line, the site of traditional injections.
Injection of the lesser occipital nerve is made with a second needle insertion just behind the
mastoid process. Often a groove can be palpated. After testing aspiration again, 1 cc of therapeutic
solution can be then injected to block the lesser occipital nerve.
The distal third occipital nerve can be injected just medial to the attachment of the conjoint tendon
on the occipital condyles, taking care to avoid the foramen magnum by angling the needle medial to
lateral and contacting bone.
Figure 19-11. Occipital injection technique.
• Fluoroscopy guided injections

Third occipital nerve blocks are often performed under fluoroscopic guidance at the level of the
C2-C3 facet.6 In patients with neck pain and headache after whiplash, the prevalence of pain
stemming from the C2-C3 zygapophysial joint was found to be 27%. Among those patients in whom
headache was the dominant feature, the prevalence increased to 53%.18 The third occipital nerve
most often crosses the C2-C3 joint opposite the center of the C3 superior articular process, but it
may run lower or higher than this plane. Because of anatomic variations, a radiofrequency needle is
placed opposite the middle of the joint as well as above and below this point19 (Figure 19-12).
Occipital adhesiolysis or suboccipital decompression is a technique developed by Dr Gabor Racz
to approach the high cervical entrapment of the occipital nerve. A blunt-tipped, curved, winged
needle (Figure 19-13A), called a Stealth ™ needle, is introduced from cephalad to caudad (Figure
19-13B), hugging the inferior occipital bone. This allows fluid to be used to lyse adhesions around
the occipital nerve to decompress the nerve (Figure 19-13C).
Figure 19-12. Radiofrequency sites for third occipital nerve denervation.18

Figure 19-13. (A) Stealth needle (Epimed International). (B) Fluoroscopic view of contrast during
suboccipital injection. (C) CT 3D reconstruction after suboccipital injection. (Used with permission from
• Ultrasound injections
Using ultrasound, the occipital nerve can be identified as it crosses the inferior oblique muscle
(Figure 19-14). Greher et al20 described an anatomic study using ultrasound to compare the
traditional injection site at the nuchal ridge with a more proximal technique (Figure 19-15). Using
0.1 cc injections of dye, they used ultrasound to identify the GON bilaterally in 10 cadavers (Figure
19-16). They reported successful injection of the GON distally in 16/20 dissections, while 20/20 of
the proximal GON was stained with dye.
Figure 19-14. Occipital nerve entrapment internal oblique.

Figure 19-15. Location of ultrasound transducer (1 = standard occipital nerve injection site; 2 = Trescot
approach injection site; 3 = Greher et al20 approach).
Figure 19-16. Ultrasound image of the occipital nerve on the inferior oblique. (Used with permission
from Andrea Trescot, MD.)
• Because the scalp is highly vascular, a hematoma can form; thus, manual pressure should be applied for
several minutes to ensure both hemostasis and adequate coverage of the nerve branches.
• Postprocedure, most patients will report that the back of the neck and head now feels “numb,” or
“frozen.” Many patients who were in the midst of a severe cervicogenic headache will report
immediate improvement of neck pain and headache symptoms.
• The patient should be encouraged to rest in the waiting room for about 10 minutes, if no IV sedation
was administered.
• Although counterintuitive, hypoesthesia over the occipital area does not appear to be necessary for
headache relief. Alfridi et al4 reported that decreased pin-prick sensation occurred in only 12 of 23
injections that resulted in complete pain relief, and in 20 of 35 with partial relief. Supplemental
pharmacotherapy is often indicated, such as anticonvulsants, anti-inflammatories, and muscle relaxants,
and is synergistic with well-performed greater and lesser occipital blocks. The reader is referred to
standard references for discussions of the pharmacotherapy of headache, since drug therapy for
“migraines” is sometimes helpful for occipital neuralgia and cervicogenic headache. Physical therapy
is also sometimes added to the above injections and drug therapy, particularly in instances of whiplash
or athletic neck injury.
• Postoperatively, mild ataxia and unsteadiness can be anticipated in most subjects, particularly when
looking downward, owing to the loss of tonic neck reflexes. The patient can expect the unsteadiness to
gradually subside, especially if visual cues including fixing on the horizon are utilized. Patients should
not drive a car until their ataxia and unsteadiness has completely resolved.
• Alopecia and skin atrophy can occur after steroid injections.21
• Infection of the injection site can occur, but is uncommon if proper aseptic technique is used.
• Patients with a history of blunt trauma to the occiput or prior posterior fossa surgery may have a defect
in the skull, allowing, direct entry into the cranial vault, which may result in a total spinal anesthesia or
brain injury.22
• Monitoring of potential complications
Inadvertent intravascular injection is rare, if one aspirates before injecting.
Inadvertent injection into the foramen magnum is theoretically possible, although even rarer.
Nevertheless, as with any interventional procedure, cardiorespiratory resuscitation equipment,
automatic blood pressure cuff, ECG monitor, IV lines, laryngoscope and endotracheal tubes,
plus oxygen and Ambu bag and ACLS-trained personnel must be immediately available.
Specific identification of the foramen magnum prior to injection (see Trescot technique above)
should decrease that risk.

• Occipital nerve blocks are simple office procedures that are underutilized in the treatment of occipital
neuralgia and cervicogenic headache.
• Anatomically and physiologically, occipital nerve blocks approximate C2 and C3 nerve root blockade,
and a first set of injections can be performed easily—even at the conclusion of the patient’s first office
visit.
• Occipital nerve injections have proven useful in the diagnosis and treatment of many forms of
cephalgia, including occipital neuralgia, extracranial “migraine,” cervicogenic headache, whiplash and
“cluster” headache. Its utility as a diagnostic technique capable of discriminating between these related
types of headache has not been well studies, primarily because of the lack of standardized techniques.
• Lasting therapeutic benefit in occipital neuralgia and/or cervicogenic headache usually requires a
series of a several injections.
• Combining this minor interventional procedure with appropriate pharmacotherapy and physical therapy
yallows many patients a lasting beneficial outcome.
• Persistent pain that responses only temporarily to low volume occipital nerve injections may respond
to botulinum toxin (to release the trapezius entrapment), cryoneuroablation of the GON/LON,
radiofrequency lesioning of the third occipital nerve, occipital stimulation, or regenerative injection
therapy (prolotherapy).
Suggested Reading
Trescot AM. Headache management in an interventional pain practice. Pain Physician. 2000;3:197-200.
Trescot AM, Irwin D. Occipital neuralgia. In: Manchikanti L, Singh V, eds. Interventional Techniques in
Chronic NonSpinal Pain. Paducah, KY: American Society of Interventional Pain Physicians
Publishing; 2009: chap 22.
Ashkenazi A, Levin M. Greater occipital nerve block for migraine and other headaches: is it useful? Curr
Pain Headache Rep. 2007 Jun;11(3):231-235.
Levin M. Nerve blocks in the treatment of headache. Neurotherapeutics. 2010 Apr;7(2):197-203.
References
1. Perelson HN. Occipital nerve tenderness: a sign of headache. South Med J. 1947;40:653-656.
2. Luff AP. On the various forms of fibrositis and their treatment. Br Med J. 1913 Apr 12;1(2728):756-
760.
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5. Biondi DM. Cervicogenic headache: a review of diagnostic and treatment strategies. J Am Osteopath
Assoc. 2005 Apr;105(4)(suppl 2):16S-22S.
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7. Madhavi C, Holla SJ. Triplication of the lesser occipital nerve. Clin Anat. 2004 Nov;17(8):667-671.
8. Gille O, Lavignolle B, Vital JM. Surgical treatment of greater occipital neuralgia by neurolysis of the
greater occipital nerve and sectioning of the inferior oblique muscle. Spine. 2004 Apr 1;29(7):828-
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9. Bogduk N. The clinical anatomy of the cervical dorsal rami. Spine. 1982 Jul-Aug;7(4):319-330.
10. Becser N, Bovim G, Sjaastad O. Extracranial nerves in the posterior part of the head. Anatomic
variations and their possible clinical significance. Spine. (Phila Pa 1976). 1998 Jul 1;23(13):1435-
1441.
11. Bovim G, Bonamico L, Fredriksen TA, Lindboe CF, Stolt-Nielsen A, Sjaastad O. Topographic
variations in the peripheral course of the greater occipital nerve. Autopsy study with clinical
correlations. Spine. 1991 Apr;16(4):475-478.
12. Ashkenazi A, Levin M. Greater occipital nerve block for migraine and other headaches: is it useful?
Curr Pain Headache Rep. 2007 Jun;11(3):231-235.
13. Caputi CA, Firetto V. Therapeutic blockade of greater occipital and supraorbital nerves in migraine
patients. Headache. 1997 Mar;37(3):174-179.
14. Kapural L, Stillman M, Kapural M, McIntyre P, Guirgius M, Mekhail N. Botulinum toxin occipital
nerve block for the treatment of severe occipital neuralgia: a case series. Pain Pract. 2007
Dec;7(4):337-340.
15. Bovim G, Sand T. Cervicogenic headache, migraine without aura and tension-type headache.
Diagnostic blockade of greater occipital and supra-orbital nerves. Pain. 1992 Oct;51(1):43-48.
16. Peres MF, Stiles MA, Siow HC, Rozen TD, Young WB, Silberstein SD. Greater occipital nerve
blockade for cluster headache. Cephalalgia. 2002 Sep;22(7):520-522.
17. Trescot AM. Headache management in an interventional pain practice. Pain Physician. 2000
Apr;3(2):197-200.
18. Bogduk N, Marsland A. On the concept of third occipital headache. J Neurol Neurosurg Psychiatry.
1986 Jul;49(7):775-780.
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ultrasound-guided blockade of the greater occipital nerve: a comparison of two selective techniques
confirmed by anatomical dissection. Br J Anaesth. 2010 May;104(5):637-642.
21. Shields KG, Levy MJ, Goadsby PJ. Alopecia and cutaneous atrophy after greater occipital nerve
infiltration with corticosteroid. Neurology. 2004 Dec 14;63(11):2193-2194.
22. Brown D. Occipital block. In: Brown D, ed. Atlas of Regional Anesthesia. Philadelphia, PA:
Elsevier; 2006:53-55.
CHAPTER 20
Periorbital Nerve Blocks (Supraorbital,

Supratrochlear, and Infraorbital Nerves)
Sanford Silverman
INDICATIONS
Blockade of the periorbital nerves (supraorbital, supratrochlear, and infraorbital) is useful for surgical
anesthesia of the face, treatment of painful facial conditions, and can provide diagnostic information for
the possibility of neurolytic blocks and neuromodulatory techniques. The indications are summarized in
Table 20-1.
TABLE 20-1. Indications for Periorbital Nerve Blocks
ANATOMY
• The supraorbital and supratrochlear nerves are terminal branches of the ophthalmic division of the
trigeminal nerve (V1).
• The infraorbital nerve is a terminal branch of the maxillary division of the trigeminal nerve (V2).
• V1 provides cutaneous innervation above the eye, forehead, and along the medial aspect of the nasal
bridge.
• V2 provides cutaneous innervation below the eye and the areas medial to the zygomatic arch to the
nostril and the lateral forehead (Figure 20-1).
• The supraorbital, supratrochlear, and infraorbital nerves lie along a vertical plane, which extends from
the supraorbital notch to the corner of the mouth, bisecting the pupil.
• The supraorbital notch is located above the pupil in the orbital rim, the supratrochlear groove is just
medial to the supraorbital notch, while the infraorbital foramen is located 1 cm below the orbital rim,
within the vertical plane.
• The nerves emanate from these foramina respectively (Figure 20-2).
• The supraorbital and infraorbital notches are relatively easy to palpate.
• The supratrochlear nerve emanates from the supratrochlear notch, which lies at the intersection of the
nasal bridge and the supraorbital ridge, medial to the supraorbital notch (Figure 20-3).
Figure 20-1. Trigeminal pattern.
Figure 20-2. Trigeminal terminal branches.
Figure 20-3. Supraorbital and infraorbital nerves.
CONTRAINDICATIONS
There are absolute and relative contraindications to performing periorbital nerve blocks, summarized
below (Table 20-2):
TABLE 20-2. Absolute and Relative Contraindications to Periorbital Nerve Blocks
Preoperative Considerations
• Pt should be thoroughly evaluated prior to any interventional pain procedure and the risks/benefits
explained.
• Although a relative contraindication, coagulopathy does not preclude the safe performance of a
periorbital nerve block.
• Many patients who are anticoagulated suffer from painful conditions of the face and can benefit greatly
from a periorbital nerve block.
• The risk/benefit ratio of stopping such medications (Plavix, Coumadin, etc) prior to the procedure may
not be acceptable in certain situations (history of stroke, MI, stent, etc).
• Use small gauge needles (25, 27, or 30 gauges) and apply appropriate pressure to the injection site
post block.
• A cold compress can be used to mitigate the effects of hematoma and ecchymosis, which can be seen
with these procedures.
• Since this area is highly vascular, systemic uptake of local anesthetic can occur and the dose of such
should be considered.
• Although usually not seen in the low doses commonly used for these blocks, local anesthetic toxicity
may occur and consists of signs such as metallic taste, altered mental status, seizures, and ultimately
hemodynamic compromise.
Positioning
The patient is placed in the supine or semi-recumbent position and monitored appropriately. The
supraorbital notch and infraorbital foramen are palpated to identify the structure and confirm the diagnosis
(Figures 20-4 to 20-5).
Figure 20-4. Supraorbital exam. (Used with permission from Andrea Trescot, MD.)
Figure 20-5. Infraorbital exam. (Used with permission from Andrea Trescot, MD.)
Typically local anesthetics such as lidocaine or bupivicaine may be utilized in small volumes, not
usually exceeding 2 cc. Small syringes (3 cc) should be used.
Technique
Supraorbital nerve (Figure 20-6):
• The supraorbital notch is identified in the vertical plane described above and sterilely prepped with
antiseptic solution with care to avoid any excess from entering the eye.
• The patient is asked to look directly in front (usually told to pick a spot on the ceiling) to ensure
midline position of the pupil. This aligns the supraorbital notch and infraorbital foramen in the same
plane.
• The skin at the notch is entered with a small gauge needle (25, 27, or 30 gauges) and directed slightly
medially to avoid entering the foramen until periosteum is contacted.
• A paresthesia may be elicited and the patient should be counseled prior to the procedure regarding this.
• If the needle enters the foramen, it should be drawn back to prevent intracranial and/or intraneural
injection.
• After careful aspiration, 1 to 2 cc of local anesthetic is injected. Large volumes may actually entrap the
nerve.
• Soft gauze should be used after the injection to apply gentle pressure to the orbital soft tissue to prevent
subcutaneous dissection of local anesthetic.
Figure 20-6. Supraorbital injection. (Used with permission from Andrea Trescot, MD.)
Supratrochlear nerve:
• The junction of the nasal bridge and the supraorbital rim is palpated and sterilely prepped with
antiseptic solution, with care to avoid any excess entering the eye.
• A needle is inserted through the skin just lateral to this point and directed medially into the
subcutaneous tissues.
• A paresthesia may be elicited and the patient should be counseled prior regarding this.
• After careful aspiration, 0.5 to 1 cc of local anesthetic is injected.
• Soft gauze should be used during injection to apply gentle pressure to the orbital soft tissue to prevent
Infraorbital nerve; extraoral approach (Figure 20-7):
• The infraorbital nerve is approached 1 cm below the orbital rim in the vertical plane passing through
the supraorbital notch and the pupil.
• The patient is asked to look directly in front (usually told to pick a spot on the ceiling) to ensure
midline position of the pupil.
• The skin is sterilely prepped with antiseptic solution, with care to avoid any excess entering the eye.
• The needle is inserted into the skin and directed 15 degrees medially to avoid entry into the foramen
until periosteum is contacted.
Figure 20-7. Infraorbital percutaneous injection. (Used with permission from Andrea Trescot, MD.)
• After careful aspiration, 1 to 2 cc of local anesthetic is injected.

Infraorbital nerve; intraoral approach (Figure 20-8):
Figure 20-8. Infraorbital intraoral injection. (Used with permission from Andrea Trescot, MD.)
• This approach to the infraorbital nerve may be desired when

– Surgical anesthesia is required for removal of lesions.
– Laceration repair is needed.
– Cosmetic considerations, such as avoiding needle puncture sites externally, are needed.
– There is inability to access the nerve using the extraoral approach.
• The infraorbital foramen is palpated and the upper lip is pulled backward.
• The alveolar sulcus is then anesthetized with a cotton ball soaked with either 10% cocaine or 2%
viscous lidocaine.
• A 25-gauge 1.5-in needle is inserted through the mucosa toward the infraorbital foramen.
• After careful aspiration, 1 to 2 cc of local anesthetic is injected.
Complications
• Intravascular injection may occur with the possible concomitant signs and symptoms listed previously.
• More common are post-block ecchymosis or hematoma formation, secondary to vascular injury.
This can be mitigated by applying a cold compress with pressure immediately after injection.
• Infection can occur with any interventional procedure and should be aggressively diagnosed and
treated.
• Infections in this area can be highly aggressive and spread into the CNS quickly.
Fluoroscopic Guidance
The supraorbital notch can be imaged under direct fluoroscopic view, which may aid in performing
periorbital nerve blocks (Figures 20-9 and 20-10).
Figure 20-9. Fluoroscopic imaging of supraorbital notch. (Used with permission from Andrea Trescot,
MD.)
Figure 20-10. 3D reconstruction; supraorbital and infraorbital foramen. (Used with permission from
Suggested Reading
Trescot AM. Headache management in an interventional pain practice. Pain Physician. 2000;3:197-200.
Sjaastad O, Stolt-Nielsen A, Pareja JA, Fredriksen TA, Vincent M. Supraorbital neuralgia. On the clinical
manifestations and a possible therapeutic approach. Headache. 1999;39:204-212.
References
1. Waldman S. Atlas of Interventional Pain Management. WB Saunders Co; 1998:30-47.
2. Brown D. Atlas of Regional Anesthesia. WB Saunders Co; 1992:121-127.
3. Brown D. Regional Anesthesia and Analgesia. WB Saunders Co; 1996:240-244.
SECTION III
SPINAL INTERVENTIONS
CHAPTER 21
Interlaminar Epidural Steroid Injections:

Cervical, Thoracic, Lumbar, and Caudal
Raj Doshi, Vikram B. Patel, and Salahadin Abdi
INTRODUCTION
Epidural steroid injections have been used for the treatment of radicular pain and spinal pathology for
many decades. The epidural space can be accessed posteriorly via the interlaminar space. Although using
an AP lateral or contralateral oblique fluoroscopically guided approach can be more precise and can also
help visualize the spread of the injectate under live fluoroscopic view, a “blind” injection performed by a
skilled practitioner using a “loss of resistance” technique to identify passage into the epidural space via
the ligamentum flavum has been utilized successfully for years. The relative simplicity of the blind
technique and one’s ability to perform it without the use of costly equipment such as a fluoroscopy unit
has provided a much-needed procedure to the masses especially in developing countries. The use of
interlaminar approach to the epidural space for injection is one of the most frequently used procedures in
the practice of interventional pain management.
INDICATIONS
• Unilateral or bilateral radiculopathy resulting from
Acute intervertebral disc herniation causing compression or impingement of spinal nerve
Acutely herniated nucleus pulposus with compression or local proinflammatory mediator release
and resultant nerve irritation
Spinal stenosis (acquired or congenital)
Foraminal stenosis
Lateral recess stenosis
Impingement from degenerative disc disease
Compression by cysts on zygapophyseal (facet) joints
• Spondylolisthesis
• Spinal deformity (eg, scoliosis)
• Postlaminectomy syndrome
• Pain from vertebral compression fractures
• Pain from herpes zoster
RELEVANT ANATOMY
• Level of interlaminar injections are initially identified via palpation between spinous processes or via
identification of the space between vertebrae on fluoroscopic imaging.
• From superficial to deep (dorsal), an epidural needle passes through the following structures for a
midline approach: skin, subcutaneous tissues, supraspinous ligament, interspinous ligament,
ligamentum flavum, and the epidural space. If the injection proceeds deeper, it comes in contact with
the dura mater and the subarachnoid space.
• From superficial to deep (dorsal), an epidural needle passes through the following structures for a
paramedian approach: skin, subcutaneous tissues, ligamentum flavum, and the epidural space.
• The epidural space is bounded by the ligamentum flavum and the lamina posteriorly, the posterior
longitudinal ligament anteriorly, and the vertebral pedicles and neural foramina laterally.
• The epidural space contains fat, lymphatics, venous plexi, connective tissue, and the spinal nerve roots.
• The ligamentum flavum can be discontinuous in the cervical and high thoracic regions, making
localization of the epidural space via loss of resistance technique potentially more challenging.
CONTRAINDICATIONS
• Absolute
Local or systemic infection
Acute spinal cord compression (injection at that level)
Untreated bleeding disorders that predispose to hemorrhage
Uncontrolled or untreated systemic disorders (cardiopulmonary, renal, endocrine) where steroid
effects may cause acute or subacute decompensation of the patient’s medical condition
Hypersensitivity or allergy to medications used in epidural steroid injection
Patient refusal
• Relative
Preprocedure evaluation in patients with immunosuppressive diseases should be undertaken to rule
out the potential for latent infection.
Considerations should be made to perform epidural injections without fluoroscopy in pregnant
women to decrease the risk of radiation exposure to the fetus.
Morbid obesity and inability to lie down (especially if there is respiratory distress).
Concurrent use of anticoagulants or antiplatelet agents (other than aspirin or nonsteroidal anti-
inflammatory medications). A careful risk assessment in patients requiring anticoagulation needs to
be performed.
PREOPERATIVE PREPARATIONS
• Fully informed consent must be obtained prior to any intervention from the patient or legal
representative.
• Preprocedure vital signs should be obtained and documented, including temperature, blood pressure,
heart rate, and oxygen saturation.
• If a cervical epidural steroid injection will be performed, some practitioners may start an intravenous
line. Occasionally, preprocedure IV access must be obtained prior to procedure for patients with a
history of vasovagal syncope.
• Preprocedure pain level and character of pain (location, duration, intensity) should be elicited prior to
procedure. If this is a repeat injection, subsequent pain relief or lack thereof should be assessed and
documented.
• The classic interlaminar injection is done with the patient in the prone position at all levels.
• Some practitioners may perform cervical epidural steroid injections with fluoroscopy with the patient
in a seated position with the head face down on the fluoroscopy table.
• Patient should be positioned appropriately on fluoroscopy table in order to maximize the spaces
between the lamina. A pillow may be placed under the patient near the level of interest to accentuate
kyphosis or reverse lordosis to maximize the width of the interlaminar space.
• Patient movement has been implicated in a significant number of cases of spinal cord injury related to
epidural injections. Judicious selection of patients requiring sedation may decrease the risk of
complications related to patient movement. (See Chapter 11.)
Equipment
1. Room
Monitor for vital signs (minimum includes blood pressure, heart rate, oxygen saturation).
Fluoroscopy machine with fluoroscopy-compatible table (CT-guidance and ultrasound guidance are
also utilized but fluoroscopy is much more common).
Lead apron (for coverage of thorax and thyroid). Use of radiation attenuating gloves and lead-lined
eye protection is highly recommended.
Pillows to improve positioning for procedure and patient comfort.
Oxygen supply (wall or tank) and suction mounted and ready to use.
Immediate availability of resuscitation equipment, including Ambu bag and/or advanced airway
devices. Devices and medications for advanced cardiac life support should be available or be
ready to be activated quickly.
2. Procedure
Epidural kits containing
Syringes for local anesthetic infiltration, preparation of epidural injection, needles for drawing
up medication and skin/tissue infiltration.
Syringe for loss of resistance.
Skin preparation solutions to sterilize the skin for the procedure.
Tuohy needle for epidural injection (gauges are practice specific but generally range from 18-
gauge to 20-gauge needles).
Labels for syringes (The Joint Commission [JCAHO] standard).
The addition of tubing to connect the epidural tubing to the syringe containing contrast can be
used to distance the provider from fluoroscopy radiation during continuous injection of contrast
and also avoid needle movement.
Sterile drape
Gauze
Sharps recovery/protective device
3. Medications
Corticosteroids (particulate or nonparticulate determined by provider)
Radiopaque water-soluble contrast
Sterile saline
Local anesthetic for epidural injection (often bupivacaine, ropivacaine, or lidocaine); lidocaine for
skin puncture analgesia
Techniques
1. Lumbar interlaminar epidural steroid injection
Identify the appropriate interlaminar space with fluoroscopy using a radio-opaque device to mark
the space (metal marker, Kelly clamp).
Prepare the skin using chlorhexidine and drape.
Infiltrate the skin and subcutaneous tissues with 1% lidocaine using a 25- or 27-gauge infiltration
needle. After initial infiltration, inject into the deeper ligamentous structures using a 22- or 25-
gauge 1.5-in needle.
With the fluoroscope in the AP position, a Tuohy or Weiss needle is placed in the midline or
paramedian approach with the tip of the needle toward the midline of the fluoroscopic image
between the spinous processes of interest for bilateral radicular symptoms or to the ipsilateral side
(of the patient’s pain), just lateral to the spinous process.
The needle is advanced until a subjective feeling of “engagement” of the ligament has been felt.
The fluoroscope is rotated to the lateral position and depth is confirmed. Prior to entry into the
epidural space, the stylet is removed and a loss-of-resistance syringe is attached filled with 1 mL
or more of saline with an air bubble. Rapid, shallow ballottement of the syringe continues as the
needle is advanced into the epidural space until there is loss of resistance and injection of saline
through the epidural needle with minimal syringe pressure.
Entry into the epidural space is confirmed by injecting 0.5 to 2 mL of nonionic contrast to verify the
spread in the epidural space.
Unilateral or bilateral spread is confirmed with fluoroscopy image capture in the AP position,
while the lateral view shows the spread of the contrast in the posterior or anterior epidural space.
Injection of steroid with or without local anesthetics and/or saline is performed.
Replace the stylet and withdraw the epidural needle.
Place gauze on needle entry site and apply pressure if there is bleeding. Place sterile dressing or
bandage over entry site.
Patient should be sat upright. Standing should always be with assistance in case there is mild
weakness after the injection or orthostatic hypotension (Figure 21-1).
Figure 21-1. (A) Fluoroscopic images of a lumbar interlaminar injection in AP view. Note the unilateral
spread of the contrast and the needle placement in the paramedian area. (B) Fluoroscopic image of a
midline lumbar interlaminar injection in AP view. Note the bilateral spread of the contrast and the needle
placement in the paramedian area. This is not the most common type of spread seen. (C) Fluoroscopic
image of a lumbar interlaminar injection in lateral view. Note the posterior and lateral spread of the
contrast. Absence of smooth contrast silhouette close to the posterior margin of the vertebral body
suggests epidural placement. (D) Fluoroscopic image of a midline lumbar interlaminar injection in AP
view. Note the presence of the bubbles (air used for the loss of resistance technique) in the cephalad area.
2. Cervical interlaminar epidural steroid injection

The technique for cervical epidural steroid injections is very similar to lumbar epidural steroid
injections with some distinct differences:
Positioning
A roll or pillows are placed under the chest so that there is mild flexion of the neck. A pillow or
padded gauze can be placed on the forehead to prevent the patient’s face from being
compressed by the table. The patient’s arms are placed at their sides.
Positioning devices are available to allow for consistent positioning of the patient’s head with
the arms flexed and placed above their head (“Superman” position).
Anatomy
There is no interspinous ligament in the cervical space. Additionally, 50% of cryomicrotomal
specimens show an absence of a midline ligamentum flavum (gaps) with absence of a posterior
epidural space above C7-T1.
Some practitioners may only perform cervical interlaminar epidurals at C7-T1 using either the
volume of injectate- or catheter-directed delivery to deposit medications to the level of interest
(Figure 21-2).
Figure 21-2. (A) Fluoroscopic image of a midline cervical interlaminar injection in AP view. Note the
presence of the air bubbles form the use of loss of resistance technique. A more reliable technique is to
use an air/fluid interface in the loss of resistance syringe as the fluid provides a noncompressible medium
and in case of an inadvertent intrathecal penetration, prevents sudden headache due to air travelling to the
intra-ventricular area in the brain. (B) Fluoroscopic image of a midline cervical interlaminar injection in
lateral view. Note the spread of the contrast medium in the posterior epidural space. Although the spread
is also in the lateral epidural space, the thinness of the contrast film viewed in a perpendicular plane
makes it nearly invisible on a lateral view.
3. Thoracic interlaminar epidural steroid injection

Positioning
Pillows may be placed under the patient while in the prone position to accentuate the thoracic
kyphosis. Arms may need to be placed either at the patient’s side (for upper thoracic injections)
or above the patient’s head (for lower thoracic injections).
Anatomic abnormalities may preclude a midline approach. A paramedian approach may be
necessary to access the thoracic epidural space (Figure 21-3).
Figure 21-3. (A) Fluoroscopic image of a midline thoracic interlaminar injection in AP view. At higher
thoracic levels, a posterior midline approach is very difficult and a paramedian approach is preferred.
(B) Fluoroscopic image of a midline thoracic interlaminar injection in lateral view. Just as in the cervical
area, thoracic epidurals in a lateral view are seen to be mainly in the posterior epidural space as the
lateral spread is too thin to be visualized in lateral view. An AP view would clearly demonstrate spread
in the lateral epidural space (see Figure 21-3A). A greater amount of contrast may show lateral spread as
in Figure 21-3C. (C) Fluoroscopic image of a midline thoracic interlaminar injection in lateral view with
contrast spreading in the lateral epidural space as well.
4. Caudal epidural steroid injection

Caudal epidural steroid injections are most commonly performed in patients with previous
laminectomies or with abnormal anatomy in the lumbar space.
Positioning
A roll or a pillow may be placed under the patients pelvis in the prone position. Tape may need
to be applied to the patient’s buttocks to laterally retract the tissue to access the sacral midline.
Preparation
Given the location of the injection, the potential injection site and the surrounding area must be
meticulously disinfected.
Technique
The sacral cornua are identified by palpation and skin site analgesia is administered using 1%
lidocaine.
The fluoroscopy machine is placed in the lateral position and the sacral hiatus is imaged and
marked with a radio-opaque marker.
If using a Tuohy needle, the needle should be bent with a convex bend to facilitate placement of
the needle within the caudal epidural space. Alternatively, a 22-gauge Quincke spinal needle
with a convex bend may also be used.
Passage of the needle though the sacrococcygeal ligament may be felt (“pop”) and the need is
advanced at a less acute angle.
Confirmation of position is performed with nonionic contrast injection.
Larger volumes of injectate may be required (about 20 mL of steroid, ±local anesthetic, and
sterile saline) to fill the caudal epidural space and to achieve cephalad spread of injectate to
the desired lumbar levels (Figure 21-4).
Figure 21-4. (A) Caudal epidural injection: lateral view with the needle through the sacral hiatus. Note
the position of the needle in the anterior epidural space. This can be achieved selectively by placing the
needle slightly more vertically. (B) Caudal epidural injection: AP view. The epidural needle tip is not
visible. (C) Caudal epidural injection: AP view. The needle tip is at approximately S3 level. In most
cases of spinal stenosis, significant amount of contrast can be seen escaping through the sacral foramina
anteriorly following the path of least resistance. Unilateral spread is not uncommon.
POSTPROCEDURE INSTRUCTIONS
• Patient should have vital signs checked immediately after the procedure.
• Patients should be able to stand without difficulty and without significant deviation from their
preprocedure neurologic status.
• If intravenous sedation was administered, the patient should be transferred to a postanesthesia care unit
(or equivalent) for observation until the patient is considered recovered from sedation.
• Patient should not engage in any strenuous activities for the rest of the day but can resume normal
activities the next day.
COMPLICATIONS AND PITFALLS

• Complications related to drug effects
Corticosteroids. Major effects include flushing, hyperglycemia, hypothalamic-pituitary-adrenal axis
suppression, fluid retention, changes in vascular tone usually resulting in hypertension.
Corticosteroids used acutely and chronically affect all organ systems, and a full account of organ-
specific effects is beyond the scope of this text.
Contrast dye-allergic reaction, flushing.
Local anesthetic-related weakness, numbness, etc.
• Complications related to procedure
Presyncope or syncope
Nausea and vomiting
Dizziness
Back pain
Feeling of “pressure” or fullness at the level of the injection
Infection (abscess, meningitis, arachnoiditis)
Spinal cord injury
Spinal cord infarction
Numbness/weakness
Paralysis
Inadvertent subarachnoid/subdural injection
Postdural puncture headache
Bleeding/bruising at skin site
Epidural hematoma
Muscle soreness from needle placement (more common with larger-gauge needles)
Air embolism (if using loss of resistance to air)
Suggested Reading
Goodman BS, Posecion LW, Mallempati S, Bayazitoglu M. Complications and pitfalls of lumbar
interlaminar and transforaminal epidural injections. Curr Rev Musculoskelet Med. 2008 Dec;1(3-
4):212-222. Epub 2008 Aug 15.
Hogan QH. Epidural anatomy examined by cryomicrotome section. Influence of age, vertebral level, and
disease. Reg Anesth. 1996 Sep-Oct;21(5):395-406.
Manchikanti L, Boswell MV, Datta S, et al; ASIPP. Comprehensive review of therapeutic interventions in
managing chronic spinal pain. Pain Physician. 2009 Jul-Aug;12(4):E123-E198 (Review).
Mulroy MF, Norris MC, Liu SS. Safety steps for epidural injection of local anesthetics: review of the
literature and recommendations. Anesth Analg. 1997 Dec;85(6):1346-1356 (Review).
Ogoke BA. Caudal epidural steroid injections. Pain Physician. 2000 Jul;3(3):305-312.
Rathmell JP. Atlas of Image-Guided Intervention in Regional Anesthesia and Pain Medicine.
Philadelphia, PA: Lippincott, Williams & Wilkins; 2006.
Stojanovic MP, Vu TN, Caneris O, Slezak J, Cohen SP, Sang CN. The role of fluoroscopy in cervical
epidural steroid injections: an analysis of contrast dispersal patterns. Spine (Phila PA 1976). 2002
Mar 1;27(5):509-514.
The Massachusetts General Hospital Handbook of Pain Management. 2nd ed. In: Jane Ballantyne, ed.
Philadelphia, PA: Lippincott, Williams & Wilkins; 2002:597. ISBN: 0-7817-2377-9.
CHAPTER 22
Transforaminal Epidural Steroid Injection

Vikram B. Patel
INDICATIONS
Transforaminal approach to the epidural space has been utilized for several decades for proper placement
of injectates at the site of inflammation. Initially called selective nerve root blocks, these injections are
more recently called transforaminal injections. The main advantages include (1) ability to place the
medication closer to the area of the pain generator and inflammation (the neuro-discal interface) and (2)
the use of less medication to achieve similar or better results than an interlaminar approach.
Lumbar transforaminal injections are commonly performed at most pain practices, but recently the
cervical transforaminal injections are now infrequently used to do an increase of the recognition of
complications from these injections. This includes catastrophic outcomes secondary to intravascular
(arterial) injections within the radicular arteries and intraneural injections leading to neuralgia and spinal
cord injuries. This chapter will focus on the lumbar transforaminal approach.
Following are some of the specific indications for these injections:
• Herniated intervertebral disc
• Lumbar radiculopathy (radiculitis) secondary to various causes such as
Herniated intervertebral disc
Spinal foraminal stenosis
Postlaminectomy syndrome causing radiculitis
RELEVANT ANATOMY
The lumbar intervertebral foramen is the exit route for the spinal nerve roots at all the levels. The
anatomic boundaries are:
• Anteriorly by the body of the vertebra superiorly and the intervertebral disc inferiorly—lined by the
posterior longitudinal ligament
• Pedicle of the superior vertebra above and the pedicle of the inferior vertebra below
• Lamina and the inferior articular process of the superior vertebra posteriorly
• Lamina and the superior articular process of the inferior vertebra—lined by the ligamentum flavum
(Figures 22-1 to 22-3)
• The spinal nerve root and the dorsal root ganglion and the sinuvertebral nerve.
• The radicular artery (segmental artery) (Figure 22-4). These arteries are not fixed in their position
relative to the foramen. These arteries enter the spinal cord through the nerve. One of the largest
arterial branches is called the arteria radicularis magna (Artery of Adamkiewicz), which enters the
spinal canal anywhere from the T9 through L1 levels. It merges with the anterior spinal artery, usually
at about T4-T6 level to supply the anterior position of the spinal cord. As it is an end-artery (without
anastomoses), blockage of this artery can lead to paralysis.
• Adipose tissue.
• Veins connecting the external and internal venous plexuses (Figure 22-5).
• Ligaments and meninges.
Figure 22-1. Spinal column. (Gray’s Anatomy.)
Figure 22-2. Sagittal section of the lumbar spine. (Gray’s Anatomy.)
Figure 22-3. Coronal section of the lumbar spine. (Gray’s Anatomy.)
The contents of the lumbar spinal intervertebral foramen include:

Figure 22-4. Graphic depiction of the segmental arteries.
Figure 22-5. Lumbar venous plexus.
THE “SAFE TRIANGLE”

• The so-called “safe triangle” (Figure 22-6) is the area posterior and inferior to the exiting nerve root.
• It can only be considered safe in relation to the nerve root as an undisplaced nerve root. It is usually
inferior to the pedicle cephalad but this triangular space also contains the artery as well as veins which
can lead to intravascular penetration by the needle.
• Some physicians advocate the use of a blunt needle for the performance of the transforaminal
injections. This school of thought postulates that a “blunt” needle may be safe as it may have less of a
chance of penetrating a blood vessel or nerve.
• However, this does not substitute the use of live fluoroscopically directed injection of contrast medium
before injection of the corticosteroid.
• It has also been thought that a nonparticulate steroid may be safer for such transforaminal injections as
the particulate material may lead to blockage of the segmental artery in case of inadvertent intra-
articular injection and cause spinal cord ischemia.
• It is the author’s belief that a blood vessel is relatively “fixed” within the confines of the intervertebral
foramen and is relatively immobile thus making it easy for a needle to cannulate it and that the blood
vessels are relatively mobile outside the foramen making them difficult to cannulate with a needle
(similar to stabilizing a vein prior to starting an IV access).
• Hence letting the needle tip remain outside or at the rim of the foramen and letting the injectate travel
transforaminally may provide added safety against intra-arterial injections.
Figure 22-6. “Safe triangle.” This so-called safe zone only means that an undisplaced nerve root may not
be encountered by a needle in this area. However, this area can contain the blood vessels which can
prove this zone to be quite unsafe if a blood vessel is damaged or penetrated and injected.
Basic concerns and contraindications

• One could potentially damage a nerve root or have an intra-vascular injection with a transforaminal
approach.
• Main contraindications include local infection, large disc herniation with significant foraminal
encroachment and lower extremity weakness (which in itself is an indication for surgical
decompression).
• Some relative contraindications are allergy to the iodine contrast material, which can be avoided with
proper preoperative preparation with steroid and antihistamine taken orally and inability of a patient to
lie down prone.
• When a patient has a true contrast allergy, noniodinated contrast can be used, or the procedure can be
performed without the aid of contrast.
• Preoperatively, a review of the MRI scan can help determine if there is enough space around the nerve
root for this procedure and to help correlate the level of pathology to the patient’s pain.
• Patient education is a must, especially about the possible complications that may result from such a
procedure.
• Patient’s body habitus and the weight should also be considered as a large patient will not only require
a longer needle but will also provide less space between the body and the fluoroscopy unit for the
placement of the needle.
• Ability of the patient to lie in a prone position should also be considered as patients with respiratory
compromise, aortic aneurysms, ileostomy, etc, will be unable to stay in a prone position for some time.
• Possibility of nerve root displacement posteriorly by a herniated disc can lead to inadvertent
paresthesiae during needle placement and the patient should be warned of such an occurrence.
• Deep sedation for this procedure is not recommended and an awake patient may be able to respond to
intraneural placement providing some safety.
• Mild sedation such as with conscious sedation technique may be appropriate for some patients who are
apprehensive about the procedure.
FLUOROSCOPIC VIEWS AND TECHNIQUE

The most important aspect of the procedure is obtaining a proper fluoroscopic view prior to staring the
procedure. Understanding the radiological anatomy of the spine is a must.
• The fluoroscopic view is first optimized for the level of intended needle placement. This is also
referred to as “squaring” the level, which basically places the x-ray beam perpendicular to the
intended intervertebral level thereby squaring off the superior and inferior vertebral end plates. (Note:
I would like a picture/drawing of this with a fluoro and patients end plates aligned.)
• The view is then further optimized with an oblique angle so that the articular elements divide the
intervertebral disc by one-third to two-thirds. The classic “Scottie dog” view (Figure 22-7).
• This view emphasizes the placement of the needle at the 6 o’clock position below the pedicle of the
superior vertebra. The needle tip is then placed within the posterior-superior quadrant of the
intervertebral foramen.
• Too much of an oblique view can lead to damage to the paraspinal structures such as the ureter and the
kidneys, where as a view that is not optimally oblique can prevent the needle from entering the foramen
altogether.
• The needle is placed initially under an oblique view and once the trajectory of the nerve is optimized
towards the target area, the view is changed to lateral so that the needle can be advanced in lateral
view thus preventing the needle from going too far anteromedially and touching the nerve root (Figure
22-8).
• The needle is halted just as it enters the intervertebral foramen.
• Contrast medium is then injected using a live/intermittent fluoroscopic views to confirm proper
placement and to identify any intravascular spread.
• The view is then changed to anteroposterior and further contrast is injected (Figure 22-9).
• The injectate can spread along the nerve root with or without any epidural spread depending on the
foraminal obstruction as well as the placement of the needle tip. Figure 22-10 shows epidural spread
of the contrast.
• A retrodiscal approach has been recently recommended where the needle is placed within the inferior
aspect of the foramen rather than the superior posterior quadrant described in the classic method of
transforaminal injection. The presence of radicular arteries along with the nerve root has prompted the
use of this approach.
Figure 22-7. (A, B) The classic “Scottie dog” view which is obtained using an oblique view. The degree
of obliquity will depend on the patient and the level of the spine and should not be considered as fixed for
a certain angle. The dot under the chin of the dog denotes the entry point for the transforaminal approach
which will place the needle lust posterior to the nerve root. Note the articular elements bisecting the disc
above by one-third laterally and two-thirds medially.
Figure 22-8. (A, B) Lateral views of the needle placement at L4-5 and L5-S1 levels.
Figure 22-9. (A, B) Anteroposterior views of the same patients as in Figure 22-8. Note the contrast
material spread along the nerve roots. In case of an intravascular spread, the contrast will not project the
same silhouette after a few seconds and in live view it can be seen taken up by the blood stream.
Figure 22-10. Epidural spread of the contrast from a transforaminal injection without much extra-epidural
spread.
EQUIPMENT
The equipment required for this procedure is no different than most of the interventional procedures for
the spine.
• A fluoroscopic machine or other advanced imaging is necessary. A machine with the capability of
digital subtraction angiography (DSA) is now preferred by some practitioners to recognize
intravascular injections.
• Regular kit for prep and drape.
• Needle choice depends on the physician. A blunt tipped or pencil point needle is recommended by
some to minimize the chances of intravascular/intraneural penetration. Others advocate smaller 22-
gauge needles to optimize patient comfort and decrease tissue disruption.
• The length of the needle is based on the patient’s body habitus and the level of the intended injection. A
3.5-in needle is considered standard, but in some cases a 5-in needle may be required for the L5-S1
level. A slight curve at the tip of the needle can help manipulate the needle without multiple
penetrations.
• Injectate includes a water soluble contrast medium, preferably a nonparticulate steroid and local
anesthetic.
• The amount of injectate should be limited to a maximum of 2 to 3 mL to prevent transient increase in
the pressure and to avoid the spread of injectate to multiple levels.
• Inclusion of a local anesthetic gives fast acting pain relief and can be confirmatory of the level of
pathology; however, a patient must be warned of its anesthetic effect and possible weakness in the legs.
POSTPROCEDURE FOLLOW UP
• Patients should be observed in the immediate postoperative period for any signs of spinal cord damage
such as lower extremity paresthesiae and weakness with or without increased back pain.
• Patient may feel increased muscle pain from the needle placement, which can be easily reduced with
an ice pack applied at the site.
• One of the most important aspects of post procedure instructions to the patient is to watch for any
lower extremity weakness from the injected local anesthetic.
• Patients are normally advised to rest for the day and resume normal activities the following day.
• A patient should also be instructed to report any fever (from infection), increased back pain, lower
extremity weakness (from a hematoma) and increased radicular symptoms (from nerve root
compression).
POTENTIAL COMPLICATIONS AND PITFALLS

• Damage to the nerve root is one of the most common occurrences if a needle is advanced too far and
touches the nerve root.
• Unrecognized intravascular injection may lead to further spinal cord damage.
• Increased myofascial pain due to muscle spasms from the needle placement.
• Loculation of the injectate can also lead to transient increase in perineural pressure. This can be easily
recognized during injection if the contrast does not get diluted while injecting the steroid and the
patient reports increase in radicular symptoms.
• Although a dural puncture is less likely form this approach, it can happen if the needle traverses too far
within the foramen.
Suggested Reading
Interventional techniques in chronic spinal pain. ASIPP, publishing.
Techniques in regional anesthesia and pain medicine, 2009;13(4):203-298. In: Diwan SA, ed. Epidural
Steroid Injections; Techniques for epidural injections, pp 217-228, Vikram B. Patel.
Interventional Techniques
Helm S II, Glaser SE, Falco FJE, Henry B. A medical-legal review regarding the standard of care for
epidural injections, with particular reference to a closed case (medical-legal review). Pain Physician.
2010;13:145-150.
Jasper JF. Lumbar retrodiscal transforaminal injection (technical update). Pain Physician. 2007;10:501-
510.
Manchikanti L, Boswell MV, Datta S, et al. Comprehensive review of therapeutic interventions in
managing chronic spinal pain EBM—guidelines. Pain Physician. 2009;12;E123-E198. Year updated
2009.
CHAPTER 23
Facet Joint Interventions: Intra-Articular

Injections, Medial Branch Blocks, and
Radiofrequency Ablations
Vikram B. Patel and Sukdeb Datta
INTRODUCTION
• The prevalence of persistent low back pain secondary to involvement of lumbosacral facet joints has
been described in controlled studies as varying from 15% to 45% based on types of populations and
setting studies. Lumbar facet joint interventions are used to diagnose as well as treat facet joint–related
pain.
• Prevalence of thoracic facet joint pain has been shown to be 34% to 48% in patients with chronic
thoracic back pain.
• Prevalence of cervical facet joint pain has been shown to be 36% to 67% in patients with chronic neck
pain.
INTRA-ARTICULAR FACET JOINT INJECTIONS AND MEDIAL

BRANCH BLOCKS
Indications
Common indications for diagnostic facet joint interventions include the following:
• Lumbar spine
Traumatic or arthritic nonradicular low back pain.
Patients can experience pain radiating in to the buttock but rarely radiating beyond the level of the
knee.
Pain on palpation is worse with extension of the lumbar spine and rotation or twisting of spine.
• Thoracic spine
Traumatic or arthritic nonradicular upper back or posterior chest wall pain.
Typically the patient experiences pain on palpation and extension and rotation or twisting of
thoracic spine.
• Cervical spine
Traumatic or arthritic neck pain, suboccipital headache, persistent and disabling axial neck and/or
upper thoracic pain or suspected cervicogenic headache
Typically pain and/or headache with neck movements in flexion, extension, and rotations
• Duration of pain of at least 3 months
• Average pain level of >5 on a scale of 0 to 10
• Intermittent or continuous pain causing functional disability
• Failure to respond to more conservative management including physical therapy modalities with
exercises and nonsteroidal anti-inflammatory agents
• Lack of evidence either for discogenic or sacroiliac joint pain
• Lack of disk herniation or evidence of radiculitis
CONTRAINDICATIONS
Common contraindications for facet joint interventions include the following:
• Suspected or proven discogenic, sacroiliac joint or myofascial pain in case of lumbar facet
interventions
• Allergies to drugs being considered for the procedure
• Inability of patient to understand consent, nature of the procedure, needle placement, or sedation
• Localized or generalized infection
• Anticoagulation therapy
• Nonaspirin combination antiplatelet therapy
• Pregnancy
• Bleeding diathesis
• Needle phobia
• Psychogenic pain
RELEVANT ANATOMY
Lumbar Spine
• Facet joints (Figure 23-1)
Figure 23-1. Lumbar spine and facet joints. Note the varying angles of the facets from top to bottom.
Lumbar facet joints are formed by the articulation of the inferior articular process of the superior
lumbar vertebra with the superior articular process of the inferior vertebra.
The lumbar joints exhibit features of typical synovial joints.
The articular facets are covered by articular cartilage, and the synovial membrane bridges the
margins of the articular cartilage of the two facets in each joint.
Surrounding the synovial membrane is a joint capsule that attaches to the articular process, a short
distance beyond the margins of the articular cartilage.
• Ligaments
Ligaments connect spinous process, lamina, and bodies of the adjacent vertebrae.
Anterior and posterior longitudinal ligaments help stabilize the joints.
The articular capsule surrounds facets and allows gliding motions.
In the lumbar spine, L4-L5 permits most flexion.
The anterior longitudinal ligament attaches to the anterior bodies and the intervertebral disk. It is
strong and prevents hyperextension.
The posterior longitudinal ligaments attaches to the posterior aspect of the vertebral bodies and
intervertebral disks. It is weaker than the anterior longitudinal ligament and permits hyperflexion.
Ligamentum flavum connects adjacent laminae of vertebrae and limits flexion. Interspinous
ligaments connect the spinous processes. These are weak ligaments. Intertransverse ligaments
connect the transverse process and are also weak ligaments.
• Innervation (Figure 23-2D)
Figure 23-2. (A-E) Cervical, thoracic, and lumbar medial branches.
The capsules of the lumbar facet joints are richly innervated with encapsulated and unencapsulated
free nerve endings.
Lumbar facet joints are appropriately equipped with sensory apparatus to transmit nociceptive and
proprioceptive information.
Each lumbar facet joint has dual innervations being supplied by two medial branches of dorsal
rami (Figure 23-2D).
Figure 23-3. Thoracic facet joints: Note the slanted angles at the middle levels and compare with the
upper and lower facets. The interspinous opening for epidural access is minimal in the mid thoracic
levels where the angles of the facets are most slanted.
The medial brunches of the L1-L4 dorsal rami have a constant and similar course.
Each nerve emerges from its intervertebral foramen and enters the posterior compartment of the
back by coursing around the neck of the superior articular process.
Hugging the neck of the superior articular process, the medial branch passes caudally and slightly
dorsally covered by mamillo-accessory ligament, hooking medially around the caudal aspect of the
root of the superior articular process to enter the multifidus muscle.
Intermediate and lateral branches arise from the dorsal ramus at the same point as the medial
branch.
The medial branch finally crosses the vertebral lamina where it divides into multiple branches that
supply the multifidus muscle, the intraspinous ligament and muscle, and ligament and the two facet
joints.
The medial branch of the L5 dorsal ramus has a different course and distribution than those of the
L1-L4 dorsal rami. Instead of crossing a transverse process, the L5 dorsal ramus crosses the ala of
the sacrum.
The L5 dorsal ramus is much longer than the typical lumbar levels.
From the L5-S1 intervertebral foramen, the medial branch of the L5 dorsal ramus runs along the
groove by the junction of the ala and the root of the superior articular process of the sacrum before
hooking medially around the base of the lumbosacral facet joint (Figure 23-2D).
Thoracic Spine (Figure 23-3)

• Facet joints
The thoracic spine has unique features that differentiate it from the lumbar spine.
Each thoracic vertebra is distinguished by costal facets on the side of the body, and all but the last 2
or 3 segments by articular facets on the transverse process, articulating respectively with the heads
and tubercles of the ribs.
The laminae are short, thick, broad, and overlap each other like roof tiles from above downward.
The typical spinous process slants posteriorly and downward overlapping between T5 and T8 and
being less oblique above and below this level.
Projecting upward at the junction of the lamina and pedicles are the superior articular processes
facing backward, upward, and laterally.
The articular processes of adjoining thoracic vertebrae form synovial joints, which permit a limited
degree of movement, primarily facilitating axial rotation.
The primary axis of rotation for the mid-thoracic segments is located close to the anterior region of
the thoracic intervertebral disk.
The lower thoracic zygapophysial joints (facets) provide specialized features with the
characteristics of this region. There is greater developmental of the mamillary processes, which
originate as extension of the superior articular process.
The mamillary process provides attachment for the multifidus muscle as it covers this medially to
attach onto the spinous process of the segments above.
Small intra-articular synovial folds may be found within the thoracic facet joints. Intra-articular
synovial folds originate medially from tissues adjacent to the ligamentum flavum and extend
varying distances into the medial joint cavity filling spaces within the joint with fibrofatty tissue.
The articular surface of the thoracic facet joint is inclined to 60 degrees from the horizontal to the
frontal plane and rotated 20 degrees from the frontal to the sagittal plane in a medial direction.
The lateral aspect of the thoracic joint is placed anterior and the medial aspect of the joint is placed
posterior.
The superior articular facet from the inferior vertebrae is almost flat and faces posterior, superior,
and slightly lateral.
The inferior articular facet is oriented in a reciprocal manner. There is variation in the inclination of
the joints by region with the mid-thoracic level approximately 60 degrees off the horizontal plane
while the upper segment has a more vertical orientation.
In contrast to the lumbar spine, the superior and inferior articular processes of the thoracic spine
cannot be identified separately because the joints are mostly in the frontal plane and do not face
sideward.
The articular pillar is wider in the thoracic level, and it extends further laterally in relation to the
vertebral bodies.
The articular facets are covered by articular cartilage, and the synovial membrane bridges the
margins of the articular cartilage of the 2 facets in each joints.
Fluoroscopic visualization is more difficult.
There is no fibrous capsule on the ventral aspect of the joint. Within interspace, the ligamentum
flavum is in direct contact with the synovial membrane.
• Innervation of the thoracic facet joints (Figure 23-2C)
The thoracic facet joints receive bisegmental innervations from the medial branch of the dorsal
ramus of the upper segment and one more cephalad level.
The medial branches of the thoracic dorsal rami were found to have a reasonably constant course
except at mid-thoracic level (T5-T8).
The medial branches of the thoracic dorsal rami at mid-thoracic levels do not run on bone. Instead,
they are suspended in the intertransverse space.
Thoracic medial branches are not that close to the facet joint as they swing laterally to circumvent
the multifidus muscle.
The dorsal ramus is separated from the ventral ramus (that is, the intercostal nerves) by the anterior
part of the superior costotransverse ligament.
In the thoracic region, the dorsal ramus is short, common trunk of 3 mm to 5 mm, which bifurcates
immediately dorsal to the superior costotransverse ligament into a medial and lateral branch.
The medial branches supply the adjacent intrinsic muscles of the back, the facet joints and skin in
the upper thoracic region; the lateral branches supply intrinsic muscles, costotransverse joint, and
the skin in the lower thoracic spine.
Spinous processes of T1-T3 and T11-T12 are located approximately at the level of the facet joint of
adjoining level and the one below; T2 spinous process relates to T2-T3 facet joint level.
Spinous processes T4-T10 are located halfway between the adjacent facet joints and the joints
below.
Cervical Spine (Figure 23-4)

Figure 23-4. Cervical spine and facets.
• Cervical facet joints from C2-C3 to C7-T1

The atlanto-occipital and the atlanto-axial synovial joints are also present in the cervical spine as
two paired joints, but are not considered to be facet joints as they are anterior rather than posterior
spinal structures. (See Chapters 14 and 15.)
The cervical facet joints are formed by the inferior articular process of the superior vertebral
segment and the superior articular process of the inferior vertebral segment.
The superior aspect of the facet joint faces forward and downward at 45 degrees, whereas the
inferior aspect of the facet joint faces backward and upward at 45 degrees.
The facet joints in the cervical spine form paired vertebral column or “pillar” which together with a
discovertebral unit provides the 3-prong structural support for this cervical segment.
The obliquity of the facet joints allows degrees of flexion, extension, and rotation.
The articular facets are covered by articular cartilage, and a synovial membrane bridges the
margins of the articular cartilage of the 2 facets in each joint.
The cervical facet joints may contain a variety of intra-articular inclusions with fibroid-exposed
meniscoid being the most common inclusions.
The average joint volume is >1 mL.
• Innervation (Figure 23-2A, B, E)
The cervical facet joints are well innervated by the medial branches of the dorsal rami. The fibrous
joint capsule is richly innervated with mechanoreceptors as well as nociceptive receptors.
The innervation of the atlanto-occipital and atlanto-axial joints is derived from C1 and C2 root,
respectively.
Cervical facet joints below C2-C3 are supplied by the medial branches of the cervical dorsal rami
above and below the joint.
The C2-C3 joint is also supplied by the third occipital nerve.
Each C3-C7 dorsal ramus crosses the same segments, transverse process, and divides into lateral
and medial branches.
The medial branch crosses around the waist of the articular processes of the same numbered
vertebra.
The medial branches are bound by fascia, held against the articular pillar and covered by the
tendinous slips of the origin of the semispinalis capitis.
Articular branches arise as the nerve approaches the posterior aspect of the articular pillar within
ascending branch innervating the joint above and a descending branch innervating the joint below.
At C7, in contrast to C3-C6, the medial branches are located at the higher level due to the transverse
process. At C7, the base of the transverse process occupies most of the lateral aspect of the
articular pillar pushing the medial branch higher.
The course of the C4 and C5 medial branch nerves has been shown to be relatively constant
crossing the waist of the respective articular pillars.
The C3, C6, and C7 medial branches show more variations compared to C4 and C5. The C3 medial
branch nerve, with its more superior location at the upper thirds of the C3 articular pillar, often
localize the third occipital nerve with the third occipital nerve being rostral through the C3 medial
branch.
The C3 medial branch and the third occipital nerve have a common origin in the C3 dorsal ramus.
The C6 medial branch crosses around the waist of the articular pillar above it, between the waist
and the superior articular process.
The majority (70%) of C7 medial branches are located high on the C7 articular pillar and across the
C6-C7 facet joint. However, a few may be lower on the C7 transverse process.
The distance between the nerves and bone varies from close proximity to separation by 2 mm
through 3 mm.
The C2-C3 facet joint is largely innervated from the third occipital nerve, which is the superficial
medial branch of the C3 dorsal ramus. The deep medial branch of the C3 dorsal ramus is referred
to as the C3 medial branch.
Articular branches may also arise from a communicating loop that crosses the back of the joint
between the third occipital nerve and the C2 dorsal ramus.
The third occipital nerve (TON) continues around the lower lateral and dorsal surface of the C2-
C3 joint embedded in connective tissue that invests the joint capsule.
• Anticoagulation is less of a concern than for epidural injections, but a concern nonetheless as there is
inherent destruction of tissue from introduction of a needle.
• Physical examination of the area for infection, skin ulceration, and necrosis and extent of disease.
• The patient must be able to lie prone for the internal length of the procedure.
• Intravenous access for IV fluid and medications for sedation or hypotension if the patient experiences
vasovagal reaction.
• Evaluation for injectable contrast allergy.
• Use of contrast agent has been area for controversy. At present, according to Medicare Guidance, use
of contrast agents for proper placement of needle is advocated.
Lumbar Facet Joint Interventions

1. Lumbar facet joint intra-articular injections
Patient position
The patient is placed in the prone position on the fluoroscopic table.
A rolled towel or a pillow can be placed under the abdomen to facilitate easier entering the
joint by reducing the lumbar lordosis.
Fluoroscopy
As with any lumbar interventions, a baseline AP fluoroscopic view of the lumbar spine is
obtained, and the fluoroscopy is oriented.
Fluoroscopy beam is rotated from the anteroposterior view toward the oblique view until the
posterior borders of the target facet joint are visible.
The upper lumbar face joints are typically aligned toward the sagittal plane and may be visible
on AP imaging, whereas the lower facet joints are typically oriented toward the coronal planes
so that oblique imaging is necessary to identify the joint lines.
Procedural steps
The target joint is then visualized under fluoroscopic guidance, and the skin may be marked.
A 22-25-gauge 3.5-inch spinal needle (depending on body habitus) is then inserted through
anesthetized area (Figure 23-5A, B).
The needle is directed downward and obliquely (from lateral to medial) toward the selected
joint under direct fluoroscopic visualization, and contact is then made with the inferior articular
process (Figure 23-5A, B).
The needle is then withdrawn slightly and redirected to the target facet joint. As the needle is
felt to penetrate the joint, advancement is stopped to prevent any potential damage to the
articular cartilage.
If there is difficulty in obtaining capsular penetration, one may try to access the articular recess
by redirection of the needle just off the margins of the inferior articular process.
Another method of getting intracapsular entry is to redirect a needle slightly medial or lateral to
the posterior joint line so that the needle gains access via its medial placement through the
insertion of the capsule on the articular process.
Once the needle is in an appropriate position, 0.2 to 0.25 mL of contrast can be injected under
low pressure into the joint to confirm proper placement (Figure 23-6A, B). An arthrographic
image can then be visualized.
During contrast injection, outline of the oval shape joint capsule should be visualized without
any vascular uptake and/or epidural spread.
After contrast confirmation of intra-articular needle replacement, the joint is injected with
anesthetic agent to complete a diagnostic block, or in combination with the steroid for a
therapeutic injection.
Figure 23-5. (A, B) Proper alignment of the lumbar facet joint posterior borders. Note that the best view
may not be the best entry point as that would represent the middle portion of the joint rather than the
posterior borders which would be visible at lesser oblique angles, especially at the lower levels. Note
the higher obliquity of the lower levels.
Figure 23-6. (A, B) Intra-articular injection. Not the contrast pattern within the joint. The upper and
lower poles of the capsule for the “S” shape of the contrast pattern. Occasional capsular foramen may be
seen with contrast spread within the epidural space.
Lumbar Medial Branch Blocks (Figure 23-7A, B)

Figure 23-7. (A, B) Lumbar medial branch blocks. The contrast pattern for the upper levels is often
described as a “blind fold” over the “Scotie dog’s” eyes (left image). The L5 medial branch is blocked at
the junction of the ala of the sacrum with its superior articular process. In this case (right image), a
common anomaly is seen. This is the winged transverse process of the L5 vertebral body which may
mimic the sacral ala.
To block the sensory innervation to the lumbar facet joint, it is necessary to block the 2 medial branch
nerves which supply the joint.
• Block the medial branch at the transverse process of the same level of the joint.
• Block the medial branch at the level below the joint.
• To block the L3-L4 facet joint, block the L2 medial branch at the transverse process of the L3, and L3
medial branch at the transverse process of L4.
• Similarly, to block the L5-S1 facet joint, block the L4 medial branch at junction of superior articular
process and transverse process of L5 and the L5 dorsal ramus at the junction of superior articular
process of sacrum with the sacral ala.
• The lumbar medial branch blocks have essentially replaced intra-articular injections in the diagnosis
of lumbar facet joint pain because they are relatively easier to perform and safer.
• Intra-articular injection of the lumbar facet joints lacks significant therapeutic utility, whereas medial
branch blocks have therapeutic utility, diagnostic utility, and can help predict the results of a
radiofrequency ablation of the nerve.
Technique for L1 to L4 Medial Branch Block
Prone position (oblique [posterolateral] approach)
The patient is positioned in the prone position with pillow under the abdomen if needed. C-arm is
adjusted to an oblique position.
To optimally visualize the landmarks for this “Scotty dog” configuration, an approximately 25 to 30
degree angle is necessary depending on the specific level from L1-L4 medial branches.
The needle is advanced toward the dorsal aspect of the root of the transverse process to ensure safe
needle depth away from the ventral ramus.
Needle placed down to contact bony endpoint utilizing oblique fluoroscopic imaging. Prior to
injection, final needle depth position should be confirmed using both AP and lateral imaging to
ensure that the needle tip is neither too deep nor too medial or by orthography.
On AP imaging, the tip of the needle should be at least in line with the lateral margin of the silhouette
of the superior articular process and if possible medial to this margin.
On lateral imaging, the needle tip should be within the confines of the shadow of the dorsal elements
and not protruding into the foramen.
The superior articular process frequently bulges laterally overlying the target point dorsally. If the
needle appears lateral to this point, it has contacted a thick transverse process instead of the
superior articular process. In this case, the needle usually needs to be adjusted dorsally until the
correct position is obtained on both the AP, oblique, or lateral views.
Before injection, the bevel opening should be medial and slightly inferior to reduce lateral and
superior flow to the intervertebral foramen, especially the needle is placed inadvertently higher than
the target position.
L5 dorsal ramus blocks
The patient is positioned prone with a pillow under the abdomen.
Begin with an AP view of the L5-S1 segment. Rotate the fluoroscope approximately 10° to 15°
oblique toward the site to be blocked to view the junctions of the sacral ala and the superior
articular process of S1.
Further obliquity usually places the medial iliac crest in front of the trajectory to the target position.
If the ilium obscures the view of the target point as the C-arm is rotated obliquely, cephalad tilt of
C-arm would usually bring the target into clear view by moving the ilium caudad within the
fluoroscopic image.
A curved needle tip will allow for adequate steering of the needle to the target despite a cephalad-
to-caudad needle entry point.
Once a clear path to the target point for the L5 dorsal ramus is identified, a skin insertion point is
chosen. The target point is recognized as a notch between the sacral ala and the superior articular
process of S1. The target point lies opposite the middle of the base of the superior articular process
and that is likely below the silhouette on top of the sacral ala.
Higher placement is associated with spread into L5-S1 epidural space and lower placement with
spread through the S1 posterior sacral foramina.
The needle is advance directly “down the beam” to the target position.
Anteroposterior imaging is obtained to verify that the needle is placed at appropriately medial to the
lateral silhouette of the S1 superior articular process.
Lateral imaging should confirm that the needle tip lies within the shadow of the posterior spinal
elements and does not protrude into the L5-S1 neural foramina.
After the needle tip confirmed to be in the proper location, the bevel opening should be rotated
medially. This has been shown to reduce the inadvertent spread to the S1 posterior foramen or the
L5-S1 vertebral foramen.
Radiofrequency Ablation of Lumbar Medial Branches (Figure 23-8A, B)
Figure 23-8. (A, B). Needle placement for RF ablation of the lumbar medial branches. Note the tangential
placement of the needle to maximize the contact with the medial branch.
• After a successful medial branch block trial done twice, one can proceed with radiofrequency ablation
of the medial branches for long-term desensitization of the facets.
• The diagnostic blocks should be performed twice using different local anesthetics in minimal amounts
(no more than 0.5 mL for lumbar region at each level).
• As mentioned earlier, each joint is supplied by two different medial branches (one at the same level
and one below) and for complete denervation of a joint both these medial branches need to be ablated.
• The fluoroscopic view is similar to the medial branch block view and should be optimized for each
level.
• The traditional method is to place the radiofrequency needle parallel to the medial branch via a
tangential approach.
• The needle entry is usually performed a level below the intended target level for a tangential approach
to the medial branch.
• Usually a 10-cm radiofrequency needle with a 10-mm active tip (straight or curved) is used for the
lumbar region.
• Once the needle tip is positioned at the junction of the superior articular process and the transverse
process of the vertebra, an AP and lateral view is obtained to confirm proper position of the needle tip
posterior to the neural foramen.
• Impedance is optimized at the tip of the needle between 300 to 500 Ohms. Lower impedance might
result from intravascular penetration and high impedance is likely from the needle being too deep
beyond the periosteum.
• Sensory and motor testing is then performed with a patient who is wide awake and responsive.
• Sensory perception is optimized at about 0.2 V with the stimulation felt only in the lower back and not
beyond the buttocks at 1 V.
• Motor stimulation is usually about 3 times higher than the sensory stimulation and should only stimulate
the lumbar paraspinal muscles at 3 V.
• This confirms that the needle tip is far away from the exiting nerve root and avoids any damage to the
nerve root.
• After the optimal stimulation is confirmed and the fluoroscopic views are optimal as well, local
anesthetic is injected. Some practitioners also like to use a small amount of steroid along with the local
anesthetic to minimize post procedural inflammation.
• Total amount of injectate should not exceed 0.5 mL to avoid spillage on to the nerve root.
• Radiofrequency lesioning is then carried out with temperature setting of 80°C for 90 seconds.
Thoracic Facet Joint Interventions (Figure 23-9A, B)

Figure 23-9. (A, B) Thoracic facet joint injections.
Intra-Articular Injections
Thoracic facet joints are not clearly evident in AP view. The location is estimated from the location of the
thoracic pedicles.
• Thoracic facet joint entry involves 22- to 25-gauge needle into the target joint.
• The target joint can be gauged to lie between the two pedicles getting the same segmental number as the
target joint.
• Thoracic facet joints cannot be entered directly from behind due to the orientation in the coronal plane,
and they cannot be entered laterally due to risk of pneumothorax.
• The surface entry from below requires an initial insertion of the needle approximately 1 to 2 segments
below the target joint.
• With intermittent fluoroscopy visualization, the needle is inserted through the skin cephalad toward the
superior articular process.
• The needle should remain on an imaginary vertical line connecting the mid portion of the target at facet
joint and the one below. If the needle stays in this line without deviation either medial or lateral, it
would be safe. Risks with deviation of the needle include entering the epidural space in the spinal cord
or the pleural space in the lung.
• After insertion of the needle approximately 4 to 5 cm, or once the needle tip is seen to lie at the mid to
inferior aspect of the pedicle, the fluoroscope is rotated away from the side being injected until the
outline of the joint is clearly visible (almost the lateral position).
• Following this, the needle is advanced through the capsule into the inferior aspect of the joint.
• After the needle is inserted into the inferior aspect of the joint, contrast is injected and after
confirmation, local anesthetic and/or steroid may be injected.
• For superior levels from T1-T2 and T5-T6, a more perpendicular approach to the facet joints is
needed. At these levels on AP imaging, skin entry is usually at the mid portion of the vertebral body
rather than its inferior aspect.
Thoracic Medial Branch Blocks (Figure 23-10)
Figure 23-10. Radiofrequency ablation. The medial branch can be lysed along its path from the junction
of the transverse and superior articular process to the interior aspect of the joint traversing over the
lamina. At this level it is not “plastered” to the lamina but rather freely floating above it. A medial to
lateral angle is preferred.
To block the nerve supply in thoracic facet joint, two medial branches must be blocked due to dual
innervation of each facet joint.
• It was originally thought that in the thoracic region, placement of the needle would be best performed
akin to the lumbar region with the needle tip ending at the junction between the superior articular
process and transverse process. However, anatomical studies have shown that the pathway of the
medial branch is not at the indicated location.
• In the thoracic region, the optimal location for a medial branch of radiofrequency neurotomy procedure
would be at the superolateral corner of the transverse process.
• The nerves through a particular joint are those that cross the transverse process above the joint and the
transverse process below the joint.
• Numerically if the joint to be blocked is the T2-T3 joint, the transverse processes required are T1-T2
to block the T2 medial branch at the T1 and T3 medial at the T2.
• For medial branch block at T8-T10, the target transverse process should be differentiated from the rib
that lies in front, and its upper margin projects slightly above the transverse process.
• At the T12 level, the medial branch of the thoracic dorsal rami assumes a course that is similar to the
lumbar region. The T12 medial branch assumes the course exactly on typical lumbar medial branch
lying at the junction of the superior articular process and the transverse process.
• For needle placement from T1-T4 and T9-T10, the needle is positioned directly overlying the target
point of the nerve. The needle must be advanced, and the contact is made with the target transverse
process, with subsequent adjustment of the needle to rest from the back of the superolateral corner of
the transverse process.
• Contrast and local anesthetic, with or without steroids may be injected at this point.
• For medial branch block at T5-T8, the aim is to position the needle on to the nerve that passes dorsally
and caudally just above and slightly dorsal to the typical target joint on the superolateral corner of the
transverse process. The depth of the needle placement is the same as the depth of the transverse
process.
• Following the confirmation of the position of the needle, contrast and local anesthetic, with or without
steroids may be injected.
Radiofrequency Ablation of Thoracic Medial Branches
of the medial branches for long-term desensitization of the facets.
(no more than 0.5 mL for thoracic region at each level).
and one below) and for complete denervation of a joint both these medial branches need to be ablated.
level.
tangential approach.
• The needle entry is usually performed a level below and slightly medial to the intended target level for
a tangential approach to the medial branch from medial to lateral angle, which helps minimize the
chances of accidental pneumothorax.
• Usually a 10-cm radiofrequency needle with a 10-mm active tip (straight or curved) is used for the
thoracic region but some prefer a smaller needle.
• Impedance is optimized at the tip of the needle between 300 to 500 Ohms. Lower impedance might
beyond the buttocks at 1 V.
the lumbar paraspinal muscles at 3 V.
nerve root.
• Total amount of injectate should not exceed 0.5 mL to avoid spillage onto the nerve root.
• Cooled radiofrequency is also a great option for thoracic region especially as the medial branches are
not exactly plastered to the bone itself and hence are sometimes missed with traditional needle
placement.
• A cooled radiofrequency lesion is much larger and spherical rather than egg shaped and has a better
chance to ablate the nerve.
Cervical Facet Joint Interventions

Intra-Articular Cervical Facet Joint Injections (Figure 23-11)
Figure 23-11. Cervical intra-articular injection. A posterior approach is safer and preferred. Although
recent evidence does not support this procedure (in favor of Radiofrequency ablations of the medial
branches), many practitioners still prefer it for inflammatory facet syndrome. The upper part of the image
shows the facets that are not aligned properly. The lower part of the image shows properly aligned facets
and articular pillars with parallax removed.
Posterior approach
The posterior approach for cervical intra-articular facet joint blocks can be performed with the
patient in a prone position, or if required in a sitting position. It involves introducing a 22- to 25-
gauge needle into the target joint from behind, along an oblique trajectory that coincides with the
plane of the joint.
The patient is placed in the prone position with a cushion under the chest with the head and neck
completely prone; however, the neck may be rotated to the side opposite the needle insertion.
Skin entry point is carried out approximately two or more segments below the target joint. The skin
entry is determined by identifying the lateral aspect of the facet joint: on prone fluoroscopic
viewing.
The needle is directed upward and ventrally through the posterior neck muscles until it makes
contact through the posterior surface of the articular pillar below the target joint. Following the
above step, the needle may be readjusted until it enters the joint cavity.
This may require inferior, posterior, anterior, and lateral fluoroscopic visualization to ensure that the
needle stays on course. Directing the needle medially toward the interlaminar space may result in
epidural or intrathecal puncture and/or spinal cord trauma.
After satisfactory localization of the needle into the joint, water-soluble contrast medium is injected
to obtain an arthrogram and verify accurate placement. Then, local anesthetic and/or corticosteroid
is injected for diagnostic or therapeutic purposes.
Due to the risk of pneumothorax and proximity of other neurovascular structures, the posterior
approach is often preferred for C7-T1 facet joints.
The C2-C3 joint may be technically more difficult to visualize and enter due to anatomic features.
The C2-C3 joint is more angulated vertically and medially and not clearly evident on lateral views.
For the C2-C3 joints, the posterior approach may be modified by rotating the patient’s head to bring
the cavity of the C2-C3 joint into view as it rotates forward on the lateral access of the vertebral
column.
Benefits of the posterior approach
The posterior approach is considered safe since the needle penetrates only the skin and partially
posterior neck muscles with the deep cervical artery the only structure at risk of inadvertent
puncture.
Posterior cervical artery poses minimal risk of morbidity as it supplies no major structures.
Risks of the posterior approach
Penetration of the anterior joint capsule moving into the neural foramen and into the vicinity of the
dorsal root ganglion, the cervical radicular artery and/or vertebral artery, epidural space, and spinal
cord.
Leakage of the local anesthetic and steroid into the dorsal root ganglion.
Lateral approach
Patient position
The patient is positioned lying on his or her side with the target side up. The shoulders are
pulleddown to avoid obscuring the joints in the fluoroscopy and rotated slightly posterior, over
25% into the plane of the upper torso and shoulders. The target joint is identified on lateral
imaging of the neck.
Fluoroscopy
Lateral fluoroscopic imaging must appropriately identify both joints so that the upper most target
joint is differentiated from the downside contralateral joint. This can be done by precisely
superimposing one joint over the other (true lateral view) or by offsetting the joints adequately to
view them independently (oblique view).
Technical steps
The needle is introduced through the skin over the midpoint of the joint. Then, the needle is advanced
deeply until it makes contact through the bone of either the superior or inferior articular process.
Once the correct joint is clearly identified, the needle is advanced until the superior articular
process is contacted just above the joint line. The needle is then directed and advanced through the
joint capsule. The needle may be felt to pierce the capsule and to enter the joint space. Only minimal
penetration is required.
The appropriate position onto the joint is confirmed by injection of a small dose of a contrast
medium to obtain an arthrogram.
The C2-C3 joint may be technically more difficult to visualize due to anatomic features. The C2-C3
joint is more angulated vertically and medially and is not clearly evident on lateral views.
Benefits of the lateral approach include: The lateral approach is considered technically less
demanding. It is more comfortable for the patient because less soft tissue is encountered. The risk of
morbidity is minimal.
Risks of lateral approach include: Aggressive maneuvering or over-penetration may enter the needle
into the epidural space or spinal cord.
With the lateral approach, to ensure safety, needle must remain posterior to the ventral ramus and the
vertebral and radicular arteries.
The C3-C4, C4-C5, and C6-C7 joint injections are easily performed using the lateral approach with
no disadvantages compared to the posterior approach.
The C7-C1 joint injection may be more easily performed at the posterior approach.
In a patient with a large neck and shoulders, C7 and T1 may not be reached from a lateral approach
and may require the posterior approach.
The C7-T1 may also require a much deeper superior to inferior approach than other mid-cervical
levels to minimize the possibility of contacting more inferior neurovascular and pleural structures.
Low volumes must be injected into the cervical facet joints. A volume of >1 mL is injected or
injection is carried out rapidly or forcefully. The joint capsule may rupture and/or medication may
spread into neighboring structures.
A communicating pathway exists in 80% of subjects within the facet joint and the interlaminar space,
the opposite facet joint, the extradural space and/or the interspinous space when volumes in excess
of 1 mL are injected.
Even with smaller volumes, extra-articular leaks have been observed in about 7% of the cases.
Cervical Medial Branch Blocks (Figure 23-12A-C)

• To block the nerve supply of single cervical facet joints, 2 medial branches much be blocked due to
dual innervation of each facet joint.
• The target points for these nerves, other than the third occipital nerves, are crossing points of the waist
of the articular pillar; these points may be reached by needles using either a posterior, lateral, or
anterior approach.
• Posterior and lateral approaches are mostly commonly utilized.
Figure 23-12. (A-C) Cervical medial branch blocks. The most important aspect of the procedure is
proper alignment of the articular pillars and removal of parallax between the right and left side. The
image on the left shows mal-aligned articular pillars which are then aligned (right image) by adjusting the
C-arm. The medial branch is blocked at the midpoint of the articular pillar. Lateral (lower image) as well
as posterior approaches are preformed.
Posterior approach
The patient is placed in prone position with a pillow under the chest. The head is maintained looking
straight downward in a neutral position or it turns to the side opposite the needle insertion. A PA
view is obtained to identify the posterior aspect of the waist of articular pillars from C3 through C7.
After the identification of the waist of articular pillars at the levels to be blocked, a 22- to 25-gauge,
2- to 3-in spinal needle is inserted through the skin.
Once the needle has made contact with the bone, it is readjusted laterally through the deepest point of
the concavity where the C3-C7 medial branches lie.
Initially directing the needle medially to bone ensures that the needle is not placed too deeply. The
needle is then directed laterally until the tip reaches the lateral margin of the waist of the articular
pillar.
The needle should barely slip off the bone laterally in a ventral direction of the deepest point of the
articular pillars concavity.
Lateral images may ensure that the needle tip rest at the centroid of the articular pillar.
Centroid is defined as an intersection of the two diagonals of the diamond shaped pillar.
The C8 medial branch is blocked by placing the needle on to the transverse process of T1 and then
directing it until it lies at the superolateral border of the transverse process.
Lateral viewing of the needle tip, location may be difficult below C6.
Moving the C-arm to an oblique projection may help to identify needle depth by moving the
shoulders out of the line of the fluoroscopic view.
Lateral approach
The lateral approach in the supine position is reported to allow for a much greater patient tolerance
by the proponent.
The lateral approach is described as a fast well tolerated effective procedure.
The direction of the x-rays is used in the procedure as a technique to avoid contact with exiting
segmental nerves.
The lateral approach may also be used with the patient’s target site.
Articular pillars are identified by lateral fluoroscopy.
The upper most articular pillar can be distinguished from the opposite side by moving the
fluoroscope. The needle will be seen to travel with the upper most articular pillar as the two
articular pillars separate on the fluoroscopic image.
This approach is suited for C3-C6 medial branches.
The needle is directed through the skin and posterolateral neck muscle toward the centroid of the
articular pillar as seen on two lateral radiographs.
To block the C7 medial branch by the lateral approach, the needle is advanced so that it stays within
the confines of the C7 articular process, which prevents excessive advancement into the C8 foramen
and toward the vertebral artery.
Once the superior articular process is contacted, anteroposterior imaging should verify that the
needle lies against the lateral aspect of the superior articular process.
With posterior and lateral approaches, contrast in doses of 0.1 to 0.2 mL may be injected to confirm
a appropriate needle placement. However, contrast injection is not mandatory.
After confirmation of the medial placement, local anesthetic with or without steroid is injected
incrementally around the nerve.
Radiofrequency Ablation of Cervical Medial Branches (Figure 23-13A-D)
Figure 23-13. (A, B) Cervical medial branch radiofrequency ablation using lateral approach. This
approach is best for pulsed RF lesioning. (C, D) Cervical RF posterior approach. Note the optimized
view with collimation.
of the medial branches for long term desensitization of the facets.
(no more than 0.25 mL for cervical region at each level).
and one above - above and below the intended facet joint) and for complete denervation of a joint both
these medial branches need to be ablated.
level. Lateral approach is preferred for pulsed RF lesions (Figure 23-13A, B) and a posterior
approach is preferable for thermal conventional RF lesioning.
posterior approach (Figure 23-13C, D).
• The needle entry is usually performed a level below the intended target level for a slightly tangential
approach to the medial branch.
• Usually a 22-gauge, 5-cm radiofrequency needle with a 4- or 5-mm active tip (straight or curved) is
used for the cervical region.
• Impedance is optimized at the tip of the needle between 300 and 500 Ohms. Lower impedance might
beyond the shoulder at 1 V.
the cervical paraspinal muscles at 2 V. Most patients cannot tolerate the motor stimulation beyond 2 V
as it becomes painful.
nerve root.
• Total amount of injectate should not exceed 0.25 mL to avoid spillage on to the nerve root and the next
level (which may hamper the test stimulation).
SIDE EFFECTS AND COMPLICATIONS

Complications from facet joint nerve blocks or intra-articular injections in the lumbar spine are
exceedingly rare.
• The most common complications of the intra-articular injections and medial branch blocks are
twofold: complications related to placement of needle and complications related to administration of
various drugs.
• Most problems such as local swelling, pain at the site of the needle insertion, and pain in the spine,
extremities, or head are short lived and self-limited.
• Complications may include dural puncture, spinal cord trauma, subdural injection, neural trauma,
injection into the intervertebral foramen, and hematoma formation, infectious complications including
epidural abscess and bacterial meningitis, and side effects related to administration of steroids, local
anesthetic, and other drugs.
• Other minor complications include lightheadedness, flushing, sweating, nausea, hypotension, syncope,
pain at the injection site, and nonpostural headaches.
• Side effects related to administration of steroids are generally attributed to chemistry or the
pharmacology of the steroids. The major theoretical complications of corticosteroid administration
include separation of the pituitary-adrenal excess, Cushing syndrome, osteoporosis, avascular necrosis
of bone, steroid myopathy, epidural lipomatosis, weight gain, fluid retention, and hyperglycemia.
• The evaluation of the effect of neuraxial steroids and weight and bone mass density show no significant
differences in the patient undergoing various types of intervention or techniques with or without
steroids.
• Radiofrequency ablations can cause increased muscular pain and spasms after the procedure especially
in the cervical region.
• Nerve root damage may occur in absence of proper placement and failure to confirm the needle tip
posterior to the foramen.
CHAPTER 24
Lumbar Facet Joint Cyst Drainage and Injection

Gerard P. Varlotta, Christopher Gharibo, and Z.T. Traeger
INDICATIONS
The indications for injections of the facet joint include:
• Facet-mediated low back pain
• Diagnostic blocks of facet-mediated low back pain
• Paravertebral spasm
• Facet joint arthritis
• Facet joint effusions
• Facet-mediated pain in rheumatoid arthritis
• Facet-mediated pain in ankylosing spondylitis
• Patients with relief from anesthetic blocks of the facet joint
• Facet joint cysts
Facet joint cysts are associated with facet joint arthropathy, degenerative disc disease, and
degenerative spondylolisthesis and cause lower back pain, unilateral radicular pain, neurogenic
claudication, and cauda equina syndrome. Most patients with lumbar cysts are in their sixties with a slight
female predominance.
RELEVANT ANATOMY
• Each spinal segment is a “three-joint complex” comprised of an interveterbral disc anteriorly and
paired posterior synovial facet joints.
• On axial imaging, the facet joints approximate a C or J shape.
• Each joint influences the other two, with degenerative changes in one, affecting the entire complex.
As the intervertebral discs degenerate and the outer annular fibers begin to fragment, the posterior load
increases and allows excessive facet joint motion to occur. This abnormal motion accounts for excessive
shear forces in the facet joint, resulting in degradation of the cartilage and joint effusion formation. The
facet capsule helps limit axial rotation.
• An intact capsule holds 1 to 2 mL of joint fluid with larger effusions implying a loss of capsular
integrity and abnormal joint motion (Figure 24-1).
• The facet joint cysts are intraspinal extradural masses, located lateral to the thecal sac and adjacent to
the arthritic facet joint ((36)) (Figure 24-2).
• They are most commonly found at the L4-L5 segment, followed by L5-S1, L3-L4, and L2-L3. ((37)).
• The cysts represent synovial exvaginations that arise secondary to recurrent joint effusions and may be
considered similar to Baker cysts in the popliteal fossa.
Figure 24-1. Facet effusions.

Figure 24-2. Facet joint cysts.
BASIC CONCERNS AND CONSIDERATIONS

The initial radiographic assessment of patients presenting with lumbar facet-mediated pain begins with
standard radiographs including AP, lateral, and oblique views. The curved configuration and sagittal
orientation of the lumbar facet joint generally limits the utility of frontal and lateral views.
• CT scan more accurately determines the extent of the degenerative changes, but it is poor for evaluation
of the presence of facet fluid or cystic formation.
• MRI scanning underestimates the extent of the severity of the osteoarthritic changes, but it is highly
sensitive to facet joint fluid and the assessment of the facet cyst.
• The classification of the facet arthropathy by CT scan or MRI can be performed using the Pathria or
Fujiwara classifications, respectively.
• Higher grades of facet joint osteoarthritis are more likely to have larger facet joint effusions and
synovial cysts.
• The facet joint cysts are usually located anterior and medial to the facet joint.
• The size, location, T2 signal of the facet cyst, and juxtaposition to the neural elements should all be
taken into consideration when determining the need for facet cyst drainage and corticosteroid
injections.
Facet joint tropism should be noted on axial images. Facet joints are more sagittally oriented in patients
with degenerative spondylolisthesis. Facet joint with >45 degrees relative to the coronal plane are 25
times more likely to develop joint effusions and degenerative spondylolisthesis (Figure 24-3). Facet joint
effusions associated with facet joint gapping of >1.5 mm are highly predictive of the development of facet
joint cysts and degenerative spondylolisthesis.
Figure 24-3. Grade 1 L4-L5 spondylolisthesis. (A) Sagittal MRI. (B) Axial MRI.
• Informed consent and proper explanation of all risks and complications.
• Anticoagulation. Since the facet joint cyst is extradural and intraspinal, precaution needs to be taken
for those on anticoagulants. It is preferable for anticoagulants to be discontinued in adequate time prior
to the procedure.
• A baseline musculoskeletal and neurologic physical examination should be performed.
• The patient must be able to lie prone for the duration of the procedure.
• IV access is not necessary for this procedure.
• Evaluate the patient for contrast allergy.
• Septic arthropathy. Lumbar facet joints are uncommon sites of hematologic spread of pyogenic
organisms. Must rule out septic arthritis typically unilaterally at L4-L5 facet level (Figure 24-4). These
patients present with:
Figure 24-4. Left L4-L5 facet joint septic arthritis with facet cyst and epidural abscess.
Severe low back pain at rest.

Activity associated with stiffness.
Fever and asthenia.
These symptoms may be present in spondylodiskitis.
Inflammatory markers including erythrocyte sedimentation rate and C-reactive protein level may be
elevated with or without leukocytosis.
An MRI with contrast and a radionuclide bone scan would be able to differentiate a facet cyst from
a septic arthropathy.
Preinjection Pearl
Identification of neurologic impairment associated with the compression of the neural structures
associated with the facet joint cyst is the most important preoperative consideration. Motor weakness is
not a contraindication for the procedure, although care is needed in pressurization and drainage of the
cyst.
Fluoroscopic Views
• Oblique view. The best view for visualization of the facet joint cyst is the oblique view after insertion
of contrast medium into the associated facet joint (Figure 24-5).
Figure 24-5. Fluoroscopic view of facet joint cyst injection. Note filling of facet cyst.
Equipment
• 25-gauge 0.5-in needle
• 20-gauge 3-in spinal needle
• Syringes: 10, 5, and 3 cc
Medications
• Anesthetic. Preservative-free lidocaine 1%
• Contrast medium. Omnipaque
• Corticosteroid. Depomedrol or Kenalog 40 mg/cc
Technique
There have been reports of a few different procedures to treat facet joint cysts:
• Interlaminar epidural corticosteroid injection under fluoroscopic guidance (extracyst injection)
• Transforaminal epidural corticosteroid injection under fluoroscopic guidance (extracyst injection)
• Cyst drainage by direct puncture (direct method) under CT guidance
• Intra-articular facet joint injection and cyst drainage (indirect method)
The extracystic placement of corticosteroids may temporarily eliminate the radicular component but
does not adequately address the cause of the radiculopathy. Direct intracyst injection allows the cyst to
reaccumulate fluid as the source of the cyst is excessive production of synovial fluid. The intra-articular
injection accomplishes all needs for addressing the pathology. It addresses the pressure of the cystic
structure by causing it to leak and treat the joint effusion.
Our Preferred Technique
• The patient is placed prone and prepped.
• The angle of the facet joint is determined by fluoroscopy.
• A lidocaine wheel is made in the skin over the facet joint.
• A 20-gauge 3-in spinal needle is placed through the paraspinal muscles and into the facet joint.
• Placement of the needle bevel entirely in the joint ensures that proper pressurization will take place.
• With the needle bevel in the facet joint, the contrast medium is inserted to confirm placement.
• Once the placement is confirmed, additional contrast material is injected into the joint by maintaining
pressure on the syringe.
• The facet joint itself should accept 1 to 2 cc contrast after which the facet cyst fills.
• Syringe pressurization and injection of contrast material continues until there is a loss of pressure
indicating a leakage of the cyst and the creation of an epidurogram (Figure 24-6).
• 0.5 to 2 cc of the 1:1 mixture of preservative-free corticosteroid with lidocaine is placed into the joint.
• The needle is withdrawn and sterile band-aid is applied.
• The procedure can be repeated if radicular pain returns.
Figure 24-6. Facet injection by CT scan. (A) Needle in facet joint. (B) Needle with contrast into facet
joint and cyst filling (curved arrow). (C) Contrast in cyst (solid arrow) and leaking into epidural space
(epidurogram) (dotted arrow).
POSTPROCEDURE FOLLOW-UP
Follow-up neurologic assessment is necessary to determine if there is change due to the expansion and
subsequent drainage of the facet joint cyst. Follow-up injections are often necessary to continue to reduce
the inflammatory response and facet joint effusion.

• Incomplete penetration of the facet joint with failure to pressurize the cyst and extravasation of
contrast.
• Failure to pressurize the facet cyst will result in incomplete cyst drainage.
• Chronic cysts with thickened capsules or thicker content may not drain well and require repeat
injections or failure of the procedure.
CLINICAL PEARLS
• These injections can be very rewarding with complete relief in pain after the initial episode of
procedural increase in radicular pain.
• Surgical options would include a laminectomy, cyst excision, and medial facetectomy. If a
spondylolisthesis is found on standing or flexion/extension radiographs, fusion may be considered.
Suggested Reading
Boden SD, Riew DK, Yamaguchi K, Branch TP, Schellinger D, Wiesel SW. Orientation of the lumbar
facet joints: association with degenerative disc disease. J Bone Joint Surg [Am]. 1996;78-A:403-411.
Brailsford JF. Deformities of the lumbosacral region of the spine. British J Surg. 1928;16:562-627.
Chaput C, Padon D, Rush J, Lenehan E, Rahm M. The significance of increased fluid signal on magnetic
resonance imaging in lumbar facets in relationship to degenerative spondylolisthesis. Spine.
2007;32(17):1883-1887.
Christophis P, Asamoto S, Kuchelmeister K, Schachenmayr W. “Juxtafacet cyst,” a misleading name for
cystic formations of mobile spine (CYFMOS). Eur Spine J. 2007 Sep;16(9):1499-1505.
Epstein NE. Lumbar synovial cysts: a review of diagnosis, surgical management, and outcome
assessment. J Spinal Disord Tech. 2004 Aug;17(4):321-325.
Hagen T, Daschner H, Lensch T. Juxta-facet cysts: magnetic resonance tomography diagnosis. Radiologe.
2001 Dec;41(12):1056-1062.
Kusakabe T, Kasama F, Aizawa T, Sato T, Kokubun S. Facet cyst in the lumbar spine: radiological and
histopathological findings and possible pathogenesis. J Neurosurg Spine. 2006 Nov;5(5):398-403.
Schmid G, Willburger R, Jergas M, Pennekamp W, Bickert U, Koster O. Lumbar intraspinal juxtafacet
cysts: MR imaging and CT-arthrography. Rofo. 2002 Oct;174(10):1247-1252.
Weishaupt D, Zanetti M, Boos N, Hodler J. MR imaging and CT in osteoarthritis of the lumbar facet
joints. Skeletal Radiol. 1999;28:215-219.
CHAPTER 25
Dorsal Root Ganglion Blocks and

Radiofrequency Procedures
Seth A. Waldman and Vladimir Kramskiy
INTRODUCTION
• The dorsal root ganglion (DRG) contains the cell bodies of first-order sensory neurons, each of which
project an axon from a peripheral receptor, and centrally to the posterior horn of the spinal cord, where
they synapse with second-order neurons.
• There is one DRG for each spinal nerve root supplying the posterior aspect of the head, the trunk and
the extremities; in the face, this function is carried out by the trigeminal ganglion.
• Unless prevented or treated, injury to the DRG often leads to the development of a chronic neuropathic
pain state. Injection procedures that target the DRG could be used in the treatment of any radicular pain
syndrome, such as primary radicular irritation, postherpetic neuralgia.
INDICATIONS
• Neuropathic pain resulting from injury to the DRG neurons, by infection, mechanical trauma, or
inflammation resulting in the development of persistent low-threshold spontaneous firing of the
neurons.
• The C2 nerve root is implicated in the production of occipital neuralgia, which may be more properly
referred to as a C2 radicular pain syndrome. Block at the DRG, particularly with cold-pulsed RF, may
be an effective treatment.
• Similarly, at all spinal levels neuropathic radicular pain may be diagnosed by selective local
anesthetic blockade of the relevant nerve root, and potentially modulated by application of cold-pulsed
RF energy.
ISSUES COMMON TO DRG BLOCKS AT ALL LEVELS

General Concerns
• RF blockade of the DRG carries the same risks as any procedure that accesses the neural foramen.
• These include inadvertent injury to nerves (the spinal root, DRG, and the spinal cord at relevant
levels), vascular injury (to the spinal arteries at thoracic and lumbar levels, and the vertebral arteries
at cervical levels).
• Infection, and hematoma.
• At cervical and thoracic levels, there is the additional risk of pneumothorax.
Neurolytic techniques directed at the DRG, including thermal radiofrequency and chemical lysis, carry
a greater risk of producing deafferentation pain, and are hard to control. Pulsed dose (low-temperature)
radiofrequency treatment of the DRG is a much safer technique.
Contraindications to Injection
• Infection
• Uncorrected coagulopathy
• Anatomic variation that limits safe visualization of the DRG
• Lack of consent
• Preoperative consultation with the patient including history, a review of diagnostic studies, and
physical examination is the standard of care.
• Physical examination should include heart, lungs, and airway; the proposed injection site; as well as a
relevant neurologic and spinal examination.
• Review of medications should pay particular attention to anticoagulants, which should be discontinued
with sufficient time to allow for normalization of clotting.
• Review of the history of allergic reactions, with particular attention to iodinated contrast sensitivity.
Use of contrast is critical to placement of the needle adjacent to the DRG, and in patients with a
contrast allergy pretreatment will be necessary to reduce this risk.
• Assessment of patient anxiety and pain level is important to allow for the selection of an appropriate
sedation technique.
• Blocks of the DRG require nerve stimulation and therefore patient communication during the procedure
is important.
• Sedation must be performed in such a way as to ensure that the patient is both comfortable and
conscious.
• Informed consent is the standard of care.
• Physicians undertaking this procedure are assumed to be adequately trained in regional anesthesia, pain
medicine, and resuscitation techniques. They must be proficient at routine spinal injection procedures
before applying these (more advanced) techniques.
Equipment
• 27-gauge 1.5-in needle (for local anesthetic administration)
• 3 cc syringe (for local anesthetic administration)
• 5 cc syringe (for contrast administration)
• Low-volume extension tubing
• Radiofrequency cannulae
22-gauge 5-cm needle, 0.5 cm active tip for cervical levels
22-gauge 10- to 15-cm needle, 0.5 cm active tip for thoracic and lumbar levels (curved and straight
should be available)
• Intravenous access supplies
• Resuscitation equipments and supplies standard to any anesthetizing location
Medications
• 1% lidocaine for cervical levels (to minimize the risk of vertebral artery uptake and seizure)
• 2% lidocaine for lumbar and thoracic levels
• Omnipaque 180 (a nonionic water-soluble iodine contrast solution)
LEVEL-SPECIFIC ISSUES FOR DRG BLOCKS

Cervical DRG at C2
Relevant Anatomy
• At the level of C2, the DRG occupies a unique position midway between the arch of C1 and C2.
• The depth of the ganglion is approximately in the middle third of the overlying C12 articulation.
• The vertebral artery is in immediate proximity to the DRG and overlays the joint.
Fluoroscopic Views
• Patient is positioned in a supine position, head is turned away from the side to be blocked (Figure 25-
1).
• The vertebral end plates are properly aligned on fluoroscopic view by adjustment of the craniocaudal
angle (Figure 25-2).
• The degree of obliquity is then determined by live fluoroscopic imaging, such that the neural foramen is
brought into sharp resolution.
• A near lateral view will be achieved in the upper cervical spine, and more operative space will be
available than with a true lateral (Figure 25-3).
Figure 25-1. Patient position C2 DRG. For the high cervical approach (at C2), the patient is positioned
supine, with the head rotated away from the foramen to be targeted. The fluoroscope is placed in a
foraminal view, using an oblique and cranial tilt.
Figure 25-2. AP fluoroscopic view C2 DRG. The tip of the needle overlays the C1-C2 articulation, over
the middle third of the joint.
Figure 25-3. Lateral fluoroscopic view C2 DRG.
For patient comfort, or operator preference, this can also be achieved with the patient in a lateral
position, provided the head is maintained in a stable and laterally neutral position, and an open mouth
view (essential for assessing the medial progress of the needle) can be obtained.
• Localize the DRG in the cervical spine at C2 midway between the arch of C1 and C2, and overlying
the C12 articulation.
• Determine the skin entry site using a straight needle coaxial with this point.
• The operator must be thoroughly familiar with the course of the vertebral artery, which overlays the
joint, and is sometimes tortuous.
• As the needle nears the foramen, these relationships should also be confirmed in an open-mouth view.
• Next, using an AP image (again, squared craniocaudal with respect to the vertebral end plates at that
level), the medial progression of the needle tip is observed.
• The final location of the needle tip should be approximately in the middle third of the overlying C12
articulation.
• 1 mL of omnipaque-180 contrast solution is then administered under live digital-subtraction
fluoroscopy, and should demonstrate a neurogram of the adjacent spinal nerve. In the cervical spine,
we use digital subtraction as our standard to demonstrate vascular uptake, possibly due to puncture of a
vertebral artery.
• The final image is saved for documentation.
• Sensory stimulation is then performed at a frequency of 50 Hz, progressing in 0.1 V increments to a
maximum of 1 V. Stimulation at approximately 0.5 V indicates that the DRG is in adequate proximity to
the active tip of the needle, and within the electromagnetic field of the lesion.
• Motor stimulation is not necessary at the C2 level due to the lack of motor function of this nerve.
• The safest lesioning technique is pulsed-mode low-temperature radiofrequency. We use a setting of
radiofrequency bursts of 20 ms, at a frequency of 2 Hz, for 120 seconds, and maintain a maximum
temperature of no more than 42°C.
Cervical DRG Block at C3-C8

Relevant Anatomy
In the cervical spine, the DRG is located in the most dorsal and cephalad aspect of the foramen,
immediately behind the middle-third of the overlying facet-joint (Figure 25-4).
Figure 25-4. Patient position low cervical DRG. For the low cervical approach, the patient is positioned
supine, with the head rotated away from the foramen to be targeted. The fluoroscope is placed in a
foraminal view, using an oblique and cranial tilt.
Fluoroscopic Views
• In supine position, the patient’s head is turned away from the side to be blocked (Figure 25-5).
• The vertebral end plates are properly aligned on fluoroscopy by adjustment of the craniocaudal angle.
• A near lateral view will be achieved in the upper cervical spine, and more operative space will be
available than with a true lateral.
Figure 25-5. AP fluoroscopic view low cervical DRG. Needle position for the low cervical block
should be approximately in the middle third of the overlying facet joint. The final position is determined
by sensory stimulation of the appropriate root level.
In the event that the lower cervical levels are still inaccessible with this technique, a posterior
approach with the patient prone in the manner of a thoracic foraminal access can also be used.
For patient comfort, or operator preference, this can also be achieved with the patient in a lateral
position, provided the head is maintained in a stable and laterally neutral position.
• The location of the dorsal root ganglion in the cervical spine C3 through C8 is in the most dorsal and
cephalad aspect of the foramen (Figure 25-6).
• Determination of the skin entry site using a straight needle must be coaxial with this point; however,
care must be taken to avoid too oblique an angle, due to the presence of the adjacent lung in the low
cervical levels.
• The operator must be thoroughly familiar with the course of the vertebral artery, which is relatively
ventral with respect to the foramen, but is sometimes tortuous.
Figure 25-6. Oblique fluoroscopic view low cervical DRG.
As the needle nears the foramen, these relationships should also be confirmed in an oblique and lateral
view.
• The final location of the needle tip should be approximately in the middle third of the overlying facet
joint.
fluoroscopy, and should demonstrate a neurogram of the adjacent spinal nerve. In the cervical spine,
vertebral artery.
• Motor stimulation is then performed at a frequency of 2 Hz, progressing in 0.1 V increments to a
maximum of 3 V. Motor stimulation of the nearby root should occur at a much higher voltage than
sensory stimulation, indicating that the electrode is adjacent to the sensory DRG, and relatively far
from the ventral motor roots.
• The safest lesioning technique is pulsed-mode low-temperature radiofrequency. We use a setting of
Thoracic DRG Block

Relevant Anatomy
In the thoracic spine, the DRG is located in the most dorsal and cephalad aspect of the foramen,
immediately behind the middle third of the overlying facet joint.
Fluoroscopic Views
• With the patient in the prone position, the vertebral end plates are made square on fluoroscopy by
adjustment of the craniocaudal angle (Figure 25-7).
• Experience is required to determine whether the oblique angle is becoming too large; thus increasing
the risk of inadvertent pneumothorax.
• If the operator is uncomfortable with their ability to safely determine this angle, the procedure should
be aborted, and consideration given to using CT guidance.
• While there is much greater radiation exposure with this technique, CT allows safe placement in the
foramen, with direct visualization of the pleura.
Figure 25-7. Patient position thoracic DRG. For the thoracic approach, the patient is positioned supine.
The fluoroscope is placed in a foraminal view, using a minimally oblique and as needed cranial tilt.

• The location of the dorsal root ganglion in the thoracic spine is in the most dorsal and cephalad aspect
of the foramen (Figure 25-8).
• Determination of the skin entry site using a straight needle must be coaxial with this point; however,
care must be taken to avoid too oblique an angle, due to the presence of the adjacent lung. It is
therefore advisable to use a curved tip needle in this circumstance.
Figure 25-8. Oblique fluoroscopic view thoracic DRG. Needle position for the thoracic DRG should
foraminal, using a curved needle, and only as oblique as is absolutely necessary, to avoid contact with the
pleura and lung. The final position is determined by sensory stimulation of the appropriate root level.
As the needle nears the foramen, these relationships should also be confirmed in a lateral view.
level), the medial progression of the needle tip is observed. The final location of the needle tip should
be approximately in the middle third of the overlying facet joint.
fluoroscopy, and should demonstrate a neurogram of the adjacent spinal nerve. In the thoracic spine,
spinal artery. The final image is saved for documentation.
• The safest lesioning technique is pulsed-dose low-temperature radiofrequency. We use a setting of
Lumbar DRG Block

Relevant Anatomy
In the lumbar spine, the DRG is located in the most dorsal and cephalad aspect of the foramen,
immediately behind the middle third of the overlying facet joint.
Fluoroscopic Views
• With the patient in the prone position, the vertebral end plates are made square on fluoroscopy by
adjustment of the craniocaudal angle (Figure 25-9).
Figure 25-9. Patient position lumbar DRG. For the lumbar approach, the patient is positioned supine,
with the head rotated away from the foramen to be targeted. The fluoroscope is placed in a foraminal
view, using an oblique and cranial tilt.

• The location of the dorsal root ganglion in the lumbar spine is in the most dorsal and cephalad aspect
of the foramen (Figure 25-10).
• Determination of the skin entry site using a straight needle must be coaxial with this point.
• As the needle nears the foramen, this relationship should also be confirmed in a lateral view.
• The final location of the needle tip should be approximately in the middle third of the overlying facet
joint.
• 1 mL of omnipaque-180 contrast solution is then administered under live fluoroscopy, and should
demonstrate a neurogram of the adjacent spinal nerve.
• The safest lesioning technique is pulsed-dose low-temperature radiofrequency. We use a setting of
Figure 25-10. AP fluoroscopic lumbar DRG. Needle position for the lumbar DRG block should be
foraminal. This can be achieved by entering the foramen using curved tip needle, and an oblique
approach. Live contrast spread should be documented around the nerve root. The final position is
determined by sensory stimulation of the appropriate root level.
CLINICAL PEARLS
• DRG injection using local anesthetic only can be diagnostic as well as therapeutic. Patients with a
short-term positive response to a local anesthetic injection may be candidates for pulsed-dose
radiofrequency (RF) ablation.
• The success of DRG blockade is entirely dependent on safely placing the needle adjacent to the
ganglion, and away from the ventral motor root.
• The only way to confirm placement, is to sequentially demonstrate:
By fluoroscopy—that the needle is in the most dorsal and cephalad portion of the foramen (except at
the C2 level)
By contrast injection under live fluoroscopy—that the needle is adjacent to the DRG
By nerve stimulation—that the electrode is able to stimulate the sensory nerve at a much lower
voltage than the motor nerve
Suggested Reading
Afifi AK, Bergman RA. Functional Neuroanatomy. 2nd ed, Lange Medical Books; 2005.
Higuchi Y, Nashold BS Jr, Sluijter M, et al. Exposure of the dorsal root ganglion in rats to pulsed
radiofrequency currents activates dorsal horn lamina I and II neurons. Neurosurgery. 2002
Apr;50(4):850-856.
Podhajsky RJ, Sekiguchi Y, Kikuchi S, Myers RR. The histologic effects of pulsed and continuous
radiofrequency lesions at 42°C to rat dorsal root ganglion and sciatic nerve. Spine. 2005;30(9):1008-
1013.
CHAPTER 26
Sacroiliac Joint Injections

Sheetal Kerkar Patil, Honorio T. Benzon, and Sudhir Diwan
OVERVIEW
The sacroiliac joint (SIJ) is the largest axial joint in the body with an abundance of nociceptive pain
fibers within the joint and surrounding ligaments. SIJ dysfunction or syndrome is pain originating in the
sacroiliac joint without demonstrable anatomic lesion and is presumed to be due to a biochemical
abnormality.1 Predisposing factors include conditions causing stress on the joint such as spinal deformity,
previous spinal surgery, and leg length discrepancy. Symptoms of SI joint dysfunction include pain in the
superior medial quadrant of the buttock, the lateral buttock, and inferior to the posterosuperior iliac spine,
with radiation to the greater trochanter, upper lateral thigh, and groin (Figure 26-1).
Figure 26-1. Distribution of pain pattern secondary to sacroiliac joint pain.
Two types of injections have been performed for SIJ pain relief: an injection of local anesthetic or
corticosteroids (or both) into the intra-articular space and the periarticular region, in particular into the
posterior ligamentous structures. Both types of injection can be effective in the treatment of SIJ pain. It is
still controversial as to which type of injection is more effective.
Several studies have evaluated periarticular vs. intra-articular. A study by Borowsky and Fagen2
retrospectively showed that patients who received intra-articular and periarticular injections did better
than the patients receiving intra-articular injections only. However, only 51.25% of patients who received
the combination of injections experienced relief at 3 months. Luukkainen et al evaluated the role of
periarticular injections in two randomized trials.3,4 Both studies showed periarticular injection of local
anesthetic with steroids to be superior, though only in a short-term follow-up.
RELEVANT ANATOMY
• The SI joint is the largest axial joint in the body, also supported by a network of muscles that help to
deliver regional muscular forces to the pelvic bones.
• Dorsally there is raised median crest with irregular surface of lateral sacrum.
• The S1 foramen too is close to PSIS and the location of S3 foramen is inferior to SIJ.
• There are ligamentous gaps on dorsal surface that extend superolaterally (Figure 26-2).
• The muscles, such as the gluteus maximus, piriformis and biceps femoris are functionally connected to
SI joint ligaments. The sacroiliac joint is innervated at its anterior and posterior aspects.
• Posteriorly, the joint is innervated by the lateral branches of the posterior primary ramus of the L4 to
S4 dorsal rami.5,6
• The predominant innervation is from the dorsal ramus of S1 and isolated dorsal innervations from S1-4
(Figure 26-3).
• The anterior innervation is from the ventral rami of L5 to S2 and via branches from the sacral plexus.5
Figure 26-2. Ligaments of the sacroiliac joint.
Figure 26-3. Lateral branches from S1 to S4 sacral foramen. Schematic drawing showing the S1-3 lateral
branches innervating the SI joint and overlying ligaments. The needles depict the approximate location for
the diagnostic LBB.
Physical Examination
Physical examination of the patient with SI joint syndrome usually reveals tenderness over the posterior
aspect of the joint and sacral sulcus with no numbness or weakness. Several provocative maneuvers can
be used to stress the SI joint and elicit pain to aid in diagnosis: the FABER, Gaenslen test, Yeoman
(extension) test, Gillet’s test, and posterior shear test.
Faber Patrick test (eg, left sacroiliac joint dysfunction) (Figure 26-4)
• Patient is in supine position.
• For left SI joint test: Left leg flexed at knee and the ankle is placed in front of the right thigh above
the knee. The physician places one hand over the right iliac crest, while the other hand pushes over
the medial aspect of the left knee.
• Positive test: Pain over sacroiliac joint region on ipsilateral side (also back, buttock, groin).
• Comment: Test stresses sacroiliac and hip joint.
Gaenslen’s test (eg, left sacroiliac joint dysfunction) (Figure 26-4)
Figure 26-4. Physical tests for evaluation of sacroiliac joint pain.
• Patient is in supine position.

• Left lower thigh and leg hang over the examination table. The examiner flexes right hip and right knee
(ie, hip joint is maximally flexed). The examiner presses downward over the left thigh (hip joint is
hyperextended).
• Positive test: Pain in the left sacroiliac joint.
• Comments: Test stresses both sacroiliac joints simultaneously by counter-rotation at the extreme range
of motion of the joint. Test also stresses the hip joint and stretches the femoral nerve (examiner should
ensure the absence of hip pathology or conditions affecting the femoral nerve to diagnose sacroiliac
joint syndrome).
Yeoman’s test, also called extension test (Figure 26-4)
• Patient is in prone position.
• Examiner places one hand above the anterior aspect of the knee and elevates it slightly, the other hand
presses downward over the crest of the ilium.
• Positive test: Pain over the posterior sacroiliac joint.
• Comments: The hip is extended and the ipsilateral ilium is rotated. Test stresses the sacroiliac joint; it
also extends the lumbar spine and stresses the femoral nerve. More specific and reliable compared to
the other tests.
Gillet’s test
• Patient is standing.
• One of the examiner’s thumb is placed on the second sacral spinous process, the other thumb is placed
on the posterior superior iliac spine (PSIS).
• Normal sacroiliac joint: When the patient maximally flexes the hip, the PSIS moves inferior to the S2
spinous process.
• Dysfunctional or fixed sacroiliac joint: PSIS remains at the level of the S2 spinous process or moves
superior to the sacrum.
Sacroiliac shear test
• Patient is in prone position.
• Palm of the examiner’s hand is placed over the posterior iliac wing. Shear thrust is directed inferiorly
producing a shearing force across the sacroiliac joint.
• Positive test: Pain in dysfunctional sacroiliac joint.
• Palpate the anatomical landmarks posterior superior iliac spine (PSIS), posterior inferior iliac spine
(PIIS) and iliac crest, and confirm under anteroposterior (AP), ipsilateral and contralateral oblique
and lateral view orientation.
• Obtain AP and oblique fluoroscopic view to superimpose anterior and posterior joint line (Figure 26-
5).
• Obtain a craniocaudal tilt so that the trajectory of the needle will be directed 30 to 45 degrees to enter
the lower one-third part of the joint.
• Use nonionic contrast for study of the joint and look for inadvertent vascular run-off.
Figure 26-5. Oblique and caudal tilt of fluoroscope for ideal needle placement with trajectory to inferior
one-third of sacroiliac joint.
Indications
• Diagnostic. As a part of work-up to rule-in or rule-out a source of chronic low back pain. To address
the potentially false-negative and false-positive results, repeat the diagnostic injections.
• Therapeutic and prognostic purpose. To decide whether or not patient should be considered for a
denervation procedure. Using steroid may provide long lasting pain relief by providing anti-
inflammatory effect.
Basic Concerns for Injection

• Immunocompromised patients are at high risk for infection.
• Patients with allergy to contrast media may require pretreatment with H1 and H2 antagonists, whereas
allergy to local anesthetics may require identification of the appropriate local anesthetic to be used for
the procedure.
• Individualize the plan based on medical comorbidities and anticoagulants.
Contraindications
• Patient refusal
• Coagulopathy
• Informed consent and proper explanation of potential complications
• Anticoagulation—this is less of a concern than for an epidural
• Physical examination of the area for infection, skin ulceration or necrosis, and extent of disease
• The ability of a patient to tolerate a prone position for the injection.
Equipments
• Isopropyl alcohol or chlorhexidine
• 22-gauge 3-in needle
• 3 or 5 mL syringe for medications
Medications
• 0.25% bupivacaine or other local anesthetic
• Corticosteroid (Dexamethasone, Triamcinolone, or Methylprednisolone)
Periarticular Technique
• The patient is positioned prone on the table, with the head to one side.
• Pillow placed under abdomen to flex the spine.
• Fluoroscopy is tilted cranially to detect the whole SIJ line.
• The posterior margin of SIJ can be divided into three equal sections (ie, upper, middle, and lower).
• A 22-gauge spinal needle can be inserted in the center of each section on the sacrum.
• Sterile prep of the area by appropriate antiseptic solution.
• The skin is anesthetized with 1 to 2 mL 1% lidocaine with a 25-gauge needle.
• A small amount of contrast is then injected to ensure there is no intravascular spread.
• After appropriate contrast spread in periarticular tissues without vascular run-off, a solution of steroid
and local anesthetic (40-60 mg of methylprednisolone or triamcinolone with 1-2 mL of 0.5%
bupivacaine or ropivacaine) is injected in divided aliquots into the top, middle, and lower regions.
Intra-Articular Technique
• The patient is positioned prone on the table, with the head to one side.
• Pillow placed under abdomen to flex the spine.
• Under straight anteroposterior (AP) view, the SI joint presents several lines that course caudocranially
in a semiparallel fashion.
• The lateral line represents the dorsal or posterior margin of the joint.7,8
• C-arm is initially rotated approximately 30 degrees caudal to axial plane to better visualize area under
posterior superior iliac spine and iliac crest.
• C-arm is angled obliquely to the contralateral side until the inferior joint space is clearly demarcated,
usually 5 to 20 degrees.
• Target is 1 to 2 cm cephalad from its most caudal end.
• Sterile prep of the area to be injected by appropriate antiseptic solution.
• The skin is anesthetized with 1 to 2 mL 1% lidocaine with a 25-gauge needle.
• A 22-gauge spinal needle is advanced coaxially toward the inferior pole of the SI joint.
• Slight curve at the tip of the needle opposite to the bevel will make steering of the needle into the joint
easier.
• Intermittent images obtained at regular intervals (every 2-4 mm advancement) to confirm trajectory.
• Once needle is in joint, typically a change in resistance is felt.
• A small amount of contrast is then injected.
• After appropriate contrast spread in the joint space and without vascular run-off, a solution of steroid
and local anesthetic (40-60 mg of methylprednisolone or triamcinolone with 1-2 mL of 0.5%
bupivacaine or ropivacaine) is injected (Figure 26-6).
• Because capacity of SI joint is small, distension may exacerbate pain so maximum volume of 2 to 2.5
mL has been recommended.7,9
• Do not inject medication under high pressure as that may disrupt the joint.
Figure 26-6. Needle placement at the inferior portion of the joint with intra-articular spread of contrast.
Other Approaches
• Another approach involves placement of the needle at the inferior end where the anterior and posterior
joints overlap, if a lucent zone is noted there.8
20 to 30 degrees contralateral obliquity, the medial and lateral planes of the joint overlap.
Needle entry is at the most lucent zone of the joint space.
Patient should be monitored closely for the following:
• Neurologic symptoms (weakness, urinary or bowel incontinence)
• Transient weakness of ipsilateral leg due to spillage of local anesthetic onto sacral nerve roots or
sciatic nerve
• Signs of local infection (warmth, erythema, purulent drainage, fever)
• Bleeding

• Infection
• Bleeding
• Nerve block; ipsilateral leg weakness
• Exacerbation of pain
• Transient difficulty voiding
• Allergic reaction to components of prep or solution
• Hematoma
Clinical Pearls
• Typically a change in resistance is felt as the needle passes through the capsular issue, and the needle
tip is deflected slightly as it traces the surface of the ilium.
• Some patients have significant osteoarthritic changes that preclude needle entry into the joint, making
periarticular infiltration necessary.
• A greater than 75% reduction of pain over the SI joint is considered to be a positive response.10
BLOCKADE OF THE L4 AND L5 DORSAL RAMUS AND

LATERAL BRANCHES OF S1-S3
Anatomy
• As noted, the posterior margin of the SIJ is innervated by the L5 dorsal ramus and the lateral branches
of S1, S2, and S3, with possible contributions from the L4 dorsal ramus.
Technique
• Patient positioned prone and C-arm is either positioned AP or angled slightly cephalocaudal to
optimize the appearance of the sacral foramina.
• Sterile prep of the area to be injected.
• After skin infiltration, 22-gauge spinal needles are advanced coaxially to a point 5 mm lateral to each
foramen between 2:00 and 5:00 o’clock positions on the right side and 7:00 and 10:00 o’clock on the
left side (Figure 26-7).
• This corresponds to the path of the lateral branch as it travels laterally and enters the ligaments of the
joint.
• The L5 dorsal ramus is blocked at the junction of the ala and the articular process of the sacrum.
• If L4 blockade desired, the C-arm is rotated obliquely to block the L4 dorsal ramus at the junction of
the transverse process of L5 and the superior articulating process.
• Once needle position confirmed, 0.5 mL 0.5% bupivacaine is injected.
• Patient instructed to keep pain diary.
Figure 26-7. Placement of RF probes at 2 o’clock and 5 o’clock positions for denervation of sacral
lateral branches from S1 to S3 foramen.
Clinical Pearls
• Can be used as diagnostic tool to predict response to radiofrequency (RF) ablation.11
RADIOFREQUENCY ABLATION OF THE SACROILIAC JOINT

Background
• Radiofrequency ablation results in a restricted neurolysis.
• May target the small, terminal sensory fibers at the posterior aspect of the joint itself (strip lesioning)
or the nerve supply to the joint.
Equipments
• Radiofrequency needles (5-10 mm active tip)
• 25-gauge needle for local anesthetic
• Sedation, if necessary
Medications
• 1% lidocaine, 0.5% bupivacaine or other local anesthetic
Technique—Strip Lesioning of SI Joint

• The technique utilizes two probes to create a bipolar strip lesion.
• The joint is visualized with the C-arm as described for the SIJ injection.
• The first RF needle (5-10 mm active tip) is inserted at the inferior margin of the joint.
• A second RF needle is placed more cephalad, at a distance of less than 1 cm from the first probe.
• After anesthetizing tissue with lidocaine, the RF probe is inserted and heated to 80°C for 90 seconds.
• Successive probes are placed less than 1 cm cephalad from the previous probe and multiple lesions
are created in a “leapfrog” manner as high in the joint as possible, creating a strip lesion in the
posterior joint.
Technique—Radiofrequency (RF) Lesioning of Lateral Branches

• Technique has been performed with traditional thermal RF and water-cooled RF.
• The patient positioned prone.
• C-arm aligned for an anteroposterior image.
• To target the L5 dorsal rami, a radiofrequency cannula placed at lateral margin of superior articular
process where it meets sacral ala.
• Because lesion created by conventional RF is smaller and is positioned along the active tip of the
probe, when using conventional RF the needle trajectory must preferably be parallel to the path of the
nerve to maximize the chances of the neural destruction.
• On lateral image, the needle tip should be no further anterior than the anterior third of the superior
articular process.7
• When using cooled RF, the lesion is larger and the tip no more anterior than the midpoint of the
superior articular process to avoid lesioning the segmental nerve root.12
• Prior to lesioning, sensory nerve stimulation is applied at 50 Hz with the goal of concordant pain being
reproduced below 0.6 V.
• Motor stimulation is applied at 2 Hz at 2 V, or 3 times the sensory threshold, to verify the absence of
muscle contraction in a radicular distribution.
• Once stimulation acceptable, sites anesthetized with 0.5 mL 1% lidocaine and lesioning begins at 80°C
for 90 seconds.
• It is customary to inject 0.5 mL of a mixture of local anesthetic (eg, bupivacaine) and steroid (eg, 8
mg/mL triamcinolone) after the lesioning for postoperative analgesia and to prevent neuritis.
• Bleeding
• Exacerbation of symptoms due to localized muscle spasms after RF lesioning
CLINICAL PEARLS
• It is now evident that diagnosing the SIJ pain has been difficult task.
• The physical examination is unreliable as the physical tests are sensitive but not specific.
• There is a poor correlation of symptoms to imaging studies.
• Placebo effects may decrease diagnostic specificity of injections.
• Though most treatment options have not been very effective, the RF neurolysis offers a promising
modality but lacks studies.
• The neuroanatomy is an extensive, mesh-like, sensory innervation makes difficult for denervation
procedures.
• There is enormous anatomical variability that includes gender to gender, person to person, and even
side to side.
• The sacral neural foramina frequently are poorly visualized and correctly identified because of pelvic
gas shadows, and may require bowel preparation for proper visualization under fluoroscopy.
• The fluoroscopic skills are extremely important to understand the obliquity of joint orientation.
• During pregnancy, the hormone relaxin from placenta relaxes SIJ to facilitate birth, may contribute to
lower back pain but does not require any treatment as pain resolves after child birth.
• Considered a synovial joint, although 75% joint is fibrosed.
• In regards to strip lesioning, the posterior superior iliac spine obscures access to the superior portion
of the joint, making only the lower third portion, or at most half, of the joint accessible to the lesioning.
• Some clinicians lesion the whole posterior border of the joint under heavy sedation.
• In RF denervation, the lesion is not created at the tip of probe but little distal, and the elliptical lesion
may produce variable coagulation and gapping between probes.
References
1. Dreyfuss P, Michaelsen M, Pauza K, et al. The value of medical history and physical examination in
diagnosing sacroiliac joint pain. Spine. 1996;21:2594-2602.
2. Borowsky CD, Fagen G. Sources of sacroiliac region pain: insights gained from a study comparing
standard intra-articular injection with a technique combining intra- and periarticular injection. Arch
Phys Med Rehabil. 2008;89:2048-2056.
3. Luukkainen RK, Wennerstrand PV, Kautiainen HH, Sanila MT, Asikainen EL. Efficacy of periarticular
corticosteroid treatment of the sacroiliac joint in non-spondylarthropathic patients with chronic low
back pain in the region of the sacroiliac joint. Clin Exp Rheumatol. 2002;20:52-54.
4. Luukkainen R, Nissila M, Asikainen E, et al. Periarticular corticosteroid treatment of the sacroiliac
joint in patients with seronegative spondyloarthropathy. Clin Exp Rheumatol. 1999;17:88-90.
5. Ikeda R. Innervation of the sacroiliac joint. Macroscopical and histological studies. Nihon Ika
Daigaku Zasshi. 1991;58:587-596.
6. Paris SV. Anatomy as related to function and pain. Orthop Clin North Am. 1983;14:475-489.
7. Bogduk N. Practice Guidelines: Spinal Diagnostic and Treatment Procedures. San Francisco:
International Spine Intervention Society; 2004:66-86.
8. Fenton DS, Czervionke LF. Image-guided spine intervention. Philadelphia, PA: Saunders; 2003:127-
139.
9. Dreyfuss P, Dreyer SJ, Cole A, Mayo K. Sacroiliac joint pain. J Am Acad Orthop Surg. 2004;12:255-
265.
10. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine.
1995;20:31-37.
11. Cohen SP, Abdi S. Lateral branch blocks as a treatment for sacroiliac joint pain: a pilot study. Reg
Anesth Pain Med. 2003;28:113-119.
12. Kapural L, Stojanovic M, Sessler DI, et al. Cooled radiofrequency (RF) of L5 dorsal ramus for RF
denervation of the sacroiliac joint: technical report. Pain Med. 2010;11:53-57.
CHAPTER 27
Sacroiliac Joint Denervation Using Synergy

System
Leonardo Kapural and Amanda Toye
INTRODUCTION
The sacroiliac (SI) joint is a common source of chronic low back pain (LBP) with a prevalence rate of
13% to 30%.1-6 There is mounting evidence that radiofrequency (RF) neurolysis may provide long-term
analgesia in this patient population. Techniques for RF neurolysis using conventional RF electrodes have
been reported achieving modest outcomes.7-9 More recently, the use of novel cooled RF electrodes for RF
neurolysis of the sacroiliac joint provided clinically meaningful efficacy over longer time intervals.10-12
Factors leading to a successful outcome following RF neurolysis include adequate diagnosis and
accurate electrode placement, which relies on a good understanding of the neuroanatomy.13,14 Accurate
electrode placement may be particularly important when treating sacroiliac-mediated pain as the precise
innervation of the SI joint has yet to be elucidated. A review of the literature demonstrates that the L5
dorsal ramus and the lateral branches of the S1-S3 are frequently implicated in SI joint pain.1-14 The L5
dorsal ramus is reliably accessible at the lateral base of the S1 superior articular pillar (Figure 27-1). It
courses along the junction formed between the base of the S1 superior articular process (SAP) and the
superior edge of the sacral ala, while the lateral branches of the sacral dorsal roots do maintain an
unpredictable distribution across the posterior sacrum.1-14
Figure 27-1. Anatomical position of dorsal ramus of the L5 nerve root. Maximum neural coagulation is
achieved by placing the electrode adjacent and parallel to the course of nerve along the base of the SAP
(A and B). The target point for electrode insertion is then identified by rotating the C-arm of the
fluoroscope until the lateral edge of the S1 SAP is clearly visible. Once the target point is identified, the
electrode is inserted using the “tunnel view.” The trajectory of the electrode is along the sagittal plane to
ensure placement of the electrode along the course of the L5DR.
RELEVANT ANATOMY
• Dissection studies revealed that the upper dorsal portion of the SI joint is primarily innervated by the
posterior dorsal ramus of L5, and the lateral branches of S1-S3 (Figures 27-1 and 27-2).
• Complete denervation of these nerves should provide at least partial sacroiliac pain relief in patients
whose pain is posteriorly mediated.
• Thus, the L5 dorsal ramus is lesioned as standard practice, in addition to the lateral branches of S1-S3,
to denervate the SI joint using cooled RF (Figure 27-3).
Figure 27-2. RF Lesions should be 8 to 10 mm from lateral edge of the sacral foramina. Target sites
should be no more than 50 degrees apart (1:40 on a clock face) to achieve optimal lesion overlap.
Epsilon (A) is used to judge distance for lesioning 8 to 10 mm from the lateral edge of the posterior
foraminal aperture. Epsilon indicates appropriate spacing between target sites; 2:30, 4:00, 5:30 (right) at
S1 and S2 and 2:30 and 5:30 for S3 (A and B). (Reproduced with permission from Kimberly-Clark
Corporation.)
Figure 27-3. Due to the spherical nature of a cooled RF lesion, variation electrode trajectory would have
no effect on the orientation of lesion. The targeted lateral sacral branches are maximally coagulated when
tip of the cooled RF electrode is positioned with sufficient proximity to any branches, regardless of
trajectory. Here illustrated is a spherical nature of achieved lesion when cooled RF is used via synergy
system. (Reproduced with permission from Kimberly-Clark Corporation.)
The advantages of cooled RF electrode are:
• It creates larger lesions than conventional RF electrodes (Figures 27-3 and 27-4).
• These larger lesions provide a means of overcoming the anatomical variation of the target nerves and
are more likely to interrupt the afferent lateral branches. These lesions are created by the much larger
focal energy delivered.
• The circulating water removes heat from the tissue adjacent to the electrode, allowing power delivery
to be increased without causing high impedance and tissue charring around the electrode (Figures 27-3
to 27-5).
Figure 27-4. (A) Three 27-gauge spinal needles are shown piercing the skin over the sacral area. (B) A
27-gauge 3.5-in Quincke needles are positioned into most lateral aspect of S1, S2, S3 posterior sacral
foramina under AP imaging. Proper positioning is then confirmed under lateral view. (Reproduced with
permission from Kimberly-Clark Corporation.)
Figure 27-5. (A) Shown here (middle, black) is a cooled electrode inserted via 1 of 2 introducers placed
appropriately in the sacral area. The electrode is connected to the generator via electrical cable (shown
black) and the tubing used for electrode cooling by the water pump (shown transparent). (B) Two
introducers are needed to facilitate the procedure, for example, while the ablation is conducted using
electrode positioned via 1 of the introducers, other is being repositioned under fluoroscopy.

Patient Selection
Candidates for lateral branch denervation using the Pain Management Synergy System must have a history
of chronic back pain originating below the L5 spinal level for >6 months and must meet the following
selection criteria.
Selection Criteria/Indications
Criteria for idiopathic sacroiliac region pain are:
• Predominant axial/mechanical pain below L5.
• >80% pain relief from two separate, low-volume, high-concentration intra-articular blocks.
• Blocks should be performed with fluorographic confirmation of needle placement and joint capsule
integrity using both anterior-posterior and lateral views.
• Positive indication of physical examination (Fortin, Patrick, Genslean, etc).
• Chronic pain for >6 months.
• Failure to achieve adequate improvement with comprehensive nonoperative treatment at minimum:
nonsteroidal anti-inflammatory and physical therapy.
• Other possible causes of low back pain have been ruled out.
• No indication of intervertebral disc involvement, and failure to obtain prolonged improvement from
facet injections, or RF rhizotomies.
Contraindications
Patients will be excluded if they meet any of the following criteria:
• New neurologic deficit
• Spinal pathology that may impede recovery such as spina bifida occulta, spondylolisthesis at L5/S1, or
severe scoliosis
• Pregnancy
• Systemic infection or localized infection at the anticipated introducer entry site
• History of coagulopathy or unexplained bleeding
Relative Contraindications
• Irreversible psychological barriers to recovery
• Radiculopathy
• Immunosuppression (eg, AIDS, cancer, diabetes, other surgery within last 3 months)
Fluoroscopic Views
• Start with anterior-posterior imaging of the L5/S1 disc space with slight cranial tilt to open the S1 and
S2 sacral foramina on the operative side. This facilitates placement of the 27-gauge 3.5-in Quincke
needles into the most lateral aspect of S1, S2, and S3 posterior sacral foramina as the internal
reference points.
• Lateral views to confirm proper marker placement and to confirm the RF electrode lesioning tips are
not in the canal.
Equipment
• Three 27-gauge 3.5-in spinal needles to be used as internal reference points
• Epsilon ruler for guidance
• Three 17-gauge cold radiofrequency synergy introducer
• Synergy radiofrequency probe
• 10-mL syringe for local anesthetic
• 25-gauge 1.5-in needle for local anesthesia
Medications
• 0.5% lidocaine for local anesthesia
• 2% lidocaine for anesthesia prior to lesioning
• 0.5% bupivacaine for anesthesia after lesioning
Brief Overview
• Moderate sedation is needed and an optional bowel prep.
• Lesions should be 8 to 10 mm from lateral edge of foramen.
• Target sites should be no more than 50 degree apart (1:40 on a clock face) to achieve lesion overlap
(see Schematic 1), and only one introducer entry point through the skin at each level (3 o’clock for a
right procedure).
• The Epsilon is used to judge distance for lesioning, which is 8-10 mm from the lateral edge of the
posterior sacral foramina (PSFA).
• Epsilon indicates appropriate spacing between target sites.
• S1 and S2: 2:30, 4:00, 5:30 (for right) positions.
• S3: 2:30 and 5:30 positions.
• Lesion DR L5 (1 lesion).
• Set temperature at 60°C to achieve target tissue temperature for 2:05 minutes; 25 second ramp time.
Procedural Technique
• The patient is placed in the prone position with a pillow under the abdomen to reduce lumbar lordotic
curvature.
• Continuous hemodynamic monitoring is initiated including blood pressure and pulse oximetry. IV
sedation is administered incrementally to allow the patient to remain comfortable and conversant
throughout the procedure.
• C-arm A/P fluoroscopy with cranial tilt is used to visualize the sacrum at the L5/S1 disc space.
• The skin is infiltrated with 0.5% lidocaine over the desired target entry sites after sterile prep and
drape.
• Three 27-gauge 3.5-in Quincke needles are placed into the S1, S2, and S3 PSFA under anterior-
posterior (AP) view to establish internal reference points (Figure 27-4).
• Beginning at the S1 level, a 17-gauge cold radiofrequency synergy introducer with stylet is inserted at
the 3 o’clock (for right reference) position (Figure 27-5) and advanced until bony contact with the
posterior sacrum.
• The introducer width is measured with Epsilon so that the tip is 8 to 10 mm from the lateral edge of the
PSFA (Figure 27-2).
• The distance between the introducer and the aperture of PSFA of S1 was measured using the Epsilon
ruler (Baylis Medical Company, Montreal; Figure 27-2). A depth marker is fixed to the level of the
skin and lateral fluoroscopy is used to confirm proper placement outside of the canal (Figure 27-6).
The stylet is removed.
Figure 27-6. Assessment of the trocar with introducer and electrode depth. Adequate depth of the trocar
with introducer needs to be achieved with tip of the trocar lying on the sacral plate (upper needle shade).
As the electrode is 2 mm shorter than trocar, there is an intentional gap from the sacral plate (lower
needle shade). This would allow better heat dissipation and should not be corrected by pushing electrode
deeper to the surface of the sacral plate.
• The RF probe is subsequently inserted via the same introducer. Correct probe placement is confirmed
in the lateral view and should be slightly off bone (Figure 27-6).
• RF energy is delivered for 2 minutes and 30 seconds at 60°C as the target electrode temperature.
Three lesions are created at the S1 level. They are about 1 cm apart from one another using the
Epsilon ruler, creating a strip of lesioned tissue lateral to the S1 foramen.
This same procedure is repeated for each subsequent sacral level; however, only two lesions are
created at S3 (Figure 27-2).
• The notch between the ala of the sacrum and the superior articular process (SAP) of the sacrum is
visualized in the AP view for L5DR denervation (Figures 27-2 and 27-7).
0.5% lidocaine is used for local skin anesthesia at this site.
• The 17-gauge cold radiofrequency synergy introducer is inserted through the skin just lateral and
inferior to the target point and directed toward the notch.
The introducer is advanced until osseous contact at the base of the S1 SAP at its lateral midline
(Figures 27-1 and 27-7).
Figure 27-7. Anterior-posterior view of the cooled radiofrequency electrode positioned just lateral to the
base of SAP.
• The depth of insertion is confirmed in the lateral view where the introducer tip is advanced no further
ventral than the AP midline of the SAP, the z-joint space (Figure 27-8). This is to avoid injury to the
segmental nerve root.
Figure 27-8. Lateral view of appropriately positioned introducer for the insertion of the cooled RF
electrode. The tip of the trocar with introducer (and later RF electrode) is positioned posterior to the
midline of the lateral fluoroscopic width of SAP.
• The stylet is removed and subsequently replaced with the cooled RF electrode.
1 to 2 mL of 0.5% bupivacaine is injected after lesioning.
• Again, RF energy is delivered for 2 minutes and 30 seconds at 60°C as the target electrode
temperature. A lesion was created around the tip of the electrode using the Pain Management Generator
(Baylis Medical Company, Montreal) at a target temperature of 60°C for 2 minutes and 30 seconds.
• Optionally, a second lesion is created 6 to 8 mm inferior to the initial target location but with the same
needle entry point.
• The patient is then monitored prior to discharge.
Complications
Most complications are minor and consistent with lumbar/sacral neurectomy.
• Some patients may experience increased pain which is typically transient and resolves within 6 weeks.
• Localized numbness over the medial quadrant of the buttock.
• Increased lower back pain.
• Prolonged itching.
Potential Complications
• Infection
• Bleeding
• Osteitis or periostitis
CLINICAL PEARLS
• Cooled RF temperatures capable of coagulating nerve tissues are achieved at a distance of 4 to 6 mm
from the electrode. Margin of safety need to be maintained and not to be confused with much lesser
forward heat dissipation from conventional electrodes.
• The use of the cooled RF electrode to lesion the L5DR (and not conventional RF electrode) may have
several advantages, to maximize the size of an effective lesion, simplify the cooled RF procedure, and
to minimize patient discomfort.
• If higher impendence than the 500 ohm is observed, the electrode repositioning needs to be performed
by reintroducing the stylet. Electrode itself should not be excessively manipulated.
• Repeated lateral fluoroscopic views add to the safety of this procedure, preventing unintended
placement into posterior sacral foramina.
References
1. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine.
1995;20:31-37.
2. Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac
pain provocation tests in 54 patients with low back pain. Spine. 1996;21:1889-1892.
3. Irwin RW, Watson T, Minick RP, Ambrosius WT. Age, body mass index, and gender differences in
sacroiliac joint pathology. Am J Phys Med Rehabil. 2007;86:37-44.
4. Cohen S. Sacroiliac joint pain: a comprehensive review of anatomy, diagnosis, and treatment. Anesth
Analg. 2005:101:1440-1453.
5. Hansen HC, McKenzie-Brown AM, Cohen S, Swicegood JR, Colson JD, Manchikanti L. Sacroiliac
Joint Interventions: A Systematic Review. Pain Physician. 2007;10:165-184.
6. Cohen S, Hurley RW. The ability of diagnostic spinal injections to predict surgical outcome. Anesth
Analg. 2007;105:1756-1575.
7. Yin W, Willard F, Carreiro J, Dreyfuss P. Sensory stimulation-guided sacroiliac joint radiofrequency
neurotomy: technique based on neuroanatomy of the dorsal sacral plexus. Spine. 2003;28:2419-2425.
8. Ferrante FM, King LF, Roche EA, et al. Radiofrequency sacroiliac joint denervation for sacroiliac
syndrome. Reg Anesth Pain Med. 2001;26(2):137-142.
9. Burnham RS, Yasui Y. An alternate method of radiofrequency neurotomy of the sacroiliac joint: a pilot
study of the effect on pain, function, and satisfaction. Reg Anesth Pain Med. 2007;32:12-19.
10. Cohen SP, Hurley RW, Buckenmaier CC, 3rd, et al. Randomized placebo-controlled study evaluating
lateral branch radiofrequency denervation for sacroiliac joint pain. Anesthesiology. 2008;109:279-
288.
11. Kapural L, Nageeb F, Kapural M, Cata JP, Narouze S, Mekhail N. Cooled radiofrequency (RF) system
for the treatment of chronic pain from sacroiliitis: the first case-series. Pain Practice. 2008:8(5):348-
354.
12. Kapural L, Sessler DI, Stojanovic PM, Bensitel T, Zovkic P. Cooled Radiofrequency (RF) of L5
dorsal ramus for RF denervation of the sacroiliac joint: technical report. Pain Medicine.
2010;11(1):53-57.
13. Willard F, Carreiro J, Manko W. The long posterior interosseous ligament and the sacrococcygeal
plexus. Third Interdisciplinary World Congress on Low Back and Pelvic Pain, 1998.
14. Ikeda R. Innervation of the sacroiliac joint. Macroscopical and histological studies. Nippon Ika
Daigaku Zasshi. 1991;58:587-596.
CHAPTER 28
Sacroiliac Joint Denervation by Using Simplicity

III
Sudhir Diwan and Nimish Davé
INTRODUCTION
The Simplicity III procedure is a technique to denervate the sacroiliac (SI) joint by creating a thermal
“strip” lesion along the sacrum lateral to the S1-S4 neural foramina and medial to SI jointline. The
procedure is usually combined with radiofrequency ablation of the ipsilateral L5 primary dorsal ramus.
Though multiple methods have been endorsed to denervate the SI joint, the Simplicity III procedure is a
convenient and effective alternative for achieving maximal disruption of nociceptive input from the SI
joint. The Simplicity III is a rigid tripolar probe with a sharp-tip that creates an adequate strip lesion that
is technically easy to perform. Its pre-curved shape closely approximates the curvature of the sacrum, and
it does not require an introducer.
ANATOMY
• The sacroiliac (SI) joint is the largest axial joint in the body and functions to provide axial stability
and to dissipate truncal loads to the lower extremities.
• It displays a great deal of inter- and intrapatient anatomical variability with respect to size, shape, and
contour (Figure 28-1A, B).
• The SI joint is classified as a diarthrodial joint because it contains synovial fluid however, only the
anterior third of the joint at the interface of the sacrum and ilium is truly synovial. The remainder of the
joint is a fibrous articulation of the sacrum and ilium, comprised of ligamentous and cartilaginous
connections.
• The joint is supported by muscles that also serve to deliver regional muscular forces to the pelvic
bones. As the musculature of the SI joint is shared with the hip joint (eg, gluteus medius/minimus,
biceps femoris, and piriformis), it cannot function independently.
• The joint is subject to shearing forces in a multitude of directions, but rotates only minimally about all
3 axes.
• From puberty onward, the joint begins to display degenerative changes, which are inevitable by the
eighth decade of life.
• Though the exact mechanism of SI joint pain is likely multifactorial and not completely understood. The
pathology of the joint has been implicated as a cause of chronic low back pain in up to 30% of all
afflicted patients.
Figure 28-1. (A) Side-to-side anatomical variation in CT scan of the same patient. (B) Side-to-side
anatomical variation in CT scan of the same patient. (Used with permission from Harold Cordner, MD)
NEUROANATOMY
• The innervation of the SI joint continues to be a topic of great debate.
• The posterior surface of the joint has been described to have sensory innervation originating as
cephalad as the medial branches of the posterior primary ramus of L4 with contributions from L5
primary dorsal ramus.
• The lateral branches from sacral nerve roots from S1 to S4 supply most of posterior surface of the SI
joint.
• The anterior joint has also been postulated to be innervated by a variety of sources, ranging from the
ventral ramus of L4 to the ventral ramus of S2.
• Along the dorsal aspect of the joint, the nerves may run along the periosteum or as far as 8 mm from the
bone.
• The diagnostic or therapeutic injections and denervation procedures are targeted to the nerve supply of
the posterior aspect of the SI joint.
INDICATIONS
The radiofrequency denervation of the SI joint for the treatment of chronic low back pain secondary to
sacroilitis is effective, as adequate evidence exists to support the therapy. However, uniform criteria to
identify those patients who would benefit most from the procedure have yet to be developed. The
Simplicity III procedure is relatively safe; however, the following criteria should be fulfilled before the
denervation of the SI joint:
• Referred pain pattern consistent with a clinical diagnosis of sacroilitis.
• Two or more positive, provocative tests consistent with sacroilitis on physical examination.
• Greater than 50% relief from two diagnostic SI joint injections, with positive intra-articular and
periarticular spread of contrast documented, when possible.

Like any intervention, the risks and benefits of this procedure should be weighed before proceeding, and
care should be taken to rule out serious diagnoses that may be coexisting with sacroiliitis, eg, neoplasm,
infection, autoimmune disease, fracture. Close attention should be paid to fluoroscopic anatomy to avoid
advancing the Simplicity III probe into one of the sacral, neural foramina, and to avoid advancing the
probe anteriorly past the sacrum subsequently entering the pelvic cavity. It should be noted that placement
of the Simplicity III probe and the creation of its subsequent strip-lesion are often associated with a
certain degree of soft-tissue damage causing postoperative myofascial pain and muscle spasm. Patients
should be informed to expect these sequalae, and appropriate medications should be prescribed.
Contraindications to Simplicity III radiofrequency neuroablation are as follow:
• Coagulopathy
• Pregnancy (teratogenic effects of radiation)
• Systemic infection, skin infection over puncture site, or immunodeficiency
• Refusal/inability to give informed consent
• Inability to tolerate the prone position
• Inability to tolerate the procedure due to coexisting medical conditions
• Informed consent should be obtained explaining of all complications including postoperative
discomfort secondary to soft-tissue damage, muscle spasm, and periosteal irritation.
• Adherence to strict aseptic technique is of utmost importance. Operating surgeons should be fully
gloved and gowned, and the patient should be surgically prepared and sterilely draped.
Selection of Anesthesia
Placement of the Simplicity III probe is inherently associated with disruption of muscular and ligamentous
tissue, as well as the periosteum along with process of denervation. Patients will differ in their ability to
tolerate the sensations accompanying placement of the probe and prone position necessary for the
procedure. Anesthetic techniques aimed at maximizing patient comfort range from local anesthetic
infiltration only, to intravenous sedation, monitored anesthesia care (MAC) and general anesthesia. Care
must be taken not to exceed appropriate dosage limits of local anesthetic. It is re-recommended to have
discussion with an anesthesiologist to determine appropriate anesthetic technique:
• Local anesthetic infiltration only
• Local anesthetic infiltration with intravenous sedation (MAC)
• Neuraxial anesthesia with intravenous sedation.
• General anesthesia with laryngeal mask airway (LMA) or tracheal intubation.
Two fluoroscopic views are used for placement of the Simplicity III probe:
Anterior-Posterior (AP) View
Start with a straight AP view of the sacrum centering on the ipsilateral SI joint and sacral neural foramina
(Figure 28-2). It is of extreme importance to identify the sacral foramina and the ipsilateral SI joint as the
lesion track will lie between these two anatomic landmarks. Care must be taken to avoid advancing the
probe into one of the sacral neural foramina.
Figure 28-2. AP view of the sacrum with expected final position of the Simplicity III probe. Note the
position of the probe lateral to the sacral neural foramina, but medial to the SI joint. The sacral foramina
have been outlined in blue, the lesion track along the simplicity 3 probe has been highlighted in red, and
the articulating portions of the SI joint have also been traced out.
Lateral View
A true lateral view of the sacrum is also of extreme importance to aid in proper placement of the
Simplicity III probe. Care must be taken to ensure that the probe is no more than 1 cm away from the
sacrum at any point along the lesion track, and also to ensure that the tip of the probe has advanced to the
sacral ala.
• Equipment
• 22-gauge 3.5, 5, and 7-in spinal needles
• 25-gauge skin needle
• 18-gauge needle
• Simplicity III radiofrequency probe
• Simplicity III cable NT1100 NeuroTherm generator
• Dispersal (grounding) pad
• 10-in RF cannula with 10 mm active tip and 10-in RF probe for radiofrequency lesioning of the L5
primary dorsal ramus
• Medications
Local anesthetic—lidocaine 1%, with or without 1:200,000 epinephrine
Triamcinolone or methylprednisone (for L5 primary dorsal ramus and for SI joint)
Bupivacaine 0.5% (for L5 primary dorsal ramus)
The Simplicity III Probe (Figure 28-3)

• It is a rigid tripolar probe with a sharp tip that fits the curvature of sacrum.
• The probe is placed transversely over the lateral branches.
• It provides multiple, independent contacts programming to create total 5 lesions.
• First 2 lesions are bipolar lesions and created in-between first, second, and third electrodes.
• The next three lesions are unipolar and created by individual electrodes.
• Needs separate radiofrequency cannula probe for L4-5 dorsal ramus.
• After activating RF lesioning, it takes 8 minutes to create sacroiliac lesion and 90 seconds for L5
dorsal ramus lesion.
Figure 28-3. Simplicity III probe.
Technique
Patient positioning. The patient should be placed in the prone position on the fluoroscopy table with a
pillow under the abdomen to reduce lumbar lordotic curvature. Dispersal (grounding) pad should be
placed on the patient’s thigh, and connected to the NT1100 NeuroTherm generator. The patient should then
be surgically prepared and sterilely draped.
Selection of skin entry point. Entry point for the Simplicity III probe should be chosen in the AP
fluoroscopic view. The optimal entry point is at the lateral, inferior border of the ipsilateral sacrum,
approximately 1 cm lateral to and 1 cm caudal to the ipsilateral S3 neural foramen (Figure 28-4).
Figure 28-4. AP view of the sacrum with final position of the Simplicity III probe. Note skin entry point
and the position of the probe lateral to the sacral neural foramina, but medial to the SI joint. The 3, radio-
opaque contacts approximate the lesion track of the “strip” lesion. The yellow “X” marks approximates
the entry point for the probe.
Define the lesion track. The lesion track should also be identified in this view, specifically a track
lateral to the S1-S4 neural foramina but medial to the SI joint.
Anesthetizing the lesion track. After selecting an entry point, a local anesthetic skin wheal should be
created there with the 25-gauge skin needle and lidocaine 1%. Subsequently, the 3.5-in spinal needle
should be advanced through the wheal until it comes into contact with periosteum lateral to the S3
foramen, where more local anesthetic is given. Thereafter, a curved 22-gauge 5- or 7-in spinal needle is
entered through the skin wheal and directed to come into contact with the periosteum at 1 to 1.5 cm
intervals along the lesion track. Each time the needle comes into contact with the periosteum, a 1- to 2-mL
aliquot of local anesthetic should be given in the vicinity of the periosteum.
An alternative method of anesthetizing the lesion track has been described, wherein a 3.5-in spinal
needle is maneuvered to lay transversely across the lesion track, and a mixture of local anesthetic and
steroid is injected as the needle is withdrawn. In our opinion, this is a technically more challenging and
time-consuming method, and the former method is preferred in our practice.
PLACEMENT OF THE SIMPLICITY III PROBE

• The Simplicity III probe should be inserted through the previously created skin wheal and advanced to
contact with the periosteum at the inferior and lateral portion of the sacrum lateral to S3 foramen.
• It is very important to advance the probe with intermittent fluoroscopic guidance in the anteroposterior
(AP) and lateral views to avoid the entry of the probe into a sacral foramen and pelvic cavity.
• Lateral fluoroscopic views are mandatory to ensure that the probe is not advanced below the inferior
border of the sacrum into the pelvic cavity.
• The probe is then advanced in a cephalad direction midway between a line passing through sacral
foramina and medial border of posterior sacroiliac joint line, keeping constant contact with the sacrum
along the previously anesthetized lesion track.
• The probe is advanced through the fibrous ligamentous tissue between the sacrum and ilium along the
anesthetized track lateral to the neural foramen and medial to the SI joint.
• Intermittent fluoroscopy in the lateral view is also useful to ensure the probe remains in close contact
(>1 cm) with the sacrum along its entire course, and that the probe is dorsal to the ilium. The probe
should be advanced until it contacts the sacral ala, and further advancement is impossible.
• The final position of the probe should be verified in the AP and lateral views (Figures 28-4 and 28-5).
• The three active radio opaque electrodes of the probe should lie adjacent to the S1-S4 pathways in the
AP view.
• In the lateral view, the probe should lie in close contact (>1 cm) with the sacrum along its curvature,
with the most dorsal contact away from the dermis to prevent skin injury.
• If the depth of the last electrode is not adequate and there is risk of skin burns, program the probe to
Simplicity II protocol to inactivate the last electrode.
Figure 28-5. Lateral view of the sacrum with final position of the Simplicity III probe. Note the lack of
separation between the probe and the dorsal sacrum and the tip of the probe against the sacral ala. Also
note that none of the contacts are close to the dermis, ensuring skin injury is prevented.
SIMPLICITY III RADIOFREQUENCY LESIONING PROTOCOL

The Simplicity III probe should be connected to the NT1100 NeuroTherm module with the provided
cable, and the preprogrammed Simplicity III, lesioning protocol carried out.
The Simplicity III protocol creates 5 sequential lesions in 5 steps. First 2 are bipolar lesions and
created between the first and second, then second and third active electrodes. Next three are monopolar
lesions and are created at each of the three active electrodes sequentially (Figure 28-6). Each of the 5
lesions is performed at 80°C, and is 1.5 minutes in duration. At the end of procedure it creates one
homogenous, consistent true strip lesion (Figure 28-7). The lesioning protocol may be adjusted to
operator preference. At the end of the protocol, the probe should be allowed to cool to body temperature
before removed, and verified to be intact.
Figure 28-6. Depiction of the Simplicity III lesioning protocol. The first 2 lesions are bipolar lesions
between the first/second and second/third electrodes. The next 3 lesions are monopolar lesions at each of
the 3 electrodes. The lesions are made sequentially, for 1.5 minutes each at 85°C.
Figure 28-7. Note the strip lesion created by the protocol on a piece of raw meat.
Radiofrequency Lesioning of L5 Primary Dorsal Ramus

This portion of the procedure may be performed prior to Simplicity III probe placement or after
Simplicity III lesioning protocol as preferred by the operator (Figure 28-8).
Figure 28-8. Picture of the RF canula in situ for lesioning of L5 dorsal ramus. Use 10-in curved RF with
10 mm active tip.
The Simplicity III radiofrequency denervation of the SI joint may be performed as an outpatient
procedure. The patient should be monitored in the postanesthesia care unit until discharge criteria at the
facility are met. The patient may be discharged with a muscle relaxant (eg, diazepam 2-5 mg PO q8h as
needed) and an oral analgesic to mitigate postoperative spasm and discomfort. Telephone follow-up 24
hour postprocedure is recommended to ensure lack of complications.

• Use an 18-gauge needle to create a stab-incision at the skin-wheal to facilitate percutaneous entry of
the Simplicity III probe.
• “Wiggle” the probe from side to side as you advance along the periosteum, so as not to get ensnared.
Optimal manipulation of the probe is accomplished using a two-handed technique, with one hand on the
probe’s handle, and one hand grasping the probe near the skin. Care should be taken to maintain the
curvature of the probe during manipulation.
• Obtain intermittent lateral radiographs as you approach the most convex portion of the sacrum to ensure
that the probe remains in close contact with the sacrum at this point and does not begin to advance
dorsally over the ilium.
• In extremely slender patients, where the third, active contact is close to the dermis and risks skin
injury, use the Simplicity II lesioning protocol. This protocol inactivates the third electrode that is
close to skin. It creates one bipolar lesion between the first and second electrodes, followed by two
monopolar lesions at the first and second electrodes. As the third contact is not used in the lesioning
protocol, the skin remains unharmed. A smaller strip lesion is created, and two such lesions could be
created to ensure complete denervation of the S1-S4 lateral branches. The same technique could be
used in patients where anatomic variation makes proper probe position impossible (ie, the sacrum is
shaped in such a way that all three contacts cannot lie in close proximity to the sacrum).
Suggested Reading
Benzon HT, Nader A. Raj’s Practical Management of Pain. 4th ed. Philadelphia, PA: Mosby Elsevier;
2008:367-385, 1063-1077.
Cohen SP. Epidemics, evolution, and sacroiliac joint pain. Reg Anesth Pain Med. 2007;32(1):3-6.
Cohen SP. Sacroiliac joint pain: a comprehensive review of anatomy, diagnosis, and treatment. Anesth
Analg. 2005;101:1440-1453.
Cohen SP, Hurley RW, Buckenmaier CC, et al. Randomized placebo-controlled study evaluating lateral
branch radiofrequency denervation for sacroiliac joint pain. Anesthesiology. 2008;109(2):279-288.
Cohen CP, Strassels SA, Kurihara C, et al. Outcome predictors for sacroiliac joint (lateral branch)
radiofrequency denervation. Reg Anesth Pain Med. 2009;34:206-214.
Ferrante MF, King LF, Roche EA, et al. Radiofrequency sacroiliac joint denervation for sacroiliac
syndrome. Reg Anesth Pain Med. 2001;26(2):137-142.
Ikeda R. Innervation of the sacroiliac joint. Macroscopical and histological studies. Nippon Ika Daigaku
Zasshi. 1991;58(5):587-596.
Kransdorf MJ. Image Guided Spine Intervention. Philadelphia, PA: Saunders; 2003:127-140.
Rupert RP, Lee L, Manchikanti L, et al. Evaluation of sacroiliac joint interventions: a systematic appraisal
of the literature. Pain Physician. 2009;12:399-418.
The Simplicity III Manual. NeuroTherm®. Middleton, MA.
Vanelderen P, Szadek K, Cohen SP, et al. Evidence Based Medicine, 13. Sacroiliac joint pain. Pain
Practice. 2010;10(5):470-478.
CHAPTER 29
Percutaneous Sacroplasty
Harold Cordner and Michael E. Frey
INTRODUCTION
Sacral insufficiency fractures are a common, but often underdiagnosed source of low back pain in the
elderly osteoporotic patient. Fractures of the pelvis are a consequence of undue stress onto a weakened
bone. Osteoporosis is the most common cause of fractures of the pelvis. Major or minor trauma is another
cause; however, spontaneous sacral insufficiency fractures are also common. The incidence of sacral
insufficiency fractures comprises of approximately 1% to 2% of pathologic fractures involving the spine
and pelvis. However, these fractures are often misdiagnosed and unrecognized. Risks of sacral
insufficiency fractures are very similar to that of vertebral compression fractures.
The treatment of sacral insufficiency fractures can either be noninterventional, interventional, or
surgical. Unstable fractures, especially with associated cauda equina syndrome, may require closed
manipulation or open reduction and internal fixation procedures. Open reduction procedures as compared
to percutaneous reduction have increased risks, especially infection.
• Conventionally, treatment in the past has been mainly bed rest, opiate analgesic management, using a
walker with partial weight-bearing and early mobilization, and lumbosacral or pelvic corsets.
• Deep venous thromboses and pulmonary emboli, reduced muscle strength with prolonged recovery,
postural hypotension and impaired cardiac function, atelectasis and pneumonia. Skin breakdown and
pressure ulcers, constipation and fecal impaction, depression and intellectual regression are known
complications of prolonged periods of inactivity.
• The overall 1-year mortality rate associated with pelvic insufficiency fractures is 14.3% and 50% of
affected patients will not return to their prior level of function.
• Although initial clinical improvement may occur rapidly, compete resolution of symptoms may not
occur for up to 9 to 12 months.
• Despite a favorable natural history, more aggressive treatments may benefit certain patients who are
incapacitated by painful sacral insufficiency fractures.
Chronic symptoms and disability related to osteoporotic insufficiency fractures are believed to be due
to fracture nonunion, micromotion, or resultant deformity related to the anemic attempts of the weakened
bone to heal. The percutaneous injection of polymethylmethacrylate (PMMA) into fractured vertebral
bodies (vertebroplasty) has been safely performed to successfully treat painful osteoporotic compression
fractures. A natural extension in the application of vertebroplasty is the percutaneous injection of synthetic
bone cement into the fractured sacrum (sacroplasty) to treat persistent symptoms and disability.
Sacroplasty was first reported in 2001 as treatment of symptomatic sacral metastatic lesions, and
subsequent reports have documented its safe and effective performance.
DIAGNOSIS
• Once suspicion of a sacral insufficiency fracture is suspected, then appropriate imaging is necessary.
Some patient may already have had normal spinal or pelvic radiographs.
• The gold standard, which yields the highest sensitivity and specificity, is a magnetic resonance imaging
(MRI). If a patient has a pacemaker or other condition that precludes obtaining an MRI, a computed
tomography (CT) is necessary to compliment the bone scan. CT scans are more sensitive; however,
nondisplaced fractures without reactive sclerosis may be missed.
• Fractures of the sacrum are best shown on coronal planes with a dedicated MRI of the sacrum.
• Traditionally, ordered MRI of the lumbar spine may miss a small percentage of fractures of the sacrum.
• Fat-suppressed T2-weighted or short T1 inversion recovery (STIR) sequences are the best imaging to
diagnose these fractures (Figure 29-1). The most sensitive but not specific study is a bone scan, which
may be positive for up to 1 year after the acute fracture. Honda sign, a typical H-shaped pattern on
bone scan is pathognomonic and represents a bilateral sacral alar fracture with a horizontal fracture
through the sacrum connecting them (Figure 29-2).
• A three-dimensional or bone scan with single photon emission CT (SPECT) may also aid in helping
diagnose sacral insufficiency fractures.
Figure 29-1. Axial view of a T2-fat suppression image demonstrating bilateral sacral insufficiency
fractures.
Figure 29-2. Honda sign on bone scan with SPECT imaging demonstrating bilateral sacral insufficiency
fractures.
Fractures can occur in several places. The most common is a bilateral sacral ala fractures. Unilateral
fractures can occur with or without a central horizontal component.
RELEVANT ANATOMY
Anatomically, the sacrum is comprised of 5 fused segments. Weight transfers can occur through the sacral
segments which can allow a unique appearance of sacral fractures. In 1988, Denis et al classified the
location of sacral fractures into 3 zones (Figure 29-3).
• Zone 1 involves the sacral ala but does not traverse the central sacral canal or foramen.
• Zone 2 involves sacral foramen but does not involve the central canal.
• Zone 3 involves the central canal. Patients with zone 3 fractures are associated with saddle anesthesia,
loss of sphincter tone as a result of cauda equina injury.
Figure 29-3. Denis classification of sacral fracture location.
The most common sacral insufficiency fractures are classified as zone 1. These fractures run parallel to
the sacroiliac join along the entire sacral ala. When viewing sacral fractures via imaging techniques,
place technical considerations when later deciding to perform sacral augmentation.
The key to successful sacroplasty depends on correctly identifying the following structures:
• Sacrum—including the posterior, anterior, and superior borders
• Four bilateral sacral foramen
• Sacroiliac joint
• Sacral canal
Other relevant that should be taken into consideration when performing Sacroplasty are:
• Rectum—this is separated from the ganglion by a layer of extraperitoneal fat and connective tissue
• Exiting nerve roots from the sacral foramen
• Sacral nerves traveling within the sacral canal
• Erector spinae muscles

As with any intervention, one must weigh the ratio of potential benefits to the potential complications. In
an average patient, and given the safety of the technique described here, sacroplasty should be considered
early on in the treatment algorithm in the properly indicated patient. However, given the associated
pathophysiology, one must carefully consider each patient individually.
Some basic concerns for injection are as follows:
• Immunocompromised patients are potentially at high risk for infection, this is of particular relevance in
patients with malignancy.
• Metastatic cancer with local masses in the region.
• Thrombocytopenia or coagulopathy.
• Prone position may be difficult if patient has associated pelvic fractures.
• Possible rectal perforation if the needle is advanced too far anteriorly.
• Possible nerve damage if the needle is advanced into the sacral canal or foramen.
Contraindications for injection include:
• Coagulopathy
• Acute neurological deficits related to the fracture
• Patient refusal
• Anticoagulation—this is less of a concern than for an epidural injection but a concern nonetheless as
there is inherent disruption of tissue from the introduction of a needle.
• Physical examination of the area for infection, skin ulceration, or necrosis.
• Patient must be able to lie prone for the intended length of the procedure.
vasovagal reaction or reaction to the PMMA cement.
Equipment
• Vertebroplasty trocars—13g or 11g
• PMMA cement and delivery system
• 5-cc syringe for medications
• 1.5- to 3.5-in 25-gauge needle for local anesthetic
• 3.5-in spinal needles for placement in sacral foramen
Technique
• Sacroplasty is performed either by fluoroscopic guidance, computed tomography (CT) guidance, or a
combination of both.
• When visualizing the sacrum under CT guidance, the choice of the entry site depends on the fracture
lines.
• For H-shaped fractures, one may chose fixation of the horizontal component by accessing the needle
puncture posterolaterally through the sacroiliac joint (Figure 29-4).
• Other alternative sites are punctures over the sacral ala with angulation of the needle between the
spinal canal and the ipsilateral sacral foramen.
• The lateral fractures can be accessed by placing the trocar more medially and advancing the slightly
laterally avoiding the sacral foramen and parallel to the fracture line.
• Sacroplasty may also be performed with fluoroscopic visualization safely if careful attention to
landmarks and anatomic structures is followed.
• Needles may be placed in the lateral aspect of the sacral foramen to help aid in visualization of the
foramen during the procedure. This describes a variation of the short axis technique using fluoroscopic
visualization.
• The patient is placed in a prone position and after an oblique view aligning the entire sacroiliac joint,
after local anesthetic infiltration, two 13-gauge vertebroplasty trocars are placed between the sacral
foramen and sacroiliac joint on the side of the fractured ala at a 45-degree angle toward the sacroiliac
joint.
• The trocars are then inserted approximately to midpoint of the sacrum, under lateral view, maintaining
the 45-degree angle (Figure 29-5).
• After mixing the PMMA cement, under AP imaging, 2 to 5 cc of PMMA are injected through each
trocar, monitoring the spread of the bone cement, to avoid medial extension toward the sacral nerve
roots (Figure 29-6).
• An alternative method is to advance the trocar from the caudal aspect of the sacrum, through the body
of the sacrum, lateral to the sacral foramen and medial to the SI joint.
• The trocar is advanced from the lower sacral segment toward the sacral ala. Fluoroscopic imaging in
both lateral and AP views is necessary. In this manner, the trocar should be parallel to the vertical
fractures (Figure 29-7). This allows for the PMMA cement to be deposited along the entire fracture
line by injecting as the trocar is withdrawn.
• Once correct placement of the trocar is confirmed, PMMA cement is injected slowly and incrementally
under constant fluoroscopic visualization (Figure 29-8).
• Constant vigilance to fluoroscopic imaging must occur to ensure cement extravasation does not occur.
• The patient should be maintained in the prone position for 10 to 20 minutes until the cement has set up
and hardened. Postprocedure, patient should be monitored for neurological deficits, systemic or
procedure related complications.
Figure 29-4. H-shaped fractures (Reprinted with the kind permission of Springer Science+Business
Media from Mathis JM, Deramond H, Belkoff SM (eds). Percutaneous Vertebroplasty and Kyphoplasty,
Second Edition. New York Springer Science+Business Media, 2006. Ch 16, Fig 16.7)
Figure 29-5. (A) Lateral fluoroscopic view of bilateral needle placement in the sacrum. (B) AP
fluoroscopic view of bilateral needle placement.
Figure 29-6. AP view of bilateral needle placement with cement placement to the bilateral sacral alae.
Figure 29-7. (A) Lateral view of the longitudinal approach under fluoroscopic guidance. (B) AP view of
the longitudinal approach under fluoroscopic guidance.
Figure 29-8. (A) AP view of cement placement with the longitudinal approach under fluoroscopic
guidance. (B) AP view of bilateral cement placement with needles withdrawn (finished product).
POTENTIAL COMPLICATIONS
• Infection
• Bleeding
• Rectal perforation
• Cauda equina syndrome
• Nerve root or intraforaminal injection
• Intravascular injection
• Osteitis or periostitis
• Hematoma
• Inadvertent cement spread may potentially lead to motor, sexual, or bowel/bladder dysfunction
CLINICAL PEARLS
• When injecting, always start in AP to ensure cement is not spreading medially.
• Under lateral view, keep the needle in the middle third of the sacral segments to decease migration of
cement.
• Always perform neurologic examination to make sure patient has adequate strength in the legs prior to
discharge.
• MRI of the lumbar spine may not be sufficient. MRI of the sacrum is gold standard.
• If the patient cannot have an MRI, get CT and bone scan with SPECT imaging.
• When using the longitudinal approach, stay lateral to the neural foremen.
• Inject small incremental amounts of PMMA with frequent visualization in both AP and lateral views.
• If cement extravasation occurs, stop injecting. Allowing the cement to harden a little at that area may
allow you to continue injecting in another area without further extravasation.
Suggested Reading
Butler CL, Given CA, Michel SJ, et al. Percutaneous sacroplasty for the treatment of sacral insufficiency
fractures. AJR Am J Roentgenol. 2005;184:1956.
Denis F, Davis S, Comfort T. Sacral fractures: an important problem. Retrospective analysis of 236
cases. Clin Orthop. 1988;227:67.
Grant M. Sacroplasty: a new treatment for sacral insufficiency fracture. J Vasc Interv Radiol.
2002;13:1265.
Kayanja M, Tsai E, Ymashita T, et al. The biomechanics of insufficiency fractures and augmentation of the
sacrum. Spine J. 2006;6(suppl 5):96.
Leroux JL, Denat B, Thomas E, et al. Sacral insufficiency fractures presenting as acute low-back pain:
biomechanical aspects. Spine. 1993;18:2502.
Lin JT, Lane JM. Sacral stress fractures. J Womens Health. 2003;12:879-888.
ME Frey, MJ DePalma, et al. Efficacy and safety of percutaneous sacroplasty for painful osteoporotic
sacral insufficiency fractures. Spine. 2007;32:1635-1640.
Waites MD, Mears SC, Mathis JM, et al. Strength restoration by sacroplasty of simulated sacral
insufficiency fractures. Eur Cells Materials. 2006;11(suppl 1):62.
Zaman FM, Frey ME, Slipman CW. Sacral stress fractures. Curr Sports Med Rep. 2006;5:37-43.
CHAPTER 30
Percutaneous Facet Fusion

Rinoo V. Shah
BACKGROUND
As surgical technology becomes less invasive, interventional pain physicians will play an increasing role
in delivering this care. Facet mediated pain has historically been treated with medial branch blocks, intra-
articular injections, and radiofrequency neurolysis. There has been an increased interest in treating facet
mediated pain from a surgical standpoint. Since facet joints are synovial diarthrodial joints, surgical
approaches have focused on joint immobilization or arthrodesis. One minimally invasive approach is
percutaneous facet fusion (PFF) with allograft bone dowels.
INTRODUCTION
PFF has emerged as a standalone and augmentative procedure to help patients with facet mediated pain.
The procedure addresses facet mediated pain due to degenerative facet arthrosis, mechanical loading, and
minor instability.
The advantages of PFF are:
• Reduced invasiveness and morbidity
• Early recovery and discharge
• Motion preservation
PFF fits well within the continuum of spinal care, with a position between interventional
(percutaneous) and reconstructive (surgical) spinal procedure.
PFF doesn’t “burn bridges.”
• The current patients will still have access to future advances in spinal surgery, eg, biologics.
• Technical feasibility, safety, and biomechanical stability have been demonstrated.
• Percutaneous facet fixation with screws and intra-articular facet joint spacers have demonstrated
efficacy.
• Finally, less invasive fusions have comparable outcomes to more invasive fusions and patient selection
continues to be subjective.
POTENTIAL INDICATIONS
• Isolated facet–based symptomatic back pain that is refractory to conservative measures
• Stabilization of the lumbar spine following decompressive procedures or where minor instability
exists or presents postoperatively
• Minor instability (1-2 mm listhesis)
• Posterior supplemental fixation to interbody fusion
• Adjunct to motion limiting devices
CONTRAINDICATIONS (RELATIVE OR ABSOLUTE) AND

INDICATIONS FOR PROCEDURE TERMINATION
• Trauma
• High-grade instability
• Tumors
• Spondylolysis (pars fracture)
• Grade 2 or greater spondylolisthesis
• Coagulopathy
• Progressive neurologic deficit
• Allergy to procedural drugs, eg, iodinated contrast
• Open wound or skin ulceration
• Poorly controlled diabetes
• Patient refusal or lack of health care proxy
• Inability to prone for the duration of the procedure
• Intraoperative recognition of foraminal trespass or epidural placement
• Severe nerve root pain during procedure
• Hypotension
RELEVANT ANATOMY
• The lumbar facet joint is a diarthrodial, synovial joint. These joints can undergo a process of
degeneration leading to arthropathy.
• The facet joint represents an articulation between the inferior articular process of the cephalad
vertebral body and the superior articular process of the caudal vertebral body.
• The inferior articular process is convex and the superior articular process is concave.
• The joint is oriented obliquely to the sagittal plane.
• The articular surfaces are lined with hyaline cartilage.
• The joint contains a synovial membrane and synovial fluid. The joint is encapsulated with a synovial
sheath. This creates a superior articular recess that is anterior and an inferior articular recess that is
posterior.
• Forward flexion opens up the inferior recess and the joint; whereas extension opens the superior
recess.
• The joint receives a rich sensory innervation by the ipsilateral medial branches, at that level and the
cephalad level.
• As the disc degeneration progresses, the facet joint may become lax and facilitate the degenerative
cascade.
• Facet arthropathy or sclerosis can be diagnosed and rated, in terms of severity, via MRI and CT
scanning. CT or MR imaging provides information about facet orientation and this helps with
procedure planning.
• There is a well-established discordance between facet arthropathy and facet mediated pain; hence, the
interventional pain community relies on comparative diagnostic blocks to diagnose facet mediated
pain. This step may be essential as a prelude to neurolysis, but is not de rigueur for PFF.
• The surgical literature relies on imaging evidence of facet arthropathy and the presence of pain, when
planning facet fusion procedures.
What is PFF?
• Percutaneous facet fusion involves the insertion of cortical bone allograft in the shape of a dowel to
achieve arthrodesis.
• These dowels are FDA approved as a bone graft to provide stability for primary and secondary healing
of bone.
• The dowels have different proprietary designs ranging from cylindrical, tapered, threaded, or
rectangular with wings/flanges.
• Different shapes exist to facilitate intra-articular placement and to mitigate “back out” or dislodgement.
• The dowels separate joint surfaces and eventually, stabilize the joint. Surgical access is similar among
different manufacturers.
• Patients should have constant pain >6/10 and functional limitations.
• Patients should have withheld coagulopathic medications for appropriate lengths of time as per ASRA
recommendations.
• Diabetic patients may need blood sugar testing.
• Female patients of childbearing age should have urine pregnancy test or a serum pregnancy test.
• Intravenous access is advised, particularly for patients receiving cervical or thoracic procedures, and
for patients who may need intravenous anxiolytics and/or analgesics.
• Cardiopulmonary safe guards and resuscitation equipment should be present within the procedure suite.
• Patients should sign witnessed informed consent, which includes an evidence-based discussion about
indications, efficacy, and safety.
• Preprocedure site marking/initialing with an indelible marker site and site verification.
Positioning of the Patient
• Prone
• Pressure points should be padded
• Eye protection may be necessary
• Neck position should be neutral
• Reduce lumbar lordosis
Needles, Medications, and Equipment

• Scalpel, #11 or #15
• 22-gauge spinal needle, 6 in
• Steinman or guide pin ×2
• Cannulated facet distractor (spatula) or directional cannula with prongs ×2
• Drill guide
• Drill bit with electrically powered drill
• Bone dowel delivery device and bone dowels ×2
• Impaction pin ×2

• Sterile patient preparation.
• Antibiotic prophylaxis.
• Fluoroscopy to visualize lucency of facet joint.
Oblique angulation (30-50 degrees)—to visualize facet joint lucency.
Angle of approach can be estimated via axial CT or MRI images.
Tip: facet joint may be curvilinear in shape—so obliquity of C-arm should accommodate dorsal
limb of facet joint.
• Under fluoroscopy, advance 22-gauge spinal needle is placed into facet joint.
• Make a stab incision with scalpel, adjacent to needle entry site.
• Advance guide (Steinman) pin into plane of facet joint (Figure 30-1).
Figure 30-1. Steinman pin placement, right L5-S1 facet joint.
Tip: use needle path to guide trajectory.

• Once guide pin contacts dorsal surface of facet joint, advance 5 mm.
Tip: the curvature of facet joint should reduce risk of foraminal trespass, but this is not applicable to
patients with osteoporosis.
• Advance cannulated facet distractor (Figure 30-2) over guide pin.
Figure 30-2. Cannulated facet distractor, right L5-S1 facet joint.
Tip: anchor guide pin and facet distractor when it enters skin, do not move this aggressively, else it
may dislodge out of facet joint.
• Tap facet distractor (spatula) (Figure 30-2) slightly into facet joint with mallet.
Tapered tip facet distractor should stop at 5 mm depth.
Tip: carefully monitor guide pin depth to avoid foraminal trespass.
• Directional cannula should be threaded over facet distractor.
• Place tip of directional cannula (2 prongs) into plane of facet joint.
• Tap the directional cannula to fully seat the device.
• Hold directional cannula and slowly remove the facet distractor and guide pin.
• Advance drill guide into directional cannula.
• Advance drill bit into cannula/drill guide.
• Use drill to core out hole in facet joint.
Tip: Trufuse uses a 1 step drill guide.
• Drill cores out superior and inferior facet joints simultaneously.
Tip: Verteloc uses a 2-step drill guide.
• Drill cores out superior facet (lateral articulating surface).
• Rotate the drill guide 180 degrees.
• Reinsert drill and core out the inferior facet (medial articulating surface).
• The drill guide has a built in stop.
Tip: saline irrigation reduces risk of thermal injury.
Tip: use lateral fluoroscopy to ensure no violation of foramen.
• Remove drill.
• Load implant holder with bone dowel or preformed dowel.
• Implant/dowel is a cortical allograft.
Tip: verify with device manufacturer about safety and reliability of cortical allograft.
Tip: implant holder has different configurations depending on shape of bone dowel.
• Verteloc: rectangular dowel with “fins”—fins are parallel to joint and body is perpendicular.
• Trufuse: cylindrical bone dowel (Figures 30-3 and 30-4).
Figure 30-3. Bone dowel, left L5-S1 facet joint.
Figure 30-4. Bone dowel, right L5-S1 facet joint.
• Nufix: threaded bone dowel.

• Advance implant holder with implant into facet joint.
• Tamp dowel into place.
• Remove instruments.
• Suture skin with 2-0 and 3-0 nylon.
• Patient bracing with a lumbosacral orthosis, for 6 to 12 weeks.
MONITORING OF POTENTIAL POSTPROCEDURE

COMPLICATIONS
• Assess for bleeding at skin entry site.
• Use lateral fluoroscopy to monitor for foraminal trespass.
• Use anteroposterior fluoroscopy to gauge anteromedial dowel placement.
• Postoperative neurologic assessment
If patient sedated, test withdrawal response on plantar surface of foot
Assess sensorimotor and reflex integrity
Voiding and ambulation status on discharge
CT scan in selected patients (Figures 30-5 through 30-7)
Figure 30-5. Axial CT scan; seated dowels at L5-S1.

Figure 30-6. Sagittal CT scan: seated dowels at L4-5 and L5-S1.
Figure 30-7. (A) 3D CT Scan of TruFUSE, (B) TruFUSE® Implanted in a sawbone. (Reproduced with
permission from Contempo Medical, LLC.)
OUTCOMES
In an abstract presentation, Trangco-Evans demonstrated that 3 out of 8 patients did well and that 5
patients did improve. The latter 5 patients had evidence of dowel back out and poor compliance with
postoperative brace utilization. Advances in dowel configuration and improving patient compliance with
brace utilization are reasonable goals to improve efficacy.
Patient safety should be monitored in the early postoperative period. Physician vigilance over infection,
pain, bleeding, dowel back out, brace compliance, nerve protection, and fall prevention are important.
ACRONYMS
CLBP chronic or nonspecific low back pain
CT computed tomography scan
MRI magnetic resonance imaging
PFF percutaneous facet fusion
Suggested Reading
Boswell MV, Shah RV, Everett CR, et al. Interventional techniques in the management of chronic spinal
pain: evidence-based practice guidelines. Pain Physician. 2005 Jan;8(1):1-47.
Fairbank J, Frost H, Wilson-MacDonald J, Yu LM, Barker K, Collins R. Spine Stabilisation Trial Group.
Randomised controlled trial to compare surgical stabilisation of the lumbar spine with an intensive
rehabilitation programme for patients with chronic low back pain: the MRC spine stabilisation trial.
BMJ. 2005 May 28;330(7502):1233. Epub 2005 May 23. Erratum in: BMJ.2005 Jun
25;330(7506):1485.
Fritzell P, Hägg O, Wessberg P, Nordwall A. Swedish Lumbar Spine Study Group. Chronic low back pain
and fusion: a comparison of three surgical techniques: a prospective multicenter randomized study
from the Swedish lumbar spine study group. Spine (Phila Pa 1976). 2002 Jun 1;27(11):1131-1141.
Fritzell P, Hägg O, Wessberg P, Nordwall A; Swedish Lumbar Spine Study Group. 2001 Volvo Award
Winner in Clinical Studies: Lumbar fusion versus nonsurgical treatment for chronic low back pain: a
multicenter randomized controlled trial from the Swedish Lumbar Spine Study Group. Spine (Phila Pa
1976). 2001 Dec 1;26(23):2521-2532; discussion 2532-2534.
Manchikanti L, Helm S, Singh V, et al; ASIPP An ALGOic approach for clinical management of chronic
spinal pain. Pain Physician. 2009 Jul-Aug;12(4):E225-E264.
McDonald M, Cooper R, Wang MY. Use of computed tomography-single-photon emission computed
tomography fusion for diagnosing painful facet arthropathy. Technical note. Neurosurg Focus. 2007
Jan 15;22(1):E2.
Park YK, Kim JH, Oh JI, Kwon TH, Chung HS, Lee KC. Facet fusion in the lumbosacral spine: a 2-year
follow-up study. Neurosurgery. 2002 Jul;51(1):88-95; discussion 95-96.
Raj PP, Shah RV, Kaye AD, Denaro S, Hoover JM. Bleeding risk in interventional pain practice:
assessment, management, and review of the literature. Pain Physician. 2004 Jan;7(1):3-51.
Shah RV. Spine pain classification: a solution. Pain Physician. 2013 Mar-Apr;16(2):E51-E59.
Shah RV. The problem with diagnostic selective nerve root blocks. Spine (Phila Pa 1976). 2012 Nov
15;37(24):1991-1993.
Shah RV, Ericksen JJ, Lacerte M. Interventions in chronic pain management. 2. New frontiers: invasive
nonsurgical interventions. Arch Phys Med Rehabil. 2003 Mar;84(3)(suppl 1):S39-S44.
Shah RV, Everett CR, McKenzie-Brown AM, Sehgal N. Discography as a diagnostic test for spinal pain: a
systematic and narrative review. Pain Physician. 2005 Apr;8(2):187-209.
Shah RV, Kaye AD. Evolving concepts in the understanding of cervical facet joint pain. Pain Physician.
2004 Jul;7(3):295-299. Comment on: Pain Physician. 2004 Jul;7(3):301-309. PMID: 16858465.
Shah RV, Kaye AD. Bleeding risk and interventional pain management. Curr Opin Anaesthesiol. 2008
Aug;21(4):433-438. Review.
Shah RV, Lutz GE. Lumbar intraspinal synovial cysts: conservative management and review of the world’s
literature. Spine J. 2003 Nov-Dec;3(6):479-488. Review. PMID: 14609693.
Shah RV, Merritt W, Collins D, Racz GB. Targeting the spinal nerve via a double-needle, transforaminal
approach in failed back surgery syndrome: demonstration of a technique. Pain Physician. 2004
Jan;7(1):93-97.
Stein M, Elliott D, Glen J, Morava-Protzner I. Young Investigator Award. Percutaneous facet joint fusion:
preliminary experience. J Vasc Interv Radiol. 1993 Jan-Feb;4(1):69-74.
Stieber J, Quirno M, Cunningham M, Errico TJ, Bendo JA. The reliability of computed tomography and
magnetic resonance imaging grading of lumbar facet arthropathy in total disc replacement patients.
Spine (Phila Pa 1976). 2009 Nov 1;34(23):E833-E840.
Trangco-Evans RA, Bejjani FJ, Shah R, Hassan SE. TruFuse Facet Fusion Outcome: a retrospective case
series. Poster 265Presented at the 2011 AAPM Annual Meeting.
http://www.painmed.org/library/posters/poster-265.
Wilson-MacDonald J, Fairbank J, Frost H, et al. The MRC spine stabilization trial: surgical methods,
outcomes, costs, and complications of surgical stabilization. Spine stabilization trial group. Spine
(Phila Pa 1976). 2008 Oct 1;33(21):2334-2340.
Websites (accessed 11/11/2011)

Nufix: http://nutechmedical.com/catalog_nufix.php
Trufuse: http://www.minsurg.com/
Trufuse: http://www.youtube.com/watch?v=rN3mDiogYFU&noredirect=1
Trufuse (FDA disclosure): http://www.trufuse.com/pdfs/No510kapproval.pdf
Verteloc: http://www.verteloc.com/
Verteloc: http://www.youtube.com/watch?v=rN3mDiogYFU&noredirect=1
CHAPTER 31
Provocative Discogram
Vikram B. Patel and Sudhir Diwan
INTRODUCTION
Discography has been practiced by interventional pain physicians for the last few decades in an attempt to
identify the pain generator in the lumbar or the cervical spine (and less commonly the thoracic spine).
Although this procedure was initially intended to identify a pain generator that can be surgically treated
with a fusion, it was eventually utilized to diagnose a contained disc herniation as well as internal disc
disruption. Evolution of intradiscal procedures such as IntraDiscal Electrothermal Treatment (IDET),
percutaneous disc decompression, cooled radiofrequency use for biacuplasty, etc, have led pain
physicians to perform these procedures as minimally invasive treatment options for disc pathology.
In a lumbar disc, the intradiscal pressure increases based on the spine position. While the pressure is at
the baseline while lying down, it does increase somewhat when standing. However, sitting can increase
the pressure to almost twice as much, as the lumbar spine flexes and the relaxed muscles do not contribute
as much in weight bearing. Bending forward while sitting can increase the pressure to almost 3 times and
adding a twisting movement can increase it to 4 times as much as standing. A patient complaining of pain
in the lower back while performing any of these activities, and does not have any obvious cause for the
back pain is a good candidate for this procedure.
Indications
• Provocation discography is performed to identify a disc that is likely source of pain.
• Other diagnostic tests have failed to clearly confirm a suspected disc as a source of persistent pain.
• Assessment of discs prior proposed fusion of segment with symptomatic discs, and whether the discs
adjacent to this segment can support a fusion.
• Assessment of candidates for minimally invasive surgery who have confirmed disc herniation.
• Evaluation of abnormal discs or recurrent pain from a previously operated disc.
• Assessment of patients in whom surgery has failed, to determine whether pseudoarthrosis or a
symptomatic disc to be the source of pain.
DIAGNOSTIC PROVOCATIVE DISCOGRAPHY

Purpose
The purpose is to simulate disc loading in a lumbar disc that happens with forward flexion and increased
intradiscal pressure. This may be reported by a patient as sitting intolerance, aggravation of back pain
while bending forward, etc. Provocative discography is the procedure performed to reproduce discogenic
pain by injecting contrast in the disc. The pain is reproduced either by chemical irritation of sensitive
tissue, or by increasing the intradiscal pressure due to volume and stretching the annular fibers of the disc.
Discography helps to evaluate disc morphology and confirms the diagnosis for consideration of surgical
intervention. It also helps to identify the normal discs.
• Diagnostic purpose to identify the pain generator for back pain which is mechanical and axial in origin
and neck pain which is axial and no other pain generator can be identified.
• Identify the painful disc as a preoperative diagnostic indicator to facilitate a surgical intervention.
• Identify a contained herniation, internal disc disruption, or a leaking disc (common cause for painful
inflammatory radiculitis).
RELEVANT ANATOMY OF THE DISC (FIGURE 31-1)
Figure 31-1. Disc anatomy. S.C., sympathetic chain; G.R., grey remi communicantes; SV.N, sinuvertebral
nerve.
The lumbar or thoracic intervertebral disc can be approached through a posterolateral approach in a
prone patient, while the cervical disc can be approached through an anterolateral approach.
• Outer annulus (annulus fibrosus)—tough fibrous multilayered but flexible structure. Made up of 15 to
25 concentric layers called lamellae
• Inner nucleus (nucleus pulposus)—softer inner core of the disc containing proteoglycans
• Bound above and below by the cartilaginous end plates
Innervation
• Recurrent sinuvertebral nerve (ascending and descending branches)—branch of the grey rami
communicantes.
• The posterior longitudinal ligament (PLL) is richly innervated by the ascending sinuvertebral nerve.
Blood Supply
• Segmental arteries located at the waist of the vertebral body and supplying the end plates through
ascending and descending branches.
• A normal disc is essentially avascular and aneural.
• A pathological disc develops neo-vascularization and proliferation of nociceptive nerve endings.
ANATOMY OF CERVICAL DISCS

Cervical discs have certain characteristics distinct from other parts of the spine.
• The posterior longitudinal ligament in the cervical region is thicker, with a double layer, enclosing the
posterior and lateral parts of the disc, while it is a much thinner, single layer, with a weaker lateral
protection in the lumbar area.
• The nuclear material of the cervical disc lies more anterior than it does in the lumbar spine; therefore,
posterior displacement difficult to occur unless great forces are applied on the disc.
• The outer annulus is substantially thicker in the posterior portion of the cervical disc, making it more
difficult for the disc to bulge posteriorly.
• The anterior aspect of the disc receives sensory innervation from the sympathetic chain and the
posterior aspect receives innervation from the sinovertebral nerves. It is thought that these nerves
provide innervation to the facet joints as well.
ANATOMY OF THORACIC DISCS

• Thoracic discs are located between the cartilaginous end plates of the vertebrae above and below it.
• The disc of the thoracic spine is characterized by a thick fibroelastic annulus that surrounds a
gelatinous nucleus pulposus.
• These annular fibers run in an oblique direction from adjacent vertebrae.
• These annular fibers receive sensory input from various sources including sinovertebral nerves
(posteriorly) and the sympathetic chain (anteriorly).
ANATOMY OF LUMBAR DISCS

• Radicular pain of discogenic origin is much more common in the lumbar region than any other region.
• Unlike the cervical region, the bony facets do not protect the nerve roots.
• The posterior longitudinal ligament of the lumbar spine is thinner and less protective. This is
especially true in the lateral aspects of the spine.
• The nuclear material in the lumbar spine is located more posterior than that of the cervical or thoracic
spine.
• The innervation of the lumbar discs is very similar to that of the discs of the cervical and thoracic
spine. The outer third of the annulus fibrosus of the disc is supplied by multiple sensory nerves.

• The risk and benefit ratio for a diagnostic discogram has to be considered and should be performed
only after all the other diagnostic and therapeutic options have been exhausted.
• Discitis remains the single most dreaded complication from this procedure and all precautions need to
be taken to avoid it.
• Lack of good blood supply to the disc makes the treatment of discitis very difficult with a prolonged
morbidity.
• Any local and systematic infection is a contraindication for these procedures.
• Patient is unable to understand the procedure and unwilling to provide the written consent.
• Proper training and experience are a must.
• Proper education of the patient is required especially as the main purpose is mostly diagnostic.
• Anticoagulant status—stop before the procedure at appropriate time depending on the anticoagulant.
• Confirm the painful side—approach from the other side so that the pain is not reproduced just by
accessing the damaged side of the disc.
• Intravenous access for antibiotic prophylaxis only. Sedation is best avoided for proper diagnostic
value of the procedure.
Fluoroscopic views (Figures 31-2 and 31-3A, B)

Figure 31-2. Fluoroscopic angles for various lumbar discs.
Figure 31-3. (A, B) “Squared” lumbar disc and entry point anterior to the lower superior articular
process (SAP).
• AP fluoroscopic view to identify the level of the lumbar discs.

• View is then angled cephalad-caudad to “square” off the intended disc endplates.
• Oblique view toward the side of entry (ipsilateral oblique view) so that the articular elements bisect
the superior end plate.
• Entry point is just lateral to the superior articular process (SAP) of the inferior vertebral body.
• Multiple AP and lateral views may be needed to properly place the needle tip within the center of the
nucleus pulposus.
Equipment
• A sterile environment with proper imaging capability is very important.
• Choice of needles depends on one’s training and experience. A single needle versus a dual needle
technique has been used.
• Although there is not much data to suggest any higher rate of infection with a single needle technique,
proponents of the dual needle technique tout the safety of using a needle through a needle and thus
minimizing the chances of possible infection.
• A dual needle technique also allows for a smaller needle to be used to access the nucleus and thus
reducing the size of the needle puncture in the annulus.
• Manometric measurements provide added information, thus improving the utility of this procedure.
• A single unit made up of a controlled injection syringe and a built in digital pressure monitor is the
latest device available. However, a controlled injection syringe connected to a separate pressure
monitor is also used. The data is presented in various formats (Figures 31-4 and 31-5).
Figure 31-4. Numeric pressure reading printout (lumbar disc).

Figure 31-5. Graphic pressure recording (lumbar disc).
• Injectate is typically made up of the radio-opaque water soluble contrast media with mixed in
antibiotic.
Technique
The approach to the intervertebral disc is typically through the posterolateral angle in the lumbar and
thoracic discs and through the antero-lateral angle in a cervical disc.
Lumbar Discogram
• Prophylactic antibiotics should be considered as per protocol.
• Patient is placed prone with a pillow under the abdomen to reduce the lumbar lordosis.
• Fluoroscopic view is optimized so that the intended disc is “squared” (the x-ray beam passing
perpendicular to the disc so that there is no parallax and the end plates are seen as a single thick line.
• The obliquity of the view is advanced up to a point where the articular elements of the lower vertebral
body bisects the upper end plate in oblique fluoroscopic view.
• The entry point is then marked just anterior to the superior articular process of the inferior vertebral
body under fluoroscopic guidance.
• A 22-gauge 13-cm styletted needle is placed through the skin and advanced to the middle of the disc of
question.
• The needle is advanced incrementally under fluoroscopic guidance in AP, lateral, or oblique views as
needed. If a paresthesia is elicited, the needle should be withdrawn and then redirected cephalad
toward the middle of the disc.
• Once the disc is contacted, the needle is advanced incrementally until the middle of the disc is
penetrated. Imaging is performed in order to avoid penetration though the back of the disc or too
laterally either into the spinal canal or the pleura (in L1 discography).
• The syringe filled with preservative-free contrast is then connected to disc pressure monitor, and
attached to the needle and zeroed. Gradual injection of the injectate is done using live fluoroscopic
view.
• 0.5 to 2.0 mL of preservative-free contrast suitable for intrathecal use is injected with careful attention
being paid to initial pressure to injection via manometry, patient’s response, and whether or not the
pressure is maintained or dissipated in the disc.
• Take note of volume of contrast injected, volume at which patient experienced pain, pressure at which
patient experienced pressure and/or pain, and pain response in terms of its location, character,
distribution, intensity, and concordance with chronic pain.
• The discogram should be evaluated to check the integrity of the disc and a decision should be made if
there is a need to evaluate the adjacent disc spaces, or to inject local anesthetic in the disc of question.
• The injection of local anesthetic into this disc space may give erroneous information if the adjacent
discs are to be evaluated. The local anesthetic can possibly track epidurally or it can anesthetize some
of the nerves that provide sensory input to the adjacent discs.
Cervical Discogram
Prophylactic antibiotic should be considered. The patient is placed in supine position with a pillow under
the shoulders and the neck extended.
• Fluoroscopic view is directed in an oblique manner with a caudad-cephalad tilt to “square” the
targeted disc.
• The obliquity is advanced to optimize the view of the foramen at the given level on the right side.
• Right side is most commonly chosen to avoid accidental puncture of the esophagus which needs to be
further pushed away with the nondominant hand.
• Important structures must be noted at this level including the trachea, carotid artery, jugular vein, and
esophagus.
• The medial border of the sternocleidomastoid muscle is palpated and local anesthetic is injected
subcutaneously at the chosen level of cervical disc.
• A short 22- or 25-gauge styletted needle is inserted under live fluoroscopy within the nucleus.
• A small amount (usually 0.3 to maximum of 0.4 mL) of contrast is injected while paying attention to
resistance to injection and patient’s response to provocation of pain.
• Make precise notes of volume of contrast injected, volume at which patient experienced pain, pressure
at which patient experienced pressure and/or pain, and pain response (location, character, distribution,
intensity, and concordance with chronic pain).
Thoracic Discography
• Prophylactic antibiotics should be considered as per the protocol.
• Patient is placed in prone position with a pillow under the lower chest in order to flex the spine.
• If CT scan is being used, make careful note of pleura, lung, ribs, nerve roots, and spinal cord.
• The area over the discs of question marked under fluoroscope wide are laterally on either side is
prepped, draped, and anesthetized.
• A 22- or 25-gauge styletted needle is placed through the skin and advanced to the middle of the disc of
question under fluoroscopic guidance.
• The needle is advanced incrementally with imaging. If a paresthesia is elicited, the needle should be
withdrawn and then readvanced toward the middle of the disc.
• Once the disc is contacted, the needle is advanced incrementally until the middle of the disc is
penetrated. Imaging is performed in order to avoid penetration of the back of the disc either into the
spinal canal or the pleura.
• Similar to the cervical discogram, 0.3 to 0.4 mL of preservative-free contrast approved for intrathecal
use is injected with careful attention being paid to resistance to injection, patient’s response, and
whether or not a pressure is maintained or dissipated in the disc via manometry.
NORMAL AND ABNORMAL FINDINGS (FIGURES 31-6A–C, 31-7,

AND 31-8)
• The images of the injected disc should be evaluated to see whether or not the disc and its components
are intact.
• The morphology of the disc will determine where the contrast will flow.
• A normal disc will appear as a lobulated mass with some posterolateral clefts and high pressure on
manometry.
• If the inner annulus is torn, a transverse pattern of contrast will show on the nucleogram or if the tears
of the annulus extend to the outer layer, a radial pattern will be noted.
• The contrast will flow into the epidural space, neuroforamen or the end plate of the vertebra if the
annulus is completely disrupted.
• Abnormal discogram shows various contrast patterns that differ from normal silhouette of the nucleus,
and may leak into annular layers or outside the annulus.
• A low-pressure abnormal disc may not be the painful when subjected to pressurization.
• Various angles of a fluoroscope may show contrast spread that could be abnormal (Figure 31-6B).
• A postdiscogram CT scan will confirm the details of disc morphology including contained herniation
(Figure 31-9).
Figure 31-6. Normal and abnormal discogram levels. (A) Shows a normal silhouette of the nucleus
denoting a normal disc. (B) Shows the L4-5 disc (below the needle) from a lateral aspect with some
leakage into the epidural space going cephalad. (C) Shows an almost ideal discography with the
degenerated disc in the middle of 2 normal discs.
Figure 31-7. Various discogram contrast spread patterns. This figure shows various possible contrast
spread patterns from a discogram. Figures 1 and 2 show a normal disc with a globular and bilobular
pattern which is contained within the nucleus. Figure 3 shows an annular tear extending into the outer third
posterolaterally. It is contained within the disc. Figure 4 shows a leaking disc. Figure 6 shows a severely
degenerated and internally disrupted disc with annular spread but still contained.
Figure 31-8. A leaking disc on discogram outlining the nerve roots. This figure shows the contrast leaking
outside the degenerated disc and spreading along the nerve roots. Note the various angles of the needles
for different levels of the lumbar spine.
Figure 31-9. A postdiscogram CT scan. Figure shows two different discs on CT scan. The upper image
shows a normal spread within the nucleus, some white areas are the bone which has the same
characteristics as the contrast. The lower image shows the contrast extruding in to the annulus as a clear
connection is seen between the contrast in the nucleus and the annulus.
OUR PREFERRED TECHNIQUE

Prep. Duraprep, Ioban adhesive drape, full body sterile drape, full scrub, gown, and gloves
Needles. Dual needle set (20 gauge 3.5 in + 25 gauge 5 in or 20 gauge 6 in, 25 gauge 8 in) (Figures 31-
10 and 31-11)
Figure 31-10. Dual needle set for discography. Yellow hub, introducer; blue hub, discography needle.
Figure 31-11. Dual needle set (curved inner discography needle).
Manometry. Syringe and Stryker Disc monitor (Figure 31-12)

Figure 31-12. Disc pressure monitor. (Reproduced with permission from Stryker.)
Injectate. Omnipaque 180 or Isovue 200 M with cefazolin 5 mg/mL

Mixing technique. Mix 1 GM cefazolin diluted with 10 mL PFNS (100 mg/mL). Take 1 mL of this
mixture and dilute it with 19 mL of preservative free contrast (100 mg in 20 mL = 5 mg/mL). Use the
other 9 mL for IV injection.
Outer or introducer needle inserted using a tunnel view and advanced to within 1 mm of the annulus. The
inner curved needle is then introduced through the introducer and advanced toward the middle of the
nucleus using AP and lateral views repeatedly to ensure central placement (Figure 31-13A, B).
Figure 31-13. (A, B) Advantage of a curved needle (dual needle set). Even if the introducer needle is not
exactly in the middle of the disc, a curved inner needle can be guided to the center of the nucleus.
(Reproduced with permission from Stryker.)
The controlled injection syringe is connected to disc pressure monitor, and then attached to the needle
and zeroed. Gradual injection of the injectate is done using live fluoroscopic view.
Appearance of the contrast within the disc marks the “opening pressure.” Injection gradually performed
with the following end points (whichever is first).
1. Pain, whether concordant or discordant
2. Pressure up to a maximum of 120 psi (lumbar disc)
3. Volume of injectate up to a maximum of 2.5 mL (lumbar disc), 0.4 mL maximum (cervical disc)
Multiple views are obtained with the fluoroscopic guidance in AP, lateral, and axial views as much as
possible using a cephalad to caudad tilt. Patient is then sent for a postdiscogram CT scan.
• Patient should obtain a postdiscogram CT scan within 30 minutes of having the procedure.
• Patient is instructed to report any fever, increased back pain, or new symptoms.
• Follow up within 1 week.

• Injury to the tissues:
Nerve root (needle too lateral or too cephalad)
Blood vessels within the neural foramen
Disc injury resulting from multiple attempts
Disc infection—discitis
Cervical level—injury to the esophagus and subsequent infection of the disc
Cervical level—injury to the great vessels
• Difficulty in needle placement—especially at the L-S1 level:
Proper cephalad to caudad angle to optimize the L5-S1 disc
Use of a curved needle may be helpful (especially using a 2-needle technique)
Suggested Reading
Lee SH, Derby R, Chen Y, Seo KS, Kim MJ. In vitro measurement of pressure in intervertebral discs and
annulus fibrosus with and without annular tears during discography. Spine J. 2004 Nov-Dec;4(6):614-
618.
Nachemson AL, Disc pressure measurements. Spine. 1981 Jan-Feb;6(1):93-97.
Peng B, Wu W, Hou S, Li P, Zhang C, Yang Y. The pathogenesis of discogenic low back pain. J Bone
Joint Surg Br. 2005 Jan;87(1):62-67.
Raj PP. Intervertebral disc: anatomy-physiology-pathophysiology-treatment. Pain Practice.
2008;8(1):18-44.
CHAPTER 32
Percutaneous Disc Decompressions

Sanjay Bakshi and Gerard W. Abrahamsen
INDICATIONS
Percutaneous disc decompression (PDD) is a minimally invasive procedure performed under
fluoroscopic guidance for the treatment of lower back with or without radiation to the lower extremities
secondary to a lumbar herniated nucleus propulsus. There are many different techniques described for
performing PDD. These include chemonucleolysis using chymopapain, automated percutaneous lumbar
decompression (APLD) using a nucleotome, percutaneous discectomy, laser discectomy, nucleoplasty,
and dekompressor.1-12 The primary goal of all of these procedures is to reduce pressure in the disc and
remove disc material.
This chapter will discuss PDD using either the Stryker Disc Dekompressor (Figure 32-1) or the
ArthroCare Nucleoplasty devices (Figure 32-2). Stryker’s Dekompressor mechanically aspirates disc
material. As a result, aspirated disc material can be visually seen and sent for histological examination.
ArthroCare’s Nucleoplasty uses Coblation, which uses bipolar radiofrequency energy to generate a
plasma field that disintegrates disc material into gases that escape through the needle.
Figure 32-1. Dekompressor.
Figure 32-2. Nucleoplasty probe.
Both procedures are designed to reduce the size of a disc herniation thereby taking pressure off the
affected nerve roots. This treatment modality is not considered a first-line therapy and should be
considered only after a patient has failed more conservative therapies such as physical therapy, oral anti
inflammatory medication, and epidural steroid injections.
Patient selection criteria for treatment with percutaneous disc decompression include:13
• Axial back pain with or without radicular symptoms
• MRI consistent with a contained disc herniation
• Imaging demonstrating greater than 50% preserved disc height
• Failed conservative treatment
• Positive diagnostic selective nerve root block
• Discography positive for concordant pain and post-discography CT scan consistent with a contained
disc herniation (this is a relative criteria and depends on surgeon preference)
RELEVANT ANATOMY
A standard percutaneous posterolateral discography approach to the disc is utilized. The Scottie dog
image is utilized for initial approach to the disc space (Figure 32-3).
Figure 32-3. Scottie dog view.
In order to minimize the risk of nerve root injury the needle is introduced in the safe triangle described
by Kambin.
It is essential to confirm that the patient has a contained disc herniation (Figures 32-4 and 32-5). This is
probably the most important thing to keep in mind to ensure success with these procedures. If the targeted
disc does not have an intact annulus, the procedure is unlikely to be successful.
Figure 32-4. Types of disc herniation.
Figure 32-5. MRI picture of contained disc herniation.

PDD is an elective, minimally invasive spinal procedure, typically performed under monitored anesthesia
care (MAC) with sedation. Therefore, a standard preoperative workup including a history and physical,
appropriate imaging studies, and tests should be performed. Patients on anticoagulant therapy will have to
stop their respective medications in a timely manner prior to the procedure to minimize the risk of
bleeding at the procedure site.
Contraindications and exclusion criteria:14
• Spinal infection
• Spinal tumor
• Spinal fracture
• Extruded disc, sequestered disc fragment, or large disc herniation
• Complete annular disruption
• Moderate to severe spinal stenosis
• Uncontrolled coagulopathy and bleeding disorder
Fluoroscopic Views
There are basically 3 fluoroscopic views that are utilized for the approach.
Initial needle entry is performed utilizing the oblique view (Figure 32-6). This is the best approach to
guide the needle through a proper path.
Figure 32-6. Oblique view.
Once the needle is on the right trajectory, the C-arm is rotated to the AP view (Figure 32-7).
Figure 32-7. AP view.
The final view is the lateral view, which is the most important view to gauge depth (Figure 32-8). This
view is the most important view for safety reasons, to ensure the needle does not penetrate the anterior
margin of the disc.
Figure 32-8. Lateral view.
Equipment
• 25-gauge 1.5-in needle for local
• Lidocaine 1% or 2%
• Iodinated water soluble contrast such as Omnipaque 240
• Stryker dekompressor probe if performing dekompressor
• Perc-D wand, 17-gauge Crawford needle and ArthroCare power generator if performing nucleoplasty
• C-arm fluoroscopy machine
• Sterile full body drapes
Technique
The basic initial steps are the same for both dekompressor and nucleoplasty. After the entry into the disc
space using the introducer needle, the technique is then a little different. With dekompressor, the disc is
decompressed mechanically with the dekompressor device. With nucleoplasty, the disc is decompressed
by coablation—a combination of coagulation and ablation.
We will first discuss the initial common steps for both the procedures. We will then mention the
differences between the steps for dekompressor and nucleoplasty.
Initial Steps
• After informed consent is obtained, patient is taken to the operating room.
• Patient lies on the operating room table in the prone position with a pillow placed under the abdomen.
• The lumbar region is prepped and draped in a sterile fashion.
• IV antibiotics are used for prophylaxis, to decrease the risk of discitis. One gram of cefazolin is the
preferred antibiotic. For patients with a history of allergy to penicillin or cefazolin, IV clindamycin or
a combination of gentamycin and vancomycin can be used.
• Light sedation is used for the procedure. The main goal of sedation is anxiolysis. The patient should not
be too deeply sedated for these procedures due to risk of nerve injury.
• At all times patient should be easily arousable and should be able to report any paresthesias from
nerve root contact during the procedure.
• Appropriate disc to be targeted is confirmed by counting down from T12, and confirming with x-rays
and MRI of the patient that should be present in the operating room during the procedure. If the patient
has had a discogram prior to the procedure, those films should be present as well.
• After the appropriate disc level has been identified, the next step is to square off the end plates at the
involved level so that the x-ray beam is perpendicular to the intended disc level.
• Now the C-arm is rotated to the oblique view, which is used to target the needle entry site (Figure 32-
6). The superior articular process should be positioned midway between the anterior and posterior
disc margins. A skin mark is now made for the needle entry point. This should be in the Kambins safe
triangle (Figure 32-9). Needle entry is preferable on the same side as the disc herniation. Local
anesthesia is now infiltrated in the skin and subcutaneous tissues. The needle is now advanced under
the oblique view of the C-arm.
• Once the needle is advancing toward the target in the oblique projection, the C-arm is rotated to the AP
projection (Figure 32-7). The needle is advanced slowly till it reaches the outer edge of the annulus in
the AP projection.
• At this point, the C-arm is rotated to the lateral position (Figure 32-8). Entry into the disc space should
always be carried out in the lateral position for safety reasons. Advance the needle into the middle of
the disc space in the lateral position.
• Careful attention should be taken while advancing the needle into the disc space. If the needle strays
too medially, it can go into the spinal canal. If it strays too laterally, it can go into the annulus, or
potentially even anteriorly beyond the vertebral margin into the peritoneal cavity. Also, in the lateral
position, it is essential to monitor the needle as it enters the disc space to ensure it does not go beyond
the anterior border of the disc space.
• Once the needle is in the center of the disc, some people prefer to inject a minimal amount of contrast
to outline the margins of the nucleus. If this approach is taken, it is important to use a minimal amount
of contrast, to avoid obscuring the field of view (Figure 32-10).15
• During the next steps, the procedure differs slightly when using the Dekompressor probe or the
Nucleoplasty wand, and will be discussed separately.
Figure 32-9. Skin mark using clamp.
Figure 32-10. Dye into disc to outline disc space.
DEKOMPRESSOR (FIGURES 32-11 THROUGH 32-14)

Figure 32-11. Dekompressor at mid-point of disc.
Figure 32-12. Dekompresor at distal end of disc in AP view.
Figure 32-13. Dekompressor in lateral view.
Figure 32-14. Dekompressor animation.
• The Dekompressor device is a mechanical device—it performs disc decompression by rotating at high
speeds to extract the disc material from the nucleus.
• The first step is to remove the stylet from the introducer needle previously placed in the center of the
disc.
• The Dekompressor device is now introduced through the introducer cannula into the nucleus.
• Confirm using fluoroscopy that the tip of the device extends beyond the introducer needle into the disc
space.
• The switch on the device is now turned on to start the discectomy procedure.
• The probe is advanced gently while on to begin decompressing the disc material by its rotating action.
• The anterior and posterior boundaries over which the probe should be passed are marked off by
adjusting the depth marker on the skin, which should be marked at the spot, where the probe tip is
anteriorly, at the junction of the annulus and the nucleus.
• There is both an audible and tactile response that is felt as the disc material is being aspirated.
• The aspiration procedure is carried out at 15-second periods, and the probe is moved back and forth
between the marked boundaries. During this process, careful attention should be paid to make sure the
probe does not advance beyond the anterior margin of the disc border.
• The device should be activated while the device is being moved forward.
• Total activation time is usually between 1 and 5 minutes, with a recommended maximum time of 10
minutes.
• Excessive pressure should not be applied to the probe.
• Visualize the collection chamber to ensure that there is nuclear material collecting in the chamber.
• Once tissue is seen at the entrance of the chamber, approximately 1 mL of tissue has been aspirated.
• If no tissue is seen after a few passes, and more than 3 minutes, remove the probe and inspect to see if
there is any tissue seen on its shaft. If no tissue is seen, ensure that the introducer cannula is still in the
nucleus of the disc.
• Disc material on the probe is removed with the black probe cleaner that is included in the kit.
• End point is reached when:
Sufficient material has been aspirated.
No disc material is aspirated after 3 minutes.
10 minutes of activated time has expired.
Collection chamber is full.
• The probe and introducer cannula are usually taken out as 1 unit.
• A band aid is applied at the entry site.
• The aspirated disc material is sent for pathology.
NUCLEOPLASTY (FIGURES 32-15 THROUGH 32-19)

Figure 32-15. Nucleoplasty probe entering disc space.
Figure 32-16. Nucleoplasty probe further into disc space.
Figure 32-17. Nucleoplasty probe into disc in lateral view.
Figure 32-18. Nucleoplasty probe in distal end of disc in lateral view.
Figure 32-19. Nucleoplasty animation.
• Nucleoplasty is performed with radiofrequency energy that dissolves the disc material using molecular
dissociation.
• Coablation technology uses a combination of coagulation and ablation.
• Coagulation denatures the proteoglycans, and the ablation process provides a controlled and localized
ablation.
• The by-products are inert gasses, which escape from the disc via the needle.
• The first step specific for nucleoplasty is once again to remove the stylet from the introducer needle
that has already been placed in the center of the disc (as described in the initial approach section).
• The Perc-D wand is introduced via the introducer cannula into the disc space.
• The wand is advanced until the distal end of the skin reference mark is positioned at the proximal edge
of the needle hub. This is the proximal limit for creating coblation channels.
• The active section of the wand tip is now outside the tip of the needle, and the location of the reference
mark identifies the proximal channel limit.
• The tip of the wand is now advanced till the tip reaches the annulus on the anterior border of the disc.
This is the distal limit for creating coblation channels. The depth gauge is advanced down the shaft to
mark off this distal limit.
• The wand is now withdrawn to the proximal marker.
• Coblation is now carried out.
• The wand is moved back and forth between the proximal and distal markers.
• A series of channels is now created in the nucleus.
• The wand is advanced 5 mm/s to the distal mark, using the ablation mode.
• The wand is withdrawn to the proximal limit, using the coagulation mode.
• The procedure is performed initially orienting the dot on the wand’s handle to the 12 o’clock position.
This is repeated creating additional channels at the 2, 4, 6, 8, and 10 o’clock position.
• After the coblation channels have been created, withdraw the spine wand from the needle, and then
withdraw the needle.
• A band aid can be applied at the needle insertion site.
• There is no tissue to be sent for pathology in this case, since there is no actual disc material that is
aspirated. The compressed disc material is broken down into gasses, which escape from the needle.
Following the procedure, patients should be discharged with a mild analgesic and advised to refrain from
strenuous activity for 24 to 48 hours postprocedure. Patients should be contacted the following day and
scheduled to follow up in office 1 week and 4 weeks following procedure to evaluate progress and or
adverse events. Patients should be educated to call the office if any of the following events occur:
• Fever
• Chills
• Weakness in extremities
• Bowel or bladder incontinence or retention
• New onset numbness or paraesthesia in extremities
• Bleeding
• Changes or exacerbation in symptoms
In many cases, patients will experience almost immediate reduction in preoperative symptoms after the
disc is decompressed. However, it is not uncommon to see a gradual improvement of symptoms days to
weeks following the procedure. Patients should be educated to refrain from heavy lifting, bending,
pushing, pulling, and twisting to reduce the risk of reherniation. Back braces are not required; however,
they are occasionally used to remind the patient that they had a spinal procedure and to prevent the
previously motioned movements and further improve surgical outcome.

Potential risks of percutaneous disc decompression include but are not limited to:
• Infection including discitis
• Bleeding
• Nerve root irritation or injury
• Exacerbation or worsening of pain
• Hematoma
• Paralysis
• Scar tissue formation
• Failure of technique requiring open surgery
• Recurrence of disc herniation
• Idiosyncratic reaction
• Anaphylaxis
• Death
CLINICAL PEARLS
• The level of evidence for managing predominantly lower extremity pain due to contained disc
herniation is level II to III for nucleoplasty,16 and level III for Dekompressor17 based on USPSTF
criteria.18 However, both of these procedures are relatively easy to perform, quick, and can be done
with minimal sedation, and with minimal risk of complications.
• The success of these procedures largely depends on good selection criteria—these procedure will be
ineffective if the disc herniation is not contained, or if the disc has lost greater than 50% of its height.
• If performed for the proper indication percutaneous disc decompression can be very efficacious.
Percutaneous disc decompression is a great alternative for patients who have failed procedures such as
epidural injections and are not usually surgical candidates.
References
1. Kambin P, Brager MD. Percutaneous posterolateral discectomy. Anatomy and mechanism. Clin
Orthop Relat Res. 1987;223:145-154.
2. Kambin P, Schaffer JL. Percutaneous lumbar discectomy. Review of 100 patients and current practice.
Clin Orthop Relat Res. 1989;238:24-34.
3. Nerubay J, Caspi I, Levinkopf, Tadmor A, Bubis JJ. Percutaneous laser nucleolysis of the
intervertebral lumbar disc. An experimental study. Clin Orthop Relat Res. 1997;337:42-44.
4. Ohnmeiss DD, Guyer RD, Hochschuler SH. Laser disc decompression. The importance of proper
patient selection. Spine. 1994;19:2054-2058.
5. Derby R, Baker RM, Lee CH. Evidence informed management of chronic low back pain with
minimally invasive nuclear decompression. Spine J. 2008;8:150-159.
6. Chen YC, Lee SH, Chen D. Intradiscal pressure study of percutaneous disc decompression with
nucleoplasty in human cadavers. Spine. 2003;28:661-665.
7. Brown MD. Update on chemonucleolysis. Spine. 1996;21:625-685.
8. Chen YC, Lee SH, Saenz Y, Lehman NL. Histologic findings of disc, end plate and neural elements
after coablation of nucleus pulposus: an experimental nucleoplasty study. Spine J. 2003;3:466-470.
9. Alo KM, Wright RE, Sutcliffe J, Brandt SA. Percutaneous lumbar discectomy: clinical response in an
initial cohort of fifty consecutive patients with chronic radicular pain. Pain Pract. 2005;5:116-124.
10. Alo KM, Wright RE, Sutcliffe J, Brandt SA. Percutaneous lumbar discectomy: one year follow up in
an initial cohort of fifty consecutive patients with chronic radicular pain. Pain Pract. 2005;5:116-124.
11. Lierz P, Alo KM, Felleiter P. Percutaneous lumbar discectomy using Dekompressor system under CT-
control. Pain Pract. 2009;9:216-220.
12. Baheti DK, Bakshi S, Gupta S, Gehdoo RP. Interventional Pain Management. A Practical Approach.
New Delhi, India: Jaypee Brothers Medical Publishers; 2009.
13. Reddy AS, Loh S, Cutts J, et al. New approach to the management of acute disc herniation. Pain
Physician. 2008;8:385-389.
14. Singh V, Derby R. Percutaneous lumbar disc decompression. Pain Physician. 2006;9:139-146.
15. Manchikanti L, Singh V. Interventional Techniques in Chronic Spinal Pain. ASIPP Publishing,
American Society of Interventional Pain Physician; 2007.
16. Manchikanti L, Derby R, Benyamin R, Helm S, Hirsch J. A systematic review of mechanical lumbar
disc decompression with nucleoplasty. Pain Physician. 2009;12:561-572.
17. Singh V, Benyamin R, Datta S, Falco F, Helm S, Manchikanti L. Systematic review of percutaneous
lumbar mechanical disc decompression utilizing Dekompressor. Pain Physician. 2009;12:589-599.
18. Berg AO, Allan JD. Introducing the third U.S. Preventive Services Task Force. Am J Prev Med.
2001;20:S3-S4.
CHAPTER 33
Hydrosurgery of Disc
Didier Demesmin and Sagar Parikh
INDICATIONS
Hydrodiscectomy is a form of disc decompression within the realm of minimally invasive discectomy that
is an effective, predictable method of nucleus removal in disc pathology such as contained disc herniation
or disc budge. Though the gold standard for surgical treatment of herniated disc disease is open
microdiscectomy, minimally invasive treatments like hydrodiscectomy has gained momentum as an
alternative treatment option. As with other forms of disc decompression, the primary goal is to remove
herniated disc material to relieve compression of a nerve root or other neural structures. Patients
requiring this procedure often have nerve impingement causing radicular pain symptoms that have not
been relieved with conservative treatment over a 2 months span or epidural steroid injections.
Hydrodiscectomy is an effective and predictable method of nucleus removal, removing hydrated or
desiccated nucleus pulposus, and poses no risk for thermal damage. Its blunt tip design minimizes risk of
end plate and annular damage. This means there is maximum safety within the disc.
The indications for hydrosurgery based on anatomical location of pain include:
• Unilateral leg pain greater than back pain
• Radicular symptoms in a dermatomal distribution correlated with MRI findings
• Positive straight leg raise test
• No improvement after 2 months of conservative treatment
• MRI evidence of contained disc protrusion/herniation
• Failed selective nerve root block ×1
• Discography positive for concordant pain
• Well-maintained disc height more than 50%
THE CONTRAINDICATIONS FOR HYDROSURGERY

As with any intervention, one must weigh the potential benefits to the potential complications. The
following are contraindications for hydrosurgery.
• Radiologic evidence of severe lateral recess stenosis
• Radiologic evidence of calcified disc herniations
• Radiologic evidence of severe degenerative facet disease or osteophytic impingement on nerve roots
• Radiologic evidence of marked ligamentum flavum hypertrophy causing spinal stenosis
• Radiologic evidence of free or extruded disc fragments within the spinal canal (extending cephalad or
caudad)
• Clinical evidence of significant progressive neurologic deficits or cauda equine syndrome
• Pathologies or conditions, such as fracture, tumor, pregnancy, or active infection that would put patient
at risk
• Disc height less than 50%
• A disc herniation that takes up more than 50% of spinal canal
• Previous surgery with scar tissue nerve root entrapment
• Bony spinal stenosis
• Active infection
• Coagulopathy
• Grade V annular tear on discography
• Lumbosacral instability on flexion/extension studies or spondylolisthesis on MRI
• Radiologic evidence of a diffuse annular bulge extending from the entire circumference of vertebral
body
• Significant end plate changes see on MRI
RELEVANT ANATOMY
The human body normally has 5 lumbar vertebrae separated by intervertebral discs. These discs act as a
shock absorber to resist compressive forces generated on the vertebral segment above and below. The
disc also provides height and widens the neuroforaminal space for a nerve root to exit the spinal column.
Each disc is composed of a core of fibrous material in a mucoproteinaceous gel called the nucleus
pulposus surrounded by multiple layers of fibrocartilage called the annulus fibrosus. The vertebral
column is supported anteriorly by the anterior longitudinal ligament and posteriorly by the posterior
longitudinal ligament.
• Access to the disc is made just lateral to the neuroforamen.
• The neuroforamen is bordered laterally by the posterior edge of the vertebral body and the
zygopophyseal joint, made up of the superior and inferior articular facets of the corresponding
vertebrae above and below.
• Superior and inferior borders of the neuroforamen are made up of the pedicle superiorly and inferiorly
of those corresponding vertebrae.
• Nerves and vessels reside in the neuroforamen; so special care must be taken to avoid the exiting nerve
root and radicular arteries.
• It is important to identify the disc of the level in question and identify the superior articular process as
your needle will be directed anterior and lateral to this structure.
• Kambin’s triangle (small triangular-shaped pathway) allows needle passage into the disc with minimal
or no contact with the nerve root.
• The annulus entry point is defined inferiorly by the caudal vertebral plate and posteriorly by the
inferior articular process of the vertebral segment.
• The exiting nerve root forms the hypotenuse of the triangle.
• Anticoagulation is a concern as there is inherent disruption of tissue from the introduction of a needle.
Stop Aspirin and Plavix prior to procedure and hold Coumadin use. INR level prior to procedure
should be below 1.2.
• Physical examination of the area for infection, skin ulceration or necrosis, and extent of disease must
be done.
vasovagal reaction.
Evaluation for contrast allergy: This is of the utmost importance as the utilization of contrast will
allow for precise needle placement.
Fluoroscopic Views (Figure 33-1)

Figure 33-1. Fluoroscopic images of hydrodiscectomy procedure. (A) Oblique view obtained with
superior articular process (SAP) lying over the disc. Entry point of needle is lateral to SAP. (B) Lateral
view of the needle placed at the posterior junction of the nucleus pulposis and annulus fibrosis. (C)
Insertion of dilator. (D) Insertion of cannula over needle and dilator followed by (E) removal of needle
and dilator. (F, G, H) Insertion of microresector.
• Oblique view (the physician must ensure that the end plates are squared. Place the needle lateral to the
SAP) (Figure 33-1A).
• Guide needle (lateral view showing that the needle is in the posterior border of the annulus at the
nuclear-annular junction) (Figure 33-1B).
• Insert dilator over the needle (make sure that the introducer needle does not advance as the dilator is
introduced) (Figure 33-1C).
• Cannula insertion over the needle and guidewire (Figure 33-1D).
• Removal of guide needle and dilator (Figure 33-1E).
• Insertion of microresector (note that the microresector is facing up). The microresector will be needed
to be rotated to extract more material (Figure 33-1F, G, and H).
Selection of Needles, Medications, and Equipment (Figures 33-2 and

33-3)
Figure 33-2. Picture of hydrodiscectomy dilator, needle, and cannula (curved and straight), along with
graphical demonstration of the resector mechanism. (Reproduced with permission from HydroCision.)
Figure 33-3. Graphical illustration of the percutaneous resector, hydrosurgery system, and basic setup.
(Reproduced with permission from HydroCision.)
• SpineJet PercResector
• SpineJet Quick Connect
• SpineJet Percutaneous Access Set:
Cannulae (curved/straight)
Spinal needle with stylet
Dilator
Guide wire
Intraoperative Technical Steps (Figure 33-4)
Figure 33-4. Graphical illustration of hydrodiscectomy procedure with initial needle insertion, followed
by dilator insertion, introduction of cannula over the dilator, subsequent removal of dilator and needle,
and advancement of the resector apparatus. (Reproduced with permission from HydroCision.)
• The patient is placed in the lateral decubitus or prone position with the lumbar spine slightly flexed.
Use a pillow under the abdomen to achieve this position.
Fluoroscopy
• Visualize a PA view using fluoroscopy depicting the radiologic anatomy pertinent to performing a
percutaneous disc procedure.
• Pertinent anatomy to see in this view are:
Inferior end plate of superior vertebral body
Superior end plate of inferior vertebral body
Intervertebral disc space
Lateral aspect of superior articular process
Anterior surface of vertebral body
Spinal canal
Procedure
• The spinous process of the vertebra just above the disc is palpated and the point just below and lateral
to that process is prepped with antiseptic solution.
• The skin and subcutaneous tissue are then locally anesthetized. (The patient must remain conscious
during the procedure to inform the operator immediately if nerve root contact is made.)
• Access to the disc is optimally visualized when the superior articular process of the vertebral body
below is positioned midway between the anterior and posterior disc margins, and the x-ray beam is
angulated slightly caudally or cephalad so that the superior end plate margins of the inferior vertebral
body align.
• Ensure that the iliac crest does not obscure the view of the superior articular process which can occur
in some cases.
• Once proper positioning is obtained the guide needle is ready to be introduced. A small incision can be
made to facilitate entry into the skin.
The needle is first advanced in a stepwise fashion parallel to and halfway between the vertebral
end plates, with the tip directed to the center of the disc until the needle tip rests slightly through the
annulus of the affected disc.
Proper care should be employed so that the needle does not advance completely through the disc.
Advance the needle into the disc first using lateral views, then intermittent A/P and lateral views
until the needle is about in the center of the nucleus midway between either end plate.
• The dilator is then advanced over the needle.
• Confirm placement with A/P and lateral views.
• The cannula is then advanced over the dilator.
Failure of properly positioning the needle/cannula could result in contact with the end plates.
• The dilator is removed and replaced by the SpineJet PercResector.
• Optimum angle must be maintained, keeping in mind the limitations and risk of entering the epidural
space, thus injuring the neural structures, or entering the retroperitoneal space and inadvertently
injuring the vital visceral organs.
• Exiting nerve root from the upper level is located well above the anticipated needle path.
• Each procedure typically removes up to 15% of the disc.
• The usual time in disc 2 to 3 minutes.
• Typically 2 to 3 g of disc material is removed.
• No shower or bathing for 24 hours
• No baths or pools for 48 hours
• PRN pain control
• No strenuous activity before post-op 6-week evaluation
• 6 weeks back brace with any activity

While this procedure offers the operator a more straightforward approach and considerably limits the
potential complications with a lateral approach with angled or curved needle, there are still obstacles that
could be encountered. The potential complications are:
• Infection
• Bleeding
• Nerve injury
• Spinal cord injury or paralysis

• Always make sure you look at both AP and lateral views before advancing the needle in the disc space.
• Discography contrast can be injected within the disc to confirm intranuclear placement.
• Advance the needle under live fluoroscopic view to prevent migration of the needle as the cannula is
being passed.
• Make sure to review MRI prior to procedure to determine the position of the disc pathology. For
example, if the disc is protruding posteriorly as in a central herniation, needle entry has to be
positioned as dorsal as possible (8-10 cm from the spinous process) to ensure dorsal placement of
needle.
Suggested Reading
Kim DH. Minimally Invasive Percutaneous Spinal Techniques. Elsevier Health Sciences; 2010.
Manchikanti L, Singh V. Interventional Techniques in Chronic Spinal Pain. American Society of
Interventional Pain Physicians; 2007.
Steven D. Waldman, Atlas of Interventional Pain Management. 3rd ed. Elsevier Health Sciences; 2009.
CHAPTER 34
Percutaneous Radiofrequency Discectomy With

Disk IT
Samyadev Datta and Vikram B. Patel
INTRODUCTION
The low back pain remains a major burden for patients and health care providers. In about 45% of
patients with low back pain, the cause is degenerative intervertebral disc. The degenerative process may
result in disc herniation or internal disc disruption. Disc herniation may be either extruded or contained.
Internal disc disruption (IDD) results in annular tears, which may be classified according to the
modified Dallas criteria (Figure 34-1). Extension of the tear into the annulus results in discogenic pain.
Figure 34-1. Modified Dallas criteria. (A) equals grade 0 - normal disc and (F) equals grade 5 tear.
Disc degeneration results in 2 separate phenomena that explain the painful process.
• Initially, there is extension of the sensory nerve fibers beyond the outer third of the annulus, an area that
previously was mechanically insensitive. These nerves may also extend into the nucleus pulposus. This
leads to pain with normal mechanical loads. Secondly, there may be fracture of the end plates. This
results in inflammation and the introduction of cytokines into the nucleus pulposus. Complete tear of the
annulus results in leakage of the contents of nucleus into the epidural space. Contents may irritate the
neural plexus in the dura, both the anterior and posterior longitudinal ligaments and dorsal root
ganglion (DRG), which may result in back pain.
• Contained disc herniations most often resolve with time and conservative measures. Internal disc
disruption is likely to continue to cause pain. Interventional pain management approaches may be of
help in these cases.
The International Association for the Study of Pain (IASP), in its taxonomy, has adapted the following
set of criteria for diagnosing IDD:
• No visible disc herniations seen on magnetic resonance imaging (MRI) or computed tomography (CT).
• During provocation discography injection of the suspected disc, recreation of the patient’s exact back,
and/or leg pain must occur.
• Injection of the disc above or below the suspect disc must be nonpainful, and this acts as a control disc
or normal disc.
• A grade 3 or 4 radial annular fissure must be demonstrated on post discography CT (Figure 34-2).
Figure 34-2. Postdiscogram CT scan with Dallas grade IV tear.
PERCUTANEOUS RADIOFREQUENCY DISCECTOMY—DISK-

IT-11
• Composed of 2 straight sharp insulated needles of 15 or 20 cm length with active tips of 20 mm.
• The proximal end of active tip has a radiopaque marker.
• In addition, 2 thermocouple electrodes of suitable length (15 or 20 cm) are needed for electro
stimulation and making radiofrequency lesion bilaterally in the annulus.
This technique can be used to help treat pain caused aby internal disc disruptions of the thoracic and
lumbar discs. The diagnosis should be made by history and physical examination. Symptoms include low
back pain with or without unilateral or bilateral radicular pain, provocation by cumulative loading, sitting
intolerance, pain on flexion, no severe neurologic deficit, tenderness over the spinous processes at the
painful level(s). The diagnosis must be confirmed by MRI and provocative discography with concordant
pain.
INDICATIONS
• Low back and thoracic back pain due to discogenic causes.
• Discogenic pain caused by internal disc disruptions and confirmed by a manometric provocation
discogram (causing concordant pain) and a postdiscogram CT scan.
CONTRAINDICATIONS
There are multiple well-defined pain generators in the spine, and not all sources can be treated with
percutaneous radiofrequency discectomy.
Following pain, generators are not treatable by radiofrequency discectomy:
• Zygapophyseal (facet) joint
• Sacroiliac joint and ligaments
• Dorsal root ganglion
• Spinal ligaments
• Paraspinal muscles
In addition, there are other relative or absolute contraindications that are common to intradiscal
procedures. These include:
• Patient refusal
• Systemic or local infection
• Irreversible coagulopathy or bleeding disorder
• Suspected history of cancer with metastasis
• Suspected unstable fracture
• Central pain syndrome
PERIOPERATIVE CONSIDERATIONS
• Important perioperative considerations include documentation of conservative measures tried
• Other sources of pain investigated and excluded
• A provocation manometric discography performed and concordant painful disc identified
• Patient education including risks, benefits, and outcomes

This procedure has been approved for thoracic and lumbar disc disruption and should not be used in the
cervical area. There is no literature suggesting that it can be safely used in the cervical area.
RELEVANT ANATOMY
• The intervertebral disc lies between the vertebral bodies, linking them together. The components of the
disc are nucleus pulposus, annulus fibrosus, and cartilaginous end-plates.
• The blood supply to the disc is only to the cartilaginous end plates.
• The nerve supply is basically through the Sino vertebral nerves.
• Biochemically, the important constituents of the disc are collagen fibers, elastin fibers, and aggrecan.
• As the disc ages, degeneration occurs, osmotic pressure is lost in the nucleus, dehydration occurs, and
the disc loses its height. The disc has its nerve supply for the annulus only. In addition, there is the
nerve supply to the end plates of the vertebral bodies. These are all sources of pain (Figures 34-3 and
34-4).
Figure 34-3. Anatomy and blood supply.

Figure 34-4. Nerve supply to disc.
• The procedure is performed in prone position.
• To overcome the lumbar lordosis use of a radiolucent pillow or any such device is recommended. This
allows for better visualization of the disc and easier placement of needles.
• Position the patient flat on the table before starting. Adjustments during the procedure are more
difficult. Use of tilting fluoroscopic table is highly recommended.
• Ensure the patient is comfortable before starting. Sometimes sedation may make the procedure difficult
to perform as patient may get restless. Needle positioning may then become difficult. Success of the
procedure is dependent on correct needle positioning.
FLUOROSCOPIC VIEWS
Comprehension on the use of fluoroscopy is essential for success. Minimal fluoroscopic exposure is
recommended.
• As this procedure involves bilateral needle placement, use of a C-arm that can rotate 45 degrees on
both sides is very helpful.
• Patient must understand the importance of being still.
• Identify the level and mark the area. Before starting, always perform a time out.

This is an intradiscal procedure and every effort must be made to take all aseptic precautions. All present
must wear cap and mask and the operator needs to be gowned and gloved. Administer preoperative
antibiotics. Intradiscal antibiotics may be considered as per protocol.
• Sterile preparation and full body drape is necessary.
• Identify the target disc. Square the end plates of the disc. Then rotate the C-arm till the superior and
inferior articular processes are at about the middle of the disc. Kambin’s triangle should be identified
(Figure 34-5).
Figure 34-5. Kambin’s triangle.
• Anesthetize the skin and needle tract, and then advance the needles into the disc. Needle entry point is
more medial. Do not bend the needle. Needle trajectory should be flatter compared to discogram as the
needle needs to be in the annulus and not nucleus pulposus. Confirm position of the needles in both AP
and lateral fluoroscopic view. Correct needle position is confirmed when the fluoroscopic image in
lateral view shows needles have traversed almost the entire length of the disc, but have not exited the
ventral margin. In the AP view, the needle is at inner margin of the pedicle on both sides (Figures 34-6
through 34-8).
Figure 34-6. Bilateral needle placement AP view. (Reproduced with permission from Neurotherm.)
Figure 34-7. Bilateral needle placement lateral view. (Reproduced with permission from Neurotherm.)
Figure 34-8. One needle in place with radio opaque marker noted and other in Kambin’s triangle.
(Reproduced with permission from Neurotherm.)

For each level of discectomy, two 20-gauge 15/20-cm introducer needles are needed. In addition,
appropriate length electrodes are required. Radiopaque contrast may be needed. The Neurotherm NT1100
machine is used for this procedure (Figures 34-9 and 34-10).
Figure 34-9. Disk IT II electrode. (Reproduced with permission from Neurotherm.)
Figure 34-10. Disk IT II introducer.
After confirmation of needle position, perform radiofrequency discectomy as per protocol set up by
Neurotherm as under:
• The NT1100 has 2 pre-programmed protocols (thermal and pulsed).
• Thermal protocol: Start with 2 minutes at 60 degrees C, followed by 2 minutes at 70 degrees C, and
finally 2 minutes at 80 degrees C.
• Pulsed protocol: 8 minutes on 60 V, 10 millisecond width and maximum temperature set at 50 degrees
C.
Resuscitation equipment must be readily available.
POSTPROCEDURE INSTRUCTIONS
• Procedure performed—percutaneous radiofrequency discectomy.
• No strenuous activity for 10 to 14 days.
• Use abdominal support if needed.
• Use pain medications prescribed as needed.
• Follow up office visit in 2 weeks.
• Start physical therapy 2 to 3 times per week for 6 to 8 weeks, 2 weeks after procedure.
Patients should expect pain relief based on symptoms. Radicular symptoms tend to get better. Axial
symptoms are less likely to respond to treatment. Axial symptoms also take longer to respond.

Immediate complications include:
• Increased pain
• Site pain and erythema
• Radicular symptoms due to possible irritation of nerve roots during needle placement
Serious complications are:
• Infection resulting in discitis
• End plate necrosis
• Disc herniation

• Proper selection of patient is essential for success.
• Diagnosis should be confirmed using a manometric provocation discogram and preferably with
postdiscogram CT scan.
• Good explanation of procedure, its complications and outcomes to the patient including need for
postoperative physical therapy is essential.
• Good positioning of patient is key to success. Use of an adjustable table will be helpful.
• Achieve optimal position before starting procedure.
• Working with an experienced radiology technician is recommended. Sedation may help but be aware
that a lightly sedated patient may get very restless.
• Deep sedation can be dangerous as possible complications from incorrect positioning of needles may
not be identified and potential neural damage may occur.
• Confirm position of needles in both AP and lateral views before starting radiofrequency. Success of the
procedure depends on good positioning of needles.
• Occasionally, patient may complain of pain during the procedure. Stop and review position of needles,
and if no apparent cause for pain can be identified, abandon procedure.
In summary, Disk-IT 11 is:
• The most economical way for disc treatment.
• Has the easiest placement of needles/electrode.
• Can be used in thermal RF or pulsed RF mode.
• Results are comparable to biacuplasty, annuloplasty, and IDET.
• Can be used in “black discs” due to a 20-gauge introducer.
• Less traumatic to disc.
Suggested Reading
Aprill C, Bogduk N. High intensity zone: a diagnostic sign of painful lumbar disc on MRI. Br J Radiol.
1992;65:361-369.
Manchikanti L, Glaser SE, Wolfer L, Derby R, Cohen SP. Systematic review of lumbar discography as a
diagnostic test for chronic low back pain. Pain Physician. 2009;12:541-559.
Raj PP. Intervertebral disc: anatomy-physiology-pathophysiology-treatment. Pain Practice.
2008Jan/Feb;8(1):18-44.
Rohof O. Intradiscal pulsed radiofrequency application following provocative discography for the
management of degenerative disc disease and concordant pain: a pilot study. Pain Practice. 2012
Jun;12(5):342-349.
Wolfer LR, Derby R, Lee J-E, Lee S-H. Systematic review of lumbar provocation discography in
asymptomatic subjects with a meta-analysis of false-positive rates. Pain Physician. 2008;11:513-538.
CHAPTER 35
Intradiscal Electrothermal Therapy

Jason E. Pope and Nagy Mekhail
INTRODUCTION
Discogenic pain has been implicated as the etiology of low back pain in approximately 45% of patients
with axial low back pain.1-3 Despite this relatively large incidence, discogenic pain diagnosis and
treatment remains controversial, as many patients are relegated to surgery secondary to an antiquated
treatment algorithm and lack of a clear minimally invasive alternative.
IDET was introduced by Saal and Saal in 1996 with data suggesting:4,5
• Improved outcomes
• Significant reductions in VAS
• Less disability
• Enhance functionality
• Analgesic medication reduction
Numerous studies supported its use, and although promising, critics questioned the scientific validity of
the study, noting nonrandomization, uncontrolled study design and potential observer bias.5-25 Mekhail and
Kapural demonstrated a 78% decrease in VAS as well as significant improvement in activities of daily
living in properly selected patients.20 Pauza et al performed a randomized, placebo controlled trial with a
sham control arm.5 Forty percent of the treatment arm had at least 50% pain reduction, 21% experienced
more than 80% pain reduction. The authors concluded that IDET was a viable therapy for an intractable
discogenic pain.6 However, the technique has fallen out of favor due to a lack of reproducible outcomes,
which is probably due to a poor patient selection, as well as inadequate and inconsistent reimbursement
by third party payers. Although challenges remain, IDET is a viable therapy for selected patients.
ANATOMY AND PATHOGENESIS

• The intervertebral disc is composed of the nucleus pulposus (NP) encased by the annulus fibrosis
(AF), sandwiched between the vertebral endplates.
• The disc is bound posterolaterally by the facet joints, anteriorly by the anterior longitudinal ligament
(ALL), and posteriorly by the posterior longitudinal ligament (PLL).
• The NP is composed of proteoglycans, collagen, and water.
• The AF composed of concentric fibrocartilaginous fibers running obliquely and inserting into the
vertebral end plates via the Sharpley fibers, with more reinforcement anteriorly.
• There is no direct vasculature to the intervertebral, and consequently, diffusion of nutrients is required.
• The segmental radicular arteries, entering near the anterior-cephalad portion of the neuroforamina,
supplies the vertebra body and indirectly the disc.
The nerve supply of the disc is complex, as the sinuvertebral nerves (via the Luschka nerves) provide
posterior coverage, while branches of the lumbar ventral rami, along with the gray ramus communicans,
innervate ventral annulus as four separate ramus communicans nerves innervate each disc. Pain receptors
have been identified in the outer third of the AP, the PLL, periosteum, paraspinal musculature, ligaments,
and facet joints, as shown in Figure 35-1.
Figure 35-1. Anatomy and innervation of the intervertebral disc.
The pathogenesis of discogenic pain is multifactorial. It can be a result of mechanical or chemical

irritation of the aforementioned nerves secondary to an internal disc disruption (IDD).
IDD is defined as:
• A disruption of the NP
• Commonly by fissures extending to the AF
• Creating chronic inflammation
• Neovascularization
• Neoinnervation of nociceptive origin, specifically A delta and C fibers, with a graded system of
increasing severity, as shown in Figure 35-2.
Figure 35-2. Dallas discogram scale grades of annular tissues.
Indications
• Discogenic pain secondary to internal disc disruption.
• Positive provocative discogram with concordant pain.
• Presence of high intensity zone on MRI suggestive of symptomatic disc.
• Pain should be of >3 months duration.
• Failed conservative measures, including medications and physical therapy.
• Less invasive causes ruled out (facetogenic or sacroiliac pain).
• MRI, x-ray, and reliable discogram should be within 1 year of proposed IDET procedure.
Detailed history and physical examination in patients with nonspecific back pain yields proper
diagnosis in 30% of cases. Assimilation of the history, physical examination, and radiographic
investigation including provocation tests, along with a skeptical suspicion, commonly yields an
appropriate diagnosis. Patients typically have sitting intolerance and pain improves with recumbence.
Straight leg raise is negative for radicular pain. The presence of high intensity zone (HIZ) on MRI may be
suggestive of a symptomatic disc, although false positives have been reported to be near 15%.4 The gold
standard for diagnosis is a provocative, concordant pain producing, appropriately performed discogram
with mamometry, with two control levels spanning the suspected culprit painful disc. Discogram results
amenable to discogenic procedures can be described as absolute, highly probable, or discogenic pain,
based on IASP (International Association for the Study of Pain) and ISIS (International Spine Intervention
Society) guideline statements. Briefly, the components of the discogram include concordant pain with a
magnitude of at least 7 on a 0 to 10 scale, pressure testing, and presence of asymptomatic adjacent levels.
Please refer to Table 35-1.
TABLE 35-1. Discogram Findings Amenable to Intradiscal Therapy
Technique
IDET should be performed in a similar setting to discography, with the same recommendations regarding
antibiotic prophylaxis, positioning, monitoring, and premedication. It should be performed in a radiologic
or surgical suite with strict aseptic precautions.
• Perioperative antibiotics are advocated.
• The patient is positioned prone on radiolucent table and sterily prepped and draped.
• Standard intraoperative monitors are placed, including 3 lead ECG, pulse oximetry, blood pressure,
HR, and intravenous access.
• Heavy sedation is not advocated.
• A fluoroscopic examination is performed to identify the symptomatic disc by previous discography in
AP projection with squaring up superior and inferior vertebral body endplates.
• The image intensifier is then rotated until the superior articulating process appears in the midline of the
aforementioned target disc, Figure 35-3.
Figure 35-3. Oblique lunar spine radiograph showing the superior articular facet (sap) and the point of
entry into the intervertebral disc (O). (Reproduced with permission from Kallweaaed JW, Terheggan
MAMB, Groen GJ, Sluijter ME, Derby R, Kapural L, Mekhail N, van Kleef M. Evidence Based
Medicine. Discogenic Low back Pain. Pain Practice, Volume 15.)
• Local anesthetic is infiltrated along the projected needle course.

• There is no consensus regarding laterality of needle placement as compared to the sidedness of fissure.
• We advocate contralateral needle placement to the fissure.
• A 17-gauge 6-in introducer needle is inserted coaxially until it contacts the annulus fibrosis.
• Care must be taken to place the needle equidistant between the aforementioned end plates, just anterior
to the ipsilateral SAP, and just anterior to the midpoint of the disc in the lateral projection, avoiding the
nerve roots, as shown in Figure 35-4A.
Figure 35-4. (A-H) Series of sequential placement of IDET catheter in lateral (left) and AP (right)
views. (Reproduced with permission from Kuslich SD, Ulstrom CL, Michael CJ. The tissue origin of low
back pain and sciatica: a report of pain response to tissue stimulation during operations on the lumbar
spine using local anesthesia. Orthop Clin North Am. 1991;22:181–187.)
• Through the introducer, the flexible electrode is advanced until it assumes a circumferential position
adjacent to the posterior/posterolateral annulus fibrosis or between the nucleus pulposus and the
annulus fibrosis (Figure 35-4B-H).
• Effort should be made to avoid kinking the catheter, as this can lead to breakage and placing the
proximal and distal radio-opaque markers.
• When satisfactory placement is confirmed by AP and lateral images, the electrode is gradually heated
to up to 90°C and maintain at 90°C for 4 minutes as long as the patients are able to tolerate it.
This portion of the procedure is often uncomfortable for patients, as their typical back pain is
transiently exacerbated by heating. Patient may be administered analgesics, but must be able to report
radicular pain. If radicular pain is reported, heating should be stopped and the catheter repositioned.
After the procedure, patients often experience an increase in their typical pain, and this pain subsides
over the next week.
Figure 35-4A-H is stepwise of IDET catheter placement in simultaneous AP and lateral views. Figure
35-5 shows ideal position of IDET catheter (A) and kinked IDET catheter (B).
Figure 35-5. Showing ideal IDET catheter place at L5/S1 level (A) and kinked catheter due to use of
excessive force (B). Courtesy of N. Mekhail MD, PhD
Pitfalls
• Electrode coil kinking after placement within the disc has been known to occur, rarely leading to
breakage.
• If kinking of the catheter is expected, the introducer and the catheter should be removed as a unit and
reentry into the disc should be attempted, with placement of a new heating electrode.
• If the heating element of the coil comes in contact with the introducer needle, during the heating
protocol, thermal injury along the introducer needle can result, potentially injuring the exiting nerve
root, muscles, and skin.
Complications
Reported complications include:10,15,25
• Nerve root injury
• Headache
• Nondermatomal leg pain
• Dural puncture
• Infection: discitis, epidural abscess, osteonecrosis
• Bleeding
• Worsening discogenic pain
• Spinal cord injury
References
1. Kallweaaed JW, Terheggan MAMB, Groen GJ, Sluijter ME, Derby R, Kapural L, Mekhail N, and van
Kleef M. Evidence based medicine. Discogenic low back pain. Pain Practice. 2010:10:560-579.
2. Kuslich SD, Ulstrom CL, Michael CJ. The tissue origin of low back pain and sciatica: a report of pain
response to tissue stimulation during operations on the lumbar spine using local anesthesia. Orthop
Clin North Am. 1991;22:181-187.
3. Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N. The relative contributions of the
disc and zygapophyseal joint in chronic low back pain. Spine. 1994;19:801-806.
4. Saal JA, Saal JS. Thermal characteristics of lumbar discs: evaluation of a novel approach to targeted
intradiscal thermal therapy. Presented in the 13th Meeting of the North American Spine Society, San
Francisco, CA 23-28, October 1998.
5. Pauza KJ, Howell S, Dreyfuss P, Peloza JH, Dawson K, Bogduk N. A randomized, placebo-controlled
trial of intradiscal electrothermal therapy for the treatment of discogenic low back pain. Spine J.
2004;4(1):27-35.
6. Saal JA, Saal JS. Intradiscal electrothermal treatment for chronic discogenic low back pain:
prospective outcome study with a minimum 2-year follow-up. Spine. 2002;27:966-974.
7. Wetzel T, McNally T, Phillips F. Intradiscal electricothermal therapy used to manage chronic
discogenic low back pain. Spine. 2002;27:2621-2626.
8. Appleby D, Andersson G, Totta M. Meta-analysis of the efficacy and safety of intradiscal
electrothermal therapy (IDET). Pain Med. 2006;7(4):308-316.
9. Bogduk N, Karasek M. Two-year follow-up of a controlled trial of intradiscal electrothermal
annuloplasty for chronic low back pain resulting from internal disc disruption. Spine J.
2002;2(5):343-350.
10. Lutz C, Lutz GE, Cooke PM. Treatment of chronic lumbar discogenic pain with intradiscal
electrothermal therapy: a prospective outcome study. Arch Phys Med Rehabil. 2003;84:23-28.
11. Derby R, Bjorn E, Yung C, et al. Intradiscal electrothermal annuloplasty (IDET): a novel approach for
treating chronic discogenic back pain. Neuromodulation. 2000;3:82-88.
12. Cohen SP, Larkin T, Abdi S, Chang A, Stojanovic M. Risk factors for failure and complications of
intradiscal electrothermal therapy: a pilot study. Spine. 2003;28:1142-1147.
13. Spruit M, Jacobs WC. Pain and function after intradiscal electrothermal treatment (IDET) for
symptomatic lumbar disc degeneration. Eur Spine J. 2002;11:589-587.
14. Gerszten PC, Welch WC, McGrath PM, Willis SL. A prospective outcome study of patients
undergoing intradiscal electrothermy (IDET) for chronic low back pain. Pain Physician. 2002;5:360-
364.
15. Singh V. Intradiscal electrothermal therapy: a preliminary report. Pain Physician. 2000;3:367-373.
16. Endres SM, Fiedler GA, Larson KL. Effectiveness of intradiscal electrothermal therapy in increasing
function and reducing chronic low back pain in selected patients. WMG. 2002;101:31-34.
17. Freedman BA, Cohen SP, Kuklo TR, Lehman RA, Larkin P, Giuliani JR. Intradiscal electrothermal
therapy (IDET) for chronic low back pain in active-duty soldiers: 2-year follow-up. Spine J.
2003;3:502-509.
18. Lee M, Cooper G, Lutz C, Hong H. Intradiscal electrothermal therapy (IDET) for treatment of chronic
lumbar discogenic pain: a minimum 2-year clinical outcome study. Pain Physician. 2003;6:443-448.
19. Davis TT, Delamarter RB, Sra P, Goldstein TB. The IDET procedure for chronic discogenic low back
pain. Spine. 2004;29:752-756.
20. Mekhail N, Kapural L. Intradiscal thermal annuloplasty for discogenic pain: an outcome study. Pain
Pract. 2004;4:84-90.
21. Kapural L, Mekhail N, Korunda Z, Basali A. Intradiscal thermal annuloplasty for the treatment of
lumbar discogenic pain in patients with multilevel degenerative disc disease. Anesth Analg.
2004;99(2):472-476.
22. Andersson GB, Mekhail NA, Block JE. Treatment of intractable discogenic low back pain. A
systematic review of spinal fusion and intradiscal electrothermal therapy (IDET). Pain Physician.
2006;9:237-248.
23. Bogduk N, Lau P, Govind J, Karasek M. Intradiscal electrothermal therapy. Tech Reg Anesth Pain
Manage. 2005;9:25-34.
24. Djurasovic M, Glassman S, Dimar J, Johnson J. Vertebral osteonecrosis associated with the use of
intradiscal electrothermal therapy: a case report. Spine. 2002;27:325-328.
25. Schellhas KP, Pollei SR, Gundry CR, Heithoff KB. Lumbar disc high-intensity zone. Correlation of
magnetic resonance imaging and discography. Spine. 1996;21:79-86.
CHAPTER 36
Intradiscal Biacuplasty
Mark Yelle and Leonardo Kapural
INTRODUCTION
Approximately 45% of back pain can be attributed to discogenic source.1,2 Lumbar discogenic pain is
typically caused by pathophysiological changes that occur within the intervertebral disc. A loss of
hydration in the nucleus pulposus from aging, chronic abnormal posturing, or injury can lead to both,
delamination and fissuring in the annulus fibrosus (Figure 36-1A, B). This structural damage is a part of
unclear degenerative process, where in addition to described changes, there is an in-growth of the nerve
endings (nociceptors) that are normally restricted to the outer third of the annulus, extending now to the
nucleus of the affected disc. Inflammatory cytokines such as tumor necrosis factor, nitric oxide and
metalloproteinases, are also released, causing pain through several possible mechanisms. These changes
transform the disc into a primary nociceptive structure. In addition, structural changes intrinsic to the
intervertebral disc can lead to reduced mechanical load-bearing capacity resulting in altered spinal
biomechanics, which can contribute to future back pain.
Figure 36-1. Comparison between intact and fairly degenerated lumbar disc. Preparation was fixed in
10% neutral buffered formalin for 1 week. Individual lumbar segments were prepared, taking care to
preserve the posterior elements. (A) Mostly intact annulus with minor lamellar disorganization in a
minimally degenerated disc with the absence of fissuring. (B) Lamellar disorganization in a degenerated
lumbar disc with presence of radiating tear extending to the outer 1/3 of the annulus.
Intradiscal biacuplasty (Figure 36-2) is the latest minimally invasive, posterior annulus heating
procedure (annuloplasty) for treatment of discogenic pain. This technique employs two bipolar
electrodes, between which bipolar radiofrequency lesioning is conducted. The use of internally cooling
electrodes provides for stable and relatively even heating over a large portion of the posterior annulus.
Throughout the entire procedure, the patient is awake and able to communicate with the physician. This
allows feedback from the patient, and reassurance from the physician, as the probes are positioned and
radiofrequency heating conducted. With the patient laying prone, 2 TransDiscal electrodes are inserted
bilaterally via introducers using fluoroscopic guidance. Once positioned in the posterior annulus, and
confirmed by fluoroscopic imaging, RF generator delivers controlled energy to the tissue. The
temperature change is measured via strategically positioned thermocouples near the tip of the probe. Over
a period of approximately 10 minutes, the heat delivered should increase temperature of the internal
thermo sensor incrementally to 50°C, and then maintained for an additional 5 minutes. The procedure has
been shown to lead to significant pain relief at 3, 6, and 12 months, as well as the improvements in
functional capacity and patient satisfaction. While still a recently described technique, it appears to be the
most promising of all annuloplasty methods. Randomized controlled studies are ongoing, and further
evaluation is needed.
Figure 36-2. Intradiscal biacuplasty electrodes properly positioned in bipolar fashion via introducers
inside the patients back.
INDICATIONS
Currently, the approved indication for the lumbar biacuplasty is a persistent discogenic lower back pain,
despite comprehensive conservative treatment, including physical therapy and a directed exercise1,2
programs. Additional patient selection criteria which, if used, may yield better clinical results include:
lack of neural compressive lesion on lumbar spine magnetic resonance imaging (MRI) and reproduction
of concordant pain in the lower back area during the provocative discography at a low pressurization in 1
or 2 lumbar intervertebral discs.

• Contraindications for intradiscal biacuplasty are consistent with contraindications for other disc
annuloplasty procedures, and include presence of disc height of less than 50% then adjacent disc when
measured on lateral radiographs, and presence of disc degeneration at greater than 2 lumbar levels on
sagittal planes of spinal MRI.3
• Relative contraindications for biacuplasty also include significantly overweight patients4 and patients
receiving workman’s compensation benefits.4-6 Inclusion criteria for past studies evaluating the
efficacy of intradiscal thermal annuloplasty could also be used to aid in identification of patients with
the highest potential to benefit from biacuplasty. This criteria could be considered additional relative
contraindications and include positive straight leg raise, the presence of any inflammatory arthritis,
nonspinal conditions that can mimic lumbar pain, or previous surgical intervention at the symptomatic
intervertebral disc level.
SUMMARY OF INDICATIONS/CONTRAINDICATIONS
Primary Indication
• Chronic discogenic low back pain unresponsive to nonoperative/conservative care >6 months
Discogenic pain evidenced by:
Positive provocative discography at low pressurization (>=7/10, at a pressure of <=50 psi above
opening pressure with a central disc injection)
Concordant pain reproduction present on provocative discography
Positive Candidate Selection Criteria

• Disc height more than 50% of adjacent disc height on sagittal imaging
• Single level disease or 2 levels of disease without evidence of additional degenerative changes
Absolute Contraindications
• Evidence of compressive radiculopathy
• Symptoms or signs of the lumbar canal stenosis
• Evidence of internal nucleus pulposus herniation on MRI
• Lack of consent
• Pregnancy
• Local infection at injection site
• Systemic or CNS infection
Relative Contraindications
• Obesity
• Workman’s compensation claim
• Inflammatory arthritis
• Underlying psychological pathology
• Prior surgery at the symptomatic level
Relevant Anatomy
Intervertebral disc is cartilaginous enclosure between 2 vertebral bodies. Posterior to the disc, 2 facet (or
zygapophysial) joints, composed of the superior articulating process of the vertebral level below the disc
and the inferior articulating process of the vertebral level above the disc, articulate and provide
protection against excessive flexion and extension of the spine and also limit sheer forces on the annulus
of the disc. The nucleus pulposus (NP) is the gelatinous structure in the center of the disc that lacks any
blood supply and is composed of proteoglycan aggrecan, collagen fibrils, chondrocytes, and water. The
NP is contained by the annulus fibrosus (AF), made mostly of type I collagen, and vertebral end plates
(VE), which are cartilaginous plates that supply nutrients to the inner two-thirds of the annulus and the
entirety of the NP. An intact, healthy disc is an avascular structure. All nutrition demands of the discus
intervertebralis are met by diffusion through the VE and AF. Diffusions of these nutrients, including
oxygen, can be compromised following injury and resultant inflammation.
The innervation of the disc is quite complex.7
• Bundles of sensory nerves, branching through rami communicantes, project both above and below the
spinal nerve and ganglion.
• Direct fibers from the sympathetic truncus join to form the sinuvertebral nerve, which continue to
branch and innervate the circumference of the AF.
The sinuvertebral nerve contains nociceptive, sympathetic, proprioceptive, and vasomotor nerve
fibers.8-13 These anatomical studies have shown the close relationship between the sensory fibers and
sympathetic fibers, which could explain why lumbar sympathetic blocks14,15 and RF ablation of the ramus
communicans16 has been shown to help in patients with discogenic pain.
• The sinuvertebral nerves diverge and project fibers ventrally and dorsally and send branches into the
lateral aspects of the AF.
• As the nerve fibers reach the ventral and dorsal aspects of the annulus, they split into finer branches
forming several complicated neural networks.
• These plexiform structures innervate the anterior longitudinal ligament (ALL), ventrally and posterior
longitudinal ligament (PLL) and ventral dura, dorsal to the disc.7
• These plexi are rich with craniocaudal connections from adjacent spinal segments, as well as bilateral
(transverse) neural contributions7,17 and ultimately innervate the ventral and posterior aspects of the
disc.18
• This multi-segmented, transverse innervation pattern could account for the varied and often dynamic
complaints of patients with discogenic pain.
The key structures to successfully attaining optimal placement of the electrodes lies in identifying the
following structures:
• Spinous process
• Lamina
• Corpus vertebrae
• Superior articular process
• Inferior articular process
• Intervertebral foramen
• Pedicles or root of the vertebral arch
• Transverse process
• Posterior annulus fibrosus of the intervertebral disc
Other relevant anatomy that should be taken into consideration when performing this procedure:
• Vertebral end plates
• Existing nerve roots
• Ramus ventralis
• Vertebral arteries
• Erector spinal muscles
• Informed consent and explanation of potential complications
• Allergies
• Physical examination of lumbar area for anomalous anatomy, infection, or skin ulceration
• Ability of patient to lie prone during procedure
• IV fluids and medications for sedation/analgesia
Fluoroscopic Views
• Start procedure with oblique view of approximately 30 degrees, such that half of the disc is lateral to
the SAP. At this angle with the radiation beam parallel to the VE, the height of the disc is maximized
Figure 36-3. Initially the biacuplasty introducer is positioned from the oblique view by rotating the
fluoroscopy C-arm to position where the superior articular process of the vertebral level below is moved
to about one half the width of the vertebral column. This view allows optimal placement of two
electrodes to form a bipolar configuration with approximate distances of less than 3 cm. Notice that the
lower end plate is lined (A), pointer placed just next to SAP (B), and then introducer placed (C) via
which an electrode will be positioned.
Figure 36-4. Same procedure should be repeated on the opposite side with an introducer placed from the
oblique view. Again closeness of the introducer tip to the SAP prevents unnecessary paresthesias.
• Confirm placement of the introducers with anterior-posterior (AP) view. The introducer tips should
appear to be within the medial edge of the pedicles (Figure 36-5).
Figure 36-5. Wider angle of insertion may be necessary for large discs to maintain maximum distance
between probes to be 2.5 cm to 3 cm. Approach angle should be adjusted from 30 degrees (A) to 45
degrees (B) from the median. Increased approach angle brings probes close enough to create a confluent
lesion.
• Once the electrodes have been placed into the disc, positioning and depth should be confirmed with
both AP and lateral views with the electrodes just piercing the posterior annulus of the disc (Figures
36-5 and 36-6).
Figure 36-6. Assessment of the introducer depth in the lateral view. Notice that initially (like here with
L4-L5 disc) an introducer may be slightly deeper that final electrode position would require. However,
no adjustment of introducer is needed. Once when biacuplasty electrode is placed via introducer, it may
be pulled out slightly in order to position an active tip within last portion of the annulus.
Equipment
• 25-gauge 1.5-in needle for infiltration
Medications
• 0.5% to 1% lidocaine
Technique
The intradiscal biacuplasty procedure is a minimally invasive annuloplasty technique using
radiofrequency heat delivery to the posterior annulus of the disc.
• Intravenous access should be obtained and 5-lead electrocardiogram, continuous pulse oximetry, and
noninvasive blood pressure monitors are placed.
• Prophylactic intravenous antibiotics were administered 15 to 40 minutes prior to beginning of the
procedure.
• The procedure is completed under fluoroscopy, with the patient lying prone and minimal sedated.
• The C-arm of the fluoroscope should be positioned obliquely at approximately 35 to 45 degrees, until
the lateral aspect of superior articular process (SAP) is located in the axial middle of the disc.
• With the C-arm properly positioned, a 17-gauge TransDiscal introducer is advanced in parallel with
the radiation beams (tunnel view) and directed just lateral SAP approaching the disc posterolaterally at
approximately the center of the disc height. This ensures that the electrodes are away from both the
nerve roots and the vertebral end plates to increase the safety of the procedure.
• The introducers are advanced until the tips appear to be within the medial edge of the pedicles in an
anteroposterior (AP) view.
• Next, an 18-gauge TransDiscal probe (Figures 36-5, 36-7, and 36-8) is advanced through the
introducer and positioned inside the disc.
Figure 36-7. Schematic explains on how such wider angle of introducer insertion is achieved within a
larger discs to maintain that optimal distance between the probes. Typically, angle taken is about 45
degrees.
Figure 36-8. Two level biacuplasty in progress with already positioned electrodes within the L4-L5
intervertebral disc and 2 introducers just placed into L5S1 disc observed from the lateral fluoroscopic
view. Notice that the tips of the introducers just pierced into the posterior annulus of L5S1 disc.
• Appropriate positioning and depth of probe are assessed by checking AP and lateral views of the
lumbar spine (Figures 36-5, 36-8, and 36-9). This procedure is repeated on the opposite side, so that
when positioned, the two probes form a bipolar configuration.
Figure 36-9. Two common mistakes when biacuplasty electrodes positioned within the lumbar discs. (A)
Angles on which introducers were positioned are small and distance between 2 electrode tips is greater
than 3 cm. Not sufficient to achieve an effective bipolar configuration with optimal level of heat in the
middle. (B) One of the electrodes is too close to the end plate even after upper end plate was lined up in
anterior-posterior view. That can produce an extensive heat and damage to the end plate of the disc.
• The generator controls the delivery of RF energy by monitoring the temperature measured by a
thermocouple at the tip of the probe.
• The temperature increases gradually over a period of 10 minutes to 50°C, with final heating at 50°C
for another 5 minutes.
• It should be noted that, although the temperature is set to 50°C on the RF generator, tissue temperature
reaches 70 to 75°C because of ionic heating.
• Throughout the entirety of the procedure, the patient is minimally sedated, but awake and able to
communicate with the physician, reducing the risk of neurological injury.
• Delivery of the heat to posterior annulus itself usually is not painful, frequently patients report mild
transient back discomfort without significant leg pain.
• Once the procedure is completed, patients were transferred to a recovery area and monitored for 45
minutes prior to discharge with postprocedural instructions and a stabilizing brace to be worn when
awake.
Following completion of the procedure, the patient should go through a specific physical therapy program
over a rehabilitation period.
• Written post-op instructions should be provided to the patient.
• Oral opioid may be used for 1 to 2 weeks, after which nonsteroidal anti-inflammatory drugs (NSAIDs)
should be adequate.
• The use of muscle relaxants is optional and should be based on patient’s symptomatology.
• A lumbar sacral orthosis (LSO) should be worn for 4 to 6 weeks after the procedure.
• A lumbosacral functional restoration program is highly recommended and is further described below.
• Patient education should be provided on how to prevent re-injury and return to work or usual activities
carefully planned.
Written post-op instructions should contain the following:
1. Activity restrictions/guidelines
2. Proper use of orthosis
3. Emergency telephone numbers and appointment date for follow-up
4. Explanation of expectable postprocedure pain, and recommendations on the adjunctive use of ice/heat.
These directions should also contain a brief description of the warning signs of post-op complications
such as:
• Stiff neck
• Increasing pain
• Lower extremity paresthesia
• Motor deficits
• Bladder or bowel dysfunction
• Wound site drainage
Special emphasis should be placed on appropriate post-op orthosis use. California LSO is frequently
well tolerated, although other orthoses can be used.
The orthosis should be carefully fit to the patient with about 15 degrees of lordosis and patient should
be instructed to bring it to operation room for immediate post-op use. The brace may be removed briefly
for personal hygiene activities.
FUNCTIONAL REHABILITATION AFTER BIACUPLASTY

Week 1:
Short periods of walking after procedure
No driving
10 lb lifting limit only
Week 2:
Gentle stretches
Lifting restrictions of 20 to 40 lb × 12 weeks
Avoid strenuous activity, twisting or sustained flexion
Option to begin gentle lumbar stabilization exercises with neutral bias and abdominal strengthening
Instruct therapist to avoid truncal rotation
No manual therapy
Weeks 3-4:
Therapist guided stretching, strengthening, ROM. Begin neutral-biased dynamic stabilization program.
May remove orthosis during PT sessions.
Limit L/S flexion to 40 degrees and torsion to 30 degrees during these weeks.
If not well tolerated in first sessions, may convert to aquatherapy based program.
Minimize driving ≤30 minutes only.
Weeks 5-6:
Progressive strengthening, endurance exercises
NSAID PRN
Education to avoid reinjury
Weeks 6-8:
Advance physical therapy to dynamic lumbar stabilization as tolerated with limited truncal rotation.
Exercise may include swimming, bicycling, and supervised aerobic exercises.
Discontinue use of orthosis.

Overall, the prevalence of reported complications following intradiscal biacuplasty remains zero.
However, complications like discitis, epidural abscess, and bacterial meningitis may occur as the number
of the completed procedures increases. Potential complications after any minimally invasive intradiscal
procedures can be divided into procedural complications and postprocedural complications.
Procedural Complications
Procedural complications may include:
• Acute paresthesias,
• Muscle spasm, or
• Even bleeding
During the provocative discography excessive amounts of local anesthetic injected deep, close to the
disc/foramina, prior to intradiscal needle placement,4 puncturing an intervertebral disc with a needle
could potentially lead to progressive disc disruption.19
With the high temperatures used in biacuplasty, electrode placement could lead to nerve injury or
osteonecrosis of end plate, causing radicular pain, axial pain, or even transient paralysis. Commonly
listed risk factors for postsurgical spinal complications, such as obesity, history of leg pain, smoking,
diabetes mellitus, and duration of the back pain, are unlikely to predict higher risk for complications after
annuloplasties.
Other possible complications include:
• Radicular signs and symptoms (from burning sensation to foot drop)
• Discitis, septic or aseptic
While never reported after biacuplasty, but has been described following IDET procedure.21-23
• Postprocedural disc herniation
Also reports as a complication IDET, but not after biacuplasty.4
Up to this date, no complications were reported in the literature on biacuplasty24-26 or by the electrode
maker (author’s correspondence).
CLINICAL PEARLS
• More strict selection criteria may improve clinical results of biacuplasty.
• Strong candidates for biacuplasty include patients with evidence of 1 or 2 levels of disc degeneration
on MRI and 1 or 2 levels positive on provocative discography.
• The ideal distance between the bipolar electrodes is 2.5 cm to 3 cm or less.
• This optimal positioning is achieved by using an oblique view with the fluoroscopy C-arm rotated to
where the superior articular process of the vertebrae 1 level below the disc is ½ the width of the
vertebral column.
• Postprocedure rehabilitation program is required to ascertain a good outcome.
References
1. Kuslich SD, Ulstrom CL, Michael CJ. The tissue origin of low back pain and sciatica: a report of pain
response to tissue stimulation during operations on the lumbar spine using local anesthesia. Orthop
Clin North Am. 1991;22(2):181-187.
2. Schwarzer AC, et al. The relative contributions of the disc and zygapophyseal joint in chronic low
back pain. Spine (Phila Pa 1976). 1994;19(7):801-806.
3. Kapural L, et al. Intradiscal thermal annuloplasty for the treatment of lumbar discogenic pain in
patients with multilevel degenerative disc disease. Anesth Analg. 2004;99(2):472-476.
4. Cohen SP, et al. Risk factors for failure and complications of intradiscal electrothermal therapy: a
pilot study. Spine (Phila Pa 1976). 2003;28(11):1142-1147.
5. Mekhail N, Kapural L. Intradiscal thermal annuloplasty for discogenic pain: an outcome study. Pain
Pract. 2004;4(2):84-90.
6. Webster BS, Verma S, Pransky GS. Outcomes of workers’ compensation claimants with low back pain
undergoing intradiscal electrothermal therapy. Spine (Phila Pa 1976). 2004;29(4):435-441.
7. Groen GJ, Baljet B, Drukker J. Nerves and nerve plexuses of the human vertebral column. Am J Anat.
1990;188(3):282-296.
8. Bogduk N, Tynan W, Wilson AS. The nerve supply to the human lumbar intervertebral discs. J Anat.
1981;132(Pt 1):39-56.
9. Edgar MA, Ghadially JA. Innervation of the lumbar spine. Clin Orthop Relat Res. 1976;115:35-41.
10. Kimmel DL. Innervation of spinal dura mater and dura mater of the posterior cranial fossa. Neurology.
1961;11:800-809.
11. Pedersen HE, Blunck CF, Gardner E. The anatomy of lumbosacral posterior rami and meningeal
branches of spinal nerve (sinu-vertebral nerves); with an experimental study of their functions. J Bone
Joint Surg Am. 1956;38-A(2):377-391.
12. Stilwell DL Jr. The nerve supply of the vertebral column and its associated structures in the monkey.
Anat Rec. 1956;125(2):139-169.
13. Wyke B. The neurological basis of thoracic spinal pain. Rheumatol Phys Med. 1970;10(7):356-367.
14. El-Mahdi MA, Abdel Latif FY, Janko M. The spinal nerve root “innervation”, and a new concept of
the clinicopathological interrelations in back pain and sciatica. Neurochirurgia (Stuttg).
1981;24(4):137-141.
15. Nakamura SI, et al. The afferent pathways of discogenic low-back pain. Evaluation of L2 spinal nerve
infiltration. J Bone Joint Surg Br. 1996;78(4):606-612.
16. Oh WS, Shim JC. A randomized controlled trial of radiofrequency denervation of the ramus
communicans nerve for chronic discogenic low back pain. Clin J Pain. 2004;20(1):55-60.
17. Suseki K, et al. Sensory nerve fibres from lumbar intervertebral discs pass through rami
communicantes. A possible pathway for discogenic low back pain. J Bone Joint Surg Br.
1998;80(4):737-742.
18. Kallewaard JW, et al. 15. Discogenic low back pain. Pain Pract. 2010;10(6):560-579.
19. Carragee EJ, et al. 2009 ISSLS Prize Winner: Does discography cause accelerated progression of
degeneration changes in the lumbar disc: a ten-year matched cohort study. Spine (Phila Pa 1976).
2009;34(21):2338-2345.
20. Biyani A, et al. Intradiscal electrothermal therapy: a treatment option in patients with internal disc
disruption. Spine (Phila Pa 1976). 2003;28(15 Suppl):S8-S14.
21. Ackerman WE III. Cauda equina syndrome after intradiscal electrothermal therapy. Reg Anesth Pain
Med. 2002;27(6):622.
22. Hsia AW, Isaac K, Katz JS. Cauda equina syndrome from intradiscal electrothermal therapy.
Neurology. 2000;55(2):320.
23. Wetzel FT. Cauda equina syndrome from intradiscal electrothermal therapy. Neurology.
2001;56(11):1607.
24. Kapural L, Mekhail N. Novel intradiscal biacuplasty (IDB) for the treatment of lumbar discogenic
pain. Pain Pract. 2007;7(2):130-134.
25. Kapural L, et al. Histological changes and temperature distribution studies of a novel bipolar
radiofrequency heating system in degenerated and nondegenerated human cadaver lumbar discs. Pain
Med. 2008;9(1):68-75.
26. Kapural L, et al. Intervertebral disc biacuplasty for the treatment of lumbar discogenic pain: results of
a six-month follow-up. Pain Med. 2008;9(1):60-67.
CHAPTER 37
Endoscopic Discectomy
Sudhir Diwan, Kiran Patel, Kenneth Chapman, and Vikram B. Patel
INTRODUCTION
Endoscopic discectomy is a minimally invasive treatment for disc herniation, protrusion, or extrusion.
The goal of endoscopic discectomy is to provide relief from nerve root compression through the removal
of herniated nuclear material. Endoscopic discectomy is also a therapeutic option for cases of advanced
degeneration with proven discogenic pain. Endoscopic discectomy can be approached differently for the
2 basic types of disc herniations, contained and noncontained, both of which can be carried in an
outpatient setting. The focus of this discussion is on contained herniations or disc bulges.
INDICATIONS
• Contained disc herniations within the annulus or posterior longitudinal ligament (typically 6-10 mm)
• Unilateral leg pain greater than back pain
• Radicular/neurological symptoms in a specific dermatomal distribution that correlates with
MRI/CT/discography findings
• Positive straight leg raising test or positive bowstring sign, or both
• No improvement after 6 weeks of conservative therapy
• Well maintained disc height of 60% or more
• Alleviation of radicular pain with low volume selective nerve root block on the affected side at the
operative level
• Facet joint pain should be excluded
Endoscopic discectomy should be strongly considered in patients with herniation within the far lateral
recess beyond the intervertebral foramen. Such patients are difficult to treat with the traditional approach
of microdiscectomy which may require removal of a large portion or the entire facet.
CONTRAINDICATIONS
• Diffuse annular bulge involving the entire circumference of the vertebral body
• Severe lateral recess stenosis
• Calcified disc herniations
• Severe degenerative facet disease
• Ligamentum flavum hypertrophy
• Free or extruded disc fragments within the spinal canal
• Clinical evidence of significant progressive neurologic deficits and/or cauda equina syndrome
• The existence of other pathologies or conditions, such as fracture, tumor, pregnancy, or active infection
• An absolute contraindication for endoscopic discectomy includes significant (>= 3 mm) migration of
disc fragment
RELEVANT ANATOMY
• The central nucleus pulposus contains collagen fibers organized randomly, and elastin fibers arranged
radially; these fibers are embedded in a highly hydrated aggrecan-containing gel.
• Interspersed at a low density are chondrocyte-like cells sitting in a capsule within the matrix.
• The annulus fibrosus is made up of a series of 15 to 25 concentric rings, or lamellae, with the collagen
fibers lying parallel within each lamella. Elastin fibers lie between the lamellae.
• The posterior lamellar annular layers are thinner than in the anterior spine, which assists in spinal
flexion and extension but also predisposes the posterior annulus to disruption.
• Trauma and internal disc derangement can lead to disc herniation, which consists of protrusion of the
nucleus pulposus through the annulus fibrosus.
• The morphology of the macroscopic annulus fibrosus and the microscopic anatomy both undergo
changes in disc herniation.
• The posterior concavity of the disc is often reduced or inverted, whereas the cellular structure itself in
the annulus fibrosus undergoes a transformation from spindle-shaped cells to rounded chondrocytes at
the area of disc herniation.
• The pathology of disc herniation is often a narrow neck of disc protruding through annular fibers with a
“mushroom” head of the nucleus pulposus compressing the nerve roots, posterior longitudinal ligament
(PLL), or dura.
• As the sinuvertebral nerve innervates the dura and PLL, inflammatory cytokines exuding from the
exposed nucleus pulposus can cause back pain without leg pain.
• Compression of the nerve root by the disc herniation often produces dermatomal numbness,
dysesthesia, reflex changes, and weakness.
• If the nerve root is not directly mechanically compressed, there may be radicular pain from the
inflammatory response of the DRG to the chemicals and enzymes from the nucleus pulposus, but
without the other signs of radiculopathy.
• The increased blood flow to the nerve root after discectomy suggests the mechanism of neurologic
deficit is partially related to vascular ischemia from compression of the nerve root.
Other considerations for endoscopic discectomy include patient size, location of the disc herniation,
neuroforaminal size, presence of furcal nerves, presence of overlying annular inflammatory membrane,
disc height, anatomic impediments to access (osteophytes in the neural foramen, iliac crest morphology),
and applicability to the technique selected.
BASIC CONCERNS
• Disc herniations are of two basic types: contained and noncontained. Contained herniated discs have
an intact outer annulus with displaced disc material being held within the outer annulus of the contained
herniated disc. In contrast, noncontained herniated disc has localized displacement of disc material
beyond the intervertebral disc space and a breach in the outer annulus.
• Using the standard foraminal posterolateral approach, the morbidly obese patient presents anatomic
limitations to treatment of disc herniations. The straight anteroposterior skin-to-skin measurement may
be 15 cm or more. Using a 45-degree-angled insertion of a needle for endoscopic discectomy in a
standard extrapedicular approach (as used in discography) would require a needle length of 21 cm or
more (>8 in). Therefore, depending on the access needles or cannulas available, obese patients may
not be candidates for endoscopic discectomy.
• Location of the disc herniation is less likely to be a significant determinant of success with most
decompression systems utilizing an “inside-out” technique.
• A small neural foramen predisposes to injury during disc access with large needles because of the
exiting nerve root being displaced inferiorly in the neural foramen. The “safe triangle” for disc access
is smaller when there is significant apical foraminal impingement.
• The presence of osteophytes also causes some difficulties when there is zygapophyseal hypertrophy or
vertebral body osteochondrosis.
• A calcified annulus fibrosus also causes some difficulty with disc access.
• The presence of a high iliac crest poses significant problems with rigid cannula or needle systems at
L5-S1 because trajectory of the disk entry will predispose to damage to the superior S1 end plate, in
addition to posing problems when nonflexible instruments are used through the cannula.
• Furcal nerves are accessory nerves present in approximately 15% of the population, and are found
primarily at L4-L5. They traverse the foramen quite laterally and exit with the L5 nerve root.
Compression of the furcal nerves with a lateral disc herniation can cause L4 and L5 symptoms. These
are primarily sensory nerves and can be injured by a needle placed across the neural foramen into the
disc.
• Inflammatory membranes over the surface of the annulus fibrosus are exquisitely sensitive to pressure
and may make posterolateral needle placement quite painful.
• Informed consent and proper explanation of all potential complications including nerve root injury,
infection, bleeding, development of spinal instability, damage to end plate, and disc space collapse.
• Anticoagulation should be corrected.
• Thorough physical examination of the lumbar region and lower extremities for assessment of
neurologic symptoms as well as the absence of infection or skin ulceration.
• Intravenous access for IV fluid and medications for sedation. Sedation may be administered, but the
patient’s level of consciousness must be carefully monitored to ensure that the patient can still respond
to pain.
• Evaluation for contrast allergy.
• Strict sterile conditions are essential to reduce the potential for postoperative discitis.
• The patient should be administered cefazolin 1 to 2 gm intravenously 30 minutes prior to the
procedure. Alternatively, if the patient is allergic to cephalosporin medication, Clindamycin 600 mg IV
may be administered.
FLUOROSCOPIC VIEWS
Anterior-Posterior. The procedure is started with an anterior-posterior (AP) image of the lumbar spine
with the desired level in view. The fluoroscopic beam should be aligned with cranial-caudal tilt such that
it is parallel to the end plates of the vertebral bodies and the end plates appear “crisp” or on the edge.
Oblique. From the AP view, the C-arm is rotated in an oblique manner so that the superior articular
process (SAP) of the inferior vertebra is in the midposition of the disc space and subsequently creates a
inverted triangular opening to approach the disc, eg, for the L5-S1 level, the SAP forms this triangle’s
medial border, the lateral border is made up by the iliac crest and superior border by the vertebral body
end plate.
The lumbar discs superior to L5-S1 are typically easier to enter because the iliac crest lies lower and
typically does not obstruct the view of the disc space. The L5-S1 disc space will typically require the
most cranial tilt. Less cranial tilt is needed as one progresses to superiorly adjacent discs. Typically, a
straight anteroposterior view is sufficient for the L3-4 disc and the L2-3 disc will actually need somewhat
of a caudal tilt. For entrance to all disc levels, the SAP should be at the midpoint of the disc with the
edges of the end plates clearly visualized.
Lateral. During penetration into the outer annulus and advancement into the nucleus pulposus, multiple
AP and lateral images of the disc are obtained. The goal is to prevent unnecessary instrumentation and
decrease the possibility of penetration into the anterior nucleus or annulus.
EQUIPMENT
See Figure 37-1. This image shows the Disc-FX kit with accessories available for the postero-lateral
access to the intervertebral disc.
Figure 37-1. Disc-FX kit with accessories for posterolateral. (Reproduced with permission from
Elliquence.)
EQUIPMENT FOR POSTEROLATERAL INTRADISCAL

APPROACH
• Monitor, camera, and light source
• Bipolar system
• Spine scope sheath
• Spine scope with camera
• Standard IV tubing
• Spinal needle 18 or 16 gauge × 8 in
• Guidewires (thin and thick)
• Scalpel #11
• Tapered dilator
• Cannula, beveled
• Cannula depth stop
• Trephine
• Cannula, straight
• Graspers
• 10-cc syringe for local
• 10-cc syringe for Indigo carmine
EQUIPMENT FOR TRANSFORAMINAL APPROACH

• Multichannel, 20-degree oval spinal endoscope with 2.7 mm working channel and integrated
continuous irrigation (inflow and outflow) ports
• Multichannel, 70-degree oval spinal endoscope
• 7-mm working cannula with various open slotted, beveled, and tapered ends
• 2-channel tissue dilator/obturator
• Specialized single and double action rongeurs for visualized fragmentectomy
• Larger straight and hinged rongeurs for discectomy and targeted fragmentectomy
• Trephines for annulotomy and foraminoplasty
• Micro rasps, curettes, and penfield probes
• Annulotomy knife
• Flexible bipolar radiofrequency probe
• Fluid pump for continuous irrigation
• Video endoscopy tower
Medications
• Lidocaine 1%
• Omnipaque
• Indigo carmine
• Normal saline for irrigation
Technique
The most common technique is through a postero-lateral approach described below:
POSTEROLATERAL TRANSDISCAL APPROACH

Step 1: Insertion of Needle into the Disc (Figure 37-2)
Figure 37-2. Step 1. Needle insertion by using posterolateral approach via Kambin’s triangle.
• The patient is placed in the prone position with a pillow or bolster to lessen the lumbar lordosis.
• Start with an AP image of the lumbar spine where the spinous processes of the operative levels are
centered between the pedicles.
• Using a marking pen, draw lines connecting the spinous processes and lines across the disc space.
Using a lateral view, disc inclination angles are drawn and the cephalad/caudal entry point is
determined by the intersection of these lines.
• Once the entry point is determined, the skin window and subcutaneous tissues are infiltrated with local
anesthesia.
• A 6-in, 18-gauge needle is then inserted from the skin window at the desired trajectory, using a
posterolateral approach into the intervertebral disc via Kambin’s triangle, typically at a 30-degree
angle to the floor (coronal plane) and passed anteromedially toward the anatomic disc center,
infiltrating the needle tract with local anesthetic while advancing the needle.
• The lateral projection of C-arm should confirm correct annular location of the tip of the needle at the
annular window (annular entry point).
• In the AP view, the needle tip should be at the disc between the pedicles. In the lateral view, the
correct needle tip position should be just touching the posterior annulus surface. These two views of
the C-arm confirm that the needle tip has engaged the safe zone, the center of the foraminal annular
window.
• While monitoring the AP view, advance the needle tip though the annulus to the midline (anatomic disc
center).
• Then check the lateral view. If the needle tip is in the center of the disc on the lateral view, it reflects a
good position for central nucleotomy.
• For paracentral herniations, the needle tip should ideally be in the posterior one-third of the disc.
Step 2: Perform the Discogram

• Perform a confirmatory contrast discography. It is optional if the discogram has been performed before.
• The contrast mixture of a water-soluble contrast such as Iohexol and Indigo carmine dye is used.
• This combination of contrast ratio gives readily visible radiopacity on the discography images and
intraoperative light blue chromatization of the pathologic nucleus and annular fissures help guide the
targeted fragmentectomy.
Step 3: Insertion of the Guidewire through the Needle (Figure 37-3)
Figure 37-3. Step 3. Insertion of the guidewire through the needle; needle removed.
• Insert the guidewire through the 18-gauge needle channel. Advance the guidewire tip, 1 to 2 cm deep
into the annulus, then remove the needle.
Step 4: Insertion of Cannula and Dilator over the Guidewire (Figure

37-4)
Figure 37-4. Step 4. The cannula and dilator passed over the guidewire.
• Make a 2-cm stab incision at the skin entry of the guidewire to facilitate placement of the dilating
obturator.
• Slide the bluntly tapered tissue dilating obturator over the guidewire until the tip of the obturator is
firmly engaged in the annular window.
Step 5: Perform Annulotomy (Figure 37-5)
Figure 37-5. Step 5. Insertion of trephine or annulotome over the guidewire.

• Advance the bluntly tapered obturator, use mallet if required. Annular fenestration is the most painful
step of the entire procedure. Advance the obturator tip deep into the annulus and confirm again with AP
and lateral fluoroscopic views.
• Slide the beveled access cannula over the obturator toward the disc. Advance the cannula until the
beveled tip is deep in the annular window with the beveled opening facing dorsally.
• Remove the dilator and insert trephine to perform the annulotomy.
Step 6: Perform Nucleotomy (Figures 37-6 and 37-7)
Figure 37-6. Step 6. Guidewire, trephine and dilator removed, and nucleus debulking forceps inserted.
Figure 37-7. Nucleus debulking forceps.
• Remove the trephine or annulotome, insert the dilator and cannula, and advance to the center of nucleus
pulposus.
• Remove the dilator and guidewire, and insert tissue debulking forceps or nucleotome to remove the
disc material. The disc material is sent for biopsy.
• Enlarge the annulotomy medially to the base of the herniation with cutting forceps. This is performed to
release the annular fibers at the herniation site that may pinch off or prevent the extruded portion of the
herniation from being extracted.
• Directly under the herniation, a large amount of blue stained nucleus is usually present.
Step 7: Perform Radiofrequency Ablation (Figure 37-8)
Figure 37-8. Step 7. The debulking forceps removed and flexible radiofrequency bipolar probe is
inserted for nucleus ablation and annulus modulation.
• The flexible radiofrequency bipolar probe is used to contract and thickened the annular collagen at the
herniation site. It is also used for hemostasis throughout the case.
Step 8: Endoscopic Visualization (Figure 37-9)

Figure 37-9. Step 8. Optional endoscopic observation of nucleotomy and annulus modulation.
• The disc visualization is optional to see the cavity created after the removal of disc material.
TRANSFORAMINAL APPROACH
• Most steps of this approach are similar up to steps 5 of the posterolateral transdiscal approach.
• The patient is positioned in the prone position with a pillow or bolster under the abdomen to lessen the
lumbar lordosis.
• Using a posterolateral access, a 16- or 18-gauge spinal needle is introduced into the intervertebral disc
via transforaminal approach.
• After an optional discography, a guidewire is placed through the needle.
• The needle is removed and a small skin incision of 2 mm is made for introduction of the dilator and
working cannula.
• The dilator and working cannula are placed on the intervertebral disc annulus over the guidewire.
• An initial endoscopic inspection is carried out along with fluoroscopy, to ensure correct positioning.
The 3 main steps of the procedure will be done through the placed cannula.
• Free subligamentary material is removed with the rongeur or the annulus is opened with the trepan
provided for additional intradiscal work. Additional intervertebral disc material is then removed
manually.
• The bipolar probe is inserted into the nucleus, and nuclear ablation is performed with a defined energy
and frequency modulation. It is also possible to continue the nucleotomy using the rongeur.
• The relieved nucleotomy region can be checked with another endoscopic inspection.
• Modulation of the dorsal annulus can be performed by placing the bipolar probe on the pathological
region and sweeping it dorsally.
• Subsequent retraction of the working cannula with a simultaneous endoscopic view can show the
epidural space and the nerve roots after the decompression. If necessary, the instruments can be used
again for continued decompression.
PERFORM ANNULOTOMY
• Advance the bluntly tapered obturator, use mallet if required. Annular fenestration is the most painful
step of the entire procedure.
• Advance the obturator tip deep into the annulus and confirm again with AP and lateral fluoroscopic
views.
• Slide the beveled access cannula over the obturator toward the disc.
• Advance the cannula until the beveled tip is deep in the annular window with the beveled opening
facing dorsally and caudally (8 o’clock position).
• Remove the dilator and connect adaptor to end of cannula. Connect suction to cannula.
• Connect light source and white balance. Connect irrigation fluid.
CAVITY CREATION
• With cannula in the posterior and lateral third of the disc space, insert working channel into cannula.
• Dissection is performed with the rongeur and elliquence Trigger-Flex bipolar probe.
• With the opening of the bevel facing toward the spinal canal, dissection is continued to the posterior
annular fibers.
• Nucleus pulposus near the herniation will stain blue secondary to the Indigo carmine.
• The herniated disc is extracted under direct visualization.
• Examine site for other.
• Radiofrequency can be used to thicken the annular collagen fibers at the herniations.
A procedure that does not result in substantial relief of pain should not be considered a failure until at
least 6 weeks have passed postoperatively.
• Analgesics and anti-inflammatory medications can be given for a short period after the procedure.
• Closely monitor for procedure-related complications such as infection and/or bleeding.
• If the patient has a very inflamed nerve root, consider an image guided selective nerve root block to
facilitate recovery.
• Postoperative physical therapy can be very helpful to facilitate recovery and prevent a re-herniation.
Postoperative discitis should be considered in all patients who develop:
• New or different back pain
• Radiation of pain to other areas of the body
• Tenderness around the spine
• Inability to bend without aggravation of pain
These patients may or may not exhibit systemic symptoms such as fever, chills, or weight loss. The
appropriate work-up includes an erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), white
blood cell count (WBC), and CT scan or MRI.

Potential complications of endoscopic discectomy include:
• Nerve root injury
• Infection
• Bleeding
• Dural tears
• Scar tissue formation
• Development of spinal instability
• Damage to end plates and disc space collapse
Because the transforaminal endoscopic approach passes adjacent to the exiting spinal nerve root and
dorsal root ganglia, there is potential for nerve irritation, dysesthesias, or overt nerve damage.
CLINICAL PEARLS
• For the oblique fluoroscopic view, positioning the SAP at the midpoint of the superior end plate will
ensure that the nerve root is out of the introducer needle’s trajectory and decrease the risk of injury.
• A stab incision prior to placement of the introducer needle may facilitate appropriate needle placement
and decrease the introduction of excessive force.
• During probe activation, the probe tip should be monitored under live fluoroscopy to decrease the
possibility of inadvertently advancing the probe into the anterior annulus.
• In some systems, an eccentric parallel channel in the obturator allows for four-quadrant annular
infiltration using small incremental volumes of local anesthetic in each quadrant, enough to anesthetize
the annulus, but not the nerves.
• The use of local anesthesia and conscious sedation rather than general anesthesia or spinal anesthesia,
and the use of standardized needle placement can decrease the occurrence of intraoperative nerve
injury.
• The vast majority of herniations can be treated via the uniportal technique.
• Biportal technique allows better approach for large central herniations. This allows the use of larger
articulating instruments that fit through the contralateral 7-mm access cannula under direct endoscopic
vision.
Suggested Reading
Chang M. Discography and endoscopic discectomy. Minimally Invasive Spine Surgery. Springer;
2009:chap 12.
Herkowitz H. Posterolateral lumbar endoscopic discectomy. Rothman-Simeone The Spine. 6th ed.
Elsevier; 2011:chap 59.
Mayer HM. Microtherapy in low back pain. Minimally Invasive Spine Decompression. Springer;
2006:chap 30.
Phillips FM. Disc herniation. The Lumbar Intervertebral Disc. Theime Medical; 2010:chap 2.
Yeung A. Minimally invasive techniques for the management of lumbar disc herniation. Orthop Clin N
Am. 2007;38:363-372.
Yue JJ. Bertagnoli R, McAfee PC, An HS. Motion Preservation Surgery of the Spine: Advanced
Techniques and Controversies. Lumbar Endoscopic Posterolateral (Transforaminal) Approach.
Elsevier; 2011.
CHAPTER 38
Minimally Invasive Lumbar Decompression

(MILD procedure)
Lora L. Brown
INTRODUCTION
• MILD (minimally invasive lumbar decompression) is an FDA cleared percutaneous, fluoroscopically
guided procedure developed as a less destabilizing bone and tissue sparing alternative to more
invasive surgical decompression options.
• The removal of hypertrophied ligamentum flavum tissue during the mild procedure creates spinal canal
space, thereby reducing intraspinal pressures, relieving nerve compression and alleviating complaints
associated with neurogenic claudication.
• The traditional treatment algorithm for spinal stenosis ranges from the least invasive conventional
therapies to the most invasive surgeries with fusion (Figure 38-1).
Figure 38-1. Lumbar spinal stenosis treatment algorithm.

INDICATIONS
• Lumbar spinal stenosis secondary to ligamentum flavum hypertrophy on MRI or CT imaging
• Symptomatic neurogenic claudication in patients with lumbar spinal stenosis
• The absence of spinal instability
• The absence of grade II or greater spondylolisthesis
• The absence of severe foraminal or lateral stenosis presumed to be causing the symptoms
CONTRAINDICATIONS
There are no FDA contraindications for the mild procedure. However, relevant clinical contraindications
are listed:
• Spinal instability
• Severe neurologic deficit
• The absence of a laminar shelf at the level to be treated
• Inability to appreciate the epidurogram at level and side to be treated
• Infection
• Conventional surgical contraindications such as bleeding disorders and/or active anticoagulation, as
well as, systemic or local infections should be considered.
RELEVANT ANATOMY
• Interlaminar space
• Ligamentum flavum
• Facet joint
• Intervertebral disc
• Epidural space
PATHOPHYSIOLOGY OF SPINAL STENOSIS

• Degenerative changes in the lumbar spine include hypertrophy of the ligamentum flavum, facet joint
arthritic changes, and bulging intervertebral discs.
• There is structural narrowing of the vertebral canal resulting in nerve root compression and
symptomatic neurogenic claudication.
• Neurogenic claudication presents as severe pain in the lower back, buttocks, and/or legs that
progressively worsens as the individual stands or walks and is relieved with forward flexion—
releasing pressure on the neural elements.
• Neurogenic claudication symptoms do not follow specific dermatomal patterns and, unless associated
with severe stenosis, usually are not associated with neurologic deficits.
• Patients often complain of lower extremity numbness or paresthesiae.
• Pain is typically not initiated with nonweight bearing positions such as sitting or lying supine.
• Compared to vascular claudication, patients with neurogenic claudication present with pain during
prolonged erect standing and walking, but tolerate cycling due to flexed positioning, and also have
palpable pedal pulses.
• In combination with patient symptomatology, radiologic evidence often used to define spinal stenosis is
a canal area of less than 100 mm2.
• As confirmed radiologically, the most common level affected by lumbar spinal stenosis is L4-5,
followed by L3-4, L5-S1, L2-3, and L1-2 (see anatomical Figure 38-2).
Figure 38-2. Lumbar spine anatomy.
As the vertebral canal narrows, there is a transient pressure elevation at the level of stenosis that is
provoked by weight bearing. Symptomatic lumbar spinal stenosis can be related to this pressure
elevation. It is postulated that as the pressure rises, venous congestion and neural ischemia occur. Flexion
of the lumbar spine expands the canal diameter to its maximum diameter, thus providing a decrease in
canal pressure and symptomatic relief. Positions that decrease the force of gravity on the spinal canal also
provide symptomatic relief in lumbar canal stenosis. When seated, the counter force provided by the chair
counteracts that of gravity, providing an overall decrease in canal pressure. When supine, the effect of
gravity on the spinal canal is eliminated totally, as the force of gravity is now perpendicular to the spine.
MECHANISM OF ACTION
• The mechanism of action for the mild procedure is based upon these pressure-volume relationships.
• It is well known that a small change in volume can create a much larger change in pressure.
• By decompressing the spinal canal with even a small volume of tissue, the associated pressure change
may decompress neural structures and restore venous flow, thus providing symptomatic relief.
LIGAMENTUM FLAVUM HYPERTROPHY

• Ligamentum flavum hypertrophy contributes significantly to spinal stenosis.
• The ligament can become quite thick, and according to current literature, may contribute up to 85% of
the induced narrowing of the spinal canal.
• Although relative in regard to patient size, ligamentum flavum tissue greater than 2.5 mm in diameter,
as measured perpendicular to the midpoint of the lamina, may be considered enlarged by radiologic
criteria.
• Ligamentum flavum hypertrophy occurs when collagenous tissue collects posterior to the fibrous
ligamentum flavum anterior border (Figures 38-3 and 38-4).
Figure 38-3. This is a photo of an axial cut MRI image of the lumbar spine demonstrating spinal stenosis
with ligamentum flavum hypertrophy (black V-shaped tissue in posterior canal). (Used with permission
Courtesy of Wade H.M. Wong, DO.)
Figure 38-4. The ligamentum flavum measurement is taken at the midpoint of the pedicle and is measured
in a perpendicular direction from the pedicle as demonstrated in this photo. A measurement of 2.5 mm or
greater is considered hypertrophic. (Used with permission from Charles Stevens, MD.)
• The change in thickness of ligamentum flavum tissue appears to occur in the presence of chronic micro-
instability that slowly develops over time.
• This process is especially evident in adjacent segmental disease associated with patients who have
had previous laminectomy procedures.
• These patients almost always develop ligamentum flavum hypertrophy as a result of the shear stress
associated with adjacent level postsurgical changes.
It has been observed that mild is extremely effective in treating spinal stenosis associated with adjacent
segmental disease, provided there is no preexisting spinal instability. The posterior anatomical position
of this tissue makes it amenable to percutaneous decompression. The mild procedure utilizes a 12-gauge
working port through which decompression instruments are placed. The optimum approach for effective
decompression is in line with the inferior lamina. The working port is positioned in such a manner that it
parallels the superior surface of the inferior lamina. Although minor adjustments may be indicated based
upon individual patient anatomy, this approach provides the most consistent position for maximum tissue
resection.
The ligamentum flavum tissue is accessed through the interlaminar window. The size and shape of this
space varies by patient and spinal level. In addition, degenerative changes, including shingling of the
lamina, as well as intraoperative positioning of the patient, may influence access through the interlaminar
space. Preoperative imaging studies are extremely important to ensure optimum access and
decompression.
EPIDUROGRAM
An important and key aspect of the mild procedure is the epidurogram. An epidurogram is utilized as a
safety feature allowing the mild decompression to proceed while avoiding device contact with the dura,
cauda equina/nerve roots and major blood vessels, thus preventing potential patient injury.
• It is beneficial to place the epidurogram at the same level and on the ipsilateral side of the level being
treated.
• This permits minimal use of contrast, which is recommended to ensure appreciation of the contralateral
oblique fluoroscopic view of the epidurogram at the treatment site during decompression of the
ligamentum flavum.
• An alternative, but less desired approach would be placement of the epidurogram one level below the
treatment level. This approach demands greater contrast volumes, which may affect visualization.
• The epidurogram provides an anterior working border that should be respected at all times.
Maintaining all decompression efforts posterior to the epidurogram ensures avoidance of the spinal
canal and neural structures.
• Informed consent with proper explanation of potential complications.
• Anticoagulation—patients must have normal coagulation status.
• The patient must be able to lie prone.
• Anesthesia—the patient must be able to endure light sedation or monitored anesthesia care.
• Intravenous access is necessary.
• Evaluation for contrast allergy—minimal amounts of epidural contrast is used. Gadolinium may be
substituted but visualization of epidurogram must be verified.
Mild is considered a minimally invasive outpatient procedure. It is performed in a sterile operating or
procedure room with utilization of fluoroscopy. The patient’s imaging studies should be present and
available for reference during the procedure.
The preoperative workup for the mild procedure is similar to that of other minimally invasive spine
surgical interventions, ie, implantation of spinal cord stimulators or intrathecal pumps. Patients should
have appropriate medical or cardiac clearance per treating facility’s anesthesia guidelines. Normal
coagulation studies should be confirmed and anticoagulation medication use suspended.
Preoperative intravenous antibiotic administration is desirable. Most mild patients require light
conscious sedation. In the rare case that conscious sedation is contraindicated, a general anesthetic may
be used. Occasionally physicians have found their patients to be comfortable during the procedure using
only local anesthetic.
INDICATIONS
Mild is cleared by FDA to perform lumbar decompressive procedures for the treatment of various spinal
conditions. The mild devices are specifically designed to access the interlaminar space from a posterior
approach, enabling removal of small portions of the lamina, then preferentially resecting and debulking
the thickened ligamentum flavum, thus accomplishing a lumbar decompression.
FLUOROSCOPIC VIEWS
• Mild is a fluoroscopically guided procedure. Utilization of a proper epidurogram is paramount to the
success of mild.
• Begin in the posterior-anterior (PA) view. Align the inferior end plate of the level being treated in
parallax. This view will open the apex of the interlaminar space allowing the epidural needle to be
placed optimally in the apex.
• Utilize PA and lateral views for placement of your epidural needle. The epidural needle is best placed
in the ipsilateral apex of the interlaminar space of the level being treated.
• PA and contralateral oblique views are used for cannula placement.
• All resection is done utilizing the contralateral oblique view. Use frequent PA visualization during
resection to confirm medial-lateral instrument positioning.
Although AP and lateral fluoroscopic views are appreciated, the bulk of this procedure is performed
utilizing a contralateral oblique fluoroscopic view.
• This view is obtained by “obliquing” the C-arm between 40 and 45 degrees to the contralateral side of
the planned treatment side.
• In this view, the superior articular process of the level being treated should be positioned at the
junction of the posterior and middle thirds of the vertebral body. In this view, the trajectory of the
fluoroscopic beam is parallel to the inferior lamina of the ipsilateral treatment side.
• In the contralateral view, the epidurogram presents as a sharp, crisp line representing the posterior
border epidural quadrant being treated.
• The epidurogram may have a “scalloped” appearance, representing ligamentum flavum enlargement.
• The reduction in the “scalloped” shape, or a thickening and straightening of the epidurogram, is
expected as decompression of the ligamentum flavum tissue occurs.
• Only a small amount of contrast is required to obtain the necessary epidurogram (typically <1 cc).
Intraoperative replenishing or “blushing” of the epidurogram (using <0.5 cc of contrast) may be needed
for optimum visualization (Figures 38-5 and 38-6).
Figure 38-5. The “contralateral oblique” fluoroscopic approach is used during tissue resection. This
view provides maximum visualization of the lamina and the epidurogram at the level of resection.
Figure 38-6. A typical scene of a physician performing the mild procedure. (Used with permission from
Wade H.M. Wong DO.)
Depth of instrument placement during the mild procedure is observed in the contralateral oblique
fluoroscopic view. All advancement of instruments, and the entire decompression procedure should be
performed utilizing this view.
While all aspects of the procedure should be conducted in the contralateral oblique fluoroscopic view
with constant visualization of the epidurogram, it is prudent to frequently stop and check the AP view. The
AP view allows verification of the mild instruments’ medial to lateral position within the posterior spinal
space.
POSITIONING THE PATIENT

• Prone position
• Lumbar flexion with abdominal bolster or radiolucent frame
• Arms elevated to allow lateral and contralateral fluoroscopic visualization
Patients undergoing the mild decompression procedure are placed in a prone position with the abdomen
bolstered to reduce lordosis. Reduction of lumbar lordosis opens the interlaminar window facilitating
access to the posterior spinal space. It is important to appreciate the degree of laminar shelving that may
exist. In some elderly patients with significant degenerative changes to the spine, the lamina can overlap
or “kiss,” making interlaminar entry difficult. Increased lumbar flexion can aid in these cases (Figure 38-
7).
Figure 38-7. A properly positioned patient for the mild procedure is demonstrated. The patient is prone
with reduction of the lumbar lordosis. (Used with permission from Wade H.M. Wong DO.)
Conversely, it is also important not to over-flex the lumbar spine. Hyperflexion of the lumbar spine
extends the epidural space as well as the posterior spinal tissue. Too much extension of these tissues can
increase the difficulty of decompression. In addition, once the epidural space is extended, the
epidurogram will lose its scalloped shape associated with ligamentum flavum hypertrophy making it more
difficult to identify the procedure endpoint (a straighter, thicker epidurogram).
Abdominal bolstering can be accomplished utilizing multiple techniques. Pillows can be used under the
abdomen. Sometimes with this technique, the pillows become too compressed and the patient can sink,
thus reducing the intended lumbar flexion. Another technique utilizes rolling of sheets or blankets into logs
8 to 12 in in height, depending on patient’s body. These logs are then placed under the patient’s iliac
crests and under the clavicles. Finally, radiolucent devices such as Wilson and Camden frames may be
utilized.
EQUIPMENT
• The mild procedure is performed using a mild kit provided by Vertos Medical Inc. (Aliso Viejo, CA).
The kit contains much of what is needed to perform the procedure. Contained within the kit is the 5.1
mm portal, trocar and handle, a bone resecting device (mild Bone Sculpter Rongeur), a soft tissue
resecting device (mild Tissue Sculpter), a portal stabilizer, a depth guide, and a surgical clamp (Figure
38-8).
Figure 38-8. The mild kit contains the Tissue Sculptor, the Bone Sculptor Rongeur, the mild portal, the
mild trocar and handle, the mild portal stabilizer, the mild depth guide, and the mild surgical clamp.
• The mild Bone Sculpter Rongeur is utilized to remove small portions of bone along the superior and
inferior laminar border. This enables the removal of small osteophytes and disengages the ligamentum
flavum attachments along the posterior lamina. This disengagement of ligamentum fibers from the
lamina facilitates the ultimate removal of ligamentum tissue.
• The mild Tissue Sculpter is uniquely designed to excise hypertrophied ligamentum flavum tissue in a
nontraumatic manner. It has a blunt, curved distal tip and a superior positioned cutting edge to capture,
cut, and then retains tissue in the shaft of the instrument. This device can accommodate multiple tissue
cuts per pass, but should be cleaned frequently to avoid over filling. The posterior end of this
instrument has a tissue eject trigger allowing contained tissue to be ejected from the device and
discarded.
• Not included in the kit, but needed for the procedure is an epidural needle (recommend 20 gauge), loss
of resistance syringe, IV extension tubing and syringe and needles for infiltration of local anesthesia.
• The contrast utilized should be a nonionic substance. Isoview M200 is the author’s choice. For patients
with contrast allergies, gadolinium may be considered provided it creates a visible epidurogram.
• Other equipment needed for this procedure includes a radiolucent procedure table and a C-arm.
• Prior to beginning, the procedure one should carefully map out the exact location of the hypertrophied
ligamentum flavum on the MRI. This will allow one to define trajectory and approaches to the stenosis.

• Step 1: Patient position.
Position patient prone with reduction of lumbar lordosis (see patient positioning above). Check
pressure points prior to implementation of anesthesia.
• Step 2: Fluoroscopy.
Using fluoroscopy, identify and superficially mark the midline as well as the medial pedicular
borders bilaterally at the intended treatment level(s).
These markings will prove useful later in the case as they can serve as a reminder of instrument
distal tip orientation.
For example, if the proximal end of the portal is positioned extremely lateral, outside of the skin
markings, it is likely the distal tip has crossed midline, thus requiring repositioning (Figure 38-9).
Figure 38-9. Superficial skin markings are made to identify the midline and the medial pedicular borders.
• Step 3: Epidural needle placement.

Align the inferior end plate of the level to be treated with the fluoroscope. This will open the
superior aspect of the intervertebral space.
The goal is to place the epidural needle as high in the apex of the intervertebral space and as close
to midline as possible while remaining ipsilateral to the treatment side.
This will provide the best epidurogram with the needle as far out of the working zone as possible.
Utilize a “loss of resistance” technique with a continuous pressure placed on the hub of the syringe.
A bounce loss of resistance technique will more often than not result in a wet tap in these patients.
Once loss of resistance is confirmed, inject a small quantity on contrast (1 cc or less) to confirm
epidural spread in the contralateral oblique fluoroscopic view. Injection of contrast is facilitated
with the use of a high-pressure IV extension tube.
With severe stenosis, it may be necessary to place the epidural needle at the level above or below
the level of the stenosis.
• Step 4: Skin entry site and trajectory planning.
The skin entry site is usually one and one half levels below the treatment site on the ipsilateral side.
This typically falls at the level of the pedicle, one level down.
The best approach is usually about 15 degrees off of midline, but may need to be adjusted based on
the patient’s spinal anatomy.
Create a skin wheel with local anesthetic. Use a 5-in 22-gauge spinal needle to advance toward the
inferior lamina.
Utilize an AP fluoroscopic view to direct the needle approximately half way to determine the
medial to lateral trajectory needed at this level on this side. (Imaging studies should be reviewed
preoperatively for trajectory planning and available throughout the case for reference.)
• Once the medial to lateral trajectory of the needle has been determined, change the fluoroscopic view
to a contralateral oblique view for advancement to the lamina.
• Advancement of the needle in the AP view does not allow visualization of instrument depth.
• Do not advance the instrument unless utilizing direct visualization in the contralateral oblique view.
• The needle track may need to be adjusted until it lies parallel to the superior surface of the inferior
lamina at the treatment level.
• Copious injection of local anesthetic along the periostium, as well as along the needle track (upon exit
of this needle) ensures adequate local analgesia.
• Step 5: Insertion of tissue access device.
• Once the track has been determined, a 15 blade is used to make a skin puncture wound.
• The portal, when cannulated with the handled trocar, is referred to as the mild Tissue Access Device.
This access device is advanced along the same track until the distal end is positioned on the
superior surface of the inferior lamina, within the posterior half of the lamina (Figures 38-10 and
38-11).
Figure 38-10. The mild portal is loaded with a trocar and is positioned parallel to the superior surface of
the inferior lamina.
Figure 38-11. A photograph of a contralateral oblique fluoroscopic image demonstrating the epidural
needle positioned high in the L4-5 intralaminar space with visible epidurogram. The trocar is positioned
parallel to the superior surface of the inferior lamina. The tip of the trocar is seen here at the posterior
edge of the inferior lamina.
• Step 6: Removal of trocar.

Release and remove the trocar by gently turning the locking screw on the handle.
• Step 7: Placement of portal stabilizer.
Next slide the portal stabilizer over to the portal and snap into place.
The stabilizer has a roller ball mechanism that allows pivoting of the cannula, which may facilitate
tissue removal.
The portal stabilizer simultaneously provides some stability as it serves to control the angle of the
mild portal against the skin surface.
• Step 8: Depth guide placement.
Next, attach the depth guide to the distal end of the portal.
This device provides a stop that limits the depth (forward motion) of any instrument inserted into
the portal.
It has a dial mechanism that allows instruments to extend in 5 mm increments from 0 to 25 mm
beyond the tip of the port and into the interlaminar space (Figure 38-12).
Figure 38-12. The mild Portal Stabilizer serves to control the angle of the mild portal against the surface
of the skin. The mild depth guide serves to adjust the depth of the Bone Sculpter Rongeur and the Tissue
Sculpter within the intralaminar space in 5 mm increments.
• Step 9: Bony tissue decompression.

Decompression is initiated with the use of the mild Bone Sculpter Rongeur.
This instrument is inserted through the port and used to resect and excise superior and inferior
laminar tissue.
It is a single bite instrument that must be withdrawn from the port and emptied after each pass.
It is recommended that a systematic technique be utilized starting at the medial surface of the
inferior lamina and working toward the lateral end.
Then, beginning at the medial surface of the superior lamina, work toward the lateral end to include
the lateral intervertebral border (Figure 38-13).
Figure 38-13. The mild Bone Sculpter Rongeur is being used along the inferior edge of the superior
lamina.
• Step 10: Ligamentum flavum debulking.

Once an adequate amount of bone has been resected, the mild Tissue Sculpter is placed within the
port and utilized to resect remaining soft ligamentum flavum tissue.
This device may be used for multiple bites, but must be withdrawn from the port regularly and
tissue sufficiently discharged to avoid overfilling, which could affect normal action of the trigger
mechanism.
The instrument design requires a scooping upward motion from inferior to superior direction
combined with activation of the trigger, which implements the cutting action.
Repositioning of the tissue sculpter with each cut ensures additional tissue resection. It is suggested
that a thoughtful plan of resection be utilized beginning at the medial aspect of the interlaminar
space and working laterally.
Continual visualization of the epidurogram is required throughout the procedure. Care is taken to
avoid passage of instruments beyond the epidurogram.
Maintaining a position posterior to the epidurogram with all instrumentation throughout the
procedure ensures that neural structures are protected (Figure 38-14).
Figure 38-14. The mild Tissue Sculpter is being used to remove ligamentum flavum tissue from the
posterior intralaminar space.
• Step 11: Repeat epidurogram.

With adequate ligamentum flavum tissue resection, a change in the epidurogram is observed.
Typically, the epidurogram is visualized as straighter and/or thicker.
This finding is considered the end-point of the procedure and all instruments are withdrawn
(Figures 38-15 and 38-16).
Figure 38-15. (A, B) Per-mild. Note the shape of the epidurogram before the mild procedure as a thin
scalloped shape.
Figure 38-16. (A, B) Post-mild. Note the shape of the epidurogram after the mild procedure as thicker
and straighter indicating improved flow of contrast after debulking the hypertrophied ligamentum flavum.
• Step 12: Wound dressing.
The wounds are then cleaned and closed using a sterile adhesive-strip and a sterile dressing. The
patient is taken to PACU (Figure 38-17).
Figure 38-17. Small 5.1 mm incisions are covered with a small dressing post procedure.
• Post mild patients are recovered in the same fashion as other outpatient spinal procedures.
• Typical PACU monitoring protocols should be implemented in addition to neurological checks no less
than 3 times every 15 minutes.
• Postoperative oozing from the wound site is frequently observed. Re-enforcement of the dressing may
be indicated prior to discharge.
• Nearly all patients treated with mild are discharged on the day of the procedure. Postoperative ice and
mild analgesics are appropriate.
• Postprocedure discomfort maybe reported for up to 7 to 10 days in some cases. Once neurological
exams have been confirmed as normal, these complaints should be treated conservatively.
• Most patients undergoing the procedure have become deconditioned over a period of years.
Postoperatively a course of physical therapy may be required to functionally rehabilitate the patient.

Pearls
• Selection of patients: As with most procedures, optimal mild patient selection is critical to success.
These patients should demonstrate clinically significant symptomatic neurogenic claudication and have
verifiable ligamentum flavum hypertrophy. Patients with severe foraminal or lateral recess stenosis
outweighing the potential benefit of a percutaneous decompression procedure should be avoided.
• Positioning is extremely important to the success of this procedure. While reduction of lumbar lordosis
is important to facilitate access to the interlaminar space, it is important not to over flex the lumbar
spine. Over flexion of the lumbar spine creates taut posterior tissues making excision of ligamentum
flavum tissue difficult.
• Trajectory planning for port placement is an important aspect of the procedure. Begin with the port
placed parallel to the superior surface of the inferior lamina.
• Placement of the epidural needle is one of the most important aspects of this procedure. To ensure the
best placement, attempt to position the epidural needle as close to the apex of the intervertebral space
as possible. This is best achieved by first aligning the fluoroscopic view at the level to be treated such
that the inferior end plate of the superior vertebral body is in alignment. For example, if decompressing
the L4-5 level, the inferior end plate of L4 should be aligned to ensure apical access of the L4-5
interlaminar space.
• “Less is more” when it comes to contrast. Take care not to inject too much contrast. As the volume of
contrast is increased, it begins to flow around the epidural space, thus diminishing the resolution of the
epidurogram in the contralateral oblique view. It is important to note that what is needed from the
epidurogram in the contralateral oblique view is a fine crisp line that layers along the quadrant of the
epidural level being treated at that time.
Pitfalls
• Forgetting to create superficial skin markings delineating the midline and the bilateral medial pedicular
borders can lead to intraoperative confusion. These markings are used intraoperatively for orientation
of the distal end of working instruments during the case.
• Advancing the local anesthetic needle or the trocar or any instrument in the AP fluoroscopic view is
dangerous. Advancement in this view does not allow one to adequately visualize depth. All
advancements should proceed in the contralateral oblique view.
• Advancement of an instrument beyond the epidurogram poses the risk of a serious complication
including nerve injury and dural puncture. The procedure as described maintains all instrumentation
posterior to the epidurogram. When performed as recommended, this is the safest decompression
procedure currently available.
SUGGESTED READING
Abbas J, Hamoud K, Masharawi YM, May H, Hay O, Medlej B, Peled N, Hershkovitz I. Ligamentum
flavum thickness in normal and stenotic lumbar spines. Spine. 2010;35(12):1225-1230.
Basu S. mild ® procedure: single-site experience with prospective IRB approved clinical outcomes
research. Clin J Pain. 2011.
Castro-Menéndez M, Bravo-Ricoy JA, Casal-Moro R, Hernández-Blanco M, Jorge-Barreiro FJ. Midterm
outcome after microendoscopic decompressive laminotomy for lumbar spinal stenosis: 4-year
prospective study. Neurosurgery. 2009;65:100-110.
Chopko B. A novel method for treatment of lumbar spinal stenosis in high-risk surgical candidates: pilot
study experience with percutaneous remodeling of ligamentum flavum and lamina. J Neurosurg Spine.
2011 Jan;14:46-50.
Chopko B, Caraway D. MiDAS I (mild ® Decompression Alternative to Open Surgery): a preliminary
report of a prospective, multi-center clinical study. Pain Physician. 2010;13:369-378. ISSN 1533-
3159.
Deer T, Kapural L. New image-guided ultra-minimally invasive lumbar decompression method: the mild
® procedure. Pain Physician. 2010;13:35-41. ISSN 1533-3159.
Deer T, Mekhail N, Lopez G, Amirdelfan K. The evolving use of minimally invasive surgery for the
treatment of pain—minimally invasive lumbar decompression for spinal stenosis. J Neurosurg Spine.
2011.
Lingreen R, Grider J. Retrospective review of patient self-reported improvement and post-procedure
findings for mild ® (Minimally Invasive Lumbar Decompression). Pain Physician. 2010;13:555-560.
ISSN 1533-3159.
Mekhail N, Benyamin R. Long-term results of percutaneous lumbar decompression mild ® for spinal
stenosis. Pain Practice. 2011 Jun 16. Online ISSN 1533-2500.
Sairyo K, Biyani A, Goel V, et al. Pathomechanism of ligamentum flavum hypertrophy: a multidisciplinary
investigation based on clinical, biomechanical, histologic, and biologic assessments. Spine.
2005;30:2649-2656.
Schomer D, Solsberg D, Wong, Chopko B. mild ® lumbar decompression for the treatment of lumbar
spinal stenosis. Neuroradiol J. 2011 Aug15.
Weinstein JN, Tosteson TD, Lurie JD, et al. Surgical versus nonsurgical therapy for lumbar spinal
stenosis. N Engl J Med. 2008;358:794-810.
CHAPTER 39
Vertebral Augmentation
Ramsin Benyamin, Ricardo Vallejo, Atiq Rehman, and Allen Burton
INTRODUCTION
The aging population gives us cause for great concern especially in those suffering from osteoporosis.
Rates are climbing, especially in women. Osteoporosis has reached epidemic proportions and is a major
public health issue for an estimated 44 million Americans and 200 million people world wide. According
to the 2005 annual report of The National Osteoporosis Foundation, 1 in every 2 women and 1 in every 4
men aged 50 and older suffered from osteoporosis-related fracture. Vertebral compression fractures
(VCFs) constitute the most frequent complication of osteoporosis, with nearly half of all of the 2 million
bone fractures caused by osteoporosis. The estimated medical cost in 2005 was over $16.9 billion. The
prevalence of VCFs increases with age, reaching 40% in women over 80 years of age. Women with
clinically diagnosed VCFs have a 15% higher mortality rate and are 2 to 3 times more likely to die of
pulmonary causes. Over 50% of people with 1 or 2 VCFs, require self-care assistance, which is
significantly higher compared to 8% of osteoarthritis patients suffering from low back pain. It is
noteworthy that each VCF increases the chance of another VCF by 19.2% within the same year. Two
VCFs increase the probability of a third fracture by 24% within a year.
• The severe pain caused by VCFs is exacerbated by movement and weight-bearing activity and is linked
to significant morbidities and impaired quality of life, the majority of which is caused by pain and
immobility, which can lead to:
Chronic pain which is often accompanied by depression and/or anxiety.
Reduced FVC by 9% leading to an increased risk of atelectasis and pneumonia.
Worsening of osteoporosis. Bone mineral density is reduced at a rate of 2% per week.
1% to 3% muscle wasting per day.
Decubitus ulcers.
Higher risk of developing deep vein thrombosis and subsequent pulmonary embolism, which may be
fatal.
• Opioid medications that are prescribed for the treatment of pain can often cause loss of appetite,
nausea, constipation, changes in mental status, ie, confusion and are associated with an increased risk
of dependence and addiction.
• The morbidity and mortality associated with osteoporotic vertebral fractures demand the need for more
aggressive treatment. Vertebral augmentation techniques have been used as a viable treatment option
providing the possibility for rapid pain relief and improved mobility. Percutaneous vertebroplasty has
been considered a developing standard of care for VCFs.
• Vertebral compression fractures may also be secondary to tumor infiltration. The most frequent
malignant lesions of the spine include osteolytic metastasis and myeloma. Current cancer therapy
prolongs life expectancy, although the increasing risk for these patients to develop metastatic vertebral
involvement and collapse persists.
• Galliber, Deramond, and colleagues performed the first case of percutaneous vertebroplasty in France
in 1984. It was not until 1993 that Jensen and colleagues at the University of Virginia performed the
first vertebroplasty in the United States.
• Vertebroplasty has gained widespread popularity, mostly because of significantly high rates of success,
low incidence of complications or adverse events, brief surgical time and recovery period, limited
sedation, and short to no hospital stay.
• Kyphoplasty was introduced in 2000, as the first vertebral augmentation technique, with proposed
advantage of restoring fracture height and reducing kyphosis.
• Vertebroplasty involves the use of acrylic bone cement to stabilize and treat painful VCFs.
• Vertebral augmentation techniques (ie, kyphoplasty) initially create a cavity in the vertebral body and
then the cavity is filled with bone cement material. In the case of kyphoplasty, cavity creation is
facilitated by an inflatable bone tamp.
• The mechanism by which cement injection attenuates pain remains unclear. Theories include thermal
necrosis, chemotoxicity of the interosseous pain receptors, mechanical stabilization, and neurotoxicity
mediated by the cement monomer.9,10
• The main goal of treatment should be pain relief and resumption of mobility.
This is contrary to “conventional conservative treatment,” which prescribes bed rest and the
administration of pain medications, usually from the opioid family of prescription drugs.
In an effort to reduce the risk of leakage from liquid bone cement, multiple new products including
high viscosity cement and Cortoss have been introduced. The main advantages are higher viscosity
resulting in less liquidity, lower exothermic temperatures that will not cause tissue necrosis, no
monomer release, stiffness, and mechanical strength that is similar to bone and, lower adjacent
level fracture.
INDICATIONS
• Vertebral augmentation and vertebroplasty are indicated for the treatment of painful vertebral
compression fractures (VCFs) that are acute or subacute (as evidenced by T2-weighted MRI) resulting
from osteoporosis, trauma, and tumor infiltration.
Preferably the facture should have less than 50% height loss.
Measurement of the height and comparative calculations should be made with a radiograph
performed in supine position during inspiration because weight bearing and exhalation may
exaggerate bone collapse.
RELEVANT ANATOMY
• VCFs typically occur at the anterior third of the vertebral body where trabecular bone is less
prominent.
VCFs alter the biomechanics of the spine, making adjacent vertebral bodies more vulnerable to
fracture.
It should be noted that above the level of T8, the relationship between the vertebral body and the
pedicle is different than the rest of the thoracic spine. The pedicles are almost perpendicular to the
vertebral body and if a practitioner tries to reach the vertebral body through the pedicle in an
oblique view, they will probably end up directly in the spinal canal. Hence, a parapedicular
approach is recommended above T8 level.

• Osteoporotic VCFs are associated with significant morbidities and impaired quality of life, the
majority of which is caused by pain and immobility.
Standard contraindications are as follows:
Presence of pain with radicular symptoms that do not correspond to the area of the fracture
More than 20% retropulsion of vertebral body fragment as evidenced by computed axial
tomography (CT) or MRI
Active localized or systemic infection
Known allergy to PMMA (polymethylmethacrylate)
Uncorrected coagulopathy
Painless compression fracture
Complete vertebral collapse
Epidural tumor
Patient unable or unwilling to give informed consent
• The main indication for the procedure is painful compression fracture. In other words, pain needs to be
consistent with imaging findings.
In order to establish the correct diagnosis clinically one may also perform examination under
fluoroscopy, which is also equally important for assessing the feasibility of safe needle placement
and performing a successful procedure (Figure 39-1).
Figure 39-1. A diagrammatic sketch showing the commonly used routes of spinal needle entry into the
vertebral body during the percutaneous vertebroplasty procedure. Due to the broad-based pedicles, (A) a
transpedicular approach is often used in the lumbar territory. (B) The costopedicular or (C) paravertebral
approaches are usually employed in the thoracic region as the pedicles possess a narrow needle entry
point. These alternative approaches are also used in situations where there is significant tumor destruction
of the pedicles.
If the patient is too osteoporotic and bony landmarks are not clearly identifiable to safely see the
pathway for proper needle placement, the procedure should be performed under CT guidance.
Utilize CT guidance for factures T6 and above.
For additional safety, injection of cement needs to be performed under real-time imaging. Usually
this is not feasible with standard CT scanners; therefore, we advocate use of fluoroscopy in
conjunction with CT scan (Figure 39-2A, B).
Figure 39-2. (A, B) C-arm fluoroscopy is placed in lateral view to monitor real-time imaging 1B while
injecting bone cement, following placement of needles under CT-guidance.
IMAGING
• X-rays are usually the first step in radiologic diagnosis of vertebral compression fractures, but the age
and extent of VCF can be confirmed with MRI.
STIR images and T2-weighted fat suppression images have the highest diagnostic value.
In case of contraindication for MRI (ie, pacemakers, spinal cord stimulators, etc) a CT or bone scan
may provide relevant information. A CT scan will also be valuable in diagnosing the presence and
severity of retropulsed bone fragments and, mapping the needle approach for the procedure.
Although not considered an absolute contraindication, the presence of retropulsion will require
extra vigilance to avoid acute spinal canal stenosis caused by further retropulsion of the fragment
dorsally and or leakage of cement (Figure 39-3A-C).
Figure 39-3. (A, B) Two-dimensional fluoroscopy in AP and lateral view. (C) Ideal view is an axial
view that could be obtained with CT scan.
TECHNIQUE
• Vertebroplasty involves the use of acrylic bone cement to stabilize and treat painful vertebral
compression fractures.
• Vertebral augmentation (ie, kyphoplasty) utilizes a bone tamp: an inflatable balloon inserted into the
vertebral body and inflated to create a cavity for the bone cement.
• Both procedures are performed under sterile conditions, local anesthesia and IV sedation or monitored
anesthesia care (MAC).
Prophylactic antibiotics like cefazolin 1 g IV (or clindamycin 600 mg IV in case of allergy) are
administered 30 minutes prior to skin penetration.
Appropriate padding during positioning is essential to avoid new osteoporotic fractures in areas
like the ribs. If possible, it is advocated to ask the patients to position themselves to avoid any
unrecognized pressure points.
• Most of the time, a minimal dose of IV anesthetic is used at the time of local anesthetic injection for
skin and subcutaneous tissue. This allows for a continuous and meaningful interaction with the patient
during the procedure. If the periosteum is well anesthetized, the patient will tolerate the procedure and
further sedation is not needed.
• Vertebroplasty is most commonly performed by using a transpedicular approach but due to anatomical
differences above T8 level, a parapedicular approach is advocated.
The target point for needle is the junction of anterior and middle third of the vertebral body.
There still remains controversy over the advantage of using unipedicular (one needle) versus
bipedicular approach and some recommend the bipedicular approach for the novice practitioners.
TRANSPEDICULAR VERSUS PARAPEDICULAR APPROACH

• Following site preparation and sterile draping, the fluoroscope is rotated to the oblique view until the
pedicles of the VBFs are in a “Scottie dog” view (Figure 39-4). Then, the C-arm is tilted (rostral-
caudal rotation) until the pedicle (the eye of the Scottie dog) (Figure 39-5) is in the upper half of the
vertebral body.
Figure 39-4. Initial “Scottie dog” view of vertebral body.
Figure 39-5. Oblique view of the vertebroplasty needle in the pedicle.
• Skin and subcutaneous tissues are anesthetized with lidocaine 1% to 2%, using a 25-guage, 1.5-in
needle, which can reach the periosteum most of the time. If it does not, the direction of the needle needs
to be reevaluated.
• Multidirectional fluoroscopic guidance may help to expedite the procedure if it is available. One C-
arm is placed in lateral position, while the other is switched between anterior-posterior (AP) and
oblique views.
• Under fluoroscopic guidance at the level of the pedicle (oblique view), an 11-gauge vertebroplasty
needle for the lumbar vertebrae, or a 13-gauge needle for thoracic vertebrae, is inserted in the tunnel
view directed to the “eye” of the Scottie dog, which will be the upper outer half of the face of the
pedicle (Figure 39-6).
Figure 39-6. AP view of the vertebroplasty needle in the pedicle.
• Once the needle is stable in the pedicle (Figure 39-7) the C-arm is rotated to lateral view to make sure
that the needle follows the axis of the pedicle (Figure 39-8A-D). If one follows proper angulations, the
tip of the needle will reach the target point at the junction of the anterior and middle third of the
vertebral body.
Figure 39-7. Lateral view of the vertebroplasty needle in the pedicle.
Figure 39-8. (A) Lateral view of the vertebroplasty needle in the final position. (B, C) Final needle
placement using transpedicular approach. (D) Basivertebral venous complex. Note the intricate
latticework of the vertebral vasculature; this venous complex must be avoided when injecting cement.
It is advantageous to have a good view of the intervertebral foramen and to confirm that the needle
is angled away from it.
• Advancement of the needle is best achieved by holding and stabilizing the needle with one hand and
using a mallet with the other. This will ensure safe and controlled advancement of the needle. Then,
gradually advance the needle through the pedicle into the vertebral body.
• To avoid the risk of spinal injury, it is imperative to avoid the needle violating the medial border of the
pedicle (in AP view), while the needle is in the pedicle (in lateral view). Once the pedicle has been
passed, the C-arm should be placed in lateral view and the needle slowly advanced until it reaches the
junction of the anterior third and the middle third of the vertebral body (Figure 39-8b,c).
There is still controversy over the advantage of using the unipedicular (one needle) versus
bipedicular approach (Figures 39-9 and 39-10). In our practice, if the initial needle is located
close to the midline, we do not place a second one.
Figure 39-9. AP view of the bipedicular approach.
Figure 39-10. Lateral view of the bipedicular approach.
• Once the needle is correctly placed, the cement is prepared according to manufacturer’s
recommendations. The cement is allowed to reach the consistency of a thin paste (eg, like that of
toothpaste) before deemed suitable for injecting. Then, the stylet is removed from the needle and the
cement is slowly injected under continuous (real-time) fluoroscopic imaging (Figures 39-11 and 39-
12).
Figure 39-11. Final AP view of vertebroplasty.
Figure 39-12. Final lateral view of invertebroplasty.
• Safe deposit area (Blue)—target area of cement deposit in anterior two-third of vertebrae
• Danger zone (Red)—posterior area to be avoided (Figure 39-13)
Figure 39-13. Blue area is the area for cement injection, the red area should be avoided.
Total amount to be injected varies according to the area.

In the lumbar region, a total of 3 to 6 mL is usually enough, while 2 to 3 mL is sufficient in the
thoracic area.
If there is any sign of cement extrusion or if it moves toward the intervertebral foramen, the
injection should immediately stop.
If a decision is made to place the second needle on the opposite side, it should be done before
mixing the cement.
• In our practice, total fluoroscopy time, using pulse mode, may range between 30 and 60 seconds per
level treated. The patient may be discharged from recovery once the usual discharge criteria are met.
PARAPEDICULAR APPROACH
• Above the T8 level, the relationship between the vertebral body and the pedicle is different in the
thoracic spine. At this level, the pedicle is almost perpendicular to the vertebral body. If one tries to
reach the vertebral body through the pedicle in an oblique view (Scottie dog), one will end up directly
in the spinal canal. Therefore, a parapedicular approach is recommended above this level.
The lateral aspect of the pedicle is identified and marked with the patient in prone position, and the
C-arm in AP view.
Skin and subcutaneous tissues are anesthetized, using a 25-gauge 3.5-in spinal needle. The
advantage of such a long needle is that it will be able to reach the vertebral body and anesthetize
the periosteum.
After local anesthesia has been applied; the 13-gauge vertebroplasty needle is inserted, following
the trajectory used with the spinal needle. In an AP view, the C-arm is rotated to lateral, and the
needle is advanced in a plane parallel to the pedicle, with the needle aiming to the point
immediately below the junction of the pedicle and the vertebral body, after the needle has
transfixed the skin. Then, the C-arm is continuously rotated between AP and lateral views.
In the AP view, one should make sure that the needle is kept lateral to the middle aspect of the
pedicle until bone has been contacted.
A mallet may be used to facilitate the vertebroplasty needle’s passing through the periosteum.
A second needle in the contralateral side is recommended because the needle placement is more
difficult with this approach.
The steps for cement injection should be followed as with the transpedicular approach, with special
attention to cement extrusion.
• The entry point in AP view is lateral and superior to transverse process. Once needle is engaged in
bone, need to check in lateral view to confirm correct trajectory (Figure 39-14A-C).
Figure 39-14. (A-C) The entry point in AP view is lateral and superior to transverse process. Once
needle is engaged in bone, need to check in lateral view to confirm correct trajectory.
VERTEBRAL AUGMENTATION (IE, KYPHOPLASTY)

PROCEDURE
• Kyphoplasty is similar to vertebroplasty in terms of draping, imaging, view, and use of anesthetics.
• The additional steps made for the kyphoplasty procedure are:
The needle is replaced with a cannula and introducer system over a guide pin.
The introducer fits inside, and extends beyond the cannula.
The beveled tip allows the introducer to be inserted into the vertebral body using a mallet.
The introducer is then advanced to the posterior aspect of the vertebral body (Figure 39-14A-C).
Leaving the cannula in place, the introducer is exchanged for a hand-operated drill. The drill is
carefully advanced to the anterior aspect of the vertebral body, 3 to 4 mm posterior to the anterior
cortical margin (Figure 39-15).
Figure 39-15. Cannula of the kyphoplasty system positioned in posterior third of vertebral body with drill
advanced to the anterior third to create a working channel for the introduction of the kyphoplasty balloon.
A near-midline position of the needle tip on the AP view is optimal.

The drill is removed and the deflated balloon is inserted into the small cavity (Figure 39-16).
Figure 39-16. Deflated balloon inserted through the cannula and advanced until the proximal mark if
visualized out of the cannula. Fluoroscopic guidance helps to determine that the distal aspect of the
balloon is in the anterior one-third of the vertebral body.
Then a second introducer is placed from the contralateral side in a similar manner.
Each balloon is configured with a locking syringe with digital manometer and is slowly inflated
with iodinated contrast using pressures of 160 to 400 psi.
The inflation is monitored both with the pressure transducer and intermittent fluoroscopy.
Inflation continues slowly until 1 of the following 3 conditions is met (Figure 39-17):
Figure 39-17. Kyphoplasty balloons inflated within the vertebral body.
1. The system reaches maximum pressure or maximum balloon volume.

2. The balloon tamp reaches one of the cortical margins.
3. The kyphotic deformity
is corrected.
The balloon is then deflated and removed.
• Cement placement in kyphoplasty
Sufficient time is allowed for the PMMA cement to reach a doughy toothpaste-like consistency.
The delivery system is connected to the cannula and the cement is slowly injected under real-time
fluoroscopic guidance.
The cement fills the cavity from anterior to posterior, matching or slightly exceeding the volume of
the cavity created by the inflated balloon.
The delivery system is then removed and manual compression is used to achieve hemostasis.
The practitioner should be aware and cautious that poor visualization of osseous structures on
fluoroscopy increases the risk of improper needle placement and cement leakage but can be
overcome with the use of CT scanner (Figures 39-18 and 39-19).33
Figure 39-18. Intravertebral cement extravasation—AP view (most likely due to medial needle
placement violating pedicle).
Figure 39-19. Lateral view of same patient.
• To achieve homeostasis, manual pressure is applied to the skin after the needles are removed.
• Bacteriostatic cream and bandages are used to cover the puncture sites.
• Patients are logrolled with extreme care from the operating table to the stretcher to avoid new
fractures.
• Vital signs, and especially neurological monitoring, should be evaluated frequently during patient’s
stay.
• Patients may start ambulation after complete recovery that may take about 1 hour.
• Patients are discharged home after ambulating, and are instructed to contact an emergency 24-hour
service in case of developing signs of possible complications.

• The majority of complications are mild, transient, and self-limited.
• Potential complications include hemorrhage; infection; spinal stenosis; death; pulmonary emboli; local
trauma to nerve roots, spinal cord, or kidney; and fracture of the lamina, pedicle, or ribs.
• Transient radiculopathy has been reported in 3% to 6% of patients and has been successfully treated in
the majority of cases with steroids and anti-inflammatory medications.14
• In the early years of performing vertebroplasty, a higher incidence of cement extrusion (30%-80%)
was noted, probably related to the low viscosity of cement (used in the initial studies) and the high
pressure required to inject cement into the cancellous matrix of the vertebral body.15,16
• Using higher viscosity filling/stabilizing materials may reduce this risk.
• There are many routes by which cement may leak from a vertebra: paravertebral leakage, venous
leakage, or leakage into the spinal canal and intervertebral foramen.17,18 Dispersing of the cement in the
bony structures shows nonuniform margins. Therefore, noticing cement with smooth and uniform
margins should raise the suspicion of cement extrusion into the paravertebral muscles. This can cause
severe localized pain due to the exothermic reaction during polymethylmethacrylate cement curing and
the effect of the mass of cement on muscle motion.
• Leakage of cement into the venous circulation can produce generalized toxic reactions and, when
entering the inferior vena cava, possibly life-threatening pulmonary embolization.19-24 Leakage of
cement into the epidural space may compress the spinal cord and/or nerve roots.25-29 The incidence of
this complication is low (1%-2% of the cases), and it is usually self-limiting.
• A postoperative CT scan is recommended if the physician suspects cement extrusion. If one is
suspecting this complication, we suggest a short course of oral steroids, anti-inflammatory
medications, or an epidural steroid injection. Only in extreme cases, a decompressive laminotomy or
foraminotomy may be required.
Intradiscal cement extrusion is seen in 5% to 10% of the cases.
The concern of increased risk of adjacent fractures is currently unsubstantiated but the risk was
shown to be reduced by using Cortoss®.
Rib fractures during these procedures have been previously reported and are related to the
positioning of the patient.
• The AP view of the intravertebral cement extravasation can be seen in Figure 39-18. (Most likely due
to medial needle placement violating pedicle.)
• The lateral view of the same patient can be seen in Figure 39-19. Note: Cement extravasation in thecal
sac.
Posterior Leakage
• More complications arising from the needle placement being too medial causing cement being
deposited in the posterior versus the anterior of the vertebral body (see Figure 39-20A-C).
Figure 39-20. (A-D) Complications from cement deposited in posterior vertebral body.
• Note the intradural leakage from taking a needle position too medial (Figure 39-20D).
Massive Pulmonary Embolism

• Insufficient polymerization of the injected cement, most likely due to an unbalanced monomer-to-
powder ratio.
• Aortic embolism (Figure 39-21)
Figure 39-21. Aortic embolism.
• Right laterovertebral artery

• 3 images of 3 different complications:
L4 radiculopathy where nerve root is severed at the dorsal horn (Figure 39-22)
Figure 39-22. Nerve root severed at the dorsal horn.
Pedicle fracture (Figure 39-23)

Figure 39-23. Pedicle fracture.
Cement deposited in the spinal canal and none in the vertebral body
• PMMA embolization and PMMA embolism into the lungs
• PMMA embolization in cerebral circulation after vertebroplasty in a patient with patent foramen ovale
CLINICAL PEARLS
• Vertebroplasty and vertebral augmentation techniques like balloon kyphoplasty are minimally invasive
vertebral augmentation procedures involving injection of polymethyl methacrylate cement (or other
bioactive material) under radiologic control into a fractured vertebral body. They strengthen the bone
and improve the intense pain caused by fracture secondary to osteoporosis, metastasis, or trauma and
refractory to conservative therapies such as analgesic use, bed rest, and bracing.30
• Although the main indication for percutaneous vertebroplasty and vertebral augmentation technique is
painful vertebral compression fracture, osteoporotic patients may also suffer from other sources of
spine pain like spinal stenosis, disc degeneration and facet arthropathy that need to be treated
separately.
• The cause and source of every compression fracture needs to be evaluated. In patients with known
history of cancer and those with no previous history of osteoporosis, it is prudent to perform bone
biopsy prior to injecting cement into the fracture.
• Both percutaneous vertebroplasty and vertebral augmentation techniques offer therapeutic benefit,
significantly reducing pain and improving mobility in patients with vertebral fracture without
significant differences in terms of outcomes.
• Both percutaneous vertebroplasty and vertebral augmentation techniques rely on imaging devices like
C-arm fluoroscopy and CT scan for safe placement of needle and injection of stabilizing material.
Injection of cement has to be performed under real-time imaging, in order to avoid detrimental cement
leakage.
• Best suited physicians for performing these procedures are interventional pain or spine physicians with
advanced knowledge of anatomy and experience in performing percutaneous image-guided
procedures.31
• The most crucial part of procedure is correct and safe placement of needle and then, injection of
stabilizing material in the target zone. Fluoroscopy has definite shortcomings: needle placed in blind
spots (as depicted in red triangles) will be viewed (in both AP and lateral) as it is placed in the
vertebral body (Figure 39-24).
Figure 39-24. Needle guide for vertebral augmentation.
• It is of utmost importance to advance the needle while checking AP and lateral view frequently to
avoid deviation of needle too medially or too laterally. As long as the needle has not passed the
pedicle into vertebral body on the lateral view, in the AP view it should not violate the medial
pedicular (facet) line. The AP and lateral views below depict the correct placement of needle in
pedicle, prior to entering the vertebral body (Figure 39-25A, B).
Figure 39-25. (A, B) AP and lateral views for correct needle placement.
• Deviation of needle medially (toward spinal canal) will have more serious consequences and should
be avoided by judicious use of imaging. The following diagrams show the needle trajectories that are
off the safe pathway (Figure 39-26A, B).32
Figure 39-26. (A, B) Unsafe needle trajectories.
ACKNOWLEDGEMENT
The authors wish to thank Daniel E. Dolen for his assistance in preparing this manuscript and for
providing his artistic skill for our anatomical drawings for this chapter.
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CHAPTER 40
Epidural Lysis of Adhesions

Rinoo V. Shah
INTRODUCTION
Epidural lysis of adhesions refers to a percutaneous spinal procedure for pain relief (Racz procedure).
Pain may occur due to epidural inflammation, nerve root compression, venous engorgement, and scar
tissue. Under contrast-enhanced fluoroscopy, a steerable radiopaque catheter is used to deliver several
drugs to the target “pain generator”; these include local anesthetics, hyaluronidase, hypertonic saline, and
steroids. Contrast epidurography identifies correct placement and permits early detection of
subarachnoid, subdural, or intravascular placement. Local anesthetics reduce intraoperative and
postprocedural pain. An enzymatic agent (hyaluronidase) or mechanical motions (moving the catheter
back and forth) are used to “loosen” peridural scar tissue. Hypertonic saline (10%) is used to reduce
intraneural edema. Steroids modulate inflammation. This procedure was initially developed for patients
with symptomatic epidural scarring, ie, post-laminectomy syndrome. Published studies report safe and
efficacious outcomes following epidural lysis of adhesions for several spinal pain etiologies: failed back
surgery syndrome, post-laminectomy syndrome, spinal stenosis, lumbar radiculopathy, and cervicalgia.
INDICATIONS
• Back/neck pain and sciatica (with or without surgery)
• Chronic low back pain
• Radiculopathy (mono- or polysegmental)
• Failed back surgery syndrome
• Lumbar spinal stenosis
• Post-laminectomy syndrome
• Spinal stenosis
• Neurogenic claudication
• Degenerative disc disease
• Herniated/prolapsed intervertebral disc
• Epidural scarring
• Sympathetically independent pain
RELEVANT ANATOMY
• The epidural space is a potential space that surrounds the dural sac and is contained within the bony
spinal canal.
• Ventrally, the epidural space is bounded by the vertebral body, intervertebral disc, and longitudinal
ligament.
• Dorsally, the epidural space is bounded by the ligamentum flavum, lamina, and spinous processes.
• Laterally, the epidural space is bounded by the pedicles, facet joints, articular processes, and
“foramina.”
• The bony spinal canal is contiguous from the foramen magnum to the sacral hiatus.
• Epidural needle access should be attempted at the sacral hiatus, interlaminar space, and only rarely, at
the intervertebral foramen.
• The sacral hiatus is dorsally covered by the sacrococcygeal ligament and is laterally bounded by the
sacral cornua. In thin patients, the hiatus is palpable.
• For the cervical, thoracic, and lumbar levels, a paramedian approach to the interlaminar space is
advised.
• The interlaminar window may be optimally visualized when utilizing cephalocaudal angulation, during
fluoroscopy.
• Optimal patient positioning helps with access.
• The lumbar lordosis should be reduced; the cervical or thoracic kyphosis should be accentuated. This
“opens up” the interlaminar space and facilitates needle entry.
Patient selection and choice of this technique depend on an individualized risk/benefit analysis and a
review of prior therapies. For instance, epidural lysis of adhesions may be the index procedure in a
patient with failed back surgery syndrome. On the other hand, this procedure may be used late in the
treatment algorithm for patients with spinal stenosis.
Contraindications (relative or absolute) and indications for procedure termination include:
• Coagulopathy
• Progressive neurological deficit
• Allergy to procedural drugs, eg, iodinated contrast
• Open wound or skin ulceration
• Poorly controlled diabetes
• Patient refusal or lack of health care proxy
• Inability to lie prone or on the side, for the duration of the procedure
• Intraoperative recognition of subarachnoid, subdural, or vascular uptake
• Severe pain during injection
• Hypotension
PREOPERATIVE PREPARATION
• Patients should have constant pain >6/10 and functional limitations.
• Withhold coagulopathic medications for appropriate lengths of time as per protocol.
• Diabetic patients may need blood sugar testing.
• Female patients of childbearing age should have an AM urine pregnancy test or a serum pregnancy test.
• Airway, cardiopulmonary, and neurological assessment is required as per protocol.
• Intravenous access is advised, particularly for patients receiving cervical or thoracic procedures.
• These are mandatory for patients receiving intravenous anxiolytics and analgesics.
• Cardiopulmonary safe guards, such as resuscitation equipment, should be present within the procedure
suite.
• Patients should sign witnessed informed consent, which includes an evidenced based discussion about
indications, efficacy, and safety.
• Preprocedure site marking/initialing with an indelible marker site and site verification is utilized in
most US-based hospitals. This reduces the risk of wrong site or wrong location surgery.
PATIENT POSITIONING
Prone or lateral decubitus
• Tip: accentuate cervical/thoracic kyphosis and reduce lumbar lordosis, by using properly placed
pillows.
FLUOROSCOPIC VIEWS
• Anterior-posterior (AP) image of the spine (cervical, thoracic, and lumbar), sacrum, or coccyx
Localize level
Identify midline
• Cephalocaudal angulation
“Opens up” interlaminar window
• Lateral
Guides depth
Best view to identify sacral hiatus

• Intravenous sedation: fentanyl, meperidine, midazolam
Patient should be able to communicate
Real time sensory and motor monitoring
• Prone position
Pillow under abdomen to flatten back
Pillow under the chest to accentuate cervical kyphosis
• Noninvasive monitoring: pulse oximetry, electrocardiography sensors, blood pressure
• Sterile prep and drape; extended drape over feet
Legs abducted and toes pointing inward (pigeon toes) for caudal approach
Arms to the side or swimmer’s position for cervical approach (optimize lateral view)
• Fluoroscopy
Palpate and identify sacral hiatus or spinous process (especially for cervical access)
Confirm with fluoroscopy
• Sacral hiatus access
Local anesthetic skin wheal (1%-2% lidocaine)
1 to 2 cm below sacral hiatus
18-gauge venipuncture needle to puncture skin
Introducer needle (angiocatheter, RX Coude needle)
Advance under lateral fluoroscopy
• Interspinous access (cervical-thoracic-lumbar)
Palpate and identify C7, T1, T2 spinous processes
Local anesthetic skin wheal 3 to 4 cm below level
Tip: use intermittent lateral (depth), posteroanterior (direction), and lateral (depth) views
Tip: advance epidural access needle to base of spinous process (spinolaminar line)
Tip: shallow angle of entry, 30 degrees
• Rotate C-arm to posteroanterior view
Tip: at sacral hiatus, do not advance needle past S3-4 foramen
• Remove stylet and replace with pulsator syringe
Loss of resistance
Tip: flat or shallow needle entry into epidural space is optimal
• Confirm negative aspiration of blood, cerebrospinal fluid
• Real-time fluoroscopic contrast instillation (iohexol, iopamidol)
Nonionic, iodinated dye
Limited literature on gadolinium or gadopentetate in iodine allergies
• 1 mL to evaluate for vascular uptake, subarachnoid (myelographic), or subdural spread
Subarachnoid—enter at different level or abandon procedure
subdural injection—consider repositioning
Muscular spread (short segmental muscles)—contrast dorsal to spinous process—advance further
Dorsal coccygeal spread—reposition needle to enter sacral hiatus
• 5 to 9 mL to identify epidurogram—“Christmas tree” pattern
Tip: this step may be optional
Lysis of adhesions was developed in a period predating MRIs, hence the need for identifying
epidural filling defects
Tip: in my practice, I inject 1 to 2 mL to confirm epidural placement at this stage
• Radiopaque catheter introduction (Tunl-XL or Brevi-XL catheter)
Directional steering can be carried out by rotating needle or “aiming” needle
Catheter will then pass in the direction of the needle
Alternatively, the catheter may be bent 15 degrees about 2 cm proximal to the tip
Tip: an early trajectory is the best approach, since distal manipulation is harder
Tip: at cervical, thoracic, or lumbar levels, the catheter can be passed ipsilaterally or
contralaterally to the target site
Tip: the catheter may have to be pulled back into the needle
Tip: needle orientation should be the same when pulling back the catheter, as when pushing it out (to
reduce risk of shearing)
• Steered under fluoroscopy to ventrolateral epidural space
Catheter resistance may be encountered due to adhesions, disc bulging, stenosis, epidural fat,
hardware
Mechanical catheter manipulation may be necessary to place catheter effectively
• Contrast (water soluble, nonionic) is instilled via the catheter to confirm epidurogram or “neurogram”
Injection resistance may be present due to the high viscosity of contrast
Tip: verify that the catheter is not kinked
Contact with nerve may elicit dysesthesias along arm, chest well, or leg
Check for absence of vascular, subarachnoid, and subdural spread
• Epidural filling defect may or may not be present
• Medication delivery
Local anesthetic (5-10 mL)
Lidocaine 1%
Ropivacaine 0.25%
Bupivacaine or levobupivacaine 0.25%
Steroids
Betamethasone (6 mg)
Dexamethasone (4 mg)
Triamcinolone (40 mg)
Methylprednisolone (40 mg)
Hyaluronidase 900 to 1500 units (dose depends on spinal level)
Cervical (900 units)
Thoracic (1200 units)
Lumbosacral (1500 units)
10% preservative free hypertonic saline (3-10 mL may be used)
Slow delivery or slow infusion
3 mL increments over 10 to 15 minutes (no neurological changes prior to instillation)
If spasms are present, consider reinstillation of lidocaine 1%
• Remove needles
• Bandage
• Dressing applied
• Neurologic examination should not change
• Pain may be exacerbated
• Monitoring of potential complications
• Temperature, heart rate, respiratory rate, blood pressure, neurologic examination, orientation status,
pain relief, self-ambulation, and voiding should be noted prior to discharge. Sedation may require
monitoring for 1 hour. Patients are not allowed to drive for up to 24 hours

• Liberal use of lateral and posteroanterior views are needed
• Use a 2-handed technique for obtaining loss of resistance
One hand on the pulsator syringe
The other hand is on the patient’s skin and slowly advancing the needle (if the patient suddenly
moves backward, the second hand can stabilize the needle)
• Proper patient positioning is imperative, particularly in obese and osteoporotic patients
Use pillows to facilitate access
OUTCOMES
Several large clinical trials have attested to the safety and efficacy of epidural lysis of adhesions.
Suggested Reading
Anderson SR, Racz GB, Heavner J. Evolution of epidural lysis of adhesions. Pain Physician. 2000
Jul;3(3):262-270.
Kobayashi S, Takeno K, Yayama T, et al. Pathomechanisms of sciatica in lumbar disc herniation: effect of
periradicular adhesive tissue on electrophysiological values by an intraoperative straight leg raising
test. Spine (Phila Pa 1976). 2010 Oct 15;35(22):2004-2014.
Manchikanti L, Cash KA, McManus CD, Pampati V, Singh V, Benyamin R. The preliminary results of a
comparative effectiveness evaluation of adhesiolysis and caudal epidural injections in managing
chronic low back pain secondary to spinal stenosis: a randomized, equivalence controlled trial. Pain
Physician. 2009 Nov-Dec;12(6):E341-E354.
Manchikanti L, Pampati V, Cash KA. Protocol for evaluation of the comparative effectiveness of
percutaneous adhesiolysis and caudal epidural steroid injections in low back and/or lower extremity
pain without post surgery syndrome or spinal stenosis. Pain Physician. 2010 Mar-Apr;13(2):E91-
E110.
Manchikanti L, Singh V, Cash KA, Pampati V, Datta S. A comparative effectiveness evaluation of
percutaneous adhesiolysis and epidural steroid injections in managing lumbar post surgery syndrome:
a randomized, equivalence controlled trial. Pain Physician. 2009 Nov-Dec;12(6): E355-E368.
Raj PP, Shah RV, Kaye AD, Denaro S, Hoover JM. Bleeding risk in interventional pain practice:
Shah RV, Ericksen JJ, Lacerte M. Interventions in chronic pain management. 2. New frontiers: invasive
nonsurgical interventions. Arch Phys Med Rehabil. 2003 Mar;84(3 suppl 1): S39-S44. Review.
Shah RV, Kaye AD. Bleeding risk and interventional pain management. Curr Opin Anaesthesiol. 2008
Aug;21(4): 433-438. Review.
Trescot AM, Chopra P, Abdi S, Datta S, Schultz DM. Systematic review of effectiveness and
complications of adhesiolysis in the management of chronic spinal pain: an update. Pain Physician.
2007 Jan;10(1):129-146.
CHAPTER 41
Vascular Complications of Spinal Interventions

Scott E. Glaser, Rinoo V. Shah, and Peter S. Staats
INTRODUCTION
Minimally invasive procedures/injections are used to diagnose and treat pain emanating from
intervertebral joints, spinal nerves, nerve roots, spinal cord, and sympathetic ganglia. These procedures
are performed in the lumbosacral, thoracic, and cervical spinal canal. Vascular complications can and do
occur in all areas of the spine and are of grave concern to all practitioners secondary to their
irreversibility (Figures 41-1 and 41-17).
Figure 41-1. Spinal cord infarction following left L3-4 transforaminal ESI. (Reproduced with permission
from Murthy, et al. Mayo Clinic Department of Radiology.)
Figure 41-2. Original description of “safe triangle” in the anterior and superior aspect of foramen on an
A-P view. Note lack of description of vascular contents.
Figure 41-3. Lateral view of “safe triangle” in the anterior and superior aspect of foramen. Again, note
lack of acknowledgement of vascular contents.
Figure 41-4. Typical course of arterial blood supply to spinal cord around waist of vertebra into the
anterior and superior aspect of the intervertebral foramen—the location of the “safe triangle.”
Figure 41-5. Typical segmental artery traversing waist of vertebra with radiculomedullary artery
traveling through anterior and superior portion of foramen just under pedicle—the “safe triangle.”
Figure 41-6. Enlarged segmental artery consistent with artery of Adamkiewicz traversing waist of L2
vertebra and entering L2-3 foramen in the anterior and superior aspect.
Figure 41-7. Parasagittal MRI slice revealing artery of Adamkiewicz entering anterior and superior
aspect of L1-2 foramen just under pedicle after traversing waist of vertebra.
Figure 41-8. Example of dye injection following “safe triangle” approach for transforaminal injection.
Presence of typical dye flow appearance is not a guarantee of safety as mechanism of injury may be
related to vascular injury and not steroid embolism.
Figure 41-9. Location of the Kambin triangle with hypotenuse formed by exiting nerve root, base of
triangle formed by superior endplate of inferior vertebra, and posterior aspect of triangle formed by the
anterior facet joint.
Figure 41-10. Oblique approach to L4-5 transforaminal injection with pointer at skin entry site utilized
for the Kambin triangle technique. End of pointer identifies skin entry site just lateral to SAP. Angle of
obliquity slightly more than “safe triangle’ technique to ensure needle passes by lateral edge of SAP but
remains medial enough to obtain adequate distribution of injectate. (Used with permission from Scott E.
Glaser, MD.)
Figure 41-11. Coaxial technique for needle placement in the Kambin triangle. The needle has just been
“walked” off the lateral edge of the SAP. (Used with permission from Scott E. Glaser, MD.)
Figure 41-12. Final needle location for transforaminal injection using the Kambin triangle technique.
Needle bevel posterior to disc, and inferior in foramen. (Used with permission from Scott E. Glaser,
MD.)
Figure 41-13. Appearance of dye flow on lateral view following the Kambin triangle technique. Note dye
in anterior epidural space posterior to disc. (Courtesy of Scott E. Glaser, MD.)
Figure 41-14. AP view following injection of dye using the Kambin triangle technique. Note excellent
outline of nerve root and excellent dye flow medially and posterior to disc. (Used with permission from
Scott E. Glaser, MD.)
Figure 41-15. AP view of transdiscal celiac plexus block. Skin insertion site and needle trajectory
similar to the Kambin triangle technique. (Used with permission from Scott E. Glaser, MD.)
Figure 41-16. Lateral view of transdiscal celiac plexus block. Note dye flow in prevertebral fascial
plane. (Used with permission from Scott E. Glaser, MD.)
Figure 41-17. Cervical spinal cord infarction following cervical transforaminal epidural steroid
injection. (Used with permission from Timothy Maus, MD.)
Based on the literature and expert opinions, it is clear that these complications occur more commonly
following procedures performed in the cervical spine. This is based on a few factors including:
• Lower margin of safety because of the proximity of arteries supplying the brain and the proximity of the
spinal cord itself.
• Random nature of the location of the vascular feeder arteries to the spinal cord within the cervical
foramen and the lack of a foolproof strategy for avoiding them while performing procedures.
• Complications following cervical procedures appear to be related to the injury or transection of these
arteries or embolism from injections into them.
In contradistinction to the cervical spine, the arterial supply to the thoracolumbar spinal cord follows a
regular and recurring path along the vertebra and within the thoracic and lumbar foramen. The critical
knowledge of vascular contents of the foramen cannot be ignored as the procedures performed in all three
areas of the spine, especially transforaminal interventions, carry the risks of disastrous complications.
Poor anatomicak knowledge has led to multiple cases of spinal cord damage and death documented in the
peer reviewed literature and even more undocumented cases throughout the world.
The incidence of vascular complications following procedures in the thoracolumbar area of the spine
clearly can be mitigated based on the knowledge of the location of the arterial blood supply. The
following section of this chapter describes the important anatomy and provides a strategy for avoiding
these arteries during procedures that put them at risk. Following that is a section on the cervical spine and
the increased risks of procedures performed in that area of the spine and the pros and cons of strategies to
reduce the risk of vascular complications.
THE RISK OF VASCULAR COMPLICATIONS IN THE

THORACOLUMBAR SPINE
Indications for interventional procedures in the thoracolumbar spine include pain that originates from:
• Facet joints (arthropathy, synovitis)
• Intervertebral discs (herniated, degenerative)
• Spinal nerves
• Spinal stenosis
• Vertebral compression fractures
• Sympathetically maintained pain from the abdomen, pelvis, and lower extremities
• Neuropathic lower extremity pain
• Shingles and postherpetic neuralgia
• Coccygodynia
• Intercostal neuralgia
• Metastatic carcinoma
Representative procedures in the thoracolumbar spine include:
• Transforaminal epidural steroid injections
• Interlaminar epidural steroid injections
• Intra-articular facet joint injections
• Sacroiliac injections and neurolysis of medial and lateral branches
• Medial branch nerve blocks and neurolysis
• Sympathetic nerve blocks and neurolytic procedures
Splanchnic nerves
Celiac plexus
Paravertebral sympathetic ganglia
Superior hypogastric nerves
Ganglion of Impar
Epidural adhesiolysis
Vertebroplasty, kyphoplasty, and sacroplasty
Spinal cord stimulation
Intrathecal pump
Rami communicans nerve blocks and neurolysis
Discography
Intradiscal procedures
Injections
Decompressive procedures
Annular ablative procedures
Complications associated with these procedures include the following:
• Postdural puncture headache
• Nerve damage
• Spinal cord injury
• Paraplegia
• Epidural hematoma
• Epidural abscess
• Pulmonary emboli
• Discitis
• Intrathecal granulomas
• Surgical site infections
• Intracranial hypotension
• Blindness.
• Pneumothorax
SPINAL CORD INJURY
Spinal cord injury and paraplegia, due to vascular ischemia, is one complication of grave concern; this
complication has a unique association with thoracolumbar transforaminal epidural steroid injections. At
least nineteen cases have been reported in the peer reviewed literature. The actual incidence is known to
be much higher and may be increasing. Spinal cord damage has occurred following transforaminal
procedures in multiple lumbar foramina including the right side and including the L5-S1 level.
Unfortunately, many cases are not reported. The confidential nature of the legal process and physician’s
reluctance to report complications limits disclosure.
In the case of lumbar transforaminal epidural steroid injections, the term “safe triangle” was
appropriated for the recommended needle placement zone (Figures 41-2 and 41-3). Keeping the
controversy of “safe triangle” in mind, authors suggest you make an explicit attempt to understand the
vascular anatomy of this “safe” zone. We emphasize that the term “safe” should not be taken at literal
value without extreme cautions. The major, if not the only, focus of this technique is to avoid injury to the
nerve root and/or spinal cord.
The root cause is vascular injury that interrupts the blood supply to the thoracolumbar spinal cord.
Downstream neurological ischemia and spinal cord damage occur.
VASCULAR INJURY
• The vascular injury occurs secondary to direct needle trauma, with or without injectate.
• The underlying pathophysiology is due to an intimal flap, arterial wall muscular spasm, complete
transection, arterial dissection, and/or embolization of fresh thrombus after arterial dissection.
• Another theory is the embolization by injected particulate steroids.
• The other salient factor is an injury to the artery of Adamkiewicz—the major vascular supply to the
spinal cord.
• For this reason alone, knowledge of spinal cord vascular anatomy is arguably the most important
element in the performance of these procedures.
RELEVANT ANATOMY
• Radiculomedullary arteries provide the arterial blood supply to the spinal cord.
• The major source of blood supply to the anterior thoracic and lumbar spinal cord is the artery of
Adamkiewicz or arteria radicularis magna (ARM).
• The radiculomedullary arteries including the ARM follow a predictable course from the aorta, around
the waist of the vertebrae, and are predictably found in the anterior and superior aspect of the foramen
• The ARM can be found in any thoracic or lumbar foramen.
Complex Vascular Supply of Spinal Cord

• The penultimate arterial supply to the spinal cord is mediated by the radiculomedullary arteries. They
travel posteriorly, following a well-established course alongside the vertebral body (Figures 41-4 and
41-5).
• These vessels enter the spinal canal, while passing through a relatively constant position within the
thoracic and lumbar foramina (Figure 41-5).
• This foraminal location is just inferolateral to the pedicle and in the upper anterior portion of the
foramen (Figure 41-5).
• The radiculomedullary vessels have a constant location within any foramen—the upper anterior
portion of the foramen (Figure 41-5).
• Moreover, the major conduit (artery of Adamkiewicz or arteria radicularis magna [ARM]), with a
remote anastomosis to the anterior spinal artery, may traverse any foramen (Figure 41-6).
• The vascular anatomical variation carries a high risk of spinal cord injury and is not routinely
addressed during the informed consent process and decision making by treating physician.
• The ARM is the major blood supply to the thoracolumbar spinal cord.
• Injury to the ARM carries a very high risk of spinal cord injury.
Radiculomedullary Arteries
• In the thoracic spine, radiculomedullary arteries are formed by posterior intercostal arteries.
• In the lumbar spine, radiculomedullary arteries are formed by paired lumbar arteries.
• At the thoracic levels 6 to 8, posterior intercostal arteries pass laterally and then, posteriorly along the
anterolateral margin of the vertebral body towards the intervertebral foramen.
• This is the shortest route between the aorta and spinal cord.
• After the intercostal artery wraps around the lateral vertebral body groove, it passes medially under
the pedicle.
• In the lumbar spine, the arteries originate more cephalically as they pass from the aorta en route to the
foramen. Hence, they lie close to the superior endplate of the lumbar vertebral body.
• Each artery divides into a series of major branches (abdominal wall, intermediate or spinal canal, and
the posterior body wall branches) just outside the level of the intervertebral foramina.
• The spinal canal (intermediate) branches divide into the anterior spinal canal, the nervous system, and
the posterior spinal canal branches.
• The nervous system branches are the radiculomedullary arteries and they arise from this segmental
artery, located just outside of the spinal canal.
• As the segmental artery courses around the posterior aspect of the vertebra, the arterial branches that
comprise the radiculomedullary arteries course upwards toward the pedicle.
• They reach the superior edge of the adjacent nerve root, located just outside or within the foramen; they
run along the dural nerve root sleeve for a short distance.
• These arteries supply blood to the spinal cord via direct cord penetration or regional anastomoses with
the anterior spinal artery.
Artery of Adamkiewicz
• The unique radiculomedullary vessel, also known as arteria radicularis magna [ARM], is the artery of
Adamkiewicz (Figures 41-6 and 41-7).
• This vessel is the major contributor to the anterior spinal artery.
• This artery does not directly supply the spinal cord but remotely anastomoses with the anterior spinal
artery to supply the majority of the blood supply to the thoracolumbar spinal cord.
• After passing through the foramen, the ARM turns sharply and travels cephalad for several segments.
• Then this vessel makes a characteristic downward “hairpin” turn to anastomose with the anterior
spinal artery.
• The most salient fact is that the ARM may enter the spinal canal at any intervertebral foramen, spanning
T5 to L5 (Figures 41-6 and 41-7).
• In one study, in greater than two-thirds of cadavers, the ARM was found along the lumbar nerve roots.
This anatomic study highlighted the “remarkable variability of the ARM origin” (Figures 41-6 and 41-
7).
• The ARM enters the spinal canal on the left 69% to 85% of the time, based on anatomic and radiologic
studies; and it enters the right side 15% to 31% of the time.
• The ARM might be duplicated in some individuals. It has also been shown in some patients to be split
ipsilaterally between adjacent foramina or bilaterally between contralateral foramina.
• Like the other radiculomedullary arteries, the ARM will join the nerve root at the foramen.
• The artery then courses medially through the superoanterior part of the foramen, in close juxtaposition
to the dorsal root ganglion-ventral root complex underneath the pedicle.
• The artery of Adamkiewicz can potentially be found at the mid vertebral body and the superior anterior
foramen at every thoracic or lumbar level, care must be taken to perform procedures in a manner which
minimizes the risk of the needle or instrument encountering the artery.
• This strategy is the only foolproof method to avoid vascular complications.
• It is important to detect intravascular injections of particulate steroid through the use of appropriate
positioning of the fluoroscope, dye injection during live fluoroscopy, and digital subtraction imaging,
to minimize potential embolization complication.
However, these techniques only prevent complications assuming one mechanism of injury, embolism of
steroid. Strategies to detect intravascular uptake, although important, will not protect the patient from
other mechanisms of injury including transection of the artery, intimal flap, and muscle spasm, local clot
formation, and/or embolization of fresh thrombus after arterial dissection.
PROCEDURES WHICH PUT THE ARTERIAL BLOOD SUPPLY

TO THE SPINAL CORD AT RISK
These procedures require placement of the bevel of a needle between the aorta and the foramen or in the
foramen risk encountering the ARM as it traverses the mid vertebra and enters the foramen. These
include:
• Transforaminal injections
• Sympathetic nerve blocks
• Procedures involving the rami communicans
Transforaminal Epidural Steroid Injections

• In the authors’ opinion, the key to safely performing transforaminal epidural steroid injections in the
thoracic or lumbar spine is to avoid the superior anterior aspect of the foramen (“safe triangle”)
secondary to the presence of the radiculomedullary arteries in this area (Figure 41-8).
• Our preferred technique is alternative locations for the placement of the needle include the inferior
foramen, just posterior to the disc (the Kambin triangle) (Figure 41-9).
• Transforaminal epidural steroid injections performed by placing the needle in the Kambin triangle
eliminates the risk of interrupting blood supply to the spinal cord as it eliminates the risk of
encountering the artery of Adamkiewicz (Figures 41-8 and 41-9).
• The most important difference between the Kambin triangle technique and the “safe triangle” technique
is that the needle will be placed in the foramen below the exiting nerve root and that the superior and
anterior aspect of the foramen will be avoided (Figures 41-8 and 41-9).
• Performing transforaminal injections in this manner will obviate the risk of placing the needle in the
area of the foramen that contains the blood supply to the spinal cord
• This eliminates the risk of encountering the artery of Adamkiewicz thereby minimizing the risk of
spinal cord damage and paraplegia.
Our preferred technique utilized for performing transforaminal injections in the Kambin triangle is
described below:
• Oblique approach, as with safe triangle approach, is utilized (Figures 41-10 and 41-11).
• Skin entry site is at mid discal level or lower, just lateral to SAP (Figures 41-10 and 41-11).
• Lateral edge of SAP can be used as depth gauge as well as intermittent lateral fluoroscopic views.
• Final needle position is at mid discal line or lower on A-P and lateral view (Figures 41-12 and 41-
14).
• Final needle position is in pedicular line on A-P (Figure 41-14).
• Final needle position is in posterior to disc in foramen (Figures 41-12 and 41-13).
Sympathetic Blocks or Neurolytic Procedures

These include thoracic splanchnic, celiac, lumbar paravertebral, and superior hypogastric blocks:
• When performing interventions involving the sympathetic ganglia in the thoracic or lumbar region, care
should be taken to avoid the mid portion of the vertebral body secondary to the presence of the
radiculomedullary arteries in this area (Figures 41-15 and 41-16).
• Alternative locations for needle or instrument placement include the anterolateral aspect of the
vertebral body close to the superior or inferior endplate or anterolateral to the disc.
• Another option is a transdiscal approach to the sympathetic chain (Figures 41-15 and 41-16).
• Oblique approach with lateral edge of transverse process even with lateral aspect of vertebral body is
utilized.
• Skin entry site is lined up with lateral edge of vertebral body just inferior to superior endplate or
superior to inferior endplate.
• Needle advanced to anterolateral aspect of vertebral body.
• Alternatively, a transdiscal approach may be utilized to obtain excellent needle placement in the
prevertebral space while avoiding risk of spinal cord damage.
Clinical Pearls
• Concerns about an increased risk of discitis secondary to increased risk of intradiscal injections using
this technique for TFESI may be unfounded.
• Should discitis occur, although serious, this is a complication that responds to appropriate treatment.
• In authors’ opinion, the outcomes using this technique for TFESI appear to be better than utilizing the
safe triangle technique. This may be secondary to the fact that a higher concentration of medication is
being deposited at the disc/nerve interface rather than tracking above the nerve and superiorly.
• In authors’ opinion, this technique also appears to improve outcomes for patients being treated for
spinal stenosis or discogenic pain. This is presumably due to a higher concentration of medication
being deposited in the epidural space just posterior to the disc.
THE RISK OF VASCULAR COMPLICATIONS IN THE

CERVICAL SPINE
The indications for cervical procedures are included in the list at the start of the chapter. Many of the
procedures listed in the start of the chapter are performed in the cervical spine as well. In addition,
interventions directed at the sympathetic chain include stellate ganglion procedures such as ganglion
blocks and neurolytic procedures. Other procedures performed in the cervical spine include:
• C1-2 joint injections
• Atlanto-occipital joint injections
• Occipital nerve blocks
The complications listed at the start of the chapter also occur following cervical interventions. In
addition, other complications that have occurred include:
• Spinal cord infarction (Figure 41-17)
• Quadriplegia
• Hemiplegia
• Seizure
• Coma
• Death
• Locked in syndrome
• Cerebellar herniation
• Brainstem infarction
• Brain infarction
Procedures in the cervical spine carry a greater risk of vascular and neurologic complications for the
following reasons:
• One is the presence of the internal carotid artery in the carotid sheath and the vertebral artery which
may be encountered by the needle or instrument or injected into during the procedure (Figure 41-19).
• The vertebral artery is especially at risk in the cervical spine based on its proximity to the foramen,
pedicle, and vertebral body (Figures 41-18 and 41-19).
• This artery passes through the foramen transversum in the transverse process located in the upper 6
cervical vertebra just anterior to and in close proximity to the foramen (Figures 41-18 and 41-19).
Figure 41-18. Note foramen transversum located immediately anterior to pedicle and foramen.
Figure 41-19. The course of the vertebral artery to the cranium. Again, note proximity to foramina, the
C1-2 joint, and the atlanto-occipital joint.
• However, in 8% of the cases it passes through a foramen transversum in the seventh cervical vertebra.
Knowledge of this anatomical variation is extremely important especially when performing stellate
ganglion blocks. The theories regarding the mechanism of injury leading to vascular complications with
involvement of the vertebral artery include:
• Embolism of particulate steroid
• Arterial intimal flaps
• Arterial dissection
• Dislodgement of plaque causing embolism
• Arterial smooth muscle spasm
• Embolism of fresh thrombus following disruption of the intima
In some cases of mortality following a procedure, vertebral artery trauma and in one case dissection
was found at post mortem. These complications have occurred following transforaminal injections, facet
joint treatments, and stellate ganglion blocks.
BLOOD SUPPLY OF CERVICAL SPINAL CORD

In contradistinction to the vertebral artery which follows a predictable course except at C7 and which can
be avoided utilizing appropriate techniques and safeguards, the location of the arterial blood supply to the
cervical spinal cord in the foramina is variable (Figure 41-20).
Figure 41-20. Anatomy of cervical intervertebral foramina. Note spinal segmental artery in posterior
foramen. (From Atlas of Image Guided Interventions, Rathmell JP.)
• The radicular arteries supplying arterial supply to the spinal cord occur posteriorly and anteriorly and
have been found running along both the anterior and posterior nerve roots.
• They supply the spinal cord in addition to the anterior spinal artery and the paired posterior spinal
arteries.
• They are branches of the vertebral, costocervical, and thyrocervical trunks of the subclavian artery.
More than one branch may enter the foramen at each level although usually only one radicular artery is
found anteriorly.
• Most radicular arteries are small and supply only the nerve roots but in the areas of the spinal cord
with higher metabolic requirements, the cervical and lumbar enlargement, some radicular arteries may
supply the gray matter in the spinal cord.
• In addition, in the cervical spine, segmental medullary arteries, after supplying the dorsal or ventral
nerve root, will continue on to reach and anastomose with the spinal arteries providing additional
blood supply to the cord.
• There is more than one of these medullary arteries in the cervical spine whereas typically the
lumbosacral cord is supplied by one such artery, the artery of Adamkiewicz.
• The fact that these medullary arteries may be found anywhere in the cervical foramen and that makes
procedures performed in or near those foramina extremely dangerous (Figure 41-20).
• Additionally, it has been shown that there are variable anastomoses between vertebral and cervical
arteries in the foramen leading to further risks of indirect injection into the vertebral artery through an
anastomosis.
Unlike the lumbar and thoracic spinal canal where the segmental reinforcing artery, the artery of
Adamkiewicz, can be reliably avoided using appropriate landmarks and techniques, the cervical arterial
blood supply is always at risk during procedures in this area of the spine. In other words, it is not
possible to reliably avoid interaction with these radicular and segmental arteries without a preprocedure
angiogram as one cannot predict which foramen they are in or where in that foramen they are traveling.
Thus, if one chooses to perform these procedures, one should choose one or more technique modifications
to avoid injecting into or injuring the artery. Below are representative fluoroscopic pictures of a cervical
transforaminal injection performed utilizing the most common technique in the posterior foramen (Figures
41-21A-C).
Figure 41-21. Left C5-6 cervical transforaminal approach, “selective nerve root block” with curved
blunt needle; note dual contrast outline of exiting C6 spinal nerve, along with epidural and lateral
muscular spread (needle orifice is proximal to needle tip—accounting for lateral contrast extravasation).
(Used with permission from Rinoo Shah, MD, MBA.)
Many modifications of “traditional” techniques have been proposed and much written about them. The
majority of these strategies hinge their success in preventing neurologic complications on the detection of
intravascular uptake and the prevention of embolism.
FLAWS WITH “EMBOLISM” THEORIES OF VASCULAR

INJURY
The flaws with this theory of injury only by embolism that it is possible to perform the safe and
atraumatic cannulation and then decannulation of an artery without the benefit of direct observation. The
assumption underlying these theories regarding the protective effect of detecting intravascular uptake rests
on the belief that these small arteries can be entered and exited without any sequela as far as damage to
that artery, This assumption also defies the fact that anatomic studies reveal that these radicular and
medullary arteries are reliably smaller than a 22- or 25-gauge needle in their diameter. These theories
also assume that after the cannulation of the artery, the injection of a particulate steroid leads to embolism
distally leading to infarction.
The embolism only theory has led to much speculation in the literature. Unfortunately, the exact
mechanism of injury is not known and is difficult if not impossible to prove. Also, and perhaps most
importantly, there are other more logical mechanisms of injury with substantial support in the literature.
As interesting as these theories may be, it is virtually impossible to assess their efficacy in reducing intra-
arterial injections. And, once again, it is even more difficult to assess if there is any protective effect
since any such effect is based on preventing only one unproven mechanism of injury, embolization of
steroid.
The other mechanisms of injury leading to these complications include:
• Transection of the artery
• Creating arterial intimal flaps
• Traumatic arterial dissection
• Arterial smooth muscle spasm
• Embolization of fresh thrombus after arterial dissection
All of these mechanisms of injury or a combination of them may lead to cessation of arterial flow and
infarction. These mechanisms also explain multiple cases found in the literature where dye flow appeared
normal during the procedure yet catastrophic vascular complications occurred.
Technique modifications to detect intravascular uptake include:
• Minimum injection of dye under live fluoroscopy.
• Use of digital subtraction angiography (DSA) that can be performed with many of the fluoroscopes in
use today can increase the ability of the operator to detect intravascular uptake.
• It has also been recommended that local anesthetic test doses should be employed with an appropriate
waiting period to monitor the patient for side effects associated with intra-arterial injection of local
anesthetic (seizures, loss of consciousness, transient neurologic deficits, etc).
• Another technique modification, the use of nonparticulate steroid, based on the assumption that
embolization occurs by injecting particulate steroid intra-arterially during these procedures.
• Use of blunt needles.
• Use a cervical interlaminar approach coupled with a steerable catheter.
The assumption is that the injection of nonparticulate steroid prevents the effects of embolism, ie,
infarction secondary to blockage of blood flow. Supporters point to the fact that there are no documented
cases of vascular complications following the use of these steroids. Unfortunately, the number of cases
known, although increasing, is low and the use of nonparticulate steroid is low as well.
The authors are concerned that the use of nonparticulate steroid may lead to a false sense of confidence
for 2 reasons.
• Based on the other possible mechanisms of injury, it is obvious that steroid choice alone will not
protect patients from all of the other injurious events that may occur to the artery.
• Secondly, although the nonparticulate steroid may not contain crystals, it is in and of itself a nonred
blood cell containing embolus much like an air embolus and this fact may negate its protective value if,
in fact, there is any.
Another protective maneuver that has been proposed is the use of blunt needles (Figures 41-21 and 41-
22). This was not discussed in the section on thoracolumbar injections because therein risk reduction is
afforded by avoiding the “safe triangle” and not by technical modifications. However, in the cervical
spine, the lack of a regular anatomical pattern of the radicular and segmental arteries within the foramen
makes it impossible to ensure that they can be avoided. With this knowledge and the multiple possible
mechanisms of injury, the use of a blunt needle is an option, but the caveat is that the introducer is sharp
and the blunt tip may cause discomfort as it passes through tissue planes. Like proponents of
nonparticulate steroids, supporters of blunt needles point to the fact that there have been no case reports
of vascular catastrophes associated with their use. Although, once again, this may not be dispositive
because of the relatively low number of these of complications and the even lower use of blunt needles, it
nevertheless is compelling. Proponents suggest that the blunt needles do not have a cutting edge bevel and
therefore may protect against arterial injury. Like all other protective maneuvers, proving the protective
efficacy of blunt needles at this time is most likely not possible.
Figure 41-22. Epimed blunt tipped needle. (Used with permission from Gabor Racz, MD, Epimed, Int’l.)
Another option is to use a cervical interlaminar approach coupled with a steerable catheter. This may
have the combined advantages of the relative safety of the interlaminar approach and the “selectivity” of
the transforaminal approach (Figure 41-23).
Figure 41-23. Targeted cervical epidural steroid injection with catheter. (Used with permission from
Rinoo Shah, MD, MBA.)
SUMMARY
• Cervical transforaminal epidural steroid injections carry a higher risk than thoracolumbar
transforaminal injections.
• Arterial injury causing vascular interruption during a cervical transforaminal is almost always
consequential, whereas during a thoracolumbar transforaminal one has to injure the artery of
Adamkiewicz.
• Furthermore, practitioners can be reasonably confident about accessing a cervical artery irrespective
of needle location within a cervical foramen.
• In contrast, practitioners can be reasonably confident about accessing radiculomedullary vessels in the
“safe” triangle and about avoiding them in the Kambin triangle.
• Risk reduction during cervical transforaminals injections may be afforded by technical modifications
(nonparticulate steroids, blunt needles, digital substraction angiography, live contrast flow, local
anesthetic test doses, slow injection, use of extension tubing to avoid excess needle manipulation,
avoidance of heavy sedation, and patient feedback)—but many of these strategies remain unproven and
are based on anecdotal evidence.
• Practitioners and patients must have a formal discussion and document that these are higher risk
procedures and that this way, patient and practitioner are fully aware of the risks versus benefits.
• Authors’ recommendations in the thoracolumbar spine, avoid the “safe” triangle.
CLINICAL PEARLS
• Because of the increased risk associated with cervical procedures, practitioners should have extensive
experience with procedures in the lumbar spine and appropriate training and mentoring before
attempting procedures in the cervical spine.
• These procedures should only be performed in cases where failure of previous treatment, the severity
of the symptomatology, and the lack of safer alternatives lead the reasonable doctor and patient to the
conclusion that the risk is worth the benefit. An example would be a patient on opioids with a low
quality of life secondary to the pain whose only other alternative would be surgery. The patient must be
completely informed as to the doctor’s rationale and the risks and benefits.
• If these procedures are going to be performed, it is recommended that one or more protective
maneuvers as reviewed above be carefully utilized.
• We also recommend the use of low dead space extension tubing to reduce movement of the needle tip
during these extremely delicate procedures.
Suggested Reading
Alleyne CH Jr, Cawley CM, Shengelaia GG, Barrow DL. Microsurgical anatomy of the artery of
Adamkiewicz and its segmental artery. J Neurosurg. 1998;89:791-795.
Crock HV, Yoshizawa H. Origin of arteries supplying the vertebra column. In: The Blood Supply of the
Vertebral Column and Spinal Cord in Man. Chicago, IL: RR Donnelly & Sons; 1977.
Glaser SE, Shah RV. Root cause analysis of paraplegia following transforaminal epidural steroid
injections: the “unsafe” triangle. Pain Physician. 2010 May-Jun;13(3):237-244.
Huntoon MA. Anatomy of the cervical intervertebral foramina: vulnerable arteries and ischemic
neurologic injuries after transforaminal epidural injections. Pain. 2005;117:104-111.
Kambin P, Sampson S. Posterolateral percutaneous suction-excision of herniated lumbar intervertebral
discs. Report of interim results. Clin Ortho Relat Res. 1986;207:37-43.
Murthy NS, Maus TP, Behrns CL. Intraforaminal location of the great anterior radiculomedullary artery
(artery of Adamkiewicz): a retrospective review. Pain Medicine. 2010;11:1756-1764.
Park JW, Nam HS, Cho SK, Jung HJ, Lee BJ, Park Y. Kambin’s triangle approach of lumbar
transforaminal epidural injection with spinal stenosis. Annals Rehab Med. 2011;35:833-843.
Scanlon GC, Moeller-Bertram T, Romanowsky SM, Wallace MS. Cervical transforaminal epidural
steroid injections: more dangerous than we think? Spine. 2007;32(11):1249-1256.
Tiso RL, Cutler T, Catania JA, Whalen K. Adverse central nervous system sequela after selective
transforaminal block: the role of corticosteroids. Spine J. 2004;4:468-474. doi:
10.1016/j.spinee.2003.10.007.
Hilton JD, et al. The “safe” triangle, contrast material, and particulate steroids in lumbar transforaminal
injections: what are the right things to do? Clin Radiol. 2012.
SECTION IV
SYMPATHETIC BLOCKS
CHAPTER 42
Stellate Ganglion Block

Richard S. Epter
Stellate ganglion blockade has been utilized since the 1920s to treat a variety of medical conditions.
Although blind stellate ganglion blockade had been the norm for decades, the use of fluoroscopy has
allowed increased accuracy with the use of less medication and decreased complications.
INDICATIONS
The indications for stellate ganglion blockade include:
• Differentiation of sympathetically maintained (SMP) versus sympathetically independent (SIP) pain
syndromes of the head or upper extremity
• Upper extremity/facial complex regional pain syndrome: type I (reflex sympathetic dystrophy [RSD]),
type II (causalgia)
• To increase upper extremity perfusion
Raynaud disease
Upper extremity arterial embolism
Intra-arterial drug injection
• Phantom limb pain
• Cluster or atypical vascular headache
• Glaucoma
• Optic nerve neuritis
• Head and face sympathetically mediated cancer pain
• Head/neck/thoracic acute herpes zoster or postherpetic neuralgia
• Hyperhidrosis of the head/neck/axilla/thorax
• Refractory atypical chest pain
• Pulmonary embolism
• Intractable angina pectoris
• Ventricular arrhythmia secondary to sympathetic imbalance
• Post mastectomy pain
• Meniere syndrome
• Scleroderma
CONTRAINDICATIONS
• Systemic or local infection in the area of injection
• Primary or secondary coagulopathy
• Untreated allergy to any of the procedure medications
• Previous anterior lower cervical surgery
• Patient refusal
RELEVANT ANATOMY
The stellate ganglion is usually formed by the fusion of the inferior cervical and first thoracic sympathetic
ganglia (Figure 42-1). The stellate ganglion lies just anterolateral to the seventh cervical vertebral body
at the base of the C7 transverse process, lateral to the first thoracic vertebral body and over the neck of
the first rib, in the groove between the vertebral body and the transverse process. It lies anterior or
immediately lateral to the longus colli muscle (Figure 42-2) and is posterior to the vertebral and carotid
arteries. The ganglion also lies just anterior to the C8 and T1 spinal roots.
Figure 42-1. Cervical anatomy depicting cervicothoracic (stellate) ganglion. (Reproduced from Netter.
Atlas of Human Anatomy. 4th ed. Plate 130, with permission.)
Figure 42-2. Anteroposterior view of cervical sympathetic chain and stellate ganglion lying over the
longus colli muscle. (Radiofrequency Part 2 Sluijter, Fig 7-1, p. 130.)
Under fluoroscopy, the ganglion lies just lateral to the vertical line joining the uncovertebral joints in an
anteroposterior view.
• Appropriate indications have been determined
• Evaluation and treatment of bleeding diathesis, contrast, or medication allergy
• Physical examination should identify previous neck or thyroid surgery, infection at the site of needle
insertion, or decreased range of neck extension
• A detailed informed consent including the potential benefits and risks as well as realistic expectations
of sympathetic blockade
• Possible postprocedural effects should be explained to the patient including ptosis; miosis; blurred
vision; enophthalmos; anhidrosis; facial and conjunctival flushing; upper extremity numbness or
weakness; contralateral blockade; and sense of dyspnea, dysphagia, or a lump in the throat
• Intravenous access for administration of fluid or medications to treat rare hypotension, seizure, or other
complication
• Preprocedural sedation for anxiety depending on the individual
FLUOROSCOPIC VIEWS
• Begin with anteroposterior imaging along with a caudal tilt of the image intensifier that allows optimal
visualization of the C6-C7 disc space and the C7 uncinate processes to clearly identify C7 (Figure 42-
3).
Figure 42-3. Fluoroscopic anteroposterior view with needle seen in perpendicular view at the base of
the uncinate process. Note the midline spinous processes.
• For oblique approach. Then obtain an oblique image of approximately 25 to 30 degrees off the median
sagittal plane to obtain a foraminal view of the lower cervical foramina. The target point is at the base
of the C7 uncinate process on the anterolateral aspect of the C7 vertebral body (Figure 42-4).
Figure 42-4. Fluoroscopic oblique view with needle seen in tunnel view at the base of the C7 uncinate
process. Note the cervical foramina and the squared off superior endplate of C7.
• For anterior approach. Then identify the C6 vertebral body and Chassaignac tubercle. The target point
after retracting the sternocleidomastoid muscle and carotid sheath is Chassaignac tubercle or slightly
medial to this structure on the transverse process. (See Figure 42-3). Note Chassaignac tubercle which
is the anterior tubercle of the C6 transverse process.
The patient is placed in a supine position on the fluoroscopy table pad with the head neutral, or slightly
rotated contralateral to the side of the procedure, and slightly extended. Arms are adducted. Pillows are
placed behind the upper thorax or shoulders to promote head extension and behind the knees.
Needles and Supplies

• 22-gauge 2.5-in Chiba or stellate block needle
• 3-mL syringe for skin local anesthetic
• 3-mL syringe for contrast
• 5-mL syringe for injectate
• 12-in extension tubing
• Kelly clamp
Medications
• Preservative-free 0.25% bupivacaine or 0.2% ropivacaine or 1% lidocaine
• Iohexol 240 (nonionic water-soluble contrast)
• Triamcinolone or methylprednisolone (optional)
Equipment
• Blood pressure monitor
• Pulse oximeter
• Oxygen available
• Resuscitation equipment and medications
• Fluoroscopy (ultrasound, CT, or MRI may also be utilized)

Different techniques have been described for stellate ganglion blockade.
Oblique Approach
This is the preferred technique of the author.
• The patient is placed in a supine position with a pillow beneath the upper thorax to promote head
extension with the head maintained in a neutral median plane or slightly rotated contralateral to the side
of the procedure.
• The skin is prepped with a 4% chlorhexidine gluconate solution three times and a sterile drape is
placed with the opening over the cervicothoracic junction.
• The lower cervical and upper thoracic spine is identified under fluoroscopy.
• An anteroposterior view is obtained with a slight caudal tilt of the image intensifier to optimize the C6-
C7 interspace and the C7 uncinate processes. This allows absolute identification of the C7 vertebral
body (see Figure 42-3).
• An oblique view is obtained allowing optimal visualization of the lower cervical foramina. This view
affords the safest approach to the target.
• A Kelly clamp is utilized as a marker on the skin for needle insertion and for holding the hub to guide
the needle using tunnel vision.
• The tip of the Kelly clamp is placed on the skin at a target point where the base of the ipsilateral
uncinate process meets the anterolateral C7 vertebral body.
• A 25-gauge 1.5-needle is used to inject 2 mL of skin local anesthetic (0.25% bupivacaine or 0.2%
ropivacaine or 1% lidocaine).
• A 22-gauge Chiba needle with a slightly bent tip is gently advanced under intermittent tunnel vision
fluoroscopic guidance until bone is contacted (see Figure 42-4).
• The contrast syringe is attached to the needle via the extension tubing and the needle is withdrawn 2-3
mL so that the tip is just anterior to the longus colli muscle.
• Following a negative aspiration for blood or cerebrospinal fluid an injection is made with 2 to 3 mL of
Omnipaque 240 (Figures 42-5 and 42-6). The initial 0.5 mL of the injection is observed under real-
time fluoroscopy to rule out early intravascular absorption.
Figure 42-5. Fluoroscopic oblique view with 3 mL Omnipaque 240 injected via extension tubing. Note
dye spread to top of C5 and extending below T1.
Figure 42-6. Fluoroscopic lateral view with 3 mL Omnipaque 240 injected. Note dye spread to top of C5
and extending below C7 the view is obscured by the shoulders.
• The desired contrast pattern should result in flow parallel to the axis of the spinal column. Dye spread
is observed for flow down to the C7-T1 level.
• The dye syringe is removed from the extension tubing and the injectate syringe containing 4 mL of
preservative-free 0.25% bupivacaine (or 0.2% ropivacaine or 1% lidocaine) with 40 mg of
triamcinolone (or methylprednisolone) is attached.
• Following a negative aspiration, a 0.5-mL test dose is made.
• A slow injection with the remaining injectate is performed under intermittent fluoroscopy. Dilution of
the dye is observed to visualize spread down to the C7-T1 level where the stellate ganglion is located
Figure 42-7. Fluoroscopic anteroposterior view with 5 mL injectate displacing Omnipaque. Note
injectate spread to C4 and extending to T2.
Figure 42-8. Fluoroscopic oblique view with 5 mL injectate displacing Omnipaque. Note injectate
spread to C4 and extending to T2.
• The needle may be flushed with saline and is then removed.

• A band aid or sterile dressing is applied.
Anterior Paratracheal Approach

This is the classic technique.
• For this approach the practitioner must stand on the ipsilateral side of the patient.
• The patient is placed in a supine position and the skin is prepped and draped as above.
• The lower cervical and upper thoracic spine is identified under fluoroscopy.
• An anteroposterior view is obtained with a slight caudal tilt of the image intensifier to optimize the C6-
C7 interspace and the C7 uncinate processes. This allows absolute identification of the C7 vertebral
body.
• The nondominant hand retracts the ipsilateral sternocleidomastoid muscle and the carotid sheath
laterally (Figure 42-9).
Figure 42-9. Schematic transverse view of cervical anatomy illustrating sternocleidomastoid retraction
and the sympathetic chain at C6. (Reproduced with permission from Brown D, Atlas of Regional
Anesthesia, 2e.)
• If a C6 procedure is desired, Chassaignac tubercle is targeted.

• If a C7 procedure is desired, the anterolateral C7 vertebral body at the base of the uncinate process is
targeted.
• The remainder of the procedure is performed in a similar fashion as described above.
Posterior Approach
This is rarely used when the oblique or anterior approach is not desired (anterior neck trauma, tumor, or
infection) and therefore will not be discussed further.
• The patient should be monitored and observed for at least 30 minutes following the procedure.
• Identify if sensory or motor block is present versus selective sympathetic blockade.
• Ipsilateral temperature monitoring may be done to confirm sympathetic blockade.
• Pain score changes are recorded prior to discharge.
• The patient may be contacted the day following the procedure for follow-up and any questions or
concerns.
• A discharge sheet is provided with instructions to call the pain center for any procedure-related
complications.

There are multiple dangerous structures in this region, including the carotid and vertebral arteries
(Figures 42-10 and 42-11). The patient should be observed for any of the following:
Figure 42-10. Gross anatomy of stellate ganglion with cervical sympathetic and upper thoracic
sympathetic chain in right anterior, slightly oblique view. At the top, small wire is exiting the vertebral
artery; the attached vertical wire overlies the cervical sympathetic chain leading to the stellate ganglion
(wire loop); the vertical wire caudad to the stellate overlies the thoracic sympathetic chain. (Dissection
used with permission of Frank H. Willard, Ph.D.)
Figure 42-11. Gross anatomy of stellate ganglion with the thoracic sympathetic chain in lateral view. At
the top a small wire comes straight out of the vertebral artery; the uppermost loop surrounds the cervical
sympathetic chain; the lower loop surrounds the stellate ganglion; the vertical wire overlies the thoracic
sympathetic chain; the transverse wires overlie intercostal nerves. Visualize the convergence of the lower
cervical and uppermost thoracic ganglia forming the stellate ganglion within the lower loop. Note the
stellate in this case is located at T1 and how posterior the thoracic sympathetic chain lies in relation to
the thoracic vertebrae. (Dissection used with permission of Frank H. Willard, Ph.D.)
• Hypotension
• Bradycardia
• Heart block
• Dyspnea
• Hematoma
• Intravascular puncture and injection of vertebral, carotid, or subclavian arteries
• Loss of consciousness or seizure from vertebral artery injection or local anesthetic toxicity
• Intrathecal or epidural injection
• Prolonged Horner syndrome that may occur with cervical sympathetic chain or stellate ganglion
blockade
• Hoarseness and dysphagia from blockade of the recurrent laryngeal nerve
• Upper extremity weakness secondary to brachial plexus blockade
• Infection or fever
• Diaphragmatic paralysis from phrenic nerve blockade
• Pneumothorax
• Thoracic duct injury
• Esophageal perforation

• Absolutely identify C7 as described above for accuracy of needle placement. If too caudal a view is
utilized, one may mistake C6 for C7 resulting in inadequate block.
• Use caution at the C7 level not to target just lateral to the vertebral body where the transverse process
begins, as the vertebral artery is exposed to potential puncture.
• Use of fluoroscopy and tunnel vision (eye through the needle) technique is extremely important due to
the proximity of important structures including the carotid, vertebral, and subclavian arteries; cervical
discs; spinal nerve roots; and the dome of the lung.
• Real-time fluoroscopy at the time of dye injection is critical to avoid unrecognized intravascular
injection—especially vertebral artery injection—that may result in seizure with as little as 0.25 mL of
local anesthetic.
• Small amounts of local anesthetics (3-5 mL) do not reliably block all fibers to the hands because
contributions from T2 and T3 (Kuntz fibers) may be present.
Suggested Reading
Abdi S, Zhou Y, Patel N, Saini B, Nelson J. A new and easy technique to block the stellate ganglion. Pain
Physician. 2004;7:327-331. ISSN1533-3159.
Hahn M, McQuillan P, Sheplock G. Regional Anesthesia. St Louis, MO: Mosby; 1996.
Raj P. Textbook of Regional Anesthesia. New York: Churchill Livingstone; 2002.
Raj P, Lou L, Erdine S, Staats P. Radiographic Imaging for Regional Anesthesia and Pain Management.
Philadelphia, PA: Churchill Livingstone; 2003.
CHAPTER 43
Thoracic (T2-3) Ganglion Block

Michael Stanton-Hicks
INTRODUCTION
The functional separation of the vagi (vagal nerves) and sympathetic trunks can be attributed to Estienne
(1544),1 but it was Winslow who, in 1732,2 described the sympathetic trunk as the paravertebral chain.
Many anatomists, including Michener and Auerbach, explored the sympathetic fibers and trunk. But as a
functional component of the autonomic nervous system, the association had to wait until Langley and
Dickerson in 1899.3
During the 20th century, many physicians (including Mandal,4 Kapppis,5 Brunn,6 Adriani,7 Loeser,8
Arnulf,9 Seabelund10) introduced their own variations on the best approach to the sympathetic trunk.5
However, they all involve variations of paravertebral techniques, the most recent being that described by
Butler and Charlton in 2001.11
INDICATIONS
• The anterior approaches to the sympathetic trunk in the neck (stellate ganglion) are easily performed
and are most commonly used; however, a posterior approach to the sympathetic trunk at the T2, T3
level provides the most reliable and consistent block of sympathetic activity to the upper extremity.12
• 20% of patients have sympathetic fibers that bypass the stellate ganglion called Kuntz fibers. These
patients may not reliably achieve sympathetic blockade with a stellate ganglion block.
• Neurolytic techniques of the stellate ganglion have a significant risk of prolonged or permanent Horner
syndrome, as well as damage to the phrenic and recurrent laryngeal nerves.
• The thoracic sympathetic block avoids these potential complications.
• The thoracic sympathetic block is indicated for all the same conditions as a stellate ganglion block.
INDICATIONS
Pain Syndromes
Common indications are as follows:
• Complex regional pain syndrome 1 and 2
• Herpes zoster (shingles)
• Postherpetic neuralgia (early)
• Postradiation arteritis
• Neuropathic pain associated with CNS pathology
• Paget disease
• Phantom limb pain
• Angina pectoris
The general indications for sympathetic block are shown in Table 43-1.
TABLE 43-1. Indications for Sympathetic Blocks
Vascular Insufficiency
Therapeutic applications for sympathetic block include:
• Raynaud disease
• Facial spasm
• Frost bite
• Microvascular pathology
• Embolic vascular disease
• Spasm of the ophthalmic artery
• Hyperhidrosis
• Buerger disease
• Stroke
• Vascular headaches
RELEVANT ANATOMY
The autonomic nervous system:
• The autonomic nervous system is divided into sympathetic and parasympathetic components, each
made up of preganglionic and postganglionic neurons.
• Their axons travel along the anterior roots of the spinal nerve as white rami communicantes that project
to the paravertebral sympathetic chain and then cephalad to synapse with postganglionic fibers in
sympathetic ganglia.
• The stellate ganglia consist of a fusion of the first and inferior cervical ganglia.
• The inferior cervical ganglion is large (15-7 mm), tending to lie anterolateral to the head of the first
rib.
• C7 and T1 ganglion cells form the stellate ganglia in about 82% of cases.
Thoracic ganglia
• Cell bodies of preganglionic sympathetic axons arise from cell bodies in the intermediolateral horn of
the spinal cord between T1 and T9.
• Fibers to the upper extremity synapse mainly in the T2 ganglia; but some also synapse in the T3
ganglia, stellate (C7, T1), and middle cervical ganglia.
• Preganglionic axons that supply the heart have their cell bodies in the intermediolateral column
between T1 and T5.
• Their preganglionic white rami synapse with postganglionic cell bodies in the paravertebral
sympathetic chain between T2 and T5, and the middle cervical and stellate ganglia.
• Gray rami fibers pass from these ganglia to the heart and great vessels.
• The right and left pulmonary plexuses include both vagal and sympathetic postganglionic fibers.
• The thoracic sympathetic trunks lie on the necks of the ribs just lateral to their costovertebral articular
processes and anterior to the intercostal vessels and nerves.
• Between T11 and T12, the sympathetic ganglia and chain lay anterolaterally on the side of the vertebral
bodies.
• The T2 ganglion is anterior to the medial portion of the neck of the rib, but ganglia between T3 and T6
are located anterior to the heads of their corresponding ribs.
• T7 through T10 ganglia are more laterally displaced to lie anterior to the costovertebral joints, while
T11 and T12 ganglia are more anterior placed to lie on the vertebral bodies.
• Because the first 4 thoracic ganglia lie in front of the upper portion of the necks and heads of each rib
compared to the lower thoracic ganglia, it is almost impossible to reach them by a paravertebral
approach (Figure 43-1).
Figure 43-1. Sympathetic trunk on the right. Note that the positions of the first and second sympathetic
ganglia are on the necks of their respective ribs whereas the third through eighth are on the heads of their
ribs.
• Specific anatomy that has a bearing on radio frequency ablation (RFA) procedures is the anatomical
disposition of the intercostal vessels. These lie posterior to the upper three ganglia. The lower thoracic
ganglia lie inferior and in front of the intercostal vessels and nerves.
• The anterior primary rami of the segmental (spinal) nerves that form the intercostal and collateral
intercostal nerves lie posterior and inferior to the ganglia except the upper T2-T4 ganglia to which
their immediate posterior relation is the posterior primary ramus of the segment above.
• As the parietal pleura reflects from the ribs, it is separated from the ganglia by a small amount of
adipose tissue.

Many techniques have been described, but because of the risk of pneumothorax, the posterior approach is
generally restricted to patients in whom fascial barriers or anatomic anomalies may prevent diffusion of
local anesthetic from its anterior deposition at C6/C7 to the upper thoracic sympathetic trunk or when
precise neurolytic procedures are planned.
When obtaining informed consent, the potential benefits, risks and complications, or any prolonged side
effects, should also be clearly explained, but within the context of the expected response and its value to
the patient and physician. It is essential to have IV access prior to the procedure. It may also be necessary
to provide some form of sedation, depending on the circumstances and disposition of the patient, who may
be a child.
Fluoroscopic Views
Anteroposterior to oblique views, and then cephalocaudal tilt for oblique approach: Follow two
radiologic landmarks, specifically the tubercle of the costotransverse articulation and the costovertebral
articulation (“head of the rib”) to achieve a comparatively straightforward approach to thoracic ganglia,
in particular T2 and T3 (Figure 43-2). This procedure was described by Stanton-Hicks in 2001.12 The
approach can be performed at any level of the sympathetic trunk with minimal risk of pneumothorax, in
contrast with the incidence of pneumothorax associated with most paraspinous techniques.
Figure 43-2. Articular facets on the transverse process and vertebral body for the corresponding rib are
shown. Radiologic landmarks for the oblique technique require identification of the nonarticular eminence
and head of the same rib. (Reprinted with permission of the Cleveland Clinic.)
Advantages of this approach are provided by the local anatomy itself:

• The parietal pleura forms a triangular space with the neck of the rib from which it reflects medially and
anteriorly as it passes away from the angle of the rib.
• The prevalence of pneumothorax is less than 1% and generally occurs when bony landmarks are
radiologically indistinct because of osteoporosis or other inflammatory processes.
• Almost all approaches to the sympathetic ganglia require either a direct posterior or slight oblique
direction using a bony landmark such as a transverse process.
• Remember that these approaches were earlier undertaken without supportive imaging and required
strict adherence to their bony landmarks for safe completion.
Equipment
• 10-cm 21-gauge spinal needle
• Image intensifier (C-arm x-ray machine)
• Telethermometer-infrared or thermistor
Medications
• Bupivacaine 0.75%
• Lidocaine 2.0%
TECHNIQUE FOR PARASANOUS APPROACH

Patient Preparation
The reason for performing a sympathetic block should be clearly explained to the patient. The expected
duration and choice of local anesthetic will help the patient understand what they will be asked to
observe during the course of the block. While sympathetic blocks may be diagnostic, prognostic, or
therapeutic, the patient should be clearly informed of the purpose for the particular procedure they are to
undergo.
• With the help of good imaging techniques, the needle must pass through the superior costotransverse
ligament and is then advanced from 7 to 10 mm, at which point it lies within the thoracic cavity (Figure
43-3A, B).
Figure 43-3. (A, B) The paraspinous approach to the sympathetic trunk. As the needle passes through the
costotransverse ligament it will travel a further 1.5 cm before reaching the sympathetic trunk. (Note that a
needle inserted at T3 will pass above the sympathetic ganglion, being “hidden” by the head of the rib.
(Reproduced with permission of the Cleveland Clinic.)
• As described above, the relationship is such that the needle should contact the upper portion of the
ganglion at T2 and T3.
• This approach is suitable for a local anesthetic block, but will also allow a radiofrequency lesion if a
curve-tipped RF needle such as the Finch needle (Radionics Instruments, Inc, Burlington, MA) is used.
• This technique applies in particular to radiofrequency lesions. Even with a curved needle, unless the
exposed tip is parallel to the ganglion surface, the generated heat will be insufficient to achieve a
satisfactory lesion.
• However, it should be noted that the lower thoracic ganglia cannot be reached by this approach.
• Most techniques designed to access the sympathetic trunk within the thoracic region carry a risk of
pneumothorax.
• Nevertheless, a good understanding of the anatomy, strict adherence to the technique, and good
imagining techniques with fluoroscopy or CT scan can minimize the incidence of pneumothorax.
INTERCOSTAL OBLIQUE APPROACH TO THE THORACIC

SYMPATHETIC GANGLIA
A thorough knowledge of the thoracic costovertebral anatomy is necessary. This approach relies on two
radiologic landmarks:
• The tubercle of the rib (costotransverse articulation)
• The head of the rib
Ribs and Their Articulations

• As can be seen in Figure 43-2, the principal parts of the ribs are the head, neck, tubercle (articular
eminence and nonarticular eminence), and curved body of the shaft.
• The costal groove contains intercostal vessels and nerves. The costal articulations should be noted.
• These, together with the tubercle and head of the rib, comprise the radiological landmarks that are
required by this technique.
• It should be observed that a line drawn from the tubercle to the head of each rib is almost parallel with
the neck of the corresponding rib; that is, the line is drawn from the inferior surface of the tubercle to
the antero-inferior surface of the costovertebral transverse articulation (head of rib), and will pass
under the neck of the rib. This line will lie adjacent and lateral to the parietal pleura (see Figure 43-
3B).
Positioning the Patient

• The patient must first be placed prone on a radiolucent table with a chest roll that allows the scapula to
move laterally with the arm either supported on an arm-board, or allowed to hang dependant.
• Patients undergoing this procedure should be lightly sedated.
• Verbal contact with the patient must be maintained at all times.
• Temperature probes (thermistors) should be placed on corresponding thumb pads for continuous
monitoring.
Technical Steps
Once the patient is in position, and sterile preparation and draping have been carried out, the image
intensifier (x-ray C-arm) is then placed at a right angle to the spine, and over the center of the vertebra
and costovertebral articulation representing the target ganglion. The view should be a true anteroposterior
(AP) projection (Figure 43-4A-C). The C-arm is then rotated to an oblique position determined by the
superimposition of the costotransverse nonarticular tubercle and the costovertebral articulation (head of
the rib) (Figure 43-5B).
Figure 43-4. (A) Position of fluoroscopy arm (C-arm)—anteroposterior with cephalad tilt. (B) True
anteroposterior projection showing the angle taken by the needle when the oblique technique is used. (C)
X-ray showing needle position in PA projection.
Figure 43-5. (A) “Gunsight” view of needle and target under the superimposed costotransverse and
costovertebral articulations. (B) X-ray view (gunsight view) of needle in oblique transverse projection.
(C) Depicting needle and target seen in oblique transverse projection.
• A C-arm with a laser sighting device will facilitate the procedure because the index can be placed
precisely at the antero-inferior edge of the costovertebral articulation.
• This placement of the index simplifies the initial position taken and increases accuracy as the needle is
advanced.
• Without such a device, the needle is inserted so that when seen “end-on” it appears as a dot (gun-sight
side view) at the inferior surface of the superimposed tubercle and antero-inferior margin of the
costovertebral articulation (Figure 43-5A-C).
• Great care should be taken to ensure this alignment, for it will allow accurate and safe needle passage
to the target ganglion.
• The needle is advanced carefully, taking 1 or 2 AP views with the C-arm during insertion until it
contacts the inferior outer edge of the rib.
• After passing underneath the rib, it is advanced in the thoracic cavity until it impacts the costovertebral
articulation.
• A lateral projection will show the needle tip to be just anterior to the costovertebral articulation and
above the vertebral foramen (Figure 43-6A, B).
Figure 43-6. (A) Lateral projection of the fluoroscopy arm (C-arm) showing correct needle position at
costovertebral articulation and so-called “hockey stick” that identifies the landmarks, foramen,
costovertebral articulation and disc. (B) Anatomy of the final needle position seen from a lateral view.
• The image seen in this view can be likened to a “hockey stick,” where the handle of the hockey stick is
the disc and the blade is the vertebral foramen.
• A small amount (0.1 mL) of water-soluble contrast should outline part of the capsule of the
costovertebral articulation in the lateral view and in an AP projection, it will appear to follow the
undersurface of the rib (neck) at an angle of 5 to 7 degrees.
• If a curved (Finch) RFA needle is used, it should be passed through a 16-gauge intravenous cannula
that is first introduced to the rib.
• The RFA needle is then rotated until it passes under the rib, at which time it is rotated back again so
that the convex surface of the distal curve of the needle faces the parietal pleura.
• As with a regular 10-cm 21-gauge needle, the RFA needle is introduced in the same manner described
above until it reaches the costovertebral articulation.
• To achieve a sympathetic block, a small amount of 0.75% bupivacaine or ropivacaine (0.25-0.5 mL) is
injected at T2 or T3 depending on the indication.
• Alternatively 0.25 to 0.5 mL of 2% lidocaine will achieve complete interruption of sympathetic fibers
to the upper extremity.
Neurolytic Procedure
• Neurolysis using 10% to 16% phenol in a volume of 0.25 to 0.5 mL will achieve a prolonged block of
each ganglion and in addition, those sympathetic fibers that are destined for the upper extremity.
• RFA of individual ganglia can be undertaken after first ensuring that no motor or sensory stimulation
occurs.
• Motor stimulation should be undertaken at 2 Hz and 1.5 V and sensory stimulation at 50 Hz and 0.8 V.
• In the absence of sensory and/or motor effects, RFA can be carried out at a temperature of 80°C for 80
seconds.
• This can be repeated with rotation of the needle through 180 degrees.
• Determine duration of procedural effect—whether it helped or not.
• May need a chest x-ray if there is any possibility of pneumothorax.
• Assess the sympatholysis to plan the further management.

• Procedure related general complications like infection, bleeding
• Pneumothorax—patient should be monitored for late onset of pneumothorax
• Epidural and/or intrathecal injection, and neurological deficit
• Intercostal neuritis, very rare
CLINICAL PEARL
• The oblique intercostal approach is a technique used in lieu of stellate ganglion block that is more
reliable in achieving complete interruption of sympathetic elements to the upper extremity.
References
1. Estienne C. De Dissectione Partium Corporis Humani Libri Tres. Paris: Apud Simonem Colinaeum;
1545.
2. Winslow JB. Exposition Anatomique de la Structure du Corps Humain. Paris: Guillaume Desprez et
Jean Desessartz; 1732.
3. Langley JN, Dickerson WL. On the local paralysis of the peripheral ganglia and on the connexion of
different classes of nerve fibres with them. Proc Roy Soc (Lond). 1889;46:423-431.
4. Mandl F. Die paravertebrale Injektion. Vienna, Austria: J. Springer; 1926.
5. Kappis M. Weitere Erfahrungen mit der Sympathektomie. Klin Wehr. 1923;2:1441.
6. Brunn F, Mandl F. Die paravertebrale Injektion zur Bekämpfung viszeraler Schmerzen. Wien Klin
Wschr. 1924; 337:511.
7. Adriani J. Labat’s Regional Anesthesia: Techniques and Clinical Applications. 3rd ed. Philadelphia,
PA: Saunders; 1967.
8. Loeser JD, Bonica’s: The Management of Pain. Philadelphia, PA: Lippincott Williams & Wilkins;
2001.
9. Arnulf G. Pratique des Infiltrations Sympathiques. Lyon, France: Camugli; 1984.
10. Skaebuland C, Racz G. Indications and technique of thoracic (2) and thoracic (3) neurolysis. Curr Rev
Pain. 1999;3:400-405.
11. Butler SH, Charlton JE. Neurolytic blockade and hypophysectomy. In: Loeser JD, ed. Bonica’s
Management of Pain. Philadelphia, PA: Lippincott Williams & Wilkins; 2001:1967-2006.
12. Stanton-Hicks M. Thoracic sympathetic block: a new approach. Tech Reg Anesth Pain Manag.
2001;5:94-98.
CHAPTER 44
Splanchnic Nerve Blocks

Andrea Trescot
INDICATIONS
The splanchnic nerves transmit the majority of nociceptive information from the viscera. Classically
performed for patients with intra-abdominal cancer, indications recently have expanded to include:
• Chronic abdominal pain1
• Chronic pancreatitis pain2
• Differential diagnosis of somatic versus visceral pain3
• Treatment of patients who have failed to obtain relief from celiac plexus blocks3
• Palliation of the acute pain of arterial embolization of the liver for cancer therapy3
• Treatment of pain of abdominal “angina” associated with visceral arterial insufficiency3
CONTRAINDICATIONS
• Local infection
• Sepsis
• Coagulopathy
• Respiratory insufficiency or pleural adhesions (due to risk of pneumothorax)
• Tumors that distort the relevant anatomy
• An abdominal or thoracic aneurism4
RELEVANT ANATOMY
• The sympathetic innervation of the abdominal viscera originates in the anterolateral horn of the spinal
cord.5
• Preganglionic fibers from T5-T12 travel with the ventral roots to join the white communicating rami,
pass through the sympathetic chain, and synapse on the celiac ganglia.
• The greater, lesser, and least splanchnic nerves are the major preganglionic of the celiac plexus.
• The greater splanchnic originates from the nerve roots of T5-T10 and travels along the vertebral body,
through the crus of the diaphragm, and into the ipsilateral celiac ganglion.
• The lesser splanchnic nerve originates from the T10/T11 nerve roots, while the least splanchnic nerve
arises from T10-T12; these also travel through the diaphragm to the ipsilateral celiac ganglion6 (Figure
44-1).
Figure 44-1. Splanchnic nerve anatomy: A = greater splanchnic; B = lesser splanchnic; C = least
splanchnic. (Used with permission from Andrea Trescot, MD.)
• These nerves are bound in a narrow compartment made up of the tibial body and pleura laterally, the
posterior mediastinum ventrally, and the pleural attachment to the vertebral body dorsally and the crua
of the diaphragm caudally.
• The volume of this compartment is approximately 10 cc on each side.7
• Documentation of coagulation status and fully informed consent are necessary. Prior to considering
neurolysis, the patient should have obtained good but only temporary relief from diagnostic splanchnic
blocks, and should be fully aware of the risks of postprocedure diarrhea and orthostatic hypotension
form the sympathetic blockade.
• Prior imaging (CT or MRI of the abdomen) should be reviewed preoperatively. Patients usually need
sedation, and therefore should be NPO as per the ASA guidelines.
• IV access is mandatory because of the potential hypotension for a successful sympathetic block, and
patients are usually pretreated with 500 to 1000 cc of balanced salt solution.

Because it has traditionally been used only for malignant pain, if the splanchnic nerve block is for
chronic, nonmalignant pain, such as chronic pancreatitis, documentation of failure of medication therapy
is warranted.
Fluoroscopic Views
Although the technique was originally described as a blind technique, relying on topographic guidance
alone,8 fluoroscopic or CT imaging is used. With fluoroscopy, the T12 vertebral body is “squared off”
and obliqued to the ipsilateral side.
Patient is positioned prone, usually with a pillow underneath the abdomen. However, patients with
ascites or severe abdominal pain may not be able to tolerate the prone position. An anterior approach to
the splanchnic nerves is also described below.

• Needles
This technique was originally described utilizing 22-gauge 15-cm Chiba needles. An alternative
approach utilizes 22-gauge 3.5-in Quincke (spinal) needles.9 Use of a blunt-tipped, curved needle with
an introducer allows the needle to “hug” the vertebral body, stay very medially, and theoretically
decrease the risk of pneumothorax. RF needles should be at least as long as those used for the
diagnostic procedure, curved and ideally blunt-tipped, with a 10- to 15-mm active tip.
30-gauge needle for skin infiltration
• Extension tubing
• Syringes
2 syringes 5 or 10 cc for medication and contrast.
1 syringe 3 cc for skin infiltration
• Contrast
Nonionic contrast such as Isovue or Omnipaque
• Local anesthetic
For diagnostic and prognostic splanchnic nerve blocks, volumes of local anesthetic ranging from 5 to
10 cc of 1% to 1.5% lidocaine or 0.5% bupivacaine have been described.10 To decrease the risk of
local anesthetic toxicity, all local anesthetic should be administered in divided doses.
• Neurolytic agent
For neurolytic injections, 10 cc of absolute alcohol or 6% to 10% aqueous phenol is recommended.10
The phenol can be mixed with contrast.

Fluoroscopic Imaging (Posterior Approach)
The original procedure was performed virtually identical to the classic retrocrural approach to the celiac
plexus, starting at L1, except that the needles were aimed more cephalad so as to end up at the anterior
lateral margin of the T12 vertebral body.11 An alternative approach utilizes 22-gauge, 3.5 in Quincke
needles placed 3 to 4 cm lateral to the midline, just below the T12 ribs with slightly mesial trajectory, so
that the tip of the needle ends up at the anterolateral margin of T12.
• The patient is placed prone, with a pillow underneath the abdomen, and the T12 vertebral body
identified and “squared off” fluoroscopically (Figure 44-2).
Figure 44-2. T12 vertebral body, AP view. (Used with permission from Andrea Trescot, MD.)
• The fluoroscope is then angled obliquely to the ipsilateral side about 45 degrees10 (Figure 44-3).
Figure 44-3. Splanchnic injection site, oblique view. (Used with permission from Andrea Trescot, MD.)
• If the diaphragm overlies the T12 vertebra and its rib, then the T11 vertebral body is identified
instead.4
• The needle (or introducer if a blunt-tipped needle is used) is then introduced through the skin just over
the lateral border of the vertebral body (Figure 44-4). The point of entry for either level (T11 or T12)
is at the junction of the rib and vertebra.
Figure 44-4. Initial needle placement, oblique view. (Used with permission from Andrea Trescot, MD.)
• Placing the entry point slightly caudad of the most narrowed portion of the vertebral body (the waist)
will allow the needle to be repositioned slightly superiorly if bony contact was made prior to optimum
needle placement.
• In the lateral view, the needle is advanced until it reaches the junction of the anterior one-third and the
posterior two-thirds of the vertebral body (Figure 44-5). If using a curved needle, keep the curve
pointing medially, rotating the tip laterally briefly if contact with bone is made too early.
Figure 44-5. Final needle placement, lateral view. (Used with permission from Andrea Trescot, MD.)
• Once the final needle placement is confirmed, nonionic contrast is injected to confirm that the tip of the
needle is not vascular or intrapleural (Figure 44-6).
Figure 44-6. Contrast injection, oblique view. (Used with permission from Andrea Trescot, MD.)
• Reconstruction CT images may help with visualization of the approach (Figure 44-7A-C)
Figure 44-7. (A-C) CT reconstruction splanchnic needle placement. (A) AP view, (B) oblique view, (C)
lateral view. (Used with permission from Andrea Trescot, MD.)
Diagnostic blocks
5 to 10 cc of local anesthetic should give good relief.
The author uses 1% lidocaine for quick, good relief on the table, followed by same volume of 0.5%
bupivacaine about 5 minutes later.
Because of the risk of intravascular injection, all local anesthetic injections should be instilled in
divided doses.
Neurolytic blocks
12 to 15cc of absolute alcohol or 6% to 10% phenol is used.10
Because of the likelihood of pain on injection, a similar volume of local anesthetic should be
injected first.
Radiofrequency ablation
The needle is placed as for the diagnostic injection, in the mid-third of the vertebral body.
Once the needle is in place, the stylet is removed and RF probe is placed through the needle.
Impedance should be less than 250 Ω.
Using sensory stimulation up to 1mV, the patient should report stimulation into the epigastric
region.10
If the patient reports a band-like stimulation pattern, they are describing intercostal stimulation, and
the needle should be advanced slightly.
Motor stimulation up to 2mV should not cause intercostal stimulation.
After the needle is in the proper position, confirmed by stimulation and fluoroscopy patterns, 2 cc of
2% lidocaine is injected through the needle to provide analgesia for the lesioning.
It is important to wait for a few (2-3) minutes to allow the local anesthetic to take effect. The author
recommends lesioning for 60 seconds at 85 degrees and then repeating after rotating the needle 180
degrees; Waldman and Pratt10 describe 90 seconds at 80 degrees.
After lesioning, inject 2 to 5 cc of 0.5% bupivacaine (with or without 40 mg of methylprednisolone
or Sarapin®) to provide postoperative analgesia.
Fluoroscopic Transdiscal Approach

Plancarte et al12 described a transdiscal posterior approach to the splanchnic nerves.
• The patient is placed in the prone position with a pillow beneath the abdomen. Prophylactic antibiotic
should be given intravenously 30 minutes before the procedure.
• The T11-T12 interspace is identified under fluoroscopy.
• Next, the fluoroscopy is obliqued 15 to 20 degrees.
• After local anesthetic infiltration of the skin and the subcutaneous tissues, a 22-gauge, 10-cm needle is
introduced lateral to the inferior aspect of the facet joint and advanced through the disc.
• 0.5 cc of contrast solution is administered to verify needle position within the disc by lateral and AP
views.
• The needle is then advanced further under lateral fluoroscopic control, using saline in a 3-cc syringe
for loss of resistance.
• When the needle has passed outside the disc space, 3 mL of contrast is administered to verify its final
position. The dye spread should be a vertical line.
• Plancarte et al used 5 cc of 10% aqueous phenol injected through the needle followed by 0.5 cc of air
before drawing the needle back to prevent the spread of the neurolytic solution within the disc
material.
• When the needle was drawn back in the disc, cefazolin 50 mg in 1 mL was administered to the disc to
prevent discitis, prior to removing the needle completely.
CT Imaging (Anterior Approach)

The theoretical advantages of an anterior CT approach to the splanchnic nerves include:
• Reduced discomfort by avoiding a prolonged prone position
• CT evaluation of anatomic distortions (from tumor or surgery)
• Less sedation for critically ill patients
Mercadante et al13 described an anterior CT approach, using a 20-cm-long needle with a stylet inserted
under CT guidance, passing through the space between aorta and vena cava, choosing the best trajectory
to avoid organ perforation and to place the tip of the needle in the retrocrural area bilaterally. Two
milliliters of contrast medium were injected through both needles to confirm the proper spread.
Neurolysis was achieved by injecting 12 mL of alcohol through each needle. An anterior approach
involves the passage of the needle through the viscera; however, this is not usually associated with
relevant complications.14
Postprocedure Considerations
The risks of splanchnic nerve blocks are similar to those of celiac plexus blocks, though the rate of
pneumothorax, thoracic duct injury, and unexpected spread of injected drugs onto the somatic nerve roots
are reportedly higher than those for transcrual approaches to the celiac plexus.7 It would be prudent to
perform a chest x-ray postoperative to rule out an early pneumothorax, because the needle passes so
closely to the lung (Figure 44-8), a reason to consider blunt-tipped needles. Because of the risk of
pneumothorax, extreme caution should be used if performing this injection bilaterally at the same sitting.
Figure 44-8. CT axial view showing proximity of the needle to the lung. (Used with permission from

• Because this is a sympathetic block, there is a potential for hypotension, and therefore IV access is
necessary. Without fluid prophylaxis (500-1000 cc of balanced salt solution), clinically significant
hypotension can be expected in 30% to 60% of patients.15
• Patients also need to be warned regarding orthostatic hypotension and diarrhea as potential side
effects.
• Pneumothorax is most obvious potential complication, and patient should be counseled to present to an
emergency room if they develop shortness of breath pain or chest pain. Bilateral procedures at the
same sitting should be avoided if possible.
• On the left side, chylothorax is a possibility, due to trauma of the thoracic duct.
• Subarachnoid or epidural injections were more common with the blind techniques.15
• Retrograde flow of local anesthetic or neurolytic agents have been described, causing the potential for
subarachnoid or epidural injections as well as paraplegia or nerve injuries.10
• Imaging would be expected to decrease the risks of this procedure; however, a large review of
complications in 1988 did not show any decrease in complications when using radiologic guidance.16

Given the higher incidence of pneumothorax associated with splanchnic nerve block relative to celiac
plexus block, splanchnic nerve block perhaps should be reserved for patients with upper abdominal and
retroperitoneal pain that fails to respond to celiac plexus block. Waldman and Pratt10 described keeping
the tip of the curved RF needle facing laterally initially until it passes the foramen. Then the tip can be
turned medially once it reaches the lateral surface of the vertebral body. This ensures the needle remains
medial to the interpleural surface and in close contact with the vertebral body. As a reminder, the phrenic
nerve also transmits nociceptive information from the upper abdominal viscera, referred to the
supraclavicular region and should be considered in all patients with upper abdominal pain.3
Suggested Reading
Loukas M, Klaassen Z, Merbs W, Tubbs RS, Gielecki J, Zurada A. A review of the thoracic splanchnic
nerves and celiac ganglia. Clin Anat. 2010 Jul;23(5):512-522.
Raj PP, ed. Interventional Pain Management; Image-Guided Procedures. 2nd ed. 2008:chap 12.
Waldman SD, ed. Atlas of Interventional Pain Management. 3rd ed. Philadelphia, PA: Saunders;
2009:chap 75.
Waldman SD, ed. Interventional Pain Management. 2nd ed. Philadelphia, PA: WB Saunders; 2001:chap
44.
References
1. Garcea G, Thomasset S, Berry DP, Tordoff S. Percutaneous splanchnic nerve radiofrequency ablation
for chronic abdominal pain. ANZ J Surg. 2005 Aug;75(8):640-644.
2. Bradley EL III, Bem J. Nerve blocks and neuroablative surgery for chronic pancreatitis. World J Surg.
2003 Nov; 27(11):1241-1248.
3. Waldman SD. Splanchnic nerve block: single-needle technique. In: Waldman SD, ed. Atlas of
Interventional Pain Management. 3rd ed. Philadelphia, PA: WB Saunders; 2009.
4. Erdine S, Talu GK. Sympathetic blocks of the thorax. In: Raj PP, Lou L, Erdine S, Staats P, eds.
Interventional Pain Management: Image-Guided Procedures. Philadelphia, PA: WB Saunders;
2008:255-265.
5. Bonica J. Autonomic innervation of the viscera in relation to nerve block. Anesthesiology.
1968;29:793.
6. Gest TR, Hildebrandt S. The pattern of the thoracic splanchnic nerves as they pass through the
diaphragm. Clin Anat. 2009 Oct;22(7):809-814.
7. Abram S, Boas R. Sympathetic and visceral nerve blocks. In: Benumof J, ed. Clinical Procedures in
Anesthesia and Intensive Care. Philadelphia, PA: JB Lippincott; 1992:787.
8. Thompson GE, Moore DC, Bridenbaugh LD, Artin RY. Abdominal pain and alcohol celiac plexus
nerve block. Anesth Analg. 1977 Jan-Feb;56(1):1-5.
9. Parkinson S, Mueller J, Little W. A new and simple technique for splanchnic nerve block using a
paramedian approach and 3-1/2 inch needles. Reg Anesth. 1989;14(2):41.
10. Waldman SD, Patt RB. Celiac plexus and splanchnic nerve block. In: Waldman SD, ed. Interventional
Pain Management. 2nd ed. Philadelphia, PA: WB Saunders; 2001:493-506.
11. Kappis M. Die Ansthesierung des Nervus splanchnicus. Zentralbl. 1918;45:709.
12. Plancarte R, Guajardo-Rosas J, Reyes-Chiquete D, et al. Management of chronic upper abdominal
pain in cancer: transdiscal blockade of the splanchnic nerves. Reg Anesth Pain Med. 2010
Nov;35(6):500-506.
13. Mercadante S, La Rosa S, Villari P. CT-guided neurolytic splanchnic nerve block by an anterior
approach. J Pain Symptom Manage. 2002 Apr;23(4):268-270.
14. Mercadante S, Nicosia F. Celiac plexus block: a reappraisal. Reg Anesth Pain Med. 1998 Jan-
Feb;23(1):37-48.
15. Moore D. Celiac (splanchnic) plexus block with alcohol for cancer pain of the upper intra-abdominal
viscera. In: Bonica J, Ventafridda V, eds. Advances in Pain Research and Therapy. New York:
Raven; 1979:357.
16. Lieberman R, Lieberman S, Cuka D. Celiac plexus block and splanchnic nerve block: A review.
Semin Intervent Radiol. 1988;5:213.
CHAPTER 45
Celiac Plexus Block Using CT Guidance

Kenneth D. Candido and Nebojsa N. Knezevic
INDICATIONS
The major indications for celiac plexus block (CPB) include abdominal pain which is nonresponsive to
less aggressive analgesic interventions and which emanates from:
• The pancreas1,2
• The liver
• Gallbladder
• Omentum
• Mesentery
• The alimentary tract from the stomach to the transverse large colon,3 which is of a visceral and not a
somatic nature
These indications include pathology that is both of a benign as well as a malignant etiology.
Neurolytic CPB is typically reserved for cancer-related pain, while it is more common that local
anesthetic and occasionally steroid injections are reserved for benign type of pain. Following
performance of CPB using 50% to 100% alcohol for malignant pain, an early meta-analysis found that
pain relief was “good or excellent” in 89% of 989 patients for the first 2 weeks following the block.4
• Determine the etiology of painful processes of the abdomen. It is essential to rule out nonvisceral
causes.
• Perform somatic blocks prior to undertaking CPB.
• Intercostal nerve blocks (ICNB) may be one such approach to using somatic blocks in an effort to
differentiate somatic from visceral etiologies.
• Judicious use of local anesthetic agents for ICNB may help determine whether or not a pathologic
process has primarily a somatic origin versus a sympathetic one.
RELEVANT ANATOMY
• Several of the abdominal viscera receive innervation through the celiac plexus.
• Sympathetic innervation is derived from the anterolateral horn of the spinal cord as axons from T5 to
T12 leave the spinal cord with ventral nerve roots to join white rami communicantes (WRC) in route
to the sympathetic chain.
• These axons do not synapse in sympathetic chain; instead, they pass through the chain to synapse at
distal sites.
• The celiac plexus includes several ganglia, these being the celiac, aortic, renal, and superior
mesenteric ganglia.
• Postganglionic nerves accompany blood vessels to visceral structures.
• Preganglionic fibers from T5 to T9 travel caudally from the sympathetic chain along the lateral and
anterolateral aspects of the respective vertebral bodies.
• The greater splanchnic nerve arises from the T9 and T10 levels.
• The celiac plexus (Figure 45-1) sits anterior to the aorta, epigastrium, and crus of the diaphragm.
Fibers comprising the celiac plexus arise from preganglionic splanchnic nerves, parasympathetic
preganglionic nerves from the vagus nerve (CN X), some sensory nerves from the phrenic and vagus
nerves, and postganglionic sympathetic fibers.
Figure 45-1. Anatomy of the celiac plexus and surrounding visceral structures.
• Complete sympathetic denervation of the gastrointestinal tract, such as may occur following CPB
renders an individual likely to develop increased peristalsis due to unopposed parasympathetic
nervous system activity.
The celiac plexus is in actuality the confluence of three distinct pairs of ganglia; the celiac, superior
mesenteric, and aorticorenal ganglia, respectively. Afferent nociceptive fibers are the identified targets of
the CPB. The CPB is useful as a diagnostic and as a therapeutic tool for managing pain of diverse
intraabdominal etiologies including both benign as well as malignant causes.
• Obtain an informed, written consent.
• Confirm the absence of contrast allergies or anticoagulant medications.
• It is useful to refer to standard references such as those published by the American Society of Regional
Anesthesia (ASRA) concerning anticoagulants and regional anesthesia prior to commencing to
determine the suitability of prospective block candidates prior to proceeding.
• Standard American Society of Anesthesiologists (ASA) monitors are applied and baseline vital signs
are assessed and documented.
• An intravenous cannula should be placed for the purposes of administering intravenous fluids and
supportive drugs in the event of either an inadvertent event or following the expected orthostatic
hypotension resulting from a successful block.

• 20 or 22-gauge 12- or 18-cm spinal type needle (Quincke)
• Water-soluble, iodine-based contrast
• Local anesthetics (0.2% ropivacaine; 0.125% bupivacaine; 0.5% lidocaine)
• CT scanner or fluoroscopy equipment
• Endoscopic ultrasound equipment (for endoscopic technique only)
INTRAOPERATIVE TECHNICAL STEPS (FIGURES 45-2 TO 45-

17)
Figure 45-2. Posterior CPB. Axial CT scan slice at the T12-L1 level demonstrating a left-sided
approaching needle in a para-aortic approach to single-injection CPB. Technique demonstrated is a trans-
crural approach. (Figure courtesy of Kenneth D. Candido, MD.)
Figure 45-3. Posterior CPB. Same patient as above. 5 mL of iodine-based, water-soluble contrast has
been injected through the needle, with the beginnings of a para-aortic spread being identified. (Figure
courtesy of Kenneth D. Candido, MD.)
Figure 45-4. Posterior CPB. Same patient as above. 10 mL of contrast is now shown beginning to extend
circumferentially toward the right side, in addition to the left side. (Figure courtesy of Kenneth D.
Candido, MD.)
Figure 45-5. Posterior CPB. Same patient as above. Spread of 15 mL of contrast moves deeper in the
para-aortic space bilaterally. (Figure courtesy of Kenneth D. Candido, MD.)
Figure 45-6. Posterior CPB. Same patient as above. 20 mL of contrast demonstrate bilateral spread in a
para-aortic fashion. (Figure courtesy of Kenneth D. Candido, MD.)
Figure 45-7. Anterior CPB. Needle advancement, midline at T12 level. Bright, hyperintense areas in
abdomen represent recent surgical clips from an “open-and-shut” laparotomy performed 6 days earlier.
(Figure courtesy of Kenneth D. Candido, MD.)
Figure 45-8. Anterior CPB. Same patient as above. Needle approaches the aorta, midline at T12 level.
(Figure courtesy of Kenneth D. Candido, MD.)
Figure 45-9. Anterior CPB. Same patient as above. 5 mL of contrast spreading ventral to the aorta in the
suspected location of the bilaterally paired celiac plexus. (Figure courtesy of Kenneth D. Candido, MD.)
Figure 45-10. Anterior CPB. Same patient as above. 10 mL of contrast begins to spread bilaterally.
Extensive scarring in the abdomen prevents material from extending posteriorly toward the vertebral body
of T12. (Figure courtesy of Kenneth D. Candido, MD.)
Figure 45-11. Anterior CPB. Same patient as above. Now, with the injection of 15 mL of contrast, the
contrast material adheres to the anterior and lateral walls of the abdominal aorta, inhibited only by the
intraabdominal scarring from prior surgical interventions. (Figure courtesy of Kenneth D. Candido, MD.)
Figure 45-12. Transaortic CPB. Green arrow points to needle tip advancing medial to the left kidney and
lateral to the T12 vertebral body. (Figure courtesy of Kenneth D. Candido, MD.)
Figure 45-13. Transaortic CPB. 2 mL of contrast has been injected after stylet removal demonstrated
bright red backflow of blood. (Figure courtesy of Kenneth D. Candido, MD.)
Figure 45-14. Transaortic CPB. 5 mL of contrast have been injected, demonstrating a crescent-shaped,
half-moon, para-aortic spread beginning to spread bilaterally. (Figure courtesy of Kenneth D. Candido,
MD.)
Figure 45-15: Transaortic CPB. Additional 2 mL of contrast spreading further bilaterally. (Figure
courtesy of Kenneth D. Candido, MD.)
Figure 45-16. Transaortic CPB. A total of 10 mL of contrast has now been injected, demonstrating
excellent spread bilaterally, in a para-aortic fashion, covering the suspected distribution of the celiac
plexus. (Figure courtesy of Kenneth D. Candido, MD.)
Figure 45-17. Transaortic CPB. A total of 12 mL have been injected, demonstrated a spread equivalent to
the posterior approach technique shown above which required almost 20 mL to completely encapsulate
the abdominal aorta and extend to the bilateral celiac plexus. (Figure courtesy of Kenneth D. Candido,
MD.)
CPB may be undertaken using one of a variety of approaches, including those which utilize fluoroscopic
or computed tomography (CT) guidance and those for which ultrasound or endoscopy is determined to be
appropriate as an adjunct to identifying the relevant anatomy. In 2012, it is probably not feasible to
consider performing CPB absent some type of imaging technique. The celiac plexus may be approached
using 1 of the 3 basic anatomical techniques:
1. Posterior para-aortic (Figures 45-2 to 45-6)
2. Anterior2 (Figures 45-7 to 45-11)
3. Posterior transaortic (Figures 45-12 to 45-17)
Posterior Para-Aortic Approach

• The patient is placed in the prone position.
Placing a pillow or bolster beneath the abdomen may help reduce the normal lumbar spinal lordotic
curve.
• A full surgical sterile skin preparation and draping is next undertaken.
• When imaging is used, it is imperative to obtain a scout film of the lower thoracic and upper lumbar
spinal areas, seeking to identify the T12 and L1 vertebral bodies by visualizing their respective
spinous processes.
• The inferior border of the 12th rib is identified and marked using a sterile marking skin pen.
• A local anesthetic skin wheal is raised using a hypodermic needle and a small-gauge needle,
approximately 7 to 8 cm from the anatomical midline, at the inferior border of the 12th rib.
• Next, a 20- or 22-gauge, 12- or 18-cm spinal type needle (Quincke) is advanced from posterior to
anterior toward the ventral surface of the T12-L1 intervertebral space, as defined by the intervertebral
disc, taking care not to penetrate the actual disc.
The goal of needle advancement is to remain in close proximity to the lateral aspect of the vertebral
bodies during the entire course of needle penetration towards the target.
Starting out farther than 8 cm from the anatomical midline poses a risk of renal injury due to
penetration by the advancing needle tip.
If the starting point is beneath the lateral tip of the 11th, and not the 12th rib, there is a distinct risk
of producing a pneumothorax.
With CT-guided techniques, of course, many of these same concerns are rendered moot, as the
anatomy is more easily reconciled (Figures 45-2 to 45-17).
• The needle (a left-sided approach may be attempted using a single-needle, or alternatively, bilateral
needles may be placed if there is not a satisfactory spread of contrast using a unilateral approach) is
advanced toward the T12-L1 interspace using CT or fluoroscopic imaging.
A left-sided approach has been demonstrated to more reliably block the celiac plexus when a
single-needle is utilized.5
In the viewpoint of these authors, who have performed >500 CPBs, it has been decidedly the rare
occasion that more than a single needle has ever been necessary to successfully attain bilateral
contrast spread using the described technique(s).
• If the needles are directed more cephalad, toward the spinous processes of T12 or T11, it is likely that
a splanchnic and not a celiac plexus block is in actuality being performed.6
• Penetration or nonpenetration of the crus of the ipsilateral diaphragm while performing a posterior
approach to CPB determines whether the block is a “true” CPB or whether in fact it is a splanchnic
nerve block (SNB).7
If the needle is posterior to the crus, the block is an SNB; anterior to the crus is a true CPB (Figure
45-4).
• The optimal angle for needle insertion varies using a left-sided approach but has been calculated to be
between 18 degree (at T12) and 19 degree (at L1).8
• Once the vertebral body has been contacted, the needle is advanced laterally until it slips off lateral
surface of the bone.
It helps to place a curve at the distal tip of the block needle so that it may be steered off the bone
without the requirement to actually withdraw it and reinsert it to bypass the lateral vertebral
margin.
Alternatively, avoiding bony contact altogether may reduce patient discomfort during performance
of CPB.9
• Once the needle passes through the psoas fascia, a distinct “pop” may be appreciated, although this is
by no means noted for every case. It is imperative to recall that the aorta will be found on the left of the
vertebral body (Figure 45-1) while the inferior vena cava will be on the right side.
• Once the needle(s) are in a satisfactory anatomical position, the next step is to perform some type of
contrast injection when CT or fluoroscopic imaging is being used.
When ultrasound is the selected imaging technique of choice, it is just as imperative to identify the
relevant vascular structures which identify the location of the celiac plexus, as the structure itself is
not likely to be visible even when using low-frequency curvilinear probes needed for their greater
depth of penetration for such a block.
• A water-soluble, iodine-based contrast agent is next injected, the volume of which is determined by a
real-time assessment of the spread of the agent.
• The present authors suggest using a volume commensurate with bilateral, para-aortic spread (under CT
guidance; Figures 45-6, 45-11, 45-16, 45-17).
• Importantly, the actual volume of local anesthetic used for the analgesic phase of the block should be
determined largely based upon how the contrast spreads, as it makes no sense to use predetermined or
“cook-book” volumes of solutions in disregard of the anatomical confines identified using the
aforementioned imaging modalities.10-12
Anterior Para-Aortic Approach2

• An anterior approach may be selected, especially for individuals who cannot or who will not be able
to lie prone. A common scenario of this nature would be someone who has recently undergone a
surgical procedure who has significant abdominal pain when assuming the prone position.
• Advantages to using the anterior approach include the ability to advance a single block needle from
anterior to posterior toward the abdominal aorta.
• Disadvantages include the requirement to insert that needle directly through the abdominal viscera as
the target of the block cannot be approached without doing so.
• The use of CT imaging (Figures 45-7 to 45-11) enhances an appreciation of the targeted and
nontargeted structures directly in the pathway of the advancing block needle.
After the usual skin disinfection and after the preparation of the patient as described above for the
posterior approach has been undertaken, a local anesthetic skin wheal is placed anterior to the T12
vertebral body as seen on imaging, followed by the insertion and advancement of a 20- or 22-gauge
12- or 18-cm spinal type needle (Quincke) directed toward the abdominal aorta.
• Contrast use as described above is then undertaken.
• Recent evidence suggest that a single-needle anterior CPB may not effectively spread contrast (and
neurolytic agent) into all four quadrants (upper right and left and lower right and left), which may also
affect the resultant analgesic response to neurolysis.2
Posterior Trans-Aortic Approach

• Occasionally during the performance of a posterior CPB, whether intentionally or unintentionally, the
abdominal aorta will be punctured (Figures 45-12 to 45-17).
• It is obviously much more likely that this situation will be identified when CT imaging is used than
when standard (nondigital subtraction angiography-DSA) imaging is undertaken.
• When the needle stylet is withdrawn under such circumstances, a few drops of bright red blood may be
identified at the hub of the needle, but seeking a “gush” of blood is typically pointless as this rarely
occurs. This is due to the characteristics of fluid flow in these longer, fine needles (20- and 22-gauge)
typically used for CPB as determined by the Hagen-Poiseuille equation which states that:
ΔP = 8 μLQ/πr4
where:
ΔP is the pressure drop from the aorta to the hub of the needle
L is the length of the block needle
μ is the dynamic viscosity of blood
Q is the volumetric flow rate
r is the radius of the nerve block needle
π is the mathematical constant 3.14
• If the vessel is penetrated, it is prudent to advance the needle until blood flow from the hub ceases.
• Under these circumstances, the procedure is then undertaken in a manner virtually identical to that
described above for posterior para-aortic CPB including the injection of contrast followed by a dilute
local anesthetic in concentrations sufficient to block the sympathetic nerves while sparing sensory and
motor nerves (ie, 0.2% ropivacaine, 0.25% bupivacaine, 1.0% lidocaine, for example).
ENDOSCOPIC TECHNIQUES13-22
Recently, interest has focused on using nonfluoroscopy and non-CT guided approaches to performing
CPB. Techniques have been described using endoscopic ultrasound equipment (EUS) to avoid radiation
exposure and are purported to reduce complications such as pneumothorax and paraplegia from the
posterior approaches.13 Some physicians believe that EUS should be considered first-line therapy in
patients suffering from pancreatic cancer who require CPB.13
• Endoscopic ultrasound approaches to CPB have been performed for at least the past 16 years.13
• A linear array ultrasound endoscope and a prototype needle-catheter were transgastrically positioned
to inject the plexus using bupivacaine and 98% dehydrated absolute alcohol in 30 patients. 88% of
patients had persistent improvement in pain scores and used less opioid analgesics at the 12-week
follow-up evaluation.14
• A prospective evaluation of the technique performed in 58 patients using the same approach with a 6-
month follow-up. 78% of patients had a reduction in pain scores associated with a reduction in
narcotic consumption. Only 5 episodes of abdominal pain and no major complications were
identified.15
• A meta-analysis of EUS-guided CPB to manage chronic abdominal pain associated with chronic
pancreatitis or pancreatic cancer reported that EUS-guided CPB was 51.46% effective in managing
chronic abdominal pain from pancreatitis but was 72.54% effective for managing the pain of pancreatic
cancer.16
• While the technique of EUS-guided CPB continues to evolve and mature,18 there is need for controlled
studies to compare this approach with alternative imaging techniques, as all the evidence is derived
from observational and uncontrolled case series.19
• EUS has been touted as being able to identify the actual celiac ganglia comprising the celiac plexus.
• It is as a hypoechoic, small, and either multilobulated or confluent series of small spheres with
hypoechoic bands of tissue.20
• Visualization of the ganglia is noted to be the single-most significant predictor of successful block.21
• Patients with visible ganglia are 15 times more likely to respond favorably than those wherein the
ganglia are not visible.21
• In one study comparing EUS with fluoroscopically-guided CPB using 10 mL of 0.25% bupivacaine and
40 mg of Triamcinolone, in patients suffering from chronic pancreatitis, 70% of EUS patients showed
an improvement in pain scores versus 30% in the fluoroscopy group.22 However, by the end of 24
weeks, almost all patients had returned to their baseline levels of pain.22
Complications occurred in 2% of patients, yet the studies included 32% of cases performed without the
benefit of any imaging whatsoever.4 When neurolytic CPB is performed for pancreatic cancer, it appears
that cancers of the head of the pancreas respond more favorably than those associated with lesions
elsewhere in the pancreas.23 Not only is neurolytic CPB favorable as an analgesic adjuvant in pancreatic
cancer pain, it may also elevate patient’s mood, reduce pain interference with activity, and possibly
increase life expectancy by some unknown mechanism.24
Monitoring of Potential Complications25-32

Nevertheless, it should be pointed out that there is the potential for severe and often grave consequences
of CPB which may occur even in the face of image-guidance and expertly performed procedures. Among
the known risks, the following have been reported25,26:
• Hypotension
• Paresthesias of lumbar somatic nerves
• Intravascular injection (arterial or venous)
• Lumbar somatic nerve root injury
• Subarachnoid or epidural injection
• Diarrhea
• Renal injury
• Paraplegia
• Pneumothorax
• Chylothorax
• Vascular thrombosis or embolism
• Vascular trauma
• Perforation of cysts and tumors
• Intradiscal injections and disciitis
• Injection into the psoas muscle
• Abscess
• Peritonitis
• Retroperitoneal hematoma
• Ureteral injury
• Ejaculation failure
• Pain both during or after the procedure
• Failure to derive an analgesic response

• Celiac plexus block is a valuable adjunctive therapy for managing abdominal pain associated with a
visceral pathology.
• Pain reduction is consistently demonstrated following successful block, and there is the potential for
reducing opioid consumption and opioid-related side effects and complications.
• Whether or not the implementation of neurolysis using this technique enhances or prolongs life
expectancy in terminal cancer, however, remains to be seen.
• A variety of imaging techniques and approaches to the plexus are available, each of which boasts some
advantage over the others.
• The clinician undertaking CPB should be well-versed in not only abdominal and retroperitoneal
anatomy, but also in the anatomy and physiology of spinal nerves and the spinal cord, and should be
prepared to deal with the many expected and occasionally unexpected sequelae following CPB.
• It should be appreciated that alternative therapies exist for treating the above-mentioned pain states
including the use of videothoracoscopic splanchnicectomy (VSPL). VSPL has been shown to be almost
as effective as neurolytic CPB in patients suffering from chronic pancreatitis pain.27 As pain is
commonly identified in pancreatic cancer patients (up to 70% of cases), perhaps the VSPL may be an
effective treatment modality employed for that disease as well.28
• For unresectable pancreatic cancer cases, neurolytic CPB reduces opioid consumption and opioid-
induced constipation in a majority of patients.29 One study, however, found little difference in opioid
consumption between neurolytic CPB, thoracoscopic splanchnicectomy, or patients receiving neither
treatment.30
• Clearly, this is an area worthy of additional analysis before final conclusions may be drawn.
• It is also clear that careful selection of appropriate candidates for block, in conjunction with technical
factors aimed at enhancing the specificity of blocks, may lead to improved outcomes for pain,
increased functionality, and reduction in opioid consumption.31
• A recent National Institutes of Health State-of-the-Science statement on Symptom Management in
Cancer highlighted the lack of properly designed comparative analgesic trials for cancer pain,
including those consisting of CPB patients.32
References
1. Arcidiacono PG, Calori G, Carrara S, McNicol E, Testoni P. Celiac Plexus block for pancreatic
cancer pain in adults (Review). Cochrane Database Syst Rev. 2011;3.CD007519:1-22.
2. DeCicco M, Matovic M, Bortolussi R, et al. Celiac plexus block: injectate spread and pain relief in
patients with regional anatomic distortions. Anesthesiology. 2001;94:561-565.
3. Yamamuro M, Kusaka K, Kato M, Takahashi M. Celiac plexus block in cancer pain management.
Tohoku J Exp Med. 2000;192:1-18.
4. Santosh D, Lakhtakia S, Gupta R, et al. Clinical trial: a randomized trial comparing fluoroscopy
guided percutaneous technique vs. endoscopic ultrasound guided technique of celiac plexus block for
treatment of pain in chronic pancreatitis. Aliment Pharmacol Ther. 2009;29:979-984.
5. Yang Y, Oraee S, Viejo C, Stern H. Computed tomography celiac trunk topography relating to celiac
plexus block. Reg Anes Pain Med. 2011;36:21-25.
6. Loukas M, Klaassen Z, Merbs W, Tubbs R, Bielecki J, Zurada A. A review of the thoracic splanchnic
nerves and celiac ganglia. Clin Anat. 2010;23:512-522.
7. Yang Y, Oraee S, Viejo C, Stern H. Transcrural celiac plexus block simulated on 200 computed
tomography images. Br J Anaesthesia. 2011;107:972-977.
8. Kim W, Lee C, Sim W, Shin B, Ahn H, Lim H. Anatomical analysis of computed tomography images
for determining the optimal oblique fluoroscope angle for percutaneous coeliac plexus block. J
International Med Res. 2011;39:1798-1807.
9. Yang I, Oraee S. A modified approach to transcrural celiac plexus block. Reg Anes Pain Med.
2005;30:303-307.
10. Busch E, Kay D, Branting S. Low volume neurolytic celiac plexus block with computed tomography
guidance. Anesthesiology. 2003;99:1243-1244.
11. Kambadakone A, Thabet A, Gervais D, Mueller P, Arellano R. CT-guided celiac plexus neurolysis: a
review of anatomy, indications, technique, and tips for successful treatment. RadioGraphics.
2011;31:1599-1621.
12. Wang P, Shang M, Qian Z, Shao C, Wang J, Zhao X. CT-guided percutaneous neurolytic celiac plexus
block technique. Abdom Imaging. 2006;31:710-718.
13. Michaels A, Draganov P. Endoscopic Ultrasonography guided celiac plexus neurolysis and celiac
plexus block in the management of pain due to pancreatic cancer and chronic pancreatitis. World J
Gastroenterol. 2007;13:3575-3580.
14. Wiersema M, Wiersema L. Endosonography-guided celiac plexus neurolysis. Gastro Endo.
1996;44:656-662.
15. Gunaratnam N, Sarma A, Norton I, Wiersema M. A prospective study of EUS-guided celiac plexus
neurolysis for pancreatic cancer pain. Gastro Endo. 2001;54:316-324.
16. Puli S, Reddy J, Bechtold M, Antillon M, Brugge W. EUS-guided celiac plexus neurolysis for pain
due to chronic pancreatitis or pancreatic cancer pain: a meta-analysis and systematic review. Dig Dis
Sci. 2009;54:2330-2337.
17. Kaufman M, Singh G, Das S, et al. Efficacy of endoscopic ultrasound-guided celiac plexus block and
celiac plexus neurolysis for managing abdominal pain associated with chronic pancreatitis and
pancreatic cancer. J Clin Gastroenterol. 2010;44:127-134.
18. Soweid A, Azar C. Endoscopic ultrasound-guided celiac plexus neurolysis. World J Gastrointest
Endosc. 2010;6: 228-231.
19. Sahai A, Wyse J. EUS-guided celiac plexus block for chronic pancreatitis: a placebo-controlled trial
should be the first priority. Gastro Endo. 2010;71:430.
20. Sakamoto H, Kitano M, Komaki T, Imai H, Kamata K, Kudo M. Endoscopic ultrasound-guided
neurolysis in pancreatic cancer. Pancreatology. 2011;11(suppl):52-58.
21. Ascunce G, Ribeiro A, Reis I, et al. EUS visualization and direct celiac ganglia neurolysis predicts
better pain relief in patients with pancreatic malignancy (with video). Gastro Endo. 2011;73:267-
274.
22. Eisenberg E, Carr D, Chalmers T. Neurolytic celiac plexus bock for treatment of cancer pain: a meta-
analysis. Reg Anes Pain Management. 1995;80:290-295.
23. Rykowski J, Hilgier M. Efficacy of neurolytic celiac plexus block in varying locations of pancreatic
cancer. Anesthesiology. 2000;92:347-354.
24. Staats P, Hekmat H, Sauter P, Lillemoe K. The effects of alcohol celiac plexus block, pain, and mood
on longevity in patients with unresectable pancreatic cancer: a double-blind, randomized, placebo-
controlled study. Pain Medicine. 2001;2:28-34.
25. Erdine S. Celiac Plexus block. Agri. 2005;17:14-22.
26. Carroll I. Celiac plexus block for visceral pain. Curr Pain Headache Report. 2006;10:20-25.
27. Basinski A, Stefaniak T, Vingerhoets A, et al. Effect of NCPB and VSPL on pain and quality of life in
chronic pancreatitis patients. World J Gastroenterol. 2005;11:5010-5014.
28. Adolph M, Benedetti C. Percutaneous-guided pain control: exploiting the neural basis of pain
sensation. Gastroenterol Clin N Am. 2006;35:167-188.
29. Yan B, Myers R. Neurolytic celiac plexus block for pain control in unresectable pancreatic cancer.
Am J Gastroenterol. 2007;102:430-438.
30. Johnson C, Berry D, Harris S, et al. An open randomized comparison of clinical effectiveness of
protocol-driven opioid analgesia, celiac plexus block or thoracoscopic splanchnicectomy for pain
management in patients with pancreatic and other abdominal malignancies. Pancreatology.
2009;9:755-763.
31. Erdek M, Halpert D, Gonzalez Fernandez M, Cohen S. Assessment of celiac plexus block and
neurolysis outcomes and technique in the management of refractory visceral cancer pain. Pain Med.
2010;11:92-100.
32. Wong G, Schroeder D, Carns P, et al. Effect of neurolytic celiac plexus block on pain relief, quality of
life, and survival in patients with unresectable pancreatic cancer. JAMA. 2004;291:1092-1099.
CHAPTER 46
Celiac Plexus Block Using Fluoroscopic

Guidance
Kenneth D. Candido, Peter S. Staats, Corey W. Hunter, and Sudhir Diwan
INDICATIONS
The celiac (coeliac) plexus (CP) is a group of 1 to 5 ganglia of varying sizes that are interconnected by a
dense mesh-like network of neural fibers, located in the upper abdomen, anterolateral to the aorta at the
level of the first lumbar vertebrae. The CP carries afferent innervation of the upper abdominal viscera,
from the distal esophagus and stomach to the mid-transverse colon, as well as the pancreas, kidneys, gall
bladder, adrenals, and portions of the small bowel. CP blocks are indicated for the diagnosis and
treatment of upper abdominal pain as it can be performed to help separate out visceral from somatic
pains, and can be used as a treatment for chronic cancer–related pain as well as non-cancer-related pain.
It is important to note that pain carried by somatic nerve fibers will not be affected when the CP is
blocked.
Local anesthetic blocks, with or without steroids and alcohol neurolytic blocks are all performed. The
literature is relatively clear that alcohol neurolysis is effective in reducing pain in patients with
pancreatic and other upper abdominal cancers as well as retroperitoneal structures. CP blocks can be
very effective when opiate therapy is causing significant side effects and can decrease the amount of
opiates necessary to control pain, improves mood, and may improve life expectancy.1 The role of alcohol
neurolysis in nonmalignant pancreatic pain is more controversial.
This is extremely successful in the treatment of upper abdominal cancer pain and should therefore be
considered early on in the treatment algorithm.2
The indications for a celiac plexus block include:
• Treatment of visceral, poor localizing, abdominal pain, with or without malignancy
• Diagnostic block to differentiate somatic versus visceral complaints
• Pancreatic adenocarcinoma3
• Cholangiocarcinoma3
• Abdominal visceral pain syndrome
• Upper abdominal malignancies2
• Retroperitoneal malignancies
• Hepatobiliary disorders, including biliary sphincteric disorder
• Abdominal angina
• Pancreatitis, acute or chronic
RELEVANT ANATOMY
• The innervation of visceral abdominal structures largely comes from the sympathetic terminals of T5-
T12.
• The preganglionic fibers leave the spine with the exiting nerve root and travel with the white
communicating rami to the level of the celiac ganglion.
• The greater splanchnic nerves (T5-T9) lesser splanchnic nerves (T10-T11) and least splanchnic nerves
(T11-T12) travel along the lateral border of the thoracic vertebral body and dive anterior to travel
through crus of the diaphragm to become the celiac ganglion.
• The greater, lesser, and least splanchnic nerves travel together to become the celiac plexus. The celiac
plexus lies anterior to the vertebral body at approximately T12 to L1, and usually lies near the takeoff
of the celiac and superior mesenteric artery, which can be visualized on a preoperative computerized
topography (CT) scan.
• The celiac plexus lies posterolaterally to the aorta at the level of the T12, L1 interspace on AP
orientation.
• It is important to note that in a minority of patients, the artery of Adamkiewicz can leave the aorta in the
low thoracic spine.
• The most important vertebrae to identify under fluoroscopic imaging are T12, L1, and L2.
Other relevant anatomy that should be taken into consideration when performing this injection is:
• Aorta
• Celiac and superior mesenteric arteries
• Anterior spinal artery (ie, the artery of Adamkiewicz)
• Adrenal glands and kidneys—located just lateral to the CP
• Diaphragm
• Renal arteries—inferiorly
• Exiting nerve roots of the lower thoracic and upper lumbar spinal cord

The well-documented efficacy of this procedure for the treatment of pain caused by upper abdominal
malignancy should direct the astute pain physician to consider this procedure early on. However, given
the vast array of possible comorbidities likely suffered by a patient that could potentially benefit from a
CP block, one must also consider added risk that would not typically be present in the average patient—
as well as the basic risks inherent to the injection, itself.
• Immunocompromised patients are potentially at high risk of infection, this is of particular relevance in
patients with malignancy.
• Patients with metastatic cancer pain may have local masses in the region.
• Patients may have thrombocytopenia secondary to chemotherapy.
• Prone position may be difficult if pain is too intense in the abdomen or if patient has abdominal
distension.
• Skin breakdown from radiation treatment.
• Hypotension in a cancer patient who may already be dehydrated and hypovolemic.
Contraindications include:
• Coagulopathy
• Neoplasm or metastasis obstructing or potentially obstructing the intended path of the needle
• Patient refusal
• Informed consent listing the risks and proposed benefits of the procedure.
• Discontinuation of anticoagulation prior to procedure.
• Physical examination of the area of intended skin entry for infection, skin ulceration, or necrosis.
• The patient will need IV access. Pretreat with 500 to 1000 cc of lactated ringers to minimize the risk of
symptomatic hypotension.
• Check for contrast allergies.
• Verify tumor anatomy.
• When alcohol is being considered for neurolysis and the patient is taking antabuse, it should be
discontinued before performing an alcohol neurolysis.
• The aid of an anesthesiologist or the ability to administer sedation as it can be quite painful.
Fluoroscopic Views
• Start with an anterior-posterior (AP) image of the lumbar and lower thoracic vertebra with T12 in
view and centered. The craniocaudal orientation of the C-arm should be adjusted to “square off” the
vertebral bodies. The skin inferior to the T12 rib on the left side approximately 5 to 7 in lateral to the
spinous process of L2 or even L3 is marked.
• Lateral view—when positioning the patient prone, the physician must take care to have the patient’s
arms place toward the head so as to prevent view obstruction when obtaining lateral images. This
view will allow for control of the depth and visualize the anterior advancement of the needle.
Equipment
• 22-gauge 7-in spinal needle—2 needles
• 20-cc syringe for alcohol if neurolysis is to be performed
• Connector tubing (extension)
Medications
• Omnipaque 240
• 1% lidocaine with epinephrine
• 0.25% or 0.5% bupivacaine
• Occasionally steroids are added for pancreatitis
• For neurolysis—10 to 20 cc 50% to 100% alcohol
Technique
Different techniques have been advocated in the performance of the celiac plexus block. All techniques
should use some type of advanced imaging in performance of the block. Fluoroscopic guidance, CT
guidance, and ultrasound guidance have demonstrated to be effective. Advocates of fluoroscopic guidance
point to dynamic imaging and the rapidity with which the procedure can be performed. CT guidance can
be done in the prone or supine position and can demonstrate aberrant anatomy and flow of contrast more
carefully. Ultrasound guidance is now being performed from a transesophageal approach, usually by the
gastroenterologist, and can be done at the time of an endoscopy. The superiority of one approach over
another has not been demonstrated.
We will describe here the classic retrocrural approach via fluoroscopy in the prone position using 2
needles.

• The arms are placed toward the head and out of view of lateral images.
• AP views of the lumbar and low thoracic spine are obtained.
• The skin inferior to the T12 rib on the left side approximately 5 in lateral to the spinous process of L2
or even L3 is marked. It is key that the needle is below the inferior rib of the T11 or T12 rib margin.
• The skin is then draped and prepared in a typical sterile fashion.
• The skin and deep structures are anesthetized with 1% lidocaine using the 25-gauge needle.
• A 7-in needle is advanced anterior to the aorta at the vertebral body and at the T12 L1 level taking an
angled approach (Figures 46-1 and 46-2).
Figure 46-1. Lateral fluoroscopic image demonstrating left-sided needle advancing approximately 1 in
anterior to the T12-L1 vertebral interspace for CPB. (Used with permission from Kenneth D. Candido,
MD.)
Figure 46-2. Lateral fluoroscopic image of CPB showing needle in place on the left side at T12-L1 with
initiation of contrast injection demonstrating para-aortic spread. (Used with permission from Kenneth D.
Candido, MD.)
• Initially the needle is placed from the left side and angled with intermittent fluoroscopic images to the
region about 1 in anterior to the vertebral body at the inferior pole of the T12 level (Figure 46-3).
Pulsations of the aorta can frequently be identified.
Figure 46-3. Anterior-posterior image of left-sided needle placed at T12-L1 for CPB. Initiation of
contrast injection. No vascular uptake noted. Needle is curved intentionally to assist in negotiating lateral
wall of the L1 vertebral body. (Used with permission from Kenneth D. Candido, MD.)
The patient should be followed into a postprocedural recovery area to ensure no immediate
complications result as well as by telephone the next day (Table 46-1). The patient should be advised to
call the pain service for any procedure-related complications and/or any unexpected neurological deficits
or other changes. The patient should be monitored closely for the following:
TABLE 46-1. A list of the potential symptoms one can experience after the procedure
and the most likely causes
• Abdominal cramping and/or diarrhea
• Dizziness
• Weakness
• Hematuria
• Shortness of breath
• Urinary or bowel incontinence
• Fever
• Bleeding
• Numbness

The majority of complications or adverse events that will take place postprocedurally are related to the
loss of sympathetic tone and now unopposed parasympathetic input.
• Orthostatic hypotension—leading potential complication which likely results from vasodilation to the
abdominal vasculature due to the loss of sympathetic tone. As mentioned above, pretreatment with a
fluid bolus of 500 to 1000 cc of lactated ringers is recommended.
• Diarrhea—this can result from the now unopposed parasympathetic innervation of the alimentary tract.
Cancer patients who are currently on opioids have a minimal risk.
• Intravascular injection—seizures can result from local anesthetics injected into the venous circulation.
Careful fluoroscopic monitoring and use of a test dose can minimize the risk.
• Injection into the kidney.
• Pneumothorax.
• Paralysis—spasm of the artery of Adamkiewicz injection of particulate matter or alcohol into a feeding
vessel of the cord, or direct spread of alcohol.
• Infection.
• Bleeding.
• Neurolytic injection into nerve roots.
• Nerve root injection (neuritis).
• Intravascular injection.
• Osteitis or periostitis.
• Hematoma.
CLINICAL PEARLS
• When performing celiac plexus neurolysis for pancreatic cancer, it is not necessary to perform a
separate diagnostic block and neurolytic block. When the needle is placed for the neurolytic block and
contrast demonstrates appropriate flow, use local anesthetics to assess pain relief. If after 3 to 5
minutes a patient has pain relief with the local anesthetic block, and they are able to move their lower
extremities, it is acceptable to proceed with the neurolytic block.
• Keep the patient prone for 15 minutes post procedure for a neurolysis. This allows the
neurodestructive agent to remain in the same position it is placed and minimizes the chance of aberrant
posterior spread.
• As one advances the needle toward the aorta via a retrocrural approach, both the pulsations of the
aorta and breathing patterns will be identified in the pulsations of the needle. This helps confirm that
the needle is approaching the appropriate plane.
• If patients have significant tumor spread or scar tissue in the area of the celiac plexus, consider a more
proximal splanchnic nerve block along the thoracic vertebral body.
• If pain recurs months after a neurolytic block, it is reasonable to repeat the block.
References
1. Staats PS, Hekmat H, Sauter P, Lillimoe K. The effects of alcohol celiac plexus block, pain, and mood
on longevity in patients with unresectable pancreatic cancer: a double-blind, randomized, placebo-
controlled study. Pain Medicine. 2001;2:28-34.
2. de Oliveira R, dos Reis MP, Prado WA, The effects of early or late neurolytic sympathetic plexus
blocks on the management of abdominal or pelvic cancer pain. Pain. 2004; 1110:400-408.
3. Fishman SM, Ballantyne JC, Rathmell JP. Bonica’s Management of Pain. 4th ed. Baltimore, MD:
Lippincott; 2010.
CHAPTER 47
Lumbar Sympathetic Block

Joshua P. Prager
SYMPATHETIC NERVE BLOCKS
Indications
Pain specialists use sympathetic nerve blocks for diagnostic, prognostic, prophylactic, and therapeutic
purposes (Table 47-1). Sympathetic nerve blocks have been used to:
TABLE 47-1. Neural Blockade as Part of Integrated Pain Management

Diagnostic blocks
• Determine source of chronic pain.
• Determine contribution of sympathetic nervous system to patient’s pain.
• Differentiate peripheral from central pain.
• Evaluate the patient’s reaction to treatment.
Prognostic blocks
• Allow patients to experience pain relief of the nerve block.
• Can predict the effect of spinal cord stimulation.
Prophylactic blocks
• Delay onset of postoperative pain.
• Prevent exacerbation of chronic pain syndromes, such as complex regional pain syndrome,
when trauma (such as surgery) is anticipated.
Therapeutic blocks
• Optimize short-term pain relief.
• Provide pain relief that permits more effective physical therapy and rehabilitation.
• Improve peripheral blood flow.
• Gain patient’s cooperation in addressing physiologic and psychologic aspects of pain.
• Diagnose sympathetically mediated pain

• Control pain during surgery
• Treat pain associated with complex regional pain syndrome (CRPS)
• Treat herpes zoster infections
• Treat Raynaud disease
• Treat phantom limb pain
• Treat scleroderma
• Treat cancer pain
Sympathetic nerve blocks are used routinely to provide short-term regional analgesia, and their efficacy
for this application is well established. Though the effect of local anesthetics can be prolonged by the
addition of epinephrine, any resulting analgesia eventually diminishes. Thus, even successful therapeutic
blockade is not curative. In the context of interdisciplinary pain management, however, sympathetic
blocks can be used to facilitate rehabilitation in patients with chronic noncancer pain.
Although the popularity of sympathetic blocks has generally decreased, mainly due to the scarcity of
evidence from randomized controlled trials, the procedure continues to be valuable in treating CRPS. An
interdisciplinary treatment protocol for CRPS, developed under the aegis of the International Association
for the Study of Pain, positions sympathetic blocks early to support physical rehabilitation (Figure 47-1).
If blockade is not sustained or progressively longer with each injection, sympathetic blockade should be
abandoned and a trial of spinal cord stimulation (SCS) initiated. Among the advantages of sympathetic
blocks and SCS are that both are minimally invasive and neither involves neuroablation.
Figure 47-1. Multidisciplinary care continuum for complex regional pain syndrome. This algorithm
was developed by the International Association for the Study of Pain for the multidisciplinary treatment of
complex regional pain syndrome. It emphasizes functional rehabilitation utilizing various forms of
progressive physical therapy, with adjuvant interventional pain management techniques, including
neuromodulation and behavioral therapy. (Adapted from Stanton-Hicks, et al. Pain Pract. 2002;2:1-16.)
• Sympathetically maintained pain requires a coupling of sympathetic noradrenergic neurons and primary
afferent neurons in the periphery of the body.
• The long-lasting pain relief achieved by temporary sympathetic blockade clearly implies that
sympathetic neurons, which are of central origin, maintain a positive feedback circuit through the
primary afferent neurons.
• A temporary block of the sympathetically mediated activity—lumbar sympathetic ganglia (anterior L2
and L3), for example—affects both the central state of hyperexcitability and the afferent neurons.
• Sympathetic blocks consist of injecting local anesthetic around the sympathetic paravertebral ganglia
that communicate with affected body part.
• The contribution of the sympathetic system to a patient’s pain can be determined by selectively
blocking autonomic pathways that are separate from somatic nerve fibers.
• Injection of local anesthetics near sympathetic ganglia is intended to disrupt pain transmission
temporarily and may reset sympathetic tone to a normal state.
• Tissue damage may also be minimized by the increase in peripheral blood flow that accompanies
sympathetic block.
• Pain relief or reduction following the procedure confirms that the patient’s acute or chronic pain was
sympathetically mediated.
• Decreased pain may allow inflamed tissues to heal and physical therapy or rehabilitation to commence.
• There is also some evidence that early sympathetic blocks may prevent development of CRPS.
Contraindications
Patients who should not receive a sympathetic block include those patients who:
• Cannot discontinue their anticoagulant medication
• Have a bleeding diathesis
• Have an active infection near the injection site
RELEVANT ANATOMY
Anatomy
• The lumbar sympathetic chain consists of 4 to 5 paired ganglia that are located over the anterolateral
surface of the second through fourth lumbar vertebra.
• Lumbar sympathetic ganglia are variable in number and location from one individual to another.
• The cell bodies that connect to the lumbar sympathetic ganglia lie in the anterolateral region of the
spinal cord from T11 to L2 and contributions vary from T10 to L3.
• The preganglionic fibers exit the spinal canal via the corresponding ventral spinal nerve root, and join
the sympathetic chain as white rami communicantes and then synapse within the corresponding
ganglion.
• Postganglionic fibers leave the chain to join the diffuse perivascular plexus around the femoral and
iliac arteries, via the grey rami communicantes to join the nerve roots that produce the lumbar and
lumbosacral plexuses.
• Sympathetic fibers associate with all major nerves to the lower extremities and produce the majority of
sympathetic innervation to the lower extremities.
• The largest portion of the lumbar sympathetic ganglia is located in the area of the lower second and
upper third lumbar vertebrae. Thus, blockade of these ganglia result in near complete sympathetic
block of the lower extremities.
• In the lumbar region, the two-bilateral sympathetic chains are connected segmentally to the spinal cord
by preganglionic neurons, whose cell bodies are situated in the lateral horn, intermediate nucleus, and
paracentral nuclei of the thoracolumbar spinal cord. These nerves are responsible for vasoconstriction
in the lower limbs.
• The preganglionic fibers travel as the white rami communicans, which communicate in the
paravertebral ganglia with postganglionic efferents and in the prevertebral ganglia by postganglionic
efferents leaving the sympathetic trunk as gray rami communicans.
• Each lumbar sympathetic chain enters the retroperitoneal space under the right and left crura,
continuing inferiorly between the anterolateral aspect of the vertebral bodies and the psoas muscle to
enter the pelvis.
• The sympathetic ganglia of the lumbar sympathetic chain are variable in numbers, size, and position.
Landmarks
The needle is placed 1 cm below the ipsilateral rib approximately 8 cm from the midline (depending on
body habitus). The needle is then directed to the anterolateral aspect of the body of L2 and then, after the
needle is withdrawn, to the body of L3.
Sympathetic blocks should be performed by experienced pain specialists, because diagnostic and
prognostic information can be lost if the block is not properly performed or evaluated. Requirements for
optimal results are listed in. The procedure should be performed where the patient can be adequately
monitored and managed should an adverse event occur (Table 47-2).
TABLE 47-2. Obtaining Optimal Results from Sympathetic Blocks

Physician requisites
• Thorough knowledge of pain syndromes and their pathophysiology, and of the range of
diagnostic and therapeutic measures available for each patient.
• Understanding of the risks and benefits of sympathetic blocks.
• Knowledge of anatomy, pharmacology of local anesthetics, expected results and possible
side effects.
Patient evaluation and communication
• Physicians must be willing to devote adequate time to the patient’s previous and current
history, physical and neurologic examination, and to continued pain assessment and
management.
• Should be conducted within the framework of a multidisciplinary pain program where
nerve block is not the only available option.
• Patients should understand that nerve block is not curative.
Requirements for diagnostic or prognostic blocks
• Target nerve should be identified with localized radiography. Contrast media should be
used to determine appropriate flow of the medication. Even with appropriate needle
placement, it is possible to move medication into the wrong tissue plane or intrasvascularly
(Figure 47-2K).
• Small volumes of local anesthetic should be used to avoid block of adjacent nerves.
• The duration of the block should be correlated with subjective pain relief.
• Sedation should be avoided when blocks are performed for diagnostic and prognostic
purposes, because the effects of sedation can confound the results.
Assessment by medical personnel
• Note patient’s reaction to initial needle insertion as indicator of personal pain threshold.
• Assess block with neurologic examination.
• Evaluate efficacy of block in relieving pain.
• Correlate duration of pain relief with duration of neural block.
• Accurately record results in patient’s record.
Limitations
• Nerve block is not a panacea.
• Results of a nerve block must be interpreted in the context of all of the diagnostic and
prognostic information available.
• Blocks represent only part of a multimodal rehabilitation or management program for
chronic pain.
Before performing a sympathetic block for noncancer pain, the physician should review the patient’s
previous and current history, perform a physical and neurologic examination, and discuss any prescription
and over-the-counter medications the patient is currently taking. This evaluation should be conducted in
the context of a multidisciplinary pain program, where nerve block is not the only available option, and
patients should understand that sympathetic block is not curative. The patient’s response to the block
should be carefully noted if it is being performed for diagnostic or prognostic reasons.
Fluoroscopic Views
Lateral, AP and anterolateral views are helpful in correctly positioning needles for injection.
For a lumbar sympathetic block, the patient is placed in the prone position.

Equipment includes:
• 18-gauge needle to use as radiological marker at L2
• Sterile towels
• Multiple 10-mL syringes with local anesthetic
• Sterile gloves
• Marking pen
• 6- to 7-in, 22- or 25-gauge spinal needles
• 3-mL syringe with 30-gauge needle to anesthetize skin
• 18-gauge introducer
• 5-mL syringe for contrast with extension tubing
Medications include:
• Lidocaine 1% with bicarbonate for skin
• 10 mL 0.25% bupivacaine per level
• Contrast (Isovue or Omnipaque)
If performing bilateral sympathetic blockade, it is essential to administer 500 to 1000 mL of normal
saline or lactated Ringer’s solution prior to the procedure to avoid hypotension or orthostatic hypotension
from the sympathetic blockade. It is also essential that vasopressors be available in the room and be
readily identified prior to starting the procedure, although they need not be opened because they are rarely
needed.

• For a lumbar sympathetic block, with the patient in the prone position, the body of L2 is
radiographically marked.
• Approximately 1 cm below the ipsilateral costal margin and about 8 cm from the midline (depending
on body habitus), the skin is infiltrated with short-acting local anesthetic with bicarbonate using a fine
needle.
• With the 2-needle technique, an introducer is placed and then a 6- to 7-in sharp spinal needle is
inserted through the introducer (Figure 47-2A).
Figure 47-2. Radiographic imaging of sympathetic blockade. (A) AP view of the radiographic marker
at L2 with placement of the needle at L3. (B) Lateral view of the needle at L3. (C) Lateral view of
injection of contrast media at L3. (D) AP view of contrast media at L3. (E) Lateral view of inadvertent
intravascular injection, lumbar sympathetic block, see text. (F) AP view of needle and radiographic
marker at L2. (G) AP view of radiographic marker and needle at L2 after contrast injection. (H) Lateral
view of contrast media at L2 before local anesthetic. Note contrast at L3 from prior injection. This view
should be utilized when first injecting contrast. (I) AP view of contrast media followed by local
anesthetic at L2. (J) Oblique needle placement. (Used with permission from Dr. Andrea Trescot.) (K) CT
view of needle placement. (Used with permission from Dr. Andrea Trescot.)
• The needle is then advanced to L2 or L3. In the lateral view (Figure 47-2B), after negative aspiration,
nonionic contrast solution is injected at L3 (Figure 47-2C, D).
• Special care should be exercised to avoid and detect immediately intravascular injection (Figure 47-
2E). In Figure 47-2E, the needle can be seen in the appropriate position and yet, even after negative
aspiration, almost all the contrast is seen intravascular. The flow extends into the spinal canal from
anterior to the spine. Care should be applied to ensure that injection of medication be avoided if
such intravascular flow is noted. Typically, 10 mL of local anesthetic is injected around the
anterolateral aspect of the L3 vertebral body under fluoroscopic guidance.
• The needle in this case is moved to L2 where it and the marker is again visualized (Figure 47-2F).
• Contrast media is injected at L2 (Figures 47-2G AP), Figure 47-2H in a lateral view with needle at L2
(note the contrast diluted with local anesthetic at L3 from the prior injection).
• Medication is injected following the contrast injection (Figure 47-2I). Injection at L2 generally blocks
the leg. For better results near the foot, a second block at L3 must be performed.
Alternative Technique
• Use ipsilateral oblique fluoroscopy view of the needle.
• The camera is obliqued until the transverse process is at the edge of the vertebral body (Figure 47-2J).
• The needle is then advanced to the target area.
• Both lateral and AP views should still be used to assure appropriate placement of the medication.
Pain relief can be measured by subjective means (visual analogue scale, quality of life measure), as well
as by assessing function and use of pain medication postprocedure.
• Pain relief: YES. The patient may be asked to move the painful body part shortly after injection.
• Increased temperature: YES. Temperature monitoring of the involved part should be performed before
and after the first block. Increased warmth or redness may be noticeable at first, but this effect usually
resolves within 4 to 18 hours.
• Motor or sensory deficit: NO. After a lumbar block, the legs should never feel weak or numb.

As with any invasive procedure, sympathetic nerve blocks carry some risks, but complications are rare
when the procedure is performed by an experienced physician and the patient is adequately monitored.
Patients should be monitored using the same protocol as for epidural anesthesia. Infection, hematoma,
vascular puncture, local anesthetic toxicity, nerve injury, and hypotension are possible complications.
Infection can be minimized by using strict aseptic technique and avoiding multiple needle punctures. The
risk of local anesthetic toxicity is greater with large volumes of long-lasting anesthetics than with smaller
volumes of shorter-acting medications. This is particularly true for older and frailer patients. Local
anesthetic should never be injected if a patient complains of pain or if resistance is felt during injection.
Hypotension can occur and may result from sympatholysis. This is unusual with unilateral block except in
the frail or intravascularly depleted patient.

Epidural Sympathetic Blockade
• Low-concentration continuous epidural infusions have been used in lieu of pure lumbar sympathetic
blockade in CRPS to facilitate physical therapy. Although more popular in the past, this technique is
still commonly used.
• An advantage of this approach is that it obviates the need for frequent repeat injections.
• Disadvantages include diminished normal sensation, including proprioception, which can hamper or
render unsafe some aspects of physical therapy.
• Spinal cord stimulation can diminish sympathetically-mediated pain without disturbing normal
sensation.
• Historically, there was belief that sympathetic fibers could be selectively blocked in the epidural space
by using low concentrations of local anesthetic. This belief was based on the concept that sympathetic
fibers are nonmyelinated and small, and therefore, more likely to be affected differentially by local
anesthetic before other nerve fibers. There are no data to verify this belief.
• Single-shot epidural sympathetic blockade should never be used diagnostically or prognostically.
• Low concentration of local anesthetic will inevitably block normal sensory fibers and it will not be
possible to determine whether the pain is sympathetically mediated using epidural technique.
Lumbar Sympathetic Neurolysis

Destruction of the lumbar sympathetic chain (lumbar sympathectomy), chemically, surgically or by radio
frequency is likely to have excellent short-term success if pure lumbar sympathetic blockade has been
successful but of insufficient duration. Meta-analysis by Furlan et al suggests that long-term risks are
potentially significant, and that informed consent for such procedures should include discussion of
persistent neuropathic pain, among other sequelae, as a consequence.
Some physicians perform lumbar sympathetic block at L3 and L4 rather than at L2 and L3. This often
spares the leg from sympathetic blockade despite good results at the foot.
Suggested Reading
Boswell MV, Trescot AM, Datta S, et al. Interventional techniques: evidenced-based practice guidelines
in the management of chronic spinal pain. Pain Physician. 2007;10:7-111.
Cepeda MS, Carr DB, Lau J. Local anaesthetic sympathetic blockade for complex regional pain
syndrome. Cochrane Systematic Rev. 2005:4:art. no. CD004598.
Furlan AD, Lui PW, Mailis A. Chemical sympathectomy for neuropathic pain: does it work? Case report
and systematic literature review. Clin J Pain. 2001;17(4):327-336.
Prager J, Aprill C. Complications related to sedation and anesthesia for interventional pain therapies.
Pain Med. 2008;9(S1):S121-S127.
Stanton-Hicks MD, Burton AW, Bruehl SP, et al. An updated interdisciplinary clinical pathway for
CRPS: report of an expert panel. Pain Pract. 2002;2:1-16.
CHAPTER 48
Superior and Inferior Hypogastric Plexus Blocks

Agnes Stogicza
INTRODUCTION
The hypogastric plexus is the extension of the aortic plexus in the retroperitoneal space, below the aortic
bifurcation. The upper part, the superior hypogastric plexus, is located anterior to the L5 vertebral body
and the sacral promontory, whereas the inferior hypogastric plexus lies within the bilateral presacral
tissues on either side of the rectum at S2, S3, and S4 levels. Pain from the lower abdominal as well as the
pelvic and perineal area is transmitted through the hypogastric plexus.
Chronic noncancer and cancer pain of the pelvic structures are often challenging to treat and
interventional approaches may well be invaluable tools. Plancarte et al described the superior
hypogastric block in 1990, and found that sympathetically mediated pain was significantly reduced or
eliminated in all cases without serious complications. Although this injection was originally developed
for the treatment of pelvic cancer pain, as with many procedures originally limited to the terminal cancer
patient in pain, these techniques are now commonly used in the nonmalignant pain. Patients have
frequently failed to respond to less invasive procedures, such as lumbar or caudal epidural injections.
INDICATIONS
The indications for performing the two types of blocks have some overlap. A diagnostic block of the
hypogastric plexus with local anesthetic if positive can be followed by a neurolytic procedure, which
could potentially provide long-term relief.
The superior hypogastric plexus block is indicated for chronic intractable lower abdominal and/or
pelvic pain:
• Gynecologic disorders like endometriosis, pelvic inflammatory disease, and pelvic adhesions
• Nongynecologic disorders like interstitial cystitis, irritable bowel syndrome
• Sympathetically maintained pelvic pain (pelvic CRPS)
• Pain secondary to neoplasm in the pelvic area
The inferior hypogastric plexus block is indicated for chronic intractable lower abdominal and/or
pelvic pain:
• Sacral or perineal pain
• Bladder conditions
• Penile pain
• Prostatitis
• Vaginal pain/vulvodynia
• Rectal/anal pain
• Irradiation-induced tenesmus
• Perineal, sacral, and lower pelvic pain caused by malignant causes
• Sympathetically maintained pelvic pain (pelvic CRPS)
• Lower pelvic endometriosis
• Acute herpes zoster
• Postherpetic neuralgia of the sacral area
CONTRAINDICATIONS
• Infection (systemic or localized)
• Coagulopathy
• Patient refusal
Other Considerations
The risks and potential contraindications need to be weighed carefully when performed in patients with
cancer pain and noncancer pain.
• Although this injection is performed outside the neuroaxis, there are large blood vessels (iliac arteries
and vein) in close proximity, and therefore an adequate coagulation status is warranted.
• In the same way, injections into or through an area of infection should be avoided.
• Psychological status in cancer pain patient appears to be less of an issue, as long as the patient or
health care surrogate is capable of providing informed consent.
• However, for the nonmalignant pain patient, because of the dramatic psychological overlay often seen
in patients who suffer from chronic pelvic pain, including a history of medication abuse and altered
self image, it is probably prudent to rule out major psychiatric disorders prior to performing this
advanced procedure.
• Immunocompromised patients are potentially at high risk for infection.
• Patients with cancer may have local masses in the region.
• Anticoagulation is a concern because of the amount of tissue penetrated and also the vicinity of major
blood vessels.
• Aspirin alone is considered safe, but the combination of aspirin with other antiplatelet therapies may
increase the risk of bleeding and hematoma.
• Patients must be able to lie prone for the intended length of the procedure which may be difficult with
pain and abdominal distension.
RELEVANT ANATOMY
The superior and inferior hypogastric plexuses innervate the lower pelvic viscera including the distal end
of the alimental canal, bladder, ureters, prostate, penis, ovaries, uterus, and vagina.
Superior hypogastric plexus
• It is the extension of the celiac, then aortic plexus in a caudad direction, below the aortic
bifurcation.
• It receives fibers from the aortic plexus, as well as contributions from L3 and L4 splanchnic nerves.
• It is situated on the ventral aspect of the L5-S1 and on the disc between L5 and S1.
• The superior hypogastric plexus is close to the sympathetic chain at this level, the common and
internal iliac arteries and veins on each side.
• The ureter is located just lateral to the structures in close proximity to the anterolateral aspect of the
L5 vertebral body.
• As the aorta is shifted more toward the left, the superior hypogastric plexus and hypogastric nerves
are located somewhat to the left as well.
• Descending into the pelvis it bifurcates as the right and left hypogastric nerves. These “nerves”
aren’t really what is traditionally thought of as a nerve, they are more like meshwork than solid
nerve trunks.
• These nerve meshwork diverge lateral to the rectum on both side and curve outward and backward
as they make their way down into the pelvis. They interconnect the superior and inferior hypogastric
plexuses, contain no ganglia.
Inferior hypogastric plexus
• It is found by following the superior hypogastric plexus and hypogastric nerves in caudad direction
as a network of nerves within the connective tissue around the rectum.
• Extensions of inferior hypogastric plexus, which include the medial rectal and vesical plexuses,
continue along the branches of the internal iliac artery to innervate autonomic effector of the pelvis
(Figure 48-1).
Figure 48-1. Illustration of the superior and inferior hypogastric plexus with relation to nearby
anatomical structures on the left. (From Schultz DM. Inferior hypogastric plexus blockade: a transsacral
approach. Pain Physician. 2007 Nov;10(6):757-763.)
The key to successfully locating the superior hypogastric plexus lies in identifying the following:
• Iliac crest
• Sacral ala
• L4 and L5 vertebral body and transverse processes
• L5-S1 disc
• Assessing the depth from the skin to the anterior portion of L5
• Iliac arteries and veins
• Ureters at the lateral aspects of L5 vertebral body
• L5 nerve root
The key to successfully locating the inferior hypogastric plexus lies in identifying the following:
• S2 or S3 neural foramina, both posterior and anterior openings
• Anterior surface of the sacrum
• Iliac arteries and veins
• S1-S4 exiting nerve roots
• Rectum is separated from the anterior surface of the sacrum by a layer of extraperitoneal fat and other
connective tissues.
Preoperative considerations like in all sympathetic blocks, attention should be paid to the potential for
sympathetic lysis of vasoconstriction, contributing to hypotension. In addition, review of the CT or MRI
performed is mandatory, paying close attention to any abnormal structures present anterior to the sacral
promontory or sacral concavity. As there is a significant amount of tissue which the needle must go
through, this procedure can be uncomfortable. There is also a significant risk of paresthesia, either at the
L5 nerve root for the superior hypogastric block or sacral nerve roots for the inferior hypogastric
block.
Preparation of the Patient

• Physical examination of the area for infection, skin ulceration or necrosis, and extent of disease.
• Intravenous access for IV fluid and medications for sedation or hypotension caused by sympathectomy
or vasovagal reaction.
• Evaluation for contrast allergy—this is of the utmost importance as the utilization of contrast will
allow for precise needle placement just anterior to the promontory or the anterior sacral surface.
Documentation for Off-Label Indications

As noted above, this technique was developed for patients with intractable cancer pain, and was often
performed with neurolytic agents, with or without a preceding diagnostic block. However, it has recently
shown promise as a diagnostic and potentially therapeutic technique for patients with chronic intractable
pelvic pain, including interstitial cystitis and chronic pain caused by prostatitis. Although technically
potentially difficult to perform, the procedure itself has relatively few risks, and therefore may provide
benefit to a larger group of patients. However, as with all procedures for nonmalignant pain, conservative
therapies including medication, psychological interventions, and more standard interventions such as
epidurals should be tried first.
Superior Hypogastric Plexus Block

Medication
• 1% lidocaine
• Iohexol 180 (nonionic water-soluble contrast)
Although some authors recommend the use of steroids in sympathetic blocks, there appears to be a little
evidence to support this.
Equipment
Technique
Various techniques have been described for needle passage to gain access to the superior hypogastric
plexus: lateral approach, transdiscal approach, and anterior approach (Figure 48-2).
Figure 48-2. Superior hypogastric plexus block. Lateral approach, skin entry at L4 level (red needle),
lateral approach, skin entry at L5 level (blue needle), transdiscal approach (green needle), and the
anterior approach (orange needle). (Used with permission from Dr. Agnes Stogicza.)
Lateral Approach
Patient Position
Patient is positioned in the prone position with a pillow under the abdomen to decrease the lumbar
lordosis.
Fluoroscopic Views
This procedure, unlike most of our other interventional techniques, does not necessarily benefit from an
oblique view. The use of three-dimensional imaging helps the clinician to better visualize the eventual
needle location.
• Start with anteroposterior image of the lumbosacral area, centered on L5 vertebral body. Note the L5
transverse process, the sacral ala and iliac crest, as the needle has to be advanced anteriorly at the
bone-free space. A cephalad tilt of the C-arm is likely to increase the visibly bone-free area.
• Lateral view allows the physician to control the depth of the needle tip as it advances anteriorly past
the anterior surface of the L5-S1 disc. This is also the view in which contrast will be injected to verify
the position of the tip.
• After the L5 vertebral body endplates optimized, an imaginary line is drawn from the tip of the
transverse process of L4 or L5 inferiorly to the midline S1 spinous process. The decision to use a
higher (L4) or lower (L5) entry site is dictated by the height of the iliac crests.
• After sterile prep and drape, lidocaine is infiltrated subcutaneously lateral to the transverse process,
and the spinal needle is directed anteriorly and inferiorly toward the midline S1 sacral promontory.
• Care must be taken around the L5 nerve root, since the path of the needle may pass close to the root
itself, so the patient should be warned about possible paresthesias.
• If the vertebral body is encountered, the needle needs to be withdrawn and repositioned more
anteriorly.
• Once the needle is placed, the position is confirmed by injection of a small amount of contrast with
firm location anterior to the promontory and to also confirm the lack of vascular uptake (Figures 48-3
and 48-4).
Figure 48-3. Superior hypogastric plexus block. Lateral approach: needles are in the final position.
Contrast spreads anterior to L5 vertebral body and the promontorium. Lateral view (A), anteroposterior
view (B). Contrast spreads more laterally and then, ideal, bilaterally. (Used with permission from Dr.
Agnes Stogicza.)
Figure 48-4. Superior hypogastric plexus block, lateral approach, 3D reconstruction. The image was
taken with ALLURA Xper FD 20 Phillips. Final needle position and contrast show contrast spread
anterolateral to the L5 vertebral body, L5-S1 disc and promontorium. Needles pass between the sacral ala
and L5 transverse process. (Used with permission from Dr. Agnes Stogicza.)
• Although the optimum amount of local anesthetic has not been defined, 6 to 8 cc of local anesthetic on
each side appears to usually adequately cover the sacral promontory. Using short-acting local
anesthetic first, and if the patient notes relief on the table but no complication, following with the
bupivacaine is a safe and efficient approach.
• Needle is removed, and the area is covered with a Band-Aid.
Because it is relatively difficult to get contrast truly midline with this approach, the procedure almost
always has to be repeated on the contralateral side so that medication will flow bilaterally.
Transdiscal Approach
Patient Position
Patient is positioned in the prone position with a pillow under the abdomen to decrease the lumbar
lordosis.
Fluoroscopic Views
• The fluoroscopic image should be centered on the L5 vertebra in anteroposterior view, then the C-arm
rotated cephalad until the end plates at L5-S1 are as sharp as possible.
• The C-arm is then obliqued slightly toward the ipsilateral side in order to position the superior
articular process into the distal one-third of the disc.
• After sterile prep and drape and local anesthetic infiltration subcutaneously, the needle is introduced in
a “down the barrel” view, taking care to direct the needle laterally instead of medially to avoid
entering the nucleus pulposus. As the annulus is expected to be difficult to inject and the prevertebral
tissue easy to inject, Trescot recommends a loss of resistance technique utilizing saline, lidocaine, or
contrast.
• Verify needle position in a lateral view. The tip of the needle should be slightly anterior to either the
L5 body, L5-S1 disc, or promontory.
• Contrast should also spread at L5-S1 area, retroperitoneally (Figures 48-5 and 48-6).
Figure 48-5. Superior hypogastric plexus block, transdiscal approach, needles are in the final position.
Contrast spreads anterior to L5 vertebral body and the promontorium. Lateral view (A), anteroposterior
view (B). (Used with permission from Dr. Agnes Stogicza.)
Figure 48-6. Superior hypogastric plexus block, transdiscal approach. 3D reconstruction, oblique view
(A) and transsection (B). Final needle position and contrast spread anterior to the L5 vertebral body, L5-
S1 disc and promontorium. Needles pass between the sacral ala and L5 transverse process. The image
was taken with ALLURA Xper FD 20 Phillips. (Used with permission from Dr. Andrea Trescot.)
• 6 to 8 mL of bupivacaine 0.25 % is injected on each side after negative aspiration.

Since the needle is placed more medially, the local anesthetic often passes bilaterally, obviating the need
for a second needle placement (Figure 48-7). This technique has the distinct advantage of being very
familiar to those who have performed discograms, and perhaps avoids some of the risk of paresthesia.
However, because the needle passes through the disc, there is a theoretical risk of discitis. The patient
should probably receive IV antibiotics before the procedure and certainly should be advised of the
potential risk of discitis. In my experience, this procedure has been significantly less traumatic for
patients who have undergone aforementioned standard techniques.
Figure 48-7. Superior hypogastric plexus block, transdiscal approach, single needle technique. Contrast
spreads anterior to L5-S1 disc in the midline. Lateral view (A), anteroposterior view (B). (Used with
permission from Dr. Agnes Stogicza.)
Anterior Approach
Patient Position
Patient is placed in supine position with pressure points protected.
Fluoroscopic Views
• Using an AP view the L5 vertebral body is identified.
• The tunnel view can be utilized to guide the needle until bony contact on L5.
• Lateral view is used to verify the needle tip placed on either L5 vertebral body or L5-S1 disc.
• After sterile prep and drape lidocaine is infiltrated subcutaneously about 5 cm below the umbilicus.
• A 22-gauge 3.5-in needle is advanced until bony contact.
• Contrast is injected to verify medication spread.
• 10 to 15 cc of 0.25% bupivacaine is injected through the needle.
Even though this approach might be the easiest of all, it is rarely utilized because of the potentially
increased risk of infection.
Inferior Hypogastric Plexus Block

Equipment
Medications
• 1% lidocaine
• Iohexol 180 (nonionic water soluble contrast)
Although some authors recommend the use of steroids in sympathetic blocks, there appears to be a little
evidence to support it.
Fluoroscopic Views
• Start with anterior-posterior image of the sacrum and identify the sacral foramina. Choose the foramen
that is most easily visible. This block can be performed through S2, S3. Cephalo-caudad and
ipsilateral rotation is likely to optimize foraminal view.
• Lateral view allows the physician to control the depth of the needle tip as it advances anteriorly past
the anterior surface of the sacrum.
This is also the view in which contrast will be injected to verify the position of the tip
Technique
The inferior hypogastric plexus block was first described by Schultz in the journal Pain Physician.
Utilizing the ability to fluoroscopically line up the foramen between the posterior and anterior sides,
Schultz recommends finding the most visible foramen (usually S2 or S3, and slightly obliquing the C-arm
ipsilaterally to optimize superimposing the posterior and anterior foramen).
• After sterile prep, drape, and local anesthetic infiltration of the subcutaneous tissues, a 25-gauge 5-in
needle is utilized.
• The needle is passed through the posterior tissues onto the lateral edge of the posterior foramen and
then walked anteriorly.
• Switching to a lateral view, the needle is advanced just anterior to the anterior sacral plate.
• Contrast shows a thin layer, hugging the anterior border of the sacrum area (Figure 48-8).
Figure 48-8. Inferior hypogastric plexus block. Schematic picture (upper): needle is in the S3 foramen.
Lateral view (left): needle is in final position; contrast spreads at the anterior surface of the sacrum.
Anteroposterior view (right): needle is passing through the S3 foramen, toward medial to the anterior
surface of the sacrum. (Used with permission from Dr. Agnes Stogicza.)
• Then 5-cc of local anesthetic, first lidocaine, followed by bupivacaine 5 cc, is injected to anesthetize
the inferior sacral plexus.
Because these are sympathetic blocks, there is a potential for vascular dilation leading to hypotension.
There is also at least a theoretical risk of increasing gastrointestinal motility in the lower abdominal
region, leading to the potential for diarrhea. The patient should be counseled to monitor pain relief,
ideally with a pain diary to confirm the diagnostic aspects and also the therapeutic effects. Patient
education about the signs and symptoms of infection or bleeding is necessary.
Monitoring Potential Complications

During the procedure, blood pressure, heart rate, and Sao2 are monitored for potential epidural or
intravascular injection, allergy, or bleeding caused by complications.
Postprocedure complications include bleeding (which would be expected immediately after the
procedure), acute and late infections, and, for the inferior hypogastric, local anesthetic bathing of the
lower extremity nerves, leading to weakness and difficulty walking. There is at least a theoretical risk of
loss of sensation of the bladder and bowel that would normally trigger the urge to urinate or defecate, and
therefore the patient should be counseled to attempt to urinate and defecate on a regular schedule.

• Performing a superior hypogastric block from a lateral approach, starting first at the L4 transverse
process especially in males with high riding iliac crests, will provide the most straightforward
injection with a low risk of L5 paresthesia. The temptation to start low should be avoided (Figure 48-
9).
Figure 48-9. Skin entry points for superior hypogastric block, lateral approach. The red dot corresponds
to the L5 and the blue dot corresponds to the L4 transverse process. In this male patient, with high riding
iliac crest the recommended entry level is L4. (Reproduced with permission from Schultz DM. Inferior
hypogastric plexus blockade: a transsacral approach. Pain Physician 2007: 10:757-63.)
• The transdiscal approach, though associated with the potential for discitis, may well prove to be the
easiest on the patient and therefore the easiest on the operator, because it is a familiar view. It has
proven to be the easiest approach to teach; after one attempt on a cadaver, almost all participants are
able to place the needles appropriately.
• The injections can be diagnostic as well as therapeutic. The patients with positive diagnostic injections
are generally candidates for neurolysis by phenol or alcohol.
• The superior hypogastric block does not necessarily cover the areas innervated by the inferior
hypogastric plexus.
• Most studies report no or only transient complications, and complications mostly arise from the wrong
needle placement and injection:
Transient paresthesia is the most common complication.
Rectal puncture is easily avoided with using lateral views with the fluoroscope.
The most vulnerable structures are at the iliac artery and vein, so although it increases costs, using a
blunt needle for the superior hypogastric plexus block is reasonable and might minimize risks and
complications.
Suggested Reading
Erdine S, Yucel A, Celik M, Talu GK. Transdiscal approach for hypogastric plexus block. Reg Anesth
Pain Med. 2003 Jul-Aug;28(4):304-308.
Gamal G, Helaly M, Labib YM. Superior hypogastric block: transdiscal versus classic posterior
approach in pelvic cancer pain. Clin J Pain. 2006 Jul-Aug;22(6):544-547.
Gregory D Cramer, Susan A Darby. Basic and Clinical Anatomy of the Spine, Spinal Cord and ANS.
1995.
Kitoh T, Tanaka S, Ono K, Ohfusa Y, Ina H, Otagiri TJ. Combined neurolytic block of celiac, inferior
mesenteric, and superior hypogastric plexuses for incapacitating abdominal and/or pelvic cancer pain.
Anesthesiology. 2005;19(4):328-332.
Laxmaiah M, Vijay S. Interventional Techniques in Chronic Non-Spinal Pain. ASIPP Publishing; 2009.
P. Prithvi Raj, Leland Lou, Serdar Erdine, Peter S Staats. Radiographic Imaging for Regional
Anesthesia and Pain Management. Elsevier Sciences; 2003.
Plancarte R, Amescua C, Patt RB, Aldrete JA. Superior hypogastric plexus block for pelvic cancer pain.
Anesthesiology. 1990 Aug;73(2):236-239.
Plancarte R, de Leon-Casasola OA, El-Helaly M, Allende S, Lema MJ. Neurolytic superior hypogastric
plexus block for chronic pelvic pain associated with cancer. Reg Anesth. 1997 Nov-Dec;22(6):562-
568.
Schultz DM. Inferior hypogastric plexus blockade: a transsacral approach. Pain Physician. 2007
Nov;10(6):757-763.
CHAPTER 49
Ganglion Impar Block

Corey W. Hunter and Sudhir Diwan
INDICATIONS
The ganglion impar, also known as the ganglion of Walther or sacrococcygeal ganglion is a singular
retroperitoneal structure located at the level of the sacrococcygeal junction (SCJ). It is of particular
importance when considering patients who suffer from pain in the pelvic and perineal structures as it
provides nociceptive and sympathetic supply to those regions. It receives afferent innervation from the
perineum, distal rectum, anus, distal urethra, and distal vagina. Plancarte et al first reported the successful
relief of perineal pain through the blockade of the ganglion impar in 1990.1 The initial approach as
offered by Plancarte involved a bent spinal needle. Through the years, techniques have evolved with the
use of fluoroscopy, computed tomography (CT), and ultrasound, and the utility for its potential relief of
patient remains relatively unquestioned.
The indications for blockade based on anatomical location of pain include:
1. Perineal pain, with or without malignancy
2. Rectal/Anal pain (proctitis)
3. Distal urethral pain
4. Vulvodynia
5. Scrotal pain
6. Female pelvic/vaginal pain (distal 1/3)
7. Sympathetically-maintained pain to the region (ie, Complex Regional Pain Syndrome)
8. Endometriosis
9. Chronic prostatitis
10. Proctalgia Fugax
11. Coccygodynia2
12. Radiation proctitis3
13. Postherpetic neuralgia4
14. Burning and localized perineal pain associated with urgency
RELEVANT ANATOMY
Each sympathetic trunk in the pelvic area is positioned anterior to the sacrum, situated medially to the
anterior sacral foramina. There are 4 or 5 small sacral ganglia with the ganglion impar being the most
caudal segment of the confluence of the sacral sympathetic chain as it passes anteromedially over the
sacrum. More specifically, the ganglion Impar is the terminal fusion of the 2 sacral sympathetic chains and
is located with some anatomical variability between the SCJ and the lower segment of the first coccyx.
The fusion of the 2 chains typically positions the ganglion midline, which makes it relatively easy to find
(Figure 49-1). However, there is a wide range of variability in the anatomical location with respect to the
SCJ (Figure 49-2).5
Figure 49-1. Illustration of the ganglion Impar with relation to nearby anatomical structures on the left.
The illustration on the right represents the path and trajectory of the needle through the sacrococcygeal
disc at the SCJ to the ganglion impar.
Figure 49-2. Illustration of variable locations of the ganglion Impar with respect to the SCJ and the
coccyx as reported by Chang-seok et al. Distances of the ganglion impar were measured using a digital
caliper and a relative index was calculated. The percentages at each respective index are reported
above.5
The key to successfully locating the ganglion Impar lies in identifying the following structures:
1. Sacral hiatus
2. Coccyx
3. SCJ
4. The 4 bilateral sacral foramina—for correct assessment of anteroposterior image under fluoroscopy
5. Sacral and coccygeal cornua—manually palpated to assess the surface anatomy and compared with the
image
1. Rectum—this is separated from the ganglion by a layer of extraperitoneal fat and connective tissue
2. Exiting nerve roots from the sacral foramen
3. Coccygeal nerve traveling within the sacral canal
4. Erector spinae muscles
5. Sacral canal
6. Lateral and posterior sacrococcygeal ligaments—that can produce resistance while advancing the
needle if calcified

As with any intervention, one must weigh the potential benefits to the potential complications. In the
average patient, and given the relatively less invasive nature of the technique described here, a blockade
of the ganglion Impar should be considered early on in the treatment algorithm in the properly indicated
patient. However, given the wide array of pathological conditions that could benefit from this injection
and the associated pathophysiology, one must carefully consider each patient individually. For example, a
patient suffering from radiation proctitis may have skin breakdown in the area, which might contraindicate
injection.
Some basic concerns for injection are:
• Immunocompromized patients are potentially at high risk for infection, this is of particular relevance in
patient with malignancy.
• Patients with allodynia could benefit from this injection may also have pain in the very area of the
injection which could complicate the ability of one to tolerate the procedure.
• Prone position may be difficult if patient has abdominal distension.
• Possible rectal perforation may occur if the needle is advanced too far anteriorly.
• Coagulopathy
• Rectal fistula in proximity of ganglion (Figure 49-3)
Figure 49-3. Fluoroscopic image demonstrating contrast spreading through a fistula into the rectum.
• Patient refusal
1. Informed consent and proper explanation of all potential complications
2. Anti-coagulation—this is less of a concern than for an epidural injection but a concern nonetheless as
there is inherent disruption of tissue from the introduction of a needle
3. Physical examination of the area for infection, skin ulceration or necrosis, and extent of disease
4. Patient must be able to lie prone for the intended length of the procedure.
5. Intravenous access for IV fluid and medications for sedation or hypotension if the patient experiences
vasovagal reaction
6. Evaluation for contrast allergy—this is of the utmost importance as the utilization of contrast will allow
for precise needle placement just anterior to the SCJ
Fluoroscopic Views
1. Start with anterior-posterior (AP) image of the sacrum with the coccyx in view. A slight caudal tilt
will allow for proper visualization of the SCJ given the curvature of the sacrum and coccyx.
Diligently mark the middle of SCJ to insure a midline approach, making sure the sacral foramina are
equidistant from the spinous processes of the sacrum (Figure 49-4).
Figure 49-4. Image on the left demonstrates the initial positioning of the C-arm over the patient for an AP
view. The image on the right is the corresponding fluoroscopic view in AP.
2. Lateral view: This is most important view. It allows the physician to control the depth of the needle
tip as it advances anteriorly past the disc of the SCJ. This is also the view in which contrast will be
injected to verify the position of the tip (Figure 49-5).
Figure 49-5. Image on the left demonstrates the C-arm positioned about the patient for a lateral view. The
image on the right is the corresponding fluoroscopic view.
EQUIPMENT
1. 22-gauge 3.5-in spinal needle
2. 25-gauge 1.5-in needle
3. 3-cc syringe for local anesthetic
4. 5-cc syringe for contrast
5. 10-cc syringe for medications
6. Connector tubing (extension)
MEDICATIONS
1. 1% lidocaine
2. 0.25% or 0.5% bupivacaine
3. Iohexol 180 (nonionic water-soluble contrast)
4. Triamcinolone or Methylprednisolone
Technique
Varying techniques have been described for needle passage to gain access to the ganglion Impar.
• Anococcygeal approach with single-bent needle
• Anococcygeal approach with curved needle
• Trans-sacrococcygeal approach
• Coccygeal (transdiscal) joint approach
• Paramedian approach with double-bent needle
• Sub-transverse process of coccyx approach
• Needle-in-catheter technique for Cryoneurolysis
• Two needles approach for radiofrequency neurolysis
As previously mentioned, Plancarte pioneered the initial anococcygeal approach by utilizing a curved
needle that makes initial contact with the skin between the anus and coccyx and directing the needle
anteriorly between the coccyx and rectum.1 In using this approach, there is inherently a greater risk of
contact with the rectum and often requires the physician to place a finger in the rectum to help facilitate
proper needle placement. This particular technique can be uncomfortable for the patient with rectal
pathology or allodynia in the area. Moreover, this approach can present a particular challenge when
attempting to maintain sterility. The angulated or bent needle renders the operator unable to use the stylet,
makes it more difficult to maneuver, potentially causes more tissue damage and may lead to needle
breakage (Figure 49-6).
Figure 49-6. Illustration of the various configurations to a 22-gauge spinal needle for the alternative
techniques described.
In an attempt to correct these predicaments, a curved needle technique6 was described which avoided
some of the aforementioned problems but resulted in difficulty when attempting to pass through a calcified
anococcygeal ligament; however, the overall flaws of the procedure were still the same. In the sub-
transverse process approach, a curved needle is advanced just caudal to the transverse process of the
coccyx.7 This results in less discomfort to the patient and allows the operator the choice of positioning the
patient either prone or lateral. There is, however, still an increased risk of contact to the rectum as the
curve could potentially pass too far anterior. A paramedian approach was described by McAllister et al8
where the operator uses a lateral approach using a double-bent needle to allow for better approximation
to the ganglion Impar. This is difficult for patients with rectal pain as it also requires a finger to be placed
in the rectum.
TRANSSACROCCYGEAL APPROACH
We advocate the most direct approach to the ganglion Impar. The transsacroccygeal approach was first
described by Wemm and Saberski (Figure 49-1).9 This technique minimizes the potential risk of rectal
perforation as advancing the needle is precisely controlled and monitored in the lateral view of
fluoroscopy. It also circumvents the problems with altering the needle’s shape, while avoiding needle
passage through the skin in close proximity to the patient’s pain complaints.

1. The patient is placed in a prone position with a pillow under the abdomen to reduce the lumbar
lordotic curvature (Figure 49-7).
Figure 49-7. Patient positioned in the prone position with pillow under the abdomen.
2. The skin overlying the SCJ is identified with an AP fluoroscopic image, marked and prepared in a
typical sterile fashion (Figures 49-4 and 49-8).
Figure 49-8. Image on the left shows the skin marked for injection. Image on the right demonstrates a
representation of the underlying bony anatomy.
3. 1% lidocaine is then used to infiltrate the skin overlying the SCJ using the 25-gauge 1.5-in needle to
provide adequate skin analgesia.
4. Contrast is drawn up into the 5-cc syringe with the connector tubing attached and primed.
5. Injectate is drawn up in the 10-cc syringe which consists of 40-mg of either triamcinolone or
methylprednisolone and 4-cc of 0.25% bupivacaine. Total 5-cc volume of injectate is recommended
to cover the area of the elongated ganglion Impar.
6. The 22-gauge 3.5-in spinal needle is then advanced anteriorly through sacrococcygeal joint under
fluoroscopic guidance into the most midline aspect.
7. Once the needle is suspected to have contacted the SCJ, the fluoroscopic view changed to lateral
(Figure 49-5) to monitor the depth of the needle tip into the SCJ (Figure 49-9a).
Figure 49-9. (A) Image on the left is a lateral fluoroscopic view of the needle with the tip lying in the
SCJ. (B) Image on the right is a lateral fluoroscopic image of the needle as the tip has passed just anterior
to the SCJ and now lying in the retroperitoneal space.
8. The needle is then carefully advanced 1 millimeter at a time until the tip passes just anterior to the
disc of the SCJ—this can be felt as a “loss of resistance” if the local anesthetic syringe is kept on the
needle (Figure 49-9b).
9. Once the needle is suspected to be just anterior to the SCJ, the syringe containing contrast is attached
to the spinal needle via the connector.
10. The needle is then aspirated to ensure that the needle is not intravascular.
11. Contrast is injected under live-fluoroscopy into the retroperitoneal space and the spread of the dye
should give a “reverse comma” appearance when seen on the lateral view (Figure 49-10).
Figure 49-10. Lateral fluoroscopic image (left) with the needle tip just anterior to the SCJ in the
retrorectal space (between the sacrum and the rectum) and contrast spread in the “reverse coma”
appearance. The image on the right is an illustration of the fluoroscopic image.
12. Careful examination should be made to ensure there is no unintended contrast spread—within the
SCJ itself, intravascular, or outside the space containing the ganglion Impar.
13. Once proper placement has been ensured, the 5-cc syringe is removed and 10-cc syringe containing
the injectate is attached to the tubing.
14. The injectate is then injected slowly.
15. The needle is then flushed and withdrawn.
16. Sterile dressing is applied.
If additional control is desired, as well as extra assurance to avoid needle fracture, one can use a
“needle-inside-needle” approach.
1. The technique described by Munir et al12 utilizes a 22-gauge 1.5-in needle inserted over the
sacrococcygeal disc at the superior aspect of the intergluteal crease, just below the sacral hiatus.
2. The needle is then advanced under lateral fluoroscopic imaging until the tip is through the disc.
3. Then a 25-gauge 2-in spinal needle is introduced through the 22-guage introducer—the remaining steps
are the same as those described above.
If the patient receives excellent but only temporary relief, the same procedure can be repeated using 1%
lidocaine followed by 6% phenol in glycerin for neurolysis.
NEEDLE-IN-NEEDLE TECHNIQUE FOR RF

This technique is used for radiofrequency neurolysis of the ganglion Impar. The Teflon coating of an RF
cannula can be damaged while advancing through the often calcified sacrococcygeal joint. The tougher,
larger 22-gauge needle is introduced first, and then RF cannula is passed through the first needle to place
it anterior to the SCJ (Figure 49-11).
Figure 49-11. Needle-in-needle technique. A sturdy larger needle is used to enter the sacrococcygeal
joint to minimize the damage to Teflon coating of the radiofrequency cannula.
Post-Procedure Follow-Up
The patient should be followed up by telephone the next day for the potential complications and queried
regarding immediate pain relief secondary to the local anesthetic effect. The anti-inflammatory effect of
the steroid will not be apparent for several days. The patient should be advised to call the pain service
for any procedure-related complications and/or any unexpected neurological deficit. Patient should be
monitored closely for following:
1. Weakness
2. Urinary or bowel incontinence
3. Fever
4. Bleeding
5. Rectal bleeding
6. Numbness
7. Exacerbation of symptoms

While the transsacroccygeal offers the operator a more straightforward approach and considerably limits
the potential complications compared to a lateral approach with angled or curved needle, there are still
obstacles that could be encountered. This approach can be challenging in those patients with a history of
coccygectomy, arthritis of SCJ, or calcification of the tissue between the sacrum and coccyx.4 This can be
of particular concern in the elderly and those exposed to radiation treatment to the area. Other potential
complications are:
1. Infection (Figure 49-12)
Figure 49-12. Magnetic Resonance Image (MRI) of a patient with coccygeal osteomyelitis.
2. Bleeding
3. Rectal perforation
4. Neurolytic injection into nerve roots or rectal cavity
5. Cauda Equina Syndrome
6. Nerve root injection (Neuritis)
7. Intravascular injection
8. Osteitis or periostitis
9. Sacrococcygeal discitis
10. Hematoma
11. Inadvertent spread may potentially lead to motor, sexual, or bowel/bladder dysfunction
Clinical Pearls
1. These injections can be diagnostic as well as therapeutic. The patients with positive diagnostic
injections are generally candidates for radiofrequency (RF) ablation, cryoneurolysis, or neurolysis by
phenol or alcohol.
2. The success of this procedure is most dependent on the exact location of the ganglion Impar relative to
the SCJ. As mentioned above, there is anatomical variability of the location of the ganglion, which
can create variable results.
3. Patients can expect anywhere from 50% to 100% pain relief.1,10,11
Suggested Reading
De Andres J, Chaves S. Coccygodynia: a proposal for an algorithm for treatment. J Pain 2003;4:257-
266.
Trescot AM. Chapter 26: Interventions in managing female pelvic pain. In: Manchikanti L, Singh V, eds.
Interventional Techniques in Chronic Non-Spinal Pain. American Society of Interventional Pain
Physicians Publishing, Paducah, KY 2009.
Antalok SJ. Chapter 32: Interventions in managing male pelvic pain. In: Manchikanti L, Singh V, eds.
Interventional Techniques in Chronic Non-Spinal Pain. American Society of Interventional Pain
Physicians Publishing, Paducah, KY 2009.
References
1. Plancarte R, Amescua C, Patt R, et al. Presacral neurectomy of the ganglion impar (Ganglion of
Walther). Anesthesiology. 1990;73:A751.
2. Datir A, Connell D.: CT-guided injection for ganglion impar blockade: a radiological approach to the
management of coccydynia. Clinical Radiology. 2010;65:21-25.
3. Waldman SD: Altas of Interventional Pain Management, 2nd ed. Philadelphia, PA: WB Saunders;
2004.
4. McAllister RK, Carpentier BW, Malkuch G. Sacral postherpetic neuralgia and successful treatment
using a paramedical approach to the ganglion impar. Anesthesiology, 2004; 101: 1471-1474.
5. Chang-seok Oh et al. Clinical implications of topographic anatomy on ganglion impar.
Anesthesiology. 2004;101: 249-250.
6. Nebab EG, Florence IM. An alternative needle geometry for interruption of the ganglion impar.
Anesthesiology, 1997;86:1213-1214.
7. Huang J. Another modified approach to the ganglion of Walther block (ganglion of impar). Journal of
Clinical Anesthesiology. 2003;15:282-283.
8. McAllister RK, Carpetier MD, Malkuch, G. Sacral postherpetic neuralgia and successful treatment
using a paramedical approach to the ganglion impar. Anesthesiology. 2004;101:1472-1474.
9. Wemm K, Saberski L. Modified approach to the ganglion impar (Ganglion of Walther). Regional
Anesthesiology, 1995;20:544.
10. Toshniwal GR, Dureja GP, Prahanth SM. Trans-sacrococcygeal approach to ganglion impar block for
management of chronic perineal pain: A prospective observational study. Pain Physician. 2007;10:
661-666.
11. Swafford JB, Ratzman DM. A trans-articular approach to blockade of the ganglion impar (ganglion of
Walther). Regional Anesthesiology and Pain Medicine. 1998;23:103.
12. Munir MA, Zhang J, Ahmad M. A modified needle-inside-needle technique for the ganglion impar
block. Canadian Journal of Anesthesiology. 2004;51:915-917.
SECTION V
MUSCULOSKELETAL INJECTIONS
CHAPTER 50
Fluoroscopy and Ultrasound-Guided Joint

Injections
Jennifer Solomon, Christine Roque-Dang, and James Wyss
IMAGE-GUIDED PERIPHERAL JOINT INJECTION

INDICATIONS
The most common clinical indication for an image-guided interventional procedure is pain in the targeted
anatomic location, which has either failed other conservative treatments or as an adjunctive treatment.
The primary advantage of image-guided interventional procedures over blind injections includes needle
placement confirmation and the ability to view the targeted area and relevant anatomy.
Corticosteroid injections are frequently used as conservative treatments in the management of various
conditions, including osteoarthritis, tendonitis, bursitis, and impingement conditions. Injectate mixtures
typically comprise a local anesthetic and a corticosteroid (triamcinolone or methylprednisolone). In
addition, patients at higher risk for developing nonsteroidal anti-inflammatory drug (NSAID)–induced
renal dysfunction or gastric and duodenal ulcers are candidates for intra-articular steroid injections to
avoid the potential systemic effects that occur with oral anti-inflammatory medications. However, the
detrimental effects of repeated steroid injections on soft tissue structures like articular cartilage and
tendons have not yet been determined.
The advantages of ultrasound-guided percutaneous interventional procedures are as follows:
• Real-time assessment
• Guidance, and continuous needle visualization
• Lack of radiation exposure
• Technological portability
• Relatively low cost
• Improved accessibility
Fluoroscopic guidance also allows real-time needle visualization and the acquisition of imaging frames
throughout the injection course. The visualization occurs at different C-arm angles. The primary
disadvantage of fluoroscopy is radiation exposure to both the patient and physician.
With therapeutic interventions, the benefits and risks of the procedure must be considered. Generally,
peripheral joint corticosteroid injections are considered to be safe and conservative treatments. However,
each patient’s risk factors for complications must be carefully considered prior to undergoing the
procedure.
Some basic concerns for injection are following:
• Patients with primary or metastatic tumors in the target area
• Immunocompromised patients, who are at increased risk for infection
• Patients with thrombocytopenia
• Patients who may be unable to tolerate positioning
• Patients with allodynia or complex regional pain syndrome (CRPS), who will be unable to tolerate the
procedure
• Patients on anticoagulant medications, who have been unable to stop these medications at an
appropriate time interval
• For fluoroscopically guided procedures with the use of contrast dye, patients with allergies to contrast,
shellfish, or iodine may be considered for interventional procedures without contrast
• Coagulopathy
• Pregnancy for fluoroscopically guided procedures
• Patient refusal
GENERAL IMAGE-GUIDED INTERVENTIONAL PROCEDURE

• Informed consent must be obtained and the risks and benefits of the procedure should be properly
explained to the patient or consenting individual.
• The area must be examined for infection, skin lesions, and disease extent.
• Proper exposure of the targeted area is necessary. If clothing is restrictive, the patient should be
requested to change into a gown.
• Ideally, the patient should be able to remain in the appropriate position throughout the procedure.
• Intravenous access is not necessary, but may be considered if the patient has a history of
postprocedural vasovagal or hypotension responses.
• The patient must be asked whether he or she takes any anticoagulant medications (ie, aspirin, NSAIDs,
etc) and, if applicable, when these medications were stopped prior to the procedure. If stopping the
anticoagulant medications increases cardiac risks, it is highly recommended to obtain medical
clearance from the patient’s cardiologist.
• The physician performing the procedure should have access to fluoroscopy or ultrasound.
• For fluoroscopically guided procedures, female patients in reproductive age should be asked about
potential pregnancy and may require a urine pregnancy test.
• For fluoroscopically guided shoulder injections, the patient must be asked about prior allergic
reactions to contrast, shellfish, and iodine.
BASIC ULTRASONOGRAPHY
Depending on the ultrasound probe and machine used, the shoulder, hip, and elbow regions may be
examined with high-frequency (>10 MHz) linear array transducers. If the patient has a large body habitus,
a mid-range frequency transducer (6-10 MHz) may need to be used to optimize image resolution and
facilitate proper examination. An appropriate initial depth is 3 cm. Also, the frequency may be adjusted to
visualize deeper structures (ie, glenoid labrum or labrum of the hip) or shallower ones (ie,
acromioclavicular joint [AC] joint).
For ultrasound examination, tissues are described by their properties of echogenicity, echotexture,
degree of anisotropy, compressibility, and blood flow on Doppler examination. Blood vessels are not
susceptible to anisotropy, but exhibit compressibility and presence of blood flow on Doppler
examination. In the shoulder, rotator cuff tendons display a high degree of anisotropy, which is
particularly pronounced at the musculotendinous junction.
Tissue echogenicity is characterized as hyperechoic, hypoechoic, anechoic, or isoechoic. Due to lack of
echoes, anechoic structures have a black appearance. Isoechogenic tissues have similar brightness in
comparison with surrounding tissues. Hyperechoic structures (ie, normal tendons and ligaments) appear
brighter than adjacent tissues. In contrast, hypoechoic structures appear darker than surrounding
structures. Both muscles and nerves have mixed echogenicity patterns. Blood vessels either appear to be
hypoechoic or anechoic.
Echotexture refers to the internal pattern of echoes and may vary based on the axis used to assess the
structure. Both tendons and ligaments have “broom end” appearance when viewed in the transverse axis
and a fibrillar pattern when viewed in the longitudinal axis. Nerves have a “honeycomb” appearance on
transverse imaging and a fascicular pattern on longitudinal imaging. Muscles have a “starry night”
appearance on a transverse axis and a pennate or “feather like” pattern on a longitudinal axis [7, 9].
BASIC POSTPROCEDURE FOLLOW-UP

The patient should be contacted via telephone on the day following the interventional procedure to
determine pain relief achieved from the local anesthetic and if there were any complications. If the patient
received a corticosteroid injection, the patient should be reminded that the anti-inflammatory property has
a variable onset and may take up to 2 to 3 weeks to achieve symptomatic improvement. The primary
postinjection concern is infection. Therefore, the patient should monitor the injection site for erythema,
warmth, increased swelling or systemic features of an infection, including fever and chills. If the patient
develops any complications, he or she should be advised to contact the injectionist for further guidance.
For severe procedurally related adverse events, ie, fever >101°F, weakness, dyspnea, severe pain
exacerbation, etc, the patient should be recommended to seek immediate emergency medical services and
to notify the injectionist. All adverse reactions should be properly documented in the patient’s chart.
Clinical Pearls
• Image-guided interventional procedures are powerful diagnostic and therapeutic tools to aid in the
diagnosis and management of various musculoskeletal disorders.
• The duration of benefit is variable, but steroid injections tend to produce substantial short-term relief
of symptoms (eg, pain, swelling) with variable duration of relief (1-3 months).
• Body habitus may influence the image-guided approach used. In obese patients, fluoroscopy may be
used to improve visualization of deeper anatomic structures that would be more difficult to visualize
under ultrasound guidance. Conversely, in leaner patients, use of ultrasound guidance eliminates
radiation exposure and usually most anatomic structures can be easily identified.
• Success of image-guided procedures is dependent on numerous factors, which include target
localization through use of anatomic landmarks, patient cooperation, and the experience of the
physician with image-guided interventions.
• Image-guided injections are well tolerated and have an excellent safety profile.
• These procedures can be repeated to manage recurrent symptoms, but patients should be cautioned that
the detrimental effects of repeated steroid injections on soft tissue structures, ie, articular cartilage and
tendons have not yet been determined.
THE GLENOHUMERAL (GH) JOINT OF THE SHOULDER

Indications
The glenohumeral joint of the shoulder is susceptible to premature arthritic development from various
conditions that may damage the joint cartilage. Of these conditions, glenohumeral osteoarthritis is the most
common form of arthritis that results in shoulder joint pain. The indications include:
• Glenohumeral osteoarthritis
• Rotator cuff arthropathy
• Post-traumatic osteoarthritis
• Acute and chronic adhesive capsulitis
• Rheumatoid arthritis
• Collagen vascular diseases
Oftentimes, patients present with generalized shoulder and upper arm pain and it may be difficult to
localize the primary pain generator intra-articular glenohumeral joint injections are excellent diagnostic
tools, which can aid in elucidating the primary pain generator. Therapeutically, intra-articular
glenohumeral joint corticosteroid injections are relatively safe interventional procedures. These
procedures may be performed if shoulder pain remains refractory to more conservative measures such as
occupational therapy, pharmacologic intervention, and activity modification. Accuracy of blind
glenohumeral joint injections has been found to be extremely variable, ranging from 25% to 95%
accuracy. Image-guided intra-articular glenohumeral joint injection enables dynamic real-time
visualization of the process, improves needle visualization, augments target accuracy, reduces damage to
surrounding structures, ie, glenoid labrum, and decreases the risk of neurovascular injury, particularly to
the brachial plexus.
Relevant Anatomy
The large and round head of the humerus articulates with the relatively flat glenoid fossa of the scapula to
form the glenohumeral (GH) joint. The articular surface is covered with hyaline cartilage. Due to the
relative incongruence of these surfaces, the glenohumeral joint is susceptible to degenerative changes and
instability. The glenoid labrum is a fibrocarti-laginous layer, which envelops the rim of the glenoid fossa.
With humeral dislocation and subluxation, the glenoid labrum is exposed and has an increased risk for
trauma. The glenohumeral joint is encompassed by a lax capsule that permits a wide range of motion of
the joint. However, this laxity compromises joint stability. The glenohumeral joint is lined by a synovial
membrane, which attaches to the articular cartilage and forms synovial tendon sheaths and bursae. These
synovial structures are particularly vulnerable to inflammation. The glenohumeral joint are innervated by
the axillary and suprascapular nerves.
The glenohumeral, transverse humeral, and cora-cohumeral ligaments are the major ligaments of the
shoulder joint. The rotator cuff muscles that surround the shoulder joint are the supraspinatus,
infraspinatus, teres minor, and subscapularis muscles. The rotator cuff musculature and ligaments provide
strength to the joint. However, due to misuse and overuse injuries, the rotator cuff muscles and their
tendons are susceptible to trauma and inflammation.
The key to successfully locating the glenohumeral joint from a posterior approach is identifying the
following structures (Figure 50-1):
• Humeral head, which is the primary bony landmark for locating the GH joint
• Posterior labrum
• Infraspinatus muscle and tendon
• Tendon sheath of the bicipital tendon
Figure 50-1. Illustrations of the posterior (left) and anterior (right) views of the right glenohumeral joint
with relation to nearby anatomical structures.
From an anterior approach, the following structures should be identified (Figure 50-1):
• Lesser tubercle of the humerus
• Coracoid process
• Tendon sheath of the bicipital tendon
Other relevant anatomy that should be taken into consideration while performing these injections is:
• Brachial plexus, which is at increased risk for neurovascular injury from the anterior approach
• Calcifications of the rotator cuff muscle and bicipital tendons
Preoperative Considerations for GH Joint Injections

• For the ultrasound-guided approaches to the glenohumeral joint, the patient must be able to sit upright
for the procedure duration. Preferably, the patient will be able to sit upright on a stool with a rotating
seat, but without wheels.
• Alternatively, the patient may lie prone or supine on the examination table for, respectively, ultrasound-
guided posterior and anterior approaches to the glenohumeral joint. However, assessment and
procedural efficiency would likely be sacrificed.
• For most fluoroscopic interventional procedures, the patient should be able to maintain his or her
position for the length of the procedure. For glenohumeral joint injections utilizing the posterior
approach, the patient must be able to lie prone. For the anterior approach, the patient must be able to
supine.
Selection of Needles, Medication, and Equipment

Needles
• 22-gauge 3.5-in spinal needle or, for ultrasound-guided injections, a 22-gauge echogenic needle, which
will be connected to extension tubing
• 22-gauge 1.5-in needle to prepare the injectate medication
• 25-gauge 1.5-in needle for local anesthetic
• 3-cc syringe for fluoroscopically guided procedures with contrast
• 6-cc syringe for GH effusion aspiration (if applicable)
• Ultrasound machine or fluoroscope
Medications
• 1% lidocaine: 4 to 5 cc for local analgesia
• Injectate mixture
1% lidocaine or 0.25% bupivacaine or 0.5% bupivacaine: 2 to 4 cc
Triamcinolone or methylprednisolone 40 to 80 mg (40 mg/mL)
Please note that medication doses are dependent on factors including patient body habitus and
condition severity
• Iohexol 180 (nonionic water-soluble contrast) for fluoroscopically guided procedures
• Total injectate volume: 5 to 8 cc
Ultrasound Views
• Ideally, a brief ultrasound-guided examination of the shoulder should be performed to assess the
glenohumeral joint and periarticular structures. Performance of a routine ultrasound-guided
examination of the targeted area ensures that errors of omission are evaded.
• Initially, the ultrasound probe is aligned in the long axis of the myotendinous junction of the
infraspinatus muscle. The humeral head is the critical bony landmark to visualize. Due to the curved
geometry of the rotator cuff tendons, anisotropy is usually present at this area.
• Transducer repositioning may be used to differentiate anisotropy from other pathological conditions.
Great care should be taken to identify the other primary landmark, the glenoid labrum.
• The infraspinatus muscle and glenoid labrum are located superior to the glenohumeral joint. Whereas,
the humeral head is located slightly inferolateral to the glenohumeral joint. Prior to needle entry site
demarcation, the intended target should be viewed in 2 orthogonal planes, which are the long and short
axes.
• Scan the area for the presence of a glenohumeral joint effusion to aspirate. The bicipital tendon sheath
directly communicates with the glenohumeral joint and may have fluid due to either an extension of the
glenohumeral joint effusion or a local tenosynovitis.
• Orient the ultrasound probe in the long axis view of the glenohumeral joint with the glenohumeral joint
centered on the screen.
Ultrasound-Guided Injection Techniques

Primarily, the anterior and posterior approaches have been described for needle passage to gain access to
the glenohumeral joint. Due to the increased risk of neurovascular injury to the brachial plexus with the
anterior approach, we advocate the posterior approach to the glenohumeral joint. Contributing to this
preference, other rationales include heightened patient anxiety with direct needle visualization and
enhanced sensitivity of flexor surfaces compared with extensor surfaces.
Our Preferred US-Guided Technique: The Posterior Approach to the GH Joint
• The patient is seated on a stool and is positioned facing away from the injectionist.
• For the shoulder, a high-frequency (17-5 MHz) ultrasound transducer should be selected and ultrasound
gel should be applied to the transducer.
• The ultrasound transducer is aligned in the long axis of the myotendinous junction of the infraspinatus
muscle with visualization of the humeral head and glenoid labrum as the primary landmarks.
• When inspecting the target area, the depth and gain may be adjusted to optimize structure visualization
[9].
• Scan the area for glenohumeral joint effusion to aspirate.
• To relieve the pressure from teres minor and infraspinatus muscles against the posterior capsule or to
increase the amount of fluid in the posterior recess of the glenohumeral joint and facilitate ultrasound-
guided arthrocentesis, the targeted upper limb may be externally rotated.
• Orient the ultrasound probe in the long axis view of the glenohumeral joint with the glenohumeral joint
centered on the screen and the needle entry point should be clearly demarcated approximately 1 cm
from the medial transducer edge (Figure 50-2).
Figure 50-2. Image demonstrates the ultrasound transducer alignment in the long axis of the glenohumeral
joint in the posterior view. The needle entry point is clearly demarcated 1 cm medial to the ultrasound
probe edge.
• The skin overlying the demarcated needle entry site and the glenohumeral joint should be prepared
using aseptic technique.
• 5 cc of 1% lidocaine is infiltrated into the skin and surrounding soft tissues to ensure appropriate local
analgesia using a 25-gauge 1.5-in needle.
• Using the 22-gauge 1.5-in needle, the 1% lidocaine/triamcinolone injectate mixture is drawn up into a
6-cc syringe. Depending on the patient’s body habitus, the amount of 1% lidocaine will range from 2 to
4 cc and the amount of triamcinolone will range from 40 to 80 mg. The total injectate volume should
range from 3 to 6 cc.
• Invert and revert the injectate syringe several times to ensure adequate mixing of the medications.
• The injectate syringe should be attached to the connector tubing with the 22-gauge 3.5-in spinal needle
and primed.
• The 22-gauge 3.5-in spinal needle is inserted at the demarcated needle entry point and directed toward
the glenohumeral joint. In the long axis view, the needle should appear as a hyperechoic and linear
structure.
• Throughout the entire procedure, the needle tip position should be visualized. To enhance need
conspicuity, the needle should be maintained as parallel as possible to the ultrasound probe and may be
gently moved without advancement, which is termed jiggling.
• The needle should take an oblique course from medial to lateral, which facilitates the gliding of the
spinal needle above the humeral head and below the posterior labrum and the infraspinatus tendon.
• As the needle is advanced, the needle path should be adjusted to access the posterior recess of the
glenohumeral joint, which lies deep to the free margin of the labrum and tangential to the curve of the
humeral head.
• With proper intra-articular needle positioning at the posterior recess of the glenohumeral joint, the
needle tip should be located beneath the infraspinatus tendon and glenoid labrum and adjacent to the
hyaline cartilage of the humeral head (Figure 50-3). The hyaline cartilage should appear hypoechoic
against the hyperechoic humeral head [4].
Figure 50-3. Ultrasound image (left) with needle tip inferior to the infraspinatus tendon and glenoid and
adjacent to the hyaline cartilage of the humeral head in the glenohumeral joint. The image on the right is an
illustration of the ultrasound image.
• The needle is aspirated to ensure that the needle is not located intravascularly.
• With real-time ultrasound, the 1% lidocaine/triamcinolone mixture is slowly injected into the posterior
recess of the glenohumeral joint.
• Correct intra-articular positioning is confirmed by the dynamic and visual expansion of the posterior
recess with injectate mixture fluid and hydrodissection, which should appear relatively hyperechoic on
ultrasound.
• Consequently, the needle is flushed and withdrawn.
• The overlying skin is cleansed and a sterile dressing is applied.
Alternative US-Guided Technique: The Anterior Approach to the GH Joint
An anterolateral approach may be used. The patient is positioned lying supine on an examination table
with his or her head rotated to the contralateral side. The needle would be visualized in the longitudinal
view. The 22-gauge spinal needle would be inserted on the anterior surface between the coracoid process
and the lesser tuberosity of the humerus. Then, the needle would be aimed in the posterolateral direction
toward the spine of the scapula and the medial border of the humeral head. The needle tip should be
positioned at the glenohumeral joint. Due to the increased risk of neurovascular injury, the area should be
assessed for the presence of nerves, which appear as honeycombed structures on transverse views and
fascicular patterns on longitudinal views. Also, vascular structures may be evaluated with power Doppler
imaging.
Fluoroscopic Views
• Start with an anterior-posterior (AP) image of the glenohumeral joint in view. Diligently mark the
center or inferolateral quadrant of the humeral head as the needle entry site to ensure a medial
approach to access the glenohumeral head.
• A lateral view may be helpful to determine needle depth.
Fluoroscopy-Guided Injection Techniques

As with ultrasound-guided glenohumeral joint injections, the anterior and posterior approaches have been
described for needle passage to gain access to the glenohumeral joint. Again, due to increased potential
complications including neurovascular injury, patient anxiety, and sensitivity of dorsal surfaces, we
advocate the posterior approach to the glenohumeral joint.
Our Preferred Fluoro-Guided Technique: The Posterior Approach to the GH Joint
• The patient is positioned in the prone position with the arm on the side of the symptomatic shoulder in
either a neutral or slightly internally rotated position.
• Starting in the AP view, the symptomatic shoulder should be elevated until the glenohumeral joint is
visualized tangentially.
• A radio-opaque marker is utilized to localize the center or the inferolateral quadrant of the humeral
head and, consequently, the skin overlying this area should be clearly demarcated.
• The skin overlying the demarcated needle entry site and the glenohumeral joint should be prepared in a
typical sterile fashion.
• 5 cc of 1% lidocaine is infiltrated into the skin and surrounding soft tissues to ensure appropriate local
analgesia using a 25-gauge 1.5-in needle.
• 3 cc of contrast should be drawn up into a 3-cc syringe. Then, the extension connector tubing with a 21-
gauge 3.5-in spinal needle should be attached and primed.
• Using a 22-gauge 1.5-in needle, the 1% lidocaine/triamcinolone injectate mixture is drawn up into a 6-
cc syringe. Depending on the patient’s body habitus, the amount of 1% lidocaine will range from 2 to 4
cc and the amount of triamcinolone will range from 40 to 80 mg. Including contrast, the total injectate
volume should range from 5 to 8 cc. The injectate syringe should be inverted and reverted several
times to ensure adequate mixing of the medications.
• The 22-gauge 3.5-in spinal needle is inserted at the demarcated needle entry point and directed toward
the cartilage of the humeral head and the glenohumeral joint (Figure 50-4).
Figure 50-4. Fluoroscopic image (left) demonstrates the posterior approach with the 22-guage spinal
needle directed towards the center of the humeral head and the glenohumeral joint in the AP view. Image
on the right demonstrates the glenohumeral joint arthrogram with capsular distension achieved with
injected iodinated contrast media.
• With fluoroscopic guidance, needle is advanced vertically in the oblique view to the cartilage of the
humeral head.
• Once the needle is suspected to be at the glenohumeral joint and the needle tip contacts the center of the
humeral head, the syringe with contrast is attached to a spinal needle via the connector.
• With real-time live fluoroscopy, the iodinated contrast media is injected to obtain an arthrogram
(Figure 50-4). If this isn’t observed, rotate the bevel of the needle 90 to 180 degrees, maintain contact
with the humeral head and repeat.
• Careful examination should be made to ensure that the contrast spread remains confined to the
glenohumeral joint and that no intravascular uptake occurred.
• Once proper needle placement has been confirmed, the 5-cc syringe containing the iodinated contrast is
removed and the 5-cc syringe containing the injectate mixture is attached to the extension tubing.
• Prior to pushing the injectate mixture, the needle should be aspirated again to ensure that the needle is
not located intravascularly.
• The needle injectate should be pushed slowly.
• With repeat fluoroscopic imaging, contrast spread throughout the GH joint and “washing out” of the
contrast dye adjacent to the needle tip should be visualized.
Alternative Fluoro-Guided Technique: The Anterior Approach to the GH Joint
An anteroposterior approach may be utilized. The patient lies supine on the fluoroscopy table with his or
her arm in slight external rotation. With this technique, a straight AP view would be obtained. The needle
entry point should be demarcated for the inferolateral border or center of the humeral head. After sterile
skin preparation and local anesthetic infiltration, a 22-gauge spinal needle should be directed toward the
glenohumeral joint and the inferolateral quadrant or center of the humeral head under fluoroscopic
guidance. Consequently, iodinated contrast media is injected to confirm intra-articular needle position.
With the anterior fluoroscopically guided anterior approach to the GH joint, it is particularly important to
aspirate prior to injection, inject iodinated contrast media, and obtain an arthrogram.

Although image-guided interventional procedures of the glenohumeral joint offers the advantages of real-
time assessment, needle visualization, and guidance, various obstacles may be encountered. In patients
with a history of prior shoulder surgeries, history of prior shoulder trauma, abnormal or complicated
anatomy, and calcifications of the rotator cuff tendons and bicipital tendon, all of these approaches may be
challenging to the injectionist. With fluoroscopy, these procedures may be a particular concern for elderly
patients and those exposed to radiation in other body regions. Patients should be cautioned that
corticosteroid injections to the GH joint may not completely alleviate the pain and may be potentially
ineffective. Other potential complications include:
• Neurovascular injury, particularly to the brachial plexus
• Infection
• Bleeding
• Hematoma and ecchymoses
• Neuritis
• Tendon rupture
• Myalgias
• Chronic regional pain syndrome development
THE HIP JOINT

Indications
In clinical practice, intra-articular hip injections are utilized for diagnostic and therapeutic purposes.
Many patients present with a history of hip and lumbar osteoarthritis (OA) and differentiating the etiology
of the pain can be difficult without diagnostic hip joint injections. Therefore, intra-articular anesthetic hip
injections can help rule in or out the suspected source of pain. For therapeutic purposes, intra-articular
steroid injections are often considered as the next step of treatment for intra-articular sources of hip pain
(eg, OA or labral pathology) that is nonresponsive to more conservative measures (eg, oral medications
such as NSAIDs, physical therapy, activity modifications and other lifestyle changes).
Image guidance has been recommended for many years for specific anatomic reasons related to the hip
joint; including the deep location of the joint and the close proximity of the anterior hip joint to the
femoral artery, vein, and nerve (Figure 50-5). Therefore, image guidance can improve the accuracy of
proper needle placement, and theoretically improve the safety profile of the injection with less risk of
neurovascular injury [23].
Figure 50-5. Illustration of the hip joint and its proximity to the neurovascular bundle, including the
femoral vein, femoral artery, and femoral nerve.
Relevant Anatomy
A thorough understanding of intra-articular and extra-articular structures of the hip is absolutely necessary
in the management of various hip conditions. For the purposes of intra-articular hip injections, a solid
understanding of the surface anatomy of the hip and the bony anatomy of the proximal femur is most
important. This will provide the clinician with the ability to locate the site of entry and then allow for
proper navigation of the needle into the joint space. In addition, to avoid complications, the location of
the femoral neurovascular bundle (femoral nerve, artery, and vein) must be understood since they are in
close proximity to the anterior hip joint.
The key to successfully locating the hip joint from an anterior approach is identifying the following
structures (Figure 50-6):
Figure 50-6. Illustration of the hip joint with relation to nearby anatomical structures.
• Inguinal crease/ligament
• Location of neurovascular bundle (femoral artery, vein, and nerve)
• Proximal quadriceps, rectus femoris, and sartorius
• Iliopsoas tendon
• Anterior inferior iliac spine (AIIS)
• Anterior superior iliac spine (ASIS)
• Greater trochanter and abductor tendons
• Origin of the adductor muscle group
Other relevant anatomy that should be taken into consideration while performing these injections are:
• Femoral head, neck, and head-neck junction
• A thorough understanding of the location of the joint capsule attachments which extends down to the
intertrochanteric line on the anterior femur (Figure 50-7)
Figure 50-7. Illustration on the left demonstrates the hip capsule anterior attachments, including the
iliofemoral ligament to intertrochanteric line of the femur and the pubofemoral ligament to the lesser
tuberosity of the femur. On the right, a posterior view of the hip capsule and ischiofemoral ligament is
illustrated.
• The acetabulum and its bony anatomy with labrum
Preoperative Considerations for Intra-Articular Hip Injections

• For the image-guided approaches to the intra-articular hip joint, the patient must be able to lie supine
for the procedure, which should take approximately 10 to 15 minutes.
• If ultrasound is not available or the clinician prefers to use fluoroscopic guidance, the fluoroscopically
guided approach can be utilized.

Needles
• 22-gauge 3.5-in spinal needle or, for ultrasound-guided injections, a 22-gauge echogenic needle, which
will be connected to extension tubing
• 25-gauge 1.5-in needle for local anesthetic
• 3- or 5-cc syringe for local anesthetic
• 10-cc syringe for aspiration
• 5-cc syringe for fluoroscopically guided procedures with contrast
• Ultrasound machine or fluoroscope
Medications
• 1% lidocaine: 1 to 3 cc for local analgesia
1% lidocaine: 2 to 4 cc
Triamcinolone 40 to 80 mg (40 mg/mL) or methylprednisolone 40 to 80 mg (40 mg/mL)
0.25% or 0.5% bupivacaine (optional): 2 cc
Please note that medication doses are dependent on factors including patient body habitus and
condition severity.
• Iohexol 180 (nonionic water-soluble contrast) for fluoroscopically guided procedures
Techniques
Two primary techniques have been described for intra-articular hip injections:
1. Anterior approach (patient supine, hip in full extension and neutral rotation)
2. Go from medial to lateral in order to avoid hitting vital structures. Lateral approach (patient supine
with the hip in full extension)
The anterior approach with fluoroscopic or ultrasound guidance, with the patient supine and the hip in
full extension with neutral rotation is commonly utilized by clinicians. The advantages includes the ability
to palpate key landmarks, easy positioning of tools for image guidance (C-arm or ultrasound probe) and
most importantly avoidance of important intra-articular structures (eg, articular cartilage, acetabular
labrum) because the target is either the middle of the femoral neck on AP fluoroscopic image or the
femoral head-neck junction on ultrasound image. The primary disadvantage includes the potential for
neurovascular injury to the femoral nerve, artery, or vein; even injury to the lateral femoral cutaneous
nerve is possible.
The lateral approach, with the patient supine and the hip full extension, is another approach commonly
utilized by clinicians. The primary advantage over the anterior approach may be improved accuracy if
image guidance isn’t utilized. The primary disadvantage includes injury to intra-articular structures, such
as articular cartilage and/or acetabular labrum.
Ultrasound Views
• The ultrasound probe is placed longitudinal to the femoral neck and positioned to obtain a long axis
view of the femoral head-neck junction.
Ultrasound-Guided Injection Techniques

Our Preferred Technique: Anterior Approach to the Intra-Articular Hip Joint With Ultrasound
Guidance
We advocate this approach for many reasons. This technique allows for comfortable positioning of the
patient, confirmation of intra-articular placement via ultrasound visualization of the needle tip and
injectate filling pattern, and the patient and operator is able to avoid ionizing radiation and the use of
contrast agents which theoretically decrease the risk of allergic reactions. In our experience, this
approach is tolerated very well by the patient and is an accurate approach that may be confirmed with
real time visualization by the operator. The literature supports a high rate of accuracy and safety with this
approach.
• The patient is placed in a supine position with the hip in full extension and neutral rotation, slight
internal rotation may be utilized to obtain a better image of the femoral head-neck junction.
• The ultrasound probe is then used to mark the location of the femoral nerve and vessels, then the probe
is placed longitudinal to the femoral neck and positioned to obtain a long axis view of the femoral
head-neck junction.
• The site of needle entry is marked with a pen on the skin just distal (approximately 2-3 cm) to the
probe.
• The injection site is then prepared in a sterile fashion and a sterile cover is applied to the ultrasound
probe.
• Up to 3 cc of 1% lidocaine is then infiltrated into the skin overlying the site of the injection to provide
adequate skin analgesia using a 25-gauge 1.5-in needle.
• The injectate is drawn up using a 10-cc syringe which consists of 40 to 80 mg of either triamcinolone
or methylprednisolone and 2 to 4 cc of 1% lidocaine with the option to include additional 2 cc of
0.25% bupivacaine.
• The 22-gauge 3.5-in spinal needle with this 10-cc syringe attached is then advanced at approximately a
45-degree angle, in the plane of the ultrasound beam to allow real time visualization of the needle tip
and shaft.
• The trajectory of the needle is adjusted to visualize the needle tip at the femoral head neck junction.
Expect a slight increase in resistance as the needle pierces the iliofemoral ligament and anterior
capsule. In our experience, passing the needle through these tissues produces anterior hip pain for the
patient, and warning them prior to this may be helpful.
• Once the needle tip contacts the femoral neck and can be visualized on ultrasound, aspiration is
performed and if negative for blood, a test injection of 1 to 2 mL is used to confirm filling along the
femoral head-neck junction along with anterior capsular distension (Figure 50-8). If this isn’t
observed, rotate the bevel of the needle 90 to 180 degrees and maintain contact with the femoral neck
and repeat.
Figure 50-8. Ultrasound image (left) with needle tip contacting the femoral neck with anterior capsular
distension along the femoral head-neck junction. The image on the right is an illustration of the ultrasound
image.
• The remainder of the solution is injected under real time visualization to continue to confirm filling
pattern along the femoral head-neck junction along with anterior capsular distension.
• At the conclusion of the procedure, the needle is clearly withdrawn and sterile dressings are used to
apply pressure.
• The area is cleansed with alcohol solution, dried, and a dressing is applied over the site of the
injection.
Fluoroscopic Views
• Start with an AP view of the pelvis, center the femoral neck, and magnify the image. Mark the middle
of the femoral neck (Figure 50-9).
Figure 50-9. Fluoroscopic image of the right hip (top left) demonstrates the posterior approach with the
22-guage spinal needle directed toward the femoral neck in the AP view. Image on the top right
demonstrates the injection iodinated contrast media into the right intra-articular hip joint. The bottom
image demonstrates filling of a left hip capsule with contrast media.
Fluoroscopically Guided Technique

• The patient is placed in a supine position on the table, with the hip in full extension and neutral
rotation.
• An AP view of the pelvis is obtained, then femoral neck on the side of the injection is centered.
• The site of needle entry is marked with a pen on the skin at the center of the femoral neck.
• The injection site is then prepared in a sterile fashion.
adequate skin analgesia using the 25-gauge 1.5-in needle.
• The injectate is drawn up using a 10-cc syringe, which consists of 40 to 80 mg of either triamcinolone
or methylprednisolone and 2 to 4 cc of 1% lidocaine +/1 an additional 2 cc of 0.25% bupivacaine.
• A 22-gauge 3.5-in spinal needle is directed down to the femoral neck under fluoroscopic guidance.
• The trajectory is perpendicular to the femoral neck, in the beam of the fluoroscope, attempting to obtain
a hub view. Expect a slight increase in resistance as the needle pierces the iliofemoral ligament and
anterior capsule. In our experience, passing the needle through these tissues produces anterior hip pain
for the patient, and warning them prior to this may be helpful.
• Once the needle tip contacts the femoral neck and is visualized fluoroscopically (still using an AP
image), aspiration is performed and if negative, the extension tubing is connected to the spinal needle
and contrast dye is injected to obtain an arthrogram (Figure 50-9). If this isn’t observed, rotate the
bevel of the needle 90 to 180 degrees and maintain contact with the femoral neck and repeat.
• Once a good arthrogram is obtained, indicating a capsular filling pattern, syringes are switched and
now the steroid and anesthetic is injected.
apply pressure.
injection.
EXTENSOR CARPI RADIALIS BREVIS MUSCLE AND THE

COMMON EXTENSOR TENDON
Indications
Lateral epicondylitis, which is more commonly known as tennis elbow, is caused by overuse injuries and
chronic repetitive microtrauma to the forearm extensor tendons. The most common area of pain is located
at the origin of the extensor carpi radialis brevis tendon at the lateral epicondyle of the elbow. Rarely,
lateral epicondylitis pain may originate at a more distal site, which is where the ECRB overlies the radial
head. With chronic overuse or misuse of the forearm extensors, the inflammatory response may spread to
adjacent tissues. With lateral epicondylitis, the abnormality consists primarily of degeneration, tendinosis,
and potential tendon tear. The primary indication for extensor carpi radialis brevis muscle and common
extensor tendon injection is lateral epicondylitis.
Relevant Anatomy
The extensor carpi radialis brevis muscle extends the wrist with radial deviation. The origin of the
extensor carpi radialis brevis muscle is located at the lateral epicondyle via the common extensor tendon,
the radial collateral ligament, and the antebrachial fascia. The distal insertion is located at the base of the
third metacarpal. The extensor carpi radialis brevis muscle is innervated by the deep branch of the radial
nerve. Overuse and misuse injuries of the extensor carpi radialis brevis muscle are associated with the
development of lateral epicondylitis.
The common extensor tendon is located at the lateral elbow in the posterior compartment. The lateral
collateral ligament lies immediately deep to the common extensor tendon. The radial head lies beneath the
lateral collateral ligament. The deep fibers primarily contain contributions from the extensor carpi
radialis brevis. The superficial tendon receives fibers from the extensor carpi radialis brevis, extensor
carpi ulnaris, extensor digitorum, and extensor digit minimi muscles.
The key to successfully locating the ECRB muscle and common extensor tendon is identifying the
following structures (Figure 50-10):
Figure 50-10. Illustration of the lateral view of the elbow, highlighting the location of the lateral
epicondyle, common extensor tendon, and extensor carpi radialis brevis muscle to nearby anatomical
structures.
• Lateral epicondyle
• Radial head
• Lateral collateral ligament
• Common extensor tendon
• Extensor digiti minimi muscle
• Extensor carpi ulnaris muscle
• Extensor digitorum communis muscle
Other relevant anatomy that should be taken into consideration while performing these injections
includes the deep radial nerve.
• For this procedure, the patient must be able to lie supine or seated for the procedure duration.

Needles
• Ultrasound machine
Medications
1% lidocaine: 2 to 3 cc
Triamcinolone: 1 cc (40 mg/mL)
Ultrasound Views
• Ideally, a brief ultrasound-guided examination of the lateral elbow and forearm should be performed to
ensure that errors of omission are evaded.
• Initially, the ultrasound probe is aligned in the long axes of the extensor carpi radialis brevis muscle
and common extensor tendon. The radial head and lateral epicondyle are the critical bony landmarks to
visualize. Also, the lateral collateral ligament, which is immediately deep to the common extensor
tendon, should be identified (Figure 50-11).
Figure 50-11. Image demonstrates the ultrasound transducer alignment in the long axis view of the
attachment site of the extensor carpi radialis brevis muscle to the common extensor tendon. The needle
entry point is clearly demarcated 1 cm proximal to the ultrasound prove edge.
• Prior to needle entry site demarcation, the intended target should be viewed in both the long and short
axes.
Ultrasound-Guided Injection Technique

The patient should lie supine with the arm adducted at the patient’s side and the elbow flexed the palm
down or halfway between pronation and supination. The patient’s hand should be placed atop a raised
surface or folded towel to relax the common extensor tendon.
• Alternatively, the patient may be seated with the arm resting on the table and the elbow flexed to 70 to
80 degrees. In this position, the wrist should be pronated.
• For the elbow and forearm, a high-frequency (17-5 MHz) ultrasound transducer is an appropriate
ultrasound probe to select and ultrasound gel should be applied to the transducer.
• Structures of interest in the lateral elbow include the common extensor tendon, lateral epicondyle, the
lateral collateral ligament complex, the radial head, annular recess, capitulum, extensor carpi radialis,
extensor digitorum, extensor carpi ulnaris, and extensor digiti minimi. While performing the
sonographic examination, the wrist and finger extensor musculature may be identified by having the
patient move their wrist or finger(s) accordingly.
• The ultrasound transducer is aligned in the long axis view of the attachment site of the extensor carpi
radialis brevis muscle to the common extensor tendon (Figure 50-11). To guide the examination, the
lateral epicondyle, lateral collateral ligament, and the radial head, which lie deep to the common
extensor tendon and ECRB muscle, should be identified and examined in a longitudinal plane. To aid in
ECRB identification, the patient may be asked to extend and radially deviate the wrist. The common
extensor tendon origin has a uniform hyperechoic triangular configuration, which is seen traversing the
radiocapitellar joint.
• Scan the area for neurovascular structures, including the deep branch of the radial nerve. The deep
branch of the radial nerve should appear to have a “honeycomb” appearance on a transverse view and
a fasicular appearance on longitudinal view.
• When inspecting the target area, the depth and gain may be adjusted to optimize structure visualization.
• Once the ECRB muscle and common extensor tendon are identified, these structures should be
evaluated in 2 orthogonal planes, which are longitudinally (long axis) and transversely (short axis).
• The extensor carpi radialis brevis component of the common extensor tendon is most commonly
affected in lateral epicondylitis. Sonographically, tendinosis appears as thick and hypoechoic. Also,
there may be concomitant swelling of the involved tendon with possible hyperechoic calcification with
chronic cases. Also, bone irregularity may be present. Hyperemia on color or power Doppler imaging
is variable, but may be present with soft tissue inflammation. Superimposed partial-thickness tears
appear as hypoechoic or anechoic clefts and incomplete fiber discontinuity with linear [33].
• Orient the ultrasound probe in the long axis view of the ECRB muscle and its attachment to the common
extensor tendon centered on the screen. The needle entry point should be clearly demarcated
approximately 1 cm from the proximal transducer edge (Figure 50-11). With the long-axis approach,
the needle tip and shaft are positioned collinearly with the long axis of the ultrasound probe. This
optimizes the needle visualization approach to the target.
• Following sterile preparation of the skin overlying the posterolateral aspect of the joint, the lateral
epicondyle is identified.
• Using the 22-gauge 1.5-in needle, the 1% lidocaine/triamcinolone injectate mixture is drawn up into a
5-cc syringe.
• The 22-gauge 1.5-in needle is inserted at the demarcated needle entry point and directed toward the
centered ECRB muscle attachment to the common extensor tendon. In the long axis view, the needle
should appear as a hyperechoic and linear structure. Throughout the entire procedure, the needle tip
position should be visualized. To enhance need conspicuity, the needle should be maintained as
parallel as possible to the ultrasound probe. Also, the needle may be gently moved without
advancement, which is termed jiggling.
• The needle should take a longitudinal course from proximal to distal.
• With proper needle positioning at the ECRB muscle attachment to the common extensor tendon, the
needle tip should be located adjacent to the target area (Figure 50-12). Care must be taken to ensure
that the common extensor tendon is not directly injected to avoid tendon rupture.
Figure 50-12. Ultrasound image (left) with needle at the musculotendinous junction of the extensor carpi
radialis brevis and the common extensor tendon. The image on the right is an illustration of the ultrasound
image.
• With real-time ultrasound, the 1% lidocaine/triamcinolone mixture is slowly injected into the area
adjacent to the musculotendinous junction of the ECRB muscle. Correct positioning is confirmed by the
dynamic and visual expansion of the area with fluid and hydrodissection, which should appear
relatively hyperechoic on ultrasound.

Although ultrasound-guided interventional procedures of the extensor carpi radialis brevis muscle and
common extensor tendon has the distinctive advantages of dynamic real-time assessment, needle
visualization, accessibility, and portability, various challenges may be encountered. This approach may
be difficult to utilize in patients with a history of prior elbow or forearm surgeries, history of prior elbow
or forearm trauma, abnormal or complicated anatomy, and calcifications of the common extensor tendon.
Patients should be cautioned that corticosteroid injections for lateral epicondylitis may not completely
alleviate the pain and may be potentially ineffective. Performance of the corticosteroid injection
superficial to the ECRB should be avoided due to the increased risk of skin depigmentation and fat
atrophy. Other potential complications include:
• Common extensor tendon rupture
• Neurovascular injury, particularly to the deep radial nerve
• Infection
• Bleeding
• Hematoma and ecchymoses
• Neuritis
• Myalgias
• Chronic regional pain syndrome development
CHAPTER 51
Viscosupplements and Steroid Injections

Jennifer Solomon and Vijay Vad
INTRODUCTION
Steroids and viscosupplements (VS) are two commonly injected substances used to provide mobility of
and relief to osteoarthritic joints. Steroids presumably provide relief by controlling inflammation of
peripheral joints, while VS seek to reestablish the elasticity and viscosity of the joint’s normal synovial
fluid. VS are also reported to have anti-inflammatory effects through the reduction of leukocyte function
and inflammatory mediators.1,2 The efficacy of both injections for temporarily alleviating joint pain has
been demonstrated in various clinical trials.3-5
The FDA approved the use of VS in 1997 for the treatment of knee osteoarthritis (OA) and VS have
since gained widespread use.6 Although off-label use of VS occur in everyday clinical practice, such as
its use for hip and shoulder,7,8 this chapter will focus on the use of these agents for their current FDA
indication, the treatment of knee OA.9
See Table 51-1 for a list of current FDA-approved VS.
TABLE 51-1. Manufacturer and Brand Information for Viscosupplements

INDICATIONS
According to the American College of Rheumatology (ACR), the indications for treating a swollen
inflamed knee are:
• Failed conservative measures (oral medications such as nonsteroidal anti-inflammatory drugs
(NSAIDs), physical therapy, activity modifications, and other lifestyle changes).
• Patients who have or are at higher risk for developing NSAID-induced renal dysfunction or
gastroduodenal ulcers are excellent candidates for intra-articular steroid injections because they avoid
the potential systemic effects that occur with oral NSAIDs.
If there is persistent pain and impaired quality of life following a knee steroid injection, or only short-
term benefit from the steroid injection, then VS is the next treatment option to consider. Although steroid
injections are reported to have quicker acting pain relief than VS, VS-derived pain relief may last
considerably longer, from 4 to 26 weeks.13,54 Therefore, in some cases the patient will experience short
duration but significant relief following a knee steroid injection and this duration of relief may be
extended with the use of knee VS injection(s).
The clinical criteria for the diagnosis of knee osteoarthritis based on anatomical location of pain
include14,15:
• Persistent knee pain that typically worsens with weight bearing and activity
• Morning stiffness
• Tenderness of the bony margins of the joint
• Bony enlargement
• Crepitus with motion
• Lack of palpable synovial warmth
Radiographic evidence of knee osteoarthritis, including the presence of osteophytes, subchondral cysts,
and joint space narrowing, helps to confirm or support clinical suspicion.
Recent findings suggest that the most useful diagnostic criteria are:
• Three symptoms: persistent knee pain, limited morning stiffness, and reduced function
• Three signs: crepitus, restricted movement, and bony enlargement
Assuming a 12.5% background prevalence of knee OA in adults aged ≥45 years, the estimated
probability of having radiographic knee OA increased with increasing number of positive features to 99%
when all 6 symptoms and signs are present.16
RELEVANT ANATOMY
A thorough understanding of intra-articular and extra-articular knee structures and three-dimensional
surface anatomy is absolutely necessary in the management of various knee conditions and intra-articular
knee injections. This will provide the clinician with the ability to locate the site of needle entry and then
allow for proper navigation of the needle into the joint space.17
The key landmarks to identify before considering an intra-articular knee injection are (Figure 51-1):
Figure 51-1. AP view of knee.
• Patella, including the inferior, superior, medial, and lateral poles

• Femoral condyles (medial and lateral)
• Tibial plateau (medial and lateral)
• Quadricep tendon
• Patellar tendon
Other relevant anatomy that should be considered prior to and during the injection is:
• A thorough understanding of the location of the synovial lining/joint capsule (Figure 51-2).
Figure 51-2. Lateral view of knee.
• The infra-patellar fat pad is important to understand and consider, depending on the injection approach
utilized.
• Medial and lateral meniscus
• Medial and lateral collateral ligaments
• Quadriceps, including vastus lateralis and medialis

Steroid injections and viscosupplements are routinely recommended after other conservative measures
have failed to provide adequate relief of symptoms for patients with knee osteoarthritis. In the majority of
cases, the potential benefit greatly outweighs the potential risks and these injections are well tolerated
and have an excellent safety profile.4 The patients with significant medical comorbidities and multiple
medications may be more susceptible, and certain adverse events and the risks/benefits of the procedure
must be reassessed. Therefore, the medical history of each patient must be considered before
administration to avoid further complication.
Basic concerns for the injections include:
• Injection of steroid or VS in intravascular or extra-articular areas from inaccurate needle placement
can result in local and systemic complications.
• Patients may experience postprocedure pain at the site of the injection.
Some contraindications include:
• Coagulopathy
• Distorted or complicated anatomy (may be an indication for image guidance, even contrast
enhancement)
• Patient refusal
• Known hypersensitivity to hyaluronan
• Product specific (Hyalgan, Supartz): Known allergy to avian products
• Product specific (Orthovisc): Known allergy to gram-positive bacterial proteins
INTRA-ARTICULAR KNEE INJECTION FOR

ASPIRATION/STEROID INJECTION
• Anticoagulation. This is less of a concern than for spinal injections but since there is trauma to the
tissues from the introduction of a needle both subcutaneously and intra-articularly, there is an inherent
risk for hematoma or hemarthrosis.
• Physical examination of the area for signs of infection or skin breakdown, and the ability to properly
palpate bony landmarks of the knee.
• Patient must be able to lie supine for brief procedure. The head of the bed/examination table may be
slightly elevated for patient tolerance during the procedure.
• Intravenous access is not necessary but may be considered if the patient has a history of vasovagal
reaction and hypotension responses post injection.
Efficacy of the injections is dependent upon accurate needle placement in the joint space, and not by
patient’s age or gender. The knee joint can be accessed through a multitude of approaches and the majority
of studies show that there is no significant difference in the accuracy of needle placement between the
various approaches.18,19
Fluoroscopic or Ultrasound Guidance
Fluoroscopic or ultrasound-guided injections generally are not necessary since accurate knee intra-
articular needle placement can be obtained without guidance. If anatomical guidance (eg, palpation of
anatomic landmarks) appears to be too difficult due to body habitus, distorted or complicated anatomy, or
other factors, then fluoroscopic or ultrasound guidance may be considered.19
However, recent studies suggest that the use of imaging during injection significantly increases the
needle placement accuracy rates. In the absence of imaging, up to 20% of injections are inaccurate.18
Equipment
• 22-gauge 2-in needle (an 18-gauge needle may be required for large-volume aspiration)
• 3-cc syringe for local anesthetic (optional)
• 10-cc syringe for intra-articular steroid/anesthetic
Medications
• 1% lidocaine
• 0.25% or 0.5% bupivacaine (optional)
• Triamcinolone or methylprednisolone
Technique
Varying techniques have been described for intra-articular knee injections and aspiration:
• Medial or lateral parapatellar approach. Patient seated or supine position with knee flexed 45 to 90
degrees. This approach is also described as an anteromedial or anterolateral approach.20
• Medial or lateral suprapatellar approach. Patient in supine position, with knee in full extension.
• Medial or lateral retropatellar approach. Patient in supine position, with knee in full extension. This
approach is also described as an medial or lateral midpatellar approach.20
The medial or lateral parapatellar approaches, with the patient seated and the knee flexed 90 degrees
are commonly utilized by clinicians.
The advantage includes:
• Relatively easy access to the joint due to gravitational distraction forces on the knee that increases the
tibio-femoral joint space.
The disadvantages include:
• The potential for infrapatellar fat pad injection that is very painful for the patient
• Inability to aspirate mild effusions in the flexed knee position
• Difficulty handling vasovagal responses for a seated patient
The medial or lateral suprapatellar approach, with the patient in supine position and the knee in full
extension, are another approach commonly utilized by clinicians (Figure 51-3).
Figure 51-3. Positioning.
The advantages include:

• Safer positioning for management of potential vasovagal responses during or after the injection
• The ability to aspirate joint effusions and confirm intra-articular needle placement
• The ability to avoid infra-patellar fat pad injections
• Accuracy remains high with this approach.
The disadvantage includes:
• A potentially narrower joint space to navigate
The medial or lateral retropatellar approaches have similar advantages and disadvantages as those
described for the suprapatellar approaches.
Medial Suprapatellar Approach

We advocate the medial suprapatellar approach. In our opinion, this technique minimizes the potential
risk of a painful injection that may occur due to inadvertent infrapatellar fat pad injection, allows
confirmation of intra-articular placement if an effusion is present, and allows for easier management of
vasovagal responses. In our experience, this approach is tolerated very well by the patient and is a very
accurate approach in regards to intra-articular needle placement.21,22

• The patient is placed in a supine position with the knee in full extension (see Figure 51-3).
• The skin overlying the knee is marked, using key anatomical landmarks (eg, medial and superior poles
of the patella and medial femoral condyle) (Figure 51-4).
Figure 51-4. Photo of anatomical landmarks on the right knee. The circle outlines the patella,
infrapatellar tendon is outlined as well and a small horizontal line represents the superior pole of the
patella.
• The injection site is prepared in a typical sterile fashion (Figure 51-5).

Figure 51-5. Site of needle entry marked with an X, and sterile preparation of the injection site.
• Up to 3-cc of 1% lidocaine is then infiltrated into the skin overlying the site of the injection to provide
• The injectate is drawn up into the 10-cc syringe which consists of 40 mg of either triamcinolone or
methylprednisolone and 2 to 4 cc of 1% lidocaine +/–, an additional 2 cc of 0.25% bupivacaine.
• The 22-gauge 2-in needle with an empty 10-cc syringe attached (an 18-gauge needle may be required
for large-volume aspiration) is then advanced at approximately a 45 degree from the Sagittal plane.
The needle will be directed in a slightly lateral, inferior, and posterior direction to enter the capsule of
the knee joint (Figure 51-6). The patella may be tilted slightly to open up the joint space (Figure 51-7).
Figure 51-6. Needle placement photo and line drawing of needle placement.
Figure 51-7. Image of Patella Tilt, preformed to slightly elevate the medial facet of the patella.
• Once the needle is suspected to have entered the joint capsule, the needle is then aspirated to confirm
intra-articular placement (and for therapeutic reasons) and to ensure that the needle is not intravascular.
• Once proper placement has been achieved, the 10-cc syringe used for aspiration is removed and 10-cc
syringe containing the injectate is attached.
• Then the injectate is instilled into the knee joint.
apply pressure.
• The area is cleaned with an alcohol solution, dried, and a dressing is applied over the site of the
injection.
INTRA-ARTICULAR KNEE INJECTION OF

VISCOSUPPLEMENT
• Please refer to the section Intra-articular Knee Injection for Aspiration/Steroid Injection.
Fluoroscopic or Ultrasound Views
• Please refer to the section Intra-articular Knee Injection for Aspiration/Steroid Injection.
Equipment
• 25-gauge 1.5-in needle (optional)
• 3-cc syringe for local anesthetic (optional)
• Syringe of viscosupplement
Medications
• 1% lidocaine
• Viscosupplement (one preloaded syringe of preferred viscosupplement)

• The patient is placed in a supine position with the knee in full extension.
• The skin overlying the knee is marked, using key anatomical landmarks (eg, medial and superior poles
of the patella and medial femoral condyle) (see Figure 51-4).
• The injection site is prepared in a typical sterile fashion (see Figure 51-5).
• The 22-gauge 2-in needle with an empty 10-cc syringe attached (an 18-gauge needle may be required
for large-volume aspiration) is then advanced at approximately a 45 degree from the sagittal plane. The
needle will be directed in a slightly lateral, inferior, and posterior direction to enter the capsule of the
knee joint (see Figure 51-6). The patella may be tilted slightly to open up the joint space (see Figure
51-7).
• Once the needle is suspected to have entered the joint capsule, the needle is then aspirated to confirm
intra-articular placement (and for therapeutic reasons) and to ensure that the needle is not intravascular.
• Once proper placement has been achieved, the 10-cc syringe used for aspiration is removed and a
preloaded syringe of preferred viscosupplement is attached.
• Then the viscosupplement is instilled into the knee joint.
apply pressure.
injection.
The patient should be instructed to contact the office if there are any concerns for potential complications.
It is important to advise the patient that the antiinflammatory effect of steroid will not be apparent for 48
to 72 hours and maximal benefit may take up until 1 or 2 weeks postinjection. The primary concern
postinjection is for infection (cellulitis or joint infection), therefore, the patient should monitor the
injection site for erythema, warmth, increased swelling, or systemic features of an infection:
• Fever or chills
In addition, depending on the viscosupplement chosen, the patient will need to return to the office to
repeat this injection an additional 2 to 4 times. Treatment with viscosupplement, with the exception of
Synvisc-One, follows a protocol recommended by the manufacturer for a treatment series of 3 to 5 total
injections.
Because of the percutaneous approach, there are limited potential systemic complications from this
treatment. The most commonly reported adverse events with VSN and steroid injections are transient and
occur at the injection site. The potential complications include:
• Mild pain
• Swelling or effusion
• Warmth
• Redness
• Allergic reactions to the medications.
• Iatrogenic knee joint infections or local skin infections.
• Hemarthrosis of the knee joint
Product-specific instances of pseudosepsis were found in patients who received Synvisc
injections.10,11,23 In rare cases, patients reported various systemic effects.10,24 The long-term effects of
repeated steroid injections and VSN on the joint are conflicting. A number of studies have concluded that
repeated injections of VSN are safe and have no known long-term complications.4,25 A more recent study
found increased levels of a cartilage breakdown marker postprocedure, suggesting that long-term VSN
use increases the rate of joint degradation.26,27
Similarly with steroids, there is some fear that repeated injections will lead to more rapid joint
deterioration; however, there is little current evidence supporting or denying this claim.3,28 The potential,
but rare, complications from steroid injections also include skin depigmentation and subcutaneous fat
atrophy.29-33
CLINICAL PEARLS
• These injections are effective therapeutic tools for the management of knee OA.
• The duration of benefit is variable
• Steroid injections tend to produce substantial short-term relief of symptoms (eg, pain, swelling),
whereas VS tend to produce longer duration relief (3-6 months) but with a slower onset of relief.
• These injections are well tolerated and have an excellent safety profile. If patient compliance for a
series of injections may be a problem, then consider Synvisc-One.
• No specific VS has been proven to be superior to another, so clinicians can help their patients to make
individualized choices. The variables include but are not limited to patient allergies (eg, egg allergies
require avoiding those VS made from avian products) or the patient’s ability to return to the office
weekly for repeated injections.
• Many needle approaches can be utilized, all with relatively good accuracy, but our preferred approach
is the medial supra-patellar approach. The patient remains relaxed in the supine position, with the knee
extended and a 22-gauge 2-in needle is guided percutaneously under the supero-medial aspect of the
patella into the joint capsule.
• These procedures can be repeated to manage recurrent symptoms (eg, knee pain, joint effusion) and
maintain quality of life.
• Typically, the use of steroids is best in patients with concurrent acute synovitis and arthritis versus
viscosupplementation which is best utilized in patients with knee osteoarthritis without synovitis.
References
1. Forrester JV, Balazs EA. Inhibition of phagocytosis by high molecular weight hyaluronate.
Immunology. 1980;40(3):435-446.
2. Ghosh P. The role of hyaluronic acid (hyaluronan) in health and disease: interactions with cells,
cartilage and components of synovial fluid. Clin Exp Rheumatol. 1994;12(1):75-82.
3. Raynauld JP, Buckland-Wright C, Ward R, et al. Safety and efficacy of long-term intraarticular steroid
injections in osteoarthritis of the knee: a randomized, double-blind, placebo-controlled trial. Arthritis
Rheum. 2003;48(2):370-377.
4. Bellamy N, Campbell J, Robinson V, Gee T, Bourne R, Wells G. Viscosupplementation for the
treatment of osteoarthritis of the knee. Cochrane Database Syst Rev. 2006;(2)(2):CD005321.
5. Bellamy N, Campbell J, Robinson V, Gee T, Bourne R, Wells G. Intraarticular corticosteroid for
treatment of osteoarthritis of the knee. Cochrane Database Syst Rev. 2005;(2)(2):CD005328.
6. Marshall KW. Viscosupplementation for osteoarthritis: current status, unresolved issues, and future
directions. J Rheumatol. 1998;25(11):2056-2058.
7. Fernandez Lopez JC, Ruano-Ravina A. Efficacy and safety of intraarticular hyaluronic acid in the
treatment of hip osteoarthritis: a systematic review. Osteoarthritis Cartilage. 2006;14(12):1306-
1311.
8. Migliore A, Tormenta S, Martin LS, et al. Open pilot study of ultrasound-guided intra-articular
injection of hylan G-F 20 (Synvisc) in the treatment of symptomatic hip osteoarthritis. Clin
Rheumatol. 2005;24(3):285-289.
9. Caglar-Yagci H, Unsal S, Yagci I, Dulgeroglu D, Ozel S. Safety and efficacy of ultrasound-guided
intra-articular hylan G-F 20 injection in osteoarthritis of the hip: a pilot study. Rheumatol Int.
2005;25(5):341-344.
10. Goldberg VM, Coutts RD. Pseudoseptic reactions to hylan viscosupplementation: diagnosis and
treatment. Clin Orthop Relat Res. 2004;(419)(419):130-137.
11. Puttick MP, Wade JP, Chalmers A, Connell DG, Rangno KK. Acute local reactions after intraarticular
hylan for osteoarthritis of the knee. J Rheumatol. 1995;22(7):1311-1314.
12. Aviad AD, Houpt JB. The molecular weight of therapeutic hyaluronan (sodium hyaluronate): how
significant is it? J Rheumatol. 1994;21(2):297-301.
13. Bannuru RR, Natov NS, Obadan IE, Price LL, Schmid CH, McAlindon TE. Therapeutic trajectory of
hyaluronic acid versus corticosteroids in the treatment of knee osteoarthritis: a systematic review and
meta-analysis. Arthritis Rheum. 2009;61(12):1704-1711.
14. Altman R, Hochberg M, Moskowitz R, Schnitzer T. Practice Guidelines: Recommendations for the
Medical Management of Osteoarthrits of the Hip and Knee.
http://www.rheumatology.org/practice/clinical/guidelines/oa-mgmt.asp. Published May 12, 2000.
Updated 2000. Accessed June 18, 2011.
15. Altman R, Asch E, Bloch D, et al. Development of criteria for the classification and reporting of
osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria
Committee of the American Rheumatism Association. Arthritis Rheum. 1986;29(8):1039-1049.
16. Zhang W, Doherty M, Peat G, et al. EULAR evidence-based recommendations for the diagnosis of
knee osteoarthritis. Ann Rheum Dis. 2010;69(3):483-489.
17. Netter F. Atlas of Human Anatomy. 4th ed. Philadelphia, PA: Saunders Elsevier; 2006:506-507, 508,
509, 510, 511.
18. Daley EL, Bajaj S, Bisson LJ, Cole BJ. Improving injection accuracy of the elbow, knee, and
shoulder: does injection site and imaging make a difference? A systematic review. Am J Sports Med.
2011;39(3):656-662.
19. McGarry JG, Daruwalla ZJ. The efficacy, accuracy and complications of corticosteroid injections of
the knee joint. Knee Surg Sports Traumatol Arthrosc. 2011.
20. Esenyel C, Demirhan M, Esenyel M, et al. Comparison of four different intra-articular injection sites
in the knee: a cadaver study. Knee Surg Sports Traumatol Arthrosc. 2007;15(5):573-577.
21. Walsh NE, Eckmann M. Frontera WR, DeLisa JA, Gans BM, Walsh NE, Robinson LR, eds. DeLisa’s
Physical Medicine and Rehabilitation, Principles and Practice. Vol II. 5th ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2010:1866-1867.
22. Sarwark JF. Knee and Lower Leg. In: Sarwark JF, Koh J, eds. Essentials of Musculoskeletal Care.
4th ed. Rosemont, IL: The American Academy of Orthopaedic Surgeons; 2010:647-648, 649.
23. Synvisc, Hylan G-F 20 (prescribing information). In: Ridgewood, NJ: Genzyme Biosurgery; 2010.
24. Hamburger MI, Lakhanpal S, Mooar PA, Oster D. Intra-articular hyaluronans: a review of product-
specific safety profiles. Semin Arthritis Rheum. 2003;32(5):296-309.
25. Ozturk C, Atamaz F, Hepguler S, Argin M, Arkun R. The safety and efficacy of intraarticular
hyaluronan with/without corticosteroid in knee osteoarthritis: 1-year, single-blind, randomized study.
Rheumatol Int. 2006;26(4):314-319.
26. Gonzalez-Fuentes AM, Green DM, Rossen RD, Ng B. Intra-articular hyaluronic acid increases
cartilage breakdown biomarker in patients with knee osteoarthritis. Clin Rheumatol. 2010;29(6):619-
624.
27. Garnero P, Ayral X, Rousseau JC, et al. Uncoupling of type II collagen synthesis and degradation
predicts progression of joint damage in patients with knee osteoarthritis. Arthritis Rheum.
2002;46(10):2613-2624.
28. Balch HW, Gibson JM, El-Ghobarey AF, Bain LS, Lynch MP. Repeated corticosteroid injections into
knee joints. Rheumatol Rehabil. 1977;16(3):137-140.
29. Ayral X. Injections in the treatment of osteoarthritis. Best Pract Res Clin Rheumatol.
2001;15(4):609-626.
30. Noerdlinger MA, Fadale PD. The role of injectable corticosteroids in orthopedics. Orthopedics.
2001;24(4):400-5; quiz 406-7.
31. McColl GJ, Dolezal H, Eizenberg N. Common corticosteroid injections. An anatomical and evidence
based review. Aust Fam Physician. 2000;29(10):922-926.
32. Rozental TD, Sculco TP. Intra-articular corticosteroids: an updated overview. Am J Orthop (Belle
Mead NJ). 2000;29(1):18-23.
33. Wada J, Koshino T, Morii T, Sugimoto K. Natural course of osteoarthritis of the knee treated with or
without intraarticular corticosteroid injections. Bull Hosp Jt Dis. 1993;53(2):45-48.
CHAPTER 52
Trigger Point Injections

Ricardo A. Nieves and Rinoo V. Shah
INDICATIONS
• Trigger point injections (TIs) are commonly used as a treatment option in patients with acute and
chronic muscle pains associated with an irritable, tight or taut muscle band, or palpable knot within a
muscle that can radiate pain into specific distant or referred pattern called the “reference pain zone.”
• Pain can be present at rest, with poor posture or with overuse activity increasing the stress of a
particular muscle or muscles involved. It can be the primary pathology in a muscle injury due to trauma
or accident (ie, Whiplash) or secondary to underlying problem such as disk herniations, facet joint pain
or bone, nerve injury.
• Trigger points are commonly present in patients with myofascial pain syndrome. This is a chronic
regional localized pain syndrome with several trigger points limited to a particular area of the body.
The neck and upper and lower back are commonly involved areas.
• In the cervical and thoracic area common muscles involved include the paraspinal muscles: splenius
capitis, sternocleidomastoid, trapezius, levator scapulae, rhomboids, latissimus dorsi, serratus
posterior inferior.
• In the lumbar spine, it commonly involves the quadratus lumborum (both deep and superficial), psoas,
internal oblique, iliocostalis, longissimus or deep semispinalis, and multifidus.
• Trigger points in the shoulder rotator cuff muscles (supraspinatus, infraspinatus, subscapularis, and
teres minor) and shoulder blade area such as serratus posterior superior, latissimus dorsi, teres major,
coracobrachialis, serratus anterior can present with referred pain patterns that can mimic or be
confused with nerve root or radicular distribution.
• Similarly, trigger points in the gluteus medius, minimus, and piriformis muscles can refer down the
posterior lateral thigh and be confused with sciatica.
• Trigger points are not to be confused with tender points commonly present in patients with
fibromyalgia in which pressure in the tender points cause pain but no distant reference zone.
PHYSICAL EXAMINATION
• Physical examination findings include a knot, tight or taut muscle band.
• Associated with muscle spasm, irritable muscle with positive “jump sign,” histamine reaction.
• Painful on resistance to movement as during manual muscle strength testing.
• Referred pain in a “reference pain zone.”
• And at times, muscle twitch presents with pressure or when needle is inserted in the muscle.
• A pressure algometer can be use to quantify abnormal pressure pain sensitivity over trigger points and
to identify the most painful trigger points for injection.
• Increase of pressure pain threshold by 2 to 3 kg immediately after TPI indicates that the injection was
effective.
• A trigger point is called active when the referred pain is present spontaneously and latent when the
referred pain is elicit with pressure or muscle activity.
TYPICAL REFERRED PATTERNS

Goal of Trigger Point Injections
The primary goal of the trigger point injections is to inactivate the trigger points by destroying and
anesthetizing the primary area of pain through needling and infiltration with injectable solution.
Equipment and Supplies (Figure 52-1)
Figure 52-1. Picture of the tray.
• Sterile gloves
• Betadine and/or alcohol solution or other antiseptic solution
• Ethyl chloride spray
• 1% lidocaine (usual anesthetic of choice) and/or 0.25% or 0.5% marcaine, +/– steroid
• 10-cc syringe
• 25-gauge 1.5-in needle for superficial muscles and 25-gauge 3.5-in needle for deeper muscles
Procedure
• Patient is positioned to optimize access to the affected muscle, ie, prone for posterior muscles and
supine for anterior muscles (ie, sternocleidomastoid, pectoralis, abdominals, biceps, quadriceps); see
Figure 52-2.
Figure 52-2. Patient positioning.
• Ensure comfortable breathing and body positioning by using a head rest, pillows under the chest or
abdomen and pillow under the legs.
• In the neck and upper back, the sitting position can be used but prone position preferably due to
potential vasovagal reaction.
• Identify and mark with sterile marker trigger point locations (Figure 52-3) and more painful area
within the trigger point.
Figure 52-3. (A–D) Examples of common trigger points with reference zone marked.
• Clean area to be injected with antiseptic solution of choice. Spray the area to be injected (the taut
band) with ethyl chloride to slight frost point.
• Utilizing a 25-gauge 1.5 in needle for deeper muscles insert the needle into the muscle slowly (Figure
52-4).
Figure 52-4. Example of injection.
• Give yourself time to feel the needle advancing through skin, subcutaneous tissue, normal muscle, and
contacting the trigger point or fibrotic tissue and find trigger point (ideally muscle twitch present)
through needling technique moving the needle back and forth through the trigger point.
• After negative aspiration of blood, fluid, or air inject a total of 3 mL of solution per trigger point
location.
• Following the injection ethyl chloride stretch and spray can be of help.
• Also acupuncture needle placement and left to disperse for 10 to 15 minutes or gentle massage in the
area injected.
POSTINJECTION INSTRUCTIONS
• No heavy activity or exercise except for gentle stretching on the day of the procedure and apply heat to
the injection site for 15 minutes with a barrier between skin and heat 2 to 3 times a day.
• Postinjection stretching and stabilization program and instructions/education on proper posture, spine
mechanics and extremities ergonomics.
• Infection, bleeding, reaction to the medications used (keep total lidocaine used to no >20 mL),
vasovagal reaction, injection site pain (temporary flare up) or more serious complications such as
pneumothorax.
• If using steroid be aware of potential skin depigmentation changes and possible skin atrophy
particularly on thin patients and with superficial muscles.
CLINICAL PEARLS
• While among the safest procedures, they are not without risk.
• Risk of pneumothorax when performing procedure either posterior or anterior over the lung margins
(ie, cervical upper thoracic and anterior injections).
• When using a 25-gauge needle it can deflect without the operator being aware of what is happening at
the tip of the needle.
• Patients may cough at the time of the procedure or have a strange taste in the mouth. Certainly shortness
of breath can occur.
• Other concerns include injection of local anesthetic into superficial arteries in the neck.
• Vertebral and carotid injections with even low volume of local anesthetics can cause seizures and
death.
• As with all interventional procedures, it is important to use caution and carefully weigh the risks and
benefits of the proposed procedures.
Suggested Reading
Fischer AA. Pressure threshold measurement for diagnosis of myofascial pain and evaluation of treatment
results. Clin J Pain. 1987;2:207-214.
Fischer AA. Documentation of myofascial trigger points. Arch Phys Med Rehabil. 1988;69:286-291.
Fischer AA. Local injections in pain management. Trigger point needling with infiltration and somatic
blocks. Phys Med Rehabil Clin North Am. 1995;6:851-870.
Fischer AA. Myofascial pain. In: Windsor RE, Lox DM, eds. Soft Tissue Injuries: Diagnosis and
Treatment. Philadelphia, PA: Hanley & Belfus; 1998:85-100.
Fischer AA. Treatment of myofascial pain. J Musculoskeletal Pain. 1999;7:131-142.
Garvey TA, Marks MR, Wiesel, SW. A prospective, randomized, double-blind evaluation of trigger point
injection therapy for low-back pain. Spine. 1989;14:962-964.
O’Connor T, Abram S. Atlas of Pain Injection Techniques. Churchill Livingstone; 2003:101-112.
Scott NA, Guo B, Barton PM, Gerwin RD. Trigger point injections for chronic non-malignant
musculoskeletal pain: a systematic review. Pain Med. 2009;10(1):54-69.
Simons DG. Myofascial pain syndromes due to trigger points. In: Goodgold J, ed. Rehabilitation
Medicine. St. Louis, MO: Mosby; 1988.
Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Vol. I.
Baltimore, MD: Williams & Wilkins; 1983.
Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. The Lower
Extremities. Vol. II. Baltimore, MD: Williams & Wilkins; 1992.
CHAPTER 53
Neuroma Injections
Rinoo V. Shah and Ricardo A. Nieves
INTRODUCTION
Neuromas are considered “tumors” of neural structures. For purposes of this chapter, we refer to non-
neoplastic neuromas. Neuromas typically form following surgical transection, trauma, or entrapment.
Neuromas are considered to be discrete enlargements. If superficial, they may be palpable. If deeper, they
may be visualized with noninvasive imaging tools (MRI, ultrasound).
Like trigger points, a neuroma can be stimulated with normal palpation (allodynia). Painful stimuli over
a neuroma may lead to an excessive or prolonged pain response, ie, hyperalgesia and hyperpathia. Due to
dysfunction of this neural tissue, there may be impairment in conduction. Motor function and sensory
processing may be dysfunctional. Autonomous and maladaptive reflexes may be present.
Infiltration with a local anesthetic and steroid may be therapeutic. Perineural infiltration is preferred,
since intraneural injections may lead to permanent nerve damage and paradoxically, a deafferentation pain
syndrome.
INDICATIONS
Neuroma injections (NIs) are commonly used as a treatment option in patients with acute and chronic
pain. Pain can be present at rest or with movement. Neuroma pain may be exacerbated with constriction,
eg, stump and the Morton neuromas.
Trigger points are commonly present in patients who have undergone surgery. This is especially true
when the surgical scar injured a peripheral nerve, eg, limb amputation or rib resection or retraction.
Neuromas may be found in the surgical bed:
• In areas exposed to repetitive trauma
• Or, in areas exposed to overuse
Neuromas may be confused with tender points, as is usually found in patients with fibromyalgia. Unlike
fibromyalgia, neuromas are typically isolated and develop secondary to a specific event.
PHYSICAL EXAMINATION
Physical examination findings include:
• A palpable and tender swelling that is painful with light touch (allodynia).
• Deeper pressure leads to a more protracted (hyperpathic) and heightened (hyperalgesic) pain response.
• The scar should be healed.
• Poorly healing scars or ulcers should be addressed, before considering neuroma injections.
• Some healed surgical scars may demonstrate dystrophic or color changes.
• There may be a significant amount of allodynia, distributed around the scar.
• In this situation, there may be a heightened sympathetic response in addition to the presence of
neuromas.
• Passive stretching of the scar or focal neuroma compression should elicit pain.
• This pain should be eliminated following a neuroma injection.
• Arguably, a pressure algometer, as described in the trigger point injection chapter, may be useful: “an
increase in the pressure pain threshold by 2 to 3 kg, immediately after the NI will indicate an effective
injection.”
GOAL OF NEUROMA INJECTIONS

The primary goal of the neuroma injections is to inactivate the neuromas by anesthetizing the primary area
of pain through needling and infiltration with an injectable solution.
EQUIPMENT AND SUPPLIES

• Sterile gloves
• Betadine and/or alcohol solution or other antiseptic solution, eg, chlorhexidine
• Ethyl chloride spray
• 1% lidocaine (usual anesthetic of choice) and/or 0.25% or 0.5% marcaine, +/– steroid (40 mg depo-
medrol, 3 to 6 mg betamethasone, and 2 to 4 mg dexamethasone).
• 10-cc syringe
• 25-gauge 1.5-in needle for superficial neuromas and 22- to 25-gauge 3.5-in needle for deeper
neuromas
• Image guidance (fluoroscopy, ultrasound)
PATIENT POSITIONING
• Patient is positioned in the supine, prone, or side lying position depending on the location of neuroma.
• Assurance of comfortable breathing and body positioning by using a head rest, pillows under the chest
or abdomen and pillow under the legs.
• In the neck and upper back, the sitting position can be used but prone position preferably due to
potential vasovagal reaction.
PROCEDURAL STEPS
• Identify and mark with sterile marker the neuroma locations.
• Area to be injected is cleaned with an antiseptic solution of choice.
• Spray the area to be injected (the taut band) with ethyl chloride to slight frost point.
• Utilizing a 25-gauge 1.5-in needle or 22- to 25-gauge 3.5-in needle for deeper neuromas, insert the
needle into the skin.
• One should feel the needle advancing through skin, subcutaneous tissue, normal muscle, and contacting
the neuroma or fibrotic tissue.
• Pain should be elicited.
• The needle trajectory should be at a 45-degree angle to the skin. This is especially important near the
chest wall.
• After negative aspiration of blood, fluid or air inject a total of 1 to 5 mL of solution per neuroma
location.
• Following the injection ethyl chloride stretch and spray can be of help, also acupuncture needle
placement and left to disperse for 10 to 15 minutes or gentle massage in the area injected.
POSTINJECTION INSTRUCTIONS
• No heavy activity or exercise except for gentle stretching on the day of the procedure.
• Apply heat to the injection site for 15 minutes 2 to 3 times a day for 3 days with a barrier between skin
and heat.
• Postinjection stretching and stabilization program and instructions should be provided along with
education on proper posture, spine mechanics, and extremities ergonomics.
• Infection
• Bleeding
• Reaction to the medications used (keep total lidocaine used to no more than 20 mL)
• Vasovagal reaction
• Injection site pain (temporary flare up) or more
• Serious complications such as pneumothorax if injected in thoracic area
• If using steroid be aware of potential skin depigmentation changes and possible skin atrophy
particularly on thin patients and with superficial muscles.
CHAPTER 54
Myofascial Injections (Trigger Point, Piriformis,

Iliopsoas, and Scalene Injections)
Clark C. Smith, Farooq Khan, Juan Francisco Asenjo, and Honorio T. Benzon
OVERVIEW OF MYOFASCIAL INJECTIONS

Myofascial pain is a common source of pain in the neck, low back, and other areas of the body. The term
“myofascial pain” encompasses muscle strain, myofascial trigger points, and specific muscle pain
syndromes. These syndromes include piriformis syndrome, iliopsoas related pain, and pain associated
with the scalene muscles (trigger points, neurogenic thoracic outlet syndrome).
RELEVANT ANATOMY
Skeletal muscle consists of muscle fibers under somatic nervous control. Each nerve root innervates a
muscle or group of muscles known as a myotome. The muscle belly of skeletal muscles is connected by
tendons to bone. Trigger points occur in the muscle body, most often located in the center of the muscle.
TRIGGER POINT INJECTIONS

• Trigger points are hyperirritable localized taut bands of skeletal muscle that produce characteristic
referral patterns.
• A trigger point (TP) may occur in isolation or concomitantly with myofascial pain syndrome or other
pain generating syndromes.
• Trigger points are diagnosed by history and physical examination.
• A patient will complain of a localized pain or regional pain located in or around any skeletal muscle.
• The neck, shoulder girdle, and low back are the most common areas involved. Commonly involved
muscles are the trapezius, splenii, cervical and lumbar paraspinal muscles, and the quadratus
lumborum.
• On examination, localized taut bands of muscle are noted and palpation produces characteristic non-
dermatomal referral patterns.1
• Trigger points may be active or latent. Active trigger points produce spontaneous pain, while latent
trigger points produce pain only when palpated.
• Active trigger points may result from trauma, overload or overuse injury, or due to a muscle being in a
prolonged contracted or shortened position.
• Treatments for active trigger points include physical therapy (stretching and strengthening,
conditioning, therapeutic modalities); trigger point injections; acupuncture; biofeedback;
transcutaneous nerve stimulation (TENS); and some medications.2-4
• Trigger point injections are intramuscular injections of local anesthetic with or without corticosteroids
thought to work by local anesthetic effect, interruption of pain transmission, mechanical effects on the
muscle itself, and disruption of ephaptic transmission.

• Immunocompromised patients, patients at high risk for infection.
• Patients with allodynia in the area of injection.
Contraindications
• Coagulopathy
• Patient refusal
• Refer to ASRA guidelines, consider the risks and benefits.
• Anticoagulation—this is less of a concern than for an epidural.
• The ability of a patient to tolerate a supine, prone, lateral decubitus, or seated position for the
injection.
Equipments
• 3, 5, or 10 mL syringe for medications
Medications
• 0.25% bupivacaine or other local anesthetic
• Corticosteroid (dexamethasone, triamcinolone, or methylprednisolone)
Technique
• The muscle is palpated and the trigger points are identified and marked. Ultrasound may be used to
identify hypoechogenic TPs.
• Sterile prep of the area to be injected.
• The needle is inserted into the trigger point. When the patient verbally identifies the painful area, and
after negative aspiration, local anesthetic is injected with or without steroid. Botolinum toxin A, 6-12.5
units per muscle, total dose not to exceed 300 units.
• The authors use a nonparticulate steroid, dexamethasone (4 mg in 30 mL bottle of local anesthetic), or a
low dose of particulate steroid (eg, 20-40 mg of methylprednisolone diluted in the local anesthetic
solution) may also be used.
• Pain relief can be obtained with 1 to 3 mL of injectate per trigger point this may be done in a fanwise
technique.
• There should be no paresthesia, blood, or cerebrospinal fluid (CSF) with needle insertion.
• Bleeding
• Depending on the location of the injection, the patient should be instructed on the signs and symptoms
of pneumothorax (neck, shoulder, thoracic, and anterior chest wall injections), or local nerve blockade
(eg, inadvertent median nerve block in injection of flexor carpi ulnaris).

• Infection
• Bleeding
• Nerve block
• Hematoma
Clinical Pearls
• The success of the procedure of the procedure is dependent on the diagnosis and localization of the
trigger point.
• Patients with chronic widespread pain or psychological disorders may be less likely to respond to
TrPs.
• Patient’s can expect days to weeks or months of 50% to 100% relief. In some instances of acute TrPs in
the absence of other pain generators, a TrP injection is curative when combined with physical therapy
or a home exercise program.
PIRIFORMIS INJECTIONS
• Piriformis syndrome (PS) is a painful condition consisting of pain in the buttock with or without
radiation in the distribution of the sciatic nerve.
• It is a relatively uncommon disorder though some suggest it may contribute to up 8% of buttock pain.
Piriformis syndrome is a diagnosis of exclusion.
• There are no standardized diagnostic criteria for PS.
• Piriformis syndrome can be a consequence of an abnormal relationship between the sciatic nerve and
the piriformis muscle (PM), resulting in irritation of the sciatic nerve.
• A hypertrophic muscle, infection or the invasion of the muscle by tumor can cause pressure/irritation
on the nerve.
• In 78% to 84% of the population, the sciatic nerve passes in front and medial to the muscle, but in 12%
to 21% of individuals the divided nerve passes through or posterior to the muscle being exposed to its
contractions triggering sciatic symptoms.5,6
• Piriformis syndrome should be considered in patients who present with buttock pain, tenderness to
palpation over the PM, and have a positive response to several provocative maneuvers including5:
Pace sign: pain and weakness with seated abduction of the hip against resistance
Lasegue sign: pain with unresisted flexion, abduction, and internal rotation of the flexed hip
Freiberg sign: pain with forced (ie, against resistance) internal rotation of the extended hip
Due to its small size, its proximity to neurovascular structures, and its deep location, the piriformis
muscle is usually injected under radiographic or ultrasound guidance. Piriformis injections under CT or
electromyographic guidance have also been described.7,8 In this chapter, we will discuss flouoroscopic
and US-guided piriformis injections.

Piriformis injections are relatively safe procedures. However, the same conditions noted in the section on
trigger point injections are causes for concern.
Contraindications and Preoperative Considerations

These are the same as the ones noted in the section on trigger point injections.
Equipments
• Insulated nerve-stimulating 15-cm block needle
• Nerve stimulator
• 3, 5, or 10 mL syringe for medications
Medications
• 0.25% bupivacaine or 1% lidocaine
• Corticosteroid (dexamethasone, triamcinolone, or methylprednisolone)
Fluoroscopic Technique
• The patient is placed prone on a fluoroscopy table, and the inferior margin of the sacroiliac joint is
imaged and marked.
• The patient is prepped and draped in sterile fashion.
• The needle insertion site is 1 to 2 cm caudal and 1 to 2 cm lateral to the inferior margin of the SI joint.
• The insertion site is anesthetized with 2 to 3 mL of 1% lidocaine.
• The insulated needle is inserted and advanced with the nerve stimulator on (1 mA, 2 Hz, 0.1 ms) until a
sciatic nerve evoked motor response is achieved (dorsiflexion, plantar flexion, eversion, inversion) at
0.4 to 0.6 mA.
• The needle is slightly withdrawn until the sciatic stimulation disappears. This is to avoid intraneural
injection.
• Steroid (40 mg of either methylprednisolone or triamcinolone) plus 5 mL of saline is injection around
the sciatic nerve.
• The needle is pulled back 1 cm into the belly of the piriformis muscle and 1 to 2 mL contrast is
injected.
• The contrast should outline the piriformis muscle belly with no sign of spillage, ie, the margins are
clean (Figure 54-1).
Figure 54-1. The piriformis muscle was outlined after a dye injection. (Reproduced with permission
from Mackenzie-Brown, Chekka K, Benzon HT. Reprinted from: Musculoskeletal injections: Iliopsoas,
quadratus lumburom, piriformis, trigger point injections. In Huntoon M, Benzon HT, Narouze, S. Spinal
Injections and peripheral nerve blocks. In Deer T. Interventional and Neuromodulatory Techniques in
Pain Management. New York: Elsevier – Churchill Livingstone, 2011.)
• After the characteristic dye spread is achieved, the local anesthetic solution and steroid are
administered. Typically, good pain relief can be attained with an injection of 5 mL of 0.25% or 0.5%
bupivacaine plus 40 mg of methylprednisolone (or triamcinolone).
Ultrasound-Guided Piriformis Injections

Ultrasound-guided technique permits not only a direct view of the PM, but also examines its relationship
to the sciatic nerve and rule out some an anatomic variation.9
Patient Position
The patient is in prone position with the US machine on the opposite side.
Equipment
• A curved, low frequency US probe (2-6 MHz) is used to scan a wider and deep area.
• US machine should have Doppler to help identifying the inferior gluteal artery medial to the sciatic
nerve and anterior to the PM.
• A 20- to 22-gauge 10- to 12-cm-long needle is recommended.
Preparation as described above.
Scanning Procedure
There are 2 recommended scanning techniques:
1. The classic technique
• Position the transducer in short-axis (transverse) over the SIJ where medially the sacrum will be
visible and laterally the ilium/gluteus maximus muscle (GMM) complex will be observed.10
• Keep the SIJ in the center of the screen and move the transducer caudal until the lateral view of
the ilium is lost, indicating that the transducer is over the greater sciatic notch.
• In that position the operator will see the hyperechoeic lateral portion of the sacrum medially.
• In the center of the image, the following are visualized: the skin and fat in the near field, then the
GMM and deeper to it and originating from the anterior/lateral sacral edge is the piriformis
muscle with the typical longitudinal fibers.
• Clockwise rotation on the right gluteal area and counter clockwise on the LEFT gluteal area.
Move the transducer slightly lower and with mild clockwise rotation, the sciatic nerve will be
visible deeper in the medial aspect of the piriformis and the ischium appears initially as a curved
hyperechoeic line (posterior acetabulum) and more caudally it becomes a flat line deeper to the
piriformis (Figure 54-2).
Figure 54-2. The piriformis muscle over the ischium and the sciatic nerve and under the gluteus maximus
muscle (GMM). The red dashed arrow shows the in-plane needle trajectory.
2. Alternative technique
• Place the transducer over the line between the greater trochanter and the ischial tuberosity.
• Once the sciatic nerve is identified, it is followed cephalad until the PM and the GMM are seen
over the sciatic nerve.
Two Pearls with Either Approach

• To confirm the view of the PM, flex the knee in 90 degrees and rotate the hip of the patient
internally/externally to see the PM sliding over the ischium as opposed to the stable position of the
GMM (Figure 54-3).
Figure 54-3. Typical movement to identify the piriformis muscle over the ischium when flexing the knee
in 90 degrees and rotating the hip internally externally.
• When observing the sciatic notch it is useful to identify the ischial spine since other muscles in similar
position to the PM insert in the area (ie, the gemelli and obturator muscles) and should be
differentiated from the PM.
Needle Insertion
• The more perpendicular the needle is to the US beam, the better is the view.
• With the patient in prone position, the PM runs almost horizontal between the sacrum and the femur.
• We suggest a lateral to medial, in-plane approach with the needle entering the skin at 3 to 4 cm lateral
to the lateral edge of the transducer to achieve a rather flat trajectory that makes it much easier to see.
• After local anesthetic infiltration, the needle should cross the skin and fat in a lateral-to-medial,
posterior-to-anterior direction, enter the GMM and then the PM in its medial half, where it is thicker.
• Hydrodissection with normal saline (NS) 1 mL may help in confirming the position of the tip before
injecting into the PM.
• A steroid (methylprednisolone or triamcinolone) with local anesthetic bupivacaine or lidocaine is then
injected.
Patient should be advised to call pain medicine service for any procedure related complications and/or
any unexpected neurological deficit. Though complications are uncommon, patient should be monitored
closely for following:
It is common for the patient to have weakness or numbness in the distribution of the sciatic nerve for
the expected duration of the local anesthetic.
• Bleeding

Same as in the section on trigger point injections plus sciatic nerve blockade.
Clinical Pearls
• The success of the procedure is dependent on the diagnosis of piriformis syndrome.
• Patients with other spine or SI joint comorbidities, chronic widespread pain or psychological
disorders may be less likely to respond.
ILIOPSOAS INJECTIONS
Overview
Pain emanating from the iliopsoas muscle is relatively uncommon, but a very real cause of low back, hip,
or inguinal pain. Patients typically present with unilateral low back or anterior hip pain, though pain can
frequently refer into the thigh or inguinal area.
On examination:
• An antalgic gait may be noted as the patient enters the examination room, due to a shortened stride on
the affected side.
• The patient may also have pain and/or weakness when squatting to sit or when transitioning from a
seated position to a standing one.
• The psoas muscle can be palpated deep in the abdomen, medial to the anterior superior iliac spine,
when the ipsilateral hip is flexed.
• Pain on palpation while flexing the hip against resistance is an excellent diagnostic tool for psoas
myopathy, but may be extremely uncomfortable for the patient due to pain and privacy reasons.
Provocative tests:
• Are not specific for the iliopsoas muscle, but can be used to aid in the diagnosis via active and passive
extension of a painful muscle.11
• Thomas test—inability of the patient to completely extend the affected hip when lying supine, with
contralateral hip fully flexed, due to tightened hip flexors
• Yeoman test—pain with passive extension of affected hip when lying prone, typically a sacroiliac joint
test, but can cause anterior hip pain with passive iliopsoas extension
• Gaenslen test—pain with maximal extension of affected hip (leg hangs off examination table) and
maximal flexion of contralateral hip (knee held to chest), typically a sacroiliac joint test, but can cause
anterior hip pain with passive iliopsoas extension
• FABER test—pain with Flexion Abduction and External Rotation of affected hip
• Snapping hip test—“snapping” or “clicking” when hip is rotated from flexion and abduction to
extension and adduction—this rules out coxa saltans or “snapping hip syndrome”
Relevant Anatomy
• The psoas major muscle is located in the retroperitoneal space and is composed of two layers.
• A deep layer that originates from the transverse processes of L1-5.
• A superficial layer that originates from the lateral portions of T12-L4.
• The lumbar plexus is located between these two layers of muscle.
• The psoas major also has fibrous attachments to all of the lumbar discs except the L5-S1.
• According to their position, the attachments are categorized as either “anterior” or “posterior.”
• The attachments located on the vertebral bodies and intervertebral discs are referred to as anterior
fascicles, while those located on the transverse processes are known as the posterior fascicles.12
• The psoas joins the iliacus muscle, which arises from the ilium, to form the iliopsoas muscle within the
iliac fascia.
• This muscle then runs anterolaterally through the iliopubic (iliopectineal) eminence, through the
muscular lacuna beneath the inguinal ligament, then forms a tendon that sits anterior to the hip joint and
finally inserts onto the lesser trochanter of the femur.13
• Innervation of the psoas muscle is achieved via the lumbar plexus from the ventral rami of L1-3, while
the iliacus muscle is innervated by the femoral nerve from the ventral rami of L1-4.
Imaging
Once the diagnosis is suspected, it can be confirmed through history and physical examination alone,
without the aid of special imaging. However, diagnostic imaging is often required due to the uncommon
nature of the syndrome, and a diagnosis is frequently made based on incidental findings. Multiple imaging
modalities, including ultrasound, CT scan, and MRI can be useful in providing rapid and accurate
information. CT scanning can be used to outline the extent of affected tissue and may provide a diagnosis,
such as infection or tumor.
Basic Considerations
The same concerns that apply to any myofascial injection will apply to iliopsoas injections as well. Care
must also be taken to ensure that the muscle is free of tumor, abscess or hematoma before proceeding with
an injection. Additionally, the practitioner must always be cognizant of the muscle’s intimate relation to
the spinal column and major vascular structures.

See section on trigger point injections.
Contraindications
Include the following, in addition to the ones noted in the section on trigger point injections:
• Known allergy to contrast
• Pregnancy (for fluoroscopy only)
See section on trigger point and piriformis injections.
Equipment (for fluoroscopy-guided injections)

• Sterile prep and drape
• 3.5-in 22- or 25-gauge spinal needle
• 1.5-in 25-gauge needle for infiltration
• 2 × 3 mL syringes (for contrast and local anesthetic)
• 5 mL syringe (for injectate)
• Extension tubing (flush air out)
• Local anesthetic with/without steroid
• Iodinated contrast
• Fluoroscopy or ultrasonography
Medications
• Long or short acting local anesthetic (0.25% or 0.5% bupivacaine)
• Steroid (methylprednisolone or triamcinolone)
• Sedation if needed for procedure (midazolam)
Fluoroscopic Technique
• Perform “timeout”
Verify patient, procedure, side, allergies, and contraindications.
Verify all necessary equipment is prepared.
• Place patient prone on examination table.
Ensure patient is comfortable and can remain still.
Place pillows beneath abdomen as needed to correct lumbar lordosis.
Apply monitors as needed.
• Perform sterile prep and drape.
• Visualize L4 transverse process on AP fluoroscopy.
Place radiopaque marker or coaxial laser guide on inferior edge of transverse process.
• Infiltrate with local anesthetic.
Initial skin wheal
Infiltrate deep subcutaneous tissues in plane of anticipated injection.
• Place needle in subcutaneous tissue in plane with fluoroscopy beam.
• Adjust the needle as it is advanced to achieve “gun barrel” view.
• The needle is advanced approximately 1.5 cm to touch the transverse process.
• For the psoas muscle injection, the tip of the needle touches the superior aspect of the middle or the
lateral one-third of the transvers process. The needle is then advanced 1 cm beyond the transverse
process.
• Remove stylet, attach extension tubing and contrast syringe.
Ensure tubing is air free before injecting.
Aspirate to assess extravascular location before injecting.
• Inject approximately 1 mL of iodinated contrast under fluoroscopy.
Observe distinct muscle striation pattern, “sail like” (Figure 54-4).
Figure 54-4. Right psoas muscle injection. (The muscle outlined on the left is the quadratus lumborum.
Note that it is lateral to the tip of the transverse process.) (Reproduced with permission from Mackenzie-
Brown, Chekka K, Benzon HT. Reprinted from: Musculoskeletal injections: Iliopsoas, quadratus
lumburom, piriformis, trigger point injections. In Huntoon M, Benzon HT, Narouze, S. Spinal Injections
and peripheral nerve blocks. In Deer T. Interventional and Neuromodulatory Techniques in Pain
Management. New York: Elsevier – Churchill Livingstone, 2011.)
Observe contrast spreading in discrete muscle sheath.

Confirm no arborization or disappearance of contrast.
• Obtain lateral confirmatory imaging.
• Attach local anesthetic/steroid syringe to extension tubing.
Aspirate, then slowly inject medication.
STOP injecting if needle moves out of place, patient complains of severe pain, or aspiration is
positive.
Document patient’s pain before, during, and after injection.
• Usually 6 to 8 mL local anesthetic (0.5% bupivacaine) and steroid (40 mg methylprednisolone or
triamcinolone) is injected.
• Remove needles, clean patient’s skin, apply hemostatic dressing.
• Assess patient for any immediate complications or side effects.
Weakness, bleeding, increased pain
ULTRASOUND-GUIDED TECHNIQUE
Single shot procedures as well as catheter placements can be accomplished safely with US guidance.
Sedation as mentioned above is recommended. Two US-guided techniques are presented in this chapter.
Lateral Approach (modified from the one proposed by Kirchmair et

al)14
This technique is recommended in patients with BMI lower than 35 since the US view is impaired by the
thick abdominal wall.
• The patient is placed in lateral decubitus with a mild anterior tilt.
• Extensive skin prep is done from the posterior midline to the anterior axillary line and from the iliac
crest to the lower costal margin.
• A low-frequency (2-6 MHz) curved probe is recommended covered with a sterile plastic sheet.
• The transducer is initially placed lateral to the spine, in cross-sectional view, just above the iliac crest
(Figure 54-5).
Figure 54-5. Needle in position lateral to the vertebral body in the psoas muscle.
• The image is optimized in terms of gain, depth, texture, etc.

• The scan is moved laterally identifying the following structures as the probe is kept still and
perpendicular to the skin over the posterior axillary line (PAL): skin, fat, lateral part of the erector
spinae muscle, quadratus lumborum, part of the external and internal oblique muscles and transverse
process of L4.
• At this level, it is unlikely that the kidney is seen, unless the patient takes a very deep breath.
• The transducer is then moved slowly toward a more lateral position between the PAL and the mid
axillary line and the hyperechoeic lateral portion of the vertebral body is seen; lateral to it is the cross-
sectional cut of the psoas muscle.
• Gentle and slow scanning on the psoas muscle and looking at the medial-posterior area will show the
nerve root coming into the muscle along with an artery.
• We recommend an in-plane access with an entry point in the skin about 4 cm medial to the medial end
of the transducer.
• Anesthetize the skin with lidocaine deep in the planned trajectory of the needle.
• Use a 12- to 15-cm-long 20-gauge needle for single shot injections or a long epidural needle for
insertion of a catheter in the muscle.
• The needle is advanced from lateral to medial, from posterior to anterior in the plane of the US directly
toward a point which represents the junction between the posterior and the middle third of the muscle
(in the anteroposterior plane) and the medial and the median third in the lateral plane, almost at the
center of the body of the muscle.
• The needle is easily visible because of the almost perpendicular angle with the US beam (Figure 54-
6).
Figure 54-6. Position of the patient, transducer, and needle for the in-plane posterolateral psoas
compartment block technique.
• If catheter used, the catheter should be advanced 2 to 3 cm beyond the needle tip under direct vision
with the bevel of the needle facing cephalad along the fibers of the muscle.
• The same volumes and drugs as in the radioscopy-guided approach are recommended.
US-Guided Posterior Approach

• Position the patient prone with a pillow under the abdomen to obtain a flat, more superficial spine
position.
• The area that is prepped and draped includes the iliac crest to the last rib area. In this approach, the
transducer probe case is initially positioned longitudinally over the spinous process at the level of L3-
L4.
• The spinous processes are identified and the transducer is moved laterally showing the laminae, then
the masses of the facet joints and finally the transverse processes of L2-L3-L4 like a trident.15
• Carefully observe while the patient pushes his/her ipsilateral knee against the table, will show the
fibers of the psoas muscle deeper, in between the transverse processes.
• Local anesthesia is applied to the skin 2 to 3 cm distal to the inferior edge of the transducer and then
deep in the trajectory of the needle.
• The needle is advanced in between the transverse processes of L3 and L4 about 1.5 cm deeper from
the distance measured from the probe to the posterior surface of the transverse process.
• When injecting in that position not much will be seen and no liquid should be seen superficial to the
transverse processes.
• If catheter used, the catheter can be advanced as in the lateral approach above.
• Expect some degree of immediate relief with local anesthetic effect
• Expect from 2 to 5 days to start steroid effect
• Assess patient for lower extremity weakness
• Assess patient for any signs of intravascular anesthetic injection
• Avoid submersion in water (eg, swimming, bathtub) for 24 to 48 hours
• Keep pain log

• Intravascular injection into aorta or vena cava (needle is too anterior)
• Intrathecal or epidural injection (needle is too medial or larger volumes are injected)
• Lumbar plexus block (psoas compartment injection)
• Hematoma formation
• Abscess formation
• Allergy to any component of procedure
Clinical Pearls
• Thorough history and physical examination to ensure accurate diagnosis.
• Utilize preprocedural imaging to aid in diagnosis and plan injection.
• Ensure the muscle is free of abscess, hematoma, or tumor.
• Meticulous needle direction under fluoroscopy to avoid too medial or anterior placement.
SCALENE MUSCLE INJECTIONS

Overview
Scalene muscle injections are indicated for neurogenic thoracic outlet syndrome (TOS), as diagnostic and
therapeutic tools for either presurgical planning or pain management. The diagnosis of TOS itself can be
controversial, but since 1956, when it was first described, it was thought to result in upper extremity
symptoms due to neurovascular compression in the cervicoaxillary canal.16
• The incidence of TOS varies anywhere from 3 to 80 cases per 1000 people and there exist 3 different
forms of the syndrome: neurogenic, venous, and arterial.
• The most common type, neurogenic, accounts for 95% of all cases and results from brachial plexus
compression between the anterior and middle scalene muscles and the first rib.
• Patients often present with unilateral paresthesia and/or weakness of the upper extremity, and variable
other symptoms such as headache and cold intolerance.
• The diagnosis is often difficult to achieve due to a lack of specific diagnostic criteria, relative
insensitivity of imaging modalities and other diagnostic testing, and a lengthy list of confounding
diagnoses on the differential.17
A procedure that has proved useful in the diagnosis and management of neurogenic TOS has been local
anesthetic injection into the anterior scalene muscle alone or both the anterior and middle scalene
muscles. The result of this block relaxes the muscle(s) elevating the first rib and mimics the effects of a
first rib resection or scalenectomy. The quality of relief achieved by this technique has been shown to
correlate well with successful physical therapy and surgical treatments.18 In order to be predictive of
surgical success however, care must be taken to avoid blockade of the brachial plexus and cervical
sympathetic ganglia. In fact, successful treatment of TOS with scalene muscle injection has been shown to
be independent of any brachial plexus injection effect.19
Imaging
Even the most sensitive imaging modality (eg, MRI) fails to reveal abnormalities causing TOS in patients.
However, there are several reasons to obtain some form of high resolution imaging before performing any
procedure in the posterior triangle of the neck. First, aberrant anatomy is frequently found in this region,
from muscle anomalies (scalene minimus muscle presence, sickle-shaped middle scalene) to bone
abnormalities (cervical rib, prolonged transverse process) which may confuse needle placement. Second,
isolated or repeated trauma is a factor in up to two-third of neurogenic TOS cases, from whiplash injuries
to repetitive motion stress due to work or sports activities. In these cases, evaluating the surrounding soft
tissue for evidence of other injury (eg, rotator cuff tear) will aid in the diagnosis and management of the
patient. Finally, a very small percentage of TOS cases are acquired through tumor metastases,
osteomyelitis or other uncommon sources, that will greatly impact the treatment strategy for the patient.20

Same as in the sections on trigger point and piriformis injections
Contraindications
Same as in the previous sections
Same as in the previous sections
Equipment
• Sterile prep and drape
• 1.5-in 22- or 25-gauge needle (hyperechoic)
• 1.5-in 25-gauge needle for infiltration
• 2 × 3 mL syringes (for infiltration and local anesthetic injection)
• Extension tubing (flush air out)
• Botulinum toxin (optional)
• Ultrasonography with 10 to 12 MHz probe
• Ultrasound gel
• 4 × 4 in gauze
Medications
• Choice of long or short acting local anesthetic 2 to 3 mL (0.25% bupivacaine)
• Botulinum toxin 20 (12-15 units per muscle)
• Sedation if needed for procedure (midazolam)
Techniques
The injections can be done blindly, which is not recommended, until fluoroscopy (to see spread of
contrast within the muscle), under CT guidance, or with ultrasound which is the preferred technique.
Ultrasound-Guided Technique
• Perform “timeout.”
Verify patient, procedure, side, allergies, and contraindications.
Verify all necessary equipment is prepared.
• Place patient supine or lateral decubitus on examination table.
Ensure patient is comfortable and can remain still.
Place pillows as needed to optimize exposure.
Apply monitors as needed.
• Perform sterile prep and drape.
Sterile ultrasound sheath or Tegaderm dressing.
Apply sterile gel to ultrasound probe and skin.
Identify medial and lateral on US probe.
• Identify external landmarks (clavicle, sternocleidomastoid, trapezius).
Place probe in axial oblique plane at level of cricoid cartilage/C6 vertebra.
Move laterally from trachea.
Identify carotid artery then internal jugular vein (compressible).
Move laterally to identify brachial plexus in interscalene groove.
• Another approach via identification brachial plexus at supraclavicular area.
Place probe in supraclavicular area similar to a supraclavicular plexus block.
Identify brachial plexus lateral to artery.
Follow the brachial plexus cephalad.
Identify the anterior and middle scalene muscles on either side of the brachial plexus.
• Identify scalene muscles.
Anterior scalene muscle is medial to brachial plexus.
Middle scalene muscle is lateral brachial plexus.
Brachial plexus roots/trunks appear as round and hyperechoic between muscles.
Sliding probe inferiorly visualizes subclavian artery and vein.
• Infiltrate with local anesthetic.
Initial skin wheal
Shallow subcutaneous infiltration
• Place needle in subcutaneous tissue in plane with ultrasonography beam.
Utilize out-of-plane technique to avoid traversing the fascia on the interscalene grove, allowing
leakage of the local anesthetic and causing brachial plexus blockade19 (Figure 54-7).
Figure 54-7. An out-of-plane needle approach to scalene muscle injection. AS, anterior scalene muscle;
MS, middle scalene muscle; arrows display location of injection. (Reproduced with permission from
Benzon HT, Rodes ME, Chekka K, et al. Scalene muscle injections for neurogenic thoracic outlet
syndrome: Case series. Pain Pract 2011 Jun 2.)
Connect extension tubing to needle.
Flush tubing with local anesthetic to eliminate air.
• Adjust the needle as it is advanced to penetrate anterior or middle scalene muscle.
Advance the needle using “hydrodissection,” ie, injecting very small amounts of saline to visualize
the tip of the needle.
Avoid deviation into surrounding tissues.
Place the tip of the needle in the belly of the scalene muscle, preferably away from the brachial
plexus.
• Attach local anesthetic/botox syringe to extension tubing.
Aspirate, then slowly inject medication.
Inject 1 to 2 mL of 0.25% bupivacaine per muscle.
STOP injecting if needle moves out of place, patient complains of severe pain, or aspiration is
positive.
Document patient’s pain before, during, and after injection.
• Remove needles, clean patient’s skin, apply hemostatic dressing.
• Assess patient for any immediate complications or side effects.
Weakness, bleeding, increased pain
• Expect relief of symptoms shortly after injection with local anesthetic
• Expect relief of symptoms in 2 to 3 days with botox
• Keep log of symptoms post procedure
• Keep area clean and dry

• Horner sign
• Brachial plexus block
• Dysphonia
• Dysphagia
• Sensory blockade and weakness of the upper extremity
• Intravascular placement
• Spinal accessory nerve (CN XI) injury
Clinical Pearls
• Thorough history and physical examination to ensure accurate diagnosis.
• Utilize preprocedural imaging to aid in diagnosis and plan injection.
• Ensure the muscle is free of abscess, hematoma, or tumor.
• Meticulous needle direction under ultrasonography to avoid brachial plexus or intravascular
placement.
References
1. Borg-Stein J, Simons DG. Focused review: myofascial pain. Arch Phys Med Rehabil. 2002;84:S40-
S49.
2. Han SC, Harrison P. Myofascial pain syndrome and trigger-point management. Reg Anesth.
1997;22:89-101.
3. Testa M, Barbero M, Gherlone E. Trigger points: update of the clinical aspects. Eur Med Phys.
2003;39:37-43.
4. Cummings TM, White AR. Needling therapies in the management of myofascial trigger point pain: a
systematic review. Arch Phys Med Rehabil. 2001;82:986-992.
5. Benzon HT, Katz JA, Benzon HA, Iqbal MS. Piriformis syndrome: anatomic considerations, a new
Injection technique, and a review of the literature. Anesthesiology. 2003; 98:1442-1448.
6. Peng PWH, Tumber PS. US-guided interventional procedures for patients with chronic pelvic pain—a
description of techniques and review of the literature. Pain Physician. 2008;11:215-224.
7. Porta M. A comparative trial of botulinum toxin type A and methylprednisolone for the treatment of
myofascial pain syndrome and pain from chronic muscle spasm. Pain. 2000;85:101-105.
8. Fishman SM, Caneris OA, Bandman TB, Audette JF, Borsook D. Injection of the piriformis muscle by
fluoroscopic and electromyographic guidance. Reg Anesth Pain Med. 1998;23:554-559.
9. Chen, WS. Bipartite PM: an unusual cause of sciatic nerve entrapment. Pain. 1994;58:269-272.
10. Smith J, Fredrich-Hurdle M, Locketz AJ, Wisniewski J. Ultrasound-guided piriformis injection:
technique description and verification. Arch Phys Med Rehabil. 2006;87:1664-1667.
11. Ingber RS. Iliopsoas myofascial dysfunction: a treatable cause of “failed” low back syndrome. Arch
Phys Med Rehab. 1989;70:382-386.
12. Bogduk N, Pearcy M, Hadfield G. Anatomy and biomechanics of psoas major. Clin Biomech.
1992;7:109-119.
13. Platzer W. Color Atlas of Human Anatomy, Vol. 1: Locomotor System. Thieme Medical Publishers,
Stuttgart, Germany 2004;234.
14. Kirchmair L, Entner T, Kapral S, Mitterschiffthaller G. Ultrasound guidance for the psoas
compartment block: an imaging study. Anesth Analg. 2002;94:706-710.
15. Karmakar MK, Ho AMH, Li X, Kwok WH, Tsang K, Ngan Kee WD. Ultrasound-guided lumbar
plexus block through the acoustic window of the lumbar ultrasound trident. Br J Anaesth.
2008;100:533-537.
16. Peet RM, Henriksen JD, Anderson TP, et al. Thoracic-outlet syndrome: evaluation of a therapeutic
exercise program. Proc Staff Meet Mayo Clin. 1956 May;31:281-287.
17. Brooke BS, Freischlag JA. Contemporary management of thoracic outlet syndrome. Curr Opin
Cardiol. 2010 Nov;25:535-540.
18. Torriani M, Gupta R, Donahue DM. Sonographically guided anesthetic injection of anterior scalene
muscle for the investigation of neurogenic thoracic outlet syndrome. Skeletal Radiol. 2009;38:1083-
1087.
19. Pain Pract. 2012;12:66-70 Epub Jun 2, 2011
20. Laulan J, Fouquet B, Rodaix C, et al. Thoracic outlet syndrome: definition, aetiological factors,
diagnosis, management and occupational impact. J Occup Rehabil. 2010 Dec 31.
CHAPTER 55
Intra-Articular Joint Injections

Michael N. Brown
INTRODUCTION
In the past, the purpose for gaining intra-articular access of joints has been predominant for aspiration of
synovial fluid and injection of corticosteroid. Over recent years, other options of intra-articular injections
have been emerging, including viscosupplementation as well as biologic therapies such as platelet-rich
plasma and stem cell therapy. It is anticipated that many more options will be available in the future and
physicians carrying for patients with joint pathologies will want to develop expertise in performing intra-
articular injection techniques.
Physicians treating musculoskeletal diseases have been taught an understanding of pathophysiology,
functional anatomy, and biomechanics. In addition, physicians need to develop injection experience and a
kinesthetic sense of feel as the needle traverses tissue planes and anatomical structures. Physicians who
have gained significant fluoroscopic-guided injection experience typically have a much better respect for
traversing tissue planes and understanding how a needle behaves when it is guided toward a target. An
intra-articular injection is often part of a complex diagnostic and treatment algorithm, and physicians need
to have a specific plan as to what will be the next step based on response to the procedure. A patient who
benefits for 7 to 14 days may require much more complicated management and planning treatment than the
patient who benefits for 6 months after the injection.
Anatomical Landmarks
A key to intra-articular injections is the process of identifying specific anatomical and topographical
landmarks. It is recommended to utilize a systematic approach of anatomical landmark localization and
skin marking before every procedure. In addition to understanding landmarks, one also needs to have a
keen understanding of the anatomy that needs to be avoided during the procedure, such as nerves, vessels,
ligaments, tendons, etc.
Selection of needles, medications, and equipments:
• Sterile gloves
• Sterile fenestrated drape
• 4 × 4 gauze soaked with povidone-iodine solution (Betadine)
• 30-gauge 0.5- or 1-in needle for subcutaneous infiltration
• 25-gauge 2-in needle, 25-gauge 3.5-in Quincke needle, 22-gauge 3.5-inch Quincke needle, 22-gauge 5-
in Quincke needle
• Quincke needles are styleted, and have a relatively dull tip that does not cut into articular cartilage as
readily as a standard sharp beveled needle
• 3-cc syringes
• Hemostat, especially if intra-articular access is for the purpose of aspiration, in order to stabilize the
needle to switch syringes.
• Extension tubing to facilitate syringe changes from local anesthetic, to contrast, to injection solution. It
also keeps the syringe and hands out of the way of the radiographic picture during fluoroscopic
injections.
• Local anesthetic (lidocaine, bupivacaine)
• Proposed injectate (deposteroid, viscosupplement)
• Skin marker
• Radiographic marker for fluoroscopic identification of structures
• Paperclip or similar object for ultrasound identification of structures
Indications
• Symptomatic degenerative shoulder joint disease
• Fluid aspiration for diagnosis and treatment
• Viscosupplementation (not FDA approved)
Contraindications
Contraindications to any intra-articular injection will include:
• Uncooperative or noncompliant patient
• Allergy to previous or proposed medications
• Previous severe steroid flare
• Adjacent osteomyelitis
• Bacteremia
• Hemarthrosis
• Impending joint replacement surgery within days
• Infectious arthritis
• Joint prosthesis
• Osteochondral fracture
• Periarticular cellulitis
• Poorly controlled diabetes mellitus
• Uncontrolled bleeding or coagulopathy
Relative contraindications include crystalline steroid injections near critical arteries or weight bearing
joints. Large crystalline steroids potentially may have mechanical erosive effects with weight-bearing
activity immediately following corticosteroid injection and therefore it has been recommended by some to
limit weight-bearing activity for a time following a steroid injection.1 It is this author’s preference to use
triamcinolone (a smaller particle) rather than Depo-Medrol (a larger particle). Betamethasone may also
be an option. Steroids can cause a significant, though transient, increase in blood glucose.2,3 Diabetic
patients should therefore be counseled to monitor for hyperglycemia after the procedure.
• Risk factors for avascular necrosis (AVN)
• Diabetes
• Patients on dialysis
• Hemoglobinopathy
• Previous steroid use
• Cushing’s syndrome
• Radiation exposure
• Hyperglycemia in diabetic patients
• Immune deficiency or elevated risk for potential infection
• Anticoagulation therapy or patients with coagulation disorders
Every physician doing intra-articular injections on a regular basis will eventually have to face the
decision as to whether or not one should inject into the intra-articular space of a total joint arthroplasty.
The complication of an infection in a total joint arthroplasty can be disastrous, involving removal of the
hardware, insertion of devices imbedded with antibiotics, months of antibiotic treatment, and revision of
the arthroplasty procedure. However, there may be times when the benefit outweighs the risk and the
physician may perform the procedure. One needs to be concerned about the potential activation of latent
infections such as Mycobacterium tuberculosis, Nocardia, Cryptococcus, Pneumocystis, Borrelia
burgdorferi, toxoplasmosis, etc, when utilizing corticosteroids.
Reducing Pain of Injection

Reduction of the pain of the procedure will also reduce the anxiety and stress in the patient, and can
reduce patient concerns and fear of a possible repeat procedure. Simple technical considerations can be
made which can substantially reduce pain associated with intra-articular injections, which often require
only a slight change in technique or just an extra minute of time. The following are a few brief techniques
that can be utilized to reduce the pain of an injection:
• Quick insertion of the needle through skin that has been placed under tension. Depending on the
location on the body, skin can have different tensions and texture. On occasion, simply placing a finger
or thumb on the skin and stretching the skin taut and quickly (but smoothly) inserting the needle can
have a substantial effect on reducing pain.
• The use of topical vapocoolant over the skin can reduce the pain of an injection, there are some
questions regarding its sterility. Therefore, weigh the potential risk in a specific patient and specific
location before considering a topical vapocoolant.
• Perform a brief sterile skin prep followed by vapocoolant and a subcutaneous injection of 1% buffered
lidocaine, and then a complete sterile skin prep prior to the procedure.
• Use buffered lidocaine subcutaneously to provide substantial reduction in the pain. Lidocaine is acidic
and has a characteristics sting when injected because of the acidity. Buffering the acidity and creating a
neutral pH offers significant reduction in the pain of the injection.
A single dose vial of buffered lidocaine can be made as follows:
• In a 50-cc vial of 1% lidocaine, removed 5 cc from the vial and discard it. Then inject 4.5 cc of 8.4%
sodium bicarbonate into the vial. This provides you 49.5 cc of 1% buffered lidocaine.
• Alternatively, in a syringe, mix lidocaine and 8.4% sodium bicarbonate at a ratio of 10:1.
Some more tips to reduce the pain of injection:
• Utilize a 30-gauge 0.5″ or 1″ needle to inject local anesthetic subcutaneously prior to injection. Raise
a small skin bleb to reduce the pain of injection and patient anxiety prior to the injection procedure.
• Application of distractive maneuver. Touch, pressure, or skin stimulation in a location away from the
site of injection or a simple tissue pinch just prior to needle insertion or at the time of needle insertion
can provide a distraction which can reduce pain of a needle insertion.
• Utilization of sedatives. Although IV conscious sedation is rarely indicated for simple intra-articular
injections, on occasion the utilization of an anxiolytic prior to injection can reduce anxiety and the pain
experienced by anxious patients. Alternatively, consider oral benzodiazepine before the procedure.
Postprocedural Considerations
• Apply gentle pressure with gauze for hemostasis and apply sterile bandage.
• Observe the patient for any signs of syncope, lightheadedness or dizziness immediately following the
procedure.
• Perform a passive range of motion to determine subjective response to local anesthetic.
• For weight-bearing joints (hips and knees), support the patient when first standing, to avoid potential
collapse from limb weakness.
• Evaluate patient’s symptomatic response of the injection.
• Give patient a pain diary to monitor symptomatic response over the course of 5 to 7 days post
injection.

The patient is to contact the physician if there is any increased skin temperature, erythema, swelling, or
signs of infection.
ULTRASOUND-GUIDED JOINT INJECTIONS

Ultrasound-guided interventional procedures are rapidly becoming a popular emerging technology. With
imaging resolution improving and the portability of new ultrasound technology as well as elimination of
radiation exposure, ultrasound is anticipated to continue to grow in popularity. Images of confirmed initial
needle placement as well as post injection position should be saved. Ultrasound-guided injections should
be performed with the following basic principles:
• Perform a baseline ultrasound assessment and explore clinical anatomical landmarks for the planned
injection.
• The choice of transducer depends on the size of the patient and the depth of the structure. Use 7.5 to 15,
higher frequency transducer for shoulder and curvilinear only 3.5 to 7 for obese patients.
• Find the optimal ultrasound window that will allow visualization of the needle at the tissue target. The
use of a paperclip (Figure 55-1) or similar localizing device will aid in the rapid identification of the
injection site.
Figure 55-1. Ultrasound marker.
• Create a sterile technique protocol so that the surface of the probe and skin is sterile during the
injection procedure.
• Place a thin layer of sterile gel on the skin surface.
• Monitor the progress of needle progression directed toward target site continuously with particular
focus on the needle tip.
• Needles typically have to be slightly larger for visualization during ultrasound-guided procedures.
• Visualize the injected solution during and after the injection.
• Save or print visualized image with properly placed needle before and after the injection for purpose
of documentation.
There are a few additional steps to maintain sterility when performing ultrasound-guided intra-articular
injections. Utilization of ultrasound requires an assistant to maintain sterility. The ultrasound transducer
head can be held upright by the cord using an assistant and the physician with sterile gloves can apply a
large sterile bio-occlusive dressing (such as Tegaderm) over the transducer head (Figure 55-2A-C). The
transducer head is now sterile and can be handled by the physician with sterile gloves. An assistant prior
to the procedure can then apply a thin layer of Betadine gel or sterile surgical lubricant (Figure 55-3)
over the transducer head. Alternatively, one can use a sterile sleeve and sterile ultrasound gel (Figure 55-
4), being sure to place gel on the transducer before placing it in the sleeve, securing it with the supplied
sterile rubber bands, and then using sterile gel between the sleeve and the patient.
Figure 55-2. Ultrasound probe with bio-occlusive cover (A, B, C).
Figure 55-3. Sterile surgical lubricant.

Figure 55-4. Ultrasound sterile sleeve.
INTRA-ARTICULAR INJECTION OF GLENOHUMERAL JOINT

The functional anatomy and biomechanics of the shoulder is complex. There are 4 basic approaches to the
intra-articular space of the shoulder discussed in this chapter.
1. Anterior approach
2. Posterior approach
3. Superior approach
4. Lateral approach
The intra-articular injections can be performed by:
• Non-image-guided blind technique
• Fluoroscopy-guided technique
• Ultrasound-guided intra-articular injections
BLIND JOINT INJECTIONS

Disadvantages of blind injections:
• Poor accuracy rates of blind injections, which can be as low as 27% to 42% relying on anatomical
landmarks and palpation alone.
• Misplaced injections can result in an intra-tendinous injection (which can lead to tendon weakening),
skin depigmentation, soft tissue damage.
• Negative effects on clinical outcome.
Advantages of blind injections:
• Simple and safe injection to perform as an in-office procedure
• No exposure to ionizing radiation
• Reduced expense
Each anatomical approach and method offers advantages and disadvantages. Utilizing image-guided
injections obviously offers confirmation of intra-articular placement and resolves some of the inherent
inaccuracies of blind procedures. A posterior approach avoids the subclavian artery, subclavian vein, and
neural elements of the brachial plexus as well as offers a psychological advantage of the needle being out
of the patient’s field of vision. In contrast, the anterior approach offers the advantage of more
reproducible bony landmarks such as the coracoid process to help to guide the injection.
Glenohumeral intra-articular injections may be done for the purpose of diagnostic or therapeutic
maneuvers. If intra-articular contrast is being injected for the purpose of MRI arthrogram, one needs to
consider the approach and avoid a needle traversing through structures that may be of clinical interest.
For example, an anterior approach may need to be avoided if one is interested in the subscapularis,
glenohumeral ligament or anterior labrum, and it may be more appropriate to utilize a posterior approach
in preparation for this particular patient’s MRI.4 If a therapeutic injection is being considered, one may
need to consider what imaging may need to be performed after the procedure, since certain types of
injections can create abnormal signal on an MRI following an injection, which may interfere in
interpretation. Physicians should have knowledge of multiple approaches to the glenohumeral joint to
avoid creating an abnormality on MRI in the future or to overcome anatomical variations and body habitus
issues.
The technology of ultrasound-guided procedures will probably overcome many of the issues of blind
injections and maintain acceptable accuracy rates for intra-articular placement.5-10 Some who defend
blind injections will state that clinical experience may play a role in accuracy of intra-articular
injections.11 Regardless of a physician’s preference of blind versus image-guided glenohumeral
injections, it is important for a physician to possess the skills for blind injection procedures. There can be
great variability in the techniques and approaches for glenohumeral joint injections.7, 8 and 12
Relevant anatomy (Figure 55-5):
Figure 55-5. Anterior shoulder landmarks (Gray’s anatomy): A = lateral acromiom, B = anterior
acromiom, C = distal clavicle, D = coracoid process.
• Humeral head
• Biceps tendon
• Acromion
BLIND GLENOHUMERAL INJECTION WITH ANTERIOR

APPROACH
There are 2 anterior approaches that will be discussed in this section. The first is the standard anterior
approach and the second is the rotator interval approach.
Anterior Schneider Technique

The anterior Schneider technique is one of the most commonly used blind intra-articular glenohumeral
joint injection.13 Accuracy of this approach can vary, but in a cadaver study of 50 shoulders, 96% of
injections were accurately administered into the glenohumeral joint with only 4% in the surrounding soft
tissues and capsule.13-15 This technique is more commonly performed in a supine position, which is the
author’s preferred position.
Positioning of the patient:
• Position patient in supine position. Place a small pillow or rolled towel under the elbow to eliminate
extension of the shoulder (Figure 55-6).
Figure 55-6. Position of patient for anterior approach.
• Externally rotate the humerus to open the joint space and move the biceps tendon further away from the
injection site (Figure 55-7).
Figure 55-7. Anterior shoulder injection position.
Intraoperative technical steps:

• Carefully palpate the tip of the coracoid process and mark skin for reference. Pressure-mark the skin
with a retracted ballpoint pen at a location just below and slightly medial to the coracoid process.
• Sterile skin prep this region and raise a skin bleb utilizing a 30-gauge 1-in needle with 1% buffered
lidocaine.
• Attached to spinal needle to a 3-cc syringe filled with 1% buffered lidocaine, and while guiding the
needle to the target site, infiltrate local anesthetic sequentially for purpose of loss of resistance
technique.
• Advanced the needle in a trajectory that will place the needle tip at the distal humeral head just
anterior to the joint line (Figure 55-8). You will experience a distinct fibrous end-feel when you
contact the articular capsule overlying the humeral head.
Figure 55-8. Anterior shoulder injection.
• Inject local anesthetic while passing through the thick fibrinous capsule and you will experience a
slight loss of resistance when the needle tip traverses the articular capsule and enters the joint space.
Another option is to have the patient sitting with the patient’s hand in the lap and the shoulder muscles
relaxed.
• The glenohumeral joint can be palpated by placing the fingers between the coracoid process and the
humeral head.
• As the shoulder is internally rotated, the humeral head can be felt turning inward and the joint space
can be felt as a groove just lateral to the coracoid process (Figure 55-9).
Figure 55-9. Anterior glenohumeral examination.
• Position the patient with the humerus slightly externally rotated to open the joint space.
• Skin mark the coracoid process and sterilely prep the anterior shoulder region.
• Raise a skin bleb of 1% buffered lidocaine just lateral to the coracoid process. Remember that the
coracoacromial artery lies medial to the coracoid.
• The needle is directed in a posterior direction, slightly medial. Infiltrate local anesthetic as the needle
is advanced into the fibrous capsule.
• Once loss of resistance is experienced after traversing the articular capsule, the needle tip will be
within the intra-articular space of the shoulder.
• It is helpful to direct the needle slightly superior as well to avoid the neurovascular bundle.
Clinical Pearl
• This technique is helpful for heavier patients. With the contralateral sterile glove hand, place one
finger above the insertion site and one finger below the insertion site and feel for the joint line and the
humeral head. Guiding the needle toward the humeral head is then facilitated and avoids the needle
contacting the glenoid labrum.
The Rotator Interval Method

A modified anterior approach is through the rotator cuff interval, which is a thick, dense triangular space
found between the supraspinatus and subscapularis tendons (Figure 55-10).16 The needle is advanced to
the medial upper quadrant of the humeral head, which avoids penetration of the subscapularis tendon and
traversing important structures such as the glenohumeral ligaments and labrum, which may be of interest
on MRI arthrogram if the injection is being done for that purpose. It may interfere with imaging findings if
the coracohumeral ligament and rotator cuff interval are in question. Therefore, one needs to consider any
potential imaging and the structures that will be of interest following the injection. This technique can be
done in a supine or sitting position. We will describe this method in a supine position. This technique is
used to avoid key structures such as the subscapularis, glenohumeral ligaments, glenoid labrum.
Figure 55-10. Rotator interval approach.
Relevant anatomy:
• Sulcus between humeral head and coracoid
• Patient is positioned supine with the arm externally rotated to open up the joint space and move the
biceps tendon further away from the needle insertion.
• Palpate the coracoid process and mark the skin site.
• Palpate between the humeral head and the coracoid process (Figure 55-9).
• Mark the region just lateral to the coracoid process and leave a skin impression with the tip of a
retracted ballpoint pen.
• Sterile prep this insertion site and perform subcutaneous local anesthetic injection with 1% buffered
lidocaine via a 30-gauge needle.
• A 3-cc syringe filled with 1% buffered lidocaine on a 25-gauge 2-in spinal needle (or other needle of
choice) is guided from the point just lateral to the coracoid process posterior and slightly medial as
well as 5 to 10 degrees cephalad.
• Infiltrate local anesthetic as the needle is advanced into the fibrous capsule. Once loss of resistance is
experienced after traversing the articular capsule, the needle tip will be within the intra-articular space
of the shoulder.
• Inject local anesthetic and deposteroid.
• This technique provides a means to perform an intra-articular injection without penetrating important
anatomical structures such as to glenohumeral ligament, subscapularis, and avoiding the glenoid
labrum.
• This is a popular technique with radiologists performing gadolinium injections prior to MRI for
purpose of MRI arthrogram.
Anterior-Superior Approach
This is a rather novel approach that one should be aware of to perform in certain circumstances. Since the
needle does enter the superior aspect of the joint, one must keep in mind that the biceps tendon wraps
around the humeral head and inserts at the superior glenoid. Utilizing this technique, it has been shown
that periodically the needle can pierce the biceps tendon, potentially weakening the tendon.
This technique utilizes the anterior aspect of the acromioclavicular joint as the predominant landmark
(Figure 55-11).
Figure 55-11. Superior approach to the anterior glenohumeral joint.
• Notice the relationship of the anterior margin of the acromion, the anterior margin of the distal clavicle
and the tip of the coracoid.
• These structures will provide a slight protuberance palpated under the skin.
• The physician performing the procedure should be well acquainted with topographical anatomy and not
confuse the coracoid for the anterior margin of the acromion. This would place the needle into a
neurovascular bundle.
• It is helpful to mark the skin at the lateral acromion (A), anterior margin of the acromion (B), anterior
distal clavicle (C), and coracoid process (D) to avoid this confusion (Figure 55-12).
Figure 55-12. Superior approach to the anterior glenohumeral joint.
Indications:
• This technique provides an alternative access to the glenohumeral joint capsule when an alternative
approach may be needed.
• Place patient in the seated position with the elbow flexed and the arm externally rotated in order to
rotate the bicipital tendon away from the traversing needle (Figure 55-13).
Figure 55-13. Arm positioned with elbow flexed and arm externally rotated.
Selection of needles:
• Use a 25-gauge 2-in needle so that the needle traversing near the biceps tendon is small and, if it
inadvertently does pierce the biceps tendon, it causes less damage.
• Palpate and mark the coracoid process, the distal clavicle and the anterior lateral aspect of the
acromial process. A skin bleb is raised just anterior to the distal clavicle.
• The arm must be positioned in an externally rotated position to rotate the long head of the biceps
tendon away from the needle. It is still possible to traverse the long head tendon at the superior aspect
of the joint if one directs the needle to the most superior aspect of the acromion.
• Utilizing a 3-cc syringe filled with 1% lidocaine, infiltrate small amounts of local anesthetic and then
slowly advanced the needle sequentially to maintain adequate local anesthesia. After the needle meets
the resistance of the fibrous capsule, a slight loss-of-resistance can be felt while injecting the local
anesthetic. With the needle in place, gently passively internally and externally rotate the shoulder. If
this rotation movement is accompanied by movement of the needle, the tip should be in proper
position.17
• This injection technique has demonstrated issues of inaccuracy when compared to other approaches.
• One of the problems with this approach is that the needle can pierce the biceps tendon as it wraps
around over the superior humeral head to attach to the superior labrum damaging the biceps tendon.
BLIND GLENOHUMERAL INJECTION BY POSTERIOR

APPROACH
Indications:
• When there is a need to avoid anterior glenohumeral soft tissues and structures for purposes of MRI
arthrography or for other medical reasons, a posterior approach offers an excellent option for gaining
intra-articular access.
Relevant anatomy:
• Posterior-lateral acromion
• Teres minor muscle
• Infraspinatus muscle
• The patient is typically placed in a seated position.
• A prone position can also be utilized.
• Identify posterior-lateral edge of the acromion.
• Mark the needle entry zone 3 to 4 cm below the acromion and 2 cm medial to the posterior-lateral
margin of the acromion. This point corresponds to the transition between the teres minor muscle and
the infraspinatus muscle18 (Figure 55-14).
Figure 55-14. Posterior shoulder anatomy: Sup = supraspinatus, Inf = infraspinatus, TMi = teres minor,
TMa = teres major, X = injection site.
• Inject a skin bleb with 1% buffered lidocaine utilizing a 30-gauge 0.5-in needle.
• Attach a 3-cc syringe to the spinal needle and hold the needle with a dominant hand; with the
nondominant hand anterior to the shoulder, place a finger directly over the coracoid process. The
coracoid process and the palpation finger will be a guide to the trajectory of the needle.
• Direct the needle horizontally, being careful not to allow the needle drift cranially or caudally. Guide
the needle to the distal humeral head, just lateral to the joint line (Figure 55-15).
Figure 55-15. Posterior approach to the shoulder.
• Perform sequential infiltration of local anesthetic as needed for patient comfort while advancing the
needle. Once the needle comes into contact with the fibrous capsule, perform a slight infiltration of
local anesthetic and watch for a slight loss-of-resistance as the needle is advanced further. The needle
tip should now be within the intra-articular space of the shoulder (Figure 55-16).
Figure 55-16. Posterior shoulder needle position.
• Aspirate to ensure that the needle had not entered into a vessel and then remove the lidocaine syringe
and attach the syringe containing the injectate solution.
FLUOROSCOPIC-GUIDED GLENOHUMERAL INJECTIONS

The main advantage of fluoroscopic-guided glenohumeral joint injection over blind injection is that the
needle position can be confirmed and injection of contrast medium can be controlled. For an accurate
diagnostic injection, and for those patients with an altered anatomy, fluoroscopic-guided glenohumeral
joint injections are important techniques.
Figure 55-17. Shoulder fluoroscopic landmarks.
• Humeral head
• Glenoid and glenoid labrum
Fluoroscopic views:
• Anterior-posterior view tilted parallel to angle of the scapula (25-30 degrees) (Figure 55-18).
Figure 55-18. Fluoroscopic positioning.
• Patient also can be positioned slightly obliquely to the ipsilateral side with the fluoroscopy unit to
remain in a straight posterior-anterior without tilt.
• Patient is positioned supine on the fluoroscopy table for the anterior approaches and prone for the
posterior.
Selection of needles and medications:
• Use a 25-gauge 2-in needle
• Extension tubing to facilitate syringe exchanges from local anesthetic, to contrast, and to injection
solution. Extension tubing keeps the syringe and hands out of the way of the radiographic image.
• Nonionic contrast for intra-articular confirmation and documentation of contrast spread.
• Viscosupplementation material (not FDA approved).
• 4 approaches can be utilized
Anterior interval approach
Anterior approach
Lateral approach
Posterior approach
Anterior Approach
• Place radio opaque marker, and mark the skin just inferior to and lateral to the coracoid process under
fluoroscopy (Figure 55-19).
Figure 55-19. Injection site marked.
• After sterile skin prep, perform local anesthetic infiltration.

• Insert spinal needle with extension tubing attached performing sequential local anesthetic injections
through the trajectory for patient comfort until contact was made with the fibrous capsule at the distal
humeral head.
• The target is the distal humeral head and not the glenoid.
• Avoid trying to put the needle into the joint space between the humeral head and glenoid to avoid
potential damage to the glenoid labrum.
• Inject contrast and confirm arthrography (Figure 55-20).
Figure 55-20. Anterior intra-articular injection.
• Save image for documentation.

• Switch syringes and complete injection.
Anterior Interval Approach

• Use similar radiographic positioning over the region 1 cm lateral to the coracoid process, and skin
mark this region.
• Sterile prep and drape the skin and inject 1% buffered lidocaine subcutaneously and into deeper
tissues.
• Insert Quincke needle attached to the extension tubing, directed toward the distal upper outer quadrant
of the humeral head.
• Attached a 3-cc syringe filled with 1% buffered lidocaine and perform sequential local injections as
needed through the trajectory until gentle contact was made with the fibrous capsule just over the head
of the humerus.
• Inject local anesthetic while passing through the fibrous capsule, performing a loss-of-resistance
technique until contact was made with the humeral head. It is helpful to place the bevel against the
humeral head.
• Inject contrast and confirm intra-articular placement.
• Remember that the interval approach avoids the subscapularis tendon, the glenohumeral ligaments, and
the glenoid labrum.
Lateral Approach
• Patient is positioned supine, and the lateral aspect of the proximal humerus identified by fluoroscopy.
• Skin entry point is marked at the inferior border of the capsule (at the inferior border of the humeral
tuberosity) at the lateral or anterolateral aspect of the humerus (Figure 55-21).
Figure 55-21. Lateral shoulder approach.
• Sterile prep the skin and drape, and inject 1% buffered lidocaine subcutaneously and into deeper
tissues.
• Insert Quincke needle attached to the extension tubing and direct toward the proximal outer quadrant of
the humeral head.
• Attached a 3-cc syringe filled with 1% buffered lidocaine and perform sequential local injections as
needed through the trajectory until gentle contact was made with the fibrous capsule just over the head
of the humerus.
• Inject local anesthetic while passing through the fibrous capsule performing a loss-of-resistance
technique until contact was made with the humeral head.
• Inject contrast and confirm intra-articular placement (Figure 55-22).
Figure 55-22. Lateral shoulder arthrogram.

• Capsular adhesions may require large volumes (10-20 cc) of normal saline or very dilute local
anesthetic to perform “adhesiolysis” (Figure 55-23).
Figure 55-23. Lateral shoulder approach “adhesiolysis.”
Posterior Approach
• The posterior fluroscopic-guided approach requires special prone patient positioning. Once
positioning is optimized, a posterior approach utilizing fluoroscopy is a simple procedure. This
technique avoids the glenohumeral ligament, subscapularis tendon, and the glenoid labrum.
• Patient will need to be positioned in a oblique posterior-anterior position of approximately 25 degrees
(Figure 55-24), a Grashey view,19 or the C-arm will need to be obliqued until the joint line is sharp.
Figure 55-24. Posterior shoulder approach position.
• Externally rotate the humerus to create a laxity of the posterior capsule, which can help with needle
placement.
• Once patient is positioned, use radiopaque pointer to target the distal humeral head just lateral to the
joint space (Figure 55-25).
Figure 55-25. Posterior shoulder approach.
• Skin prep and drape this region and perform subcutaneous local anesthesia injection with 1% buffered
lidocaine.
• Guide Quincke needle with attached extension tubing to the humeral head similar to what was done
with the anterior approaches.
• Perform local anesthesia sequentially through the trajectory for patient comfort and use a loss-of-
resistance technique while entering the articular capsule.20
• The target is the humeral head just lateral to the joint line.
• Avoid trying to insert the needle into the joint space between the humeral head and glenoid.
• Inject contrast, confirm intra-articular placement (Figure 55-26).
Figure 55-26. Posterior shoulder arthrogram.
Clinical Pearls
• It is helpful to apply slight downward pressure during the injection of the contrast solution to ensure it
is through the posterior capsule and enters the intra-articular space.
• Keep in mind that a true AP view requires obliquing the fluoroscopy unit or tilting the patient.
• Many radiologists prefer a posterior approach because the needle does not traverse important anterior
structures that are often of clinical interest in magnetic resonance imaging studies such as the anterior
capsule, anterior glenoid labrum, and subscapularis tendon.
• If one suspects posterior labral pathology or pathology in the posterior shoulder, then an anterior
approach or a rotator cuff interval approach may be more appropriate if the intra-articular injection is
performed for the purpose of MRI arthrogram.
ULTRASOUND-GUIDED ANTERIOR GLENOHUMERAL
INJECTION
Studies have demonstrated the efficacy of ultrasound when performing intra-articular glenohumeral
injections.6, 21, 22 More recently, ultrasound-guided glenohumeral joint injection was found to be
significantly less time consuming and more successful on the first attempt compared to fluoroscopic
imaging.23 The ultrasound method described below is a technique initially described by Valls.27
• Patient positioned in a seated or supine position.
• The author’s preference is to have the patient supine with the head turned and with the arm externally
rotated to move the biceps tendon further away from the trajectory of the needle.
Ultrasound transducer:
• An ultrasound transducer 7.5 MHz linear array is typically utilized.
• If the patient is significantly obese, a lower frequency curved ultrasound transducer may need to be
utilized to penetrate to deeper tissues.
Relevant anatomy under ultrasound:
• Conduct a brief examination prior to procedure and identify key anatomical structures required for the
procedure, which include the coracoid process and the anteromedial portion of the humeral head.
• Transducer head will be positioned transversely as noted in Figure 55-27.
Figure 55-27. Ultrasound of the anterior shoulder.
• The coracoid process will be identified as a hyperechoic structure approximately 1 cm wide

protruding anteriorly.
• The medial humeral head will appear as a homogeneous curvilinear or rounded structure with a
hyperechoic layer; subchondral bone may show a hypoechoic layer (articular cartilage) (Figure 55-
28).
Figure 55-28. Ultrasound probe location.
• Identify the region just lateral to the coracoid process.

• Utilizing a paperclip under the ultrasound head, apply pressure to the skin to mark the needle entry zone
(Figure 55-1).
• Wipe the gel off and then sterilely prep and drape this region of the shoulder in preparation for the
injection.
• After ultrasound localization of injection site.
• Sterile skin prep and subcutaneous local anesthetic
• A 22-gauge spinal needle attached to extension tubing is directed from the region just lateral of the
coracoid to the medial aspect of the humeral head.
• Images should be saved of the initial needle placement as well as postinjection confirmation.
• Remove the needle, clean the skin, apply pressure, then sterile bandage.
Clinical pearls and pitfalls:
• Gentle contact is made on the humeral head just lateral to the joint space with the bevel of the needle
toward the bone.
• This provides a way for the bevel to “hug” the articular cartilage and improve injection within the
intra-articular space.
ULTRASOUND-GUIDED POSTERIOR GLENOHUMERAL

APPROACH
• Patient can be positioned sitting or prone or lateral decubitus on the contralateral shoulder.
Sonographic transducer:
• 7.5- to 14-MHz linear array transducer is used.
procedure, which include the humeral head and glenoid labrum.
• Position the probe transversely across the joint.
• The humeral head will appear as a curvilinear homogeneous hypoechoic structure (articular cartilage)
overlying a hyperechoic layer (cortical bone).
• You should be able to visualize the hyperechoic triangular glenoid labrum found between the humeral
head and the glenoid at the joint margin (Figure 55-29).
Figure 55-29. Ultrasound of posterior shoulder approach.
• Skin mark the region corresponding to the anterior medial aspect of the humeral head by sliding a
paper clip under the transducer head and pressure mark the skin at this region.
• Wipe the gel off and then sterilely prep and drape this region of the shoulder in preparation for the
injection.
• Perform subcutaneous local anesthesia with 1% buffered lidocaine over the sterilized prepped area
and skin marked previously.
• Direct a 22-gauge needle “in plane” toward the distal humeral head just medial to the joint line.
• Turn the bevel toward the humeral head and allow the bevel to hug the bone.
• With continuous sonographic monitoring, infiltrate the intra-articular space of the humerus.
• This is the favorite approach of most physicians, since it avoids the neurovascular bundle.
INTRA-ARTICULAR INJECTIONS OF THE

ACROMIOCLAVICULAR JOINT
• The acromioclavicular joint allows full abduction of the shoulder by acting as a pivot joint. The AC
joint may be a source of pain from inflammation, arthritis, or impingement from spurs.
Indication:
• Patients with predominately acromioclavicular joint pain typically describe pain greater with
horizontal adduction (cross chest) motions.
Relevant anatomy:
• Distal clavicle.
• Acromion.
• Acromioclavicular capsule.
• Coracoclavicular ligament.
• Coracoacromial ligament.
• The angle made by the junction of the distal clavicle and acromion can vary from individual to
individual. It is helpful to palpate and identify this angle prior to injection.
• The joint space is slightly wider in the anterior than the posterior, which is helpful when inserting a
needle (Figure 55-30).
Figure 55-30. Acromioclavicular joint anatomy.
Preoperative considerations:
• Patient with significant osteoarthrosis of the acromioclavicular joint may be at risk for impingement of
the rotator cuff tendon (predominantly supraspinatus), secondary to a joint spur extending from the
anterior surface of the joint.
BLIND AC JOINT INJECTIONS

Blind AC joint injections require some experienced palpation skills, though the injection can be mastered
with practice. If the injections are not placed intra-articularly, patients will not have symptomatic pain
relief. It is not helpful to inject steroid over the superior aspect of the joint without entering the intra-
articular space.
• The patient is placed in a seated position.
• It can be helpful for the patient to relax the shoulder and hold a heavy book, object or have an assistant
gently distract the humerus downward to open the acromioclavicular joint.
Selection of needles, medications, and equipments:
• The author’s preference is to utilize a 27-gauge 1.5-in needle for this injection, although a 30-gauge 1-
in needle can be used on thinner patients.
• With the patient seated, carefully palpate the acromioclavicular joint (Figure 55-31).
Figure 55-31. Blind acromioclavicular landmarks.
• Mark the skin overlying the exact location of the palpated joint line where the needle will be inserted.
• Inject 1% buffered lidocaine with a 30-gauge 0.25-in needle for local skin anesthesia.
• Direct a 27-gauge 1.5-in or 30-gauge 1-in needle downward and slightly medial into the joint.
Due to the variability in the acromioclavicular joint and a joint with osteoarthritic spurs, the needle
may need to be redirected if the needle comes into contact with bone.
Postprocedural considerations:
• Perform passive movements of the patient’s shoulder, especially with horizontal adduction motion, to
determine symptomatic response during the anesthetic phase of the injection.
• The subacromial bursa and articular capsule of the acromioclavicular joint can on occasion be
contiguous, and therefore injections into the intra-articular acromioclavicular joint space can infiltrate
into the subacromial bursa. This can confuse the diagnosis if the physician is unaware of this
relationship.
• In patients with hypertrophic changes and osteoarthritis, it is sometimes helpful to do some local
anesthetic injections over the superior aspect of the joint so that, in the event that bone was contacted
and the needle had to be redirected, the patient will not experience significant discomfort.
FLUOROSCOPIC-GUIDED AC JOINT INJECTIONS

Those who are skilled to perform blind AC joint injection will find it very simple to do fluoroscopically
guided AC joint injections. Patients who are quite obese can be a challenge, and fluoroscopy offers a
quick and simple injection, which requires less manipulation of the needle, thus reducing pain and patient
anxiety with the procedure.
Relevant anatomy:
• Acromion
• Clavicle
• Humeral head
• Typically the patient is placed in a supine position; however, if one does not have a fluoroscopy table,
the patient can be positioned seated and the C-arm brought over the joint in a seated position.
• We will describe the procedure in supine position.
Fluoroscopic imaging:
• The angle of the fluoroscopy unit for AC joints will vary based on the joint angle of the patient.
• Typically, it does not require as much tilt as for the glenohumeral joint.
• Thus, start at approximately AP, take a single view and then adjust accordingly (Figure 55-29).
Selection needles and medication:
• Utilize a 27-gauge 1.5-in needle, although a 25-gauge needle for this injection.
• If contrast is to be used for confirmation, then extension tubing will be helpful to make syringe change
easier without needle manipulation.
• With a radio-opaque pointer, mark the skin overlying the center of the AC joint (Figure 55-32).
Figure 55-32. Acromioclavicular joint location.
• After a sterile prep and skin anesthesia, the needle is directed into the intra-articular space.
• Contrast can be injected for arthrogram confirmation but only a small volume should be used (Figure
55-33).
Figure 55-33. Contrast in the acromioclavicular joint.
• Following arthrogram confirmation, switch syringes and complete the injection.

• Remember that the AC joint orientation varies widely and the fluoroscopic view therefore must be
individualized.
• Use of an x-ray marker will greatly speed up the procedure by quickly localizing the skin insertion site.
ULTRASOUND-GUIDED AC JOINT INJECTION

• Patient can be positioned sitting or supine.
• A 7.5- to 14-MHz liner array ultrasound transducer is used with this injection.
procedure, which include the joint itself, the clavicle, and the acromion.
• With the patient sitting, arm at the patient’s side, the acromioclavicular joint is evaluated in both the
sagittal and coronal planes.
• In the coronal position, the clavicle will often sit slightly higher than the acromion.
• Move the transducer slowly anterior to posterior to examine the joint and the joint space (Figure 55-
34). You will notice that the joint space is often wider in the anterior aspect.
Figure 55-34. Acromioclavicular joint under ultrasound.
• Once the joint space is identified, there are 2 ways to accomplish the injection.
• One is to simply identify the exact location of the joint on the surface of the skin with ultrasound and
then do the injection without guidance (“ultrasound localization”).
• The alternate technique is to guide the needle into the joint under continuous ultrasound observation
(“ultrasound guidance”).
• The transducer is placed midline over the joint when doing diagnostic ultrasound, but, when
performing an ultrasound-guided injection, the transducer head must be positioned medially, placing
the transducer head over the lateral aspect of the joint if you plan to do an “in plane” injection.
• Utilizing a paperclip under the ultrasound head, apply pressure to the skin to mark the needle entry
zone.
• A 27-gauge needle is directed in the transverse position or “out of plane.”
• The needle is more difficult to track when “out of plane” because the needle is not guided until the
needle tip become visible under the ultrasound head.
• In-plane injections can be done but one has to slide the ultrasound head all the way over to the right or
left and attempt to track the needle toward the joint.
• Another option is to track the needle down to the distal clavicle, which typically is slightly higher than
the acromion, and, once the distal edge of the clavicle is contacted, remove the ultrasound head, tip the
needle and syringe upright and then insert the needle into the intra-articular space.
• It is typically more efficient to do ultrasound localization (ultrasound assisted) rather than ultrasound
guidance.
INTRA-ARTICULAR INJECTIONS OF HIP JOINT

The techniques of intra-articular injections of the hip are rather simple, since the articular capsule extends
over the head of the femur and onto the neck, which makes it relatively simple to place the needle tip into
the capsule. In this section, we will cover techniques for blind intra-articular injection as well as
fluoroscopy and ultrasound-guided hip injection.
Indications:
• Symptomatic degenerative hip joint disease
• Fluid drainage for diagnosis and treatment
• Viscosupplementation
Figure 55-35. Hip anatomy.
• Femoral head
• Acetabulum
• Greater trochanter
BLIND INTRA-ARTICULAR HIP INJECTIONS

These injections have recently come under research scrutiny.9, 24 Kurup reported that utilizing anatomical
landmarks resulted in a success rate with blind injections of only 65.1%. Based on this result, he
suggested that hip injection should be carried out by a trained specialist under radiologic guidance.1 Ziv
et al reported an overall success rate in 40 cadavers of 77.5%. He also indicated that in all 9
unsuccessful injections, the dye typically was located distal to the joint along the lateral aspect of the
femoral neck. He did not find any dye from the injections located near neurovascular structures. Based on
this, he concluded the accuracy of blind hip joint injections were similar to blind knee injections and
therefore could be used safely in the standard office setting. The decision to accept the potential error rate
of a blind intra-articular injection is a clinical decision that will have to be made based on the merits of a
particular case. There may be circumstances where a blind intra-articular injection would be appropriate
and other times when it would not. Blind intra-articular injection should not be utilized when the
injections are performed as diagnostic. It is inappropriate to consider placement of a
viscosupplementation injection into the intra-articular space of the hip joint without image-guided
confirmation.
Relevant anatomy:
• Lateral aspect of greater trochanter.
• Superior aspect of greater trochanter.
Positioning os patient:
• Although the patient can be placed in the supine position, it is the author’s preference to use a lateral
position. The patient is placed on the contralateral hip with the knee slightly flexed. However, the
supine position may be more appropriate for bilateral positions, to avoid repositioning and re-
prepping.
Selection of needles:
• A 3.5- to 5-in Quincke needle is used.
• Palpate and mark the superior aspect of the greater trochanter as well as 2 cm above the superior
aspect of the greater trochanter.
• Prep and drape the superior aspect of greater trochanter.
• 1% buffered lidocaine injected subcutaneously 2 cm above the superior aspect of the greater
trochanter. Local anesthetic can also be injected into deeper tissues along the proposed trajectory of
the needle.
• Position the needle perpendicular to the skin and directed the needle perpendicular to the skin surface
or slightly inferior. Exercise caution not to apply pressure on the needle that would cause the needle to
curve or skive off course (Figures 55-36 and 55-37).
Figure 55-36. Blind hip injection.
Figure 55-37. Blind hip injection
• Carefully feel for a fibrous end feel at the needle as the needle tip enters the articular capsule. If a bony
end feel is encountered without the feel of the fibrous capsule, withdraw the needle completely and
redirect the needle.
• Estimate the patient’s size and the potential depth of the injection. If the needle appears to be traveling
too deep for the suspected endpoint, pull the needle back once again and redirect, because more likely
the needle has skived off course.
• Do not inject unless you have contacted the fibrous capsule and gently tapped bone.
• Aspirate to reassure that the needle tip is not in a blood vessel, and then inject solution.
• Remove the needle and apply gentle pressure and sterile bandaid.
• You must take into consideration the amount of adipose tissue or soft tissue overlying the greater
trochanter when estimating the exact location of the superior aspect of the greater trochanter.
• The most common location for needle malposition is distal to the capsule. If the needle tip is felt to
strike bone before one feels the capsule, then withdraw the needle and angle typically slightly more
inferiorly; the needle tip should then enter the hip capsule.
FLUOROSCOPY GUIDED INTRA-ARTICULAR HIP INJECTION

Figure 55-38. Fluoroscopic hip structures.
• Lateral aspect of greater trochanter

• Superior aspect of greater trochanter
• Acetabulum
• Femoral neck
• Femoral head
Fluoroscopic views:
• Straight anterior-posterior fluoroscopy view; no tube tilt required
• Supine position with leg slightly externally rotated.
Selection of the needles and medications:
• Occasionally a 5-in Quincke needle may be needed for the significantly obese patient.
• Nonionic contrast for intra-articular confirmation and documentation of medication spread.
• Viscosupplementation material (not FDA approved).
• Bring the fluoroscopy unit to center over the head of the femur.
• With a radio opaque pointer, confirm the location of the neck of the femur.
• Sterile skin prep and drape.
• 1% buffered lidocaine injected subcutaneously at the location noted below (depending upon technique)
as well as inject into deeper tissues through the proposed trajectory of the needle.
• 2 approaches can be utilized: anterior and lateral.
Anterior approach (Figure 55-39):
Figure 55-39. Intra-articular hip injection-anterior approach.
• Palpate anterior superior iliac spine and palpate the femoral pulse.
• Mark the region of the skin 2 cm below and 3 cm lateral to the palpated femoral pulse.
• Following local anesthesia, position the spinal needle, directing the needle at an angle of
approximately 50 degrees to the skin.
• Advanced the needle directed to the top of the surgical neck below the head of the femur.
• The needle will be advanced through the capsular ligament, encounter a fibrous end feel with the
needle tip, and then gently contact os.
• Inject small 1 to 2 cc of contrast for confirmation of position and save image for documentation.
• Switch syringes and inject proposed medication and removed the needle.
Lateral approach (Figure 55-40):
Figure 55-40. Intra-articular hip injection—lateral approach.
• Identify the greater trochanter and the femoral neck by fluoroscopy.

• From the lateral aspect of the thigh, advance the needle to the junction of the acetabulum and femoral
neck, using a “loss of resistance” technique with the lidocaine syringe.
• Aspirate to ensure the needle tip is not in a blood vessel.
• Inject small 1 to 2 cc of contrast for confirmation of position and save image for documentation.
• Switch syringes and inject proposed medication and remove the needle.
• Do not attempt to place the needle tip between the acetabulum and the femur head but rather through the
fibrous capsule just below the femur head.
• Because of the potential for pseudo-septic reactions if viscosupplementation material is not intra-
articular, these injections should usually be performed under fluoroscopy or ultrasound guidance
ULTRASOUND-GUIDED INTRA-ARTICULAR HIP INJECTION

• Position patient in supine position with hips slightly externally rotated.
• Consider body habitus and determine whether a higher or lower frequency ultrasound transducer will
need to be utilized to maximize visualization of anatomical landmarks.
• A higher frequency 7 to 15 MHz or 6 to 12 MHz linear array transducer can be utilized for
visualization of the femoral head.
• It may be necessary to use lower frequencies in order to gain deeper penetration or change the
ultrasound head to a 3- to 5-MHz curvilinear array transducer to gain better penetration on heavy
patients.
procedure, which include:
Femoral nerve, artery, vein
Anterior superior iliac spine (ASIS)
Femoral head
Femoral neck
Acetabulum
Acetabular labrum
Iliofemoral ligament
• Ultrasound transducer is oriented in the sagittal plane just medial to the ASIS (Figure 55-41).
Figure 55-41. Ultrasound transducer for hip injection (head to the right).
• Transducer is moved medial until the hyperechoic, rounded appearance of the femoral head is seen
(Figure 55-42).
Figure 55-42. Ultrasound of the hip: FH = femoral head.
• Visualize the anterior acetabular labrum.

• Now rotate the transducer into the transverse plane and move transducer medially to identify the
femoral nerve and vein. Confirm location of neurovascular structures and then move transducer back
over the anterior hip joint in the sagittal plane.
• Rotate the inferior end of the transducer laterally approximately 30 degrees until the femoral neck
comes into view.
• Note the hyperechoic iliofemoral ligament and hip capsule as well as overlying hypoechoic articular
cartilage over the femoral head.
• Utilizing a paperclip under the ultrasound head, apply pressure to the skin to mark the needle entry
zone.
• Wipe the gel off and then sterilely prep and drape this region of the hip in preparation for the injection.
• Maintain a 30-degree position of the transducer in the plane of the femoral neck and place the
transducer as far laterally on the head-neck junction as possible.
• Marked the skin at the inferior end of the transducer.
• After ultrasound localization of injection site, sterile prep, and subcutaneous local anesthetic, a 22-
gauge spinal needle attached to extension tubing is directed through the previously marked skin in the
longitudinal plane of the ultrasound transducer and parallel to the femoral neck.
• Reposition transducer head to visualize the combination of the femoral neck and head as previously
imaged.
• Tract the needle to the neck of the femur until the needle tip reaches the fibrous articular capsule and
advance through the capsule, entering the intra-articular space (Figure 55-43).
Figure 55-43. Ultrasound hip anatomy and needle.
• Inject local anesthetic (1-2 cc) to confirm intra-articular placement of the needle tip.
• Inject hip with planned injection solution and confirm echoic fluid entering the intra-articular space.
• Remove the needle, clean the skin, apply pressure, then sterile band-aid.
• Sonographic-guided intra-articular hip injections have been shown to have an accuracy of 96% to
100%.25-27
INTRA-ARTICULAR INJECTIONS OF KNEE JOINTS
The knee joint contains the largest synovial space in the body and in the joint most often injected. There
are several approaches to the intra-articular injections have been documented. Arthrocentesis of the knee
is easy and relatively painless in a joint that is distended with fluid or when boggy synovial proliferation
is present, though it may be much more difficult in joints with severe degenerative changes or distorted
anatomy. The non-image-guided blind, fluoroscopy-guided, and ultrasound-guided intra-articular
injections of the knee will be discussed below. Each approach and method offers advantages and
disadvantages. Utilizing image-guided injections obviously offers confirmation of intra-articular
placement and resolves some of the inherent inaccuracies of blind procedures. For most knee injections,
the usual point of entry is on the extensor surface, avoiding the large nerves and major vessels that are
usually present on the flexor surface. Optimal joint positioning should be accomplished to stretch the
capsule and separate the joint ends to produce maximal enlargement and distraction of the joint or
synovial cavity to be penetrated.
Indications:
• Symptomatic degenerative knee joint disease
• Synovial fluid aspiration for diagnosis and treatment
• Viscosupplementation
Figure 55-44. Knee anatomy.
• Palpation of knee joint line

• Patellar tubercle
• Patellar tendon
• Inferior pole of patella
• Aspirate and document the volume and character (clear, cloudy, thin, etc) of the synovial fluid
• Viscosupplementation is relatively ineffective in patients with large-volume effusions.28, 29
BLIND INTRA-ARTICULAR INJECTIONS

There are multiple approaches for a blind intra-articular needle placement. Four approaches are common:
• The anteromedial approach
• Anterolateral approach
• Lateral mid-patellar approach
• Medial mid-patellar approach
The highest accuracy is seen in anterolateral and lateral mid-patellar approaches and the lowest is the
medial mid-patella approach, which is why this author prefers the anterolateral approach.30 The lateral
mid-patella approach has also shown to be quite accurate.31, 32
Confirmation of intra-articular injection can be made by injecting a small amount of air following the
injection and then flexing and extending the knee and listening for a “squishy sound” caused by air
bubbles within the fluid.
Intraoperative Technical Steps

Suprapatellar Approach
This approach is considered extra-articular because the needle does not enter the joint space directly, but
still within the joint space because of the connection between the suprapatellar bursa and the joint space.
As a result, fluid can be aspirated and medication injected without direct needle trauma to the articular
cartilage. However, it is not an adequate approach for viscosupplementation, because of the high
likelihood of extravasation:33
• Patient is placed supine with the knee in full extension.
• Palpate the superior aspect of the patella.
• Mark the skin 1 cm cephalad and 1 cm either medial or lateral of midline.
• Prep and drape the knee and inject subcutaneous 1% buffered lidocaine with a 30-gauge 1-in needle
and then inject additional lidocaine in the trajectory of the needle to be used with the procedure.
• Depending on the injection substance, a 27-gauge 1.5-in needle, 25-gauge 1.5-in, or 22-gauge 1.5-in
needle can be utilized. Smaller gauge needles can be used for injection and larger gauge needles for
aspiration and viscosupplementation.
• If aspiration is to be performed, utilize a hemostat clamp once the needle is in place to stabilize the
needle for purpose of switching syringes during the aspiration process.
• Enter the skin approximately 45 degrees from horizontal, aiming caudally and medially toward the
middle of the patellar (Figure 55-45).
Figure 55-45. Suprapatellar approach knee injection. (From FPnotebook.com.)
Midpatellar Approach
• Patient is placed supine with the knee in full extension.
• Carefully palpate the superior and inferior aspect of the patella and mark the skin 1 cm lateral to the
mid patella position.
• Enter the skin obliquely, from a medial or lateral approach, aiming approximately 20 to 30 degrees
medially toward the inferior patellar pole.
Infrapatellar Approach (Anteromedial Infrapatellar, Anterolateral Infrapatellar)

• The infrapatellar route is useful when the knee cannot be fully extended or only minimal fluid is
present.
• Patient can be sitting or be placed in a supine position with the knee flexed 30 to 40 degrees (Figure
55-46).
Figure 55-46. Positioning for the infrapatellar approach knee injection.
• The author’s preference is to slide the physician’s flexed knee under the patient’s knee for support and
control (Figure 55-46).
• Carefully palpate and identify the injection site lateral or medial and inferior to the patella. Palpate the
patella tendon, and then fall off the patella tendon to either the medial or lateral side.
• This depression or dimple is typically the best insertion site.
• Insert a 25- or 27-gauge 1.5-in needle toward the inferior one-third of the patellar pole. Once the
needle slides under the patella, the needle tip should be within the intra-articular capsule (Figure 55-
47).
Figure 55-47. Infrapatellar approach knee injection.
• To test for intra-articular placement, inject small amount of local anesthetic. If the patient experiences
pain with the injection, this typically signifies that the needle is still within the patellar fat pad.
Reposition the needle slightly toward the inferior patellar pole. Once inside the intra-articular space,
infiltration of the local anesthetic should not cause pain.
• Aspirate prior to injection. If synovial fluid aspiration is planned, one may want to choose a larger
gauge needle for the aspiration procedure rather than the smaller 27- or 25-gauge needle.

• The most common reason for inaccurate needle placement or extra-articular needle placement is
inadvertent injection into the patellar fat pad.
• Because the fat pad is richly innervated, it is painful when injected by any solution. The patient should
not feel any pain with the injection. If the patient feels pain with the initial injection, it may be because
the needle tip is within the fat pad and not in the intra-articular space.
• Increased pain and “pseudo-septic” reaction experienced by some viscosupplementation injections is
caused by inadvertent injection into the patellar fat pad. Avoidance of this almost eliminates this
problem.
• If the patient complains of pain, redirect the needle more toward the region just under the inferior
patellar pole.
• Once the needle slides slightly under the patella it should reach the intra-articular space.
• Begin reinjecting again and monitor the patient’s subjective response. The initial discomfort the patient
reported should resolve and the injection should be able to be carried out painlessly.
• This technique is an excellent way to ensure intra-articular placement of the needle.
FLUOROSCOPY-GUIDED INTRA-ARTICULAR INJECTION OF

KNEE
Relevant anatomy:
• Medial and lateral patella femoral condyle
• Medial or lateral patellar facets
• Patellar tendon
• Medial and lateral tibial plateau
• Lateral and medial femoral condyles
Fluoroscopic views:
• Fluoroscopic views can be obtained in both the anterior-posterior as well as lateral views (Figure 55-
48), based on preference of the physician and the injection technique utilized.
Figure 55-48. Fluoroscopic knee image.
• Some physicians prefer to rotate the image intensifier toward the feet until the joint line is as sharp as
possible (Figure 55-49).
Figure 55-49. Knee joint line optimized.

• The patient is placed in supine position with a small pillow under the knee to place the knee in slight
flexion of approximately 15 degrees (Figure 55-50).
Figure 55-50. Knee support.
Selection of needles and medications:

• A 25-gauge 1.5-in needle can be used; however, some physicians prefer a 23-gauge or 22-gauge needle
because it is better visualized under fluoroscopic imaging.
• Nonionic contrast for intra-articular confirmation and documentation of medication spread.

Anterolateral or Anteromedial Patella Approach
Mark the area one fingerbreadth lateral or medial to the patella. Perform a sterile prep and drape.
Choice of lateral or medial depends on the patient’s greatest area of pain and the size of the joint space.
Fluoroscopy allows the delivery of medication to the narrowest of joint spaces (Figure 55-51), which
may be therapeutically valuable, especially with the use of viscosupplementation.
Figure 55-51. Medial joint line narrowing.

Anesthetize the region with 1% lidocaine with a 30-gauge needle.
• The needle is inserted shallowly in the soft tissues and then directed into the joint space.
• With an anterior-posterior view, the needle should be angled approximately 45 degrees medially and
45 degrees inferiorly toward the infrapatellar pole.
• With the rotated view, the needle is directed straight into the joint space.
• Position the fluoroscopy unit for a lateral projection and correct the angle of the trajectory if needed
and guide the needle into the intra-articular space.
• The lateral view is not usually needed if a “loss of resistance” with local anesthetic, saline, or air is
used.
• Aspirate, and then inject 1 to 2 cc of contrast to confirm intra-articular injection and save image for
documentation, which can be done in the anterior-posterior or lateral view.

• Any of the approaches of intra-articular knee injection can be done with a simple anterior-posterior, a
rotated, or a lateral fluoroscopic view with confirmation using nonionic contrast.
• With the current use of ultrasound-guided injections, the exposure to ionizing radiation, and the
potential allergic reaction to contrast, fluoroscopic-guided intra-articular injection are beginning to be
less attractive.
• However, the contrast may identify capsular disruptions and extra-articular spread of (which would be
a contraindication to the use of viscosupplementation medications) or intra-articular adhesions (which
would limit the therapeutic spread of medications).
• Neither of these conditions would be identified under ultrasound.
ULTRASOUND-GUIDED INTRA-ARTICULAR INJECTION OF

KNEE
• Patient can be positioned sitting or supine with a pillow under the knees.
• A 5- to 12-MHz linear transducer is usually used.
procedure:
Femoral condyles
Tibial plateau
Medical and lateral joint line
Infrapatellar fat pad
• Place the ultrasound probe in the transverse plane over the anteromedial aspect of the knee so that the
ultrasound transducer head will be positioned at right angles to the needle traversing through the joint
from the opposite side (Figure 55-52).
Figure 55-52. Ultrasound positioning for the lateral knee injection.
This will allow image-guided needle trajectory to the point of contact of the femoral condyle.
• Identify the lateral part of the knee similar to that which was described in the blind technique. This
represents a small depression or dimple that lies inferior to the patella and lateral to the patellar
tendon.
• Skin mark the region corresponding to the joint line by sliding a paper clip under the transducer head
and pressure mark the skin at this region
• Wipe the gel off and then sterilely prep and drape this region of the knee in preparation for the
injection.
• Inject subcutaneous 1% buffered lidocaine at the site where the needle will be inserted.
• The 22-gauge needle is directed in a slightly upward angle toward the inferior patellar pole and the
medial femoral condyle (Figure 55-53).
Figure 55-53. Ultrasound knee labeled.
• Gently contact the femoral condyle before performing confirmatory lidocaine injection or performing
the therapeutic injection.
Clinical pears and pitfalls:
• Studies have demonstrated that if the needle is not gently in contact with the femoral condyle, there was
a 22% failure rate to accomplish the intra-articular injection under ultrasound guidance; therefore, one
needs to make sure a gentle contact is made with the medial femoral condyle before injection.34
• The advantage of the technique of using the medial instead of lateral port is that it does not require a
sterile preparation of the ultrasound head and gel. This makes the injection quicker and more efficient.
Suggested reading
European Society of MusculoSkeletal Radiology: Musculoskeletal Ultrasound Technical Guidelines
(knee) http://www.scribd.com/doc/17528261/European-Guidelines-of-Musculoskeletal-Ultrasound
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6. Cicak N, Matasovic T, Bajraktarevic T. Ultrasonographic guidance of needle placement for shoulder
arthrography. J Ultrasound Med. 1992; 11:135-137.
7. Demirhan M, Sonmez M, Kahraman S, Esenyel M, Ozbaydar M, Senel B. Accuracy of anterior
glenohumeral injections: a cadaver study. Arch Orthop Trauma Surg 2010;130:297-300
8. Eustace J, Brophy D, Gibney R, Bresnihan B, FitzGerald O. Comparison of the accuracy of steroid
placement with clinical outcome in patients with shoulder syndromes. Ann Rheum Dis.
1997;56(1):59-63.
9. Kurup H, Ward P. Do we need radiological guidance for hip joint injections? Acta Orthop Belg. Apr
2010;76(2):205-207.
10. Sethi P, Kingston S, Elattrache N. Accuracy of anterior intra-articular injection of the glenohumeral
joint. Arthroscopy. 2005;21(1):77-80.
11. Hodler J. Technical errors in MR arthrography. Skeletal Radiol. 2008:37:39-18.
12. Tobola A, Cook C, Cassas K, et al. Accuracy of glenohumeral joint injections: comparing approach
and experience of provider J Shoulder Elbow Surg. Apr 12 2011:1058-2746.
13. Schneider R, Ghelman B, Kaye J. A simplified injection technique for shoulder arthrography.
Radiology. 1975;114(3):738-739.
14. Schneider R, Ghelman B, Kaye J. A simplified injection technique for shoulder arthrography.
Radiology. 1975;114:738-739.
15. Esenyel C, Esenyel M, Yeslitepe R, al. e. The correlation between the accuracy of steroid injections
and subsequent shoulder pain and function in subacromial impingement syndrome. Acta Orthop
Traumatol Turc. 2003;37(1):41-45.
16. Porat S, Leupold J, Burnett K, Nottage W. Reliability of non-imaging-guided glenohumeral joint
injection through rotator interval approach in patients undergoing diagnostic MR arthrography. AJR
Am J Roentgenol. Sept 1 2008;191(3):66-69.
17. Micheo W, Rodriguez R, Amy E. Joint and soft-tissue injections of the upper extremity. Phys Med
Rehabil Clin N Am. 1995;6(4):836-837.
18. Wahl C, Warren R, Altchek D, eds. Shoulder arthroscopy. 3rd ed. Philadelphia, Pa:: Saunders; 2004.
Rockwood C, Matsen F, Wirth M, Lippitt S, eds. The shoulder.
19. Farmer K, Hughes P. MR arthrography of the shoulder: fluoroscopically guided technique using a
posterior approach. Am J Roentgenol 2002;178(2):433-444.
20. Malfair D. Therapeutic and diagnostic joint injections. Radiol Clin North Am. May 2008;46(3):439-
453, v.
21. Valls R, Melloni P. Sonographic guidance of needle position for MR arthrography of the shoulder.
AJR. 1997;169:845-847.
22. Zwar R, Read J, Noakes J. Sonographically guided glenohumeral joint injection. AJR. 2004; 183:48-
50.
23. Rutten M, Collins J, Maresch B, et al. Glenohumeral joint injection: a comparative study of ultrasound
and fluoroscopically guided techniques before MR arthrography. Eur Radiol. 2009;19:722-730.
24. Ziv YB, Kardosh R, Debi R, Backstein D, Safir O, Kosashvili Y. An inexpensive and accurate method
for hip injections without the use of imaging. J Clin Rheumatol. Apr 2009;15(3):103-105.
25. Smith J, Hurdle MF, Weingarten TN. Accuracy of sonographically guided intra-articular injections in
the native adult hip. J Ultrasound Med. Mar 2009;28(3):329-335.
26. Atchia I, Birrell F, Kane D. A modular, flexible training strategy to achieve competence in diagnostic
and interventional musculoskeletal ultrasound in patients with hip osteoarthritis. Rheumatology
(Oxford). Oct 2007;46(10):1583-1586.
27. Pourbagher MA, Ozalay M, Pourbagher A. Accuracy and outcome of sonographically guided intra-
articular sodium hyaluronate injections in patients with osteoarthritis of the hip. J Ultrasound Med.
Oct 2005;24(10):1391-1395.
28. Waddell D, Marino A. Chronic knee effusions in patients with advanced osteoarthritis:
implications for functional outcome of viscosupplementation. J Knee Surg. Jul 2007;20(3):181-184.
29. Conrozier T, Bertin P, Mathieu P, et al. Intra-articular injections of hylan G-F 20 in patients with
symptomatic hip osteoarthritis: an open-label, multicentre, pilot study. Clin Exp Rheumatol. Sep-Oct
2003;21(5):605-610.
30. Esenyel C, Demirhan M, Esenyel M, et al. Comparison of four different intra-articular injection sites
in the knee: a cadaver study. Knee Surg Sports Traumatol Arthrosc. May 2007;15(5):573-577.
31. Jackson DW, Evans NA, Thomas BM. Accuracy of needle placement into the intra-articular space of
the knee. J Bone Joint Surg Am. Sep 2002;84-A(9):1522-1527.
32. Glattes RC, Spindler KP, Blanchard GM, Rohmiller MT, McCarty EC, Block J. A simple, accurate
method to confirm placement of intra-articular knee injection. Am J Sports Med. Jun
2004;32(4):1029-1031.
33. Bum Park Y, Ah Choi W, Kim Y, Chul Lee S, Hae Lee J. Accuracy of blind versus ultrasound-guided
suprapatellar bursal injection. J Clin Ultrasound. Jan 2001;40(1):20-25.
34. Chavez-Chiang CE, Sibbitt WL Jr., Band PA, Chavez-Chiang NR, Delea SL, Bankhurst AD. The
highly accurate anteriolateral portal for injecting the knee. Sports Med Arthrosc Rehabil Ther
Technol. 2011;3(1):6.
CHAPTER 56
Tendon Injections
Robert Balch III
INDICATIONS
• The indications for tendon or ligament injections can fall into 1 of 2 categories: diagnostic and
therapeutic. Infiltration of local anesthetic along the tendon sheath can confirm the suspected diagnosis
through symptom relief. Indications for therapeutic injections include decreased mobility and range of
motion, pain, and the need to place medication in the area of pathology as a therapeutic adjunct to other
forms of treatment.
• Common tendon/soft tissue–related conditions for which diagnostic and therapeutic injections are
indicated:
Bursitis
Ischial
Trochanteric
Pes anserine
Patellar
Tendinopathy/tendonosis
Bicipital tendonitis
Supraspinatus tendonitis
De Quervain tenosynovitis
Patellar tendonitis
Achilles tendonitis
Medial/lateral epicondylitis
Levator scapulae tendonitis
Enthesopathy
Iliolumbar ligament
Sacrococcygeal ligament
Sacrotuberous ligament
Sacrospinous ligament
Sacroiliac ligament
Interspinous ligament
Supraspinous ligament
Neuromas/ganglion cysts
Fasciitis
Plantar fasciitis
Entrapment syndromes
CONTRAINDICATIONS
• Relative contraindications
Needle phobia
Underlying coagulopathy/bleeding diathesis
Failure to respond to two previous injections
Anticoagulation therapy
Uncontrolled diabetes mellitus
Pregnancy
• Absolute contraindications
Local cellulitis
Acute fracture
Septic arthritis
Bacteremia
History of allergy or anaphylaxis to injectate
Local tumor
Inability of patient to understand consent
RELEVANT ANATOMY
Bicipital Tendonitis/Tendonosis
• The long head originates at the greater tuberosity of the humerus, glenoid labrum, and supraglenoid
tubercle (Figure 56-1).1
Figure 56-1. Anatomical depiction of the long head of the biceps inserting onto the greater tuberosity of
the humerus (arrow).
• The short head originates at the coracoid process. These sites are common areas of inflammation in
bicipital tendonitis.
• Arterial supply via the circumflex humeral artery1
• Most commonly the long head of the biceps becomes inflamed where it passes through the bicipital
groove.
The tendon may become impinged between the head of the humerus, acromion, and coracoclavicular
ligaments with elevation and internal rotation of the arm.
• Distal inflammation along the insertional site is less common.
• The musculocutaneous nerve (C5C6) provides innervation to the biceps muscle.
Clinical Anatomy
• Point tenderness in the bicipital groove
• Anterior shoulder pain with referral to the arm
• Positive Yergason test—anterior shoulder pain with flexion of elbow to 90 degrees and resisted
supination of the wrist
Levator Scapula
• Originates at the lateral mass of C1-C4 and the tendon inserts on the superior medial angle of the
scapula (Figure 56-2)
Figure 56-2. Anatomical depiction of the levator scapula originating at the lateral masses of C1-C4 and
inserting on the superior medial angle of the scapula.
• Motor innervation by dorsal scapular nerve (C5)
Clinical Anatomy
• Pain along the superior medial angle of the scapula
• Painful, stiff neck
• Limited cervical rotation
• Pain at the angle of the neck, where the levator emerges from beneath the anterior border of the upper
trapezius muscle
Lateral Epicondylosis/Epicondylitis
• Wrist extensors and supinators attach to the humerus at the lateral epicondyle
• These muscles pass laterally over the radiocapitellar joint
Clinical Anatomy
• Inflammation and enthesopathy occur with repetitive motion (Figure 56-3)—carpenters, typists, tennis
players (especially backhand)
Figure 56-3. MRI images of lateral epicondyle (T1 on the left and T2 on the right).
• “Coffee cup sign”—pain worse when holding a coffee cup or thick phone book, turning a door knob
• Pain worse with resistive extension
Supraspinous/Interspinous Ligaments
• The supraspinous and interspinous ligaments course from spinous process to spinous process (Figure
56-4).
Figure 56-4. Supraspinous and interspinous ligaments.
• The supraspinous ligament is found from C7-L3 as opposed to the interspinous ligament which courses
the entire length of the spine.2
• Protects against spinal separation and flexion.
• Innervated by the medial dorsal primary rami.
Clinical Anatomy
• Afferent nociceptors are activated by tearing or micro-tears in the ligament, typical of deceleration or
acute flexion-extension injuries resulting in midline spine pain.
• Micro-tearing can lead to ligamentous laxity over time, which promotes poor posture and mechanical
derangement of the spine with ensuing chronic spine pain (Figure 56-5).
Figure 56-5. Interspinous/supraspinous ligamentous laxity depicted by the arrow from C7-T3.
Distal Piriformis
• Originates at the anterior surface of the inferior lateral angle of the sacrum.
• Inserts on the medial side of the superior surface of the greater trochanter (Figure 56-6).3
Figure 56-6. Distal piriformis tendon depicted inserting onto the greater trochanter.
• In 20% of patients, all or part of the sciatic nerve passes through the piriformis muscle.3
• Innervated by the piriformis nerve (L5, S1, S2).
Clinical Anatomy
• Lateral thigh pain
• Buttock pain
• Low back pain
• Pain with paresthesia can be noted in the posterior thigh, and hip with radiation into the distal leg and
foot
• Point tenderness along the posterior superior greater trochanter
• Symptoms aggravated by prolonged sitting and with a combination of hip flexion, adduction, and
medial rotation
Iliolumbar Ligament
• The iliolumbar ligament originates from the L-5 transverse and is made up of an anterior and posterior
band (Figure 56-7).
Figure 56-7. Iliolumbar ligament originating at L5 transverse process and inserting on the iliac crest.
• The anterior band is broad and flat and has two different anatomic varieties.
Type 1 originates from the anterior aspect of the inferiolateral portion of the L-5 transverse process
and fans out widely before inserting on the anterior portion of the iliac tuberosity.
Type 2 originates anteriorly, laterally, and posteriorly from inferiolateral aspect of the L-5
transverse process and fans out before inserting on the anterior portion of the iliac tuberosity.
• The posterior band of the iliolumbar ligament originates from the apex of the L-5 transverse process
and becomes fusiform just prior to inserting on the anterior margin and apex of the iliac crest.4
Clinical Anatomy
• Unilateral or bilateral low back pain
• Exquisite tender point at the posterior iliac crest (Figure 56-8)
Figure 56-8. Exquisite tender point at the posterior iliac crest.
• Positive hip flexion test and Patrick maneuver

• Constant ache aggravated by prolonged sitting and standing—referral pain to the greater trochanter and
into the groin (“my testicles are in a vice”)
• Anticoagulation/bleeding diathesis/thrombocytopenia.
• Physical examination of the target area for singes of infection, skin ulceration or necrosis, and extent of
disease.
• Patient must be able to lie still for the intended length of the procedure.
• Consider intravenous access for IV fluid and medications for sedation or hypotension if there is
concern for a vasovagal reaction.
• Evaluation for contrast allergy—this is of the utmost importance if using fluoroscopy, since the
utilization of contrast will allow for precise needle placement. This is not a concern for ultrasound-
guided injections.
FLUOROSCOPIC/ULTRASOUND VIEWS
• When using fluoroscopic guidance for supraspinous/interspinous, levator, iliolumbar and distal
piriformis tendon/ligament injections, always start with anterior-posterior (AP) images to confirm your
location and to line up the anatomical structures.
Slight cephalad tilt with ipsilateral obliquity may enhance visualization of the superior medial
portion of the greater trochanter for distal piriformis tendon injections (Figure 56-20A).
Cephalocaudal adjustments in the AP view should be done to square up the end plates and line up
the spinous processes midline when performing supraspinous and interspinous ligament injections
(Figure 56-17).
• Cephalad tilt with ipsilateral oblique can enhance visualization of the PSIS when performing an
iliolumbar ligament injection (Figure 56-19A).
• Lateral views should always be done to verify depth (Figure 56-18B).
EQUIPMENT
• 22- or 25-gauge 1.5- to 3.5-in spinal needle
• 30-gauge subcutaneous needle
• 5 cc syringe for local anesthetic/deposteroid
• 3 cc syringe for contrast
• Extension tubing
MEDICATIONS
• 0.5% bupivacaine
• 1% lidocaine
• Deposteroid
• Nonionic contrast (Omnipaque 240 or Isovue 300)
• Prep solution

Bicipital Tendon Injection
• The tendon is palpated in the bicipital groove of the humerus.
• After a sterile prep and subcutaneous local anesthetic infiltration, a 25-gauge 1.5- or 2-in needle is
inserted into the skin over the area of maximum tenderness and directed into the groove at an angle near
parallel to the groove itself.
• The goal is to enter the sheath of the biceps tendon and not the tendon itself (Figure 56-9).
Figure 56-9. Bicipital tendon injection (fluoroscopy).
• Increased resistance to injection indicates intra-tendinous placement and the needle should be
withdrawn slightly until there is very little resistance to injection.5
• After negative aspiration and no resistance, 2 to 3 cc of 0.5% bupivacaine with deposteroid is injected
slowly
Zhang et al describe an ultrasound-guided approach.6
• The patient is positioned supine with the torso and upper body and the ipsilateral arm alongside the
body with the elbow flexed 90 degrees.
• The skin surrounding the needle entry point is cleaned with Betadine solution and sterile drapes
placed.
• The ultrasound transducer is protected with a sterile cover containing a small amount of gel.
• A preliminary ultrasound evaluation is performed with an ultrasound unit with multi-frequency linear
transducers.
The transducer frequency is chosen based on the depth of the individual anatomic structure.
• Color Doppler is used to identify local vascular structures.
• On the transverse scanning of proximal humerus, the brachial bicipital groove and the biceps brachii
tendon can be seen clearly (Figure 56-10A). The tendon appears as an echogenic ellipse within the
groove.
Figure 56-10. (A) Transverse ultrasonogram at the level of brachial bicipital groove shows the biceps
brachii tendon in the groove and the tendon appearing as an echogenic ellipse within the groove. (B)
Transverse ultrasonogram of the biceps brachii tendon at the level of the brachial bicipital groove after
injection of medication (corticosteroid and lidocaine). Note the distention of the peritendon sheath space
and circumferential spread of medication around the tendon. (Both the images were reproduced with
permission from Zhang et al. Ultrasound guided injection for the biceps brachii tendinitis: Results and
Experience. Ultrasound in Med. & Biol., Vol. 37, No. 5, pp. 729–733, 2011.)
• A lateral to medial approach using a 25-gauge, 1.5-in needle is performed. The needle is visualized in
the long axis of the probe and advanced under ultrasound guidance.
• Once the needle tip is seen within the brachial bicipital groove, the corticosteroid is delivered under
real-time monitoring (Figure 56-10B).
Levator Scapula Tendon Injection

• The patient is positioned seated, if no fluoroscopy is being used, or prone if using fluoroscopy.
• The tendon insertion site is marked over the superior angle of the scapula and the area of max
tenderness is identified (Figure 56-11).
Figure 56-11. Levator injection site.
• After sterile prep, the skin is infiltrated with 1% lidocaine; then a 25-gauge 1.5-in spinal needle is
inserted under fluoroscopic guidance using a coaxial technique.
• The needle is advanced until it contacts bone along the superior angle of the scapula (Figure 56-12).
Figure 56-12. Levator scapula injection without fluoroscopy.
• Then, the needle is walked off the bone until it is seated in the tendon sheath.
• After negative aspiration, 1cc of contrast is injected to ensure proper placement and no
vascularization.
• Then, 3 cc of 0.5% bupivacaine with deposteroid is injected.
• Laying an RF probe across the enthesopathy may denervate the periosteum, giving pain relief (Figure
56-13).
Figure 56-13. Radiofrequency lesion, right levator.
Lateral Epicondyle Injection

• For the nonfluoroscopic injection, the elbow is held in the noninjecting hand, and the lateral epicondyle
identified by palpation (Figure 56-14).
Figure 56-14. Lateral epicondyle examination.
• Fluoroscopically, the radial head is identified (Figure 56-15).

Figure 56-15. Fluoroscopic location of lateral epicondyle.
• The radial nerve lies medial to the tendon, so the injection needs to be kept laterally.
• The injection is placed at the base of the tendon attachment (Figure 56-16).
Figure 56-16. Lateral epicondyle injection.
Supraspinous/Interspinous Ligament Injection

• The patient is placed prone.
• After sterile preparation and drape, the spinal interspace of interest (the area of tenderness) is located
by fluoroscopy (Figure 56-17).
Figure 56-17. Midline tenderness at L5S1.
• Local anesthesia of the skin and subcutaneous tissues is performed with 1% lidocaine.
• Then, a 22-gauge spinal needle is advanced under fluoroscopic guidance between the affected spinous
processes so that the tip of the needle is placed directly between the affected spinous processes on the
PA image (Figure 56-18A).7
Figure 56-18. (A) PA view of interspinous injection. (B) Contrast infiltrating the space between the L3
and L4 spinous processes. (Both the images were reproduced with permission from Lamer et al.
Fluoroscopically-Guided Injections to Treat “Kissing Spine” Disease. Pain Physician: July/August
2008:11:549-554.)
• Lateral views are then taken to verify that the needle is placed midway along the dorsal-ventral axis of
the processes.7
• Then, after negative aspiration, 1 cc of contrast is injected to reveal contrast spread between the
targeted spinous processes (Figure 56-18B).7
• This is followed by the injection of 2 cc of 0.5% bupivacaine and deposteroid.
Iliolumbar Ligament Injection

• The target site of injection is the posterior iliac crest identified by fluoroscopy (Figure 56-19A).
Figure 56-19. (A) Bone spur seen on fluoroscopy at the iliolumbar ligament insertion site. (B) Final
needle placement at the iliolumbar ligament insertion site.
• After sterile prep and drape, the skin and subcutaneous tissues are infiltrated with 1% lidocaine.
• Then a 22- or 25-gauge 3.5-in spinal needle is inserted under fluoroscopic guidance using a coaxial
technique.
• The needle is advanced under fluoroscopic guidance until it contacts bone along the posterior iliac
crest (Figure 56-19B).
• The needle is then walked of the bone medially until it is seated in the tendon sheath.
• After negative aspiration, 1 cc of contrast is injected to reveal contrast spread along the tendon and to
ensure proper placement without vascularization.
Distal Piriformis
• Patient is placed prone.
• AP views of the lumbosacral junction and hip of the target side are visualized. Slight cephalad tilt with
ipsilateral obliquity will help enhance visualization of the target at the medial superior portion of the
greater trochanter (Figure 56-20A).
Figure 56-20. (A) Fluoroscopic view depicting the needle target along the distal piriformis tendon
insertion on the greater trochanter. (B) Final needle placement at the distal piriformis insertion site.
• After sterile prep and drape, the skin and subcutaneous tissues are infiltrated with 1% lidocaine.
• Then a 22 or 25 gauge 3.5 inch spinal needle is inserted under fluoroscopic guidance using a coaxial
technique (Figure 56-20B).
• The needle is advanced under fluoroscopic guidance until it contacts bone along the medial superior
portion of the greater trochanter.
• The needle is then walked of the bone medially until it is seated in the tendon sheath.
• After negative aspiration, 1 cc of contrast is injected to reveal contrast spread along the tendon and to
ensure proper placement without vascularization.
• The patient should be followed up by telephone next day for the potential complications and immediate
pain relief secondary to local anesthetic. The anti-inflammatory effect of steroid will not be apparent
until 1 or 2 weeks. Patient should be advised to call pain service for any procedure related
complications and/or any unexpected neurological deficit. Patient should be monitored closely for the
following:
Weakness
Swelling
Fever
Bleeding
Numbness
Exacerbation of symptoms

• The overall incidence of side effects after local corticosteroid injection for tendon lesions is
unknown.5
• Tendon rupture
• Exacerbation of pain
• Infection
• Nerve damage
• Weakness
• Numbness
• Damage to the tendon itself
• Allergic reaction to the injectate
• Tissue atrophy
CLINICAL PEARLS
• As early as 1930, Leriche pointed out that, after infiltration of a tender ligament or tendon with
procaine, there was not just temporary relief of discomfort but a more prolonged effect than what one
would expect from the anesthesia.8
• Corticosteroid injections are one of the most commonly used treatments for chronic tendon lesions.
• Despite their popularity, the evidence for long-term effectiveness is lacking.5
Many of the studies have had inadequate design.
Problems include small sample sizes, unsuitable outcome measures, short term follow up,
inadequate blinding, lack of a true placebo, and the inclusion of heterogeneous study populations.5
• Tendinitis may be inflammatory, but the primary problem is often degeneration with attempted repair,
ie, tendinopathy or tendinosis rather than true tendinitis.9
References
1. Ahrens et al. The long Head of the biceps and associated tendinopathy. J Bone Joint Surg. 2007
Aug;89-B(8).
2. Cuccurullo SJ. Physical Medicine and Rehabilitation Board Review. New York: Demos Medical
Publishing; 2004:153-154, 264.
3. Travell J, Simons D. Travell and Simons’ Myofascial Pain and Dysfunction, the Trigger Point
Manual. Pages 187, 188, 191, 192, 193.
4. Rucco et al. Anatomy of the iliolumbar ligament: a review of its anatomy and a magnetic resonance
study. Am J Phys Med Rehabil. 1996 Nov-Dec;75(6):451-455.
5. Speed CA. Corticosteroid injections in tendon lesions. BMJ. 2001 Aug18;323.
6. Zhang J, Ebraheim N, Lause GE. Ultrasound guided injection for the biceps brachii tendonitis: results
and experience. Ultrasound Med Biol. 2011;37(5):729-733.
7. Lamer et al. Fluoroscopically-guided injections to treat “kissing spine” disease. Pain Physician.
2008 Jul/Aug;11:549-554.
8. Naeim F. Treatment of the chronic iliolumbar syndrome. West J Med. 1982 Apr;136(4):372-374.
9. Rasmussen OS. Sonography of tendons. Scand J Med Sci Sports. 2000;10:354-360.
9. Mitra et al. Interspinous ligament steroid injections for the management of Baastrup’s disease: a case
report. Arch Phys Med Rehabil. 2007 Oct;88:1353-1356.
11. Nosir HR. Upper extremity joint injections. In: Manchikanti L, Singh V, eds. Interventional
Techniques in Chronic Non-Spinal Pain. Paducah, KY: ASIPP Publishing; 2009:361-388.
SECTION VI
PERIPHERAL NERVE BLOCKS

CHAPTER 57
Intercostal Nerve Block

Amitabh Gulati
INTRODUCTION
The intercostal nerve block was first described in 1907 by Heinrich Braun1 to treat acute and chronic
pain of the posterior and anterior portions of the superficial thorax and upper abdomen. The intercostal
nerves are mixed nerves of with motor and sensory components. Elaborate on the function of the ICN.
INDICATIONS
Intercostal blocks are useful in relieving post-traumatic and postoperative pain, and more recently,
chronic nonmalignant and from malignancies processes involving the thoracic wall (Table 57-1).2-4
Blockade of the intercostal nerve may ameliorate painful nerve impulses associated with chronic
neuropathic pain. Local anesthetic blocks can also be used to diagnose pain problems when both thoracic
and visceral sources are suspected. Similar techniques can be used to perform neurolysis (cryoablation,
radiofrequency ablation, or chemical neurolysis).
TABLE 57-1. Indications for Intercostal Nerve Blocks3,5,6

• Severe pain from rib fractures
• Dislocation of costochondral joint
• Chest wall pain from acute herpes zoster or postherpertic neuralgia
• Postoperative pain management (thoracotomy, sternotomy, upper abdominal surgery)
• Chronic intercostal nerve-related pain (eg, postthoracotomy pain)
• Cancer-related pain of the chest wall
• Idiopathic neuropathic pain of the intercostal nerve
• Establish a diagnosis
CONTRAINDICATIONS
While there are few absolute contraindications to an intercostal nerve block, extra caution must be taken
in patients to whom a pneumothorax may be detrimental. These patients may include:
• Respiratory decompensated patients
• Patients with a single lung on the side of the planned procedure
• Patients on positive pressure ventilations
• Postsurgical patients
General relative contraindications include blood dyscrasias, local or uncontrolled systemic infection,
or unknown anatomical changes (eg, unknown rib resection).
Advantages
As with other regional techniques, intercostal nerve blocks are associated with:
• Decreased need for parenteral or oral opioids.3,5
• In thoracic surgery, the use of intercostal nerve blocks allows for improved respiratory function in
FEV1 and Peak expiratory flow rate.5,7
• Decreasing oral or parental opioids may reduce the incidence of nausea, vomiting, urinary retention,
itching, and hypotension.
Complications
While complication rates vary, performing the block with imaging may reduce some of the associated
risks described below (Table 57-2).
TABLE 57-2. Complications Associated with Intercostal Nerve Blocks3

• Bleeding along the path of needle or hematoma
• Infection
• Toxicity to injectate (local anesthetic, etc)
• Pneumothorax
• Hematoma
• Nerve damage
• Spinal cord injury from uptake of alcohol
• Epidural or spinal injection
• Muscle trauma
ANATOMY
The intercostal nerve travels along the intercostal groove of each corresponding rib. Each intercostal
nerve, bilaterally from T1-T12, emerges from the intervertebral foramen of the respective vertebra. From
the foramen, each thoracic nerve root divides into four branches:
• The white and gray rami communicate (traveling anteriorly to join the sympathetic ganglion).
• The posterior dorsal ramus.
• The ventral ramus (which becomes the intercostal nerve).5,8
The Ventral Ramus

• The ventral ramus joins with the corresponding thoracic artery and vein, forming the neurovascular
bundle, which carries both sensory and motor fibers (Figure 57-1).
Figure 57-1. Cross-sectional view of the intercostal space from a cephalocaudal transection. This cross
section is a common view obtained with ultrasound-guided procedures involving the intercostal nerve.
EICM, external intercostal muscle; IICM, internal intercostal muscle; IM ICM, innermost intercostal
muscle; V-A-N = intercostal vein, artery, and nerve, respectively. (Adapted from Cousins & Bridenbaugh,
1998.)
• Within this bundle, the vein is positioned superior to the artery and nerve, with the intercostal nerve
sitting most inferiorly (V-A-N configuration).
• About 3 cm away from the intervertebral foramen, the neurovascular bundle first transects the internal
intercostal membrane, where it then runs parallel with the rib traveling in the intercostal groove,
located on the internal surface of inferior border of the rib.
• At this point, the intercostal nerve is situated between the innermost intercostal muscle and the internal
intercostal muscle.
The first major branch of the intercostal nerve is the lateral cutaneous branch, occurring at midaxillary
line (Figure 57-2). The remaining intercostal nerve continues to travel anteriorly and terminates into the
anterior branch at the sternum. Along the course of the nerve, smaller branches may separate from the
intercostal nerve (ie, anterior and posterior cutaneous branches). The intercostal muscles and parietal
pleura are innervated by small branches of the intercostal nerves of T1-T6.
Figure 57-2. Cross section of vertebral body. Path and branches of the intercostal nerve are marked. The
thoracic nerve root leaves the vertebral body and lies inferior to the corresponding rib. (Adapted from
Cousins & Bridenbaugh, 1998.)
The T12 intercostal nerve:

• The T12 intercostal nerve does not run as closely to the intercostal groove of its accompanying rib as
the other intercostal nerves do, making it a more difficult nerve to identify and anesthetize.5
• A substantial part of the T12 ventral rami ultimately joins the ventral ramus of L1, forming the
iliohypogastric, ilioinguinal, and genitofemoral nerves.
• The remaining portion transects the transverse abdominis muscle and lies between that and internal
oblique muscle.8
Lateral cutaneous branches:
• The lateral branches of the intercostal nerve pierce the internal and external intercostal muscles,
dividing into anterior and posterior branches that innervate muscles and skin of the lateral aspects of
the chest.
• The lateral anterior divisions of T7-T11 supply the skin extending to the lateral edges of the rectus
abdominis muscle. The lateral posterior division supplies the skin overlying the latissimus dorsi
muscle.8
Anterior cutaneous branches:
• The anterior cutaneous branches of T2-T6 travel through the external intercostal and pectoralis major
muscles, entering into the superficial fascia at the lateral border of the sternum.
• These nerves supply the midline portion of the anterior thoracic wall.
• The anterior branches of T7-T12 supply the motor nerves to the rectus abdominis muscle as well as
sensory fibers to the skin of the anterior abdominal wall.
• Some branches continue to travel anteriorly to innervate the parietal peritoneum and the cutaneous area
of the abdominal midline.5,8
As with any regional anesthetic technique, proper preparation is essential for a safely performed
procedure. A patient’s airway, respiratory, and cardiac status and examination should be performed.
Resuscitation equipment should be nearby, and if sedation and analgesia are used, supplemental
oxygenation may be necessary. Postprocedure evaluations should include signs of pneumothorax, local
anesthetic toxicity, and intrathecal injection. Vital sign monitoring, including heart rate, rhythm, and
oxygen saturation, should be performed.
Technique
Perform a cardiac and respiratory assessment to determine the patient can tolerate the blockade of one or
more intercostal nerves. Obtain baseline vital signs and consider monitors to be placed on the patient.
Supplemental oxygenation should be available. Resuscitation cart should be accessible. Larger needle
gauges (smaller diameter) could reduce the risk of puncturing the pleura. Usually, 2 to 3 mL of solution is
sufficient to successfully block the intercostal nerve. Commonly injected local anesthetic solutions
include lidocaine (1%-2%), ropivicaine (0.2%-0.5%), or bupivicaine (0.25%-0.5%).
Anatomical Landmark Technique

The patient can be in the prone, sitting, or lateral decubitus position. The angle of the rib (where the rib
begins its bend in front of the tubercle), which is usually about 6 to 8 cm from the paraspinal muscles for
lower ribs and 4 to 7 cm for upper ribs, is located by palpation. Blocks medial to the rib angle may pose
more risks, as the nerves lie deep to the posterior intercostal membrane with very little tissue between it
and the parietal pleura.
CLINICAL PEARLS
• At the angle of the rib, the risk of a dural injection is unlikely. The rib is relatively superficial and the
subcostal groove is at the widest, minimizing the risk of a pneumothorax, hopefully.
• The intercostal nerve is oriented inferiorly to the intercostal artery, and surrounded by adipose tissue,
coursing between the internal intercostal and innermost intercostal muscles.
• Once the location is decided, apply a disinfectant preparation (consider chlorohexidine or betadine),
draping and sterile precautions.
• While retracting the skin over the rib superiorly, infiltrate the skin with local anesthetic (usually a 30-
gauge needle and 1 mL of local anesthetic is sufficient) at the puncture site. The rib palpated should
correspond to the intercostal nerve to be blocked.
• The preferred target is the inferior border of the rib.
• Introduce the needle (usually a 22- or 25-gauge 1-in spinal needle) and contact the rib. While
maintaining control of the needle, slowly walk the needle caudally with the injecting hand.
• When bony contact has ceased, slowly advance (usually about 2-3 mm) until a subtle “pop” through the
fascia of the internal intercostal muscles is felt. Use of a blunt needle can facilitate the tactile “pop.”
• The average distance between the posterior aspects of the rib to pleura may be as little as few
millimeters.9
• After negative aspiration, 2 to 5 mL of local anesthetic can be injected.
Fluoroscopy-Guided Technique
The anatomical technique can be modified such that the rib is visualized under fluoroscopy. This may be
especially beneficial when the rib cannot be reliably palpated. Again, the needle is directed to contact the
inferior border of the corresponding rib and directed caudally such that the needle is both inferior to the
rib and at the anterior border of the rib in lateral and AP view (Figures 57-3 and 57-4, respectively).
Figure 57-3. Lateral view of the intercostal nerve block under fluoroscopic guidance. The white arrow
shows the needle at the anterior border of the rib. This image can be used in conjunction with the AP view
to accurately guide the needle.
Figure 57-4. AP view of fluoroscope-guided intercostal nerve block. The needle placement is confirmed
to be at the inferior border of the rib.
• The use of ultrasonography allows for real time visualization of needle placement and local anesthetic
injection.
• This technique has the potential to reduce incorrect needle positions and pleural punctures when done
appropriately.
• The ultrasound probe (usually high-frequency linear probes) is placed in the longitudinal axis, parallel
to the posterior mid-clavicular or mid-axillary line (Figure 57-5).
Figure 57-5. Position of ultrasound probe, needle, machine, and rib markings to perform an intercostal
nerve block.
• This allows for views of two ribs in cross-sectional view (Figure 57-6).
Figure 57-6. Anatomical representation of an intercostal nerve block. Needle entry point and target is
shown. EICM, external intercostal muscle; IICM, internal intercostal muscle; IM ICM, innermost
intercostal muscle; V-A-N, intercostal vein, artery, and nerve, respectively.
• An in-plane approach for needle placement is recommended.

• Puncture site is initiated from the superior border of the rib below the intercostal nerve of interest (ie,
if T6 intercostal nerve is to be blocked, the superior border of T7 rib is the puncture site).
• After local anesthetic is given for skin anesthesia (as above), a 22- or 25-gauge needle is inserted
roughly at a 30- to 45-degree angle (Figures 57-7 and 57-8).
Figure 57-7. Intercostal nerve block under ultrasound guidance with a 22-gauge needle. Notice the needle
is easier to visualize when compared to a 25-gauge needle.
Figure 57-8. Intercostal nerve block under ultrasound guidance with a 25-gauge needle. A 25-gauge
needle may be visualized subtly with tissue distraction under real-time view using ultrasonography.
• The needle can be directed to the inferior border of the corresponding rib.
• The needle can penetrate the internal intercostal muscle and can be visualized above the pleura and
innermost intercostal muscle.
• Usually the intercostal nerve is not visualized, but the spread of solution beneath the fascia of the
internal intercostal muscle signifies a successful blockade of the intercostal nerve.
POSTPROCEDURE FOLLOW-UP AND PITFALLS

After completion of the procedure, evaluation of the patient for side effects should be performed. Of
primary concern is the presence of a pneumothorax, which can be detected with a postprocedure chest X-
ray. A pulmonary examination may help detect a severe pneumothorax or a tension pneumothorax.
Supplemental oxygen may be necessary for mild pneumothorax, while a chest tube may be necessary for
symptomatic pneumothorax.
For lower thoracic intercostal nerve blocks, the peritoneum or retroperitoneum may be punctured.
Hematoma may be considered if abdominal or back pain ensues over time. Finally, local anesthetic
toxicity should be evaluated both for neurologic and cardiac complications, including seizure and
arrhythmias.
CLINICAL PEARLS
• Intercostal nerve procedures are indicated for thoracic and abdominal pain and anesthesia.
• Intercostal nerve blocks are contraindicated for patients in which respiratory compromise would lead
to severe patient decompensation.
• Utilization of imaging can be used to assist in the placement of the intercostal nerve block.
• Postprocedure evaluation for pneumothorax is warranted.
References
1. Braun H. Operations of the Spinal Column and Thorax. Local Anesthesia, Its Scientific Basis and
Practical Use. 3rd ed. Cincinnati, OH: Lea & Febiger; 1914:278-282.
2. Barash PG, Cullen BF, Stoelting RK, Cahalan, and Stock MC. Peripheral nerve blockade. In: Tsui B,
Rosenquist RW, eds. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins;
2009:981-984.
3. Cousins MJ, Carr DB, Horlocker TT, Bridenbaugh PO. Intercostal, intrapleural, and peripheral
blockade of the thorax and abdomen. In: Harmon DC, Shorten GD, eds. Cousins and Bridenbaugh’s
Neural Blockade in Clinical Anesthesia and Pain Medicine. 4th ed. Philadelphia, PA: Lippincott
Williams and Wilkins; 2009:386-390.
4. Wong FC, Lee TW, Yuen KK, et al. Intercostal nerve blockade for cancer pain: effectiveness and
selection of patients. Hong Kong Med J. 2007;13(4):226-270.
5. Mulroy MF, Bernards CM, McDonald SB, Salina FV. Intercostal and terminal nerve anesthesia of the
trunk. In: Mulroy MF, ed. Regional Anesthesia. 4th ed. Baltimore, MD: Lippincott Williams &
Wilkins: 2009:137-146.
6. Karmakar MK and Ho, AMH. Acute pain management of patients with multiple fractured ribs. J
Trauma. 2003; 54(3):612-615.
7. Dowling R, Thielmeier K, Ghaly A, Barber D, Dine A. Improved pain control after cardiac surgery:
results of a randomized, double-blind, clinical trial. J Thorac Cardiovasc Surg. 2003;126(5):1271-
1279.
8. Gray H. Anatomy of the Human Body. 29th ed. Philadelphia, PA: Lea & Febiger: 1973:978-983.
9. Byas-Smith MG, Gulati A. Ultrasound-guided intercostal nerve cryoablation. Anesth Analg. 2006
Oct;103(4): 1033-1035.
CHAPTER 58
Supraclavicular and Infraclavicular Nerve

Blocks
David B. Albert, Robert Altman, and Lisa Doan
SUPRACLAVICULAR NERVE BLOCK

Indications
The supraclavicular nerve block is ideal for pain of the upper extremity below the shoulder. The trunks
formed by the C5-T1 nerve roots of the brachial plexus are very closely approximated at this level, so all
the branches of the brachial plexus will be successfully blocked.
Anatomy (Figure 58-1)

Figure 58-1. Relationship of the trunks of the brachial plexus to the subclavian artery as they cross over
the first rib. The subclavian artery and brachial plexus travel in a neurovascular bundle emerging between
the anterior and middle scalene muscles.
Brachial Plexus
• The nerve roots of the brachial plexus join to form the trunks.
• The C5 and C6 nerve roots (with occasional significant contributions from C4) combine to form the
superior trunk.
• The C7 nerve roots become the middle trunk.
• C8 and T1 nerve roots (with occasional contribution from T2) form the inferior trunk.
• The 3 trunks emerge from the interscalene space and continue in an anterior, lateral, and inferior
direction.
• The trunks converge near the upper surface of the first rib and as they cross the first rib around the
upper border of the clavicle, they divide into their separate anterior and posterior divisions.
The relationship of the subclavian artery and vein:
• The relationship of the subclavian artery and vein (later the axillary artery and vein, respectively) to
the trunks is an important consideration.
• When the subclavian artery passes under the clavicle, it becomes the axillary artery. Anatomically the
subclavian artery (above the clavicle) lies in front of the trunks, while distally and below the clavicle
at the level of the cords the axillary artery lies in the middle.
• The subclavian vein (above the clavicle) is separated from the subclavian artery by the anterior
scalene insertion, and therefore does not travel within the neurovascular bundle (Figure 58-2).
Figure 58-2. Relationship of the brachial plexus to the subclavian vasculature. Note the subclavian vein
is separated from the subclavian artery by the anterior scalene muscle. Thus proximal to the clavicle, the
subclavian vein does not travel in the same fascial sheath as the subclavian artery and brachial plexus.
• Distal to the clavicle, the axillary vein joins the neurovascular bundle, so that now the cords are found
around the artery but also in between the axillary artery and vein.
Techniques
The supraclavicular nerve block can be performed with either a nerve stimulator or under ultrasound
guidance. The complication most often associated with this block is a pneumothorax. Remember that the
apex of the lung is just medial and posterior to the brachial plexus as well as deep to the first rib.
Nerve Stimulator Technique

Landmarks (Figure 58-3)
Figure 58-3. Landmarks for supraclavicular block. The initial approach is similar to an interscalene
block. The posterior border of the sternocleidomastoid muscle is palpated. The fingers are then rolled
laterally over the anterior scalene muscle into the interscalene groove.
• The initial approach to this injection is identical to that of an interscalene nerve block.
• Place the patient in a supine position and draw a line at the level of the cricoid cartilage (C6).
• The arm should be at the patient’s side, pointing to the ipsilateral toes.
• The head is turned toward the opposite side. The head should be turned three-fourths lateral, so as not
to tense the neck muscles to the point where muscle bellies cannot be appreciated.
• Palpate the posterior border of the sternocleidomastoid muscle at the C6 level.
• Roll the fingers laterally over the anterior scalene muscle until a distinct groove is felt between the
anterior and middle scalene muscles.
• Move the fingers laterally and inferiorly down the interscalene groove until they are approximately 1
cm from the mid-clavicle.
• This location is the initial insertion site for the needle.
• The practitioner stands near the patient’s head and directs the needle toward the axilla.
Needles
• 22-gauge 5-cm, insulated needle
• 18-gauge 5-cm, insulated Tuohy needle for catheter placement
Stimulation
• The nerve stimulator is initially set at 1.0 to 1.2 mA.
• Proper needle placement is confirmed by flexion or extension of the digits at 0.3 mA or less.
• The brachial plexus can be deep at this location, but is often reached at 2 to 4 cm.
Pearls
• Aspiration of bright red blood suggests subclavian artery penetration, indicating the needle is too
medial.
• Stimulation of the musculocutaneous nerve (biceps contractions) usually indicates the needle is too
lateral.
• Pectoralis muscle contraction indicates the needle is anterior.
• Scapular movement indicates the needle is posterior to the plexus.
• If the needle encounters bone (the first rib), it is too anterior and must be walked posteriorly.
• Because of the close proximity of the lung, the needle should never be directed medially.
Ultrasound Technique
Probe
• High frequency linear (5-12 MHz)
• In-plane
Probe position (Figure 58-4)
Figure 58-4. Ultrasonographic anatomy for supraclavicular brachial plexus block (left panel). Right
panel shows diagrammatic relationship between brachial plexus and subclavian artery. At this level, the
trunks or divisions of the brachial plexus are lateral to the subclavian artery (SA). (Image (A) was
reproduced with permission from VAULT Virginia Ultrasound; http://www.vaultrasound.com/educational-
resources/regional-anesthesia-vascular-access/supraclavicular/.)
• Position the probe on the neck directly above the clavicle in the supraclavicular fossa.
• The probe should be placed parallel to the clavicle.
• The practitioner should identify the subclavian artery, the first rib, the pleura, and the brachial plexus.
• At this level, the plexus will be configured as trunks or divisions and is typically located lateral and
slightly superior to the subclavian artery at a depth of 2 to 4 cm.
Technique (Figures 58-5 and 58-6)
Figure 58-5. Setup of ultrasound probe and needle (left panel) and corresponding image (right panel) for
supraclavicular brachial plexus block. The needle (N) is shown piercing the omohyoid muscle (omo) as it
approaches the brachial plexus (BP). A indicates subclavian artery; L, lung; R, first rib. (Reproduced
with permission from Orebaugh, SL, Bigeleisen, P. Ultrasound Imaging in Brachial Plexus Blockade. In:
Seminars in Anesthesia, Perioperative Medicine and Pain, Volume 26, Issue 4, Dec 2007.)
Figure 58-6. Ultrasound image of in-plane lateral-to-medial needle insertion for supraclavicular brachial
plexus block. BP indicates brachial plexus; LA, local anesthetic; N, needle tip; R, first rib; SA,
subclavian artery; *, needle shaft. (Reproduced with permission from Heil, JW, Ilfeld, MD, et al.
Preliminary Experience With a Novel Ultrasound-Guided Supraclavicular Perineural Catheter Insertion
Technique for Perioperative Analgesia of the Upper Extremity, J Ultrasound Med, Oct 2010, 29:1481-
1485; Fig. 1.)
• Insert the needle at the lateral end of the ultrasound probe and advance it parallel to the ultrasound
beam until it approaches the plexus.
• The initial local anesthetic injection is made near the lowest nerve trunk, close to the subclavian artery.
• If local anesthetic spread is adequate, the entire volume is injected.
• If spread to the superior nerve trunks is deemed inadequate, the needle should be repositioned and the
remaining local anesthetic injected.
Pearls
• The brachial plexus will appear like a bundle or cluster of grapes (hypoechoic circles with
hyperechoic rings).
• If three bundles are visualized, the practitioner is at the level of the trunks.
• If 5 to 6 clusters are seen, then the practitioner is at the level of the divisions.
• Always keep the tip and shaft of the needle in view to ensure that the needle is not penetrating too deep
into the supraclavicular fossa; deep penetration can result in an inadvertent pneumothorax or vascular
puncture.
INFRACLAVICULAR NERVE BLOCK
Indications
The infraclavicular nerve block is employed for pain distal to the mid-humerus. It allows for complete
anesthesia, without the sparing of the musculocutaneous nerve distribution that plagues the axillary block.
A potential advantage of this technique over the supraclavicular approach is the sparing of the phrenic
nerve—often blocked in the supraclavicular approach.
Anatomy (Figure 58-7)

Figure 58-7. Relationship of the cords of the brachial plexus to the axillary artery in the infraclavicular
fossa.
Techniques
As with most blocks, techniques exist for performing as the infraclavicular block using either the
ultrasound or nerve stimulator approaches. With the supraclavicular block, the proximity of the lung,
though usually further from the target injection site than in the supraclavicular approach, makes
pneumothorax a potential complication. Since the nerves of the brachial plexus surround the axillary
artery, intravascular injection of local anesthetic is also a complication to be wary of. Frequent aspiration
during all portions of the injections is warranted.
Nerve Stimulator Approach

Landmarks
• The key landmarks are the midpoint of the clavicle medially, and the axillary pulse laterally.
• One must visualize the course of the axillary artery between these two points, as the needle target is
essentially the artery (with the nerves surrounding it) as it follows this course.
Technique
• The block is most easily performed with the arm abducted to roughly 90 degrees allowing for
palpation of the axillary pulse.
• One stands at the head of the patient, or on the contralateral side to the block.
• A 4 to 6 in insulated nerve stimulator needle is inserted just lateral to the midpoint of the clavicle,
entering the skin at roughly a 45-degree angle, aiming at the visualized course of the axillary artery.
• The nerve stimulator is initially set at 1.5 mA, allowing for the initial phase of searching for the
general location of brachial plexus twitches.
• Musculocutaneous (biceps) twitches are not acceptable, as this nerve has such an early high take-off
from the remainder of the plexus that local anesthetic deposited here may not fill the remaining parts of
the sheath well. This will lead to a delayed and potentially patchy block.
• As acceptable twitches are located, the fine tuning of the location of the plexus begins. This involves
interplay between slowly decreasing the twitch intensity as one maps out a more exacting location for
the nerves with increasingly finer needle repositioning.
• When acceptable twitch intensity has been reached (usually under 0.35 mA), the local anesthetic can be
injected.
• Volumes for adequate blockade are in the 30 to 50 mL range. Frequent aspiration during injection is
indicated because of the close proximity of the plexus to the axillary artery.
Pearls
• This block can require more searching for an acceptable twitch because of the depth of the block
versus the superficial skin landmarks. Therefore, very efficient use of the nerve stimulator and needle
are important. One must essentially construct a 3D mental image of the underlying anatomy as twitches
are obtained to allow one to efficiently zero in on the location of the brachial plexus.
• While a musculocutaneous twitch is not acceptable for a block, it still provides one with useful
information, namely that the needle is directed to cephalad.
• One must be wary of needle angles steeper than 45 degrees, since increasingly steep needle entry
increases the chance of causing a pneumothorax.
• Despite an acceptably low milliamperage twitch, one may still have patchy blocks. This is because of
fascial divisions inhibiting full spread of the local anesthetic in this portion of the brachial plexus
sheath.
• Unfortunately, the nerve stimulator technique does not allow for the repositioning of the needle during
the injection as once the initial twitch is lost there is nothing left to guide one in needle positioning.
• This is one clear advantage of the ultrasound technique, where one can visualize the anesthetic spread,
and reposition one’s needle during the injection.
Ultrasound Approach
Probe
• High-frequency linear probe 5 to 12 MHz using an in-plane approach.
• Some practitioners may opt for a lower frequency probe in patients with large chest walls.
Technique (Figures 58-8 and 58-9)
Figure 58-8. Setup of ultrasound probe and needle for infraclavicular brachial plexus block. CL indicates
clavicle; COR, coracoid process. (Reproduced with permission from USRA.ca.)
Figure 58-9. Ultrasound image for infraclavicular brachial plexus block. At this level, the lateral cord
(Lat) is cephalad to the axillary artery (A), the posterior cord (Pos) posterior, and the medial cord (Med)
caudad to the artery. PMM indicates pectoralis major muscle; PMi, pectoralis minor muscle; V, axillary
vein. (Reproduced with permission from Paul G. McHardy, MD.)
• The probe is oriented in a parasagittal plane so as to cut across the axillary artery in the short axis.
• The probe location can be anywhere from the mid-clavicle to the coracoid.
• Visualize two major vascular structures, the axillary artery and vein deep to the pectoralis minor
muscle belly. The artery is on the cephalad side of the vein, and is rounder and less compressible than
the vein.
• If more than two vessels are seen, slide probe medially, simplifying the image as branches of vessels
rejoin the major trunks.
• The nerves of the plexus may or may not be visualized as hyperechoic structures surrounding the artery.
• The lateral cord is on the cephalad side of the artery, the posterior cord posterior to the artery, and the
medial cord on the caudal side of the artery, often between it and the vein.
• The needle is introduced from the cephalad side of the ultrasound probe, in plane with the beam so as
to allow the needle path to be visualized from the start.
• The goal is to place the needle just alongside the cephalad portion of the artery.
• Injection of local anesthetic can then commence in small increments (with frequent aspiration to ensure
no intravascular placement).
• It is very important to pay attention to the spread of the local anesthetic, since, as mentioned
previously, there are fascial divisions described in this portion of the plexus inhibiting full spread from
a single injection site.
• If full spread of the local anesthetic around the artery is not seen surrounding it like a doughnut (except
for the most superficial side of the artery), reposition the needle under direct visualization. Usually one
repositioning is enough to complete the spread. Some practitioners like to inject separately along the
caudal side of the artery to assure better spread to this portion of the plexus sheath.
• Careful to make sure that the needle does not enter the artery or the vein during injection.
• Volumes employed are 30-40 ml of local anesthetic solution.
Pearls
• Visualization of the nerves is not critical here, as they always surround the artery. This makes this
block easier than some others under ultrasound, since nerve visualization is usually more difficult than
visualization of vessels under ultrasound.
• The vein is very compressible. As one presses with the ultrasound probe, it may be occluded and not
well visualized. This is important to remember to prevent inadvertent puncture of the vessel. This is
especially important if one is injecting on the caudal side of the artery, in the space between the artery
and the vein.
• The needle path should be visualized throughout, from right after skin entry. It is only in this way that
one can be assured that one is visualizing the tip of the needle, rather than a portion of the shaft. This is
important both in placing the needle in the correct spot for injection, as well as preventing inadvertent
puncture of a vessel or a pneumothorax.
• One of the major benefits of the ultrasound approach in this block is avoiding the patchy blocks
sometimes seen with nerve stimulator approaches due to fascial divisions inhibiting full local
anesthetic spread. It is very useful to be able to move one’s needle under direct visualization and
deposit local anesthetic in several areas around the artery to ensure more uniform spread of the
anesthetic agent.
• While not critical for the block, the nerves are often better visualized with the patient’s arm abducted,
making them more taught and more echogenic.
Suggested readings
Borgeat A, Ekatodramis G, Dumont C. An evaluation of the infraclavicular block via a modified approach
of the Raj technique. Anesth Analg. 2001;93:436-441.
Brown DL. Atlas of Regional Anesthesia. 3rd ed. Philadelphia, PA: Lea & Febiger; 1990.
Brown DL, Cahill DR, Bridenbaugh LD. Supraclavicular nerve block: anatomic analysis of a method to
prevent pneumothorax. Anesth Analg. 1993;76:530-534.
Heil JW, Ilfeld MD, et al. Preliminary experience with a novel ultrasound-guided supraclavicular
perineural catheter insertion technique for perioperative analgesia of the upper extremity. J
Ultrasound Med. 2010.
Kapral S, Krafft P, Eibenberger K, Fitzgerald R, Gosch M, Weinstabl C. Ultrasound-guided
supraclavicular approach for regional anesthesia of the brachial plexus. Anesth Analg. 1994;78:507-
513.
Mariano ER, Loland VJ, Bellars RH, et al. Ultrasound guidance versus electrical stimulation for
infraclavicular brachial plexus perineural catheter insertion. J Ultrasound Med. 2009;28:1211-1218.
Mariano ER, Sandhu NS, Loland VJ, et al. A randomized comparison of infraclavicular and
supraclavicular continuous peripheral nerve blocks for postoperative analgesia. Reg Anesth Pain
Med. 2001;36:26-31.
Neuraxiom.com, A Website of Neuraxiom LLC.
Orebaugh SL, Bigeleisen P. Ultrasound imaging in brachial plexus blockade. In: Seminars in Anesthesia,
Perioperative Medicine and Pain. 2007;26(4):.
Raj PP, Montgomery SJ, Nettles D, Jenkins MT. Infraclavicular brachial plexus block—a new approach.
Anesth Analg. 1973;52:897-904.
Sandhu NS, Capan LM. Ultrasound-guided infraclavicular brachial plexus block. Br J Anaesth.
2002;89:254-259.
Sandhu NS, Manne JS, Medabalmi PK, Capan LM. Sonographically guided infraclavicular brachial
plexus block in adults: a retrospective analysis of 1146 cases. J Ultrasound Med. 2006;25:1555-
1561.
Subramanyam R, Vaishnav V, Chan VW, Brown-Shreves D, Brull R. Lateral versus medial needle
approach for ultrasound-guided supraclavicular block: a randomized controlled trial. Reg Anesth
Pain Med. 2011;36:387-392.
Tank PW, Geest TR. Lippincott Williams and Wilkins Atlas of Anatomy. 1st ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2008.
Vongvises P, Panijayanond T. A parascalene technique of brachial plexus anesthesia. Anesth Analg.
1979;58:267-273.
Wedel DJ. Nerve blocks. In: Miller RD, ed. Anesthesia. 5th ed. Philadelphia, PA: Churchill Livingstone;
2000.
http://www.usra.ca/infrascan.php
http://www.usra.ca/isura2012/syllabus/IAPN.pdf
http://www.vaultrasound.com/educational-resources/regional-anesthesia-vascular-
access/supraclavicular/
CHAPTER 59
Ilioinguinal and Iliohypogastric Nerve Blocks

Paul J. Hubbell III
INDICATIONS
The diagnosis and treatment of:
• Ilioinguinal neuralgia
• Iliohypogastric neuralgia
• Groin pain
• Inguinal pain, especially after mesh and/or staples
• Pelvic pain
• Postherpetic neuralgia
• Lateral abdominal wall pain postincision or trocar placement
CONTRAINDICATIONS
• Inability to communicate with the patient
• Infection
• Severe anxiety to needle sticks
• Anticoagulant or nonaspirin antiplatelet therapy
• Severe scarring over entire area to be injected
• Coagulopathy
• Psychogenic pain
RELEVANT ANATOMY
Iliohypogastric Nerve
• Branch of the L1 nerve root with a contribution from T12 occasionally.
• In a study of 100 embalmed cadavers, the iliohypogastric nerve originated from T12 on 14 specimens
(7%), from T12 and L1 in 28 (14%), from L1 in 20 (10%), and from T11 and T12 in 12 (6%).1
• Follows an oblique course that takes it from L1 and T12 around the flank to perforate the transverse
abdominis muscle and is positioned between it and the external oblique muscle terminating inside the
ilium (Figure 59-1).
Figure 59-1. Ilioinguinal and iliohypogastric nerves.
• Often entrapped at the lateral edge of the rectus border (Figure 59-2).
Figure 59-2. Entrapment at rectus border.
• May also be entrapped more proximally at the edge of the external oblique (Figure 59-3).
Figure 59-3. Proximal entrapment.
• Divides into an anterior and lateral branch after the perforation of the transverse abdominis muscle.
• The lateral branch gives sensory skin innervation to the posterolateral gluteal region, whereas the
anterior branch gives skin sensory innervation to the abdominal skin above the pubis.
• Both ilioinguinal and iliohypogastric branches of this L1 nerve root may interconnect and provide
significant variation of sensory innervation.
Ilioinguinal Nerve
• Branch of the L1 nerve root with a contribution from T12 in some patients.
• In a study of 100 embalmed cadavers, the ilioinguinal nerve originated from L1 in 130 specimens
(65%), from T12 and L1 in 28 (14%), from L1 and L2 in 22 (11%), and from L2 and L3 in 20 (10%).1
• Penetrates the transversus abdominis at the anterior superior iliac spine and terminates in the ilium.
• Ilioinguinal nerve may interconnect with the iliohypogastric nerve as it passes along inferiorly and
accompanies the spermatic cord through the inguinal ring and into the inguinal canal (Figure 59-1).
• Often entrapped at the lateral edge of the rectus border (Figure 59-2).
• May also be entrapped more proximally at the edge of the external oblique (Figure 59-3).
• Innervation of the ilioinguinal nerve includes the skin of the upper portion of the inner thigh, root of the
penis, the upper scrotum in men, and the mons pubis and lateral labia in women.
• Informed consent and proper explanation of risks, complications, and benefits.
• Lateral abdominal wall, flank and lower abdominal surgeries can result in neuralgia to the ilioinguinal
and iliohypogastric nerves, such as:
Open appendectomy
Open hernia repair
Liposuction of abdominal or flank wall
Pfannenstiel incisions
Any laparoscopic abdominal procedures
Liposuction abdomen and flank
Anterior spinal fusion chevron flank or retroperitoneal incision
Blockade of these nerves can be considered in preemptive analgesia for hernia surgery utilizing local
anesthesia with or without intravenous or nitrous oxide mask sedation.
Fluoroscopic Views
• Generally not indicated for this procedure, unless obese patient or anatomy impairs palpation of
anterior superior iliac spine (ASIS)
Physical examination usually suffices (Figure 59-4)
Figure 59-4. Palpation of the iliohypogastric at the rectus border.
• Ultrasound guidance for these nerve blocks provides about 70% to 95% success2,3 (Figure 59-5).
Figure 59-5. Ultrasound localization of ilioinguinal and iliohypogastric nerves at ASIS.
Equipment
• 25-gauge 2.0-in insulated needle
• 3-cc Luer lock syringe for local anesthetic
• Sensory nerve stimulator with alligator clip or other connections for grounding ECG pad and needle
Analgesia or Surgery
• 22-gauge 6- or 8-in spinal needle
• 3-cc syringe with 25-gauge 0.5-in needle
Radiofrequency or cryoanalgesia
• Radiofrequency or cryoanalgesia machine and appropriate cables and needles and/or cannulas and
grounding pads as well as 20- or 21-gauge insulated RF needle or 12-gauge IV catheter for
cryoanalgesia
Medications
• 0.75% or 0.50%, or 0.25% bupivacaine
• 1% or 2% lidocaine
• Deposteroid
• Neurolytic
5% to 10% phenol in saline or glycerin
Absolute alcohol
Technique
Diagnostic Block
• The patient is placed in the supine position with a pillow under the knees with the legs extended to
avoid exacerbation of abdominal pain due to stretching of extended legs.
• For rectus entrapments, the lateral edge of the rectus is palpated, and the point tenderness identified
Figure 59-6. Injection at the rectus border.
• For more proximal injections, the anterior superior iliac spine on the affected side is located by
palpation. A point 2 to 3 cm inferior and medial to the iliac spine is the insertion site for the 25-gauge
insulated needle (Figure 59-7).
Figure 59-7. Injection at the ASIS.
• Insertion should be directed inferior and slightly medial toward the crease of the affected inner leg
junction with the pubis for the ilioinguinal nerve.
• For the iliohypogastric nerve, the needle angle is directed more medial and inferior toward the
umbilicus.
• Connect the nerve stimulator and grounding pad to the needle and begin testing for patient sensation
along the tested nerve with between 0.2 and 0.5 V.
• It may be necessary to project nearly the entire needle length and to make multiple deliberate parallel
needle stimulation passes in order to locate the nerves.
• Once sensation is felt between these parameters, then inject less than 1 cc of local anesthetic with
deposteroid onto each nerve and remove the needle.
Preemptive Analgesia or Surgical Block

• Utilize the same ASIS position and location of insertion of needle with the same inferior but more
perpendicular approach and inject in a fan like direction through the subcutaneous tissue.
• Then inject along an additional line of subcutaneous and intramuscular injection from the iliac spine to
the inferior umbilicus at the midline.
• Now make a new inferior injection through the subcutaneous and intramuscular tissue over the midline
starting just below the umbilicus and directed inferior to just above the pubis.
• The surgeon will frequently add injection into the spermatic cord, so calculate your total volume
allowing for 5 to 10 cc of local anesthetic by the surgeon.
Ablation by Pulsed Mode Radiofrequency
• Place needle as above for diagnostic block for each nerve, then for RF, place probe into insulated
needle.
• Begin sensory nerve stimulation until patient feels stimulation between 0.2 and 0.5 V.
• Maintain firm grip on needle with fingers resting on abdomen and treat at 42 to 45°C for 2 minutes per
nerve.
Cryoanalgesia
• Use a larger 12-gauge angiocath and follow the same technique for placing diagnostic needle.
• Remove stylet and place cryoprobe with enclosed nerve stimulator into cannula (Figure 59-8).
Figure 59-8. Cryoneuroablation probe in place.
• Test sensory nerve through the treatment probe as with RF and treat by increasing gas flow to 10 to 12
L/min.
• A series of 3 two-minute freezes with 30 seconds for defrosting between each cycle is performed.
Ablation by Phenol or Absolute Alcohol

• Injection of 1 cc of 5% to 10% phenol or absolute alcohol on each nerve after satisfactory diagnostic
block and adding the phenol or alcohol after the local anesthetic injection (to avoid injection pain).
• 5 to 10 minutes of immediate follow-up for location and presence of pain relief secondary to local
anesthetic along with telephone contact the next day for potential complications as well as significance
and length of time of pain relief.

• Since the diagnostic block, radiofrequency or cryoanalgesia procedures are primarily subcutaneous
techniques, they are associated with few complications. There is a chance of hematoma and postblock
ecchymosis.4
• The preemptive or surgical block is intramuscular and subcutaneous so the possibility of peritoneal
penetration and colon perforation exists. Also there is a possibility of hematoma formation in the area
of the cord, which is a relative complication for the surgeon by hindering visualization of the surgical
dissection.
• Destruction of surrounding non-nerve tissue is a complication of phenol and absolute alcohol.
CLINICAL PEARLS
• Ilioinguinal and iliohypogastric nerve blocks are relatively simple procedures that usually provide
near-complete pain relief.
• These injections can be diagnostic and therapeutic. The patients with positive diagnostic but not
therapeutic response are candidates for an ablation procedure using pulsed mode RF, cryoanalgesia, or
phenol/alcohol.
• Pressure should be applied to the injection site for prevention of hematoma and ecchymosis, especially
for large cannula procedures like cryoanalgesia and after surgical or preemptive blocks.
• Absolute alcohol and phenol injections should only be utilized for cancer pain patients with limited
lifespan who suffer from intractable ilioinguinal or iliohypogastric neuralgia.
• The success of the diagnostic procedure is most dependent on accurate placement of the nerve
stimulation needle and a steady hand upon location of the affected nerve until injection of the local
anesthetic.
• The success of pulsed mode RF depends on appropriate location of the insulated treatment needle more
perpendicular than parallel to the nerve and sensation along the nerve tract between 0.2 and 0.5 V. This
treatment provides 6 to 18 months of at least 50% relief.5,6 Lower percentage relief usually indicates
more than one nerve branch is involved, requiring subsequent treatment of the untreated branch(es).
• Cryoanalgesia provides 4 to 30 months of good to excellent relief for each nerve properly identified
with nerve finder stimulation.7
• Phenol provides good relief with the possibility of necrosis on and around the nerve.8,9
• Absolute alcohol provides good relief with the possibility of nerve and surrounding permanent
necrosis and damage.10
If patients present with ilioinguinal or iliohypogastric dermatomal pain and do not get relief from a
diagnostic block, then consider T12, L1, or L2 nerve root pathology. Also consider pudendal nerve
pathology in refractory cases.
• It is not unusual to block branches of both nerves with 1 injection due to the possibility of multiple
branches and overlapping innervation of both nerves.
Suggested Reading
Brown DL. Atlas of Regional Anesthesia. 4th ed. Philadelphia, PA: Saunders; 2010.
Eichenberger U, Greher M, Kirchmair L, Curatolo M, Moriggl B. Ultrasound guided blocks of the
ilioinguinal and iliohypogastric nerve: accuracy of a selective new technique confirmed by
anatomical dissection. Br J Anaesth. 2006;97(2):238-243.
Manchkanti L, Singh V. Interventional Techniques in Chronic Non-Spinal Pain. 1st ed. Kentucky,
American Society of Interventional Pain Physicians; 2009.
Waldman SD. Atlas of Interventional Pain Management. 2nd ed. Philadelphia, PA: Saunders; 2004.
Willschke H, Marhofer P, Bosenberg A, et al. Ultrasonography for Ilioinguinal/iliohypogastric nerve
blocks in children. Br J Anaesth. 2005;95(2):226-230.
References
1. Klaassen Z, Marshall E, Tubbs RS, Louis RGJ, Wartmann CT, Loukas M. Anatomy of the ilioinguinal
and iliohypogastric nerves with observations of their spinal nerve contributions. Clin Anat. 2011.
2. Eichenberger U, Greher M, Kirchmair L, Curatolo M, Moriggl B. Ultrasound-guided blocks of the
anatomical dissection. Br J Anaesth. 2006;97:238-43.
3. Willschke H, Marhofer P, Bosenberg A, et al. Ultrasonography for ilioinguinal/iliohypogastric nerve
blocks in children. Br J Anaesth. 2005;95:226-230.
4. Vaisman J. Pelvic hematoma after an ilioinguinal nerve block for orchialgia. Anesth Analg.
2001;92:1048-1049.
5. Karaman H, Tufek A, Kavak GO, Yildiim ZB, Celik F. Would pulsed radiofrequency applied to
different anatomical regions have effective results for chronic pain treatment? JPMA. 2011;61:879.
6. Trescot AM. Cryoanalgesia in interventional pain management. Pain Physician. 2003;6:345-360.
7. Racz GB, Hagstrom D. Iliohypogastric and ilioinguinal nerve entrapment: diagnosis and treatment.
Pain Digest. 1992;2:43-48.
8. Nashel DJ. Entrapment neuropathies. In: Kippel JA, Dieppe PA, eds. Rheumatology. London,
England: Mosby; 1996.
9. McGrady EM, Marks RL. Treatment of abdominal nerve entrapment syndrome using a nerve
stimulator. Ann R Coll Surg Eng. 1988;70:120-122.
10. Applegate WV. Abdominal cutaneous nerve entrapment syndrome (ACNES); a commonly overlooked
cause of abdominal pain. The Permanente J. 2002;6:1-14.
CHAPTER 60
Genitofemoral Nerve Block

Andrea Trescot
Perhaps because much of its path is intra-abdominal, the genitofemoral nerve (GFN) nerve is an under-
recognized cause of abdominal and pelvic pain.
INDICATIONS
• The diagnosis and treatment of:
Groin pain
Inguinal pain, especially after inguinal hernia repair using mesh and/or staples
Pelvic pain
Suprapubic pain (mimicking interstitial cystitis)
Vaginal or penile pain
• Used with ilioinguinal and iliohypogastric nerve blocks for inguinal herniorrhaphy
• Used with femoral nerve block for saphenous vein stripping
• Used to diagnose genitofemoral neuralgia
RELEVANT ANATOMY
Genitofemoral Nerve
• Branch of the L1 and L2 nerve root
• Pierces the psoas muscle at the level of the third and fourth lumbar vertebra behind the ureter and
divides into 2 branches (Figures 60-1 and 60-2)
Figure 60-1. Drawing of genitofemoral nerve.
Figure 60-2. Anatomy of genitofemoral nerve.
The genital branch provides the efferent and afferent components of the cremasteric reflex
The femoral branch, which supplies the anterior skin in the femoral triangle
Accompanies the external iliac artery in the femoral sheath lateral to the artery
The genital branch, which travels along the medial pelvic ring, enters the inguinal canal through the
deep (ventral) inguinal ring in 97% of patients,1 passing lateral to the pubic tubercle
In males, the genital branch travels through the inguinal canal within the spermatic cord and
supplies the cremaster muscle and the scrotal skin.
In females, the genital branch travels with the round ligament and supplies sensation to the mons
pubis and labia majora.2

• Large volumes of local anesthetic are often used for blind anesthetic blocks for surgery, but diagnostic
injections need to be low volume.
• Contraindications
Absolute
Infection
Severe anxiety to needle sticks
Severe scarring over entire area to be injected
Coagulopathy
Relative
Psychogenic pain
Inability to communicate with the patient
Anticoagulant or nonaspirin antiplatelet therapy (for the superficial injections, there is little risk of
bleeding, since these are small gauge needles)
Because of its intra-abdominal as well as abdominal wall location, the genitofemoral nerve can be
injured by conditions such as:
• Psoas abscess
• Postoperative intra-abdominal scarring
• Any laparoscopic abdominal procedures
• Transpsoas lateral interbody fusion3
• Femoral branch
Trauma to the groin
• Genital branch
Inguinal hernia repair, especially mesh repairs, when the mesh is secured to the Poupart ligament at
the symphysis pubis4,5
Pain pathology is usually distal; however, occasionally it is necessary to address the nerve proximally
at L1.
• Informed consent and proper explanation of risks, complications, and benefits must be performed.
• Anticoagulation does not necessarily need to be stopped for the peripheral injections, but
anticoagulation needs to be held for the psoas and transforaminal injections.
Fluoroscopic Views
• Although the proximal genitofemoral nerve is not visualized fluoroscopically, the genital branch can be
located fluoroscopically at the pubic tubercle (Figures 60-3 and 60-4).
Figure 60-3. Fluoroscopic imaging of GFN location at pubic tubercle.
Figure 60-4. Fluoroscopic imaging of peripheral nerve stimulator directed GFN injection at pubic
tubercle. (Used with permission from Andrea Trescot, MD.)
• The psoas muscle shadow can be visualized fluoroscopically (Figures 60-5 and 60-6).
Figure 60-5. Fluoroscopic imaging of psoas shadow. (Used with permission from Andrea Trescot, MD.)
Figure 60-6. Fluoroscopic imaging of psoas injection with contrast in the muscle. (Used with permission
• A transforaminal approach at L1 and/or L2 can be used to address the nerve proximally (Figure 60-7).
Figure 60-7. Fluoroscopic imaging of the L1 foramen. (Used with permission from Andrea Trescot, MD.)
Equipment
• Peripheral injection
30-gauge needle for subcutaneous infiltration
25- or 22-gauge Quincke needle
3-cc Luer lock syringe for local anesthetic
Sensory nerve stimulator with alligator clip or other connections for grounding ECG pad and needle
• Psoas injection
22-gauge Quincke needle
• Transforaminal injection
Blunt-tipped needle and introducer (22 gauge Whitacre or Epimed)
3-cc Luer lock syringe for local anesthetic
Extension tubing
Medications
• Depo-steroid
• Nonionic contrast for psoas and transforaminal approach
Technique
Diagnostic Injection (anterior blind approach)
The patient is placed supine with a pillow under the knees.
• Anatomic landmarks
Pubic tubercle
Inguinal ligament
Inguinal crease
Femoral artery
• There are two sites of injection
At the inguinal ring
At the pubic tubercle
• Use of a peripheral stimulator improves accuracy and allows for low volume diagnostic injections
(ideally less than 2 cc total volume).
• Note: Injections of the ilioinguinal nerve at the inguinal ring may also anesthetize the GFN, but
ilioinguinal injections at the ASIS will not affect the GFN.
Diagnostic Injection (anterior fluoroscopic approach)

• The pubic tubercle is identified by palpation and then fluoroscopy.
• The GFN lies just lateral to the pubic tubercle (Figure 60-3).
• Use of a peripheral stimulator improves accuracy (Figure 60-4) and allows for low-volume diagnostic
injections (ideally less than 2 cc total volume).
Diagnostic Injection (transpsoas approach—blind or image-guided)

The patient is placed prone and the L3 or L4 transverse process identified approximately 5 cm from the
midline (by landmarks, fluoroscopy, or CT).6
• For the blind approach, a 22-gauge subarachnoid needle is advanced between the L3 and L4 transverse
processes, using a loss-of-resistance technique to identify the anterior surface of the psoas. 10 cc of
local anesthetic is then injected.
• Fluoroscopically, the psoas muscle is identified at the level of L3 (Figure 60-5). A 22-gauge
subarachnoid needle is advanced into the body of the muscle, and 1 cc of nonionic contrast injected to
confirm the intramuscular positioning (Figure 60-6). The needle is then advanced to just anterior to the
muscle, using a loss of resistance technique. 2 cc of local anesthetic is then injected (less if a nerve
stimulator is used).
• Using CT guidance, the entry site just above the L4 transverse process is identified. IV contrast is
injected to opacify the ureters, and a 22-gauge 5-in Quincke or Chiba needle advanced through the
muscle onto the surface of the muscle.
Diagnostic Injection (transforaminal approach)

By addressing the nerve at its most proximal site, it is possible to anesthetize the nerve proximal to any
pathology.
• Identify the L1 vertebral body, and align the upper endplate using fluoroscopic image.
• Identify the pedicle and the nerve foramen below it from an AP or oblique view (Figure 60-7).
• Advance a blunt-tipped needle into the foramen (see Chapter 22 for complete details)
Use of a peripheral stimulator will facilitate identification of the nerve.
Stimulation of the posterior lumbar area reflects stimulation of the cluneal nerve, which exits
from the same foramen. In that case, the needle needs to be repositioned more anteriorly.
Nonparticulate steroid, and real-time injection of contrast are expected to decrease the risk of
transforaminal injection of the radicular artery, which has been associated with spinal cord infarct,
paralysis, and death.
Neuroablation
• If there was excellent but only temporary relief with the peripheral or transforaminal diagnostic
injections, cryoneuroablation can be used to kill the nerve (see Chapter 79).
For the peripheral technique, the cryo probe is placed on the pubic tubercle (Figure 60-8) under
fluoroscopic control. The built-in peripheral stimulator is used to find the nerve.
Figure 60-8. Cryoneuroablation of the genitofemoral nerve at the pubic tubercle. (Used with permission
An ultrasound GFN cryoneuroablation technique has also been described.7

For the transforaminal technique, the cryo probe is placed just inside the foramen (Figure 60-9).
The built-in peripheral stimulator is used to find the nerve.
Figure 60-9. Cryoneuroablation of the genitofemoral nerve at the L1 foramen. (Used with permission
• Although pulsed radiofrequency treatment has been described for several peripheral nerves, in the US
it is not a covered procedure.
• Heat radiofrequency lesioning on the anterior surface of the psoas has been described, but was not
successful.6
• Phenol injections, 4%, have been described for a variety of peripheral nerves, including the GFN.8 The
use of 7% phenol in myelographic contrast via a transpsoas approach has been described.6 Absolute
alcohol has also been used for peripheral neuralgia.
Evaluate the patient immediately after the procedure for presence of sensory block and pain relief
secondary to local anesthetic effect. Patient should be evaluated by subsequent telephone or office
follow-up for potential complications as well as significance and length of time of pain relief, including
evaluation of the effect from the deposteroid.

• Since the diagnostic block, radiofrequency, or cryoanalgesia procedures are primarily subcutaneous (at
least for the distal approaches), they are associated with few complications. There is a chance of
hematoma and postinjection ecchymosis.
• The transpsoas injection is retroperitoneal, but the possibility of peritoneal penetration and colon
perforation exists.
• Destruction of surrounding non-nerve tissue is a complication of phenol and absolute alcohol.
CLINICAL PEARLS
• Genitofemoral nerve blocks at the pubic tubercle are relatively simple procedures that can provide
near complete pain relief, at least temporarily, if the diagnosis is correct.
• These injections can be diagnostic or therapeutic. The patients with positive diagnostic but not
therapeutic effects are candidates for an ablation procedure using cryoneuroablation, pulsed
radiofrequency lesioning or phenol/alcohol.
• Pressure should be applied to the injection site for prevention of hematoma and ecchymosis, especially
for large cannula procedures such as cryoneuroablation.
• Absolute alcohol and phenol injections should only be utilized for pain patients with limited lifespan
who suffer from intractable genitofemoral neuralgia.
• The success of the diagnostic procedure is most dependent on accurate placement of the nerve
stimulation needle.
• If patients present with genitofemoral pain and do not get relief from a diagnostic block, then consider
L1 or L2 nerve root pathology. Also consider pudendal nerve pathology in refractory cases.
Suggested Reading
Broadman L. Ilioinguinal, iliohypogastric, and genitofemoral nerves. In Gay SG, ed. Regional
Anesthesia: An Atlas of Anatomy and Techniques. St. Louis, MO: Mosby; 1996:247-254.
Brown DL. Atlas of Regional Anesthesia. 4th ed. Philadelphia, PA: Saunders; 2010.
Hartrick CT. Genitofemoral nerve block: a transpsoasy technique. Reg Anesth. 1994;19(6):432-433.
Trescot AM: Chapter 8–Cryoneurolysis. In Manchikanti L and Singh V (ed): Interventional Techniques in
Chronic Non-spinal Pain. American Society of Interventional Pain Physicians Publishing, Paducah,
KY 2009.
Waldman SD. Atlas of Interventional Pain Management. 2nd ed. Philadelphia, PA: Saunders; 2004.
Rab M, Ebmer, Dellon AL. Anatomic variability of the ilioinguinal and genitofemoral nerve: implications
for the treatment of groin pain. Plast Reconstr Surg. 2001;108(6):1618-23.
References
1. Liu WC, Chen TH, Shyu JF, et al. Applied anatomy of the genital branch of the genitofemoral nerve in
open inguinal herniorrhaphy. Eur J Surg. 2002;168:145-149.
2. Broadman L. Ilioinguinal, iliohypogastric, and genitofemoral. In: Gay SG, ed. Regional Anesthesia: An
Atlas of Anatomy and Techniques. St. Louis, MO: Mosby; 1996:247-254.
3. Moller DJ, Slimack NP, Acosta FL, Koski TR, Fessler RG, Liu JC. Minimally invasive lateral lumbar
interbody fusion and transpsoas approach-related morbidity. Neurosurg Focus. 2011;31:E4.
4. Amid PK, Chen DC. Surgical treatment of chronic groin and testicular pain after laparoscopic and open
preperitoneal inguinal hernia repair. J Am Coll Surg. 2011;213:531-536.
5. Rho RH, Lamer TJ, Fulmer JT. Treatment of genitofemoral neuralgia after laparoscopic inguinal
herniorrhaphy with fluoroscopically guided tack injection. Pain Med. 2001;2:230-233.
6. Parris D, Fischbein N, Mackey S, Carroll I. A novel CT-guided transpsoas approach to diagnostic
genitofemoral nerve block and ablation. Pain Med. 2010;11:785-789.
7. Campos NA, Chiles JH, Plunkett AR. Ultrasound-guided cryoablation of genitofemoral nerve for
chronic inguinal pain. Pain Physician. 2009;12:997-1000.
8. Weksler N, Klein M, Gurevitch B, et al. Phenol neurolysis for severe chronic nonmalignant pain: is the
old also obsolete? Pain Med. 2007;8:332-337.
CHAPTER 61
Lateral Femoral Cutaneous Nerve Block

Gerard P. Varlotta and Anya Myers
INTRODUCTION
The lateral femoral cutaneous nerve (LFCN) is a purely sensory nerve from the lumbar plexus and is
derived from the L2-L3 nerve roots. LFCN pain is believed to be associated with obesity, pregnancy, or a
constricting belt. Symptoms are thought to be due to entrapment of the LFCN as it passes through or under
the inguinal ligament. The LFCN is also at risk of irritation from bone graft due to the nerves close
proximity to the iliac crest. Because it is a sensory nerve, symptoms after injury, irritation, or laceration
to the LFCN include dysaesthetic pain, numbness and paresthesias localized or radiating to the buttocks or
anterolateral thigh. The lateral femoral cutaneous nerve innervates the skin on the lateral part of the thigh
and because it is 1 of the 6 nerves that comprise the lumbar plexus, the LFC can be blocked as part of the
lumbar plexus block or on occasion with a femoral nerve block.
INDICATIONS
• Diagnosing and treating nerve entrapment (meralgia paresthetica)
• Regional aesthesia
Skin grafting from the upper thigh
Muscle biopsy
• Postoperative analgesia after hip surgery
• Repeated blocks can function as a treatment for meralgia paresthetica
• Predicting outcome of neuromodulation techniques or surgical neurolysis
RELEVANT ANATOMY
• The lateral femoral cutaneous nerve of the thigh is 1 of the 6 nerves of the lumbar plexus. It arises from
the posterior division of the second and third lumbar nerves.
• The nerve traverses the psoas muscle and emerges alone from the lateral aspect of the muscle.
• After crossing the psoas muscle, the lateral femoral cutaneous nerve follows an oblique and lateral
course between the iliac muscle and the fascia iliaca in the direction of the anterosuperior iliac spine
(ASIS).
• At this point, it provides branches for the peritoneum. It then enters the thigh by passing through or
under the inguinal ligament and over the sartorius muscle, where it bifurcates into an anterior and
posterior branch (Figure 61-1).
Figure 61-1. Dissection of the anterior thigh anatomy depicting the location of the LCFN.
• The anterior branch supplies the anterolateral part of the thigh as far as the knee. It emerges
approximately 10 cm below the inguinal ligament.
The distal most fibers communicate with the anterior cutaneous branches of the femoral nerve and the
infrapatellar branches of the saphenous nerve creating the peripatellar plexus. The posterior branch
pierces the tensor fascia lata and supplies the skin of the superior and lateral aspects of the thigh from the
greater trochanter to the middle of the thigh (Figure 61-2).
Figure 61-2. Cutaneous distribution of the LFCN.

Anatomical variations that may explain failure of anesthesia after a femoral nerve block:
• Described in 25% of cases
• Arise directly from the femoral nerve in 18% of cases
• LFCN innervation may extend medially as far as the anterior surface of the thigh in 31% of cases.
CONTRAINDICATIONS
• Coagulopathy (relative contraindication)
• Allergy to the injectate
For patients with a coagulopathy a 27-gauge needle is recommended. Meralgia paresthetica refractory to
the injection and other causes of lateral thigh pain need to be investigated. Differential diagnosis are
fractures of the anterior superior iliac spine, iliac bone graft, pelvic tumor, psoas tumor, lumbar
metastasis, tight pants, seat belt trauma, waist belts, hip arthroplasty, and obesity. The risks and benefits
of the procedure need to be explained to the patient thoroughly before the procedure.
• Informed consent including the risks and benefits of the procedure and all reasonably anticipated
complications.
• Anticoagulation is not a significant concern for an injection in this location.
• Examine the region for infection, cutaneous lesions, hip pathology, and other inguinal pathology.
• Patient must be able to lay be supine for the length of the procedure.
• Be sure that all equipment is operational.
Equipment
Materials
• Marking pen
• Sterile gloves
• Prep solution
• Sterile bandage
• 3-cc syringe with 25-gauge needle for cutaneous anesthetic injection
• 10-cc syringe for injectate
• 22- or 25-gauge 1.5- or 3-in insulated needle appropriate for injecting with peripheral nerve
stimulation
• Fluoroscopy or ultrasound for needle guidance
• Nerve stimulator
Medications
• 1 cc 1% lidocaine for skin numbing
• 1 cc of 40 mg/cc of methylprednisolone acetate or triamcinolone acetonide (Depo Medrol or Kenalog)
for injectate
• 6 cc of 1% lidocaine or 0.5% marcaine for injectate

The patient should be supine with the thigh in neutral position.
Intraprocedural Technical Steps

The Fanning Technique
• This is a common technique used for the lateral femoral cutaneous nerve block.
• Patient should be in supine position; an area 2 cm medial and 2 cm caudal from the anterior superior
iliac spine (ASIS) is marked (Figure 61-3).
Figure 61-3. Right lateral femoral cutaneous nerve localization and injection. (Reproduced with
permission from Hadzic A: The New York School of Regional Anesthesia Textbook of Regional
Anesthesia and Acute Pain Management: http://www.accessanesthesiology.com. Copyright © The
McGraw-Hill Companies, Inc. All rights reserved.)
• Sterile preparation of the area in usual fashion.

• A skin wheal can be performed, although it is not necessary as most patients tolerate the procedure
well without the wheal.
• A 25-gauge 1.5-in needle is inserted at the target site and advanced until a loss of resistance or a “pop”
is felt when needle pierces the fascia lata.
• The anesthetic/corticosteroid mixture is injected.
• The needle is removed and a Band-Aid is applied.
• Local anesthetic alone can be used for diagnostic purposes.
The Transinguinal Technique

• This is another technique that can be used to block the lateral femoral cutaneous nerve.
• Palpate the most medial part of the anterior superior iliac spine and mark a point 1 cm medial to the
ASIS.
• Then extend a vertical line caudally just below the inguinal ligament to determine the site of
introduction of the needle (Figure 61-3).
• Prepare the site with povidone iodine (Betadine) or chlorhexidine gluconate (Chloraprep) antiseptic
solution.
• A 50-mm insulated needle connected to a nerve stimulator (1.5 mA, 2 Hz, 0.3 ms) is introduced
perpendicular to the skin until paresthesia on the lateral border of the thigh is elicited.
• The needle position is adjusted to maintain the paresthesia with a current of 0.5 mA.
• After negative aspiration for blood, the anaesthetic/corticosteroid mixture is slowly injected.
• The needle is removed and a Band-aid is applied.
Ultrasound guidance with or without nerve stimulation can be used to further ensure the localization of the
needle placement (Figure 61-4). Fluoroscopic confirmation with a neurogram can be obtained, but usually
does not enhance the efficacy of the injection.
Figure 61-4. Transverse ultrasound image of the lateral femoral cutaneous nerve (LFCN). (Reproduced
with permission from Hadzic A: Hadzic’s Peripheral Nerve Blocks and Anatomy for Untrasound-Guided
Regional Anesthesia, 2nd Edition: www.accessanesthesiology.com. Copyright © The McGraw-Hill
Companies, Inc. All rights reserved.)
• Local anesthetic toxicity (central nervous system and cardiovascular toxicity)
• LFCN trauma resulting in transient neuritis or permanent injury
• Transient femoral nerve block resulting in prolonged motor blockade of the muscles of the thigh
• Hematoma formation
• Block failure
Examination postprocedure is necessary to assess for anesthesia to the region of the lateral thigh
innervated by the LFCN. Quadriceps weakness in both hip flexion and knee extension needs to be
assessed. Precautions toward ambulation and driving need to be emphasized for any prolonged anesthetic
response.
CLINIC PEARLS AND PITFALLS

• This injection can be both diagnostic and therapeutic.
• This procedure can be performed without nerve stimulation, radiographic or ultrasound guidance6 but
the use of the nerve stimulator does not increase the success rate of obtaining adequate neural
blockade.7
• With a successful block, there should be anesthesia of the upper two-thirds of the anterolateral thigh.
Suggested Reading
1. Cousins MJ, Carr DB, Horlocker TT, Bridenbaugh PO, eds. Cousins & Bridenbaugh’s Neural
Blockade in Clinical Anesthesia and Pain Medicine. 4th ed. Lippincott Williams & Wilkins;
2009:352-354.
2. Frontera WR. Delisa’s Physical Medicine & Rehabilitation: Principles And Practice. 5th ed.
Lippincott Williams & Wilkins; 2010:1835.
3. Ballantyne JC, Fields HL. Massachusetts General Hospital Handbook of Pain Management. 3rd ed.
Lippincott Williams & Wilkins; 2006:186.
4. Mulroy MF, Bernards CM, McDonald SB, Salinas FV. Practical Approach to Regional Anesthesia. 4th
ed. Lippincott Williams & Wilkins; 2009:236-237.
5. Loeser JD. Bonica’s Management of Pain. 3rd ed. Lippincott Williams & Wilkins; 2001:1916-1918.
6. Hurdle et al. Ultrasound-guided blockade of the lateral femoral cutaneous nerve: technical description
and review of 10 cases. Arch Phys Med Rehabil. 2007 Oct;88(10):1362-1364.
7. Hara K, Sakura S, Shido A. Ultrasound-guided lateral femoral cutaneous nerve block: a comparison of
two techniques. Anaesth Intensive Care. 2011 Jan;39(1):69-72.
CHAPTER 62
Pudendal Nerve Block

Susanti Chowdhaury, Gail Gray, and Andrea Trescot
Pudendal pain can often be difficult to diagnose and harder to treat. The majority of patients suffering
from this malady are female; chronic pelvic pain affects approximately 1 in 7 women.1 Frequently, they
have been to various doctors with a complaint of chronic perineal pain that may be localized to the
rectum, anus, urethra, or genitalia. This usually causes them multiple diagnoses and treatment without
resolution of symptoms. For years, patients with chronic neuropathic perineal pain were assigned a
“psychosomatic vulvovaginitis” diagnosis by exasperated physicians.2 Finally, this elusive presentation
has been recognized to have a valid biomechanical and a neuropathic basis that allow multiple modalities
for its treatment. Current treatments can improve a patient’s quality of life, and research continues to
improve outcomes.
DIAGNOSIS
The pudendal nerve is a mixed motor/sensory nerve having numerous potential entrapment sites.
Therefore, the clinical presentation varies.
• The pain of pudendal neuralgia (PN) typically waxes and wanes and is often described as burning,
tearing, stabbing, sharp, electrical, and shooting along with feelings of a lump or foreign body in the
vagina or rectum.3
• Symptoms include abnormal temperature sensations, constipation, pain and straining with bowel
movements, straining or burning when urinating, painful intercourse, and sexual dysfunction (including
uncomfortable arousal or decreased sensation). PN presents most commonly as unilateral.
• The symptoms are usually aggravated by sitting or cycling and are absent or relieved by standing,
recumbent position, and sitting on a toilet seat.4
Indications
Pudendal nerve blocks are used to diagnose and manage patients with chronic pain with possible
pudendal origin. Local anesthetic blocks can be used to diagnose pain problems. If the local anesthetic
removes the pain, the pain generator is presumed to be distal to this pathology. They can also be used to
predict results of surgical neurolysis, pudendal nerve stimulation, and as a direct treatment.
Contraindications
• Systemic infection
• Infections at the skin, injection site, ischiorectal space, rectum, vagina, or perineum
• Coagulopathy
• Contrast allergy (when used)
• Metastatic cancer in the area
• Lack of understanding or cooperation with the procedure
Relevant Anatomy
Rising from the sacral plexus and formed from contributions of the second, third, and fourth sacral nerve
roots, the pudendal nerve is a sensory and motor nerve. There are 3 branches of the nerve on each side of
the body:
• Rectal branch
• Perineal branch
• Penile/clitoral branch
Pudendal neuropathy occurs when the nerve or one of its branches becomes damaged, inflamed, or
entrapped.
• The pudendal canal runs from the lesser sciatic notch to the posterior edge of the perineal membrane.
• A space within the obturator fascia, the pudendal (Alcock’s) canal, is bound by the medial aspect of the
obturator internus muscle and the lateral wall of the ischioanal fossa.
• It contains the internal pudendal vessels and the pudendal nerves, which enter the gluteal region
through the lower part of the greater sciatic foramen.
• The pudendal nerve, when accompanied by the internal pudendal artery, is known as the pudendal
bundle. This pudendal bundle courses around the sacrospinous ligament near its attachment to the
ischial spine and passes through the ischioanal fossa and then through the pudendal canal.
• Either just before entering the pudendal canal or just within it, the pudendal bundle gives rise to the
inferior rectal (inferior anal) nerve, which crosses the ischioanal fossa toward the anal canal and the
external anal sphincter muscle.
• Within the pudendal canal, the pudendal nerve divides into two terminal branches, the perineal nerve
and the dorsal nerve of the penis or clitoris.3
• Throughout this course, there are two critical areas where compression is likely to occur—at the
ischial spine in the gluteal region or in the pudendal canal (Figures 62-1 and 62-2).
Figure 62-1. The ischial spine3.
Figure 62-2. Schematic anatomy of deep dissection of gluteal region. Most of gluteus maximus and
medius muscles have been removed. Segment of sacrotuberous ligament also has been removed, revealing
pudendal nerve. Pudendal nerve emerges from pelvis inferior relative to piriformis muscle and enters
gluteal region medial relative to sciatic nerve, superficial relative to sacrospinous ligament, and deep
relative to sacrotuberous ligament. After coursing around sacrospinous ligament, pudendal nerve reenters
pelvis.10
Diagnostic Criteria5
• Pain in the anatomical distribution of the pudendal nerve
• Pain worsened by sitting
• Patient not woken at night by the pain
• No objective sensory loss
• Positive anesthetic pudendal block
Because there are several different approaches, a decision as to the site of damage or entrapment dictates
the approach. Injections at the ischial spine anesthetize the entire length of the nerve, but will not address
pathology more proximal, at the sciatic notch. The ischial spine can be approached vaginally or
transperineally (from a lithotomy position) or from a prone approach, using peripheral nerve stimulation
or fluoroscopy or CT guidance or ultrasound. If the entrapment is more distal, injection at the ischium can
allow for more selective diagnostic and potentially therapeutic treatment.

Not applicable
Fluoroscopic Views
• Supine: AP view of the ischium
• Prone: P view, oblique to the ipsilateral side in order to visualize the ischial spine (Figure 62-3)
Figure 62-3. Ipsilateral oblique view of the ischial spine. (Used with permission from Andrea Trescot,
MD.)
• Depends on approach
Lithotomy for transvaginal or transperineal approach
Prone for posterior approach

• Transvaginal approach
Be sure to use a needle with a guide—either the Iowa trumpet (Figure 62-4) or the Kobak needle
guide (Figure 62-5)—to limit the depth of submucosal penetration and to prevent injury to the
patient’s vagina and potentially puncturing the physician’s hand.
Figure 62-4. Iowa trumpet. (Used with permission from Andrea Trescot, MD.)
Figure 62-5. Kobak needle.
Requires a 5-in 22-gauge spinal needle.

• Additional supplies for any approach
27/30-gauge needle for local infiltration (1% lidocaine)
22-gauge 3.5- or 5-in spinal needle
0.25% or 0.5% bupivacaine, approximately 10 cc (alternatively, 1% lidocaine may be used for
quicker onset and shorter duration)
Nonionic contrast if dye localization is chosen
Peripheral nerve stimulator (PNS) if chosen to reproduce symptoms
Fluoroscopy, ultrasound, and/or CT scanner if chosen

Transvaginal Approach
• To perform a left-sided block, palpate the ischial spine with the index finger of the left hand, using the
Iowa trumpet or Kobak needle guide on the index finger (Figure 62-6).
Figure 62-6. Transvaginal approach.6
• Place the end of the guide beneath the tip of the ischial spine.
• Push the needle through the guide into the vaginal mucosa.
• Raise a mucosal wheal with 1 mL of local anesthetic.
• Advance the needle through the vaginal mucosa until it touches the sacrospinous ligament 1 cm medial
and posterior to the ischial spine.
• Infiltrate the tissue with 1 mL of local anesthetic.
• Next, advance the needle further through the sacrospinous ligament for a distance of 1 cm until a loss of
resistance is appreciated.
• The tip now lies in the area of the pudendal nerve. At this point, the pudendal vessels lie just lateral to
the pudendal nerve, so care must be taken to avoid intravascular administration. Aspirate to confirm
the needle placement is not intravascular prior to injecting lidocaine.
• Subsequently, withdraw the needle into the guide and move the tip of the guide to just above the ischial
spine.
• At this new location, reinsert the needle though the mucosa and again inject.6
• (Note: An alternative to placing the needle through the vagina would be to place the needle lateral to
the labia majora but still use the hand transvaginally as a guide.)
Pararectal Approach Using PNS7

• The index finger of the nondominate hand is inserted into the anus and used to palpate the ischial spine,
introducing the needle lateral to the rectum down to the ischial spine.
• PNS is used to elicit contraction of the external anal sphincter.
Transperineal Approach Using PNS and Fluoroscopy

• Patient is placed in a lithotomy position, and an AP projection obtained.
• The inferior ramus is palpated through the perineum until a paresthesia is obtained.
• 1 cc of local anesthetic is infiltrated subcutaneously.
• A 22-guage 3.5-in needle is advanced through the perineum under PNS control until the patient
identifies a twitch in the distribution of the pain (urethral, vaginal/perineum, rectal) (Figure 62-7).
Figure 62-7. Transperineal approach. (Used with permission from Andrea Trescot, MD.)
• Alternatively, for perirectal pain, the patient can be positioned prone in a modified jackknife position.
Posterior Approach Using PNS and Fluoroscopy

• The C-arm fluoroscope is projected in the anterior-posterior position and then obliqued to the
ipsilateral side to allow visualization of the pelvic inlet and the ischial spine (Figure 62-3).8
• A 22- or 25-gauge 3.5-in needle is then advanced to the tip of the ischial spine and 1 cc of local with
deposteroid is injected.
• A peripheral nerve stimulator may help in localization, and contrast confirms the lack of vascular
injection (Figures 62-8 and 62-9).
Figure 62-8. Fluoroscopic posterior pudendal injection at the ischial spine. (Used with permission from
Figure 62-9. 3D reconstruction of fluoroscopic injection. (Used with permission from Andrea Trescot,
MD.)
Posterior Approach Using a CT Scan9

• The patient is positioned in the prone position.
• CT images are obtained from the femur head to the ischium.
• Once the ischial spine, sacrospinous and sacrotuberous ligaments as well as the falciform process are
located, 1 of 2 approaches may be utilized to block the pudendal nerve.10
• In the first, a 22-gauge needled is placed transgluteally to avoid the sciatic nerve, at the ischial spine
between the sacrotuberal and sacrospinal ligament.
• Another approach enters the medial part of the obturator internus muscle under the falciform process.
• After verifying the location of the needle, local anesthetic and deposteroid are then injected (Figure
62-10).
Figure 62-10. CT guided pudendal nerve injection. (Reproduced with permission from American Journal
of Roentgenology. Hough DM, Wittenberg KH, Pawlina W, et al. Chronic perineal pain caused by
prudendal nerve entrapment: anatomy and CT-guided perineural injection technique. AJR Am J
Roentgenol 2003; 181(2):561-7; American Roentgen Ray Society.)
Posterior Approach Using Ultrasound11

• A low-frequency curved array US transducer is used in the transverse plane to visualize the ischium
forming the lateral border of the sciatic notch.
• By moving the ultrasound probe in a cephalad-caudal direction, the ischium appears as a progressively
lengthening hyperechoic line, widest at the ischial spine level.
• The sacrospinous ligament appears as a hyperechoic line in continuity with the ischial spine, with
lower echogenicity than bone.
• The sacrotuberous ligament appears as a light hyperechoic line deep to the gluteus maximus muscle,
parallel and superior to the sacrospinous ligament.
• Doppler will show the internal pudendal artery close to the ischial spine.
• A 22-gauge spinal or stimulating needle is inserted from the medial aspect of the probe in line to the
medial aspect of the artery.
• Once the needle passes through the sacrotuberous ligament (felt as a “click” or “pop”), a small amount
of fluid is injected as contrast to confirm location (Figure 62-11).
Figure 62-11. Ultrasound pudendal injection. (Reproduced with permission from Rofaeel A, Peng P,
Louis I, Chan V. Feasibility of real-time ultrasound for pudendal nerve block in patients with chronic
perineal pain. Reg Anesth Pain Med 2008;33:139-45.)
• After verifying the location of the needle, local anesthetic and deposteroid are then injected.
Subsequent Options
• Botulinum toxin. The pudendal nerve has a close relationship with the obturator internus muscle. It has
been theorized this relationship could contribute a musculoskeletal component to the pain of pudendal
neuralgia. A particular case study from 200512 investigated the effects of botulinum toxin on a patient
that had previously been treated with multiple modalities including surgical release. The patient had
botulinum toxin injected into the right obturator internus muscle with a 90% relief of symptoms for a
period of 3 months. This was a single case study but further investigation is warranted to determine if
botulinum is a viable therapeutic option for patients with pudendal neuralgia.
• Cryoanalgesia. In her 2003 review,13 Trescot discusses how cryoanalgesia, cryoneuroablation, or
cryoneurolysis is a specialized technique for providing long-term pain relief when pain has been
shown to be caused by sensory nerves. The pudendal nerve is approached either vaginally or
percutaneously. The vaginal approach is a simple modification of the pudendal nerve block utilized by
obstetricians. Using a modified Iowa trumpet with the patient in the lithotomy position, the 2.0 mm
probe is advanced through the trumpet to the ischial spine. Cryoneurolysis at this site will lead to
profound hypoesthesia, including the possibility of loss of clitoral sensation. The transperineal
approach can be much more selective in the isolation of specific branches of the pudendal nerve. If the
pain is primarily vaginal, the patient is placed in a modified lithotomy position with the feet on the
table instead of in stirrups. The 12-gauge introducer is directed toward the sacrospinous ligament
instead of the ischial spine itself, and the 2.0-mm probe sensory stimulation is used to select the
stimulation field needed. In the same way, if the pain is primarily rectal, the patient is positioned prone
in a jackknife position, placing the 12-gauge introducer and then the 2.0 mm probe more inferiorly,
using stimulation to direct the probe toward the rectal branches.
• Radiofrequency. Continuous radiofrequency ablation (CRF) is a percutaneous minimally invasive
technique that has been in clinical use for over 25 years. Pulsed radiofrequency ablation (PRF) is a
more recent neuromodulatory technique that is felt to be less destructive than conventional CRF.
Although the exact mechanism of action for PRF is unknown, current literature supports involvement of
electromagnetic fields resulting in neuromodulation. A recent case report14 suggests that PRF may be
useful in treatment of refractory pudendal neuralgia.
• Peripheral stimulation. There have been multiple approaches proposed for electrical stimulation to
treat chronic pelvic pain—retrograde,15 antegrade through the sacral hiatus,16 transsacral,17 and on the
nerve itself.18 Discussion of these techniques is outside the scope of this chapter, and is included here
only for completeness.
Risks
• Laceration of the vagina or puncture of the rectum are possible complications.
• As with all invasive procedures, there is the potential risk of bleeding or infection.
• Vaginal, retroperitoneal, and ischiorectal hematomas from damage to the pudendal artery, particularly
with compromised coagulopathy, have been reported.19
• Although rare, systemic local anesthetic toxicity can occur. Symptoms could include: palpitations,
dysarthria, tinnitus, drowsiness, confusion, convulsions, hypotension, bradycardia, and loss of
consciousness.6
• Retropsoas or subgluteal infection is a possibility. Maintain a high titer of suspicion when there is back
or hip pain and diminished range of motion postinjection.20
• Nerve injury or vascular injury may occur from the injection itself.
• Needle stick injuries to the physician with the associated risks of blood-borne pathogens, including
HIV, may occur as the needle guide does not uniformly protect the physician.
POSTPROCEDURE FOLLOW-UP CONSIDERATIONS

• Because this injection is diagnostic as well as therapeutic, close monitoring of the immediate
postprocedure analgesia is critical.
• Because the sciatic nerve is close to the pudendal nerve (Figure 62-12), there is a risk of leg weakness
after the procedure.
Figure 62-12. Pudendal injection. Arrow shows staining from pudendal injection; asterisk shows the
sciatic nerve. (Reproduced with permission from American Journal of Roentgenology. Hough DM,
Wittenberg KH, Pawlina W, et al. Chronic perineal pain caused by prudendal nerve entrapment: anatomy
and CT-guided perineural injection technique. AJR Am J Roentgenol 2003; 181:561-7.)

2 types of complications
• Intraoperative
Due to placement of the needle
Needle injury to nerve, artery, surrounding tissues
Intravascular injection leading to toxic reaction
Monitor patient response during injection
Pain on injection or needle movement
Complaints of agitation, palpitations, nausea
• Postoperative
Bleeding, infection, steroid reaction
Monitor patient for several days after procedure, looking for orthostatic blood pressure changes,
fever, increased pain, personality changes, polyuria, muscle cramping
• Treating patients with pelvic pain is a daunting task for many interventional pain physicians, and yet the
pudendal nerve is very amenable to treatment.
• Diagnosis is made by a careful history (perineal pain, pain with sitting, history of trauma) and physical
examination (tenderness at the ischium), followed by a diagnostic injection.
• Small volumes are necessary to avoid anesthetizing unexpected or unwanted structures.
• Pudendal nerve blocks at the ischial spine may help identify in general pain related to the pudendal
nerve, but, since there are 2 potential sites of entrapment, injection at a distal entrapment site or both
sites may be necessary to provide relief.
Suggested Reading
Moore DC. Regional Block, A Handbook for the Use in the Clinical Practice of Medicine and Surgery.
4th ed. Springfield, IL, Thomas Books; 1981.
Waldman SD. Atlas of Interventional Pain Management. Philadelphia, PA: Saunders; 1998.
Hahn MB, et al. Regional Anesthesia, An Atlas of Anatomy and Techniques. St. Louis, MO: Mosby;
1996.
Scott DB. Techniques of Regional Anesthesia. Norwalk, CT: Appleton and Lange; 1989.
References
1. Mathias SD, Kuppermann M, Liberman RF, Lipschutz RC, Steege JF. Chronic pelvic pain:
prevalence, health-related quality of life, and economic correlates. Obstet Gynecol. 1996;87:321-
327.
2. Dodson MG, Friedrich EG Jr. Psychosomatic vulvovaginitis. Obstet Gynecol. 1978;51:23s-25s.
3. Popeney C, Ansell V, Renney K. Pudendal entrapment as an etiology of chronic perineal pain:
diagnosis and treatment. Neurourol Urodyn. 2007;26:820-827.
4. Prendergast SA, Weiss JM. Physical therapy and pudendal nerve entrapment. Advance. 2004;15:15-
47.
5. Labat JJ, Riant T, Robert R, Amarenco G, Lefaucheur JP, Rigaud J. Diagnostic criteria for pudendal
neuralgia by pudendal nerve entrapment (Nantes criteria). Neurourol Urodyn. 2008;27:306-310.
6. Nerve block, transvaginal pudendal. Medscape Reference, 2010.
http://emedicine.medscape.com/article/83078-overview. Accessed March 20, 2012.
7. Kim S, Song S, Paek O, Lee H, Park D, Lee J. Nerve-stimulator-guided pudendal nerve block by
pararectal approach. Colorectal Dis. 2011.
8. Abdi S, Shenouda P, Patel N, Saini B, Bharat Y, Calvillo O. A novel technique for pudendal nerve
block. Pain Physician. 2004;7:319-322.
9. Filippiadis DK, Velonakis G, Mazioti A, et al. CT-guided percutaneous infiltration for the treatment of
Alcock’s neuralgia. Pain Physician. 2011;14:211-215.
10. Hough DM, Wittenberg KH, Pawlina W, et al. Chronic perineal pain caused by pudendal nerve
entrapment: anatomy and CT-guided perineural injection technique. AJR Am J Roentgenol.
2003;181:561-567.
11. Rofaeel A, Peng P, Louis I, Chan V. Feasibility of real-time ultrasound for pudendal nerve block in
patients with chronic perineal pain. Reg Anesth Pain Med. 2008;33:139-145.
12. Gajraj NM. Botulinum toxin a injection of the obturator internus muscle for chronic perineal pain. J
Pain. 2005;6:333-337.
13. Trescot AM. Cryoanalgesia in interventional pain management. Pain Physician. 2003;6:345-360.
14. Rhame EE, Levey KA, Gharibo CG. Successful treatment of refractory pudendal neuralgia with
pulsed radiofrequency. Pain Physician. 2009;12:633-638.
15. Richter EO, Abramova MV, Alo KM. Percutaneous cephalocaudal implantation of epidural
stimulation electrodes over sacral nerve roots—a technical note on the importance of the lateral
approach. Neuromodulation. 2011;14:62-67.
16. McJunkin TL, Wuollet AL, Lynch PJ. Sacral nerve stimulation as a treatment modality for intractable
neuropathic testicular pain. Pain Physician. 2009;12:991-995.
17. Lavano A, Volpentesta G, Piragine G, et al. Sacral nerve stimulation with percutaneous dorsal
transforaminal approach in treatment of isolated pelvic pain syndromes. Neuromodulation.
2006;9:229-233.
18. George AT, Dudding TC, Nicholls RJ, Vaizey CJ. A new minimally invasive technique for pudendal
nerve stimulation. Colorectal Dis. 2012;14:98-103.
19. Kurzel RB, Au AH, Rooholamini SA. Retroperitoneal hematoma as a complication of pudendal block.
Diagnosis made by computed tomography. West J Med. 1996;164:523-525.
20. Hibbard LT, Snyder EN, McVann RM. Subgluteal and retropsoal infection in obstetric practice.
Obstet Gynecol. 1972;39:137-150.
CHAPTER 63
Obturator Nerve Block

Arthur Atchabahian
INDICATIONS
The obturator nerve innervates a portion of the hip joint, most of the adductor muscles, a variable portion
of the medial aspect of the femur, and has variable skin distribution on the medial aspect of the thigh.
The indications for blockade include:
• For acute and subacute pain
Supplementation of femoral and sciatic nerve blocks for lower extremity surgery, especially knee
surgery
For refractory adductor spasms that interferes with acute rehabilitation
• For chronic pain
As a diagnostic block for hip joint pain or for suspected neuropathy
For chronic hip pain with a local anesthetic block, with or without steroids, or using radiofrequency
lesioning
For adductor spasticity as a neurolytic block. Kwon suggests that a selective blockade of the
anterior branch may be sufficient to permit abduction more than 45 degrees.
• Another indication is to prevent the obturator reflex during transurethral resection of the bladder
(TURB). The reflex is due to the stimulation through the bladder of the obturator nerve, resulting in
sudden thigh adduction that can cause bladder perforation. Bilateral blocks have to be performed to be
effective.
RELEVANT ANATOMY
• The obturator nerve is a mixed sensory and motor branch of the lumbar plexus and derives from the
anterior divisions of the ventral rami of L2, L3, and L4 (Figure 63-1).
Figure 63-1. Anatomy of the obturator nerve.
• It typically emerges from the medial border of the psoas muscle at the level of the pelvic brim, and
divides in the obturator canal into anterior and posterior branches (Figure 63-2), although variations
are common with a multiple branching pattern.
Figure 63-2. Sagittal section demonstrating the relationship of the obturator nerve to the adductor
muscles. 1, obturator nerve passing through the obturator canal; 2, obturator externus; 3, pectineus; 4,
adductor longus, 5, adductor brevis; 6, adductor magnus; 7, medial femoral condyle; 8, femoral nerve; 9,
sciatic nerve.
• The anterior branch gives an articular branch to the hip joint (Figure 63-3), provides motor innervation
of the adductor brevis, adductor longus, gracilis, and occasionally the pectineus, and innervates a
variable area of skin; most references show an area in the medial aspect of the thigh, while others
suggest a more distal location at the level of the knee.
Figure 63-3. Contribution of the obturator nerve to the sensory innervation of the hip.
• The posterior branch provides motor innervation to the adductor magnus, obturator externus, and
occasionally the adductor brevis (in that case, this muscle is not innervated by the anterior branch), and
ends with an articular branch to the knee joint.
• The obturator nerve can be blocked with the other nerves of the lumbar plexus using the psoas
compartment approach. Despite initial claims, a perivascular inguinal block (Winnie’s “3-in-1 block”)
only rarely reaches the obturator nerve, as demonstrated by Macalou et al.
• The block can be performed using external anatomic landmarks and neurostimulation, or using imaging
guidance (fluoroscopy or ultrasound, rarely CT scan). Blockade can be performed proximally, in the
obturator foramen, before nerve division, or more distally, in the proximal thigh, between the adductor
muscles.
• The anterior and posterior branches can be blocked separately at that level, as the anterior branch lies
between adductor longus and adductor brevis, while the posterior branch lies between adductor brevis
and adductor magnus.

Absolute
• Patient refusal
• Inguinal lymphadenopathy (although a posterior approach would still be possible)
• Infection in the injection area or in the perineum
• Hematoma at the needle insertion site
• Systemic infection
Relative
• Preexisting obturator neuropathy (except if the block is used to diagnose such a neuropathy)
• Significant coagulopathy or anticoagulation (an ultrasound-guided block could be considered by a
trained operator)
• Contrast allergy if a fluoroscopic technique is used and contrast will be administered, although
premedication is feasible
• Patient unable to lie supine and achieve the desired position to be able to perform the block
• Informed consent should be obtained after thorough discussion of risks and benefits.
• Anticoagulation or coagulopathy: evaluate the risk/benefit ratio.
• Examination of the area for infection or hematoma.
• The patient should be able to lie supine.
• IV access can be considered for sedation and treatment of a possible vasovagal reaction. Vital sign
monitoring can include ECG, NIBP, heart rate, and pulse oximetry.
• Resuscitation equipment and 20% intralipid can be available to treat local anesthetic toxicity.
• Position the patient supine, with the lower extremity slightly abducted, and in slight external rotation.
Optimal positioning might be difficult to achieve in a spastic patient.
• Protect the genitalia and the perineum from the antiseptic solution.
Equipment
• 25-gauge 35-mm needle for skin anesthesia
• 3 or 5 mL syringe for skin anesthesia
• 10 or 20 mL syringe for medication
• 21- or 22-gauge, 50- to 80-mm nerve block needle, used with a peripheral nerve stimulator or
ultrasound machine
• 22-gauge 100-mm spinal needle and fluoroscopy equipment, according to the technique used
Medications
• 1% lidocaine for skin anesthesia
• 0.0625% to 0.25% bupivacaine or 1% to 2% lidocaine or another suitable local anesthetic for nerve
blockade; phenol for neurolytic block (3% phenol if only a sensory block is desired, 6% phenol to
obtain a motor block as well).
Technique Using Neurostimulation

Labat’s original technique is uncomfortable for the patient, as it requires bone contact and multiple
redirecting of the needle, and the needle may enter the pelvis if inserted too far. Wassef described an
elegant interadductor technique, but the technique described by Choquet is preferred, as it is more distal
and thus minimizes the risk of vascular injury and of entering the pelvis. One has to be aware, however,
that because the nerve is blocked more distally, the branches to the hip joint might not be blocked.
• The insertion of the tendon of the long adductor muscle on the pubic tubercle is identified, using
extreme leg abduction (Figure 63-4).
Figure 63-4. Neurostimulation technique as described by Choquet. Tendon of the long adductor muscle
(LA). Pulse of the femoral artery (FA). Needle insertion site (X).
• A line is drawn, following the inguinal crease, from the pulse of the femoral artery to the tendon of the
long adductor muscle.
• The needle is inserted at the midpoint of this line and directed cephalad at a 30-degree angle.
• After 3 to 5 cm in an average size patient, contractions of the long adductor and gracilis muscles can be
detected on the posterior and medial aspect of the thigh.
• After the current is decreased to less than 0.4 mA and the response is preserved, 5 to 7 mL of local
anesthetic are injected after aspiration.
• The needle is then redirected slightly laterally and inserted 0.5 to 1.5 cm deeper until a response from
the adductor magnus muscle is obtained on the posteromedial aspect of the thigh.
• Again, the current is decreased to less than 0.4 mA and 5 to 7 mL of local anesthetic can be injected.
Occasionally, the obturator nerve divides more distally, and both motor responses may be observed
with a single stimulation.
• Both branches can then be blocked with a single injection.
Technique Using Ultrasound Guidance

Soong et al described the ultrasonographic imaging of the obturator nerve.
• With the patient supine and the lower extremity slightly abducted, a low-frequency ultrasound probe is
placed just lateral to the tendon of the adductor longus muscle, perpendicular to the axis of the thigh.
• The muscles are identified by scanning between proximal and distal positions. The anterior and
posterior branches of the obturator nerve have typically a flat and hyperechoic (ie, white) appearance
(Figure 63-5).
Figure 63-5. Ultrasonographic appearance of the branches of the obturator nerve. The anterior branch (A)
is seen lying between, the adductor longus (AL) and the adductor brevis (AB). The posterior branch is
found between the adductor brevis (AB) and the obturator externus muscle (OE).
• The anterior branch can be found between, superficially, the adductor longus or the pectineus, and the
adductor brevis. The posterior branch is found between the adductor brevis and the obturator externus
muscle, or, if the probe is positioned more distally, the adductor magnus muscle.
• It is useful to track the nerves up and down to confirm that they are indeed continuous structures. Color
Doppler can be used to locate the obturator artery or its branches.
• The block is often performed using an out-of-plane technique, as the area is small and a needle
introduced in-plane would have to go through the adductor longus tendon medially, or might threaten
the femoral vessel immediately lateral to the ultrasound probe, but careful technique makes the in-plane
approach possible, especially if a probe with a small footprint (“hockey-stick”) is used.
• Following negative aspiration for blood, 5 to 7 mL of local anesthetic are deposited near both nerves,
although some authors recommend injecting 7 to 10 mL near one branch to block both branches by
diffusion.
Akkaya described a more proximal approach, comparable to Labat’s approach but without the need for
bone contact. The ultrasound probe is positioned parasagittally medial to the area where the femoral vein
is visualized, at the level of the inguinal ligament.
• The superior pubic ramus is identified, and a triangular hypoechoic area bound by the superior pubic
ramus superiorly, the pectineus muscle anteriorly, and the obturator externus muscle posteriorly is
defined, containing the obturator nerve (hyperechoic) and the obturator vein (Dopplerable).
• A 22-gauge needle is inserted in-plane from the distal side of the probe.
• Neurostimulation is used to confirm proximity of the needle tip with the obturator nerve (adductor
response with a current of >0.5 mA).
• 10 mL of local anesthetic is then slowly injected while monitoring solution spread under real-time
ultrasound.
Technique Using Fluoroscopic Guidance

• Labat’s approach is typically used.
• The patient is positioned supine with the leg slightly abducted.
• A 22-gauge 100-mm needle is inserted at a point 1.5 cm caudal and lateral to the pubic tubercle,
perpendicular to the skin, after raising a skin wheal with lidocaine.
• The needle is advanced until bone (the inferior pubic ramus) is contacted.
• It is then slightly withdrawn, redirected cranially and laterally, and advanced 2 to 3 cm in order to
enter the obturator canal.
• Fluoroscopy is used to confirm the needle position (Figure 63-6), and 3 mL of contrast is injected for
further confirmation.
Figure 63-6. Position of the needle in the obturator canal confirmed by fluoroscopy. (Reproduced with
permission from Viel EJ, Perennou D, Ripart J, Pélissier J, Eledjam JJ. Neurolytic blockade of the
obturator nerve for intractable spasticity of adductor thigh muscles. Eur J Pain. 2002;6(2):97-104.)
• If a stimulating needle is used, neurostimulation can be used to elicit contraction of the adductors, or to
reproduce the pain sensation.
• Anterior and posterior CT-guided techniques have also been described.
• The patient must be warned of the risk of gait or standing instability and fall, as adductor muscle tone
will be significantly decreased.
• Depending on the local anesthetic or phenol concentration injected, the duration of the blockade will
vary from a few hours to up to a year.

As this block is used only infrequently, no complication has, to our knowledge, been reported in the
literature. This is not in itself an assurance that complications cannot happen.
• A misdirected needle could pass over the superior pubic ramus and penetrate the pelvic cavity,
perforating the bladder, rectum, or spermatic cord.
• The obturator vessels travel with the nerve in the obturator canal; intravascular injection and hematoma
formation are possible.
• The corona mortis, a retropubic anastomosis between the external iliac (or deep epigastric) and
obturator arteries, is present in 10% to 30% of patients; bleeding secondary to laceration of the corona
mortis could be difficult to control.
• As with other peripheral nerve blocks, nerve trauma or local anesthetic toxicity is also possible.
CLINICAL PEARLS
• In 8% to 30% of patients, an accessory obturator nerve arises from L3 and L4, travels with the femoral
nerve and gives branches to the hip joint.
• Adductor spasm persisting after an obturator block can be due to this accessory nerve. However,
among the adductor muscles, the femoral nerve usually innervates the pectineus, and a portion of the
adductor magnus is innervated by the sciatic nerve.
• These might be sufficient to explain a persistent adductor tone following a well-conducted obturator
nerve block.
• Adductor motor strength has been shown to be decreased by about 25% following femoral nerve
blockade, and 11% following sciatic nerve blockade.
Suggested Reading
Adriani J. Labat’s regional anesthesia. In: Techniques and clinical applications. 4th ed. St Louis, MO:
Warren H. Green; 1985:331-333.
Akkaya T, Ozturk E, Comert A, et al. Ultrasound-guided obturator nerve block: a sonoanatomic study of a
new methodologic approach. Anesth Analg. 2009 Mar;108(3):1037-1041.
Atanassoff PG, Weiss BM, Brull SJ, et al. Electromyographic comparison of obturator nerve block to
three-in-one block. Anesth Analg. 1995 Sep;81(3):529-533.
Choquet O, Capdevila X, Bennourine K, Feugeas JL, Bringuier-Branchereau S, Manelli JC. A new
inguinal approach for the obturator nerve block: anatomical and randomized clinical studies.
Anesthesiology. 2005 Dec;103(6):1238-1245.
Eisenberg E. Échographie en anesthesia régionale périphérique. Arnette, Wolters Kluwer, Rueil-
Malmaison, France; 2007:106-108.
Harvey G, Bell S. Obturator neuropathy. An anatomic perspective. Clin Orthop Relat Res. 1999 Jun;
(363):203-211.
Heywang-Köbrunner SH, Amaya B, Okoniewski M, Pickuth D, Spielmann RP. CT-guided obturator nerve
block for diagnosis and treatment of painful conditions of the hip. Eur Radiol. 2001;11(6):1047-1053.
Hong Y, O’Grady T, Lopresti D, Carlsson C. Diagnostic obturator nerve block for inguinal and back pain:
a recovered opinion. Pain. 1996 Oct;67(2-3):507-509.
House CV, Ali KE, Bradshaw C, Connell DA. CT-guided obturator nerve block via the posterior
approach. Skeletal Radiol. 2006 Apr;35(4):227-232.
Jochum D, Iohom G, Choquet O, et al. Adding a selective obturator nerve block to the parasacral sciatic
nerve block: an evaluation. Anesth Analg. 2004 Nov;99(5):1544-1549.
Katritsis E, Anagnostopoulou S, Papadopoulos N. Anatomical observations on the accessory obturator
nerve (based on 1000 specimens). Anat Anz. 1980;148(5):440-445.
Kwon JY, Kim JS. Selective blocking of the anterior branch of the obturator nerve in children with
cerebral palsy. Am J Phys Med Rehabil. 2009 Jan;88(1):7-13.
Macalou D, Trueck S, Meuret P, et al. Postoperative analgesia after total knee replacement: the effect of
an obturator nerve block added to the femoral 3-in-1 nerve block. Anesth Analg. 2004 Jul;99(1):251-
254.
Marhofer P, Nasel C, Sitzwohl C, Kapral S. Magnetic resonance imaging of the distribution of local
anesthetic during the three-in-one block. Anesth Analg. 2000 Jan;90(1):119-124.
Soong J, Schafhalter-Zoppoth I, Gray AT. Sonographic imaging of the obturator nerve for regional block.
Reg Anesth Pain Med. 2007 Mar-Apr;32(2):146-151.
Tipton JS. Obturator neuropathy. Curr Rev Musculoskelet Med. 2008 Dec;1(3-4):234-237.
Viel EJ, Perennou D, Ripart J, Pélissier J, Eledjam JJ. Neurolytic blockade of the obturator nerve for
intractable spasticity of adductor thigh muscles. Eur J Pain. 2002;6(2):97-104.
Wassef MR. Interadductor approach to obturator nerve blockade for spastic conditions of adductor thigh
muscles. Reg Anesth. 1993 Jan-Feb;18(1):13-17.
Woodburne RT. The accessory obturator nerve and the innervation of the pectineus muscle. Anat Rec.
1960 Mar;136:367-369.
CHAPTER 64
Suprascapular Nerve Block

Christopher Gharibo and Steve Aydin
INTRODUCTION
The suprascapular nerve is a branch off the brachial plexus that arises from the C5-C6 nerve roots. It has
afferent, efferent, and sympathetic fibers. Seventy percent of the afferent input travels via the
suprascapular nerve; specifically, it provides sensory input from the scapula, acromioclavicular joint, and
posterior and superior shoulder joint. Its efferent component innervates the supraspinatus and
infraspinatus muscles.
The suprascapular block was first described by Wertheim and Rovenstein in 1941 for the use of
intractable shoulder pain. This initial technique was essentially “blind” in that it was solely based on
landmarks and clinical information without additional modalities that may be used today such as a nerve
stimulator, fluoroscopy, or ultrasound. Wertheim and Rovenstein relied on the patient’s perception of
paresthesias as the marker that their needle was correctly placed in the suprascapular notch where the
nerve exits. Studies have demonstrated significant benefits of the suprascapular nerve block such as pain
relief and improved range of motion. With shoulder pain affecting approximately 15% to 30% of adults,
the relative ease of this block along with its minimal risks emphasizes the importance of its use in clinical
practice.
INDICATIONS FOR SUPRASCAPULAR BLOCK

• Shoulder pain from inflammatory diseases: rheumatoid arthritis, seronegative spondyloarthropathies,
crystal arthropathies
• Postoperative pain after shoulder surgery (arthroscopy, acromioplasty)
• Adhesive capsulitis/rotator cuff disease
• Intractable pain from trauma (ie, fracture)
• Bursitis
• Acute anterior shoulder dislocation
• Diagnostic block for suprascapular nerve entrapment
RELEVANT ANATOMY
• The suprascapular nerve is arises from the C5 and C6 nerve roots of the brachial plexus.
• In 50% of instances, the nerve will also arise from the C4 nerve root.
• It runs lateral, posterior, and inferior deep to the posterior belly of the omohyoid muscle and anterior to
the trapezius muscles to reach the superior border of the scapula to the superior scapular notch.
• It then runs inferior to the transverse scapular ligament and passes under the supraspinatus muscle
through the floor of the supraspinous fossa, around the lateral border of the scapular spine and into the
infraspinaous fossa to innervate the infraspinatus muscle.
The suprascapular nerve gives off several branches including:
• Motor nerves to the supraspinatus and infraspinatus muscle
• Sensory nerve branches to the coracoclavicular, coracohumeral ligaments, acromioclavicular joint,
glenohumeral joint, and the subacromial bursa
The supraspinous fossa is an important structure to delineate as it is used for the blockade of the
suprascapular nerve in several techniques. It is bounded by the following structures:
• Spine of the scapula
• Plate of the scapula
• Supraspinous fascia
Suprascapular Notch
• The suprascapular nerve is the only neural structure that exits through the supraspinous fossa via the
suprascapular notch which also serves as point of injection for this nerve block.
• The anatomic variation of this notch can explain the incidence of suprascapular nerve injury as well as
any difficulty in placement of this block.
• In one cadaveric study, the suprascapular notch was found to be deeper in men than in women with the
average for males being 8.22 mm and for women 8.06 mm.
The suprascapular notch (Figure 64-1) can be described into 5 types.
Figure 64-1. View of the suprascapular nerve in relation to the muscle attachments and suprascapular
vasculature.
• Type 1: Lacks a distinct notch.

• Type 2: Notch is greater in transverse length than vertical length.
• Type 3: Notch is greater in vertical length than transverse length.
• Type 4: Bony foramen.
• Type 5: Notch and a bony foramen.
A specific vascular structure to recognize is the suprascapular artery which courses superior to the
transverse scapular ligament (the nerve travels inferior to the ligament) and along the scapular spine
(Figure 64-1).
Important anatomy to consider when performing this block:
• Spine of scapula
• Inferior angle of the scapula
• Trapezius muscle
• Clavicle
CONCERNS AND CONTRAINDICATIONS

Unlike other nerve blocks to the shoulder including the interscalene and supraclavicular block, the
suprascapular block is less invasive and carries a decreased risk to the patient. However, this does not
preclude the fact that each patient needs to be carefully examined and the risks and benefits be weighed
before the procedure.
Some basic concerns/contraindications as in all nerve blocks include:
• Patient refusal
• Lack of knowledge of the practitioner
• Complicated anatomy
• Infection at the site
• Coagulopathy
The preoperative considerations may vary slightly depending on the technique chosen for this nerve
block. This should therefore be taken into account.
• Proper history and physical to exclude any infectious/malignant etiology that could potentially
complicate the results
• Informed consent
• Patient needs to be able to be cooperative and alert in order to give feedback such as paresthesias
• Able to sit comfortably (for ultrasound and “blind” technique) or prone (for fluoroscopic technique)
• Allergies to any medications
Equipment Needed
These will vary based on the technique used.
Equipment for direct/indirect “blind” approach:
• 21-gauge 38-mm spinal needle
• 25-gauge needle for local administration
• 3-cc syringe for local medication
• Marking pen
Equipment for the ultrasound block will have the following added:
• Ultrasound with linear probe
• Sterile ultrasound cover
Equipment for Fluoroscopic Procedure

• 22-gauge 8- to 10-cm needle
• 25-gauge needle for local
• 3-cc syringe for local medication
• 3-cc syringe for medication
• Connector tubing
Medications
• 1% lidocaine
• Bupivacaine 0.5%
• Methylprednisolone 40 mg or triamcinolone 20 mg
• Antiseptic solution for skin preparation
Technique
There have been several different techniques illustrated for the suprascapular nerve block. These include:
• Wertheim method (“classic”) directing at suprascapular notch
• Dangoisse modified method—directing at the supraspinous fossa
• Ultrasound guided
• Fluoroscopic guided
The “Classic” Approach

• The Wertheim approach, first described in 1941, relies on surface anatomy, patient participation as the
needle produces paresthesias in proximity to the nerve.
• The patient is sitting with hands at sides and head and shoulder slightly flexed.
• Landmarks are identified and drawn on the patient.
• A line is drawn along the spine of the scapula from the base of spine to the medial border of the bone.
• A second line is then drawn from the inferior angle of the scapula and this will bisect the first line
drawn (Figure 64-2).
Figure 64-2. Technique for suprascapular nerve block. One line drawn from inferior angle of scapular. A
second line along scapular spine. The Wertheim method adds a third line bisecting in the upper outer
quadrant.
• A third line is then drawn that bisects the upper outer triangle formed from the 2 lines (Figure 64-3).
Figure 64-3. The Wertheim method adds a third line bisecting the outer quadrant.
• After sterile preparation and local anesthesia, a point 1.5 cm along this third line is the point of
introduction for the needle.
• This is directed caudally and medially until it enters the notch.
• The patient should experience paresthesias to the apex of the shoulder.
• There is a greater risk of pneumothorax with this technique rather than directing at the supraspinous
fossa, although the risk is still minimal.
The Dangoisse-Modified Method

Our preferred method is an alternative approach (still using landmarks only) that indirectly affects the
nerve and carries a reduced risk of pneumothorax.
• Patient is sitting with arms at sides and head and shoulder slightly flexed.
• Using a marking pen, a line is drawn along the scapular spine.
• A second line is drawn from the inferior angle of the spine perpendicular cephalad to bisect the first
line.
• The area is prepped in a sterile fashion.
• A 3-cc syringe attached to a 25-gauge needle is filled with 1% lidocaine which is used to infiltrate the
skin approximately 2.5 cm laterally from the bisected line along the spine.
• The 21-gauge spinal needle is inserted at the previously anesthetized area and walked off the superior
portion of the spine and advanced until the needle makes contact with the bony floor of the
supraspinous fossa.
• A 10-cc syringe with the medication is attached, aspirated, then given slowly.* This will “fill”
supraspinous fossa and thus bathe the suprascapular nerve (Figure 64-4).
Figure 64-4. Fluoroscopic image of the suprascapular nerve block under fluoroscopy (taken with patient
sitting). Contrast was given to delineate the suprascapular fossa. A, AP view; B, Neers view; C, AP view
with visualization of suprascapular fossa; D, Neers view.
• The ultrasound technique utilizes the indirect method with the added convenience of enhanced
visualization.
• The ultrasound is placed parallel to the scapular spine and moved cephalad to identify the
suprascapular fossa.
• It is then moved laterally to identify the suprascapular notch where the nerve will exit.
• The nerve is seen as a round hyperechoic structure inferior to the transverse scapular ligament. The
needle should be continually visualized while the medication is injected.
• To note, having the patient flex his/her elbow and placing it on the opposite shoulder theoretically
decrease the pneumothorax risk additionally by moving the scapular away from the posterior chest
wall.
Fluoroscopy-Guided Technique
• The fluoroscopic-guided block is mainly described in the literature when performing a radiofrequency
or pulse radiofrequency lesioning of the nerve for intractable and refractory shoulder pain.
• This is reasonable and logical method for this procedure considering the need for increased accuracy
for this technique.
• It also provides the benefit of having to use less local anesthetic due to its higher accuracy.
• The patient is placed prone on the table.
• The area is prepped and draped in a sterile manner.
• The suprascapular notch is identified by placing the C-arm in cephalocaudad and an angle slightly
oblique approximately 15 to 20 degrees (Figure 64-5).
Figure 64-5. View of RF needle placement with fluoroscopy in a suprascapular block.
• Local anesthetic is given after locating the notch and the needle is inserted carefully with subsequent
administration of the medication.
• If an RF procedure is performed, sensory and motor information is important to ascertain from the
patient before proceeding with the lesioning of the nerve.
Adequate pain relief and possible complications need to be addressed by contacting the patient the
following day.
The patient should be monitored for:
• Any chest pain or difficulty breathing possibly from a pneumothorax
• Bleeding
• Fever or other signs of infection
COMPLICATIONS
Unlike other blocks for the shoulder including the interscalene and supraclavicular blocks that have
higher risks such as inadvertent epidural or spinal anesthesia and vertebral artery injection, one of the
benefits of the suprascapular block is its minimal risks with the most cited being that of a pneumothorax.
The commonly reported complications with this procedure are:
• Pneumothorax (<1%)
• Inadvertent vascular injection and injury
• Infection
• Neuritis
CLINICAL PEARLS
• The suprascapular nerve provides 70% of sensory to the shoulder and provides motor to both the
supraspinatus and infraspinatus muscle.
• The suprascapular block is a relatively safe and easy block to perform and can be diagnostic and/or
therapeutic.
• The most cited risk is a pneumothorax which still carries only <1% chance.
• It is not sufficient to cover surgery but is helpful in the postoperative state.
Suggested Reading
Shanahan EM, et al. Suprascapular nerve block (using bupivacaine and methylprednisolone acetate) in
chronic shoulder pain. Ann Rheum. 2003;62:400-406.
Vorster W, et al. The sensory branch distribution of the suprascapular nerve: an anatomic study. J
Shoulder Elbow Surg. 2008;17:500-502.
Wertheim HM, Rovenstine EA. Suprascapular nerve block. Anesthesiology. 1941;2:541-545.
References
1. Harmon D. Ultrasound-guided suprascapular nerve block technique. Pain Physician. 2007;10:743-
746.
2. Feigl GC, Anderhuber F, Dorn C, Pipam W, Rosmarin W, Likar R. Modified lateral block of the
suprascapular nerve: a safe approach and how much to inject? A morphological study. Reg Anesth
Pain Med. 2007;32:488-494.
3. Peng P, Wiley M, Liang J, Bellingham G. Ultrasound-guided suprascapular nerve block: a correction
with fluoroscopic and cadaveric findings. Can J Anesth. 2010;57:143-148.
4. Shanahan EM, Ahern M, Smith M, et al. Suprascapular nerve block (using bupivacaine and
methylprednisolone acetate) in chronic shoulder pain. Ann Rheum Dis. 2003;62:400-406.
5. Gado K, Emery P. Modified suprascapular nerve block with bupivacaine alone effectively controls
chronic shoulder pain in patients with rheumatoid arthritis. Ann Rheum Dis. 1993;52:215-218.
6. Jones D, Chattopadhyay. Suprascapular nerve block for the treatment of frozen shoulder in primary
care: a randomized trial. Br J Gen Pract. 1999;49:39-41.
7. Wassef MR. Suprascapular nerve block. Anesthesia. 1992;47:120-124.
8. Emery P, Bowman S, Wedderburn L, Grahme R. Suprascapular nerve block for chronic shoulder pain
in rheumatoid arthritis. BMJ. 1989;299:1079.
9. Breen T, Haigh J. Continuous suprascapular nerve block for analgesia of scapular fracture. Can J
Anaesth. 1990;7:786-788.
10. Parris W. Suprascapular nerve block: a safer technique. Anesthesiology. 1990;72:580-581.
11. Karatas G. Suprascapular nerve block for pain relief in adhesive capsulitis: comparison of 2 different
techniques. Arch Phys Med Rehab. 2002;83:593-597.
12. Shah R, Racz G. Pulsed mode radiofrequency lesioning of the suprascapular nerve for the treatment of
chronic shoulder pain. Pain Physician. 2003;6:503-506.
13. Gleeson AP, Graham CA, Jones I, Beggs I, Nutton RW. Comparison of intra-articular lidocaine and a
suprascapular nerve block for acute anterior shoulder dislocation. Injury. 1997;28:141-142.
14. Hadley M, Volker K, Donntag H, Pittman W. Suprascapular nerve entrapment. J Neurosurg.
1986;64:843-848.
15. Ritchie E, Tong D, Chung F, Norris A, et al. Suprascapular nerve block for postoperative pain relief
in arthroscopic shoulder surgery: a new modality? Reg Anesth Pain Manag. 1997;84:1306-1312.
16. Vorster W, Lange C, et al. The sensory branch distribution of the suprascapular nerve: an anatomic
study. J Shoulder Elbow Surg. 2008;17:500-502.
17. Schneider-Kolsky ME, Pike J, Connell DA. CT-guided suprascapular nerve blocks: a pilot study.
Skeletal Radiol. 2004;33:277-282.
18. Cuneyt Y, Taylan A, Ozgur O, et al. Ultrasonographic evaluation and morphometric measurements of
the suprascapular notch. Surg Radiol Anat. 2009;31:409-414.
19. Chan C, Peng P. Suprascapular nerve block: a narrative review. Reg Anesth Pain Med. 2011;36:358-
374.
SECTION VII
INTRATHECAL DRUG DELIVERY

CHAPTER 65
Commercially Available Reservoir Options for Intrathecal Drug

Delivery
Corey W. Hunter and David Caraway
INTRODUCTION
The presence of abundant opioid mu receptors in the dorsal horns of the spinal cord was discovered in
the 1970s. Subarachnoid injection of morphine was soon utilized to control cancer pain. Since intrathecal
delivery of opioids provides direct access to the mu receptors, a much lower dose can achieve analgesia
than by other routes of delivery. Thus, significant activation of systemic mu receptors, such as occur in the
gut, is avoided thereby reducing unwanted side effects of opioid therapy such as constipation. The first
clinical use of an implanted intrathecal drug delivery system (IDDS) was described in 1981. Introduction
of effective bacteriostatic filters allowed safe long-term infusion. By 1991, commercially available fully
programmable implanted IDDS became available (Medtronic, Inc, Minneapolis, MN).
Presently, commercially available pumps fall into two categories: continuous infusion and
programmable rate devices. Several continuous infusion devices have been approved by the FDA (eg,
Codman 3000, Codman and Shurtleff, Inc, a Johnson & Johnson Company, Raynham, MA, US). At
present, the only programmable IDDS approved for pain indications in the US is the SynchroMed family
of pumps (Medtronic, Inc, Minneapolis, MN).
CONTINUOUS INFUSION PUMPS

Fundamentals
• Continuous infusion pumps are typically designed as two compartment devices.
1. Inner compartment containing the drug to be administered
2. Outside chamber, which is filled with a 2-phase fluorocarbon propellant, which applies continuous
pressure to the inner compartment.
• Filling the drug reservoir compresses the propellant and this pressure drives the drug from the
collapsible chamber through a flow restrictor and then into the patient’s spinal catheter.
• Flow rates are factory preset.
• The advantage of a continuous flow rate device is that it does not require an energy source or complex
programming circuitry and therefore does not need replacement because of battery life or utilize a
specialized programmer.
• The main disadvantage is that any dosage adjustment requires emptying and refilling the pump with a
newly formulated drug concentration. Additionally, potential clinical advantages such as timed bolus
dosing, varying flow rates, and on-board storage of clinical data are not possible.
There are several mechanical, continuous infusion pumps that have been available in the United States.
For example, Infusaid (Pfizer Hospital Products Group, Inc) and Isomed (Medtronic, Inc) are no longer
available (Figure 65-1). At the present time, the Codman 3000 (Codman & Shurtleff, Inc, Raynham, MA)
formerly known as Arrow 3000, and prior to that as Therex 3000, is the only approved mechanical pump
in the United States (Figure 65-2).
Figure 65-1. Medtronic IsoMed pump.

Figure 65-2. Codman 3000—16 mL (left), 30 mL (center), and 50 mL (right).
CODMAN 3000 INFUSION PUMP

Indications
• Continuous regional delivery of intraspinal (intrathecal or epidural) preservative free morphine or
baclofen
• Hepatic artery infusion for cancer treatment
Specifications
See Table 65-1.
TABLE 65-1. Specifics of Codman 3000

Design
• The Codman pump is a continuous infusion mechanical device (no battery or programmability) of the
type described previously.
• It is available in 3 reservoir sizes: 16, 30, and 50 mL.
• The manufacturer supplies multiple flow rates for each reservoir size (Table 65-1).
• A novel feature of this pump is a bypass port for bolus dosing that allows direct access to the catheter
through the same septum as the refill port (Figure 65-3).
Figure 65-3. Schematic drawing Codman 3000: bolus injection demonstrated (left) and pump refill
(right).
• A special, noncoring bolus needle is used and available from the manufacturer.
• It has a large raised domed port in the center of the pump for refill access.
MRI Compatibility
The manufacturer states: “The pump is made of surgical grade titanium which does not affect an MRI and
has had extensive testing done by Codman to confirm this.”
PROGRAMMABLE PUMPS
Fundamentals
• The programmable pump also uses a propellant stored in an outside chamber to exert constant pressure
on a bellows compartment that collapses as the drug is infused.
• Uses battery-powered electronics and motor to move the drug from the reservoir via a peristaltic pump
through the intraspinal catheter.
• The pump delivers the prescribed medication in precise amounts based on the instructions that the
clinician programs into the device.
• The device incorporates a catheter access port (CAP) that allows injection directly into the implanted
catheter for drug administration and diagnostic purposes.
• The advantage of a programmable pump is that dose changes can occur simply by the use of an external
programmer, flow rates are available over a much broader range, and the flow rates can be tailored so
that the patient can receive different doses at selected times of the day.
• Clinical information is stored in the pump’s memory including recent programming changes, drug
concentrations and flow rates, catheter length, battery life indication and refill dates. Current battery
life is estimated at 6 to 7 years.
• New technology (myPTM Personal Therapy Manager, Medtronic, Inc, Minneapolis, MA) allows for
patient activated boluses within the dosage and frequency prescribed by the managing physician. This
may facilitate treatment of patients who experience intermittent pain of varying intensity.
Regardless of the manufacturer or design of the IDDS, patient safety is of paramount importance. Best
practices recommendations and manufacturer’s instructions must be followed to avoid pocket refill,
unintended direct catheter injection and untoward medication interactions. Appropriate training and
familiarity with the device is essential.
A number of manufacturers have developed pumps, including programmable devices (eg, MedStream,
Codman & Shurtleff, Inc, a Johnson & Johnson company, Raynham, MA, US and Prometra, InSet
Technologies Incorporated, Mt. Olive, NJ, US) that are undergoing clinical trials or have received
approval in Europe or elsewhere. The focus of this chapter will be to present technical descriptions of
commercially available implantable intrathecal drug administration systems presently indicated for
treatment of chronic pain in the United States—SynchroMed EL (10 and 18 mL) and SynchroMed II (20
and 40 mL) (Figure 65-4).
Figure 65-4. SynchroMed EL (left) and SynchroMed II (right).
SYNCHROMED EL BY MEDTRONIC
This model is no longer in production by Medtronic and is succeeded by their newer model, the
SynchroMed II with the earlier model phased out after the initial FDA approval in 2004. However, as
thousands of the SynchroMed EL pumps were implanted worldwide, many patients are still actively
receiving therapy with this model. Therefore, design and clinical considerations for both pumps are
included.
Indications
• Intrathecal (or epidural) infusion of preservative-free morphine for treatment of chronic pain. (Current
labeling is for maximum concentration of 25 mg/mL.)
• Intrathecal infusion of preservative-free ziconotide (Prialt) for treatment of chronic pain. (Current
labeling is for maximum concentration of 100 μg/mL.)
• Intrathecal infusion of baclofen (Lioresal) for treatment of spasticity.
• In addition to their application for intrathecal delivery, these pumps can be utilized for intravascular
infusions of methotrexate, FUDR, doxorubicin, cisplatin, for cancer and clindamycin for osteomyelitis.
Drugs other than the FDA approved medications listed above are commonly used. However, the clinician
should be aware that compatibility with other medications and mixtures of medications has not been well
studied. Reports of corrosion, pump stall and other failures have been attributed to use of nonapproved
medications.
Specifications
See Table 65-2.
TABLE 65-2. Specifics of SynchroMed EL

Design
• 3 sealed chambers:
1. Reservoir propellant
2. Battery and electronic module
3. Peristaltic pump and drug reservoir
• The peristaltic pump is what drives the medication from the pump into the catheter and eventually out
of the tip into the intrathecal space. It is a two-roller model, which also acts as a valve that prevents
introduction of fluid into the reservoir when capacity is reached.
• Side catheter access port—access with a 25-gauge needle for either drug administration or diagnostic
purposes. There is a mesh screen covering the port; however, an external bacterial filter on the syringe
is required when injecting into the port. Any introduction of fluid through this port will flow strictly
forward through the system and out of the catheter. Therefore, one could inject radiopaque dye through
the port to perform a myelogram without fear of introducing dye into the reservoir and distorting the
concentrations of the drugs.
• Stability of morphine and baclofen has been tested and approved to 90 days with the SynchroMed EL
Figure 65-5. SynchroMed EL.
Figure 65-6. Schematic drawing of the pump.
Precautions During Implantation

• Pump needs to be warmed to body temperature prior to implantation to ensure proper function. If the
SynchroMed EL is not warmed prior to voiding of the reservoir and initial filling, incomplete emptying
can occur, which can lead to possible overfill of the reservoir and subsequent activation of the
reservoir valve.
• Since the SynchroMed EL pump did not detect if the motor was stalled (unlike the newer SynchroMed
II pump) a “pump purge” was recommended to ensure that the pump was functional.
• Implantation of the pump requires a maximum recommended depth of 1 in (2.5 cm) from the skin
surface. Greater depth can cause difficulty with programming as well as difficulties with refilling as it
can inhibit access to the pump’s septum during refilling.
Initial Programming
• The SynchroMed EL has 6 settings for drug administration:
1. Single bolus, which is programmed in drug units, ie, μg, mg, etc, over a predetermined time.
2. Priming bolus, which is programmed in volume (mL) over a predetermined time.
3. Bridge bolus, which is programmed when changing concentrations to deliver the old medication in the
catheter and pump tubing at one flow rate and the new medication at a different flow rate.
4. Continuous infusion at a predefined rate.
5. Complex continuous infusion administers the reservoir contents at multiple rates. Between 2 and 10
variations are possible, with each variation programmed at its own individual predefined rate.
6. Periodic bolus for a determined period at specific intervals.
• When using the periodic bolus setting, the pump must be set for a flow rate of at least 1.8 μL/h.
• The internal computer is also capable of storing information specific to the pump being implanted (ie,
model number and reservoir size) as well as the individual patient (ie, drugs present, concentration,
rates, catheter length, etc). However, due to limits in memory—patient identification is limited to 3
characters and drug name to 5.
• The alarm must be programmed at the initial implant for low reservoir volume.
• If using the red “Therapy Stop” button on the programmer to stop the pump, it will not obtain or
provide pump status information, and the pump will decrease its infusion rate to 0 μL/d.
MRI Compatibility
The SynchroMed EL is approved for MRI scanning. Pump performance has not been established for
greater than 3.0 Tesla (T) horizontal, closed-bore MRI scanners.
• The magnetic field of the MRI scanner will temporarily stop the rotor of the SynchroMed EL pump
motor and suspend drug infusion for the duration of the MRI exposure.
• The pump should resume normal operation upon termination of MRI exposure; however, there is the
potential for an extended delay in pump recovery after exiting the MRI magnetic field because
exposure to the MRI magnetic field may cause the motor gears within the pump to bind temporarily
without permanent damage.
• This temporary binding may delay the return of proper infusion after the pump is removed from the
MRI magnetic field.
• While extended delays in pump recovery are unlikely, reports have indicated that there is the potential
for a 2- to 24-hour delay in return to proper drug infusion after completion of an MRI scan.
• Instructions for MRI safety are provided by the manufacture.
SYNCHROMED II BY MEDTRONIC
Indications
The SynchroMed II has similar indications as its predecessor (SMII is not indicated for doxorubicin,
cisplatin, or clindamycin). It was created as an updated version of the EL and meant to improve upon the
ease of use and allow more options for increased customization (Figure 65-7).
Figure 65-7. SynchroMed II.
Specifications
See Table 65-3.
TABLE 65-3. Specifics of SynchroMed II

Design
The essential design is relatively similar to the SynchroMed EL, with several differences highlighted
below:
• Improved form factor
• 3 roller system with radiopaque ball marker on one of the roller arms for identification
• Refined mechanics and electronics allow for more precise infusion of medication as compared to the
predecessor
• Pressure-activated reservoir (compared to the volume activated valve in the EL). As the reservoir
fills, a pressure diaphragm flattens resulting in a spring-driven valve stem to form a seal—this allows
for immediate release of the seal with aspiration (EL requires continuous aspiration and time for valve
release).
• Larger catheter access port allowing for as large as a 24-gauge needle as well as a funnel design for
easier access.
Precautions During Implantation

• Does not require warming or a pump purge prior to implantation.
• Implantation of the pump requires a maximum depth of 1 in (2.5 cm) from the skin surface. Greater
depth can cause difficulty with programming as well as difficulties with refilling as it can inhibit
access to the pump’s septum during refilling.
Initial Programming
• The SynchroMed II has settings which are similar to the EL with new features that allow further
customization of dosing regimens:
1. Single bolus over a predetermined time.
2. Continuous infusion at a predefined rate.
3. Flex infusion which is similar to the complex continuous infusion of the EL. However, this version
allows up to 13 different sequences to be programmed, each with independent rates and durations.
In addition, a “basal rate” is programmed that runs whenever another sequence is not programmed.
If desired, two “patterns” can be programmed to deliver different dosing for two sets of
consecutive days throughout the week.
4. Minimum rate infusion—the minimum rate is 6 μL/d (0.25 μL/h)
5. Predetermined bolus—single bolus, priming bolus, or bridge bolus
6. Stopped pump mode—can be used for periods of up to 48 hours before an alarm will sound and
potential damage to the pump may occur.
• SynchroMed II can store a patient’s full name and drug names up to 25 characters.
• Individual drugs, their concentrations, and even physician notes for communication with other
clinicians are all possible.
• Programming/interrogation takes somewhat longer due to the increased amount of information stored
within the pump as compared to the EL.
• One tone alarm for noncritical alert (ie, low reservoir volumes, elective replacement indicator, and a
noncritical pump memory error).
• Two tone alarm for critical alert (ie, an empty reservoir, end of service, motor stall, stopped pump
duration greater than 48 hours, and a critical pump memory error).
• When stopping the pump with the “stop key,” the SynchroMed II pump will provide the pump status just
before shutting down and will also program the pump to the minimum infusion rate of 6 μL/d so as to
avoid pump damage that can occur if the pump is left completely stopped for an extended period of
time.
TABLE 65-4. Direct comparison of the SynchroMed EL to the SynchroMed II

MRI Compatibility
SynchroMed II compatibility has been established for use with up to 3.0 Tesla (T) horizontal, closed-bore
MRI scanners. SynchroMed II pump performance has not been established with magnetic fields higher
than 3.0 (T).
• The magnetic field of the MRI scanner will temporarily stop the rotor of the SynchroMed II pump
motor and suspend drug infusion for the duration of the MRI exposure.
• The pump should resume normal operation upon termination of MRI exposure; however, there is the
potential for an extended delay in pump recovery after exiting the MRI magnetic field because
exposure to the MRI magnetic field may cause the motor gears within the pump to bind temporarily
without permanent damage.
• While extended delays in pump recovery are unlikely, reports have indicated that there is the potential
for a 2- to 24-hour delay in return to proper drug infusion after completion of an MRI scan.
• The SynchroMed II pump detects motor stall and motor stall recovery.
• Medtronic does not recommend programming the SynchroMed II pump to “stopped pump mode” prior
to an MRI because of the possibility of an increased delay in the detection of an extended motor stall.
• Motor stall events are recorded in the pump event log and can be reviewed using the clinician
programmer.
• A motor stall will also cause the pump alarm to sound (2-tone alarm). Stall recovery detection should
occur within 20 minutes of exiting the MRI magnetic field. The detection of a motor stall and detection
of motor stall recovery may each take up to 90 minutes if the pump is programmed to minimum rate
mode (0.006 mL/d).

Codman 3000
• Care should be taken not to use the special bolus needle for refilling the pump—as an inadvertent
overdose is possible (IFU, Codman Refill Kit Model 3000 series REF AP-07014).
• Changes in body temperature or sea altitude can change the infusion rate, thus altering the refill
interval.
SynchroMed EL
• Variable lifespan may need replacement as early as 3 years after implant due to battery depletion from
higher infusion rates.
• Limited internal memory—can only store 3 characters of patient’s name and 5 of the drug.
• Erratic flow rates can occur at reservoir volumes below 2 mL with the potential for interruption of
therapy.
• Prior to implantation, the pump needs to be warmed to body temperature and purged to ensure proper
function.
SynchroMed II
• While the lifespan is much less variable than the EL, battery life can still be dependent on infusion
rates.
• Once the reservoir volume drops below 1 mL, erratic flow rates can occur with the potential for
interruption of therapy.
• Longer communication time required between interrogator and pump due to increased amount of
information to be transferred.
Figure 65-8. Comparison of width between models.
For both devices, compounded drugs and admixtures of unapproved medications can cause the
development of impurities within the pump resulting in damage and potential pump failure. An external
filter on the syringe should be used when injecting into the catheter access port (side port). Pump function
can be affected by radiation, lithotripsy or if the patient exposes themselves to elevated temperature or
changes in pressure for extended periods of time.
CLINICAL PEARLS
Codman 3000
• Does not require an energy source or complex programming circuitry and therefore does not need
replacement because of battery or a specialized programmer.
• Any dosage adjustment requires emptying and refilling the pump with a newly formulated drug
concentration.
• Timed bolus dosing, varying flow rates, and on-board storage of clinical data are not possible.
Several important clinical changes occurred with the introduction of the SynchroMed II:
• Reservoir size increased from 10 and 18 mL to 20 and 40 mL. This allows for longer refill intervals,
reduced costs, and improved patient satisfaction.
• Device size was reduced considerably: the SynchroMed El 18 mL pump has a displacement volume of
125 mL, while the SynchroMed II 20 mL pump displaces just 91 mL and the 40 mL reservoir pump
displaces 121 mL. This improves cosmesis and patient acceptance.
• Morphine and baclofen have been tested and approved for stability in the reservoir for 180 days—
doubling approved stability.
• Continued approval for intrathecal delivery of preservative-free morphine sulfate, preservative-free
ziconotide (Prialt), and baclofen (Lioresal).
• Design consisting of a three roller pump system with a radiopaque ball marker on one of the roller
arms (can track roller rotation for a “roller study” to detect pump stall).
• Improved accuracy of flow rates and improved memory capacity.
• Pressure diaphragm in reservoir—immediate aspiration from the reservoir.
• Newer infusion modes—flex infusion and minimum rate infusion mode.
• The myPTM device, compatible only with SynchroMed II, allows patients who experience episodes of
intermittent pain to dispense a bolus dose of medication (within physician-prescribed limits) when
needed.
Suggested Reading
Belverud S, Mogilner A, Schulder M. Intrathecal pumps. Neurotherapeutics. 2008;5(1):114-122.
Bennett G, Serafini M, Burchiel K, et al. Evidence based review of the literature on intrathecal delivery
of pain medication. J Pain Symptom Manage. 2000;20(2):S12-S36.
Codman. http://www.codmanpumps.com/Patient_pain_faq.asp#7. Accessed July 27, 2011.
Deer T, Krames ES, Hassenbusch SJ, et al. Polyanalgesic Consensus Conference 2007: recommendations
for the management of pain by intrathecal (intraspinal) drug delivery: report of an interdisciplinary
expert panel. Neuromodulation: Technology at the Neural Interface. 2007;10:300-328.
Krames ES. Intraspinal opioid therapy for chronic nonmalignant pain: current practice and clinical
guidelines. J Pain Sympt Manage. 1996;11(6):333-352.
Medtronic. http://professional.medtronic.com/products/synchromed-el-pain/mri-guidelines/index.htm.
Accessed July 27, 2011.
Medtronic. http://professional.medtronic.com/products/synchromed-II-pain/mri-guidelines/index.htm.
Accessed July 27, 2011.
Medtronic Inc. http://professional.medtronic.com/products/synchromed-II-pain/index.htm. Accessed July
27, 2011.
Medtronic Synchromed EL Implant Guide. Medtronic, Inc; 2006.
Medtronic Synchromed II Implant Guide. Medtronic, Inc; 2006.
Onofrio B, Yaksh T, Arnold P. Continuous low dose intrathecal morphine administration in the treatment
of chronic pain of malignant origin. Mayo Clinic Proc. 1981;56:516-520.
Penn RD, Kroin JS. Long-term intrathecal baclofen infusion for treatment of spasticity. J Neurosurg.
1987;66:181-185.
Science. 1976 June 25;192(4246):1357-1358.
Smith TJ, Staats PS, Deer T, et al. Randomized clinical trial of an implantable drug delivery system
compared with comprehensive medical management for refractory cancer pain: impact on pain, drug-
related toxicity, and survival. J Clin Oncol. 2002;20(19):4040-4049.
Synchromed EL/Synchromed II Programmable Pump Comparison. Medtronic, Inc; 2006.
Wang JK, Nauss LA, Thomas JE. Pain relief by intrathecally applied morphine in man. Anesthesiology.
1979;50:149-151.
CHAPTER 66
Choosing Intrathecal Medication

Philip S. Kim and Sudhir Diwan
INTRODUCTION
• Intraspinal delivery of drugs via implantable drug delivery systems (IDDS) has been available since
the early 1980s.
• These devices allow for precise delivery of drugs for treatment of pain and spasticity.
• The delivery is medications in the intraspinal or intrathecal space allows delivery of medications
directly to their site of receptor binding in the spinal column at much smaller doses than systemic
administration.
• The result is potent analgesic effect with lower systemic side effects.
IDDS comprises of a pump implanted in a subcutaneous pocket usually in the abdomen and attached to a
catheter that is tunneled under the skin and inserted in the intrathecal space of the spinal cord at the
appropriate level (Figure 66-1). The pump available is programmable or nonprogrammable. The
nonprogrammable pump runs at a constant flow rate with dose adjustments made by changes in the
concentration of medications. The programmable pump is programmed to deliver the drug or admixture at
a controlled rate based on the drug concentration and dose requirements of the patient.
Figure 66-1. Side view of implantable drug delivery device.
Complications related to the pump and catheter system:

• Complications should be addressed prior to choosing and adjusting intrathecal drug medications.1
• The most common operational problems are related to either pump programming or motor stalling.
• Pump programming errors are most likely to occur when drug concentrations are changed.
• Verification of drug concentration, daily dose, volume, and refill date is absolutely necessary.
• A motor stall is typically caused by gear shift wear. The incidence is low (0.5%-2.2%) and can be
detected with radiographic examination.2
• New SynchroMed pumps are equipped with electronic logs to detect and report motor stall issues.
• Catheter malfunctions include kinks, holes, or blockages that prevent accurate delivery of
medications.1
• Other complications include catheter fibrosis or inflammation and granuloma formation.
Granuloma:
• Development of noninfectious inflammatory mass or granuloma has been reported 0.1% to 5% of
patients with implantable pumps.3,4
• Physicians should be suspicious of possible granuloma if patient complains of increased pain that was
previously controlled and/or neurological deficits of weakness and sensory loss.
• Granulomas have been reported most frequently with morphine followed by hydromorphone and
fentanyl.
Once patient has selected for intrathecal drug therapy, drug selection is the next step. The polyanalgesic
consensus conference (PACC) panel has developed recommendations on the rational use of intrathecal
analgesics. This PACC panel has reviewed preclinical and clinical research and experience in 2000,
2003, 2007, and 2011.5 The current standard of care of intrathecal therapies reflects on current knowledge
from literature and clinical experience. Analysis of published literature is combined with clinical
experience of a large panel of scientist and clinicians to form recommendations regarding the use of
intrathecal analgesics to treat chronic pain. It is this author’s belief to follow these recommendations as a
guide and experience in clinical practice.
PACC 2011 recommendations for prevention and detection of granuloma:
• Prevention
Use lowest effective conc. and dose (Table 66-1)
TABLE 66-1. 2011 PACC Recommendations for Maximum Daily Doses and
Concentrations
Use bolus dosing instead continuous infusion

Consider placing catheter tip in lumbar region below conus medullaris
Implement nonopioid adjuvants if concerned about granuloma formation
Switch IT opioid to Ziconotide if recurrence of granuloma.
• Screening/detection
Detailed history and physical examination every 3 months.
Routinely monitor patients for prodromal clinical signs or symptoms.
Monitor yearly increase in daily dose.
Educate other physicians/radiologists about granuloma.
PACC 2011 panel recommendations:
• The current 2011 PACC panel recommendations have new algorithm tracks for neuropathic and
nociceptive pain states is an new step in improving patient care (see Tables 66-2 and 66-3).5
TABLE 66-2. 2011 Polyanalgesic Algorithm for Intrathecal Therapies in Neuropathic Pain
TABLE 66-3. 2011 Polyanalgesic Algorithm for Intrathecal Therapies in Nociceptive Pain
• Prior and current recommendations for drug selection provide clinical practice guidelines for the
optimization of IT (intrathecal) therapy with single and multidrug combination in rational and
prioritized order.
• In each arm of the algorithm, the medications are arranged in a hierarchy on the basis of efficacy and
safety.
• First line medications/combinations are supported by extensive clinical experience and published
clinical and preclinical literature.
• Typically, these medications are used to start IT therapies.
• Note that morphine and ziconotide are the two agents that approved by U.S. Food and Drug
Administration (FDA) for IT therapies.
• Nonapproved agents are commonly used among pain practitioners who manage IT pump and have been
thoroughly discussed for its safety and efficacy.
• Specific recommendations for ziconotide for neuropathic pain and baclofen for pain from spasticity.
• Recommendation made against using certain drugs intrathecally due to toxicity (Table 66-4).
TABLE 66-4. PACC 2011 Recommendations Against Using These Drugs Intrathecally
• Best practices for improved patient care and outcomes with intrathecal infusion are recommended to
minimize the morbidity and mortality.
OTHER CONSIDERATIONS
Recommendation Starting Dosages
• Starting dosages recommended by the PACC panel are shown in Table 66-5.5 Appropriate starting
dosages may vary on the basis of patient’s baseline oral intake at the time of IT therapy is started.
TABLE 66-5. Recommended Concentration and Doses of Intrathecal Agents by PACC

2011
Compounding of Medications
• The U.S. FDA regards traditional pharmacy compounding as the combining or altering ingredients by a
pharmacist in response to a licensed practitioner’s prescription so as to treat a patient’s special
medical needs.5
• When prescribing a drug for IT administration, special and strict requirements are needed to ensure
patient safety and protection of the practice.
• IT drug preparation requires strict sterile and free of contaminants to avoid potential catastrophic
effects.
• It is important that the compounding pharmacist has written policies and procedures established and
updated to remain compliant with USP 797 standards. This means compounding sterile products under
manufacturer’s labeled instructions and with other manipulations that expose the original contents to
potential contamination.
• Other considerations in evaluation and selection of a compounding pharmacy for IT drug preparation
are the following: aseptic training of personnel, segregated sterile compounding area, environmental
monitoring of air quality, calibration of equipment, clean and disinfection program, and quality
assurance program.
Drug Admixtures
• The PACC took into account drug stability information available.5
• There is infinite number of drug combinations and it is the author’s view that only drug mixtures be
utilized where drug stability information is available.
• If a study suggests that high concentration drug combinations are stable, stability can be assumed for
lower-concentration combinations of the same drugs.
• For most pharmaceuticals, there are established and published standards of solubility at room
temperature.
• While high drug combinations allow for longer refill interval and delivery of higher daily doses,
alteration in pH to develop high drug concentration solutions can result in unstable solutions that can
lead to patient and complications with the pump.
• This author has had precipitant cause catheter obstruction and failure of IT drug therapy (see Figure
66-2).6,7
Figure 66-2. Corrosion of pump components due to incompatible drug formulations. (Reprinted with
permission from Medtronic.)
• These concentration and pH can be deleterious effect on the pump catheter and tubing.
• This author has seen pump corrosion with high concentration of opioids (see Figure 66-3).8
Figure 66-3. Distal catheter obstruction due to precipitant formation. (Reprinted with permission from
Medtronic.)
• A maximum recommendation concentration and starting doses of IT drugs is cited by PACC for the
concern of solubility, stability, and granuloma (see Table 66-5).5
• These concentrations are guidelines that can be adjusted for each patient.
• This author may use higher concentrations for cancer patients to accommodate in rapid escalation pain
in the end of life.
PACC 2011 Recommendations for Compounding IT Medications

• Avoid preservatives, antioxidants, and solubility enhancers, as they may be neurotoxic.
• Use buffers that are compatible with the delivery system. Acetate buffers are not compatible with the
SynchroMed infusion system.
• Use a pH that is physiologically appropriate and is consistent with the drug solubility and delivery
system, generally in the range of pH 4 to 8.
• Use solutions that are isotonic with normal CSF (˜300 mOsm/L).
• Prepare the solution in a manner that does not alter the solubility of the constituents to minimize
neurotoxicity or incompatibility with pump.
• Verify the chemical and physical stability, and sterility of the preparation in accordance with the USP
and ASHP publications.
• Ensure appropriate control of bacterial endotoxins (pyrogens).
Drug Flow Rates and Intermittent Bolusing

Continuous IT delivery of medications is a standard mechanism. No studies exist to support the best rate
of delivering medications. Some PACC members theorize that lower flow rates may result in higher
concentration of the drug at the catheter tip and may result in higher risk of granuloma, but this has not
been proven clinically.5,6
• Constant flow pumps cannot be used to change flow rate or administer boluses. With programmable
pumps, intermittent bolusing and patient controlled analgesia (PCA) is now available.
• Bolus doses can be given by programming the pump to give doses at set times and when available, the
patient has option of self-administer boluses as needs as a (PCA) or personal therapy manager (PTM).
• Usually boluses are 5% to 20% of daily dose that is administered at a continuous rate. This manner of
drug administer is favored given a lot of patient’s pain is intermittent affected by certain activities of
daily living and time of day.
• Caution must be used as baseline doses climb with clonidine and bupivacaine.
• To avoid hypotension or motor block, the dose of clonidine should not exceed 20 mcg and the dose of
bupivacaine should not exceed 3 mg.
Trialing to Consider Permanent Intrathecal Therapy

The concept of trialing before implantation of an IT drug delivery device is based on the assumption that
it will provide information on the efficacy of the therapy. Trialing was thought to be critical prior to
implantable and is now debatable. Trialing may be considered in patients with existing implanted pumps
for which a change in IT medication is being considered.5
• Trialing may be performed prior to consideration of pump implantation.
• The issue of opioid-induced hyperalgesia (OID) cannot be addressed during a single shot trial or short-
term 72-hour drug infusion.
• Many PACC members felt trialing not needed in end-of-life cancer patients if patients have previously
tolerated the same drug by another route.
• This author feels that trialing should still be considered for most patients.
• The trial of various medications such as ziconotide will benefit patient beyond potential side effects
and toxicities.
• Trialing will allow patient to determine overall benefit in pain relief measured with quality of life and
activities scales.
• Realistic expectations can be built during trial for long-term IDDS to reduce patient’s pain and to
improve quality of life.
• Trialing can be performed by IT or epidural injection or infusion for most drugs.
References
1. Follett KA, Burchiel K, Deer T, et al. Prevention of intrathecal drug delivery catheter-related
complications. Neuromodulation. 2003;6:32-41.
2. Fluckiger B, Knecht H, Grossmann S, Felleiter P. Device-related complications of long-term
intrathecal drug therapy via implanted pumps. Spinal Cord. 2008;46:639-643.
3. Langsam A. A case of spinal cord compression syndrome by a fibrotic mass presenting in a patient with
an intrathecal pain management pump system. Pain. 1999;83:97-99.
4. Deer T, Levy R, Prager J, et al. PACC 2011: Consensus on Diagnosis, Detection, and Treatment of
Catheter-Tip Inflammatory Masses (Granulomas); 2011.
5. Deer T, Levy R, Prager J, et al. Polyanalgesic Consensus Conference 2011: Recommendations for the
Management of Pain by Intrathecal (Intraspinal) Drug Delivery: Report of an Interdisciplinary Expert
Panel; 2011.
6. Kim P. Case Series of Distal Catheter Obstruction. In: NANS Annual Meeting 2011. Las Vegas,
Nevada; 2011.
7. Medtronics. Intrathecal Distal End Catheter Occlusions as a Result of pH & Salt Concentration
Gradients Between Delivery Solution & Cerebrospinal Fluid (CSF); 2009.
8. Medtronics. SynchroMed® EL & SynchroMed II Pump Corrosion from Nonindicated Drug
Formulations Resulting in Permanent Pump Stalls Minneapolis; 2009.
CHAPTER 67
Intrathecal Drug Delivery Trialing Procedures

Richard Bowman, Timothy R. Deer, and Jason E. Pope
INTRODUCTION
• Intrathecal drug delivery system (IDDS) trials offer the clinician an ability to utilize neuraxial
medications in the patient and assess whether or not the patient has a positive response to the
medications.
• By delivering substances in this format, prior to committing the individual patient to surgical
implantation of the device, the physician can be cost-effective, selective, and most importantly improve
patient efficacy and safety.
• There are 2 major categories of patients who would be considered for intrathecal pump infusion
system trialing in the field of interventional pain management.
• The first group suffers from neuropathic, nociceptive, or mixed pain syndromes which may be related
to cancer pain or noncancer pain syndromes. Trialing often involves a primary opioid, ziconotide, or a
combination of medications to treat different types of pain.
• The second group suffers from poorly controlled spasticity, and involves the injection of baclofen.
• The mechanics of needle and catheter placement may be similar between these groups; however, the
assessment of the individual patient, with respect to outcome, differs significantly.
• Trialing in the neuroaxis also varies based on the targeted area of drug delivery.
• Options include single shot injections or catheter placement with intermittent bolusing or continuous
infusion, and the anatomical location may be the epidural space or the cerebral spinal fluid.
RELATIVE ANATOMY
Intrathecal pump infusion system trials are generally performed with placement of the needle below the
conus, and the catheter in the area of the pain generator. The needle placement, generally, is performed
between L1 and S1 in the interlaminar space. The specific anatomic points of consideration are as
follows:
• Visualization of the thoracolumbar junction at the lowest rib level
• Visualization of the pedicles and spinous processes
• Identification of the interlaminar spaces
Other relative anatomy that should be considered includes:
• The body habitus of the patient
• The relative amount of lumbar lordosis present in the patient’s position on the table
• The orientation of rotation of the spine in a patient with scoliosis
• The integrity of the skin
• The paraspinal musculature
• The spinal ligamentous structures
• The ligamentum flavum and the dura mater

There are some general concerns and considerations that would be applicable to all forms of IDDS
trialing, whether the trial is performed as a single-shot, continuous epidural infusion or continuous
intrathecal infusion.
The choice of interlaminar space:
• The location should be based not only on adequate visualization of the interlaminar space, along with
adequate space visualized to accommodate needle placement, but should also be based on entering the
spine at a level with good skin integrity.
• This includes an area absent of any evidence of skin breakdown or infection, and at a level where
previous spine surgery has not been performed.
• Areas of previous surgery may have atypical spinal anatomy, and may lead to complications.
Immunocompromised patients:
• Patients with immunocompromised status may require preprocedure consultation and special antibiotic
or preoperative care.
• They should be monitored very carefully for the development of infection, although this is a rare
complication in short-term trials.
• Significant compromise of immune response may be an absolute contraindication to the procedure, and
consultation with a infectious disease is warranted with white blood counts less than 2000.
• This may be of concern in those undergoing chemotherapy, suffering from malignancy, with advanced
age, and with other advanced diseases.
Fluoroscopy:
• Radiolucent hardware, soft tissue masses, or other obstructions to needle placement may not be
visualized on fluoroscopic imaging.
• Vigilance should be used in those cases where needle placement is difficult. Imaging may be enhanced
with contrast in cases where there is uncertainty about location.
Other concerns:
• Patients with bleeding disorders may not be candidates for the procedure.
• Patients with thrombocytopenia that have platelet counts less than 50,000 may be at high risk for
bleeding.
• Care should be administered in those with counts below 100,000 or with a downward trend.
• Platelet function is equally worrisome, and should be assessed by a hematologist if questions persist.
Difficult patient position:
• Patients with abdominal wounds or masses may have difficulty with lying in the prone position.
• Most trials can be performed with the patient in the lateral decubitus position which can be tolerated
with or without the addition of sedation in most cases.
Absolute contraindications to the procedure include:
• Active spinal infection
• Localized infection at the area of skin entry necessary to perform the procedure
• Active systemic infection
• Coagulopathy
• Allergy to infused medication
• Immunocompromised state that would preclude adequate healing after implantation of the permanent
device
PERIOPERATIVE CONSIDERATIONS FOR TRIALING

• When possible, a patient should be weaned off, or reduced to a minimum amount of oral or transdermal
opioid prior to an intrathecal drug delivery system trial.
• Preadmission testing should include screening for coagulopathies with a PT/INR, PTT, and bleeding
time.
• Additional history should be taken to screen for undiagnosed coagulopathies such as von Willebrand
disease and history should include any previous history of unusual bleeding due to surgeries or
lacerations.
• Anticoagulants should be discontinued as per ASRA guidelines prior to performance of needle-based
spinal procedures. Additionally, it is recommended that clinicians consider stopping aspirin for 1
week prior to the procedure, and herbal supplements such as fish oil that may cause bleeding for 2
weeks preoperatively.
• Preadmission testing should screen for any electrolyte abnormalities or cardiovascular risks that would
preclude a patient from undergoing a minor surgical procedure.
• Anatomical considerations such as existing hardware, skin integrity, skin masses, soft tissue masses,
tumor growth, patient tolerance to positioning and body habitus should be evaluated preoperatively in
order to determine the feasibility of needle placement at the desired location.
• Please refer to Figure 67-1.
Figure 67-1. PACC 2012 trialing algorithm.
During The Trial

• Preoperative administration of IV antibiotics in high risk patients may be considered for placement of
catheters for trialing. The choice of antibiotic should be determined with evaluation of common
pathogens in the clinician’s region. Infectious disease specialists may be helpful in making
recommendations for specific antibiotic choice and dose in each region.
• Oral or transdermal opioids should be reduced or discontinued when feasible in order to best assess
the efficacy of epidural or intrathecal infusion of opiates.
• Dosing epidural versus intrathecal: it should be noted that intrathecal dosing is generally 1:10 relative
to epidural dosing of opiates. Similar ratios apply for bupivacaine, baclofen, and clonidine.
• It is recommended that continuous pulse oximetry be utilized during continuous epidural or intrathecal
infusions.
• Vital signs should be assessed at 4-hour intervals.
• Any signs of sedation, confusion, low oxygen saturation, or hypotension should prompt discontinuation
of the infusion until the physician is contacted for instruction.
• Patients should be monitored closely for development of allergy to the infused agent for the first 2
hours after initiating infusion.
• Patients should resume pretrial doses of oral or transdermal opiates after the infusion has stopped at
discharge, or should be tapered off infused opiates prior to discharge if on no oral opiates at home.
• Blood pressure should be monitored for rebound hypertension for 24 to 48 hours subsequent
discontinuation of clonidine infusion.
• If an opiate is combined with ziconotide, all psychological complications that could occur with
administration of ziconotide would apply as described in the ziconotide trialing section.
Mechanics of Fluoroscopic Imaging

• After positioning the patient on the table, ideally in a prone position, a “true” anterior-posterior (AP)
image of the lumbosacral spine is performed. Cephalocaudal tilt is utilized to image the inferior end
plate of the vertebral body superior to the interlaminar space targeted. It is recommended to “square
off” the end plate of this vertebral body. A true AP image should visualize the spinous process at that
level as centered between the adjacent pedicles.
• Reduction of lumbar lordosis with padding or pillows placed under the abdomen, when feasible, will
help increase the interlaminar space available the desired entry level in the upper lumbar spine.
• Lateral views should be obtained at this level prior to patient prep in order to be sure that adequate
visualization of the needle tip or catheter will be feasible in the patient’s position.
• Typical interlaminar location for insertion of the intrathecal needle tip should be L2-L3 or L3-L4.
• Choosing a level below L2 or the level of the conus is suggested for intrathecal placement of needles
when feasible.
PARAMEDIAN TECHNIQUE FOR INTERLAMINAR

PLACEMENT OF NEEDLE
This preferred technique is utilized for single-shot trials as well as catheter placement for continuous
infusion, although it may be performed at different spinal levels depending on the specific technique. This
procedure applies to trialing whether for pain or spasticity.
• A paramedian technique for interlaminar placement of the needle tip is suggested with lateral to
medial, caudad to cephalad, and posterior to anterior angling is utilized.
• Fluoroscopic identification of the interlaminar space to be targeted and appropriate imaging of the
targeted level (as described under fluoroscopic views) is performed first.
• A needle insertion site is identified under fluoroscopy at approximately 2 vertebral body segments
inferior to the targeted interlaminar level with the medial border of the pedicle at that level used as a
reference point for needle insertion.
• Lidocaine is applied at the overlying skin surface with the 25-gauge 1.5-in needle and 5 to 10 cc of 1%
lidocaine. A skin wheal is created and the subcutaneous tissue is infused with lidocaine.
• A 15-blade scalpel is used to make a small stab incision at the site of needle insertion.
• The Tuohy needle is advanced through the anesthetized skin with AP imaging visualizing the
advancement in a lateral to medial, caudad to cephalad, posterior to anterior trajectory until the tip of
the Tuohy needle reaches the laminae of the vertebral level that lies along the inferior ipsilateral side
of the interlaminar space targeted.
• The needle angle utilized should be a shallow angle of 30 degrees or less, relative to the spine (Figure
67-2).
Figure 67-2. Shallow needle placement for paramedian technique.
• Adjustments to needle entry location may vary based on body habitus in order to maintain this angle
such that in individuals with more adipose tissue the needle entry point may need to be more than 2
segments inferior to the targeted site and the needle tip may lie as far lateral as the lateral edge of the
pedicular line and the inverse is true for very thin individuals.
• The needle should be guided directly to this bony landmark and should touch bone before being further
advanced.
• A lateral image to ensure appropriate location of the needle tip along the laminae in this position is
suggested (Figure 67-3).
Figure 67-3. Lateral image diagram of lumbar spine anatomy.
• Once the needle tip is confirmed to be in this location, the needle is subsequently “walked off” of the
laminae and is advanced through the ligamentum flavum into the epidural space with loss of resistance
technique using the Luer-slip syringe with 2 to 3 cc of normal saline in the loss of resistance syringe, as
well as fluoroscopic visualization confirming midline spinal placement in AP view and placement of
the depth of the posterior epidural space on lateral view (Figure 67-4).
Figure 67-4. Loss of resistance.
• Lateral imaging can further confirm the location of the needle depth. Infusion of contrast dye could be
utilized to confirm posterior epidural spread, but is not always necessary in cases where intrathecal
needle tip placement is desired.
• This is the final needle position for epidural injection or epidural catheter placement.
For advancement to the intrathecal space:
• The needle is then advanced through the dura mater into the intrathecal space for single shot intrathecal
injection or for the purpose of intrathecal catheter placement.
• Placement into the intrathecal space should be confirmed by spontaneous flow of CSF via direct
visualization or aspiration and may be confirmed by visualization of the needle tip in the central spinal
canal on lateral imaging.
INTRATHECAL PUMP INFUSION SYSTEM TRIAL FOR PAIN

Intrathecal pump infusion system trials for pain are performed preceding permanent pump placement to
assess patient efficacy and tolerability. Both pain reduction and functional improvement measures allow
the clinician to determine efficacy and patient tolerability may be determined by both subjective measures
from the patient’s perspective and objective measures from the clinician’s perspective.
The objective measures include:
• The patient’s respiratory status and oxygenation
• Blood pressure stability
• Urinary status
• Bowel function status
• Physical functioning status with respect to strength and agility
• Absence or presence of allergic reaction to the medications delivered
Continuous infusion trial:
• Trialing has traditionally been performed in multiple formats.
• Some clinicians propose intrathecal trials, as they best simulate a permanent system via delivery of the
medications to the same spinal space.
• The potential negative adverse effect of performing continuous intrathecal trials is the high likelihood
of postdural puncture spinal headache that occurs upon discontinuation and removal of the trial catheter
from the intrathecal space.
• Other clinicians prefer continuous epidural infusion. Continuous epidural infusion does simulate
intrathecal pump system infusion.
• Clinically, it appears that there is no significant difference in outcomes between continuous intrathecal
and continuous epidural trial infusion and both simulate the permanent system with equal safety and
efficacy.
• One exception is the medication ziconotide, which, due to its high molecular weight, does not appear to
cross over from the epidural space into the intrathecal space and hence requires intrathecal trialing to
simulate its potential efficacy with respect to permanent pump placement.
Single-shot trialing:
• Finally, some clinicians prefer single-shot trialing for opiate trials.
• Single injections of morphine have been traditionally shown to be successful predictors of efficacy in
permanent systems.
• While intuitively the application of continuous administration of opiate via epidural or intrathecal
infusion may seem superior in detecting efficacy with respect to pain relief and improved function in a
patient whose pain may fluctuate within the day or on a day-to-day basis.
• The 2007 Polyanalgesic Consensus Conference (PACC) recommendations for pump trialing suggest
that there is a lack of comparative data in the literature to determine superiority of continuous trialing
of opiate versus single injection trialing.
• While the current trend is to look at functionality as a predictor of efficacy with scales such as the
Oswestry Disability Index, this can be challenging in the short period of time available for assessment
that is present during a single injection trial.
PATIENT SELECTION
Patients with chronic pain generally fall into 1 of 2 categories of pain types as defined by Dr Elliot
Krames. Most patients suffer from a predominance of either neuropathic pain or nociceptive pain.
• Those who suffer primarily from nociceptive pain generally respond more favorably to opioid
medications and thus are trialed with morphine when possible.
• Those who primarily suffer from neuropathic pain may respond better to nonopioid agents and thus are
often trialed with ziconotide.
• The specific mechanism of trialing may vary based on the medications being utilized. Continuous
infusion of opioids for the purpose of trialing can be done epidurally or intrathecally.
• The advantage of continuous epidural infusion trialing is the lack of postdural puncture headache that
occurs frequently after removal of the catheter in continuous intrathecal trials.
INTRATHECAL MEDICATIONS FOR PAIN

The FDA has approved the intrathecal use of morphine, ziconotide, and baclofen for use in humans.
• Morphine is mostly effective in individuals with nociceptive pain conditions.
• Ziconotide is primarily effective in patients with a predominance of neuropathic pain.
• Baclofen: Severe spasticity can be a painful phenomenon, and the use of intrathecal baclofen may
therefore provide pain relief in those with painful spasticity.
NON-FDA-APPROVED MEDICATIONS
Consensus guidelines for the use of intrathecal medications such as those coming from the
Interdisciplinary Polyanalgesic Consensus Conference in 2007 advocate the judicious use of certain non-
FDA-approved medications for individual use or in combination with FDA-approved intrathecal
medications or as single agents as follows:
• Hydromorphone, fentanyl, and sufentanil—any one of these individual opioids may be used alone or in
combination with other suggested nonopioid agents in the case of lack of efficacy or tolerability to
morphine.
• Bupivacaine—this anesthetic is utilized for neuropathic pain generally as an adjunct to an intrathecal
opioid such as morphine.
• Clonidine—this intrathecal agent is often utilized as an adjunct to an intrathecal opioid such as
morphine and is utilized for neuropathic pain conditions.
Clinical pearls for the use of non-FDA-approved suggested intrathecal agents:
• Hydromorphone—is often dosed at 10% of the corresponding effective dose of morphine. It has a side
effect profile similar to morphine.
• Fentanyl—this lipophilic agent is an opioid with intrathecal potency approximately 100 times that of
intrathecal morphine.
• Sufentanil—this highly lipophilic agent is approximately 10 times more potent than fentanyl. Fentanyl
has similar chemical characteristics and a similar side effect profile to that of sufentanil. Both
sufentanil and fentanyl, due to their highly lipophilic state, tend to provide pain relief at only 1 or 2
vertebral segments above or below the catheter tip and are, therefore, most effective in patients who do
not have widespread pain. Anatomic localization of the catheter becomes more critical in patients who
are known to have intolerability to morphine or hydromorphone and are expected to be utilizing
fentanyl or sufentanil in their permanently implanted system.
• Bupivacaine—weakness or urinary dysfunction are often associated with epidural or intrathecal
bupivacaine infusion. Patients receiving bupivacaine should be monitored for these side effects. These
side effects are reversible upon the discontinuation of the bupivacaine.
• Clonidine—this drug potentially has opioid sparing effects in its treatment of neuropathic pain and may
reduce blood pressure. Patients should be carefully monitored for hypotension. Just as with
discontinuation of clonidine orally, discontinuation of clonidine infusion can lead to hypertension,
withdrawal or more serious complications, and should be titrated downward prior to complete
discontinuation.
• Baclofen—if continuous baclofen infusion is utilized in a trial setting, the infusion should be weaned
downward rather than discontinued abruptly due to the risk of seizure with abrupt baclofen
discontinuation.
• Other agents—other agents utilized in an intrathecal pump infusion system.
• Injectable saline—may be utilized for flushing of the pump or catheter and can be utilized for
continuous infusion.
TRIALING VIA CONTINUOUS EPIDURAL INFUSION OF

OPIATES
Equipment for needle placement (Figure 67-5):
Figure 67-5. Tools for trialing: Tuohy needle, syringe, filer, and cap. (Reproduced with permission from
MILA International, Inc.)
• Tuohy needle—16- or 17-gauge 3- to 6-in (based on body habitus)

• 10-cc syringe for local anesthetic medications
• 5-cc syringe for contrast dye
• 10-cc syringe for medication infusion
• Luer-slip loss of resistance syringe (10 cc)
• Connector (extension) tubing with stop cock
• Sterile preparation materials
Equipment for continuous epidural infusion (all of the above plus):
• Epidural catheter connector piece
• Epidural catheter 1 size smaller than the gauge of the Tuohy needle
• Antibacterial filter
• 1 catheter end cap
• Tunneling device
• Steri-strips
• Skin preparation
• Antimicrobial agent (iodine povacrylex and isopropyl alcohol or chlorhexidine gluconate may be used)
PROCEDURE OF NEEDLE PLACEMENT

• Needle placement will be performed with a Tuohy needle via the technique described as “Paramedian
Technique for Interlaminar Placement of Needle.”
• After placement and confirmation of needle placement in the posterior epidural space via the
“Paramedian Interlaminar Needle Placement Technique,” an epidural catheter is directed through the
spinal needle and guided through the posterior epidural space in a caudad to cephalad trajectory.
• Lateral imaging on fluoroscopy can confirm that the catheter remains posterior relative to the spinal
canal and AP imaging under continuous or intermittent views allows steering of the catheter from a
medial to lateral perspective as the catheter advances in a cephalad direction to its desired location
Figure 67-6. Epidural trial.
Figure 67-7. AP image.
• After the catheter tip is placed at its desired location, the catheter should be checked for flow and
catheter integrity by placing the connector and filter onto the end of the catheter and infusing 1 to 2 cc
of contrast dye (or saline if there is a dye allergy).
• Lateral imaging should always be performed at this point to confirm that the catheter tip is indeed in the
posterior epidural space.
• The catheter tip should be located medial to the medial pedicular line in order to avoid placement
adjacent to the spinal nerve root at that segment.
• Then, the connector and filter must be unattached for needle removal and/or if tunneling is desired
(Figure 67-8). If tunneling is desired, it would be performed at this step as described in the above
section titled “Tunneling of Catheters for Trialing.”
Figure 67-8. Epidural needle placement with catheter.
• When tunneling is completed and the Tuohy needle has been removed, then the catheter is confirmed to
be in its desired location by a final AP fluoroscopic image.
• Next, the catheter connector and filter are placed.
• Flush the catheter with a small volume solution, such as saline, to ensure catheter integrity, and an end
cap is placed until epidural infusion of opioid or combined agents is initiated.
Typical desired locations may be as follows:
• T10: Commonly utilized for back and leg pain from FBSS
• Sacrum: Common site for catheter placement for pelvic or rectal pain
• C3 or C4: Common location for catheter placement for head and neck pain
• T1: Often used for placement for mid-chest pain
Clinical pearls for catheter tip placement:
• Placement of the tip below the conus reduces the risk of spinal compression when intrathecal
granulomas develop.
• Lipophilic opioids such as fentanyl or sufentanil may not spread more than 1 or 2 vertebral segments
above or below the catheter tip and therefore will not control head and neck pain as well as back and
leg pain in the same individual.
TRIALING FOR OPIATES VIA CONTINUOUS INTRATHECAL
ADMINISTRATION OF MEDICATION
The efficacy of continuous epidural and continuous intrathecal trials with opiates appears to be similar
based on the literature review. The administration of opiates via continuous intrathecal infusion requires
significantly lower doses compared to epidural infusion and carries with it the possibility of postdural
puncture headaches and meningitis, both which tend to occur at a higher rate than with continuous epidural
infusion of opiates.
Procedure for Catheter Placement

• A Tuohy needle is placed via the “Paramedian Technique for Interlaminar Placement of Needle.”
• Once the needle is advanced through the dura and into the intrathecal space and free CSF flow is
observed, then an intrathecal catheter is passed through the needle into the intrathecal space and the tip
is steered to its desired location with the tip found to be medial to the medial pedicular line on AP
fluoroscopic imaging and localized in the spinal canal on lateral fluoroscopic imaging.
• If tunneling is to be performed, it would be performed via the technique described in “Catheter
Tunneling Technique for Trials.”
• After the desired catheter location is obtained and the Tuohy needle is removed, the catheter is checked
for flow integrity with the catheter connector and filter attached.
• Then, either the end cap is placed until intrathecal opioid administration is initiated.
• A 1- to 2-mL flush with normal saline of the catheter may precede end cap placement.
Single Shot Injection Opiate Trial

Some clinicians prefer single injection opiate trials to continuous infusion intrathecal or epidural
infusion.
• The advantage of a single injection is that there is potentially less risk of infection due to the lack of an
indwelling catheter.
• The obvious disadvantage is the short period of time available to make a comprehensive assessment,
not only of the patient’s response to pain, but also their potential improvement in functionality.
• The growing interest in assessing function: including gait and mobility, transfers including movement
into and out of the bed and chair, necessitates the importance in evaluating the response to spinal
delivery of opioids over a greater period of time in order to thoroughly assess function based on scales
such as the Oswestry Disability Index.
• Furthermore, since some patient’s pain fluctuates, not only throughout the course of a given day, but
from day to day, there may be some significant benefit to monitoring a patient’s response to pain over a
prolonged period of time (in days) with continuous epidural or intrathecal infusion of opiate.
Single Injection Trial Procedure for Opiate (Morphine)

• Tuohy needle is placed in the lumbar spine below the level of L2 (most typically at L2-L3 or L3-L4).
• Advance the needle into the intrathecal space via the technique outlined in “Paramedian Technique for
Interlaminar Placement of Needle.”
• Once achieving free flowing CSF, an intrathecal injection of morphine is performed. Dosing varies
greatly in the literature and is dependent on both the patient’s tolerance to opiates and pain demand.
• Resuscitation equipment, including oxygen and medications, should be immediately available in the
case of respiratory depression induced with a morphine injection.
• The patient should be monitored for several hours with respect to the potential positive effects of the
injected morphine, such as reduction in pain on a numeric pain score or visual analog score.
• The patient should also be assessed as to changes in functionality and comparison should be made
between preinjection gait, transfers and strength as compared to postinjection gait, transfers and
strength.
• Monitoring for adverse events and side effects should also be performed for several hours
postinjection.
• Common side effects would include those typical with administration of morphine, such as nausea,
vomiting, dizziness or lightheadedness, respiratory depression, sedation, confusion, somnolence, and
urinary retention.
• Itching is a common side effect and rash may be indicative of an allergy to the medication.
Post-Trial Considerations (for continuous epidural or intrathecal

infusions or single shot method)
• Respiratory depression may occur.
• Respiratory status should be closely monitored with oxygen at the bedside and pulse oximetry
monitoring.
• Meningitis may occur with intrathecal or epidural trialing and is most prevalent with intrathecal trials
and has been reported with single injection trials.
• Nausea and/or vomiting is a frequent side effect of opiates.
• Drowsiness or somnolence may occur.
• Blood pressure should be closely monitored as hypotension is a frequent side effect.
• Urinary retention may occur.
• Seizures and/or coma are an uncommon occurrence.
• Postoperative antibiotics during the course of injection are debatable and are not currently supported
by the scientific literature.
Other Adverse Events

• Bladder or bowel changes
• Paralysis
• Death
• Spinal headache
• Intrathecal hematoma
• Intrathecal abscess
• Discitis
• Injury to adjacent nerve root
• Skin infection including cellulitis and abscess
• Skin erosion
• Skin irritation or allergy to skin preparation
• Anaphylaxis from any medications utilized
• Allergy to hardware or other supplies utilized
• Catheter dislodgement (with continuous infusion)
TRIALING WITH ZICONOTIDE

Intrathecal trialing, as compared to epidural trialing of ziconotide, is necessary due to the lack of
transportation of the ziconotide molecule from the epidural to the intrathecal space, believed to be due to
its large molecular size and hydrophilic state of the molecule. Intrathecal trials are typically performed
via continuous infusion.
• The continuous infusion is proposed to be the superior trialing method by Dr David Caraway and Dr
Michael Saulino.1
• However, authors such as Dr Eric Grigsby,2 suggest that single-shot ziconotide trials are equally
predictive of long-term success of permanent pump implantation for ziconotide administration.
• According to Dr Allen Burton, et al,4 when comparing 3 methods of ziconotide trialing: continuous
infusion, bolus injection, and limited duration infusion, all 3 methods appear to be effective in
predicting patient response to long-term administration of ziconotide therapy and none prove to have
superior safety or efficacy given current scientific data.4
• Intrathecal ziconotide was developed with the purpose of treating opiate resistant neuropathic pain.
• It is a neuroactive peptide isolated from the conus magus snail, which appears to have efficacy in many
neuropathic pain conditions.
• It has been studied in FDA trials as a single agent and has more recently been studied in combination
with opiates for continuous infusion as seen by a study by Dr Timothy Deer, et al.3
Continuous Intrathecal Ziconotide Infusion

Continuous intrathecal infusion of ziconotide has been the most frequently reported method of trialing in
the literature to date. While starting doses of ziconotide for continuous infusion have varied from study to
study, a trend toward side effects occurring at higher infused doses has been identified.
• Most recently, Caraway et al have suggested a starting dose of 1.2 μg/d as compared to 2.4 μg/d as
seen in multiple previous trial results published.
• Dr Caraway’s 3-day titration schedule allows for a dose increase of 1.2 μg every 12 to 24 hours as
determined to be necessary by the clinician.
• Careful monitoring for side effects or adverse events is suggested.
• Typical ziconotide trials are performed in the hospital.
• Psychosis is a reversible, yet severe, potential side effect that may occur with escalating doses of
ziconotide and requires discontinuation of the trial.
• Management of the complications of psychosis, which may include lack of verbal response or
immobilized state, often includes admission to a psychiatric unit.
• The psychosis may take days to weeks to resolve completely.
• Other frequent side effects include nausea and vomiting (approximately 50% in some studies),
alterations in gait, somnolence, memory impairment or aphasia, and urinary retention.
• There does not appear to be any withdrawal symptoms with abrupt termination of ziconotide.
• It should be noted, however, that patients undergoing intrathecal trialing for ziconotide should either be
weaned off of their opiates preceding the trial or continued on their regular dose of opiate via oral or
transdermal administration during the course of the trial, so as to avoid opiate withdrawal.
• There does not appear to be any significant respiratory depression associated with ziconotide infusion.
Equipment for Needle Placement (as above in this chapter)

Procedure
• Placement of the Tuohy needle as described in “Paramedian Technique for Interlaminar Placement of
Needle” is performed first.
• After the needle is advanced into the intrathecal space, and CSF flow is obtained, the stylet is
removed, and the catheter is steered into the desired intrathecal location.
• If tunneling is to be performed, it should be performed as described in the section titled “Catheter
Tunneling Technique for Trials.”
• After completion of catheter placement, and ensuring proper catheter location and function, intrathecal
ziconotide infusion may begin.
• Trial length typically consists of 3 days or more of inpatient monitoring.
• Determination of efficacy is assessed by both improvements in pain and/or function.
• Monitoring includes nursing assessment of vital signs. Pulse oximetry if on opiates, mental and
cognitive status, urinary output and neurologic checks.
• Monitoring in an inpatient setting should occur at a minimum of 4 hour intervals.
• Adjustments in ziconotide dosing during the trial phase should be considered no more frequently than at
12 hour intervals.
• Slow upward titration appears to decrease the likelihood of significant side effects as most ziconotide
side effects appear to be dose dependant.
• After discontinuation of the trial, and removal of the catheter, the patient should be monitored for
postdural puncture headaches.
• Adverse events with intrathecal placement of catheters may occur and are similar to those referenced
under the section “Post-Trial Considerations” in the above opiate trialing section.
Limited Duration Infusion Trials of Ziconotide

A limited duration trial involves infusion of ziconotide via an external pump and is generally performed
over the course of a 1-hour time period.
• Typical infusion doses vary between 1 to 10 μg infusion of ziconotide into the intrathecal space during
this time frame.
• The patient is then assessed for response to the ziconotide via reduction in pain or improvement in
function over the following 4 hours.
• As with continuous infusion, monitoring for known side effects is imperative.
• The positive or negative effects of ziconotide from a limited duration infusion may persist for greater
than 24 hours.
• Limited evidence in the literature is available to suggest a specific length of time for which inpatient or
outpatient monitoring via the physician should be performed.
Equipment for Needle Placement (as above in this chapter)

• Externalized pump
Procedure for Continuous Infusion of Ziconotide

• Patients should be weaned from all spinal drugs prior to initiation of the infusion.
• Placement of a Tuohy needle via the “Paramedian Technique for Interlaminar Placement of Needle.”
• Once the needle tip is advanced into the intrathecal space, and CSF flow is obtained, then the catheter
is placed into the needle and steered into the desired location.
• If catheter tunneling is to be performed, it is performed as described in “Catheter Tunneling Technique
for Trials.”
• After catheter placement is completed and the function and continuity of the catheter has been
confirmed, then the limited duration infusion with an external pump and ziconotide dose typically
varies between 1 to 10 μg intrathecally over the course of 1 hour.
• After the 1-hour infusion, the intrathecal catheter is removed manually and patient monitoring continues
for a suggested minimum for 4 hours with the understanding that positive or negative effects of
ziconotide may persist for 24 hours.
• Any side effects or adverse events that are observed during the 4-hour monitoring period would
preclude discontinuation of patient monitoring until these effects subside.
Bolus Trials With Ziconotide by Single or Multiple Injections

• The obvious advantage of bolus trials involves the lack of necessity of an indwelling catheter for any
period of time.
• Bolus trials do appear to offer adequate efficacy with respect to the predictive value of response for
permanent pump placement as suggested by Dr Grigsby.
• Rosenblum et al reported in a randomized, double blind, placebo controlled trial, administration of up
to 4 intrathecal ziconotide injections with placebo being one potential injected substance.
• Other studies by Dr Grigsby involve administration of a single injection of 1 μg of intrathecal
ziconotide with visual analog scores assessed prior to the injection and 1 hour after the injection as
well as follow-up assessment occurring 24 hours after the injection.
• Subjective patient data was also collected to determine their satisfaction with pain relief as perceived
after the injection.
• Some patients in this trial who failed to achieve efficacy at 1 μg were later injected with 3 or 5 μg
doses.
• Monitoring included visual analog pain scores and significant reductions in pain combined with a lack
of intolerable side effects yielded a successful trial outcome.
Equipment for Single Bolus Trial (as above in this chapter)
Procedure of Single-Shot Trial of Ziconotide

• Place Tuohy Needle via the “Paramedian Technique for Interlaminar Placement of Needle.”
• Once the needle tip is advanced into the intrathecal space and free CSF is obtained, injection of the
ziconotide bolus is performed (bolus dosing in the literature varies between 1 μg and up to 50 μg with
typical doses between 1 and 5 μg).
• After bolusing, the needle is removed.
• The patient is carefully monitored for both efficacy and side effects with monitoring performed
typically over the first hour after the injection, and effects from a single bolus are often monitored for
as long as 24 hours postinjection.
• The potential for side effects or adverse events does not differ from those potentially occurring with
limited dose infusion or continuous infusion of ziconotide via catheter placement, with the exception
that catheter dislodgement could not happen and that the risk of infection or meningitis should be
minimal compared to risk seen with catheter placement.
POST-TRIAL CONSIDERATIONS (FOR CONTINUOUS

INTRATHECAL INFUSIONS OR SINGLE-SHOT METHOD)
• Psychosis commonly occurs during administration of ziconotide.
• Meningitis may occur with intrathecal trialing and has been reported with single injection trials.
• Nausea and/or vomiting is a frequent side effect.
• Blood pressure should be closely monitored.
• Postoperative antibiotics during the course of injection are debatable and are not currently supported
by the scientific literature.
Other Adverse Events

• Bladder or bowel changes
• Paralysis
• Death
• Spinal headache
• Discitis
• Skin erosion
• Catheter dislodgement (with continuous infusion)
INTRATHECAL BACLOFEN PUMP TRIALING FOR

SPASTICITY
Intrathecal baclofen pump implantation is utilized for patients with severe spasticity. Patient selection for
this modality includes those with spasticity who have one or more of the following criteria:
• Inadequate management of spasticity with physical modalities and oral spasticity agents.
• Intolerance to side effects associated with oral spasticity agents and failure of alternate modalities.
• Widespread, nonlocalized spasticity that cannot be managed with nonpharmacological modalities.
• Patient positioning challenges created by the spasticity.
• Informed consent with discussion of all possible risk or adverse events associated with the procedure.
• Preoperative planning of patient positioning based on their anatomy, degree of spasticity, and ability to
maintain prone positioning as some individuals may need to be trialed in a lateral decubitus position.
• Evaluation for allergy to baclofen, contrast dye or any of the components utilized in performing the
procedure or inherent in the system to be implanted.
• IV access and equipment for resuscitation including appropriate medications and oxygen should be
immediately available.
• Anticoagulation considerations should be discussed with the patient and dealt with in the preprocedure
clinical assessment.
• Body habitus should be assessed to determine the appropriate length of spinal needle necessary to
perform the procedure.
• Ashworth assessment on admission.
• For intrathecal shot trialing, the lumbar level chosen should be below the level of the conus (below
L2).
• Preoperative antibiotics should be considered for any patient with a presumed infection or infectious
risk or those undergoing catheter placement for continuous infusion.
• Urinary retention may worsen with intrathecal baclofen administration.
Equipment for Single-Shot Infusion (as above in this chapter)

Medications Used
• Baclofen 25, 50, 75, or 100 μg (dose chosen based on patient’s degree of spasticity and tolerance to
oral baclofen)
• 1% lidocaine
• Injectable saline
• Nonionic water-soluble contrast iopamidol
Considerations for Single-Shot Baclofen Injection

• Contraindications to iopamidol include:
Hypersensitivity to iodine containing preparations
Hypersensitivity to iodine contrast media
Severe renal disease
Multiple myeloma
Waldenstrom macroglobulinemia
Pregnancy
Postoperative antibiotics generally not needed for single shot trials
Needle Placement Technique

• A paramedian technique for interlaminar placement of the needle tip is suggested with lateral to
medial, caudad to cephalad, and posterior to anterior angling is utilized as described in the section
“Paramedian Technique for Interlaminar Placement of Needle.”
Technique for Delivery of Baclofen in Single-Shot Trials

• Administration of the 25, 50, 75, or 100 μg baclofen dose (50 μg most commonly utilized) through the
Tuohy needle with connector tubing.
• Pretrial and postinfusion monitoring of spasticity utilizing the Modified Ashworth Scale.
• Careful documentation of spasticity changes after administration of baclofen as well as evaluation of
gait, transfers and posture, and pre- and postinjection.
• Spasticity monitoring at 2 and 4 hours post single-shot dosing is commonly performed with careful
documentation of the above at these intervals.
• A 2-point reduction on the Modified Ashworth Scale with tolerability of the intrathecal baclofen is
generally considered favorable in assessment of the overall success of the trial.
Technique for Placement of Intrathecal Catheter for Continuous
Baclofen Infusion
First, needle placement as described in the section “Paramedian Technique for Interlaminar Placement of
Needle.”
• An epidural catheter of one size smaller than the needle gauge (one gauge number higher) should be
placed through the Tuohy needle (with stylet removed).
• Fluoroscopic visualization of the catheter initially exiting the tip may be assessed best in lateral view.
• Advancement of the catheter under AP view allows steering medially and laterally.
• The final position of the catheter tip should be at the midline and is often placed at the thoraco-lumbar
junction, although catheter tip placement may vary based on desired outcome.
• If tunneling of the catheter is desired, then the Tuohy needle should be left in place until tunneling is
performed.
Catheter Tunneling Technique for Trials

• The desired location for the tunnel exit site should be prepped and anesthetized with 1% lidocaine and
the projected course of the tunneled catheter should be anesthetized with lidocaine subcutaneously.
• The projected exit location of the tunneled catheter is usually positioned several inches lateral and
slightly inferior to the Tuohy needle site.
• A small stab incision with a 15-blade scalpel at the projected exit site of the tunneled catheter may be
placed into the anesthetized skin prior to the tunneling device introduction.
• The tunneling device may then enter through this stab incision and is directed subcutaneously, just
below the dermis, through the projected tunnel and over to the Tuohy needle.
• The tunneling device should then be directed so that the sharp end of the device exits the stab incision
made for the Tuohy needle.
• The sharp end of the tunneling device then lies adjacent to the Tuohy needle where the needle enters the
skin.
• The sharp center hardware of the tunneling device is then extracted from the outer sheath of tunneler.
• Carefully remove the Tuohy needle while maintaining slight forward pressure on the catheter so as not
to withdraw it from its desired location.
• Guide the catheter from the Tuohy needle skin site through the sheath of the tunneler and through the exit
site.
• Once the catheter tip extends beyond the tunnel exit site, pull the outer sheath of the tunneling device
out of the tunnel—leaving the catheter within the tunnel.
• Pull any additional catheter slack outward so that the catheter is taut and the entire catheter is
positioned below the skin level through its course over to the exit site.
• Close both 15-blade stab wound sites with steri-strip.
• Proper catheter flow should then be tested by placing the catheter hardware connector and filter onto
the catheter end and then infusing injectable saline or contrast of 1 to 2 cc thereby ensuring proper flow
into the epidural space.
• The use of contrast infusion for catheter integrity testing may be considered to ensure proper flow and
ensure that the catheter is free of any leaks.
• The catheter should then be flushed with saline and the filter end capped until the intrathecal baclofen
continuous infusion is initiated.
Post-Trial Considerations
• Respiratory depression may occur.
Respiratory status should be closely monitored with oxygen at the bedside and pulse oximetry
monitoring.
• Meningitis may occur with intrathecal or epidural trialing and is most prevalent with intrathecal trials.
• Nausea and/or vomiting is a frequent side effect of intrathecal baclofen administration.
• Blood pressure should be closely monitored as hypotension is a frequent side effect of intrathecal
baclofen administration.
• Seizures and/or coma may occur.
• Careful monitoring and notation of cognition, alertness, and basic vital signs should be performed
every 30 minutes for the first 4 hours postbaclofen injection and then at least every 2 hours between
hours 4 and 8 postinjection.
• Oral intake of food and liquid should not be resumed until the patient is shown to have adequate
alertness and cognition and at least 2 hours has passed since the single shot baclofen injection
• Postoperative antibiotics during the course of injection is debatable and is not currently supported by
the scientific literature.
Other Adverse Events for Single-Shot Trial

• Bladder changes
• Paralysis
• Death
• Spinal headache
• Discitis
• Skin erosion
• Catheter dislodgement
References
1. Caraway D, Saulino M, Fisher R. Intrathecal therapy trials with ziconotide, a trialing protocol before
initiation of long-term ziconotide intrathecal therapy is presented. Practical Pain Management.
2008;8:53-56.
2. Michiels W, McGlthlen G, Platt B, and Grigsby E. Trigeminal neuralgia relief with intrathecal
ziconotide. Clinical Journal of Pain. 2011;27(4):352-354.
3. Deer TR, Kim C, Bowman R, Tolentino D, Stewart C, Tolentino W. Intrathecal ziconotide and opioid
combination therapy for noncancer pain: an observational study. Pain Physician. 2009 Jul-
Aug;12(4):E291-6.
4. Burton, et al. Considerations and methodology for trialing ziconotide. Pain Physician. 2010;13:23-33.
ISSN 1533-3159.
Suggested Reading
Burton AW, Deer TR, Wallace MS, Rauck RL, Grigsby E. Considerations and methodology for trialing
ziconotide. Pain Physician. 2010 Jan;13(1):23-33.
Deer TR, Kim C, Bowman R, Tolentino D, Stewart C, Tolentino W. Intrathecal ziconotide and opioid
combination therapy for noncancer pain: an observational study. 2009;12:E291-E296.
Willis KD, Doleys DM. The effects of long-term intraspinal infusion therapy with noncancer pain
patients: evaluation of patient, significant-other, and clinic staff appraisals. Neuromodulation:
Technology at the Neural Interface. 1999 Nov;2(4):241-253.
CHAPTER 68
Permanent Implant
Sean Li and Peter S. Staats
INTRODUCTION
The use of intrathecal opioids dates back to August 16, 1898, when August Bier and his assistant
Hildebrandt performed “cocainization of the spinal cord” on each other. Unfortunately, Bier was also the
first to describe the complication of postdural puncture headache from his personal experience. The
mechanism of opioids on the spinal cord was later confirmed in a rat model.1 Subsequently, intrathecal
medication has been widely utilized for both anesthesia and analgesia. The use of implantable intrathecal
drug delivery systems began in the early 1980s and is now indicated for use in patients with persistent
chronic pain of malignant and nonmalignant origin that are either refractory to maximal medical therapy or
dose limited due to significant side effects, and has been demonstrated to have a better side effect profile
than systemic opiates alone.2 In addition, non-narcotic medications that can have minimal analgesia when
administered systemically can be very effective when administered intrathecally.3
INDICATIONS
• Chronic intractable pain
• Malignant and nonmalignant in origin
• Refractory pain to maximal systemic medical therapy
• Dose limiting side effect to systemic medical therapy
• Intractable spasticity
AVAILABLE MEDICATIONS
• Medications may be compounded to suit individual needs
• Medications may be used individually or compounded in combination therapy
• FDA approved and off-label medications (Table 68-1)
TABLE 68-1. List of Medications Used in Intrathecal Pumps. Currently the Only Three
FDA Approved Medications are: Morphine, Baclofen, and Ziconotide. These Medications
Can be Delivered Individually or Compounded for Combination Therapy (Deer et al,
2012)
RELEVANT ANATOMY
The preferred catheter insertion site is below the conus medullaris, usually located at vertebral levels L1-
L2 (Figure 68-1A). The catheter is anchored to the lumbodorsal fascia to prevent migration. The pump is
usually placed in the left or right lower quadrant of the abdomen in the subcutaneous fat between the
inferior costal margin and iliac crest. One may consider placing the pump in the subfacial space between
the external and internal abdominal oblique muscles in the young and/or thin patients for decreased risk of
wound breakdown and improved cosmesis (Figure 68-1B).
Figure 68-1. (A) Anatomy for needle insertion. (B) Diagram illustrating the location of IT pump.
Basic Prerequisites
• Patient has tried and failed maximal systemic pain control
Uncontrolled pain on maximal systemic medications
Uncontrolled side effects with systemic medications
• Successful intrathecal trial
Methods of Trial for Intrathecal Pump

• In-patient continuous intrathecal catheter infusion.
• In-patient continuous epidural catheter infusion.
• Single or repeated epidural injections
• Single or repeated intrathecal injections
Basic Concerns and Contraindications

• Psychological evaluation to rule out secondary gain issues
• Comorbidities
• Anticoagulation therapy
• Immunocompromised condition and high risks for infection
Patients being considered for intrathecal drug delivery pump therapy should have a multidisciplinary care
team which ideally includes a primary care physician, a pain psychologist, and a pain management
specialist. Those who fail maximal systemic therapy or have dose-limiting side effects should undergo
intrathecal trial via a single bolus lumbar puncture or an external drug delivery system through a
temporary intrathecal catheter. Concurrently, noncancer or nonterminally ill patients should have a
thorough pain psychology evaluation to rule out any potential secondary gain issues and/or untreated
psychological comorbidities. Prior to placement of permanent intrathecal drug delivery pump, patients
should undergo the necessary preoperative anesthesia evaluation. For patients who are taking
anticoagulation medications, follow the latest American Society of Regional Anesthesia and Pain
Medicine (ASRA) guidelines for neuraxial techniques. Finally, patients should have a clear understanding
of potential complications and intrathecal drug side effects.
Pump pocket site should be marked with consideration for patient comfort, activities, belt lines, rib
margins, wheelchair arms, and prostheses.
Editor’s Pearls
Prior to coming to the operating room, I like to place a nonsterile dummy pump on the abdomen to assess
the patient’s tolerance for the device relative to their belt line, rib margin, and iliac crest. It is marked
preoperatively.
Optimal pump position (Figure 68-2)
Figure 68-2. Optimal pump position.
• Superior to iliac crest.

• Below costal margin.
• Away from belt line.
• Avoid areas of previous incisions and/or radiation.
• Catheter access port should be oriented uniformly to facilitate pump refill.
• Obese patients should have pump pocket position marked in the standing position to account for
movement of large panniculus.
Patient Position
• Patient is placed in the lateral decubitus position allowing for simultaneous access to both the patient’s
lumbosacral spine and abdomen.
• The patient’s back should be perpendicular and their spine should be parallel to the floor.
• The fluoroscopy compatible surgical table is slightly flexed at the hip to further open up the space
between the patient’s rib cage and pelvic brim giving greater exposure to the abdomen for pump pocket
placement.
• The patient’s arms are placed slightly above their head to allow for C-arm access and pillows are
placed between the arms to alleviate pressure points.
• The legs are slightly flexed and padded to avoid pressure points.
• The entire abdomen and lumbosacral spine is prepped with antiseptic solution and draped with a large
Ioban dressing (3M, Minneapolis, MN) for added sterility (Figure 68-3).
Figure 68-3. Proper positioning of the patient allows for access to both intrathecal catheter placement in
the lumbosacral spine and pump placement in the anterior abdomen. (Used with permission from Dr. M.
Bottros and Dr. K. Williams, Blaustein Interventional Pain Treatment Center, Johns Hopkings Univeristy,
Baltimore, MD.)
Fluoroscopic Views
Fluoroscopic guidance should be utilized for all intrathecal catheter placements to ensure patient safety
and to verify the anatomic location of the catheter. A C-arm fluoroscope is sterilely draped and positioned
in the cross-table anteroposterior (AP) configuration during the case. This allows for C-arm access for
both AP and lateral views during the procedure. The position of the image intensifier can be positioned
either at the patient’s abdomen or back. Placement of the larger image intensifier at the abdomen allows
for added room behind the patient for placement of the intrathecal catheter, however, this configuration
may create increased scatter radiation for the surgeon and operating room staff.
Equipment
There are now multiple commercially available intrathecal drug delivery pumps include programmable
(SynchroMed II, Medtronic, Minneapolis, MN, and Prometra, Flowonix, Mt. Olive, NJ) and constant
flow (Codman 3000, Johnson and Johnson, Raynham, MA). The programmable SynchroMed II or
Prometra pump offers the versatility of dose adjustments via telemetric flow control without having to
replace the medication within the reservoir but its usage is limited by the battery lifespan (5-10 years).
Constant flow configuration of the multiple nonprogrammable pumps offers unlimited usage due to its
contained propellant design but dose adjustments require replacement of remaining drug with a refill of a
different concentration. The manufacturers offer models with various reservoir volumes ranging from 16
to 40 mL. Choice of equipment should be based on the individual medication requirements of the patient
and personal patient preference (Table 68-2).
TABLE 68-2. Comparison of The Two Commercially Available Intrathecal Delivery

Pumps
Anesthesia
The operation can be successfully performed under general anesthesia, regional anesthesia or local
anesthesia with sedation. Anesthesia with sedation allows for direct patient feedback during catheter
placement, which may help alert the surgeon of potential nerve or spinal cord injury; however, in certain
cases, patients cannot tolerate lumbar and abdominal incisions without a deeper level of sedation.
Implantation Technique
The pump implantation procedure is described in 6 simplified steps as follows:
• Accessing the intrathecal space
• Anchoring the catheter
• Creating the pump pocket
• Tunneling the intrathecal catheter
• Pump placement and catheter connection
• Wound closure and dressing
Once the patient is anesthetized or adequately sedated, a single prophylactic dose of parenteral
antibiotic is given within 60 minutes of incision.
Accessing the Intrathecal Space
• Under direct fluoroscopic guidance, the patient’s L3-L4 intervertebral space is located with
fluorography in the AP view.
• The overlying skin is infiltrated with a local anesthetic (we prefer 1% lidocaine with 1:200,000
epinephrine) with a 25-gauge needle.
• May elect to access the intrathecal space percutaneously with the 14-gauge Tuohy needle first then
create the necessary skin flaps by making a vertical incision that incorporates the needle site.
• We prefer to make the vertical paramedian skin incision prior to accessing the intrathecal space. A 3-
to 4-cm vertical paramedian incision is made over the L3-L4 intervertebral space.
• Once the skin is incised sharply with a skin blade, the dissection is carried down to the lumbodorsal
fascia with electrocautery and blunt dissection.
• Dissection is carried out laterally 1 to 2 cm to the lumbodorsal fascial plane to create small tissue
flaps and have adequate space for the anchor and excess catheter.
• Meticulous hemostasis should be obtained at this point.
• The skin is retracted with a Weitlaner self-retaining retractor.
• Next, the intrathecal space is accessed by shallow paramedian approach with a 14-gauge Tuohy
needle.
• The shallow angle of the paramedian approach reduces the potential for shearing or excess stress on
the catheter, minimizes catheter kinking, and facilitates advancing the catheter to the desired level.
• Subarachnoid position of the needle is confirmed radiographically and clinically with positive return
of cerebral spinal fluid (CSF).
• The Tuohy needle bevel is then turned cephalad, the stylet is removed and the catheter is quickly
inserted into the needle to minimize CSF leakage.
• Under live fluoroscopic guidance in the AP view, the catheter is advanced to the desired vertebral
level.
Editor’s Pearls
Minimize nerve root trauma during intrathecal needle insertion by avoiding muscle paralysis. This should
be discussed with the anesthesiologist prior to induction of general anesthesia.
Anchoring of Catheter
Once the catheter is placed, the intrathecal pump should be prepared on the back table by filling it with
the desired medication and allowing adequate time for the pump to prime.
• Before the Tuohy needle is removed, a purse string suture is made within the lumbodorsal fascia and
loosely placed around the Tuohy catheter complex. We prefer a nonabsorbable braided suture such as
an O-TiCRON (Covidien, Mansfield, MA) or O-Ethibond (Ethicon, Piscataway, NJ).
• Before the guidewire and Tuohy needle are completely withdrawn, the purse string suture is tied down
snug. This may decrease CSF leak around the catheter.
• Next the Tuohy needle and catheter guidewire are carefully removed while keeping the catheter in
place.
• Proximal catheter position is checked with fluoroscopy and a small clamp is placed at the distal tip to
prevent further CSF leakage.
• The catheter is then anchored to the lumbodorsal fascia using premade anchoring devices that are
supplied by the pump manufacturer.
• The anchor is first carefully secured to the catheter with the same nonabsorbable braided O suture and
then catheter-anchor complex is sutured to the lumbodorsal fascia.
Creating the Pump Pocket
• The pump pocket is made by first infiltrating the skin over the planned pocket site with local anesthetic.
• Using a skin blade, an 8-cm horizontal incision is made at the superior aspect of the pocket.
• Care should be taken to avoid a position too close to the rib margin. Typically 3 to 4 cm below the rib
margin is sufficient.
• This incision is dissected to a depth of approximately 1.5 cm into the subcutaneous tissue with both
electrocautery and blunt dissection.
• The pump pocket should be no more than 2.5 cm deep allowing for future programming and medication
refill.
• Keeping parallel to the skin, a pocket is created with sharp and blunt dissection. One may use the pump
as a template of pocket size.
• Meticulous hemostasis should be maintained.
Tunneling the Intrathecal Catheter
• Once the pump pocket is created, the intrathecal catheter is tunneled laterally from the insertion site to
the abdominal wall, where the pump will reside.
• A malleable tunneling device is carefully tacked in the subcutaneous plane from the abdominal incision
toward the back incision.
• It is imperative to keep the tunneling trocar superficial in the subcutaneous tissue or risk major
vascular and/or bowel injury.
• Avoid placing tunneling device in subcutaneous plane to minimize the risks of penetration through skin.
• The catheter is fed through the tunneling device and trimmed to the appropriate length.
• A gentle strain relief loop is created at the catheter insertion site.
• Catheter position should be verified radiographically and clinically with positive CSF return.
Pump Placement and Catheter Connection
• Final catheter length should be recorded as part of the standard pump parameters.
• After the catheter is properly connected to the pump, excess catheter is coiled deep to the pump.
• One may elect to use a Dacron pouch around the pump to encourage fibrosis and prevent pump
migration or flipping.
• We prefer to secure the pump directly to the external abdominal fascia with interrupted nonabsorbable
braided suture through prefabricated anchors found on the pump.
Wound Closure and Dressing
• Prior to wound closure, both incisions are irrigated with warm antibiotic impregnated saline solution.
• The incisions are closed in a layered fashion.
• Use absorbable 1-O Vicryl for inverted interrupted sutures at the deep fascial layer.
• Followed by 3-O Vicryl at the subcutaneous layer.
• The skin is closed with a running subcuticular 4-O monocryl suture.
• The closed incision is reinforced with tissue glue and left open to air.
• If programmable pump is used, the appropriate settings are verified through telemetry.
• Patient is woken up, and taken to the recovery room for postoperative monitoring and safe discharge to
floor or home.
POSTPROCEDURAL FOLLOW-UP
Most pump implantation patients are discharged home on the same day but one may elect to admit patients
with complex comorbidities overnight for observation. Close monitoring should be provided for
incisional bleeding and/or infection. All post-implant patients should be followed up with wound checks
and possible suture/staple removal within 2 weeks of surgery. Patient will require several follow-up
appointments for titration of intrathecal medication dosage.
• Acute postoperative complications
CSF leak
Postdural puncture headache
Wound infection
• Catheter-related complications
Kinking
Breakage
Granuloma
• Medication-related complications
Respiratory depression
Sedation
Pruritus
Constipation
Urinary retention
Nausea/vomiting
Sweating
Hypogonadism
Decreased libido
• Long-term complications
Pump failure
Displaced catheter
Cracked or kinked catheter
Human error in programming
PITFALLS AND CLINICAL PEARLS

• Accessing the intrathecal space below, the level of the conus medullaris will minimize spinal cord
injury.
• Keeping the needle bevel parallel to the spine at dural entry may help minimize future CSF leak.
• Placement of catheter tip near the spinal level of pain complaints will keep looking for proof in
literature.
• Prelubricating the guidewire with saline may help during removal.
• Keeping the catheter and guidewire straight during removal will prevent damage to the catheter.
• Leaving the Tuohy in place while making the purse string stitch prevents inadvertent catheter damage
from the suturing needle.
• Keeping the guidewire in distal catheter while tightening the purse string suture.
• Avoid withdrawing the catheter through the Tuohy needle to avoid shearing of the catheter.
• Keep pocket parallel to skin to avoid slanted pump position or pump flipping.
• Avoid making the incision over the final pump position.
Suggested Reading
Cohen S, Dragovich A. Intrathecal analgesia. Anesthesiol Clin. 2007;25:863-882.
Coombs D, et al. Continuous epidural analgesia via implanted morphine reservoir. Lancet. 1981;2:425-
426.
Deer T, Krames ES, Hassenbusch S, et al. Management of intrathecal catheter-tip inflammatory masses:
an updated 2007 consensus statement from an expert panel. Neuromodulation. 2008;11:77-91.
Deer TR, Levy R, Prager J, et al. Polyanalgesic Consensus Conference 2012: recommendations to reduce
morbidity and mortality in intrathecal drug delivery in the treatment of chronic pain.
Neuromodulation. 2012;15:467-482.
Deer TR, Prager J, Levy R, et al. Polyanalgesic Consensus Conference 2012: recommendations for the
management of pain by intrathecal (intraspinal) drug delivery: report of an interdisciplinary expert
panel. Neuromodulation. 2012;15:436-466.
Follett KA, Burchiel K, Deer T, et al. Prevention of intrathecal drug delivery catheter-related
complications. Neuromodulation. 2003;6:32-41.
Horlocker T, Wedel DJ, Rowlingson JC, et al. Regional anesthesia in the patient receiving antithrombotic
or thrombolytic therapy: American Society of Regional Anesthesia and Pain Medicine Evidence-
Based Guidelines. 3rd ed. Reg Anesth Pain Med. 2010;35:64-101.
Kopell BH, Sala D, Doyle WK, et al. Subfascial implantation of intrathecal baclofen pumps in children:
technical note. Neurosurgery. 2001;49:753-757.
Onofrio B, Yaksh T, Arnold P. Continuous low-dose intrathecal morphine administration in the treatment
of chronic pain of malignant origin 1981. Mayo Clin Proc. 1981;56:270-271.
Patel V, Manchikanti L, Singh V, et al. Systematic review of intrathecal infusion systems for long-term
management of chronic non-cancer pain. Pain Physician. 2009;12:345-360.
References
1. Yaksh T, Rudy T. Analgesic mediated by a direct spinal action of narcotics. Science. 1976;192:1357-
1358.
2. Smith TS, Staats PS. Reply to commentaries on “Randomized clinical trial of an implantable drug
delivery system compared to comprehensive medical management for refractory cancer pain: Impact on
pain, drug-related toxicity, and survival.” J Clin Oncol. 2003;21:2802-2803.
3. Staats PS, Yearwood T, Charapata SG, et al. Intrathecal ziconotide in the treatment of refractory pain in
patients with cancer or AIDS: a randomized controlled clinical trial. JAMA. 2004 Jan 7;1:291.
SECTION VIII
NEUROAUGMENTATION TECHNIQUES
CHAPTER 69
Spinal Cord Stimulation: Hardware Specifications

Sudhir Diwan, Karina Gritsenko, and Neel Mehta
INTRODUCTION
Spinal cord stimulation (SCS) offers hope to the estimated 75 million people who suffer from chronic
pain. SCS sends electrical impulses that trigger nerve fibers selectively in the dorsal column based on the
“gate control” theory. This interruption of pain signals traveling to the cerebral cortex causes feelings of
pleasant and soothing tingling and paresthesia replacing the painful sensation of pain. Most commonly,
SCS is utilized for the treatment of chronic neuropathic pain of the back, trunk, or extremities.
Specifically these conditions include postlaminectomy syndrome, complex regional pain syndrome,
diabetic neuropathy, as well as other off label uses have had great success with the SCS. SCS has
successfully relieved pain in thousands of patients with severe chronic painful conditions.
Neuroaugmentation techniques have become increasingly popular in the specialty of interventional pain
medicine due to its wide variety of on-label and off-label applications. Most products are manufactured
by Medtronic, St. Jude Medical, and Boston Scientific, and have been undergoing continuous evolution.
Competition and innovation in the industry has led to advanced technology allowing for variable
programming and smaller sizes to make it physically acceptable to patients. For example, the old leads
with 4 electrodes, also known as contacts, have been replaced by leads with 8 electrodes. Currently,
predominantly cylindrical leads are used for percutaneous trials and paddle leads for laminectomy
procedures. Now thinner paddle (surgical) leads, previously implanted exclusively with a laminotomy
and surgery, are now being implanted percutaneously. Although the basic device works on the principles
of the “gate control” theory, each company offers products with unique advantages.
The advantages of SCS therapy include:
• It is a nonpharmacologic option to control chronic pain.
• By avoiding medications, there are no psychosocial or medicolegal implications related to drug abuse,
addiction, or tolerance.
• The system is reversible and can be removed without any harm to the patients, unlike spine surgeries
that cannot be reversed.
• The SCS can be programmed based on the chronic pain severity and location of pain.
• Patient has ability to use multiple programs as desired for different situations, including fully turning a
device off or on.
• As pain location, quality, or characteristics may change, there is an opportunity for regulation of
electrodes to adapt to lead migration, or new location and quality of pains.
INDICATIONS FOR SCS
Chronic, intractable pain of the trunk and/or limbs, including unilateral or bilateral pain associated with
various conditions.
On-label indications are:
• Failed back syndrome (FBS) or low back syndrome or failed back
• Radicular pain syndrome or radiculopathies resulting in pain secondary to herniated disk
• Degenerative disk disease (DDD) refractory to conservative and surgical interventions
• Complex regional pain syndrome (CRPS) I or RSD
• Complex regional pain syndrome II or causalgia
• Epidural fibrosis
• Arachnoiditis
Off-label indications are:
• Extremity pain due to ischemia
• Angina resistant to other therapies
• Chronic headache not responding to other treatments
• Typical and atypical facial pain
• Postsurgical neuropathies (postherniorrhaphy, post-thoracotomy syndrome)
• Abdominal visceral pain
• Pelvic visceral pain
• Vulvodynia
• Rectal pain
• Peripheral neuropathy (diabetic or metabolic)
• Peripheral entrapment neuropathy
THE COMPONENTS OF THE SCS DEVICE

The basic components of a spinal cord stimulator include:
• Leads
• Anchors
• Connecting extensions
• Implantable pulse generators (IPG) or battery
• Programmer
• Charger
Typically, epidural leads are anchored to lumbar fascia to minimize lead migration, and then connected
to IPG directly or via connecting extensions. These pulse generators contain programmable elements of
the system and specific battery life of the device. The IPG is either nonrechargeable (conventional) or
chargeable. Nonrechargeable is also referred as primary cell battery. The implantable pulse generator is
also referred as battery or neurostimulator.
The major components of the stimulator system will be discussed below with comparison of products
of the 3 major companies: Boston Scientific, St. Jude Medical, and Medtronic including some of the
indications, advantages, and disadvantages of each system.
Epiducer lead delivery system: It simplifies the multiple lead placements:
• Allows to percutaneously insert S-lead-paddle that normally would require laminectomy.
• Allows to configure patient-specific multiple lead arrays.
SCS Leads
Depending on whether the physician is implanting the SCS leads for a trial temporarily or permanently,
the terminology referring to the lead is as a “trial lead” or a “permanent lead.” However, both leads are
essentially the similar product. The selection of leads depends on source of pain, complexity of pain
generators, physician preference and ability, and comorbidities.
Percutaneous or Cylindrical Leads

Overview
• These are cylindrical insulated catheters with multiple sequential electrodes with variable spaces
mounted near the distal end.
• Used as trial or permanent leads.
• The octrodes have 8 electrodes and quads have 4 electrodes mounted.
• The leads may vary in length, number of electrodes, spacing between contacts and diameter.
• Leads can be implanted through a needle and may not need a large surgical incision.
• The percutaneous leads are faster and easier to place.
• They are more prone to migration than paddle leads, which are placed surgically.
• The cylindrical electrodes are less energy efficient due to circumferential energy dispersion.
• 360-degree stimulation of cylindrical leads can lead to painful areas of stimulation along the posterior
epidural space.
Due to increased number of electrodes in one lead, the programming of electrode configurations and
ability to steer stimulation have expanded.
Spacing of the percutaneous leads: 4 or 8 individually current controlled contacts per lead spaced apart
depending on the number of contacts on a single lead. Usually, for a quad lead the spacing is 7 to 9 mm
and for octad 4 to 5 mm allowing twice the contacts within the same “quad” spacing for precise targeting
by a single lead (Figure 69-1).
Figure 69-1. Contacts spacing. A, quad lead with 9-mm-wide spacing; B, octad with 4-mm compact
spacing. (Image courtesy of Boston Scientific Corporation.)
The octad leads:

• A percutaneous octad lead with 8 contacts is used for single and dual lead placement and
configuration.
• Octad leads cover 2 or more vertebral segments, helping to optimize pain coverage.
• They provide electronic “repositioning” to manage changes in stimulation coverage due to vertical
lead movement.
• They provide the longest contact span and most spacing options.
• Percutaneous leads may be configured to create simple or complex contact arrays, utilizing up to 2
leads for one IPG.
Surgical or Paddle Leads

Overview
• Wide variety of designs, that provides multiple options.
• Paddle leads are flat, with insulated back and sides force current to flow anteriorly toward the dorsal
column.
• These leads are larger, and require a surgical incision as well as a laminotomy for placement, due to
the larger size and shape.
• A single column paddle lead can be placed percutaneously without a laminotomy by a specifically
designed introducer called the Epiducer lead delivery system.
• The surgical leads are less prone to migration than percutaneous leads.
• The flat shape with insulated back and sides makes them more energy efficient due to unidirectional
energy penetration, leading to longer battery life.
• The placement of leads requires a surgical procedure, and often requiring a laminotomy.
• It is not possible to trial a surgical lead percutaneously.
• Often, paddle leads are used for more complicated pain patterns and spinal anatomy.
Surgical leads are typically used for permanent lead placement, but the exception to the rule may be
when difficulty encountered accessing the epidural space.
Surgical Leads
1. Single-column paddle leads
• These leads offer benefits of paddle leads in a steerable, low profile design with extensive lead
configuration and placement options.
• Narrowest paddle available can be placed through a small laminotomy procedure, which is steerable
and provides easier insertion and reduced trauma to soft tissue and bony structures.
• Flexible, styleted paddle tip is designed to enhance steering and control.
• Insulation on 3 sides to provide an efficient, unidirectional electrical field, which focuses the
stimulation on the neural target and decreases power requirements.
• Can be combined for multiple lead configurations.
2. Two-column paddle leads
• Insulated on 3 sides to provide unidirectional stimulation for enhanced precision in energy delivery
and greater system longevity. Can be configured with other paddle leads to manage complex pain
patterns.
• Narrow leads and curved designs help facilitate midline placement and stability.
3. Three-column paddle leads
• Transverse tripolar array designed to overcome anatomical challenges and provide control in shaping
the stimulation field.
• Three columns of electrodes provide anodal blocking to confine stimulation to the midline and can be
used for hard-to-cover back pain, may create transverse tripolar array.
• Narrow leads for smaller anatomy and placement flexibility. Anatomically curved designs help
facilitate midline placement and stability.
4. Five-column (penta) paddle leads
• Smallest contacts in a five-column array for precise field control and broad lateral coverage.
• Designed to enable selective nerve fiber stimulation and predictable dermatomal activation, it
provides enhanced control for coverage of complex, multifocal pain. Broad lateral contact span
designed to accommodate anatomical asymmetries as well as placement variability.
• Small contact size designed to focus current for enhanced specificity.
• Wide-spaced leads and compact-spaced leads.
Selection of Leads
Each lead, whether cylindrical or paddle, has at least 4 contacts, but a lead can contain as many as 16
contacts. The number of contacts used depends on the condition being treated as well as the physician’s
preference. For example, more complex pain patterns, such as those involving more than one area and
more than one extremity (arms and/or legs), involve more nerve structures will require two octad leads.
Thus, additional leads with more contacts may often be required to stimulate all of these structures.
Implanting a single lead with fewer contacts than you need may result in less pain relief. In fact, many
physicians believe that it is best to implant extra contacts to make up for the unexpected change in the
intensity and location of, and for potential migration of lead/leads. If that occurs, pain relief is achieved
by “electronically repositioning” the contacts. Electronic repositioning is accomplished by
reprogramming the stimulation parameters, power, pulse width and frequency, which requires a visit to
the physician’s office.
Connecting Extensions
• Connecting extensions are used for larger patients where the length of the leads is short to reach the
IPG, and to provide slack to minimize the potential for lead migration.
• This extra piece of equipment can be a source for mechanical error if there is high impedance and poor
pain relief for a patient.
Anchors
These are small devices used to anchor the leads to reduce lead migration and breakage. Ideally, it should
be radiopaque allowing easy identification under fluoroscopy.
• Should be easy for the placement, and easily accessible in the incision to minimize lead migration and
provide security to the epidural leads.
• The locking device should lock the anchor to the lead, and unlock if repositioning of the lead or the
anchor is necessary. It should be visible under fluoroscope.
1. Boston Scientific Clik anchor (Figure 69-2)
Figure 69-2. Boston Scientific Clik anchor. (Image courtesy of Boston Scientific Corporation.)
• Locking system uses a turn of a hex wrench, providing tactile and audible confirmation that lead is
secure.
2. Medtronic anchors
• Titan anchor
• Titanium body with silicon anchor
• Further adhesive bond utilized
• Bumpy anchor
• Bi-Wing anchor
• ADT Bi-Wing anchor and lead unit
3. St. Jude Medical Cinch™ anchor
• Titanium retention sleeve provides a holding force higher than conventional silicone anchors.
• Extended distal strain relief reinforces the lead where it exits the vertebral column to reduce lead
fatigue and subsequent lead fracture.
• Radio-opacity facilitates identification under fluoroscopy.
4. St. Jude Medical Swift-Lock anchor
• Mechanical locking anchor requires a 90-degree twist to lock into place.
• The anchor can be disengaged and repositioned on the lead if necessary.
• Eliminates the need for sutures or medical adhesive to fasten the anchor to the lead.
• Extended distal strain relief reinforces the lead where it exits.
IMPLANTABLE PULSE GENERATORS
The implantable pulse generator (IPG), also called neurostimulator, is a battery powered device which
generates electrical pulses and delivers stimulation through one or more leads. The IPG system is
implanted and connected to leads directly or via connecting extensions, sending signals from the device to
the spinal cord via the electrical leads. Certain companies store the patient’s programs into the battery as
well.
Type of Stimulation Based on Energy Source

In the delivery of electrical energy to biological tissues, stimulus devices can hold either current or
voltage constant during the stimulation process of maximum 16 contacts.
• Voltage constant system. Devices that hold voltage constant at a value set by the user and allow
current to be determined by Ohm’s law are known as “constant voltage stimulators.” Medtronic uses
constant voltage.
• Current constant system. Devices that hold current constant at a value set by the user during the
stimulation process and allow voltage to be determined by Ohm’s law are called “constant current
stimulators.” St. Jude Medical has a single source current constant IPG that controls all 16 contacts.
• Independent energy source. With 10 mA on entire lead, the amplitude on each contact is individually
specified and maintained even when impedances change. BSC has the independent current system.
The system provides 3 basic parameters:
1. Pulse width
2. Frequency
3. Amplitude
A program is a specific combination of pulse width, rate, and amplitude settings acting on electrode
combination up to 16 electrodes per program. Up to 4 programs can be combined into a group. When
using more than 1 program, the pulses are delivered sequentially—first a pulse from one program, then a
pulse from next program. Pulse width, amplitude, and electrode polarity of each program within the group
can have different values.
Types of IPGs include:
• Non-rechargeable (Conventional SCS Technologies)
• Rechargeable (Advanced SCS Technologies)
• External pulse generators
The IPG devices are used to treat chronic, intractable pain of the trunk and/or limbs, including
unilateral or bilateral pain associated with the following conditions:
• Failed back surgery syndrome (FBSS) or low back pain syndrome
• Radicular pain syndrome or radiculopathies resulting in pain secondary herniated disk
• Postlaminectomy pain
• Degenerative disk disease (DDD) and herniated disk pain refractory to conservative and surgical
interventions
• Peripheral causalgia
• Epidural fibrosis
• Arachnoiditis or lumbar adhesive arachnoiditis
• Complex regional pain syndrome I (CRPS I) or reflex sympathetic dystrophy (RSD)
• Complex regional pain syndrome II (CRPS II) or causalgia
CONVENTIONAL NON-RECHARGEABLE PULSE

GENERATORS
Advantages
• Simpler to use for the patient
• Cheaper
• Fully implantable
• Primary cell battery
• Nonissue with patient compliance
Disadvantages
• Require replacement in 5 to 6 years, although variable based on usage
• May result in short life span and repeat replacement surgeries
• Radiofrequency IPG requires patient to wear external equipment to power the implant
RECHARGEABLE PULSE GENERATORS

Advantages
• Longer life span (10-12 years)
• Smaller IPG
• Reduce the need for surgical procedures due to less frequent replacement, saving expenses for the
surgical procedure and potential complications
• Increased stimulation parameters and therapy options
• Suitable for patients with high energy demands
• Supports complex programming
Disadvantages
• Complexity of recharging
• Inconvenience
• Initial higher cost
• Potential lack of compliance
Rechargeable IPG by Boston Scientific (Figure 69-3)

Figure 69-3. Precision Plus rechargeable IPG. (Image courtesy of Boston Scientific Corporation.)
• Cordless patient remote control and charger with a wireless range of up to 24 in.
• Precisely targets pain by moving the electric field between simultaneously active contacts in 1%
increments with 1 mm spaced contacts to minimize dead spots and sculpt the electrical field.
• May automatically adjust impedance changes to maintain therapy when leads scar in.
• Oval shape that may provide patient comfort.
• This company do not produce primary cell non-rechargeable IPG.
Bion Microstimulator by Boston Scientific (Figure 69-4)

Figure 69-4. Bion Microstimulator by Boston Scientific. (Image courtesy of Boston Scientific
Corporation.)
• It is a rechargeable battery powered electrode.

• Implanted near the occipital nerve for chronic HA.
• It is controlled by wireless remote control.
IPGs by Medtronic
Non-rechargeable conventional IPG (also called primary cell neurostimulator):
1. RestorePrime stimulator model 37701
2. PrimeAdvanced neurostimulator model 37702
3. Itrel 3 neurostimulator model 7425
• 39 cc, 16-electrode neurostimulator with ability to shape a stimulation field between 1- and 4-lead
arrays, which can be steered in any direction.
• Multi-programmable device may store up to 4 programs in a specific combination of pulse width, rate,
and amplitude settings acting on a specific electrode combination, up to 16 electrodes per program.
• When using more than one program, the pulses are delivered sequentially, ie, first a pulse from one
program, then a pulse from the next program.
• Option for patient to self-select parameters, enhancing comfort and self-control, minimizing office
visits.
• Pulse width, amplitude, and electrode polarity for each program within the group can have different
values.
• Rate, rate limits, ramping, and cycling for each program within the group have the same values.
Rechargeable Medtronic IPG

1. RestoreUltra neurostimulator model 37712
2. RestoreAdvanced neurostimulator model 37713
3. RestoreSensor neurostimulator model 37714
• Multi-programmable, rechargeable device which delivers stimulation through 1 or more leads in the
epidural space
• Thin, small, 22-cc, 16-electrode device with up to 4 leads with steering capacity
• May create between 1- and 4-lead arrays with patient controlled parameters
Restore Advanced Rechargeable Battery

• Multi-programmable rechargeable neurostimulator
• It listens and senses the changes in the patient position.
• It automatically adjusts and reprograms to optimize the settings per change in position.
• It has ability to record patient’s objective data.
St. Jude Medical IPGs

1. The EonC non-rechargeable IPG.
• Ideal choice for patients with low to medium power requirements and those who prefer the simplicity
of a non-rechargeable IPG.
• Wide range of pulse widths, frequencies, amplitudes which adjust to impedance and treat complex pain
patterns.
• Features greatest battery capacity of any primary cell IPG battery that does not require recharging,
making it less complex, and easier to maintain. The longevity of a primary cell IPG depends on the
energy requirements of the patient. At certain settings, small primary cell IPGs will last more than 5
years and high-capacity primary cell IPGs can last 10 years or longer.
• Compatible with a comprehensive line of neuromodulation leads and extensions for easy replacement
of depleted competitive IPGs.
• Primary cell IPGs are available in 8 or 16 contact constant current, primary cell IPG that automatically
adjusts power output to maintain prescribed stimulation as impedance levels change; patient may
control up to 8 pain areas at one time.
2. The Genesis non-rechargeable IPG
• Eight-contact primary cell IPG system
• Compact size with high battery capacity among small primary cell IPGs
• Efficient circuitry and high-capacity battery
• Suitable for stable unilateral extremity pain
• Limited power requirements
• Suitable for elderly patients or patients with limited cognitive ability
• Anxious about technology
• Life span 2 to 6 years
3. Rechargeable Eon Mini IPG
• NeuroDynamix technology enables longer battery life and time between fast recharges, expected
greater than 24 hours between recharges at high settings, with a 10-year life expectancy at high settings.
• FDA approved for last 10 years at high stimulation settings, which means patients may require fewer
replacement surgeries, and it is designed to provide consistent pain therapy for virtually any pain
profile. If lower parameters are used, a significantly longer device life is possible.
• Smallest 18 cc IPG with a deeper implant depth of up to 2.5 cm to enhance patient comfort and
placement options, less tissue erosion, and without compromising recharge efficiency.
• Dynamic MultiStim programming and 16 contact header compatibility allows control of up to 8 pain
areas simultaneously.
• Offers both MultiStim and PC-Stim (patient-controlled stimulation) capabilities, giving clinicians and
patients control of the stimulation therapy and their individual pain pattern treatments—multifocal pain
pattern.
• High power requirements.
• Patient must have cognitive ability to grasp recharging responsibility and burden.
• May not be suitable for elderly patients.
4. External radiofrequency Renew IPG
St. Jude Medical is the only company that provides a pulse generator with an external battery source. The
pulse generator is actually a receiver that receives energy by radiofrequency from external source. This
may be an alternative option specifically for peripheral nerve field stimulation.
• The Renew system consists of a radiofrequency transmitter and an external receiver for percutaneous
leads or paddle leads.
• Initial high frequency high power technology
• Powerful 8- or 16-contact systems with broad range of power outputs
• Renew radiofrequency (RF) systems are designed to sustain therapy over long periods at high output
levels. Frequency ranges up to 1500 Hz.
• Does not need to be recharged, no replacement surgery required for life time.
• Small size, may be useful for peripheral nerve field stimulation.
• Receiver internalized and the transmitter is worn externally.
• Potential skin reaction from external component
• This system is not used frequently.
THE SCS EXTERNAL TRIALING SYSTEM

The external neurostimulation trialing system is used to evaluate spinal cord stimulation during lead
placement or test stimulation. The addition of the multi-lead trialing cable to the external trialing system
provides secure, confident trialing of more than one lead with less equipment necessary. Although this
portion of the trial is often managed and supported by the representatives and technicians from the device
company being used, it is important to understand the components, process, and technology.
External trialing system components include:
• Multi-lead trialing cables
• External trialing neurostimulator
• Test leads
• Clinician programmer
• Patient programmer
The external trialing system should provide the following benefits:
• Small, thin, curved anatomical design to provide comfort during trialing.
• To individually trial leads, it should provide a multi-lead trialing cable to support any program
combination of quad or octad leads, up to 16 electrodes.
• Should be single cable and no extensions.
• The cable connections with trial leads and securing to skin externally should be easy, comfortable, and
user friendly.
The external neurostimulator and the implantable neurostimulator produce comparable symptom
suppression when set to the same parameter settings.
RECHARGING THE IPG

The primary cell conventional non-rechargeable IPG will require a simple surgery to get the battery
changed at the end of life of battery. However, if a rechargeable battery is used, periodically it will need
to be recharged via the implanted device. The amount of time it takes to charge the generator varies
according to the brand and model, and age and condition of the device (about 10 years). The same is true
for the amount of time the battery can hold a charge, ie, how long between charges. The older the battery,
the more time charging takes, and the more often you will need to recharge.
• To charge a neurostimulator battery, the charger is held over the area where the device is implanted for
a specified period of time.
• Traditional charges often either required a cord connected to a device that lies over the IPG site,
however, now, there are cordless devices that can be utilized.
• Similar to cell phones, conventional SCS systems rely on rechargeable batteries that fail or suffer
irreversible damage when over-discharged.
The available chargers are:
• Boston Scientific Precision Plus system charger powered by a zero-volt battery (Figure 69-5)
Figure 69-5. Boston Scientific Precision Plus system cordless charger. (Image courtesy of Boston
Scientific Corporation.)
• St. Jude Medical Eon Mini charging system for smaller and longer lasting rechargeable battery that
gives 10 years of anticipated life span
• Medtronic RestoreAdvanced and RestoreUltra chargers
SCS PROGRAMMERS
SCS programming involves selecting and optimizing the 4 variables for configuration:
• Stimulating electrode configuration
• Amplitude (current/voltage)
• Pulse width
• Frequency of electrical pulses
Amplitude (current/voltage) indicates the intensity of stimulation and paresthesia. This is set within a
range of 0 to 10 V according the type of electrode used and the type of nerves stimulated. Increasing the
voltage increases the area of capture in the spinal cord by recruiting nerves farther from the contacts.
However, increasing the voltage can produce discomfort. Lower voltage is chosen for peripheral nerves
and paddle type electrodes. Ideally paresthesia should be felt between 2 and 4 V.
Pulse width refers to the duration of a single stimulation pulse and usually varies from 100 to 1200 μs.
Widening the pulse width will also broaden the area of paresthesia. By SCS blocking a stimulus,
depolarization and propagation of an action potential of the nerve is prevented, avoiding the pain
response. Lower amplitudes of stimulation at wider pulse widths are better tolerated by patients.
The frequency of the pulse wave is usually between 20 and 120 Hz. It is an individual preference: some
patients choose low frequency beating sensation (low back and leg pain) whereas others prefer high
frequency buzzing (CRPS).
Selection of lowest possible setting on all parameters is important in conserving battery life of SCS.
Cycling of stimulation is also employed to save battery life. Changing the stimulator’s program may occur
during the course of therapy and follow-up as the patient heals, leads scar over, or the nature of the
patient’s pain changes.
Boston Scientific Programmer (Figure 69-6)
Figure 69-6. Boston Scientific Bionic Navigator. (Image courtesy of Boston Scientific Corporation.)
• Continuous real-time adjustment of stimulation settings allows patient to steer field to cover pain areas.
• 15-minute using navigation allows evaluation of hundreds of stimulation configurations.
• A collaborative approach to patient fitting.
• Patient assumes a greater level of control over their pain coverage.
Medtronic Programmer
Medtronic N’Vision Clinician Programmer. The Medtronic N’Vision model 8840 clinician programmer
• It is a portable device that offers a single programming platform for Medtronic implantable drug
delivery and neuromodulation devices.
• It programs the RestoreSensor, RestoreUltra, Restore Advanced, RestorePrime, and PrimeAdvanced
spinal cord neurostimulators, and SynchroMed II intrathecal pump.
• The MyStim model 37744 is a patient programmer.
• It is a handheld device that increases a patient’s ability to manage his or her own therapy, within
clinician-set parameters, while receiving spinal cord stimulation.
St. Jude Medical Clinician Programmer

Designed to capture complex, multifocal pain, the St. Jude Medical Rapid Programmer 3.0 system with
multisteering technology efficiently locates desired stimulation areas, assesses their interaction in real
time, and fine-tunes settings for optimal coverage. It also simplifies the programming of multifocal pain to
help deliver optimal therapy and meet each patient’s need.
• Provides the ability to steer current in one area while another remains active, “multisteering,”
facilitating the programming of multifocal pain.
• Enables a comprehensive evaluation of stimulation patterns to enhance the likelihood of successful
outcomes.
• Designed to produce a patient-perceived change in stimulation with each incremental step used to steer
current.
St. Jude Medical PC-Stim Programming

• Allows multiple programs to be stored in the patient programmer manually selected by the patient.
• PC-Stim programming enables the patient to self-regulate therapy according to their pain level, body
position, or activity level, for up to 24 programs.
St. Jude Medical Active Balancing Programming

• Active balancing programming allows fine-tune stimulation levels in multiple coverage areas
concurrently to improve patient’s comfort level.
• Streamlined programming can adjust levels in multiple coverage areas simultaneously to quickly
establish stimulation comfort levels.
• Intelligent amplitude control allows the system to synchronize multiple areas of coverage and enables
patients to change individual amplitudes with a master control.
St. Jude Medical Dynamic MultiStim Technology

• Rapid Programmer 3.0 is built in such that 8 independent arrays can be blended for complex pain
patterns.
• Constant current delivery and simple electrode arrays improve accurate steering of current to targeted
electrodes even when impedance changes over time.
• Real-time programming allows patients to evaluate stimulation levels to multiple coverage areas as
programming adjustments are made.
SCS CONTRAINDICATIONS
As per current United States FDA guidelines, the SCS system is contraindicated for patients with demand-
type cardiac pacemakers, although patients in Europe have safely implanted stimulators in cardiac
patients with good efficacy as reported in case reports. Thus, specifically in the US, SCS devices are
avoided in patients with pacemakers.
In addition, patients who are unable to operate the system, have not passed an appropriate
psychological evaluation for use of SCS, or failed to receive effective pain relief during trial stimulation
should not be implanted with a neurostimulation system.
Important Warnings in Regards to SCS

• Neurostimulation should not be used on patients who are poor surgical risks or patients with multiple
illnesses or active general infections.
• Electrocautery. Do not use short-wave diathermy, microwave diathermy, or therapeutic ultrasound
diathermy on patients implanted with a neurostimulation system. Energy from diathermy can be
transferred through the implanted system and cause tissue damage at the location of the implanted
electrodes, resulting in severe injury or death.
• Cardioverter defibrillators. Neurostimulation systems may adversely affect the programming of
implanted cardioverter defibrillators, although in Europe case reports have reported safe concomitant
use.
• Magnetic resonance imaging (MRI). Patients with implanted neurostimulation systems should not be
subjected to MRI. The electromagnetic field generated by an MRI may forcefully dislodge implanted
components, damage the device electronics, and induce voltage through the lead that could jolt or
shock the patient.
• Pregnant patients. Safety and effectiveness of neurostimulation for use during pregnancy and nursing
have not been established.
• Implantation of two systems. If 2 systems are implanted, ensure that at least 20 cm (8 in) separates the
implanted IPGs to minimize the possibility of interference during programming.
• Implantation of multiple leads. If multiple leads are implanted, leads and extensions should be routed
in close proximity. Nonadjacent leads can possibly create a conduit for stray electromagnetic energy
that could cause the patient unwanted stimulation.
• Postural changes. Changes in posture or abrupt movements may result in a decrease or increase in the
perceived level of stimulation. Perception of higher levels of stimulation has been described by some
patients as uncomfortable, painful, or jolting. Patients should be advised to turn down the amplitude or
turn off the IPG before making extreme posture.
• The metal screening devices. Certain devices used at entrances or exits of public establishments, and
airport security screening devices may affect stimulation. It is recommended that patients use caution
when approaching such a device and that they request assistance to bypass the device. If they must
proceed through the device, patients should turn off the IPG.
• Cellular phones. The effect of cellular phones on neurostimulation systems is unknown; patients should
avoid placing cellular phones directly over the system.
• High output ultrasonic and lithotripsy. The use of high output devices, such as an electrohydraulic
lithotripter, may cause damage to the electronic circuitry of an implanted IPG. If lithotripsy must be
used, do not focus the energy near the IPG.
• Therapeutic radiation. Therapeutic radiation may damage the electronic circuitry of an implanted
neurostimulation system. Sources of therapeutic radiation include therapeutic x-rays, cobalt machines,
and linear accelerators. If radiation therapy is required, the area over the implanted IPG should be
shielded with lead.
Availability of multiple electrodes and multiple leads has made possible to cover complex pain patterns
by multiple programming capabilities. Devices are available to insert paddle leads percutaneously.
Smaller IPG devices have led to greater comfort, and rechargeable devices have changed the reoperation
rates and overall lasting nature of these devices. Perhaps with expansion into MRI compatibility, as well
as a more expansive treatment options with increased on-label and off-label indications, including
ischemic and neuropathic therapies, we look forward to continued collaboration of industries and health
care providers for newer generations of these devices and further developments in interventional
techniques to help our patients.
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Schultz DM, Webster LR, Kosek P, et al. Sensor-driven position-adaptive spinal cord stimulation for
chronic pain. Pain Physician. Jan: 15(1):1-12.
Strand NH, Trentman TL, Vargas BB, et al. Occipital nerve stimulation with the Bion microstimulator for
the treatment of medically refractory chronic cluster headache. Pain Physician. 2011;14:435-440.
Websites
www.medtronic.com
www.tamethepain.com
CHAPTER 70
Spinal Cord Stimulation: Trialing Procedure

Richard B. North
INTRODUCTION
This chapter deals with screening trials for the use of spinal cord stimulation (SCS) to treat otherwise
intractable pain. The same general principles, however, apply to other types of neuromodulation for pain,
such as peripheral, cortical, and deep brain stimulation, and stimulation for conditions other than pain.
SPECIFIC PURPOSES OF AN SCS SCREENING TRIAL

• To identify candidates for successful therapeutic chronic use of a stimulator and save the expense and
morbidity of implantation in patients likely to be therapy failures.
• To predict the technical success of SCS (overlap of pain with a comfortable level of paresthesia and
no motor reaction).
• To predict the clinical success of SCS (usually defined as ≥ 50% pain relief despite provocative
activities, patient satisfaction with the treatment, and no increase in adjunct pain therapy).
• To determine if the patient can tolerate the sensation of paresthesia and can use the equipment
successfully.
• To confirm patient compliance and validate patient reports by tracking usage.
• To reveal the electrode level and stimulation configuration that will optimize technical and clinical
success.
• To gain information that will influence the choice of electrode(s) and the choice (rechargeable versus
non-rechargeable) and location of the pulse generator in patients who proceed to implantation.
• To comply with the requirements of Medicare and many third-party payers.
APPROPRIATE PATIENT DIAGNOSES

• In many cases, the diagnosis underlying a chronic pain problem, and thus its prognosis and optimum
treatment, is unclear.
• Experimental animal1 and human2 models indicate that SCS is more effective for neuropathic than for
nociceptive pain.
• Animal models3 and clinical results point to the effectiveness of SCS for certain types of ischemic and
visceral4 pain.
• We consider an SCS trial in a patient who has persistent or recurrent, otherwise intractable pain of the
trunk and/or limbs. To the extent that a screening trial is a relatively low-risk, low-cost procedure, it is
reasonable to offer screening liberally, ie, in cases in which the expected yield of success might be
relatively low—in conjunction with critical interpretation of the results of the trial.
OFF-LABEL INDICATIONS OF SCS FOR PAIN

• Angina pectoris has been a popular indication for SCS in Europe,5 but is considered off-label by US
manufacturers of SCS equipment. The yield of SCS screening trials in patients with angina pectoris is
so high that the trial is often abbreviated or eliminated.
• Peripheral vascular disease causing limb pain, although clearly involving the areas covered by the US
labeling language (pain of the trunk and limbs), is viewed conservatively as well. SCS can have a
positive affect on blood flow, but this is not among the US label indications.
RELEVANT ANATOMY
• The effects of SCS vary according to which neural structures are stimulated.
• The location of the electrode (vertebral level6 and distance from the physiologic midline of the spinal
cord7) dictates the anatomic area in which paresthesia can be elicited.
• The depth of cerebrospinal fluid (CSF), which conducts current from the electrode to the spinal cord,
increases from the cervical to the mid-thoracic spine.
• Movement from the supine to the prone, sitting, or standing position increases the depth of CSF, which
explains postural changes in stimulation.8
• Stimulation of large dorsal column afferents close to the pial surface of the spinal cord occurs at the
lowest threshold with a dorsal midline electrode.
• Stimulation of dorsal roots can limit paresthesia coverage by causing reflex motor effects and
discomfort. This is most likely to occur in the thoracic area where several millimeters of CSF and dura
are interposed between the electrode and the pial surface.
• A reasonably current imaging study (MRI or CT myelography) of pertinent anatomy (typically the
lumbar and thoracic spine) is essential for diagnosis and treatment planning.
• The patient’s use of any medication that can cause prolonged or excessive bleeding during surgery must
be discontinued, typically 7 to 10 days before the procedure.
Percutaneous Trial Electrode Placement

• Placement of one percutaneous disposable trial electrode should be adequate for most patients,
although such placement might be difficult to reproduce with an electrode for chronic use.
• Normal infection control precautions apply (sterile preparations, etc) and prophylactic IV antibiotic
should be administered (depending on patient’s sensitivity) within an hour before beginning the
procedure.
• Local anesthetic infiltration will control procedural pain and allow the patient to describe
pain/paresthesia overlap.
• The patient is prone or seated with the target area neutral.
• Using a Tuohy needle, make a T12-L1 or L1-2 interlaminar puncture and advance at a shallow angle
under anteroposterior (and, as necessary, lateral) fluoroscopy starting 1 to 2 segments below the target
interlaminar space depending on the patient’s girth (Figure 70-1).
Figure 70-1. Using a Tuohy needle, make a T12-L1 or L1-2 interlaminar puncture.
• Increase the degree of spinal flexion as needed to gain additional interlaminar space.
• Confirm epidural space entry with loss of resistance to a Seldinger guidewire (injected air or saline
can interfere with steering and with test stimulation).
• Stimulate using adjacent contacts (bipole, cathode cephalad) to identify the physiologic midline at each
level as the electrode is advanced incrementally along the radiographic midline to the desired
longitudinal location, repositioning as needed to achieve the requisite symmetry and pain/paresthesia
overlap.
• If targeting the low back, the electrode must be close to the physiologic midline, ie, the
bilateral/perceptual stimulation threshold ratio should be no more than 110% (Figure 70-2).
Figure 70-2. Clinically relevant stimulation falls within an amplitude that ranges from perception to
discomfort, illustrated here for configurations A and B. The amplitudes at which bilateral effects are
perceived and paresthesia overlaps low back pain can be scaled to this usage range. In this example, A
and B are comparably symmetric, in that their ratio of bilateral to perceptual threshold is similar. In A,
low back coverage occurs close to the perceptual threshold; in B, low back coverage occurs near the
discomfort threshold.
• If a patient has leg pain predominant on one side and electrode placement is to favor one side, it should
favor the side with the predominant pain.
• When the contacts are in a stable position along the radiographic midline, begin test stimulation to:
Familiarize the naïve patient with the sensation of paresthesia and the test routines.
Orient the operator to the physiologic midline, which often differs from the radiographic midline.
Record areas of paresthesia coverage at multiple amplitudes: perceptual, bilateral, usage, and
discomfort.
Map responses that might be useful clinically (even if the electrode is well below the anticipated
optimal level, eg, to cover a secondary area of foot pain).
• Leaving the percutaneous electrode in place, withdraw the Tuohy needle, and suture the lead to skin.
• Place the trial connector on the side appropriate for placement of the pulse generator, eg, the side
opposite the one the patient sleeps on.
• Occasionally, multiple electrode arrays will be inserted for a trial:
At 2 different levels to cover pain at 2 different levels, eg, the low back and the foot.
Side by side, eg, for bilateral foot pain (note that this configuration is inferior for low back pain, at
least acutely).9
In 3 columns to create transverse tripole stimulation, which is cumbersome with percutaneous
electrodes because it requires 3 needle sticks or a specialized catheter and because of the difficulty
in maintaining the relative position of the electrodes.
• A percutaneous electrode designed for chronic therapy can be used for the trial and implanted with the
expectation that it will remain in place if the trial is successful (as is common in Europe). This
requires extra steps (incision, tunneling, anchoring) and incurs some disadvantages:
Additional pain can confound trial interpretation.
The increased risk of infection might cause the trial to be expedited inappropriately.
With the most difficult step of implantation completed, a certain amount of momentum has been
gained toward proceeding with generator implantation, and the trial might be interpreted less
critically than it should.
• Note on high frequency and burst stimulation: Patients might not feel SCS paresthesia at very high
frequencies, delivered continuously or in bursts; when the use of these waveforms is contemplated,
conventional, lower frequencies can be used to guide electrode placement.
Plate/Paddle Trial Electrode Placement

• Plate or paddle electrodes should be reserved for trials in special circumstances:
Percutaneous access is not feasible (eg, after spine surgery at the planned level of insertion).
To mitigate painful side effects (such as stimulation-evoked axial pain) likely mediated by small
fibers in the ligamentum flavum.10
• Plate or paddle electrodes used for trials are typically preserved for chronic use if the trial is
successful.
• It is not necessary to use a paddle electrode to reduce migration; contemporary percutaneous electrode
anchoring techniques have reduced the incidence of percutaneous electrode migration to nearly zero.11
• Normal infection control precautions apply (sterile preparations, etc), and prophylactic IV antibiotic
should be administered (chosen subject to patient’s sensitivity) within an hour before beginning the
procedure.
• Paddle electrodes can be inserted using a variety of anesthetic techniques:
Infusion and/or intermittent boluses of IV sedation (eg, propofol) and local anesthetic minimize
discomfort for the patient while allowing for verification of electrode location as well as
intraoperative testing of neurological function.
Epidural, subarachnoid or intrathecal spinal anesthesia12 can provide local analgesia without
inducing motor or sensory blockade, while still allowing stimulation paresthesia to be elicited to
determine appropriate placement in most cases, albeit at higher amplitudes. Importantly, on the
other hand, these types of anesthesia can block pain that signals injury, which can result in a
complete motor block, making it impossible to evaluate motor function and possible spinal cord
compression until well after completion of the procedure.
General anesthesia, using evoked potential monitoring to guide placement in the physiological
midline,13 precludes patient feedback but allows for monitoring of somatosensory and motor
evoked potentials, which can provide information regarding the integrity of spinal cord pathways
relative to their preoperative status.
• With the patient prone or semilateral, use bolsters or a radiolucent Wilson frame to:
Allow precise positioning of a C-arm fluoroscope, which is helpful for verification of anatomic
midline placement.
Avoid lateral curvature or rotation of the patient’s spine, which might compromise accurate midline
placement.
Improve the surgeon’s orientation compared with the lateral position.
• Confirm that skin rolls or hyperextended posture do not impede access to the implant site(s). Orient the
C-arm to provide a true AP view, with the spinous processes positioned in the midline between the
pedicles. Aligning the C-arm beam with the end plates ensures accurate localization.
• After sterile prep and draping, infiltrate the skin and paravertebral muscles with local anesthetic.
• Under fluoroscopy, center a 1- to 2-in incision on the implantation target area, which should be just
caudal to the final position planned for the most caudal contact.
• Dissect the paravertebral muscles subperiosteally; place self-retaining retractors.
• Perform a mini laminectomy of sufficient breadth, and length, oriented to allow shallow-angle insertion
of the electrode beneath the intact lamina(e) above. Keep the force vectors in the rostrocaudal
dimension rather than down toward the dura and spinal cord.
• Some clinicians have described a minimally invasive paramedian approach using a tubular retractor
system.14 Although the least invasive approach is desirable, the highest priority is safe and technically
accurate electrode insertion, achieving a stable long-term placement.
• Perform physiological monitoring to verify electrode placement and maximize pain/paresthesia
overlap. The most straightforward method is verbal reporting from a patient who is awake.
Electrophysiological monitoring of motor and sensory evoked potentials might alert the surgeon to the
potential of spinal cord injury before permanent injury can occur. Ultimately, the choice of
physiological confirmation method depends on the experience and judgment of the surgeon.
• Anchor the lead wire to the supraspinous ligament using a sleeve/strain relief and (author’s preference)
silicone elastomer adhesive.
• Place the trial connector on the side appropriate for placement of the pulse generator, eg, the side
opposite the one the patient sleeps on.
• Because patients seldom use SCS while in the prone position in which percutaneous electrodes are
placed, promptly following electrode placement, program the temporary stimulator to optimize
paresthesia coverage of pain with the patient sitting or supine.
• Before discharge, while monitoring the patient postoperatively for neurologic and other potential
complications, continue programming and patient education as needed.
• Pay careful attention to postoperative pain medication use, which can confound interpretation of the
trial.
• Each SCS manufacturer provides a temporary external generator. (Constant current as well as constant
voltage generators are available, but we lack high quality evidence about their comparative
advantages.)
• A 1-week trial is our usual practice. The trial can be extended to approximately 3 weeks (as in many
European centers), however, or conducted in minutes while the patient is “on the table.”15
• In cases where an otherwise successful trial is accompanied by therapy-limiting side effects, such as
unwanted stimulation, a repeat trial can be conducted with an insulated plate/paddle electrode
(perhaps “on-table” during permanent implant).
• A patient who reports sufficient and satisfactory pain relief during a screening trial of reasonable
duration with stable or reduced analgesic use and a concordant increase in activity should be offered
an implanted system.

• Spinal cord or nerve injury (including epidural hematoma) requires emergency neurosurgical
management, which can include decompression.
• Dural puncture responds to bed rest, hydration, caffeine, and (when necessary) an epidural blood
patch.
• Infection (wound or skin breakdown) requires a culture specimen, removal of the system (in most
cases), and administration of appropriate antibiotics.
• Electrode migration might be mitigated by reprogramming the contacts noninvasively; if this is not
sufficient, the electrode(s) may be repositioned or replaced.
• Electromechanical failure requires revision.

• Our reliance on screening trials is presumptive. We even lack randomized controlled trial evidence,
for example, on the impact of extending or eliminating screening trials.
• For patients with failed back surgery syndrome, we routinely insert the percutaneous trial electrode at
T12-L1 or L1-L2.
Because the tip of the conus is at L1-L2, a dorsal epidural electrode below this level will be
delivering cauda equina stimulation rather than SCS. The rootlets of the cauda are mobile and
difficult to recruit consistently.
Insertion into the relatively immobile thoracic spine makes the body of the lead less subject to
stresses and strains than would be the case in mobile lumbar segments.
Rarely, the interlaminar spaces are too small at the recommended levels, and one must look lower.
Not uncommonly, the patient has had a laminectomy up to and including the upper lumbar levels, and
this constrains the approach to be more cephalad.
Even when the more caudal interlaminar spaces are available, they are less desirable because
lumbar lordosis makes it more difficult to achieve the requisite shallow angle of insertion.
Furthermore, if the patient has low back pain, introducing a needle at one of the lower lumbar
interlaminar spaces is likely to cause acute pain in the same location as the patient’s usual pain,
which might confound interpretation of the trial.
• It is commonly the case that de novo placement of an electrode for chronic use offers the opportunity
for the operator as well as the patient to improve upon results obtained with the temporary trial
electrode.
The previously naive patient has gained experience with the technical goals of the procedure, and
the operator has gained experience with the individual patient.
The operator can choose a permanent electrode based on experience with the temporary.
Thus, we prefer a strictly temporary percutaneous electrode for SCS screening trials when feasible
—as is fortunately the case in most patients.
References
1. Meyerson BA, Herregodts P, Linderoth B, et al. An experimental animal model of spinal cord
stimulation for pain. Stereotact Funct Neurosurg. 1994;62(1-4):256-262.
2. Marchand S, Bushnell MC, Molina-Negro P, et al. The effects of dorsal column stimulation on
measures of clinical and experimental pain in man. Pain. 1991;45(3):249-257.
3. Foreman RD, Linderoth B, Ardell JL, et al. Modulation of intrinsic cardiac neurons by spinal cord
stimulation: implications for its therapeutic use in angina pectoris. Cardiovasc Res. 2000;47(2):367-
375.
4. Kapural L, Narouze SN, Janicki TI, et al. Spinal cord stimulation is an effective treatment for the
chronic intractable visceral pelvic pain. Pain Med. 2006;7(5):440-443.
5. Börjesson M, Andréll P, Mannheimer C. Spinal cord stimulation for long-term treatment of severe
angina pectoris: what does the evidence say? Future Cardiol. 2011;7(6):825-833.
6. Tulgar M, He J, Barolat G, et al. Analysis of parameters for epidural spinal cord stimulation. 3.
Topographical distribution of paresthesiae—a preliminary analysis of 266 combinations with contacts
implanted in the midcervical and midthoracic vertebral levels. Stereotact Funct Neurosurg.
1993;61(3):146-155.
7. Holsheimer J, Barolat G, Struijk JJ, et al. Significance of the spinal cord position in spinal cord
stimulation. Acta Neurochir Suppl. 1995;64:119-124.
8. Holsheimer J, den Boer JA, Struijk JJ, et al. MR assessment of the normal position of the spinal cord
in the spinal canal. Am J Neuroradiol. 1994;15(5):951-959.
9. North RB, Kidd DH, Petrucci L, et al. Spinal cord stimulation electrode design: a prospective,
randomized, controlled trial comparing percutaneous with laminectomy electrodes. Part II. Clinical
outcomes. Neurosurgery. 2005;57(5):990-995.
10. North RB, Lanning A, Hessels R, et al. Spinal cord stimulation with percutaneous and plate
electrodes: side effects and quantitative comparisons. Neurosurgical Focus. 1997;2(1:3):1-5.
11. Renard VM, North RB. Prevention of percutaneous electrode migration in spinal cord stimulation by a
modification of the standard implantation technique. J Neurosurgery: Spine. 2006;4:300-303.
12. Vangeneugden J. Implantation of surgical electrodes for spinal cord stimulation: classical midline
laminotomy technique versus minimal invasive unilateral technique combined with spinal anaesthesia.
Acta Neurochir Suppl. 2007;97(pt 1):111-114.
13. Falowski SM, Celii A, Sestokas AK, et al. Awake vs asleep placement of spinal cord stimulators: a
cohort analysis of complications associated with placement. Neuromodulation. 2011;14(2):130-134.
14. Beems T, van Dongen RT. Use of a tubular retractor system as a minimally invasive technique for
epidural plate electrode placement under local anesthesia for spinal cord stimulation: technical note.
Neurosurgery. 2006;58(suppl 1):ONS-E177.
15. Feler CA, Kaufman S. Spinal cord stimulation: one stage? Acta Neurochir. 1992;117:91.
CHAPTER 71
Spinal Cord Stimulation: Implantation Techniques

Elias Veizi and Salim M. Hayek
INTRODUCTION
Electrical stimulation of neural structures is a widely used, nondestructive, reversible therapy, for chronic
noncancer related pain. It has been evolving rapidly since the “gate theory,” developed by Melzack and
Wall in 1965, which opened the door for this application. Neurostimulation may modulate pain pathways
at the central nervous system and peripheral nervous system levels. Various techniques and technologies
have been developed according to the site of stimulation: spinal cord stimulation (SCS), deep brain
stimulation (DBS), motor cortex stimulation (MCS), large peripheral nerve stimulation (PNS), peripheral
nerve field stimulation (PNFS), and more recently dorsal root ganglia stimulation (DRG-S). This chapter
looks at percutaneous surgical techniques of electrical stimulation of the spinal cord.
INDICATIONS
Chronic neuropathic pain affects a significant percentage of the population and is often inadequately
treated. It may result in low quality of life, medication overuse, and worsening of mood disorders. The
FDA has approved SCS as an instrument in treatment of chronic intractable pain of the trunk and limbs
including unilateral or bilateral pain associated with postlaminectomy syndrome, intractable low back
pain and leg pain. Besides neuropathic, low back and limb pain there is evidence for off-label use of SCS
for ischemic pain in refractory angina and peripheral vascular disease and some evidence for
effectiveness in visceral pain. The indications of SCS are:
• Neuropathic pain in upper or lower extremities related to postlaminectomy syndrome (so-called failed
back [neck] surgery syndrome—FBSS or FNSS)
• Complex regional pain syndrome (type I/II)
• Radiculopathy
• Plexopathy: traumatic (partial), postradiation
• Arachnoiditis
• Painful peripheral neuropathy including idiopathic small fiber neuropathy, metabolic (diabetic),
infectious (HIV), and toxic (chemotherapy-induced) neuropathy
• Stump pain (postamputation)
• Ischemic pain associated with peripheral vascular disease
• Ischemic pain associated with refractory angina
• Visceral pain
• SCS indications associated with lower success rate
• Axial pain following spine surgery (back and neck)
• Postherpetic neuralgia pain
• Phantom pain
• Post-thoracotomy pain
• Incomplete spinal cord injury with complete or clinically distinguishable loss of posterior column
function
• Central pain
As discerned, many of the poorer responsive conditions encompass deafferentation features of pain.
CONTRAINDICATIONS
• Any contraindication for regional anesthesia such as uncorrected coagulopathy or infection
• Pregnancy (though there are reports of uneventful pregnancies and deliveries on SCS)
• Severe central canal stenosis
• Neurologic deficit that would likely be amenable to surgery
• Significant/progressive spine instability
• Need for frequent follow up by magnetic resonance imaging as in multiple sclerosis
• Unacceptable surgical risk
• Cognitive impairment
• Active substance abuse
• Implanted pacemaker or AICD (though off label use of SCS in this setting has been reported)
• Borderline personality disorder or other psychiatric co-morbidities that preclude success
• Previous lesion of dorsal root entry zone

Documentation for off-label use should include a detailed discussion with the patient. The physician may
discuss representative original publications, review articles, book chapters, or technological review
assessments, which detail the effectiveness and relative safety of SCS for the condition at hand.
A Statement of Medical Necessity

A letter documenting a statement of medical necessity should include the following components:
• Statement of request for SCS system.
• Short description of what the procedure entails including that neurostimulation is a nondestructive and
reversible therapy.
• Detailed description of the medical decision making process (discussion of):
Clinical symptoms
Imaging
Previous failed therapy—pharmacological, physical therapy, and interventional
Pertinent selection criteria and how the patient fulfills those criteria
• Describe whether patient did undergo psychological evaluation.
• Detail the request for coverage in terms of trial, implant, professional fees, and facility fees. It should
include also tentatively scheduled dates.
MECHANISM OF ACTION
The idea of electrical stimulation for pain control was based on the initial description of the “gate theory”
by Melzack and Wall, whereby electrical stimulation of large myelinated Aβ (A beta) fibers in dorsal
columns would result in closing the “gate” and obliterating onward central pain signal transmission from
peripheral nociceptors (C fibers) (Figure 71-1). Applied electrical field in the epidural space affects
various structures (dorsal columns, peripheral nerves, spinal tracts) and SCS mechanisms of action have
been shown to be more complex than the “gate” theory. SCS mechanisms currently being researched
involve:
Figure 71-1. Spinal cord stimulation hypothesized “gate theory” mechanism. Stimulation of Aβ fibers
closes the “gate” and results in reduced input and weak activation.
• Antidromic action potential spreading caudally in the dorsal columns to activate spinal segmental
mechanisms
• Orthodromic ascending action potentials activating brainstem cells which could reinforce descending
inhibition
• Direct inhibitory actions on central sensitization mechanisms
• Restoration and sustainability of blood flow (microcirculation) to the affected site by increasing the
release of vasoactive mediators such as CGRP and SP
• Decreasing sympathetic output (important in sympathetically maintained pain) by antidromic effects
RELEVANT ANATOMY
The goal of spinal cord stimulation is to produce analgesia in the area of pain. Optimal pain relief is
achieved when the paresthesia resulting from stimulation of dorsal column Aβ fibers overlaps the area of
pain. An 80% overlap of paresthesia to area of pain has been empirically sought in SCS studies. To be
able to accomplish this, the surgeon should understand:
• The structural and functional anatomy of spine
• The fluoroscopic anatomy of the spine
• Relevant clinical neurophysiology
• Limitations and capabilities of the equipment used
• Techniques to optimize parameters of stimulation to achieve better results
Epidural Space
• The epidural space is circumferential wrapping around the dura. It is bound by:
The ligamentum flavum posteriorly
The posterior longitudinal ligament and vertebral bodies anteriorly
The vertebral pedicles and intervertebral foramina with their penetrating nerve roots form the
lateral borders
• The posterior epidural space, dorsal to the dura, is the target of lead placement for SCS to facilitate
dorsal column stimulation. This space is primarily occupied by fat tissue and small blood vessels,
lymphatics and nerve roots laterally (Figure 71-2).
Figure 71-2. Percutaneous leads positioning in the epidural space. The posterior epidural space, dorsal
to the dura, is the target of lead placement for spinal cord stimulation. This space is primarily occupied
by fat tissue and small blood vessels, lymphatics and nerve roots laterally. Dorsal CSF (dCSF) fluid
thickness along the spinal canal is the most important determinant of current spread.
• The diameter of the epidural space changes along the spinal column and should be taken into account
when deciding the level entry into the epidural space. The greatest distance between the ligamentum
flavum and the dura is found at the L2 in adults (5-6 mm), followed by thoracic spine (3-4 mm) and the
least in the cervical spine region 1.5 to 2 mm.
Dorsal Columns
Dorsal columns are the target of electrical stimulation. They are formed by large-diameter, heavily
myelinated, high conductance sensory fibers (Aβ) mediating tactile sensation and proprioception from the
extremities and the trunk. Topographically they form the fasciculus gracilis and the fasciculus cuneatus
collecting sensation from lower extremities and upper extremities, respectively. The lower extremities’
primary sensory afferent projections enter the spinal cord laterally in the lower segments and are
positioned more medially and dorsally at the upper levels of the spinal cord as the trunk and upper
extremity fibers enter the dorsal column tracts (Figure 71-3). Hence, the dorsal column’s fibers are
somatotopically organized (Figure 71-3) in the following order from medial to lateral: sacral, lumbar,
thoracic, and cervical. Smaller fibers are located more medially and conduct sensory information from
more caudad segments. The nerve root fibers enter the spinal cord several levels higher than the
corresponding vertebral entry point, as such, the leads should be placed accordingly.
Figure 71-3. Topographical arrangement of dorsal columns of the spinal cord. The dorsal column’s fibers
are somatotopically organized in the following order from medial to lateral: sacral, lumbar, thoracic, and
cervical.
CSF Space
The most important factor determining stimulation parameters is the width of the high conductance CSF
dorsal to the spinal cord (dCSF). Stimulation potentials will flow toward the path of least resistance (or
higher conductance). The depth of dorsal CSF at various spinal levels and its relation to perception of
paresthesia upon stimulation is displayed in Figure 71-4. A larger dCSF would result in lateral spread of
the electrical field and stimulation of dorsal root entry zone nerve rootlets (Figure 71-5). These contain
sensory fibers many of which are proprioceptive and involved in segmental motor reflexes. Their
stimulation is thought to be responsible for the uncomfortable sensations (twitching and pain) experienced
at the discomfort threshold.
Figure 71-4. CSF fluid thickness along the spinal canal. Thickness of dorsal CSF fluid ranges from 2 to 6
mm along the spinal canal. Perception threshold (PT) is directly dependent on dCSF thickness. As noted,
the greatest thickness occurs in the mid-thoracic spine.
Figure 71-5. Anatomy of the spinal canal. The epidural space is circumferential wrapping around the
dura and is bound by the ligamentum flavum posteriorly, the posterior longitudinal ligament and vertebral
bodies anteriorly. Vertebral pedicles and intervertebral foramina with their penetrating nerve roots form
the lateral borders. dCSF thickness is largest at T4-T8. Dorsal root entry zone (DREZ) borders dorsal
columns.
• Informed consent. Both trial and permanent implant of SCS systems are invasive surgical procedures
that carry inherent surgical risk. While the risks for serious adverse events are minimal compared to
other spine surgical procedures, patients should be informed of the following potential complications:
Bleeding
Infection (including risk of meningitis)
Spinal cord injury and paralysis
Nerve damage associated with weakness and numbness
Furthermore, patients should be made aware of the long-term risk of needing revision surgery due to:
Reduced analgesic efficacy of SCS with time
Equipment malfunction with loss of stimulation
Lead migration or damage resulting in loss of stimulation
Lead failure or breakage
Chronic pain (discomfort) around the implanted programmable generator (IPG) site or anchors
• Coagulopathy. Anticoagulated patients who may undergo SCS trial or implant should be managed
according to current American Society of Regional Anesthesia and Pain Medicine (ASRA) consensus
guidelines for neuraxial anesthesia. However, adhering to guidelines does not result in absolute
elimination of all risks of bleeding. The risks to be considered in an anticoagulated patient may extend
beyond the preoperative period and include long-term potential epidural hematoma resulting from
movement of the leads in the epidural space. Important points:
Patients should always be asked about the medications they are currently taking, including vitamins
and herbals.
Coagulation screening tests should be ordered (or hematology consult) for patients suspected of
bleeding disorder.
ASRA guidelines need to be followed for SCS procedures in anticoagulated patients.
• Examine the skin at operative field for skin breakage and erythema and other infection (cellulitis)
signs.
• IV access should always be obtained for fluid administration, antibiotics, and sedation medications.
• Preoperative prophylactic antibiotics should always be administered within 1 hour of start of trial or
incision for implant.
• Patients should be able to lie in a prone or a lateral decubitus position for a long period of time and
communicate with the physician or representative aiding in programming of the device during testing
stages of the procedures. The position should be adjusted to minimize the lumbar lordosis for lumbar
entry procedures (Figure 71-6). The neck should be in flexion for cervical SCS procedures.
Figure 71-6. Patient positioning. Patient is placed in prone position and a bolster should be placed
underneath the lower abdomen to reduce the lumbar lordosis and facilitate epidural access in the lumbar
region (A). For cervical access, with patient positioned in prone position, a bolster is placed underneath
the chest and another pillow or a soft roll at the forehead (B) with the head on flexed position.
TECHNICAL DETAILS OF PROCEDURE

Physicians performing SCS placement should be actively involved in patient positioning as positional
discomfort and lack of fluoroscopic clarity would compromise the success of the procedure. The patient
is typically positioned in the prone position and occasionally in the lateral decubitus position on a padded
surgical table.
• For lower thoracic lead tip, positioning should strive to minimize patient’s natural lumbar lordosis to
facilitate needle entry into the interlaminar space (Figure 71-6A).
• Patient’s head may be turned to the side in cases where leads are not driven into the cervical region;
otherwise it should be kept midline with the cervical spine flexed in a comfortable position (Figure
71-6B).
• In the prone position, a bolster should be placed underneath the lower abdomen to reduce the lumbar
lordosis and facilitate epidural access in the lumbar region (Figure 71-6A).
• For cervical access, with patient positioned in prone position, a bolster is placed underneath the chest
and another pillow or a soft roll at the forehead (Figure 71-6B).
• A bolster under the upper chest that allows neck flexion, facilitates lead entry and steering into the
cervical epidural space (Figure 71-6B).
• In case of lumbar access, arm boards should be positioned in such a way that they do not impede
fluoroscopic views whereas for cervical lead placement, the arms should be tucked to the side of the
patient (Figure 71-6A and B).
Modified Tuohy needles are supplied with each SCS manufacturer’s kits and are used to introduce SCS
leads. In preparation, a small gauge hypodermic needle is used for anesthetizing the skin and subcutaneous
tissue at the point of needle entry and a 3.5-in-long spinal needle is used for deeper local anesthetic
delivery along the planned path of the modified Tuohy needle. Meticulous local anesthesia delivered
along the exact path of lead entry would allow the performance of the lead placement and testing portion
of the procedure with minimal or no sedation. Lidocaine 0.5% to 1% or a mixture of lidocaine and
bupivacaine is typically used for local anesthesia.
Equipment
The basic equipment for SCS includes leads, anchors to stabilize the leads, and an implantable pulse
generator (IPG). Leads and anchors are supplied as a sterile kit opened at the instrument table. The IPG is
provided also at implant time in a sterile box. There are two types of leads currently available:
cylindrical percutaneous leads and surgical (paddle) leads.
Percutaneous Leads
Percutaneous leads are flexible cylindrical polyurethane catheters with multiple evenly spaced electrode
contacts arranged at the distal end. Circumferential design of the electrodes results in the possibility of
360-degree dispersion of the stimulation current.
• Percutaneous leads contain either 4 or 8 contacts (quadripolar or octapolar). The general trend is to
utilize octapolar leads for SCS stimulation and quadripolar for peripheral nerve and nerve field
stimulation. Greater than 8 contact leads will be coming to the market and some have been FDA
approved.
• Electrode contacts are small plates composed of platinum-iridium alloy ranging 3 to 6 mm in length.
• Edge-to-edge spacing of the electrodes ranges from 1 to 12 mm depending on the manufacturer and type
of lead. Spacing of the contacts has been shown to influence steering of the electrical field and
enhanced resolution of stimulation.
• Lead length is standard and varies with manufacturer. Commonly the lengths vary between 30 and 80
cm. Lead length should be taken into consideration for appropriate spine entry point and generator
placement.
Anchors
Anchors are used to stabilize the leads to fascia or the supraspinous ligament. Good anchoring technique
plays a major role in prevention of lead migration—the most common etiology for future treatment failure
and surgical revision. All SCS system manufacturers supply their anchoring systems. There are 2 types of
anchors: traditional silicon anchors with suture sleeves and mechanical anchors. Mechanical anchors
have been developed to provide better holding force than traditional anchors and to also bypass the step
of tying the anchor to the lead (Table 71-1).
TABLE 71-1. Mechanical Anchors Developed by Three SCS System Manufacturers

Pulse Generators
Three types of generators are available: radiofrequency (RF), primary cell (non-rechargeable) battery,
and rechargeable battery. RF systems are not used much anymore as fully implantable systems are widely
available, more convenient and preferred by patients.
• Non-rechargeable systems (IPG) were introduced three decades ago and have a variable life span of 1
to 5 years depending on patient use and parameters of stimulation.
• Rechargeable IPGs offer renewable power source and a variable life span, typically longer than 5
years while maintaining high output stimulation (Table 71-2).
TABLE 71-2. Rechargeable IPG

Parameters of Stimulation
When initiating SCS, the minimum current at which patients perceive paresthesia is defined as the
perception threshold (PT). As current continues to be increased, patients may experience discomfort at
higher amplitudes. The minimum current at which patients perceive discomfort is defined as the
discomfort threshold (DT). Typical stimulation is carried out between PT and DT.
Paresthesia coverage depends on the shape of the electrical field surrounding the nerve fibers as well
as the recruitment of the nerve fibers. There are 3 variables characterizing the electrical stimulation of the
spinal cord: frequency, amplitude, and pulse width. Fine tuning of the paresthesia field is achieved by
modifying the following parameters:
• Amplitude (A, in mA or milliamperes). Affects the intensity and extent of paresthesiae. Increasing the
amplitude expands the area of coverage but could result in uncomfortable stimulation. Typical range:
1.0 to 5 mA.
• Pulse width (PW, in μs or microseconds). PW is the duration of single delivered square stimulation
pulse. Higher pulse width may help in recruiting smaller nerve fibers in the dorsal column. Pulse width
range varies with IPG manufacturer with values ranging from 20 to 1000 μs.
• Frequency (F in Hz or hertz). Frequency is the number of pulses per second. Frequency affects the
quality of paresthesia and may be perceived by patients as “smooth” sensation or more of a “thump”
sensation.
The use of higher amplitudes, higher pulse widths, and higher frequencies would obviously increase the
energy consumption and tax recharging frequency.
INTRAOPERATIVE TECHNICAL STEPS OF PERCUTANEOUS

TRIAL OF SPINAL CORD STIMULATION
• Prior to implant of a spinal cord stimulation device, a trialing period ranging from 3 to 7 days or
longer takes place.
• Trial success may not be related to duration of trial or number of leads, though a minimum duration of 3
days should be considered except under extenuating circumstances.
• The consensus of most of the literature suggests that >50% pain relief is the outcome for judging a
successful SCS trial.
• A trial of SCS can be performed as a staged procedure or with no intention for lead reuse. If performed
as staged procedure, an incision is made and leads are secured to deep fascia and an extension is
tunneled and exteriorized to the contralateral side of future IPG implant site. In case of an unsuccessful
trial, this would require a new surgical procedure to remove the leads.
• The overwhelming majority of percutaneous implanters place leads through a modified Tuohy needle
with no intention to leave the lead in place for long-term use. These trial leads can be easily removed
in the office without requirement of any surgical procedure.
Trial Procedure
1. Patient is placed in the prone or lateral decubitus position with optimal interlaminar space exposure
and spine alignment.
2. Sterile techniques are followed throughout.
3. Epidural access is achieved with a modified Tuohy needle using the loss of resistance (LOR) technique
under guidance of fluoroscopy.
4. Needle bevels are turned to facilitate lead steering (Figure 71-7A).
Figure 71-7. Technique of lead placement. Fluoroscopic views: (A) bilateral Tuohy needle placement;
(B) lateral fluoroscopic view of confirmation of epidural access by both Tuohy needles; loss of resistance
can be performed in this view; (C) lead steering into the epidural space; (D) later view confirms needle
positioning on the posterior epidural space.
5. Lateral view is preferred while performing LOR (Figure 71-7B).

6. Needle entry level into the epidural space for percutaneous lead placement depends, in part, on
anticipated final placement of the lead(s); and should be at least 2 to 3 vertebral levels below target
lead tip position.
Technical Issues
• Common needle entry for lower extremity and/or axial low back pain occurs around the mid to upper
lumbar region (Figure 71-8).
Figure 71-8. Technique of lead placement. Posteroanterior (PA) view is used initially to visualize spine
anatomy and identify the anatomical landmarks which are marked by opaque instruments (A). Skin entry
should occur at some point between the ipsilateral two pedicles below the desired interlaminar space,
depending on patient’s body habitus and spinal anatomy (A and B). Needle entry into the epidural space
should occur as close as possible to midline (B).
• Skin entry commonly is marked along a line joining the L2, L3, or L4 pedicles (Figure 71-8). Entry into
the epidural space should be as flat as possible, depending in part, on the body habitus of the patient.
• Entry into the epidural space, should occur between one to two vertebral body levels cephalad to the
skin entry point (Figure 71-8).
• Because the epidural space is obliterated in cases of previous laminectomy/spine fusion, entry into the
epidural space should occur above such levels, at virgin sites.
• A paramedian approach should be used to avoid traction forces of the supraspinous and interspinous
ligaments as well as the possibility of the spinous processes causing fracture of a lead placed through a
midline approach.
• The percutaneous implanter should not hesitate to use a longer than standard epidural needle to ensure
the angle of approach to the epidural space is shallow (<45 degrees angle with the skin whenever
possible).
• Entry of the needle into the epidural space should occur as close as possible to the midline to ensure
posterior placement of the epidural lead (Figures 71-7 and 71-8).
• A lateral view should be taken to ensure the lead has not migrated anteriorly in the epidural space
(Figure 71-9C).
Figure 71-9. Lateral fluoroscopic view is necessary for appropriate lead placement. (A) Tuohy needle
access in the epidural space; (B) leads are floated and steered smoothly cephalad into the epidural space
toward the target continuously in the AP view; (C) lateral fluoroscopic view shows wrong placement of
the left lead on the anterior epidural space; (D) lead was withdrawn and steered into posterior epidural
space initially in the lateral view, than to appropriate location on AP view and final confirmation on the
lateral view.
• Rotation of the bevel of a near-midline Tuohy needle will determine the initial steering direction of the
leads into the epidural space.
• Leads are threaded though the needle and steered in the PA view, close to midline, after posterior
epidural positioning is confirmed.
• Once lead tips are sited at the appropriate vertebral segment (see coverage segment: “Lead Location
and Paresthesia Coverage”), they are connected through an extension to an external power source and
stimulation testing would commence. During this phase, the physician’s interaction with the patient and
the manufacturer representative assisting with stimulation parameter programming is important. Small
movements in lead position and various stimulation electrode configuration patterns and parameters
are employed to achieve >80% overlap between pain area and paresthesia coverage.
• Final lead placement should always be individualized to the patient’s response during intraoperative
mapping:
For upper extremity coverage, lead tips are commonly placed between C2 and C7. Needle insertion
may occur in the upper thoracic region between T2 and T6 (Figure 71-10). A choice exists between
the upper and lower thoracic region.
Figure 71-10. Cervical placement of SCS leads for upper extremity coverage. (A) Epidural access at T4-
T5 intralaminar space is sought for cervical spinal cord stimulation; (B) leads are steered cephalad to
C4-C6 for coverage of the upper extremity.
The upper thoracic area is a stable and good site for needle placement. Skin entry location of T2
to T6 allows the needle to advance in a shallow orientation to the epidural space; however,
placement at this level requires a high degree of operator skill and is not recommended for
novices or for physicians with limited experience and limited volume of SCS trials.
The mid-thoracic area, between T5 and T9, may be most difficult to access epidurally due to
anatomic angulation of the spinous processes.
Epidural entry into the lower thoracic spine is similar to entry into the upper lumbar epidural space.
For coverage of the lower extremities, mid to low thoracic lead tip placement is common and entry
into the epidural space is generally accomplished anywhere from T12-L1 to L4-L5 depending on
anticipated final lead tip position.
• Percutaneous leads should travel at least 2 vertebral bodies inside the epidural space for increased
lead stability.
• Given sufficient pain relief (>50% relief over baseline levels) and pleasant experience with
stimulation, leads are removed in physician’s office a few days after a temporary percutaneous trial
and the patient and implanter typically come to a consensus to proceed with a permanent implant.
• Permanent implant is scheduled a few weeks after the trial which allows sufficient time for any minor
tissue trauma to heal as well as any indolent infection from the trial to manifest prior to permanent
implant.
• In the case of no or minimal pain relief, permanent implantation is not performed.
Lead Location and Paresthesia Coverage

The following lead locations have been typically mentioned to achieve specific coverage:
• High cervical regions such as C2 can cover regions of the posterior occiput and occasionally the lower
jaw.
• C2-C4 stimulation provides coverage of the neck, shoulder, and upper extremities and the lower face
as a result of involvement of the descending nucleus of the trigeminal nerve.
• C5-C6 stimulation affects the entire upper extremity including the hand.
• C7-T1 may cover the arms, anterior chest wall, or the axilla.
Occasionally, placement between C4 and T1 may result in coverage of upper and lower extremities,
particularly when using current fractionation.
• Lateral placement at T11-T12 covers the anterior thigh.
• T11-L1 can cover the posterior thigh and the foot.
• T8-T10 midline placement of the electrodes in general seems to provide the best coverage for lower
extremity pain.
• Low back pain may be very difficult to cover because mid-thoracic stimulation can also affect the chest
and abdominal wall and stimulation at lower levels preferentially recruits lower extremity fibers; T7-
T8 levels are usual targets.
There have been case reports demonstrating 4 limb paresthesias with leads placed at C1-C2 (with
retrograde paddle surgical leads) and in the lower cervical region (and down to T2; with percutaneous
leads). This observation of 4-limb stimulation has been useful in the rare patient with pain in upper and
lower extremities and may circumvent placement of a second generator and 2 additional leads.
Fluoroscopic Views
Fluoroscopic clarity of spine anatomy is aided by appropriate patient positioning on the surgical table.
• Posteroanterior (PA) view is used initially to visualize spine anatomy and identify the anatomical
landmarks. A slight (5-10 degrees) caudal tilt helps aligning vertebral end plates of the upper lumbar
spine. According to the entry level, in the PA view:
Spinous processes should be identified and aligned precisely at vertebral midline.
Vertebral end plates should be aligned to crisp, linear horizontal position.
The pedicles at the epidural entry level and 2 levels below should be identified.
Skin entry should occur at some point between the ipsilateral 2 pedicles below the desired
interlaminar space, depending on patient’s body habitus and spinal anatomy (Figure 71-8).
Needle entry into the epidural space should occur as close as possible to midline (Figures 71-7A
and 71-8B).
• The lateral view is used to confirm needle tip positioning as well as to advance the Tuohy needle,
especially when the “loss of resistance” (LOR) technique is ambiguous. Frequent comparison between
AP and lateral views ensures correct needle tip positioning in the middle of the posterior epidural
space.
• The lateral view is particularly useful in cases whereby 2 Tuohy needles are placed unilaterally in the
same interlaminar level (Figure 71-11).
Figure 71-11. Lateral approach to SCS. Unilateral, same intralaminar space placement of Tuohy needles
using lateral fluoroscopy (A). First needle confirmed in the epidural space serves also as a guide for the
second needle access to epidural space (B).
• Lead steering is performed in PA view (Figures 71-7C, 71-9A and B, and 71-15B). However, the
lateral view may be used when driving the lead, to confirm location in the posterior epidural space
versus anterior epidural space (Figure 71-9C-D).
• Pulsed mode fluoroscopy (with half- or quarter-dose exposure, as opposed to continuous fluoroscopy)
is helpful in reducing radiation exposure while steering the SCS lead to its final positioning, slightly
off the midline over the dorsal column.
• Needle entry too far off midline and lead steering way off midline will likely result in erroneous
placement of the lead in the anterior epidural space and that can be confirmed on lateral fluoroscopy
(Figure 71-9C).
• Once final positioning is confirmed, including satisfactory patient paresthesias at acceptable
programming parameters, a single fluoroscopic image is obtained as a reference.
• Lead anchoring is then performed, either to the supraspinous ligament or fascia in permanent implants
or to skin in trials; another single frame roentgenogram is taken to confirm that the lead(s) did not move
from the desired position.
Permanent Implant
Permanent implant generally follows a successful SCS trial. Percutaneous SCS implant is typically an
outpatient procedure and patients are discharged with oral analgesics for postoperative pain and usually 2
to 3 days of antibiotic prophylaxis dependent also on risk factors and comorbidities.
• The implantable pulse generator (IPG) site is determined. Anatomical considerations, patient
preferences and esthetics determine the IPG location. This position, along with skin entry point and
lead tip target determine lead length.
• Prophylactic intravenous antibiotics should be administered within 1 hour of the permanent implant.
• The patient is taken to the OR and positioned on the surgical table (Figure 71-6A and B).
• Sterile surgical preparation takes place initially with a “defatting” isopropyl alcohol prep followed by
chlorhexidine (Figure 71-12). Many implanters use an Ioban drape over the surgical site. Surgical
gown, mask, and protective head and foot wear should be used.
Figure 71-12. Procedure steps-operative field preparation. Sterile surgical prep takes place initially with
defattening isopropyl alcohol (A) followed by chlorhexidine (B). Many implanters use an Ioban drape
over the surgical site. Surgical gown, mask, and protective head and foot wear should be used.
• Fluoroscopy and opaque instruments are used to mark anatomical landmarks (Figures 71-8 and 71-13).
Decision on the level of interlaminar space access is made. Sufficient local anesthetic is used to
anesthetize the skin and needle trajectory.
Figure 71-13. Procedure steps—fluoroscopic anatomy and incision. Fluoroscopic guidance and opaque
instruments are used to identify the anatomical landmarks. After marking the incision line (A) starting
from nearly 1.5 levels from intended intralaminar space a 4-5 cm incision is made (B).
• At this point, needle access for lead placement is achieved similarly to that described for the trial. A
skin incision before skin needle entry (Figure 71-13B) or afterward with the modified Tuohy needle in
place is made longitudinally (~5 cm) and dissection down to the fascia/supraspinous ligament is
performed with the help of electrocautery (Figure 71-14A). Local anesthetic is applied along the
needle path (Figure 71-14B). Hemostasis is achieved with electrocautery carefully, as the probe
should not come in contact with the needle.
Figure 71-14. Procedure steps—fluoroscopic anatomy and incision. Sharp dissection to the level of
fascia is commenced and electrocautery is used for good hemostasis (A). Using Tuohy needle and
following a paramedian trajectory tissues layers are anesthetized with a mixture of lidocaine 0.5% and
bupivacaine 0.25%.
• Two leads may be placed at the same interlaminar space using a paramedian approach with one needle
penetrating on each side of midline. However, superimposed placement of both needles from the same
paramedian side is also useful (Figure 71-11). The first needle placed would serve as an excellent
marker for where the posterior epidural space lies on the lateral view. Caution should be used not to
damage the lead with the second needle; hence, placement of the second needle should occur inferior to
the first needle when both needles enter the epidural space on the same side. A paramedian approach
avoids tension forces of the supraspinous and interspinous ligaments on the lead; as well as avoids
spinous processes from shearing or fracturing the lead as might occur with a midline approach.
Entry into the epidural space should be as flat as possible, depending in part on the body habitus of the
patient (Figure 71-15A). Entry into the epidural space should occur between 1 to 2 vertebral levels
cephalad to the fluoroscopic skin entry point (Figure 71-8). Implanters may access the epidural space
using fluoroscopic guidance in either PA or lateral position (Figures 71-7B and 71-8). The latter,
however, requires familiarity with the posterior epidural line in this view. Lead steering can be is
performed in AP view and under live fluoroscopy for exact positioning (Figure 71-15B-D). Occasionally
a combination of epidural and subcutaneous leads is used to achieve a better coverage for low axial
postlaminectomy pain (Figure 71-16).
Figure 71-15. Procedure steps—lead placement. Loss of resistance is performed using a glass syringe
and fluoroscopic guidance with AP or lateral views. Entry into the epidural space should be as close as
possible to each side of fluoroscopic spinal cord midline (A). Post epidural access lead should be floated
without much resistance in the epidural space (B). Lead is steered into the epidural space to the desired
level (C). Rotating the bevel of the Tuohy needle can change the initial lead direction as desired (D).
Figure 71-16. Combination of epidural and subcutaneous lead placement on a patient with
postlaminectomy syndrome.
A lateral view should be taken to ensure the lead has not migrated anteriorly in the epidural space
(Figure 71-9C), even though patients may experience discomfort during steering in the anterior epidural
space or stimulation would result in muscle twitching.
SUBCUTANEOUS CUT-DOWN AND LEAD ANCHORING

TECHNIQUES
After lead final placement, the fluoroscopic view would serve as a guide to ensure no change in the
position of the leads has occurred. Meticulous anchoring of the leads is essential to prevent subsequent
migration of the lead array. Anchors should be sited as proximally as possible on the lead with the
proximal part of the anchor end dipping into the deep fascial tissue.
Nonabsorbable sutures should be placed into deep fascial planes or around the supraspinous ligament
that will hold the anchor in place through its suture sleeves.
Currently, all manufacturers have mechanical anchors (Table 71-1) that secure the lead independent of
the need to tie a suture around both lead and anchor. A suture is still taken through the fascia/supraspinous
ligament to secure the mechanical anchor/lead complex through the suture sleeves of the anchor.
Frequent fluoroscopic images during the anchoring process and a final fluoroscopic image in both the
PA and lateral views at the end of this process ensures that there has been no lead migration.
Generator Site Location and Preparation

• Generators can be placed in the buttock, the abdominal wall, the flank, along the mid-axillary line, or
in the subclavicular area (for cervical leads with upper thoracic needle placement). For buttock
placement, the generator is placed above where the patient sits but below the belt line. However,
generator placement in the buttock may predispose patients more to lead migration. A single incision
generator placement may be performed just off the midline in patients whose body habitus may allow
such positioning (Figures 71-17 and 71-18).
Figure 71-17. Procedure steps—single incision technique. A pocked is made by dissecting above the
fascia laterally (left or right) below the incision edge (A). IPG is fixed to fascia with two Surgilon sutures
(B) to prevent rotation or even erosion.
Figure 71-18. Single incision technique images. Advantages of this technique are reduced operating time
and less postoperative pain. (A) Leads are secured onto fascia and through the same incision a
subcutaneous pocked is made by careful dissection just above the fascia; (B) fluoroscopic view of the
anchored leads; (C) fluoroscopic view of the IPG and anchors. Single incision technique (no need for
tunneling; IPG placed 2-4 cm from anatomical midline; system implanted through a single incision).
• The depth of the pocket is commonly 1 to 3 cm and recommendations vary among the companies for
actual depth of generator placement. Ideally, the generator is placed deep enough to avoid subsequent
discomfort or erosion but superficial enough to allow for recharging and interrogation of the system
with subsequent programming.
• When the generator is not sited at the lead(s) incision site, the lead(s) is/are tunneled from the anchor
site to the pocket using a specialized tunneling device. It is advisable to leave a strain relief loop in the
back incision as insurance against subsequent patient movement that might dislodge the lead(s) or
cause migration.
• The electrical contact sites on the lead should be inspected for blood or tissue products. If tainted, the
lead contacts should be cleaned with a wet, then dry, sponge prior to insertion into the generator. After
connecting to the generator, excess lead is coiled and maintained underneath the generator. The IPG is
placed with the inscription up toward the skin side.
• The integrity of the system should be confirmed with an impedance check prior to closure.
• The generator is sutured into the pocket to prevent its migration, flipping over, or twiddling by the
patient. A final AP and lateral fluoroscopic image is obtained to demonstrate no migration has occurred
during the anchoring process.
• In 2006, Pyles introduced the notion of single incision for the implantation of the SCS leads and IPG
device in the lumbar spine. Hayek reported at the International Neuromodulation Society meeting on 26
patients receiving single incision SCS implants (Figures 71-17 and 71-18). Kumar and colleagues
suggested that the traditional placement of the generator in the buttock pocket might lead to increased
strain and fulcrum effect on the leads and anchors. Having only one incision may also decrease the
amount of postoperative pain that patients experience. There is also reduced operating time that may
reduce the likelihood of time-sensitive complications such as infection, which usually occurs at the
generator incision site. A potential complication that is unique to this technique is that revision surgery
may be more difficult if the generator is enveloped in the same planes of scar tissue as the electrodes
and the anchors; should an infection occur, the potential of spread to the epidural space may be higher
given proximity of the generator to the spine.
• The patient should be followed up at the clinic on postoperative day 5-7.
• The implanted patient should be encouraged to call with any signs of infections such as fever, exquisite
pain at generator site, skin erythema and excessive edema.
• Patients are advised to call the pain service for any procedure-related complications and/or any
unexpected neurological deficit.
• Patients should be monitored closely for the following: fever, bleeding, numbness, exacerbation of
symptoms, neurological deficits, weakness, extreme pain, and positional headache suggesting dural
puncture. Most common neurological complication in SCS implantation procedures is inadvertent dural
puncture. Reports in the literature indicate an incidence of less than 1% in experienced hands.

Most complications of SCS are not life threatening and can be resolved by explanation of the system:
• Technical complications include electrode migration, electrode breakage, hardware malfunction, and
other complications related to the hardware.
• Biological complications include infection, seroma, headache, neurological sequelae, pain at the
implantation site, and allergic reaction.
• Other complications include undesirable stimulation, changes in stimulation with position changes,
system tolerance, and skin erosion.

Clinical Pearls
• A shallow needle entry angle into the epidural space greatly facilitates lead placement.
• Needle entry into the epidural space should occur as close as possible to the anatomic midline
(spinous process).
• Leads should be advanced under fluoroscopy while maintaining a course along or just off the anatomic
midline in a posteroanterior view.
• Percutaneous leads should travel at least 2 vertebral bodies inside the epidural space to allow for
improved lead stability.
• Careful anchoring of the leads and placing strain relief loops may decrease the risk of lead migration.
• Mechanical anchors may reduce the risk of lead migration.
Pitfalls
• Proper training and background is an absolute prerequisite to practicing SCS.
• Surgeon’s experience and careful patient selection are important considerations for curbing SCS
complications.
• Novices or practitioners with limited SCS experience or volume of cases should not attempt cervical
SCS placement and should refrain from tackling complex cases.
• Antibiotic prophylaxis and good surgical skills are likely to result in lower infection rates.
• Overuse of the therapy may have significant untoward consequences.
Suggested Reading
Barolat G, Massaro F, He J, Zeme S, Ketcik B et al: Mapping of sensory responses to epidural
stimulation of the intraspinal neural structures in man. J Neurosurg. 1993;78:233-239.
Cameron T. Safety and efficacy of spinal cord stimulation for the treatment of chronic pain: a 20 year
literature review. J Neurosurg. 2004;100:254-267.
Compton A, Shah B, and Hayek SM. Spinal cord stimulation: a review. Current Pain and Headache
Reports. November 16, 2011. [Epub ahead of print]
Hayek SM, Veizi IE, Stanton-Hicks M. Four-limb neurostimulation with neuroelectrodes placed in the
lower cervical epidural space. Anesthesiology. 2009;110(3):681-684.
Turner JA, Loeser JD, Deyo RA, Sanders SB. Spinal cord stimulation for patients with failed back
surgery syndrome or complex regional pain syndrome: a systematic review of effectiveness and
complications. Pain. 2004;108:137-147.
CHAPTER 72
Anterograde Versus Retrograde Lead Placement

Marshall D. Bedder
INDICATIONS
The discussion for an anterograde approach versus a retrograde approach to lead placement for spinal
cord stimulation (SCS) has evolved in relationship to optimal coverage for pelvic pain conditions. Early
attempts to treat bladder pain focused on retrograde placement of SCS leads to the S3 foramen.
Unfamiliarity of many practitioners with this technique, the more difficult technical aspects, and the
variable anatomy of the sacrum have all posed challenges to this approach. Anterograde placement with
lead positioning at the T10-T12 levels has shown great promise in pelvic pain structure coverage. It is
now known that retrograde placement is actually a peripheral nerve stimulation performed within the
spinal canal by stimulating specific sacral nerves. Whereas anterograde placement is true spinal cord
stimulation giving rise to stimulation paresthesia not only in the pelvic distribution but also in the lower
extremities. Anterograde stimulation produces an electrical field at the spinal cord activating all known
mechanisms of action, whereas it is highly unlikely that peripheral nerve stimulation activates as many
different mechanisms of action.
Indications for retrograde placement/anterograde placement include:
• Interstitial cystitis, urge incontinence, urgency/frequency
• Postoperative pelvic pain/pelvic adhesions
• Endometriosis
• Postradiation pelvic pain
• Vulvodynia
• Vaginal pain
• Coccydynia
CONTRAINDICATIONS
The basic procedural/surgical contraindications hold for a trial of retrograde or anterograde SCS. These
include:
• Anticoagulation
• Thrombocytopenia
• Sepsis
• Localized infection at or near insertion site
Added contraindications specific to SCS include:
• Implanted cardiac defibrillator
• Inability to use or understand the equipment
• Need for ongoing repeat MRIs
• Untreated psychiatric or addiction issues
RELEVANT ANATOMY
Pelvic Innervation
1. Sympathetic (T12-L2)
a. Superior hypogastric plexus—largest sympathetic contribution
b. Sympathetic chain—gray rami communicantes connect to sacral ventral primary rami
c. Sacral splanchnic nerves—smaller contribution of sympathetics to pelvic viscera
2. Parasympathetic
a. S2, S3, S4
i. Inferior hypogastric
plexus—preganglionic
ii. Postganglionic fibers innervate distal colon, rectum, bladder, genital organs
All pelvic viscera receive dual innervation, sympathetic and parasympathetic. Both converge at the
inferior hypogastric plexus and are redistributed either directly to target organs within the plexus or via
smaller subsidiary plexuses.
3. Somatic efferent and afferent innervation to the pelvis
a. S2-S4
There is a recognized midline dorsal column pathway within the spinal cord that mediates the
perception of visceral pain and if interrupted relieves visceral pelvic pain in cancer patients. Therefore,
SCS systems and settings that can drive stimulation deeper into the dorsal spinal cord may respond better.
Recent studies have shown higher pulse width settings drive activation of the more medial fibres and may
be optimized at 900 to 1000 ms. Thus, anterograde stimulation at T11-T12 with high pulse widths may
represent the best potential for achieving a bilateral pelvic analgesic response. This is in distinction to a
unilateral discreet activation that may be achieved with retrograde stimulation of individual sacral nerve
roots.
• Informed consent and full explanation of all potential risks and complications including infection both
superficial and deep including epidural abscess.
• Anticoagulation status. Patients on coumadin should have their INR normalized with consultation and
consent from their cardiologist. Antiplatelet medications should be stopped for 7 days and all other
anticoagulation medications recommendations should follow the most current ASRA guidelines.
• Physical examination of the proposed area of epidural access for evidence of infection, skin ulceration,
or rash.
• Patient must be able to lie prone on bolsters or Wilson positioning frame for intended length of
procedure.
• Intravenous access for IV fluids, preoperative prophylactic antibiotics, and medications for sedation or
any untoward reactions.
• Cefazolin 1 gm, or 2 gm for patients over 80 kg up to 1 hour pre-needle insertion. Clindamycin 900 mg
for patients with allergy to cephalosporins. Vancomycin 600 to 1000 mg for patients with previous
history of MRSA infections.
Fluoroscopic Views
• Anterograde positioning. Appropriate craniocaudal positioning to open intralaminar spaces at L2-L3
and/or L3-L4 (may use best intralaminar space from T12-L3 down). Needle placement is a paramedian
approach starting with insertion over the pedicle on the ipsilateral side one level below intended
intralaminar target entry position.
• For dual lead trials, use one level below on the ipsilateral side.
• Another option is to use the same intralaminar entry point starting on the contralateral side.
• Retrograde positioning. Appropriate craniocaudal views to open intralaminar space below L2 so that
needle insertion is below conus.
• Skin entry at either 10 o’clock or 2 o’clock position, aiming at lamina and walking off to the midline
for entry into the epidural space.
Equipment
• 14-gauge Epimed Coude needle (Pyles epidural needle another good option)
• Pulsator loss of resistance syringe
• 25- or 27-gauge needle for skin infiltration
• 18-gauge needle for skin penetration
• Mastisol
• Merit Stayfix dressing
• Opsite
• SCS leads of choice
Medications
• 1% lidocaine
Technique
Preferred Technique for Anterograde Positioning
I prefer to use a left-sided paramedian placement technique with ipsilateral placement of both leads in a
dual lead trial. This will mimic placement for a subsequent implant (if the trial is successful) as this
facilitates placement through one incision with no need to cross the midline with one lead. It also allows
the option for a “one incision technique” with development of the generator pocket lateral from the single
incision if desired.
The development of the Epimed Rx Coude tip epidural needles (Figure 72-1) has made the placement
of cylindrical SCS leads much easier and safer. The current needles on the market are the Epimed 14-
gauge Rx Coude needle, the RX-2 (Figure 72-2), and the similar gauge Pyles (Figure 72-3A-E) epidural
needles. These needles allow entry into the epidural space at a much reduced angle and facilitate easy
passage of the lead into the epidural space. Their shape also allows enhanced ability to steer the lead
right or left at the initial insertion by turning the bevel left or right in the epidural space. The RX rear heel
is rounded to resist lead shearing during placement. The RX-2 blunt obturator stylet can provide safer
rotation and advancement of the needle and is purported to deflect any neural structures during needle
rotation.
Figure 72-1. 14-gauge RX Coudé. (Reproduced with permission from Epimed.)
Figure 72-2. RX-2 Coudé with blunt obturating stylet. (Reproduced with permission from Epimed.)
Figure 72-3. (A-E) Gauge Pyles epidural needles.
Tip: Have the bevel facing caudally on initial insertion to enhance appropriate tissue penetration
toward the intralaminar space. The practitioner can then turn the bevel cephalad as he/she nears the
epidural space as viewed on lateral fluoroscopic view. There are many techniques for epidural access,
but I have used the loss of resistance technique with a Teflon-coated epidural syringe, combined with A/P
and lateral fluoroscopy. The older technique of using glass syringes is less sensitive and may pose some
risk. Any blood from contacting periosteum can coagulate in the syringe and there will be loss of glide
within the syringe potentially leading to a wet tap. In elderly patients who have significant calcified
ligamentum flavum, glass syringes have been known to break at the barrel.
• The patient is placed in a prone position with either pillows or bolster under the abdomen to reverse
the lumbar lordotic curvature (Figure 72-4). Alternatively, the patient can be positioned on a Wilson
frame for optimum stability.
Figure 72-4. Positioning.
• The 12th rib is identified under AP fluoroscopy and the best intralaminar entry site is identified.
• The pedicle corresponding to one level below the proposed intralaminar entry site is identified (Figure
72-5).
Figure 72-5. Entry point for Coude needle.
• A wide field around this region is prepped with Chloroprep. Chlorhexadine has been shown to be far
superior to iodine-based skin prep solutions in reducing skin bacteria count.
• The prepared area is draped with either squared off surgical towels or adhesive transparent 3M
Steridrapes (1010).
• An appropriate surgical aperture drape is then used for infection prevention (Figure 72-6).
Figure 72-6. Surgical draping of SCS trial patient.
• The previously identified pedicle is marked and will be the site of skin entry.
• Local anesthetic, 1% lidocaine, is infiltrated with a 27- or 25-gauge needle to provide appropriate skin
and subcutaneous analgesia.
• A skin nick is made with a 20-gauge needle to facilitate insertion of the 14-gauge epidural needle.
• The needle is inserted and directed under live fluoroscopy medially toward an imaginary midline entry
point at the desired intralaminar space one level above the pedicle insertion point. Using a long-
handled forceps can facilitate directing the needle tip under live fluoroscopy while keeping the
operators hands well out of the image intensifier (Figure 72-7).
Figure 72-7. Using a forceps to direct needle to intralaminar.
• Using A/P and lateral fluoroscopy combined with the loss of resistance technique the needle is placed
successfully into the epidural space (Figure 72-8).
Figure 72-8. Lateral view of dual lead insertion.
• The use of the lateral fluoroscopic view is important as the needle enters the epidural space. You will
be in the correct position for lead insertion to make sure the lead entry is in the posterior epidural
space.
• A second lead is placed one level below on the ipsilateral side (Figure 72-9).
Figure 72-9. Dual lead insertion ipsilateral.
• A/P fluoroscopy is then used to guide the leads to the appropriate thoracic level, usually T10-T12 for
pelvic pain, based on cutaneous stimulation paresthesia reports by the patient during the on table trial
(Figure 72-10).
Figure 72-10. Dual lead final placement.
Preferred Technique for Retrograde Placement

• Positioning, prepping, and equipment are the same as above.
• Craniocaudal tilt of the C-arm is used to open the intralaminar space at either L2 or L3, which is below
the conus of the spinal cord for safety in needle insertion.
• The desired skin entry point is overlying either the 10 o’clock or 2 o’clock position on the lamina
(Figure 72-11).
Figure 72-11. The 10 o’clock and 2 o’clock entry position.
• As opposed to the normal entry technique for anterograde epidural needle placement, the goal is to use
the periosteum as a backstop from which to advance the Coude needle into the epidural space using
direct fluoroscopy combined with the loss of resistance technique.
• The angled bevel on the Coude style needles allows for the easiest insertion in a retrograde approach.
• The needle bevel can either be directed directly medial and turned once the epidural space is entered,
or directly on an angle into the epidural space (Figure 72-12).
Figure 72-12. Retrograde needle placement.
• The lead of choice is inserted into the epidural space with no regard for anterior versus posterior
placement as this has no bearing in a retrograde placement.
• The lead must be steered and directed into the desired sacral foramen depending on diagnosis of injury
or desired level intended to treat (Figures 72-14 and 72-15).
Figure 72-13. Unilateral retrograde lead placement.
Figure 72-14. Bilateral retrograde lead placement.
Figure 72-15. Mastisol, Stayfix dressing, and Opsite.
• The lead only needs to enter the foramen and does not need to extend beyond the foramen.
• On the table, testing for appropriate stimulation paresthesia is then carried out and optimized.
Preferred Lead Fixation
• Many techniques have been described for anchoring temporary percutaneous trial leads and the
following is my preferred technique.
• The inferior lead insertion site is anchored first, with the skin swabbed with mastisol (Figure 72-16).
Figure 72-16. Apply lower lead Stayfix dressing first.
• A Merit, Stay-fix dressing is applied to the skin and the lead is carefully placed through the split into
the adhesive groove. The cover adhesive tab is then massaged onto the lead to ensure adherence
(Figure 72-17).
Figure 72-17. Two trial leads in place with Stayfix dressings.
• This is then repeated for the upper lead insertion site.

• A clear adhesive dressing is then placed over both lead anchors and tape is used along the
adhesive/skin boundary.
• As per ASC protocol, the patient is always called the next day to assess for any problems or issues.
• The patient is instructed to avoid getting the insertion sites wet, and to only sponge bathse.
• A small amount of bleeding from the needle insertion sites may occur and the patient and family are
informed of this. No significant bending or heavy lifting is allowed.
• Any signs of weakness, urinary, or bowel incontinence, significant bleeding or increased pain should
be reported.
• Assessment for correct stimulation paresthesia is verified daily by either office staff or device
manufacturer field representatives, as well the patient is seen in office mid- trial for reassessment and
reprogramming if necessary to ensure an effective trial.
Suggested Reading
Al-Kaisy AA, Khan KR. Sacral nerve root stimulation for painful bladder syndrome/interstitial cystitis.
In: Krames E, Peckham HP, Rezai AR, eds. Neuromodulation. Blackwell Publishing; 2009:931-944.
Alo KM, Gohel R, Corey CL. Sacral nerve root stimulation for treatment of urge incontinence and
detrusor dysfunction utilizing a cephalocaudal intraspinal method of lead insertion: a case report.
Neuromodulation. 2001;4(2):53-58.
Bedder MD, Bedder H. Spinal cord stimulation surgical technique for the non-surgically trained.
Neuromodulation. 2009 Apr;1-19.
Kapural L, Narouze SN, Janicki T. Spinal cord stimulation is an effective treatment for the chronic
intractable visceral pelvic pain. Pain Medicine. 2006;7(5):440-443.
McIntyre PJ, Bedder MD. Complications of spinal cord stimulation. In: Deer T, Levy R, Hayek S, eds.
Neurostimulation for the Treatment of Chronic Pain. Elsevier; Amsterdam; 2011:134-146.
CHAPTER 73
Dorsal Root Ganglion Stimulation: Anatomy, Physiology, and

Potential for Therapeutic Targeting in Chronic Pain
Jeffery Kramer, Christine E. Draper, Timothy R. Deer, Jason E. Pope, Robert Levy, and
Eric J. Grigsby
INTRODUCTION
Primary sensory neurons (PSNs) process and transmit a multitude of sensory information from the
periphery to the central nervous system. In this regard, they are a key component of the initial pathway by
which pain (as well as a variety of other sensory information) is transmitted from both peripheral and
axial structures to secondary and tertiary order neurons in the central nervous system. In an acute sense,
pain transduction serves as a safety mechanism to protect tissues from injury. Classic pain reflexes that
result in withdrawal from harmful stimuli protect tissues from damage. Unfortunately, in some cases, these
same neurologic pathways can be dramatically altered resulting in the development of chronic
neuropathic pain. One component of the sensory nervous system shown to exhibit a number of
pathophysiologic changes that may contribute to chronic pain is the dorsal root ganglion (DRG), the home
of the primary sensory neuron cell bodies.
ANATOMY OF THE DRG

One of the hallmarks of PSNs is that, anatomically, they are fairly unique in structure. They are
considered bipolar or pseudounipolar neurons, in that a single axon exits the soma and divides to form
two branches, one of which travels to the periphery and the other to the spinal cord. Positioned between
the distal and proximal axons is the T junction. Studies have shown very little variability in DRG position
among healthy individuals.
• The soma of the primary sensory neurons are housed in the dorsal root ganglion. There can be up to
15,000 primary sensory neuron soma housed in a single DRG depending upon spinal level (Figure 73-
1).
Figure 73-1. Illustration of primary sensory neuron cell bodies within the DRG.
• The soma within the DRG can be large and stretches from distal tissue structures to the spine means it
can be meters in length.
• The relative size of the soma compared to the axon is very small.
• Since much of the cell’s protein synthesis occurs in the soma, the metabolic demands on this structure
are very high.
• The DRG is typically located in the foraminal space between the medial and lateral edges of the
pedicles (Figure 73-2).
Figure 73-2. Lumbar DRGs from coronal MIP imaging. The pedicles are dark (white P) and the DRGs
are indicated by the white arrows. Notice the relatively uniform position of the DRGs relative to the
pedicles. The vast majority of DRGs from healthy volunteers lie between the medial and lateral borders
of the pedicles. (Reproduced with permission from Shen J, Wang HY, Chen JY, Liang BL. AJNR Am J
Neuroradiol. 2006 Nov-Dec;27(10):2098-103.)
• There is slight variability in DRG size as DRGs located more caudal tend to be larger.
• Sensory axons maintain a fairly consistent anatomical distribution as they travel to the spinal cord.
• There is an organized and convergent distribution of cellular fibers that eventually synapse in the
dorsal horn.
The vascular structure of the DRG provides the metabolic intermediates to support the relatively high
metabolic demands of the cells in the ganglion. This vascular structure does not create a classic blood
brain barrier due to the porous nature of the structure. To this extent, the ganglion is exposed to blood-
borne stimuli and may provide some sort of chemosensory function.
PHYSIOLOGY OF THE DRG
The physiology of the cells of the DRG is thought to be fairly stagnant. In recent years, we have realized
that neurons in many different regions of the nervous system are some of the most plastic cells in the body.
The primary function of the primary sensory neuron is to conduct action potentials from the periphery to
the central nervous system, thereby generating specific sensations.
• Action potentials originating from the periphery may not necessarily invade the membrane of the soma,
suggesting that the T junction may act as a filter.
• This allows action potentials to bypass the soma resulting in rapid conduction of action potentials from
the periphery to the spinal cord.
• The afferent impulses can originate from the DRG, suggesting that the DRG may be an additional
source of sensory input.
• The neuron contains an excitable membrane that allows the passage of selected ionic currents in a
specific sequence to generate action potential.
• Disruptions of these currents will not allow the membrane to be sufficiently excitable or it may be
hyperexcitable whereby sensations are experienced in the absence of a direct stimulus.
• The changes contributing to the hyperexcitability of DRG neurons are one of the major causes of
chronic neuropathic pain.
Animal models have demonstrated that primary sensory neurons exhibit a number of pathophysiologic
changes that may contribute to a hyperexcitable state in chronic pain. Both genetic and proteonomic
changes that alter the electrophysiological membrane properties of the DRG cells have been observed
(Figure 73-3). For example, reduced action potential thresholds, reduced Ca2+ conductance, sodium
channel functional alterations, and altered gene expression have been observed. Furthermore, spontaneous
action potentials generated in the DRG cell body have been reported. These changes have been correlated
with behavioral changes that mimic chronic pain states such as hyperalgesia and allodynia, suggesting a
relationship between the pathophysiological alterations and the development of pain.
Figure 73-3. Schematic outlining the pathophysiological changes to the DRG contributing to its
hyperexcitable state. (A) Normal sensory pathway and (B) depiction of an altered sensory pathway
whereby the primary sensory neurons are hyperexcitable, leading to the generation of neuropathic pain.
CLINICAL TARGETING OF THE DRG

Clinically, the anatomy and physiology of the DRG make it an opportunistic area to modulate nociceptive
or pain transmitting neurons. A variety of surgical and nonsurgical techniques have targeted the DRG with
varying levels of success. The therapeutic success of this procedure varies and the long-term clinical
efficacy remains unclear.
• Dorsal root entry zone lesioning and ganglionectomy are used to denervate selected dermatomes in
individuals with chronic pain conditions.
• The limited success of surgical procedures and the occurrence of deafferentation syndromes precluded
their ultimate utility and continued use.
• Radiofrequency (RF) targeting of the DRG is a less invasive technique and is used in a clinical setting.
• RF can be either destructive (continuous RF) or nondestructive (pulsed-RF). Conventional RF is
controversial in the DRG and has been used more commonly with denervation of the spinal joints.
The DRG is a robust neural structure that can withstand thermal insult and remain robust. The amount of
energy that is delivered to the DRG in radiofrequency-based techniques is immense. Yet, very low rates
of serious sensory or motor complications arising from this energy delivery have been reported.
Neuroaugmentation of DRG
Limited published data have shown that neural stimulation of the DRG may provide pain relief.
Unfortunately, design limitations of current spinal cord stimulator systems preclude the ability to
adequately study the potential role of DRG stimulation in the treatment of chronic pain. New systems are
currently being developed to address this potentially useful stimulation therapy. These systems consist of
novel leads and epidural delivery systems to aid in the placement of leads near the target DRGs (Figure
73-4). More specifically, a new system that has been developed to stimulate the DRG in the treatment of
chronic, intractable pain utilizes a slightly different lead and delivery system designed to navigate toward
the lateral epidural space and near or about the dorsal root ganglion (Figure 73-5).
Figure 73-4. Spinal modulation lead and delivery system for placement of specially designed leads for
DRG stimulation. The lead is housed within a sheath that provides protection and stability for epidural
lead placement. The lead can be deployed from the distal end of the sheath to effectively place the lead
contacts near the DRG for stimulation.
Figure 73-5. Schematic view of the procedure to place proprietary leads for dorsal root ganglion (DRG)
stimulation. (A) Epidural access is obtained using a loss of resistance technique; (B) the lead and
delivery sheath is then fed through the delivery needle, after which; (C) the lead is steered through the
epidural space toward the DRG; (D) final placement of up to 4 leads for therapy delivery.
• A small, flexible lead contained within a sheath component that provides a lead-sheath delivery
combination steering to the lateral epidural space.
• Eventually, the lead deployed in such manner so that lead contacts can provide stimulation therapy.
• Once the leads are positioned near the DRG, stimulation can be tailored via pulse generator
programming.
• Similar to other programmable stimulators, contacts are selected as anodes or cathodes and stimulation
pulse-waves are adjusted (pulse wave height, width, and frequency) to best capture the painful
anatomies.
• Paresthesias are developed and steered toward the painful areas.
• Patients can then control the stimulation therapy with a wireless programmer.
• Lead placement can vary from patient to patient depending upon several factors including differences
in spinal anatomy, and desired lead location.
Figure 73-6 depicts flexible epidural needle placement techniques to effectively deliver stimulation
leads to the desired DRG. Both ipsilateral and contralateral lead placement techniques are possible to
adjacent spinal levels or levels multiple segments away from the epidural access point. Trial procedures
are completed similar to other neurostimulator systems to gauge the level of therapy success prior to fully
implanting the neurostimulator system. Procedural and postprocedural care is similar to standards
typically utilized for fully implantable neurostimulator systems. Adverse event rates are low and
comparable to similar technologies.
Figure 73-6. Final lead placements in anterior-posterior (AP; panel A) and lateral (LAT; panel B) views.
Panel A: Note the differential epidural needle placement approaches to accommodate varying lead
delivery techniques requirements. Both contralateral and ipsilateral needle trajectories can be used to
delivery leads one or more levels away from the epidural access point. Panel B: LAT view showing
dorsal lead placement within the foramen.
PATIENT SELECTION
DRG stimulation could potentially aid in the treatment of a number of chronic pain conditions such as:
• Discogenic spine pain
• Chronic foot pain
These conditions have been treated using DRG stimulation and there are likely a number of other
indications that would benefit from this therapy, including CRPS and FBSS. The ideal patient
characteristics for this type of therapy are outlined below (Table 73-1).
TABLE 73-1. Summary of Ideal Patient Characteristics for DRG Stimulation

Ideal patient characteristics
Chronic neuropathic pain refractory to conservative therapy
Radicular symptoms
Candidate for traditional SCS therapy
Peripheral neuropathy
Postsurgical neuralgias
CRPS
Peripheral vascular disease conditions
A Case Report
Authors have performed a case of trial DRG stimulation on a 69-year-old man with a history of
neuropathy and bilateral causalgia in his shins and feet. He had experienced pain for over 9 years at the
time of treatment and had failed a number of other therapies, including spinal cord stimulation.
• Two leads were placed using a percutaneous approach at the left L4 and L5 DRGs and connected to an
external neurostimulator (Spinal Modulation, Inc, Menlo Park, CA).
• Following 3 days of trial stimulation, the patient experienced an 80% reduction in overall pain and a
70% reduction in pain in the left foot.
• He rated his overall improvement as 7 out of 10.
This case suggests that DRG stimulation may succeed in treating pain due to CRPS of the foot even in
patients for whom spinal cord stimulation has failed. However, notwithstanding, DRG stimulation can
effectively treat multiple chronic pain conditions.
POTENTIAL LIMITATIONS
As with any therapy, there are potential limitations and complications from DRG stimulation.
• DRG stimulation is similar to traditional spinal cord stimulation; therefore, one would expect to see
similar complications, such as lead migration and infection.
• Unintended motor stimulation has also been reported with nerve root stimulation.
• Specially designed leads for stimulating DRG and tools to ensure that leads are accurately placed and
secured, will likely alleviate some of these limitations.
CONCLUSIONS
• DRG stimulation is a relatively new therapy that could have important implications in the treatment of
chronic pain.
• The physiology of this neural structure suggests that it plays a role in the development and maintenance
of chronic pain.
• Many physicians suspect that DRG targeted treatments may succeed in alleviating neuropathic pain.
• While a number of therapies aimed at this structure have been attempted, recently electrical stimulation
of the DRG has been proposed and initial results seem promising.
• As new devices specifically designed to access the DRG are developed, the full potential of DRG
stimulation can be realized.
Suggested Reading
Belmonte C, Gallego R. Membrane properties of cat sensory neurons with chemoreceptor and
baroreceptor endings. J Phys. 1983;342:603-614.
Cameron T. Safety and efficacy of spinal cord stimulation for the treatment of chronic pain: a 20-year
literature review. J Neurosurg (Spine 3) 2004;100:254-267.
Devor M. Unexplained peculiarities of the dorsal root ganglion. Pain. 1999;82(suppl 1):S27-S35.
Geurts JWM, van Wijk RMAW, Wynne HJ, et al. Radiofrequency lesioning of dorsal root ganglia for
chronic lumbosacral radicular pain: a randomized, double-blind, controlled trial. Lancet.
2003;361:21-26.
Grigsby E, Deer T, Weiner R, Wilcosky B, Kramer J. Prospective, multicenter clinical trial studying
dorsal root ganglion stimulation in the treatment of back pain. North American Neuromodulation
Society Annual Meeting Proceedings; 2010.
Hasegawa T, Mikawa Y, Watanabe R, An HS. Morphometric analysis of the lumbosacral nerve roots and
dorsal root ganglia by magnetic resonance imaging. Spine. 1996;21:1005-1009.
Hogan QH. Labat lecture: the primary sensory neuron: where it is, what it does, and why it matters. Reg
Anesth Pain Med. 2010;35:306-311.
Hu SJ, Xing JL. An experimental model for chronic compression of dorsal root ganglion produced by
intervertebral foramen stenosis in the rat. Pain. 1998;77:15:23.
Lirk P, Poroli M, Rigaud M, et al. Pain mechanisms: modulators of calcium influx regulate membrane
excitability in rat dorsal root ganglion neurons. Anesth Analg. 2008;107:673-685.
Lynch PJ, McJunkin T, Eross E, Gooch S, Maloney J. Case report: successful epiradicular peripheral
nerve stimulation of the C2 dorsal root ganglion for postherpetic neuralgia. Neuromodulation. 2010.
[E-pub ahead of print]
Malik K, Benzon H, Warner D, Warner M. Radiofrequency applications to dorsal root ganglia: a literature
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calcium current in axotomized sensory neurons. Anesthesiology. 2006;105:160-168.
North RB, Kidd DH, Campbell JN, Long DM. Dorsal root ganglionectomy for failed back surgery
syndrome: a 5-year follow-up study. J Neurosurg. 1991;74:236-242.
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Proceedings of the Pain 2011 Annual Meeting.
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by 3D MR imaging. AJNR. 2006;27:2098-2103.
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CHAPTER 74
Occipital Nerve Stimulation

Erich O. Richter, Marina V. Abramova, and Kenneth M. Alo
INTRODUCTION
Occipital neuralgia (ON) is a neurological disorder that commonly involves the greater occipital and less
commonly the lesser occipital nerves.1 Trauma of the C2 root such as excessive movements (whiplash
injuries) of the head and arthritic changes of the atlantoaxial joint are considered the most common causes
of ON,1 but prolonged contraction or spasm of the posterior neck muscles from a variety of causes has
also been implicated.1 The quality of the pain is classically similar to trigeminal and glossopharyngeal
neuralgia but is localized in the occipital and periauricular areas, and may radiate into the retro-orbital
area.2 As with neuropathic pain in other nerve distributions, a constant, nonlancinating pain is also
common and may be termed as occipital neuropathic pain.
HISTORY
The concept of neuromodulation for the treatment of chronic intractable pain was developed almost 50
years ago.3 Although the Melzack-Wall gate control theory was generally accepted in the past, alternative
mechanisms have been demonstrated to be responsible for the suppression of pain during neurostimulation
such as4,5:
• Direct block of depolarization of the A-alpha, A-beta, and the A-delta fibers, as well as axonal
conduction block are currently more accepted as the mechanisms of pain modulation from nerve
stimulation.6
• Torebjork and Hallin demonstrated that repetitive stimulation of peripheral nerves results in excitation
failure of C fibers thought to be responsible for conduction of painful stimuli.7
• Alternatively, peripheral nerve stimulation may block more distal nociceptive input by inhibitory
action at the dorsal horn, brain stem, thalamus, or parietal cortex.8
The pathophysiological mechanisms responsible for pain control in ON with PNS are complex, and
much remains to be learned. In 1999, Weiner and Reed reported percutaneous implantation of cylindrical
electrodes in the vicinity of the occipital nerves for occipital neuralgia.9 Shortly thereafter, transformed
migraines, that combine the features of both migraine and tension-type headache, were also treated with
this technique.10 This relatively straightforward and less invasive approach quickly gained popularity and
developed in terms of electrode type, insertion procedure, and indications.11 In 2003, Popeney and Alo
postulated that the partial convergence of afferents from the occipital and frontotemporal region may
account for a better clinical outcome with combined stimulation of the trigeminal and occipital nerves (ie,
the trigeminocervical tract).12 This was later confirmed by others10-13 including Reed et al, who
stimulated both the occipital and trigeminal systems in patients of refractory to ONS and ongoing
holocephalic migraine.13 Their results support the need to evaluate both the C1-2-3 roots (occipital) and
the supraorbital (trigeminal V1)/superficial temporal (trigeminal V3) nerves in refractory holocephalic
headache.
INDICATIONS
PNS for the treatment of occipital neuralgia was described by Weiner9 in 1999 (Figure 74-1). Indications
later expanded to include:
Figure 74-1 AP radiograph showing bilateral 8-contact occipital nerve stimulation electrodes.
• Cervicogenic headaches14
• Occipital neuroma15
• Craniofacial neuropathic pain16
• Migraines12
• Cluster headaches17
Some of these conditions have overlapping indications with trigeminal (eg, supraorbital) nerve
stimulation. In general, indications for PNS include neuropathic pain syndromes with preserved sensation
over the painful area.18 In the occipital region, the indications are the following:
• Post-traumatic or postsurgical neuropathic pain related to dysfunction of the occipital nerve
• “Transformed” migraine localized to the occipital area
• Occipital neuralgia
• Cervicogenic occipital pain
The pain should have an anatomic distribution, be medically intractable, the patient must have
favorable neuropsychological testing, and the painful area must not be anesthetic (hypesthesia or
hyperesthesia are acceptable).18
CONTRAINDICATIONS
• Inadequately treated depression
• Somatization disorder
• Drug abuse
• Drug seeking behavior
• Secondary gains
ANATOMY OF THE GREATER AND LESSER OCCIPITAL

NERVES
The occipital nerve provides sensory distribution to the posterior aspect of the scalp, the side of the neck,
the shoulders, and the face.19 The 2 nerves primarily involved in the pathophysiology of ON are the
greater occipital nerve (GNO) and lesser occipital nerve (LON).
• The GON is formed predominantly by the posterior ramus of C2; however, additional contributions
from C1 and C3 roots have been described.1
• The LON is formed from the posterior primary rami of C2 and C3.1
• The roots have connections with the spinal accessory nerve and the superior sympathetic ganglion.19
• The nerves also receive branches from the greater auricular nerve and the trigeminal nerve.1
The GON and LON travel through the atlantoepistrophic ligament penetrating the trapezius,
supraspinatus, scalenius, and temporalis muscle.1 The GON passes backward between the atlas and the
axis in the space between the inferior oblique capitis and the semispinalis muscle.19 It pierces the
semispinalis muscle and passes through a small aperture in the aponeurosis of the trapezius muscle, and
finally emerges in the occiput.19 The nerves are relatively easy to target for stimulation, with palpable
anatomic landmarks.
• Tenderness of the GON palpable over the occipital protuberance or just lateral to the insertion of the
trapezius muscle into the occipital bone.19
• Tenderness of LON may be palpated about 3 cm superomedial to the tip of the mastoid process.19
Common injury sites, where GON is most vulnerable, are:
• Bony surfaces behind the lateral auricular masses of the atlas and axis, where it is not protected by
pedicles or facets
• Where GON perforates the atlantoaxial membrane, especially during subluxation
• Where the nerve contacts the tendinous attachment of the trapezius to the suboccipital base
The following factors may affect surgical outcome2:
• Scar tissue. Scar formation from previous surgeries or trauma can make electrode placement more
difficult.
• Integrity of the nerve. Deafferentation or discontinuity along the nerve may prevent effectiveness of
stimulation. Concern must be especially high in patients with prior ablative procedures.
• Neuropsychological clearance. Severe depression, drug abuse, unrealistic expectations, a long history
of multiple procedures, or possible secondary gains may predict unsatisfactory outcome.
• Diagnostic nerve blocks. Temporary relief of pain is one of the most important factors that predict
favorable outcome.
Criteria Used to Assess the Results of Treatment

• Visual analogue scale (VAS) at baseline, during the trial, and after permanent implantation
• Medication intake before and after the implantation of the system
• SF-36 health survey, or other validated quality of life tool, to assess the patient’s physical and mental
well-being
SURGICAL PROCEDURE
Anatomical Landmarks
• The anatomical location of the occipital nerves may vary from patient to patient.20
• The anatomical localization is best done with palpation of the GON 2 cm lateral and inferior to the
external occipital protuberance.20
• Ultrasound is useful for visualizing the neurovascular structures directly.21
Trial Stimulation
Trial stimulation is commonly performed under local anesthesia and/or sedation. General anesthesia is
often not used for the following reasons:
• To ensure adequate patient feedback and optimal coverage of the painful area using intraoperative
stimulation.
• The trial procedure is short in duration.
• The occipital nerves are superficial, sedation supplemented with infiltration of the site with local
anesthetic will typically suffice.
Patient Positioning
The patient is positioned prone on the operating table with the head midline and slightly flexed to expose
the occipital surface, with support under the chest and forehead, and prepared and draped in sterile
fashion over the occipital area and neck.
Fluoroscopic Views
The proper placement of electrodes is usually verified with anteroposterior fluoroscopy. Alternatively,
ultrasound can be used for accurate real-time localization of nervous and vascular structures.21 The
ultrasound probe is inserted at the midline just below the external occipital protuberance and slowly
advanced laterally (Figures 74-2 to 74-5).
Figure 74-2 The ultrasound probe placed in the midline just below the external occipital protuberance.
(Reproduced with permission from © 2010 International Neuromodulation Society Skaribas, I. and Aló,
K. (2010), Ultrasound imaging and occipital nerve stimulation. Neuromodulation: Technology at the
Neural Interface, 13: 126-130. doi: 10.1111/j.1525-1403.2009.00254.x.)
Figure 74-3 Sonographic image of the external occipital protuberance and bilateral occipital fossae.
(Reproduced with permission from © 2010 International Neuromodulation Society Skaribas, I. and Aló,
K. (2010), Ultrasound imaging and occipital nerve stimulation. Neuromodulation: Technology at the
Neural Interface, 13: 126-130. doi: 10.1111/j.1525-1403.2009.00254.x.)
Figure 74-4 The ultrasound probe was first placed in the midline below the external occipital
protuberance. Then it was slowly advanced laterally at the same level until images of the greater occipital
artery and nerve were obtained as 2 distinct structures: the artery as a hypoechogenic oval structure
located medially and the nerve as a hyperechogenic structure located laterally. (Reproduced with
permission from © 2010 International Neuromodulation Society Skaribas, I. and Aló, K. (2010),
Ultrasound imaging and occipital nerve stimulation. Neuromodulation: Technology at the Neural
Interface, 13: 126-130. doi: 10.1111/j.1525-1403.2009.00254.x.)
Figure 74-5 Two 8 contact stimulating leads (octrodes, Saint Jude Medical, Plano, TX, USA) as they are
positioned bilaterally after ultrasound-guided placement. This fluoroscopic picture confirms the higher
lead placement (note the level of C1-C2 compared with the level of the leads). (Reproduced with
permission from © 2010 International Neuromodulation Society Skaribas, I. and Aló, K. (2010),
Ultrasound imaging and occipital nerve stimulation. Neuromodulation: Technology at the Neural
Interface, 13: 126-130. doi: 10.1111/j.1525-1403.2009.00254.x.)
Intraoperative Steps
• The landmarks for placement of occipital nerve stimulation electrodes are C1-C2 interspace, the
occipital protuberance and the mastoid processes.
• The goal is that the electrode should cross the targeted nerve about 5 mm superficial to it. Both the
occipital artery and greater occipital nerve can be identified 1 to 1.5 cm below the skin.
• The stimulator is subsequently introduced 0.5 to 0.7 cm below the skin surface.
• Confirm the optimal positioning of the needle under fluoroscopic guidance.
• A 4-contact Quattrode electrode is inserted through the needle in such a way that all 4 contacts stay in
close proximity to the greater occipital nerve.
• The appropriate position may or may not be verified with intraoperative test stimulation of the awake
patient.
• For a good long-term result, radiating paresthesia must be obtained within the distribution of the C1-2-
3 roots (occipital nerves).
• Results may be limited if a localized grabbing or nonradiating paresthesia is generated. Experienced
practitioner may not require routine intraoperative stimulation due to the relatively reliable superficial
distribution of the greater occipital nerve.
• Some practitioners do not perform intraoperative stimulation and rely exclusively on the anatomical
positioning of electrode in proximity of the greater occipital nerve.
• After proper positioning, the electrode is draped in a sterile fashion and connected to the external
stimulation device.
• The patient is discharged home on the same day.
If the trial is successful (pain reduction of >50%), then the patient undergoes permanent implantation of
the system 1 to 1 weeks after the trial electrodes are removed in the office.
Permanent Implantation
Permanent implantation is performed under general anesthesia. An occipital incision is made, and the
anatomy of the successful trial recreated. A subcutaneous pocket is formed to allow for placement of the
internal pulse generator (IPG), typically in the subclavian area or on the back. An adequate pocket should
meet the following criteria18:
• It must be deep enough to avoid erosion
• Too deep of an insertion may interfere with programming or charging. This is dependent on the specific
model of device—consult the manufacturer’s recommendations.
• The insertion site should be in a relatively immobile location to avoid potential electrode or extension
failure due to mechanical stresses.
Tunneling involves creation of an incision and tissue dissection down to the fascia. The extension cable
is passed through a subcutaneous tunnel to the pocket site to establish a connection with the IPG.
The stimulator is turned on when the patient is awakened from the procedure to ensure adequate coverage.
Some centers allow up to several weeks before turning the device on. A comprehensive programming
session is important to ensure the most optimal coverage of painful areas. The stimulation parameters
vary from patient to patient; therefore, programming is performed on an individual basis. The surgeon
should follow their own routine protocol for wound checks and follow up, keeping in mind that the
patients may require additional visits for programming adjustments initially.
MONITORING AND POTENTIAL COMPLICATIONS

Complications can be divided into surgical complications and hardware complications.
Surgical complications:
• Infection
• Wound hematoma
• Seroma
Monitor for hardware related complications:
• Lead migration
• Lead failure
• Pulse generator failure

• The trajectory to cover the occipital nerves is based on palpable landmarks. If you span that region
with electrodes, the relevant nerves are usually covered.
• Ultrasound can clarify the primary concern of depth to generate adequate radiating paresthesia.
• Migration is a major consideration. Give adequate thought to anchoring and relaxation loops in the
planning and positioning.
• Headaches are a heterogeneous treatment group. Specifically assess the contribution of other
structures, especially the trigeminal nerves (supraorbital V1 or superficial temporal V3) before
instituting treatment of the occipital nerves alone.10,12
• The use of any implantable stimulator system for cranial peripheral nerve treatment is off-label with
the FDA and this should be mentioned during the informed consent process.
• The radiofrequency system from St. Jude Medical is currently approved for peripheral nerve
stimulation and thus indicated.
Suggested Reading
Peripheral Nerve Stimulation. Slavin KV, Lunsford LD, eds. Progress in Neurological Surgery. Vol. 24.
Karger; 2011.
Reed KL, Black SB, Banta CJ II, Will KR. Combined occipital and supraorbital neurostimulation for the
treatment of chronic migraine headaches: initial experience. Cephalalgia. 2010;30(3):260-271.
Skaribas I, Alo KM. Ultrasound imaging and occipital nerve stimulation. Neuromodulation: Technology
at the Neural Interface. 2010;13:126-130.
Weiner RL, Alo KM. Occipital neurostimulation (ONS) for treatment of intractable headache syndromes.
In: Krames P, Peckham H, Rezai R, eds. Neuromodulation. Oxford, UK, Elsevier; 2009.
References
1. Kapur N, Kamel IR, Herlich A. Oral and craniofacial pain: diagnosis, pathophysiology, and treatment.
Int Anesthesiol Clin. 2003;41:115-150.
2. Slavin KV, Nersesyan H, Wess C. Peripheral neurostimulation for treatment of intractable occipital
neuralgia. Neurosurgery. 2006;58:112-119; discussion 112-119.
3. Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965;150:971-979.
4. Campbell JN, Taub A. Local analgesia from percutaneous electrical stimulation. A peripheral
mechanism. Arch Neurol. 1973;28:347-350.
5. Mendell L. Properties and distribution of peripherally evoked presynaptic hyperpolarization in cat
lumbar spinal cord. J Physiol. 1972;226:769-792.
6. Ignelzi RJ, Nyquist JK. Direct effect of electrical stimulation on peripheral nerve evoked activity:
implications in pain relief. J Neurosurg. 1976;45:159-165.
7. Torebjork HE, Hallin RG. Responses in human A and C fibers to repeated electrical intradermal
stimulation. J Neurol Neurosurg Psychiatry. 1974;37:653-664.
8. Campbell JN, Long DM. Peripheral nerve stimulation in the treatment of intractable pain. J
Neurosurg. 1976;45:692-699.
9. Weiner RR, Reed KL. Peripheral neurostimulation for control of intractable occipital neuralgia.
Neuromodulation: Technology at the Neural Interface. 1999;2:217-221.
10. Oh M, Ortega J, Belotte J, Whiting D, Alo K. Peripheral nerve stimulation for the treatment of
occipital neuralgia and transformed migraine using a C1-2-3 subcutaneous paddle style electrode: a
technical report. Neuromodulation: Technology at the Neural Interface. 2004;7:103-112.
11. Slavin KV. History of peripheral nerve stimulation. Prog Neurol Surg. 2011;24:1-15.
12. Popeney CA, Alo KM. Peripheral neurostimulation for the treatment of chronic, disabling transformed
migraine. Headache. 2003;43:369-375.
13. Reed KL, Black SB, Banta CJ II, Will KR. Combined occipital and supraorbital neurostimulation for
the treatment of chronic migraine headaches: initial experience. Cephalalgia. 2010;30:260-271.
14. Weiner R, Alo K, Reed K, Fuller M. Subcutaneous neurostimulation for intractable C-2-mediated
headaches. J Neurosurg. 2001;94:398A.
15 Hammer M, Doleys D. Perineuromal stimulation in the treatment of occipital neuralgia: a case study.
Neuromodulation: Technology at the Neural Interface. 2001;4:47-51.
16. Slavin K, Burchiel K. Use of long-term nerve stimulation with implanted electrodes in the treatment of
intractable craniofacial pain. J Neurosurg. 2000;92:576.
17. Schwedt TJ, Dodick DW, Trentman TL, Zimmerman RS. Occipital nerve stimulation for chronic
cluster headache and hemicrania continua: pain relief and persistence of autonomic features.
Cephalalgia. 2006;26:1025-1027.
18. Slavin KV, Colpan ME, Munawar N, Wess C, Nersesyan H. Trigeminal and occipital peripheral nerve
stimulation for craniofacial pain: a single-institution experience and review of the literature.
Neurosurg Focus. 2006;21:E5.
19. Kuhn WF, Kuhn SC, Gilberstadt H. Occipital neuralgias: clinical recognition of a complicated
headache. A case series and literature review. J Orofac Pain. 1997;11:158-165.
20. Loukas M, El-Sedfy A, Tubbs RS, et al. Identification of greater occipital nerve landmarks for the
treatment of occipital neuralgia. Folia Morphol (Warsz). 2006;65:337-342.
21. Skaribas I, Alo K. Ultrasound imaging and occipital nerve stimulation. Neuromodulation: Technology
at the Neural Interface. 2010;13:126-130.
CHAPTER 75
Percutaneous Peripheral Nerve and Field Stimulation

Jason E. Pope, Timothy R. Deer, and Eric J. Grigsby
INDICATIONS
Since the advent of the Gate Control Theory, as proposed by Melzak and Wall, the applications for
neurostimulation by stimulation have exploded1. First introduced in the intrathecal space, electrical
neuromodulation has progressively been advancing into the periphery, as ablative strategies continue to
fall out of favor.
• Peripheral nerve stimulation (PNS) is the direct electrical stimulation of named nerves outside of the
neuroaxis.
• Peripheral nerve field stimulation (PNfS) is the stimulation of unnamed small nerves in the vicinity of
pain by superficial, subcutaneous lead placement.
• Unlike SCS that modulates second order nociceptors, PNS and PNfS directly inhibit primary
nociceptive afferents.
• PNS and PNfS suggest that central sensitization can be subverted by peripheral nociceptive
suppression.
• Similar to spinal cord stimulation, therapeutic PNS and PNfS replace the patients pain with a pleasant,
therapeutic paresthesia.
Historically, PNS can be performed via an open surgical or percutaneous technique, well described by
Stanton-Hicks. The percutaneous techniques for both PNS and PNfS will be reviewed here, while open
techniques will not be discussed. Further, although the scope of vagal nerve stimulation has broadened to
include the treatment of neuropathic pain, these strategies have not become commonplace and will not be
discussed.
• Like spinal cord stimulation, patient selection is crucial to treatment success.
• PNS and PNfS are indicted for chronic neuropathic pain from peripheral origin.
• Peripheral nerve and field stimulation lack strong leveled evidence.
• Percutaneous neuromodulatory stimulation devices are not approved for PNS or PNfS by the FDA and
are classified as “off label.”
Not withstanding, the current indications for PNS include:
• Complex regional pain syndrome type II
• Neuropathic pain from mononeuropathy or plexopathies
• Headache (migraine, trigeminal neuralgia, occipital neuralgia, supraorbital neuralgia, cervicogenic
headache, hemicrania continua)2
Ideal candidacy for PNS has yet to be determined, as juxtaposed opinions exist. While some advocate a
successful nerve block prior to the trial, others contend that a previous successful nerve block is
unnecessary. Notwithstanding, a trial prior to implantation is mandatory. With the open technique (not
described here), some advocate a direct implant approach in an effort to reduce repetitive procedural
morbidity44.
PNfS indications are less clear, as the mechanism is ill-defined.
• Neuropathic and nociceptive pain
• PNfS alone or in concert with epidural leads for treatment of axial back pain related to FBSS3
• Failure or contraindication to conventional and conservative strategies
PNfS candidacy is even less defined and further debated. Failure of conservative and traditional
management of neuropathic or mixed nociceptive/neuropathic pain is typically a prerequisite.
Patient selection regarding psychometric testing cannot be understated. Poor treatment outcome have
been reported in patients with presurgical somatization, depression, anxiety, and poor coping strategies.
• Comorbid psychiatric illness significantly reduces interventional treatment success rates.
• Approximately 20% to 45% of chronic pain patients have accompanying psychopathology.
• It is paramount to identify candidates suitable for concurrent treatment or exclude patients that require
psychiatric treatment primarily.
RELEVANT ANATOMY
Peripheral neuromodulatory success centers on a keen understanding of the anatomy of the peripheral
nerve (Figure 75-1).
Figure 75-1. Peripheral nerve architecture42.
• Nerves are composed of axons encompassed by Schwann cells, with or without a myelin sheath.
• The cell body of the sensory nerve is located in the dorsal root ganglion and is unipolar.
• Sensory afferent nerve cell bodies extend an axon while dendrites allow synaptic communication with
neighboring cells.
• These axons are encased within the endoneurium and bundled into fascicles and surrounded by
perineurium.
• These fascicles divide and fuse to form multiple plexi along the nerve trunk, with discrete topographic
architecture.
• The vasculature of the peripheral nerve resides in the perineurium.
• The perineural bundles are then finally encased by epineurium.
Peripheral nerves can be categorized based on their conduction velocity and diameter.
Importantly, the aforementioned nerve layers and inconsistent fascicular topographic arrangement
provide an anatomic explanation not only for the impendence requirement to overcome, but also the
cumulative effect of the cathodal stimulation employed in peripheral neuromodulation.
Relevant anatomy for the common sites of neuromodulation will be discussed in the subsequent sections
and include:
• Supraorbital nerve
• Infraorbital nerve
• Greater occipital nerve
• Ulnar nerve
• Median nerve
• Suprascapular nerve
• Intercostal nerve
• Ilioinguinal nerve
• Iliohypogastric nerve
• Genitofemoral nerve
• Lateral femoral cutaneous nerve
• Saphenous nerve
• Sciatic nerve
• Posterior tibial nerve
CONTRAINDICATIONS
• Local infection near the injection site
• Coagulopathy
• Allergy to injectate
• Comorbidities/conditions that prevent fluoroscopic needle guidance
• Inability to obtain consent
• Cognitive impairment with stimulator management
• Coagulopathy8
• The use of peripheral nerve stimulation may be more applicable to the patient with multiple
comorbidities.
• Use the guidelines and follow the classifications set forth by the American Society of Anesthesiologists
for preoperative preparation.
• A clear understanding of surgical site anatomy, utilization of image guidance, and proper surgical
technique are vital to ensure both quality treatment and reduced patient morbidity and mortality.
• Proper training is essential to good clinical outcomes.
• Mitigation of infection risk when implanting a foreign body is critical. Risk factors associated with
infections of implanted hardware:
Immunosuppressive therapy (including steroids)
Diabetes
Rheumatoid arthritis
Tobacco and/or alcohol use
Malnutrition
Obesity
Prolonged hospital stay
Multiple surgeries
Perioperative transfusion
• Reduction is surgical site infections risk factors:
Appropriate selection and timing of preoperative antibiotic therapy
Hair clipping of operative site
Proper surgical site skin prep
Adequate preoperative hand scrub
Appropriate ventilation in operative suite
• Patient education, informed consent, and patient responsibilities should be completed prior to surgery.
• Percutaneous PNS and PNfS approaches utilize devices that were designed for use in the epidural
space.

• In most cases, PNS and PNfS are not labeled for use in the neuropathic pain patient. Some devices
have achieved labeling in the past, and the issues should be reviewed with the patient prior to moving
forward.
Imaging
• The use of fluoroscopy is helpful in orienting the lead position and future issues surrounding migration.
• In large nerve targets, the use of ultrasound has been advocated.
• The choice of imaging should be based on a patient specific characteristics and operator experience.
Position of the Patient

• The position of the patient is dependent on the nerve targeted to promote appropriate surgical site and
adequate field margin preparations.
• It may be necessary to reposition the patient during surgery.

• The majority of leads, generators, and tools developed for the spine and has been adopted to use in the
periphery10.
• The goal of lead placement is to produce cathodal stimulation of a neural target.
• Although power sources can be either RF coupled or a rechargeable or non-rechargeable IPG
(implanted pulse generator), only the RF-coupled transmitter receiver is approved by the FDA for PNS
use.
• The needles used for epidural entry for spinal cord stimulation are bent to facilitate percutaneous
subcutaneous or peripheral nerve placement, while mitigating needle tip or electrode erosion.
• Unlike spinal cord stimulator lead placement, percutaneous peripheral nerve placement is dependent
primarily on needle orientation.
• Stimulation characteristics are similar to SCS stimulation parameters:
Amplitude (strength of the stimulation as determined by volts or amperage)
Pulse width (the duration of the stimulation application)
Rate or frequency (the speed at which the stimulation application occurs)

PNS and PNfS trialing and permanent implantation require a meticulous sterile preparation and wide
enough operative fields to visualize the necessary surgical targets. Further, peripheral nerve stimulation is
only limited by the ability to visualize the target nerve and IPG implantation location. Peripheral nerve
stimulation targets will be discussed separately. Deer described surgical technique for these implants in
detail, including common pearls and pitfalls.
PERIPHERAL NERVE STIMULATION

Supraorbital Nerve Stimulation Trial
• The supraorbital nerve, along with the supratrochlear nerve, are terminal branches of the ophthalmic
division of the trigeminal nerve.
• The supraorbital nerve exits the supraorbital canal (Figure 75-2).
Figure 75-2. Terminal branches of the trigeminal nerve12.
• Slavin et al described the most commonly employed technique for supraorbital stimulation9.
• The patient is positioned supine, standard prep and drape (alcohol should be avoided in the face to
avoid corneal irritation).
• Monitored Anesthesia Care is suggested.
• Fluoroscopy is used in the anterior-posterior view to approximate the target.
• A skin wheel using 1% lidocaine is raised approximately 3 to 4 cm lateral to the lateral corner of the
eye and along the needle tract.
• A stab incision is then made, where a standard 14-gauge Tuohy needle (bent to allow and follow the
contour of the face), is directed toward the midline approximately 1 cm above the supraorbital ridge
until it is approximately 1 cm from the midline (Figure 75-3).
Figure 75-3. Diagram of supraorbital lead placement13 (A) and AP radiograph of electrode under
fluoroscopy (B)14. (Reproduced with permission from Johnson RD, Green A, Aziz TZ. Implantation of an
intercostal nerve stimulator for chronic abdominal pain. The Royal College of Surgeons of England.
2010. 92, 1-3.)
• Care must be taken not to direct the needle too superficially, as this may promote lead tip erosion.
• The stylet is removed, the percutaneous electrode is placed, and the needle is withdrawn to allow for
intraoperative stimulation testing.
• Judicious use of local anesthetic at the puncture site will allow for intraoperative testing, while needle
track topicalization to the midline target will likely preclude intraoperative testing.
• The externalized lead is then secured with the supplied plastic anchor of the surgeons choosing and
nonabsorbable sutures.
• A sterile dressing is applied and the patient is taken to the recovery area.
Infraorbital Nerve Stimulation Trial

• The infraorbital nerve is one of the terminal branches of the maxillary division of the trigeminal nerve
and exits via the infraorbital canal (Figure 75-2).
• The patient is prepared, positioned, and anesthetized as for supraorbital stimulation.
• The target site is the infraorbital foramen on fluoroscopy.
• The lead is placed approximately 1 cm below the orbit and just lateral to the ipsilateral nose, as
described by Slavin et al.
• The entry point is lateral and inferior to the eye over the zygoma.
• After judicious local anesthetic use at the entry point and topicalization of the needle tract, a bent
introducer needle to accommodate the contour of the face is inserted and directed to the target zone
under fluoroscopy.
• Once the needle is in the correct position, the percutaneous cylindrical lead is introduced with care not
to direct the distal tip of the needle too superficial to avoid lead tip erosion.
• The introducer needle is withdrawn (Figure 75-4).
Figure 75-4. Diagram of Infraorbital lead placement13. (Reproduced with permission from Johnson RD,
Green A, Aziz TZ. Implantation of an intercostal nerve stimulator for chronic abdominal pain. The Royal
College of Surgeons of England. 2010. 92, 1-3.)
• The lead is sutured as previously described and a sterile dressing is applied.
Supra- and Infraorbital Nerve Permanent Implant

• For the permanent implantation of both the infra and supra orbital leads and IPG, general anesthesia is
recommended (with laryngeal mask airway if feasible).
• The patient is positioned supine with a slight contralateral head turn to provide access to the
retroauricular location.
• A meticulous sterile prep and drape is required to accommodate tunneling and IPG site location.
Commonly, the infraclavicular sight is chosen.
• The permanent percutaneous lead is inserted as described for the trial.
• Additional incisions are made in the ipsilateral retroauricular location after appropriate topicalization.
• Two techniques have been described for tunneling the lead’s IPG connection portion:
One is simply using the introducer needle with stylet in place (bent to accommodate the contour of
the head and tunneling from the retroauricular incision to the anterior incision). The stylet is then
removed, the lead introduced, and the needle withdrawn, leaving the tunneled lead.
Another technique is the “needle-over-the-stylet” technique, as described by Slavin et al. The stylet
of the needle is tunneled from the anterior to the posterior incision and then the needle is passed
over the stylet toward the anterior incision. The stylet is then removed and the lead is inserted in
the needle tunneling toward the retroauricular incision. The needle is then removed, leaving the
lead in place.
• From the retroauricular location, the lead is secured with the supplied plastic anchor using
nonabsorbable suture.
• A stress loop is recommended (~2-3 cm in diameter) and the lead is attached to the extension cable.
• Place the extension cable connection in close approximation to the retroauricular incision to allow for
easy access if reoperation is required.
• The IPG site location is largely the surgeon’s preference.
• Flexion and extension pathway changes in the infraclavicular and abdominal sites were associated
with less length changes as compared to the periscapular and gluteal sites, respectively.
• The lead extensions placed that span mobile areas, including joints, will have a higher propensity to
migrate.
• Avoid IPG placement around osteal structures to reduce pain overlying the IPG device.
• It is crucial to avoid excessive blunt dissection, provide meticulous hemostasis, and anchor the
perimuscular fascia to avoid IPG dislodgement.
• Copious nonpressurized irrigation is performed at all incision sites and layered closure is performed
with absorbable suture.
• Avoid placing sutures overlying the IPG, as this may impair wound healing and increase the chance of
wound dehiscence.
• Sterile dressing is applied and the patient is recovered in the postoperative area.
Greater Occipital Nerve Stimulation Trial

• The greater occipital nerve is also known as the second occipital nerve and is the medial branch of
dorsal primary rami of C2.
• Since the characterization of the trigeminocervical complex, the greater occipital nerve has become a
popular target for the treatment of headache.
• Anatomic dissection studies have been performed to characterize the location from osteal landmarks,
including the mastoid process and the occipital protuberance.
• It is generally found 1.4 to 1.6 cm lateral from the external occipital protuberance and 2.91 to 3.7 cm
inferior.
• The nerve is consistently medial to the occipital artery (Figure 75-5).
Figure 75-5. Greater occipital nerve diagram12 and anatomic dissection.
• There are multiple techniques described to stimulate the greater occipital nerve, with major differences
centering on target location:
C1-C2 versus nuchal ridge/retromastoid
Lead trajectory orientation (medial to lateral or lateral to medial)
Type of lead chosen (percutaneous cylindrical vs paddle) (Figure 75-6)
Figure 75-6. Diagrams of percutaneous and paddle ONS lead placements19, 20, 21.
• Muscle spasm may be subverted by placement of the electrodes at the nuchal line, as opposed to the
C1-C2 level.
• Superficial lead placement may increase the chance of erosion and burning sensations, while too deep
lead placement may cause aberrant muscular stimulation.
• The trial procedure is carried out with the patient in the prone position.
• Monitored anesthesia care or sedation is suggested for the trial.
• The surgical site is prepared by hair clipping (not shaving), and meticulous sterile prep and drape in
the normal fashion, leaving the entry site exposed.
• Image guidance is a prerequisite; fluoroscopy is commonly employed.
• After the target location is chosen (AA joint vs superior nuchal line), the incision site is identified.
• Do not to anesthetize the greater occipital nerve, and use judicious local anesthetic at the incision site
using 1% lidocaine.
The medial, nuchal line approach (Figure 75-7):
Figure 75-7. Percutaneous lead site differences19. (Reproduced with permission from Hayek SM, Jasper
JF, Deer TR, Narouze SN. Occipital Neurostimulation-Induced Muscle Spasms: Implications for Lead
Placement. Pain Physician 2009. 12:867-876.)
• An incision is made in the midline just caudal to the occipital protuberance.

• The needle is bent to accommodate the contour of the head.
• Under fluoroscopic guidance, lead is placed along the nuchal ridge ipsilateral to the target greater
occipital nerve.
• Once appropriate lead position is achieved, the needle is withdrawn slightly to allow for
intraoperative stimulation testing if desired.
• The needle is removed and the lead is secured using the plastic anchor provided and nonabsorbable
suture.
• A sterile dressing is applied and the patient is further recovered and programmed in the recovery room.
Greater Occipital Nerve Permanent Implant

• Preparation and anesthesia, and the lead placement procedure are largely the same for the occipital
nerve trial and implant.
• The surgical prep site is extended to a larger area to accommodate the IPG location.
• Like SCS, strain loops are created at the incision site by careful lateral dissection.
• Plastic anchors and nonabsorbable sutures are used to suture the lead to the dorsal fascia.
• A third incision is made and carefully dissected to accommodate the IPG.
• If extensions are needed and tunneling is required over a great distance, additional incisions with
sequential tunneling may be required.
• Irrigation is performed at all incision sites and layered closure is recommended.
• Do not create a suture line overlying the implanted device.
• Sterile dressings are applied and further programming is performed in the recovery area.
UPPER AND LOWER EXTREMITY PERIPHERAL NERVE

STIMULATION
The feasibility of distal upper and lower extremity peripheral nerve stimulation was investigated by a
series of articles by Huntoon et al, describing techniques for ulnar, median, radial, peroneal, and the
posterior tibial nerves. Careful identification of the target nerves and familiarity with ultrasound-guided
techniques cannot be understated. Formal accredited fellowship training is recommended. Some examples
of peripheral nerve stimulation techniques are described below.
Ulnar Nerve Stimulation Trial

• The ulnar nerve is the most caudal portion of the brachial plexus, arising from the medial cord with
nerve roots originating at C8-T1.
• It descends medially to the brachial artery in the proximal arm, anterior to the medial triceps of the
triceps, and it resides in the grove of the medial epicondyle at the elbow.
• Patient is positioned supine and patient preparation performed in the usual manner including sterile
prep and preoperative antibiotics.
• As described by Huntoon et al, the easily identified ulnar nerve located at the medial epicondyle is
traced in the axial sonographic view to approximately 9 to 13 cm proximal.
• Once the nerve was located, a skin wheel is raised with lidocaine 1%, and a skin nick is created.
• Under a live axial view of the ulnar nerve, the needle is then introduced vial the long axis of the probe,
placing the lead deep, adjacent and perpendicular to the ulnar nerve.
• The needle is retracted and stimulation testing commenced.
• Anchoring of the lead to the skin was performed using the plastic anchors and nonabsorbable suture
(Figure 75-8).
Figure 75-8. Diagram depicting US guided peripheral nerve stimulation6.
Median Nerve Stimulation Trial

• The median nerve arises from the C5, C6, C7, C8, and T1 roots, and is more distally from the lateral
and medial cords.
• It descends anterolateral to the axillary and brachial artery, lies medial to it and the biceps muscle
tendon in the cubital fossa.
• Moving distally in the forearm, the median nerve descends between the heads of the pronator teres
muscle, and in the wrist it resides between the tendons of the flexor carpi radialis and the flexor
digitorum superficialis (Figure 75-9).
Figure 75-9. Median nerve axial view proximal forearm27. (Reproduced with permission from Bargallo
X, Carrera A, Sala-Blanch X, Santamaria G, Morro R, LLusa M, Gilabert R. Ultrasound-Anatomic
Correlation of the peripheral nerves of the upper limb. Surgical Radiol Anat 2010. 32:305-314.)
• The patient is positioned supine and preparation is performed in the usual manner.
• The ultrasound probe is placed in the transverse position and scanned distally until approximately 4 to
6 cm distal to the antecubital fossa between the pronator teres heads.
• After careful topicalization with 1% lidocaine at the incision site only, a skin incision is made and
under ultrasound guidance.
• A 14-gauge needle is introduced in the longitudinal plane with the target nerve and maintained in the
axial plane with care to place the lead adjacent to the nerve.
• Once the lead is in the optimal position, the needle is retracted and stimulation testing is performed.
• After stimulation is achieved, anchoring of the lead to the skin is performed using the plastic anchors
and nonabsorbable suture.
• A sterile dressing is applied. The patient is then transported to the recovery room for further
programming.
Radial Nerve Stimulation Trial

• The radial nerve has origins from the posterior cord from roots C5-C8. The nerve travels obliquely to
the humerus at in the proximal arm, along with the deep brachial artery.
• The nerve is reliably located lateral to the humerus at approximately 10 to 14 cm proximal to the
lateral epicondyle deep to the lateral head of the triceps (Figure 75-10).
Figure 75-10. Radial nerve in the proximal arm27. (Reproduced with permission from Bargallo X,
Carrera A, Sala-Blanch X, Santamaria G, Morro R, Llusa M, Gilabert R. Ultrasound-Anatomic
Correlation of the peripheral nerves of the upper limb. Surgical Radiol Anat. 2010;32:305-314.)
• The patient is positioned supine and preparation is performed in the usual manner.
• The ultrasound probe is placed in the transverse position and scanned distally until approximately 10
to 14 cm proximal to the lateral epicondyle.
• After careful topicalization with 1% lidocaine at the incision site only, a skin incision is made and
under ultrasound guidance.
• A 14-gauge needle is introduced in the longitudinal plane with the target nerve maintained in the axial
plane with care to place the lead adjacent to the nerve.
• Once the lead is in the optimal position, the needle is retracted and stimulation testing is performed.
• Once therapeutic stimulation is achieved, anchoring of the lead to the skin is performed using the
plastic anchors and nonabsorbable suture to the skin.
• A sterile dressing is applied, and the patient is then transported to the recovery room for further
programming.
Median, Ulnar, and Radial Permanent Implant

• The patient preparation, anesthesia, and placement of the lead are the same as the trial procedure.
• The surgical prep site is extended to a larger area to accommodate the IPG location.
• For the permanent percutaneous placement, it is recommended to place the device in the upper chest
(infraclavicular site) or abdomen for the upper extremity.
Lead extensions and serial incisions are required to connect and tunnel the leads to the IPG. As described
previously, meticulous surgical technique is paramount, including appropriate hemostasis and dissection
to the fascia for lead anchoring. Sterile dressings are applied and programming is performed in the
recovery room.
Peroneal Nerve Stimulation Trial

• The sciatic nerve is formed from the L4 to S3 nerve roots and can be subdivided into medial and
lateral compartments.
• The medial portion of the sciatic nerve is functionally the tibial nerve, formed by the ventral branches
of the L4-L5 and S1-S3, while the posterior branches of the ventral rami make up the peroneal nerve.
• The sciatic nerve descends in the rostral portion of the popliteal fossa, splitting into the tibial nerve
medially and the common peroneal nerve laterally.
• The popliteal fossa’s borders are the semimembranosus and semitendinosus medially, the biceps
femoris laterally, and the gastrocnemius muscle caudally.
• The popliteal artery is medial to the neural targets (Figure 75-11).
Figure 75-11. Popliteal fossa41; saphenous and sural cutaneous branch stimulation.
• The patient is positioned to access the popliteal fossa of the afflicted leg. After patient preparation,
monitoring, and meticulous sterile prep and drape, as previously described.
• Axial ultrasound scanning is performed from the popliteal crease cephalad. The tibial and peroneal
nerves coalesce to form the sciatic nerve just cephalad to the aforementioned popliteal fossa.
• Identification of the popliteal artery is essential to avoid vascular entry. Once the desired nerve
location is visualized, judicious topicalization of the skin entry site with 1% lidocaine is performed.
• The introducer needle is then placed deep to the bifurcation of the sciatic nerve in a posterolateral to
anteromedial direction.
• Be careful to avoid muscular entry is essential. The lead is introduced and the needle is retracted to
allow for testing.
• Once therapeutic testing is achieved, the needle is withdrawn, the lead sutured to the fascia of the
biceps femoris muscle using the plastic anchor and nonabsorbable suture.
• Sterile dressing applied, and the patient transported to the recovery room for further stimulation testing.
Saphenous Nerve Simulation Trial

• The saphenous nerve is a purely sensory nerve that is a distal cutaneous branch of the femoral nerve
and therefore has contributions from the L2-L4 nerve roots.
• It descends along the medial aspect of the thigh and posterior to the sartorius muscle.
• In the distal thigh, the nerve lies between the tendons of the sartorius and gracilis muscles (or vastus
medialis muscle more distally), where it can be reliably located just proximal to the medial aspect of
the knee and approximates the geniculate artery (Figure 75-12).
Figure 75-12. Depiction of saphenous nerve28.
• The patient is positioned supine with slight ipsilateral extremity hip external rotation.
• Appropriate patient preparation is carried out in usual fashion.
• Axial scanning of the afflicted extremity performed for an anatomic survey. The saphenous nerve is
predominately hyperechoic and Doppler survey to identify the geniculate artery may help identifying
the target.
• After needle entry topicalization with 1% lidocaine, a small skin incision is made.
• A 14G introducer needle is introduced and directed to the facial plane between the sartorius muscle
and vastus medialis using an in-plane approach, avoiding muscle penetration.
• Once the needle approximates the nerve, the stimulation lead is placed and the needle retracted to
allow for stimulation testing.
• Once therapeutic stimulation is achieved, the needle is removed and the lead is sutured to the vastus
medialis fascia using a plastic anchor and nonabsorbable suture.
• A sterile dressing is applied and the patient is transported to the recovery area for further
programming.
Lateral Femoral Cutaneous Nerve (LFCN) Stimulation Trial

• The lateral femoral cutaneous nerve is a branch of the posterior divisions of the L2-L3 nerve roots and
is also an exclusively sensory nerve.
• It travels lateral to the border of the psoas muscle and courses toward the anterior inferior iliac spine
(ASIS).
• It then passes under the inguinal ligament, lying between the fascia lata (deep) and iliaca (superficial),
providing sensory information from the lateral thigh.
• LFCN neuropathy is called meralgia paresthetica.
• The patient is positioned supine with slight ipsilateral extremity in neutral position.
• After appropriate patient preparation, monitoring, and field prep and drape, axial scanning of the
afflicted extremity performed for an anatomic survey from the ASIS along the inguinal ligament.
• After appropriate needle entry site topicalization, a stab incision is made.
• A 14-gauge needle is introduced superficially along the longitudinal axis of the probe in close
proximity to the lateral femoral cutaneous nerve just caudal to the inguinal ligament.
• Once needle placement is optimized, the lead is introduced, placing the lead perpendicular to the
course of the nerve.
• The needle is retracted and therapeutic stimulation is achieved.
• The lead is anchored to the fascia lata with the supplied plastic anchor and nonabsorbable suture.
Intercostal Nerve Stimulation Trial

• Intercostal nerves originate as the anterior rami of the paired exiting nerve roots and travel under the
adjacent rib with close approximation to the intercostal vein and artery.
• Care must be taken not to violate the pleura.
• After aseptic preparation and monitoring as described previously, the patient is positioned either prone
or in the lateral decubitus position.
• Under fluoroscopic guidance, and 1% lidocaine skin wheel, a stab incision is made to accommodate
the introducer needle.
• The needle should be bent to follow the curve of the rib.
• Once the needle is verified to be in the correct location, the lead is inserted and the needle retracted
for stimulation testing.
• Once therapeutic stimulation is achieved, the lead is anchored with the supplied plastic anchor and
nonabsorbable suture (Figure 75-13).
Figure 75-13. Radiograph of T11 intercostal nerve percutaneous PNS40. (Reproduced with permission
from Johnson RD, Green A, Aziz TZ. Implantation of an intercostal nerve stimulator for chronic
abdominal pain. The Royal College of Surgeons of England. 2010. 92, 1-3. Copyright the Royal College
of Surgeons of England.)
Iliohypogastric, Ilioinguinal, Genitofemoral Nerves

• The iliohypogastric and ilioinguinal nerves both arise from the L1 nerve root and emerge lateral to the
psoas muscle.
• The nerves course in the anatomic plane of the internal oblique and transversus abdominal muscles.
• The genitofemoral nerve arises from the L1 and L2 nerve roots and emerges on the anterior surface of
the psoas muscle.
• It’s genital branch travels through the inguinal canal and in males supplies sensory information from the
scrotal skin.
• In contrast, the ilioinguinal nerve supplies the groin.
• These nerves are amenable to peripheral stimulation, and care must be taken to ensure appropriate
needle placement without violating the peritoneal cavity; image guidance via ultrasound is
recommended.
• As these nerves are difficult to locate, the line between PNS and PNfS begins to blur (Figure 75-14).
Figure 75-14. (A) Diagram of ilioinguinal hypogastric, and genitofemoral courses12; (B) radiograph
ilioinguinal nerve stimulation.
PERIPHERAL NERVE FIELD STIMULATION (PNFS)

As described previously, there is poor prospective data justifying PNfS. Nevertheless, the available
evidence does suggest some efficacy in treating chronic neuropathic pain syndromes. PNfS has also been
used in conjunction with SCS to treat both back and leg pain, with inter and intra lead programming.
Common areas where PNfS has been employed include:
• Axial thoracic and lumbar back pain
• Failed back surgery syndrome (FBSS)
• Greater trochanteric pain after total hip arthroplasty
• Postherniorrhaophy pain
• Chronic abdominal pain
• Knee pain
• Post-thoracotomy pain
Peripheral Field Stimulation Trial

• The patient preparation and anesthesia are the same for the aforementioned named peripheral nerve
neuromodulatory targets.
• Surgical site preparation is dependent on the area of the painful area, and therefore the patient position
needs to accommodate any easy operative field access.
• The leads can be placed with different strategies:
Placed to “bracket” the area of neuropathic pain, with the area of coverage is approximately 180 ×
90 mm.
Leads placed centrally in the painful area.
• The placement technique depends on infiltration of local anesthetic either at skin entry site only or the
entry site and the desired needle tract.
To allow for intraoperative testing
To place the lead without intraoperative testing
• A stab incision is created and the 14-gauge introducer needle is inserted near the target area
subcutaneously under image guidance.
• After needle position finalized, the percutaneous lead is introduced, the needle is withdrawn, and
stimulation testing commences.
• If unpleasant and burning sensations are reported, the lead is likely too deep and needs to be redirected
more superficially.
• The lead is then secured to the skin using a plastic anchor and nonabsorbable suture and a sterile
dressing is applied.
• The externalized lead is then connected to the externalized battery and the patient is transported to the
recovery room for more complex programming (Figures 75-15 to 75-17).
Figure 75-15 PNfS for FBSS34. (Reproduced with permission from Paicius, RM, Bernstein CA, Lempert-
Cohen C. Peripheral Nerve Field Stimulation for the Treatment of Chronic Low Back Pain: Preliminary
Results of Long-Term Follow-up: A Case series. Neuromodulation 2007. Vol 10, No 3, 279-89.)
Figure 75-16. PNfS for thigh pain following greater trochanteric bursectomy32. (Reproduced with
permission from Yakovlev AE, Resch BE, Karasev SA. Treatment of Intractable Hip Pain after THA and
GTB Using Peripheral Nerve Field Stimulation: A Case Series. Wisconsin Medical Journal. 2010, Vol
109 No 3, 149-152.)
Figure 75-17. PNfS for chronic pancreatitis33. (Reproduced with permission from Paicius RM, Bernstein
CA, Lempert-Cohen C. Peripheral Nerve Field Stimulation in Chronic Abdominal Pain. Pain Physician.
2006, 261-66.)
Peripheral Field Stimulation Permanent Implant

The peripheral nerve implant following a successful trial proceeds in the same manner as the trial with
the additional prep and draping to include the battery site. The strategies and techniques that have been
described previously can be translated to PNfS permanent placement.
The decision to provide postoperative prophylactic antibiotics continues to be a controversial topic.
Many practitioners continue to do so despite only anecdotal evidence. Monitor for postoperative infection
critically.
The signs of infectious complications are:
• Surgical site tenderness
• Accompanied erythema
• Fever of 101.4 or over
• Induration
• Purulent discharge
• Wound dehiscence
Infection if confined locally, antibiotics may be utilized to salvage the device. If systemic signs are
suspected, all hardware should be removed, an infectious disease consult sought, and the infection treated
and cleared for 6 to 12 weeks before reimplantation is attempted.
• Lead placement too superficial causes a burning sensation, while too deep create muscle recruitment.
• Therapeutic programming should be performed to optimize the devices therapeutic potential and should
be adjusted as needed.
• Successful trial stimulation is defined as at least 50% pain reduction and/or 50% improvement in
function.
• Trial periods last commonly for 5 to 7 days.
• PNS trials may be better tolerated for longer periods, as there is very low procedural morbidity or
mortality innate to the superficial nature of the device placement.
• Once a trial is terminated and deemed successful, 3 to 4 weeks is usually allowed before permanent
device placement.

Potential complications include:
• Infection
• Lead migration
• Lead tip erosion
• Overstimulation
• Hardware malfunction
• Allergic dermatitis
• Myofascial pain
• Stimulation tolerance
• Pain over the device

• Intimate knowledge of peripheral nerve anatomy is crucial to device placement success and reducing
patient morbidity and mortality.
• Image guidance is mandatory for percutaneous PNS.
• Patient candidacy for PNS and PNfS centers on treating neuropathic pain, and as with any implantable
device, requires psychological prescreening.
• Percutaneous PNS is an off-label use of a device approved for SCS, and therefore requires adaptation
of the SCS placement tools.
• Judicious topicalization at the introducer needle’s entry site is required to enable intraoperative PNS
and PNfS testing.
• Avoidance of crossing mobile areas is recommended with IPG site location and tunneling.
• The most common complication, like SCS, is lead migration.
• Overall, the morbidity and mortality associated with PNS and PNfS is low.
Suggested Reading
Bargallo X, Carrera A, Sala-Blanch X, Santamaria G, Morro R, LLusa M, Gilabert R. Ultrasound-
anatomic correlation of the peripheral nerves of the upper limb. Surgical Radiol Anat. 2010;32:305-
314.
Bedder MD, Bedder HF. Spinal cord stimulation surgical technique for the nonsurgically trained.
Neuromodulation. 2009;(12):1-19.
Bittar RG, Teddy PJ. Peripheral neuromodulation for pain. J Clin Neurosci. 2009;16:1259-1261.
Deer TR. Atlas of Implantable Devices. 1st ed. Springer Publishing; 2011.
Jasper J, Hayek S. Implanted occipital nerve stimulator. Pain Physician. 2008;11:187-200.
Mironer YE, Hutcheson JK, Satterhwaite JR, LaTourette PC. Prospective, two part study of the
interaction between spinal cord stimulation and peripheral nerve field stimulation in patients with low
back pain: development of a new spinal-peripheral neurostimulation method. Neuromodulation.
2011;14:151-155.
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3. Yakovlev AE, Resch BE, Karasev SA. Treatment of intractable hip pain after THA and GTB using
peripheral nerve field stimulation: a case series. Wisconsin Medical Journal. 2010;109(3):149-152.
4. Fishbain D, Goldberg M, Meagher BR, et al. Male and female chronic pain patients characterized by
DSMIII psychiatric diagnostic criteria. Pain. 1986;26:181-197.
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6. Huntoon MA, Burgher AH. Ultrasound-guided permanent implantation of peripheral nerve stimulation
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7. Bedder MD, Bedder HF. Spinal cord stimulation surgical technique for the nonsurgically trained.
8. Torrens K, Stanely PJ, Ragunathan PL, Bush DJ. Risk of infection with electrical spinal cord
stimulation. Lancet. 1997;349:729.
9. Slavin KV. Technical Aspects of Peripheral Nerve Stimulation: Hardware and Complications.
10. Trentman TL, Zimmerman RS. Occipital nerve stimulation: technical and surgical aspects of
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11. Johnson RD, Green A, Aziz TZ. Implantation of an intercostal nerve stimulator for chronic abdominal
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21. Oh MY, Ortega J, Bellotte JB, Whiting DM, Alo K. Peripheral nerve stimulation for the treatment of
technical report. Neuromodulation. 2004;7:103-112.
22. Schwedt TJ, Dodick D, Hentz J, Trentman TL, Zimmerman RS. Occipital nerve stimulation for
chronic headache-long-term safety and efficacy. Cephalalgia. 2007;27:153-157.
23. Oh MY, Ortega J, Bellotte JB, Whiting DM, Alo K. Peripheral nerve stimulation for the treatment of
technical report. Neuromodulation. 2004;7:103-112.
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chronic headache-long-term safety and efficacy. Cephalalgia. 2007;27:153-157.
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peripheral nerve field stimulation: a case series. Wisconsin Medical Journal. 2010;109(3):149-152.
33. Paicius RM, Bernstein CA, Lempert-Cohen C. Peripheral nerve field stimulation in chronic
abdominal pain. Pain Physician. 2006;261-266.
34. Paicius RM, Bernstein CA, Lempert-Cohen C. Peripheral nerve field stimulation for the treatment of
chronic low back pain: preliminary results of long-term follow-up: a case series. Neuromodulation.
2007;10(3):279-289.
35. Mironer YE, Hutcheson JK, Satterhwaite JR, LaTourette PC. Prospective, two part study of the
interaction between spinal cord stimulation and peripheral nerve field stimulation in patients with low
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CHAPTER 76
Surgical Treatment of Trigeminal Neuralgia

Michael G. Kaplitt
HISTORY
Facial pain can be caused by a variety of factors, including but not limited to dental pathology, trauma,
multiple sclerosis, tumors or other brain lesions, temporomandibular joint (TMJ) disorders, and
myofascial and psychogenic disorders. Although most of these are difficult to treat with either medical or
surgical therapy, it is possible to address the underlying insult (tumor removal, resolving dental
pathology, resting the TMJ with a bite block) and improve pain by eliminating the offending agent.
Trigeminal neuralgia (TM) is a specific type of facial pain syndrome which can usually be clinically
distinguished from these other disorders. Proper recognition of the disorder and accurate diagnosis of TN
is critical, since there are numerous therapeutic options that are effective for TN but these are of limited
or no clear utility for most of the other forms of facial pain. The first known report of symptoms typical of
TN came from the famous physician John Locke in 1677.1 The patient described typical severe, sharp,
unilateral pain of the face and lower jaw. Interestingly, the patient had teeth removed without relief. This
continues to occur to this day, since minor tooth pathology may lead to dental procedures or extractions in
a somewhat speculative attempt to treat facial pain that in fact is TN. Nicolas Andre coined the term “tic
douloreux,” another term still in use which describes the facial contraction and contortions that often
accompany the paroxysmal pain episodes of TN.2 Until early in this century, TN was still believed to
involve the facial nerve because of these often seen contractions, but it has long been established that this
is simply a reactive muscular contraction during the severe pain episodes.
DIAGNOSIS
• TN is usually characterized by unilateral, paroxysmal sharp or burning pain of brief duration (seconds
to minutes) in either the maxillary (V2) and/or mandibular (V3) distributions of the trigeminal nerve
beginning in patients roughly 50 to 70 years of age.
• Involvement of the ophthalmic (V1) division, bilateral symptoms, and younger age of onset can happen
but are rare and should suggest consideration of an alternative diagnosis.
• Undiagnosed multiple sclerosis can present with TN-like symptoms, and very young age of onset (20-
40-year old) should promote further testing for this possibility.
• The additional presence of more chronic, less intense, and less sharp pain does not preclude a
diagnosis of TN as long as the other type of pain is present, and this type of pain may in fact be due to
the severe facial contractions that occur in reaction to TN episodes.
• TN patients can often have periods of remission, which in some cases can last for years. However,
recurrence is common, and generally any subsequent remission periods are of increasingly shorter
duration.
• There is also often a specific “trigger” zone, which can bring on a pain episode when stimulated.
Stimuli which are frequently reported as provoking TN symptoms include chewing, brushing teeth,
rubbing the area of the trigger, and wind brushing across the face.
PATHOPHYSIOLOGY
• Eminent neurosurgeon Walter Dandy in 1934 noted during surgery to partially section the trigeminal
nerve that the nerve is frequently indented or lifted up by an artery, and he specifically speculated that
this was the cause of TN.
• The primary cause of most cases of classic TN is believed to be compression of the trigeminal nerve
by an arterial loop, usually from the superior cerebellar artery.
• On occasion, open surgical intervention (described in detail below) fails to demonstrate a clear
offending artery, but large veins have been noted to be touching the nerve.
• Whether venous compression can cause trigeminal neuralgia is unclear but this has been discussed.
• This presumably developmental variant causing onset of symptoms so much later in life is unclear, but
it may be that either volume loss with age causes slight brain shifts that bring cranial nerves in closer
proximity to vascular structures and/or pulsations over many years leads to demyelination or other
alterations in the nerve which eventually facilitates the pain response.
MEDICAL THERAPY
Medical therapy for TN is based on the belief that the progressive irritation from vascular compression
leads to inappropriate firing of the nerve and the resulting spasmodic pain. Therefore, as with other forms
of neuropathic pain, the primary medications utilized in TN are anticonvulsants and antidepressants.
Carbamazepine is frequently utilized and was recently endorsed in a consensus statement of the American
Academy of Neurology as having established efficacy based upon the strength and number of class I and
class II studies. This can influence white blood cell counts and therefore requires regular monitoring.
Oxcarbazepine is also often utilized and there are several strong clinical studies in support of this
treatment as well. Most other anticonvulsant or neuropathic pain medications, baclofen, and
antidepressant medications have all been utilized with symptomatic relief in patients, but these have been
less rigorously tested in high-quality clinical trials.
Problems With Medical Therapy

• Limited efficacy in many patients.
• Dose-limiting adverse effects and disease progression/resistance to therapy.
• More severe cases may have limited responses to medication which are inadequate to permit a
reasonable quality of life.
• Some patients who have adequate pain relief cannot tolerate the medications due to adverse effects at
doses necessary for pain control.
• These adverse effects are usually a consequence of the mechanism of medication action, which treat
TN by reducing firing of the hyperactive trigeminal nerve.
• It also can similarly reduce activity of neurons throughout the brain.
• Therefore, patients can complain of difficulty with concentration or focus, excessive lethargy or
sleeping, and personality changes.
• Mild side effects often resolve spontaneously but more significant complications can severely limit the
effectiveness and utility of medical therapy.
• Patients who may have responded to medication for months or even many years can develop worsening
pain over time either due to decreased response to medical therapy or doses can no longer be safely
increased.
SURGICAL THERAPY
Several effective surgical options are available to patients who have inadequate responses to more
conservative therapy. Given the high response rates to some of the surgical procedures outlined below, it
is not entirely clear if exhausting all medical therapies is appropriate management of patients with typical
trigeminal neuralgia. Nonetheless, understandable fears of surgery and potential risks of surgery generally
lead patients and caregivers to attempt medical therapy initially, and therefore most patients have at least
attempted medical management prior to considering surgical intervention. Most of the current surgical
therapies have been available for several decades or more, and therefore there is a large and long
experience to help provide patients with confidence regarding the known effectiveness and risks of each
procedure. However, with the use of neurostimulation for other types of pain, this is now being explored
in mostly off-label or experimental fashions and may also provide a more technologically advanced
alternative, particularly in patients who have either atypical syndromes or who have not adequately
responded to traditional surgical treatments.
MICROVASCULAR DECOMPRESSION
Microvascular decompression (MVD) is the most invasive of all surgical options for TN, but it also
appears to have the best therapeutic outcomes in most series. Roughly 90% of patients are either pain free
or have dramatic pain relief soon after surgery, with more than 70% of patients still reporting absence of
pain at 5 years in most series. The reason for such strong therapeutic efficacy is likely because MVD is
the one procedure which directly addresses the presumptive pathology causing TN.
• This is an open microsurgical procedure in which a retrosigmoid craniotomy is performed just up to
the junction between the transverse and sigmoid sinuses in order to expose the trigeminal nerve.
• The cerebellum is retracted to expose the nerve, although significant drainage of spinal fluid helps to
minimize the amount of retraction needed.
• After the nerve is identified, it must be explored throughout its entire traverse in the subarachnoid
space, extending from Meckel cave laterally to the brainstem root entry zone medially.
• Often petrosal vein branches are present in the field, and these can be coagulated and divided to
prevent hemorrhage and facilitate decompression.
• An artery (most commonly the superior cerebellar artery) is usually identified as indenting the nerve,
most commonly near the root entry zone but this can occur anywhere along the intracranial expanse.
• With modern imaging, this artery can often be observed on preoperative MRI (Figure 76-1A), and
these intraoperative findings can closely mimic imaging findings (Figure 76-1B). The artery is then
mobilized away from the nerve and then a Teflon-coated cotton pad is placed in between the nerve and
artery to cushion the nerve and relieve the compression (Figure 76-2).
Figure 76-1. Arterial compression of trigeminal nerve. This is the most common cause of typical
trigeminal neuralgia, usually as a result of compression by the superior cerebellar artery. (A) Axial
FIESTA image demonstrates compression of the right trigeminal nerve midway between Meckel cave at
the base of the skull and the entry zone into the brainstem (root entry zone). (B) Intraoperative image from
the same patient demonstrates compression of the trigeminal nerve, with slight deformation of the nerve,
by the superior cerebellar artery on the superior (left on the image) side of the nerve. Note the complex of
the seventh (facial) and eighth (vestibulocochlear) nerves inferior to the trigeminal nerve (right on the
image).
Figure 76-2. Microvascular decompression for trigeminal neuralgia. The superior cerebellar artery is
mobilized away from the trigeminal nerve and a Teflon-coated cotton pad is placed between the artery
and the nerve to maintain separation and cushion the nerve. Note the deformation of the nerve seen in
Figure 76-1B is relieved by this maneuver.
• Care must be taken to ensure that the pad is sufficiently large and properly placed to minimize
migration without being so large that it causes nerve injury.
• Any vascular structures touching the nerve at any point should be separated from the nerve, including
arteries and veins, which can be either insulated from the nerve with a pad or coagulated and divided,
depending upon anatomy and surgeon’s concerns regarding safety.
COMPLICATIONS
Several potential complications of surgery can occur and must be considered within the context of the
efficacy profile prior to making a decision in favor of MVD.
• The most common adverse effects of surgery is hearing loss in the ipsilateral ear, which can occur in
up to 10% of patients.
• The vestibulocochlear (eighth) nerve is adjacent to the trigeminal nerve, and often some dissection of
the arachnoid over this nerve is necessary to permit adequate mobilization of the cerebellum and
trigeminal nerve.
• The eighth nerve is very sensitive to injury, and retraction can nonetheless stretch the eighth nerve,
leading to dysfunction.
• Vestibular dysfunction can occur as well.
• Inadvertent injury to the tenuous vascular supply for the eighth nerve can also be a cause of total
hearing loss.
• Facial weakness due to injury to the facial (seventh) nerve can also occur, since this nerve runs in a
complex with the eighth nerve at this level, but this is much less frequent due to the relative location of
the seventh nerve and the greater resistance of that nerve to injury.
• Neurophysiological monitoring of the seventh and eighth nerves can be extremely helpful to understand
if any dysfunction is occurring during surgery.
• Either partial or total sensory loss within one or more divisions of the trigeminal nerve can also occur
following MVD, most likely due to damage to the nerve while placing the cotton pad.
• Cerebrospinal fluid (CSF) leak can also occur in most posterior fossa operations.
• Aseptic meningitis is often seen following MVD due to entry of blood into the subarachnoid space
during the dissection.
• Aseptic meningitis can be minimized by limiting the amount of blood entering the subarachnoid space
and through use of perioperative steroids.
PERCUTANEOUS LESIONING AT THE GASSERIAN

GANGLION
For patients who are poor candidates for MVD based upon risk or age or for those who simply do not
wish to undergo an open neurosurgical procedure due to risks or concern, percutaneous lesioning can be a
very effective alternative. Also, for patients in pain crises who are not being controlled with more
conservative therapies, the relative ease and rapid relief from these procedures can make them very
useful in such circumstances. The goal of the RF procedure is to create analgesia without significant
anesthesia.
• Percutaneous procedure involves placement of a needle through the foramen ovale, which is the point
of exit of the mandibular (V3) division of the trigeminal nerve from the skull into the Gasserian
ganglion composed of trigeminal nerve cell bodies. Usually this is performed in a radiology suite and
fluoroscopy is used to help confirm proper location of the needle tip in the foramen ovale, and patients
are briefly sedated for the procedure. Thin-cut computerized tomography (CT) precisely identifies the
foramen ovale on reconstructed 3D models of the skull base. The image is then rotated to match the
fluoroscopy image in order to help identify the foramen ovale based upon surrounding landmarks.
• Though single-plane fluoroscopy can be used, biplane fluoroscopy in an interventional neuroradiology
suite is recommended to maintain the same submental and lateral views (Figure 76-3) throughout the
procedure and to accelerate needle entry.
Figure 76-3. Approach for percutaneous radiofrequency lesion of the trigeminal nerve. Fluoroscopy in
two planes is generally helpful to localize the foramen ovale and the proper location of the guide needle
and lesioning probe. The V3 division of the trigeminal nerve passes through the foramen ovale, but the
trajectory allows passage of the lesioning probe into the fibers of the Gasserian ganglion and thereby
permits selective lesioning of any trigeminal division. (A) Lateral approach for a V2 lesion demonstrates
the wider bore of the guide needle just before the clival line, with the lesioning probe extending roughly 4
mm out from the end of the guide needle and the tip extending just beyond the clival line. (B) Modified
submental view demonstrates the guide needles with the attached lesioning probe passing through the
center of the left foramen ovale. In this view, the needle appears to be more to the lateral edge of the
foramen but the fluoroscopy arm was rotated in this instance to demonstrate the tip, which would be
obscured by a straight view down the center.
• The ganglion is positioned in a straight line with V2 branch, 2 to 5 mm anterior and lateral to V3, and 3
to 5 mm medial past V1 at the level of the clival line (see Figure 76-3).
• Proper location of the needle is usually accompanied by egress of CSF upon entry into the
subarachnoid space, although sometimes this is not clear and is less common in repeat procedures do
to scarring from previous surgery.
• When the needle is properly placed, radiorequency (RF) thermocoagulation method is used to create a
therapeutically effective lesion.
• An RF probe is passed through the central needle, with the tip positioned based upon the pattern of
pain distribution and landmarks for the divisional nerve fibers outlined above.
• Patients are then generally awakened from sedation and a stimulating current (1 millisecond pulse
width, 50-Hz frequency) is passed through the probe to functionally confirm proper location.
• If patients report sensing stimulation in a distribution is nonconcordant their pain pattern, then the
probe can be slightly adjusted and retested.
• If patient has difficulty speaking or opening their mouth, this might suggest stimulation of the motor
branch of the trigeminal nerve, and repositioning prior to lesioning should also be considered if this
occurs.
• Patient is then resedated for an initial lesion at low temperature (60°C for 60 seconds).
• Patient should again be awakened and tested for sensory loss.
• Subsequent lesions at 90 seconds and progressively higher temperatures (usually in increments of 5°C)
are performed, preferably with awake sensory testing in between lesions.
• After the first 2 to 3 lesions, patient can often undergo successive lesioning at the highest temperatures
with less or no sedation due to the analgesia already created, which can facilitate active sensory testing
during the higher-temperature lesions. Lesioning is usually discontinued when either a maximal
temperature is reached (80°C) or when patients begin to report decreased sensation.
• Patients usually report worsening sensory loss 24 to 48 hours after the procedure, but this generally
improves to leave patients with very limited or no sensory loss.
• Short-term pain relief following the procedure is generally excellent, with most reports indicating
success rates of 70% to 80% to complete pain relief.
• The recurrence rate is reported as high as 50% at 5 years.
• Very low rates of CSF leak, infection, carotid artery injury due to misplaced needles, and corneal
sensory loss have also been reported.
GLYCEROL INFUSION AND BALLOON COMPRESSION

As an alternative to RF lesioning, glycerol infusion or balloon compression may also be used.
Percutaneous needle placement is similar to RF lesioning. For glycerol injection, some practitioners
recommend cisternography to confirm proper placement prior to infusion, but others do not believe that
this is necessary. Similarly, some reports recommend a small test infusion of glycerol to examine sensory
changes which may reflect proper localization. For balloon compression, a balloon catheter is inserted
through the needle passed through the foramen ovale and then inflated to compress the ganglion.
Compression is usually performed for several minutes (roughly 5 minutes on average), with longer
compression times associated with better therapeutic outcomes but also greater incidence of significant
sensory loss. A major advantage of these approaches is the absence of need for repeated sedation
followed by awake testing, since little or no sensory testing is required to complete these procedures.
This usually makes these procedures much shorter than a properly performed RF lesion, and can also be
very useful if patients are not very cooperative and have some cognitive impairment or a significant
language barrier. Since they are less selective than RF, they can be associated with greater sensory loss in
nerve divisions outside of the area of pain and have been reported to have somewhat greater incidences
of V1 sensory loss and associated corneal denervation. Short-term pain relief is similar to RF, although
some studies suggest that these are slightly lower than RF, and glycerol may be more preferable to balloon
compression.
STEREOTACTIC RADIOSURGERY
Stereotactic radiosurgery (SRS), commonly referred as gamma knife surgery, is the least invasive of the
accepted surgical therapies for TN. This is a specific method of SRS that has had the longest use and has
been most widely studied. The procedure of SRS involves use of focused, high-intensity radiation to
perform a noninvasive lesion of the trigeminal nerve. Since this is a consequence of the tissue response to
radiation, the effect of SRS is often delayed from 1 to 3 months, so this may be less beneficial to patients
in crisis with urgent need of pain relief. SRS can generally be performed safely on anticoagulated
patients. Therefore, this may be a good option as well for patients who cannot safely stop anticoagulation
for any length of time.
• The center of radiation is targeted to a point on the trigeminal nerve several millimeters distal to the
brainstem and irradiate the brainstem at or less than the 20% isodose line.
• The goal is to radiate as close to the root entry zone of the nerve as possible while maintaining the
radiation limit to the brainstem itself.
• For the gamma knife procedure, a rigid stereotactic frame is physically attached to the patient’s head
using local anesthesia, followed by imaging (MRI or CT) and target planning various isodose lines
around an isocenter target.
• In most cases, a single isocenter is used, but for difficult cases multiple isocenters can be used.
• Some recent technologies for SRS do not require placement of a frame, though the accuracy, safety, and
efficacy of these devices for trigeminal neuralgia SRS have not been well established.
SRS using the gamma knife is generally very effective in the first 6 to 12 months following treatment,
although it may have a slightly lower rate of patients who are pain free without medication. Most studies
indicate that 40% to 70% of patients are pain free without medication between 6 and 12 months following
the procedure, although generally 70% to 80% of patients report satisfactory pain relief at 1 year
regardless of whether or not they have discontinued medication. As with percutaneous procedures, a
substantial rate of recurrence is seen progressively over the years. Some studies have reported success
with repeat procedures in patients with long-term recurrences. The major complication of SRS is
persistent decrease or loss of facial sensation in one or more distributions of the trigeminal nerve in 10%
of patients to be as high as 30% in some studies. Generally 70 to 80 Gy is delivered to the isocenter near
the root entry zone to achieve good outcomes, with lower doses of radiation associated with poorer
outcomes while higher doses are associated with greater sensory loss but without clear additional
therapeutic benefit. The patients who fail percutaneous lesioning or MVD are unlikely to benefit from
SRS and may in fact have an alternative diagnosis to classic TN.
NEUROMODULATION THERAPIES
Neurostimulation has long been used to treat chronic pain. Currently, spinal cord stimulation and certain
types of peripheral nerve stimulation are FDA-approved for pain in the arms, legs, and back. While
neurostimulation for facial pain is increasingly being explored, it is currently considered an off-label use
of these devices. A potential advantage of neurostimulation is that it is nondestructive and is reversible
procedure, which can be effective for difficult cases with unclear diagnosis or where multiple prior
therapies have failed. Neurostimulation for pain involves placement of an externalized lead for several
days to a week as trial followed by implantation of a permanent system. There have been two primary
types of neurostimulation used for facial pain: motor cortex stimulation and peripheral facial stimulation.
MOTOR CORTEX STIMULATION

Motor cortex stimulation (MCS) is an intracranial procedure where a stimulating electrode is placed on
the surface of the brain in order to stimulate the motor cortex. The mechanism of action remains unclear,
but it is believed that MCS may stimulate U-fibers which connect to sensory areas. MCS has been used to
treat a variety of complicated pain syndromes like:
• Phantom-limb pain
• Central pain syndromes
• Poststroke pain syndrome
• Intractable trigeminal neuropathic pain
• Patients who failed SCS or peripheral nerve stimulation
TN category includes a far broader group of patients than simply classic TN, and therefore it remains
unclear if results of treatment specifically in TN would be any better or worse than in the broader group
as a whole. Most practitioners used approved spinal cord stimulation paddle electrodes to place on the
brain, generally outside the dura to avoid intradural hemorrhage or injury. Due to the invasive nature of
this craniotomy procedure, test stimulation is usually performed by attaching the end of the paddle lead to
a second lead extension, which is then externalized from a separate stab wound behind the craniotomy
incision line. After 1-week trial, if patients report adequate pain relief, then the externalized extension is
removed and the lead is attached to a new lead extension which is tunneled to a pulse generator, usually
placed in the anterior chest wall.
Most studies have defined a good response as greater than 40% to 50% pain relief in 65% to 75% of
patients with trigeminal neuropathic facial pain at 1 year. Complications of surgery are infection,
bleeding, and hardware-related complications in 5% to 10% of patients. Ten percent of patients reported
to have perioperative seizures, and that may be due to electrical stimulation of the cerebral cortex which
is more likely to lead to seizures than subcortical stimulation. However, these appear to be isolated
seizures, as long-term epilepsy has not been reported in these patients. As the permanent complications
appear to be rare, it may be a reasonable consideration as an off-label treatment for patients who have not
responded well to conservative therapy and are not good candidates for more traditional TN surgery.
PERIPHERAL FACIAL STIMULATION

As with MCS, peripheral facial stimulation (PFS) is a nonapproved application of neurostimulator
system for certain peripheral conditions like:
• Difficult cases of post-traumatic or other forms of trigeminal neuropathic pain
• Patients with refractory atypical facial pain
• TN symptoms unresponsive to other surgical therapies
Due to relatively low morbidity of peripheral stimulation procedure, the ability to trial stimulation
prior to permanent implantation and the reversibility of this procedure favor consideration of this
technique for select appropriate patients. In this case, a thin lead used for percutaneous stimulation is
placed in the subcutaneous tissue of the face in order to stimulate branches of the supraorbital (V1) or
infraorbital (V2) sensory nerves. Mandibular stimulation can also be performed, although the extreme
mobility of the mandible on an almost continuous basis (talking, eating) raises concerns regarding lead
erosions or fractures compared with less mobile sites.
• Patients are generally sedated for these procedures, although general anesthesia can be more useful as
proper placement can be somewhat painful.
• As awake test stimulation is less critical for proper localization than for spinal stimulation, general
anesthesia can actually facilitate better placement without patient discomfort.
• Fluoroscopy is helpful to confirm that leads are placed in good position and, in particular, to confirm
that the tip of the lead is just lateral to midline.
• The lead should be placed just above V1 or below V2 the orbital rim in order to stimulate the nerves
just as they exit their respective foramina (Figure 76-4).
Figure 76-4. Localization of stimulating electrode for peripheral facial stimulation of the trigeminal
nerve. In this case, the stimulation was for pain in the V2 distribution and therefore the electrode was
placed to stimulate the infraorbital nerve. (A) Lateral skull x-ray demonstrates the infraorbital location of
the percutaneous stimulating electrode (B) AP skull x-ray from the same patient again demonstrates the
infraorbital placement of the stimulating electrode. The tip of the electrode usually abuts the lateral edge
of the nasal bones.
• A percutaneous needle is bent slightly to create a curve, with a stab incision for an entry site made just
behind the hairline.
• For a trial lead, a second stab is made in a more posterior position, and the same percutaneous needle
is used as a tunneler to tunnel the excess lead from the entry site to the more posterior site.
• The lead is anchored with a suture and test stimulation is performed for 1 week. After a successful
trial, a similar technique is used to implant a new permanent lead and this is then tunneled to a pulse
generator placed in the anterior chest wall.
• A loop of the lead should be left at the entry site for strain relief from movement of the neck.
The most widespread use of peripheral stimulation in the head and neck has been stimulation of the
occipital nerves for occipital neuralgia and migraine headaches. Some studies have reported trigeminal
peripheral stimulation for trigeminal neuropathic pain and postherpetic neuralgia. The studies reported
70% of patients to have good response to trial stimulation and go on to permanent implantation. Of those
receiving permanent implants, 50% to 75% of patients maintain greater than 50% pain relief at 2 years.
Currently this remains an off-label indication for these devices, and more studies with longer-term
follow-ups are needed.
SUMMARY
Facial pain can be one of the more difficult and refractory conditions to manage for pain specialists,
neurologists, and neurosurgeons. Medical therapy is clearly the first choice and can be effective in many
cases. However, frequently patients do not adequately respond to trials of multiple medications or they
become refractory to treatment. In these situations, a variety of surgical therapies can cure or dramatically
relieve pain. A proper initial diagnosis is essential, since most accepted surgical therapies are primarily
useful for true, idiopathic trigeminal neuralgia. However, advances in neuromodulation now provides a
variety of novel options for patients who either develop recurrence of pain following more traditional
surgery or for those who do not have classical trigeminal neuralgia. At present, these approaches use off-
label applications of devices approved for other indications, which can somewhat limit utility of these
methods. Nonetheless, these can be considered in isolated cases and further studies should help increase
both our understanding of the role of neuromodulation for refractory pain and the eventual broad
acceptance of this option.
Suggested Reading
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Cetas JS, Saedi T, Burchiel KJ. Destructive procedures for the treatment of nonmalignant pain: a
structured literature review. J Neurosurg. 2008;109:389-404.
Dhople AA, Adams JR, Maggio WW, Naqvi SA, Regine WF, Kwok Y. Long-term outcomes of Gamma
Knife radiosurgery for classic trigeminal neuralgia: implications of treatment and critical review of
the literature. Clinical article. J Neurosurg. 2009;111:351-358.
Fontaine D, Hamani C, Lozano A. Efficacy and safety of motor cortex stimulation for chronic neuropathic
pain: critical review of the literature. J Neurosurg. 2009;110:251-256.
Gronseth G, Cruccu G, Alksne J, Argoff C, Brainin M, Burchiel K, Nurmikko T, Zakrzewska JM. Practice
parameter: the diagnostic evaluation and treatment of trigeminal neuralgia (an evidence-based
review): report of the Quality Standards Subcommittee of the American Academy of Neurology and
the European Federation of Neurological Societies. Neurology. 2008;71:1183-1190.
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525.
Leal PR, Hermier M, Froment JC, Souza MA, Cristino-Filho G, Sindou M. Preoperative demonstration of
the neurovascular compression characteristics with special emphasis on the degree of compression,
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findings, in 100 consecutive patients who underwent microvascular decompression for trigeminal
neuralgia. Acta Neurochir (Wien). 2010;152:817-825.
Kondziolka D, Lunsford LD. Percutaneous retrogasserian glycerol rhizotomy for trigeminal neuralgia:
technique and expectations. Neurosurg Focus. 2005;18:E7.
Kouzounias K, Lind G, Schechtmann G, Winter J, Linderoth B. Comparison of percutaneous balloon
compression and glycerol rhizotomy for the treatment of trigeminal neuralgia. J Neurosurg.
2010;113:486-492.
Lee ST, Chen JF. Percutaneous trigeminal ganglion balloon compression for treatment of trigeminal
neuralgia, part II: results related to compression duration. Surg Neurol. 2003;60:149-153; discussion
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outcomes and complications. Br J Neurosurg. 2011.
Lovely TJ, Jannetta PJ. Microvascular decompression for trigeminal neuralgia. Surgical technique and
long-term results. Neurosurg Clin N Am. 1997;8:11-29.
Paemeleire K, Bartsch T. Occipital nerve stimulation for headache disorders. Neurotherapeutics.
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Peddada AV, Sceats DJ, White GA, et al. CyberKnife radiosurgery for trigeminal neuralgia: unanticipated
iatrogenic effect following successful treatment. J Neurosurg. 2011.
Slavin KV. Peripheral nerve stimulation for the treatment of neuropathic craniofacial pain. Acta
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and long-term results. Neurosurg Clin N Am. 1997;8:11-29.
SECTION IX
NEUROLYTIC PROCEDURES
CHAPTER 77
Neurolytic Blocks
Kenneth D. Candido and Nebojsa Nick Knezevic
INTRODUCTION
Dogliotti1 first described the technique of subarachnoid chemical neurolysis using alcohol for the
treatment of sciatic pain more than 80 years ago. That same year, Suvansa2 described intrathecal carbolic
acid for the treatment of tetanus. A quarter of a century later, Maher3,4 in his 2 landmark articles described
his experience with hyperbaric phenol and silver nitrate for subarachnoid neurolysis, stating, “It is easier
to lay a carpet than to paper a ceiling,” an obvious reference to his understanding of the baricity
properties of alcohol and phenol (carbolic acid). Over the ensuing years, however, lack of experience
with either technique and fear of the anticipated complications resulted in underuse of this neurolysis,
especially when applied to the subarachnoid space. Better understanding and increased use of neuraxial
opiates for cancer pain since the 1980s have decreased the use of subarachnoid chemical neurolysis even
further. Nonetheless, because of the physical separation of the sensory and motor roots of spinal nerves
within the spinal canal, intrathecal dorsal rhizotomy (more appropriately called rhizolysis) is the only
neurolytic procedure that allows sensory block without concomitant motor block. Because of this and
because of the relative precision with which the affected nerve roots can be blocked, the technique is
particularly useful for treating cancer pain in an extremity, where preservation of motor function is so
important. In short, the physical separation of motor and sensory fibers in the subarachnoid space
preserves forever a small but unique role for subarachnoid neurolysis in the management of cancer pain in
carefully selected patients. The present chapter will describe the techniques of:
• Trigeminal neurolysis
• Lumbar sympathetic (LSNB)
• Celiac plexus (CPB) neurolysis
• Ganglion impar and superior hypogastric plexus neurolysis
• Sacroiliac joint (SIJ) neurolysis
• Spinal and epidural including transforaminal neurolysis
INDICATIONS
Neurolysis may be used to manage recalcitrant pain syndromes of both a malignant as well as benign
etiology. Techniques have been described for blocking different types of pain:
• Pain from the cranial nerves (particularly the trigeminal nerve; CN V)
• Pain originating in the major plexuses (brachial and lumbar)
• Pain associated with sympathetic-medially pain (especially the celiac plexus, lumbar sympathetic
ganglia, ganglion impar, and superior hypogastric plexus)
• Pain originating in the periphery (sacroiliac joints)
Before considering the use of chemical or thermal neurolysis, however, it behooves the clinician to
ascertain that every alternative means of providing analgesia has been investigated with the patient. By
virtue of their irretrievable nature, chemical neurolytics are exceedingly unforgiving when placed in
contact with nonintended, nontargeted tissues. For these reasons, a caveat to the successful use of
neurolytic blocks is a predetermined analgesic response, which is unequivocal following a local
anesthetic block of the same targeted structure(s).
AGENTS
• In general, absolute alcohol or phenol may be selected for chemical neurolysis.
• Alcohol has been the drug of choice for subarachnoid block, cranial nerve block, and celiac plexus
block.
• Phenol finds utility for lumbar sympathetic nerve blocks, peripheral neurolysis like SIJ block,
Ganglion impar, and superior hypogastric plexus blocks, although various authorities have used either
drug for any of the aforementioned indications.
SELECTION CRITERIA
Because the duration of action of neurolytic agents is finite but unpredictable, great care must be
exercised in choosing appropriate candidates for these procedures. Neurolytic blockade is especially
suited to patients in whom conventional treatment regimens have failed and who have a short life
expectancy, usually less than 1 year, when the subarachnoid or epidural route is selected. More often than
not, neurolysis at other sites has been successfully used in individuals who do not have an imminently
grave prognosis. As with all neurolytic procedures, including electrical and thermal neurolysis, patients
must be completely apprised of the possibility of debilitating side effects and other serious associated
complications that can follow even a successful block, most notably, motor weakness and incontinence.
The selection criteria for subarachnoid neurolysis include the following:
• The diagnosis is well established.5
• The patient’s life expectancy is short, usually 6 to 12 months.
• The patient’s pain is unresponsive to antineoplastic therapy (chemotherapy, radiation).
• The patient’s pain has failed to respond to adequate trials of analgesic agents and adjunctive drugs.
• The pain is localized to 2 or 3 dermatomes.
• The pain is predominantly somatic in origin.
• The pain is unilateral (neurolytic blocks for bilateral pain should be staggered).6
INFORMED CONSENT
• It is crucial that not only the patient, but also the patient’s family fully understand the anticipated
procedure, its potential risks, the alternative forms of therapy available, and, most importantly, the
possibility of serious complications.
• It is important that they understand that the procedure does not simply “take away pain,” but rather
substitutes numbness (loss of sensation) for the pain.
• So important is this concept that, with rare exceptions, before the decision is made to proceed with a
subarachnoid neurolytic block, a prognostic block should be carried out using a local anesthetic so that
the patient can experience the pain relief that may be anticipated after a neurolytic block and the
accompanying sensory block.
• Although an occasional patient may decide that he or she cannot tolerate the numbness, most patients
prefer this lack of sensation to the pain and choose to proceed with the neurolytic procedure
Neurolytic blocks are usually considered in patients for whom the analgesic ladder has failed to provide
adequate analgesia. However, the pros and cons for each procedure, including a detailed knowledge of
potential complications, and other factors such as the speed of pain relief, and the improvement of quality
of life need to be weighed before making the decision. In most scenarios, diagnostic block performed
prior to the therapeutic neurolytic blocks is recommended. Temporary unexpected adverse effects can
occur due to unexpected spread of local anesthesia during diagnostic block; however, serious
complications may follow injection of neurolytic agents.
The following procedures need to be done routinely for preoperative considerations:
• Obtaining an informed, written consent.
• Ascertaining the absence of contrast allergies and no use of anticoagulant medications.
• It is useful to refer to standard references such as those published by the American Society of Regional
Anesthesia (ASRA) concerning anticoagulants and regional anesthesia prior to commencing to
determine the suitability of prospective block candidates prior to proceeding.
• Standard American Society of Anesthesiologists (ASA) monitors are applied and baseline vital signs
are assessed and documented.
• An intravenous canula should be placed for the purposes of administering intravenous fluids and
supportive drugs in the event of either an inadvertent event or following the expected orthostatic
hypotension resulting from a successful block.

All candidates for whom peripheral or central neurolysis is contemplated must understand that the use of
phenol and alcohol for these procedures represents an off-label use of these chemical agents. This critical
information must be made part of the written informed consent process.
TRIGEMINAL NEUROLYSIS (FIGURES 77-1 TO 77-9)

Figure 77-1. Neurolysis using CT-scan guidance for trigeminal neuralgia. Patient in position to enter the
CT scanner. A left-sided subzygomatic approach to the foramen ovale is demonstrated. (Used with
permission from Kenneth D. Candido, M.D.)
Figure 77-2. The needle has been placed for left-sided CT-scan guided neurolytic TGN block; patient
about to enter the scanner. (Used with permission from Kenneth D. Candido, M.D.)
Figure 77-3. Coronal CT scan view of advancing needle tip for CT-guided neurolytic TGN block,
demonstrated by arrow (coronal view). (Used with permission from Kenneth D. Candido, M.D.)
Figure 77-4. Coronal view of needle tip advancing toward foramen ovale for neurolytic TGN block; tip
denoted by arrow (coronal view). (Used with permission from Kenneth D. Candido, M.D.)
Figure 77-5. Needle tip entering foramen ovale for neurolytic TGN block (coronal view). (Used with
Figure 77-6. 1-mL iodine-based, water-soluble contrast injected through foramen ovale into Meckel cave
as prelude to neurolytic TGN block (coronal view). (Used with permission from Kenneth D. Candido,
M.D.)
Figure 77-7. Sagittal CT scan view of the same view as in Figure 77-6 with contrast injected through the
foramen ovale as a prelude to neurolytic TGN block (sagittal view). (Used with permission from Kenneth
D. Candido, M.D.)
Figure 77-8. Axial CT view of same patient showing advancing needle tip heading toward foramen ovale
for neurolytic TGN block (axial view). (Used with permission from Kenneth D. Candido, M.D.)
Figure 77-9. Contrast in Meckel cave as prelude to neurolytic TGN block; same patient as in Figure 77-8
(axial view). (Used with permission from Kenneth D. Candido, M.D.)
Relevant Anatomy
The trigeminal nerve resides in Meckel ave, located within the foramen ovale. Recalcitrant V1, V2, or V3
pain which has been shown to be responsive to local anesthetic blocks may be an indication for alcohol
neurolysis of the Gasserian ganglion.
• It is imperative that patients are offered surgical options including microvascular decompression
before seeking to undertake neurolysis.
• An informed consent must include discussion of the risks of bleeding, paralysis, and death. Patients
need to be evaluated by physicians to exclude all contraindications and must have responded favorably
to one or more local anesthetic diagnostic blocks performed at previous visits.
Contraindications
• Patient who has bleeding problems
• Taking irreversible inhibitors of platelet aggregation
• Has history of allergy to iodine-based contrast agents
• Has an infection at the injection site
• Patient who is unable to remain motionless during the procedure, which may cause unexpected injury
during the intervention
Fluoroscopic Views
• The procedure may be performed using either fluoroscopic or CT guidance, and rarely by using
ultrasound guidance.
• It is the recommendation of the present authors that only CT guidance is used for these patients, both to
ascertain that the medication is successfully placed at the target site as well as to preserve a clear and
unmistakable medical record in the case of an unforeseen outcome or inadvertent spread of agent to
nontargeted tissues.
• Supine position
• A fine-gauge hypodermic needle and 2 mL of 1% lidocaine plain will be used for local anesthesia.
• A 22- or 25-gauge Whitacre-type subarachnoid needle, 10 to 15 cm long with a distal curve and 1 mL
of absolute alcohol will be used for the neurolysis block.
Intraoperative Technique Steps

• The patient is placed supine and a full complement of American Society of Anesthesiologists (ASA)
monitors is applied. Baseline vital signs are assessed and recorded.
• The skin is cleansed using chlorhexidine.
• A skin wheal is raised approximately 3 cm lateral to the corner of the closed mouth using a fine-gauge
hypodermic needle and 2 mL of 1% lidocaine plain.
• A 22- or 25-gauge Whitacre-type subarachnoid needle, 10 to 15 cm long with a curve placed at the
distal tip is then advanced from anterior to posterior, and slightly medial and cephalad, aiming toward
the ipsilateral pupil.
• Once the needle has been advanced more than 4 cm, the patient is scanned to identify the direction of
the needle in relationship to the foramen ovale (Figures 77-3 to 77-9).
• Rostral, axial, and sagittal views with reconstruction are used to properly position the needle tip.
• Once within Meckel ave, the stylet of the needle is withdrawn, and an assessment is made for
cerebrospinal fluid.
• If there is CSF aspirated, the needle is slightly withdrawn until the flow ceases.
• If there is no CSF aspirated, one mL of high-density, water-soluble, iodine-based contrast is injected.
• An assessment is made to determine the spread of contrast.
• If the spread appears adequate and there is no vascular or CSF run-off, 1 mL of absolute alcohol may
now be injected, slowly and incrementally.
• The patient must be cautioned that this may burn somewhat, in the distribution of the ophthalmic,
maxillary, or mandibular nerves, respectively.
• The needle is then flushed with 0.5 mL of air and is withdrawn.
• Following the procedure, the patient must be observed in a monitored setting for no less than 1 hour to
assess the full effects of the procedure and to determine if there have been any adverse effects from the
block.
• The patient must be observed in a monitored setting for at least 1 hour to assess the full effects of the
procedure and to determine if there have been any adverse effects from the block.
Monitoring of Potential Complication
The following complications from the blocks which may occur include:
• Numbness, hypesthesia, or dysesthesia in the entire trigeminal nerve or in one of its branches (V1, V2,
V3)
• Reactivation of a dominant herpes simplex
• Corneal abnormalities such as absence of corneal reflex, ulceration, and keratitis
• Bleeding at the injection site or localized pain
• Intracranial hemorrhage
• Infection
• Injection into the foramen spinosum in lieu of the ovale
LUMBAR SYMPATHETIC NEUROLYSIS (FIGURES 77-10 TO 77-

13)
Figure 77-10. Lumbar sympathetic neurolytic block at L2. Curved needle advancing around lateral aspect
of the right L2 vertebral body; oblique fluoroscopy image. (Used with permission from Kenneth D.
Candido, M.D.)
Figure 77-11. Anteroposterior fluoroscopy view of needle seated at level of pedicle, anterior, and lateral
to vertebral body at the right L2 for neurolytic LSNB. (Used with permission from Kenneth D. Candido,
M.D.)
Figure 77-12. Anteroposterior view of 5-mL iodine-based, water-soluble contrast injected at L2 for
neurolytic LSNB on the right side demonstrating right-sided spread. (Used with permission from Kenneth
D. Candido, M.D.)
Figure 77-13. Lateral fluoroscopic view, neurolytic LSNB; contrast injected as a prelude to injecting
phenol; tight linear spread along ventral margin of multiple vertebral bodies without extravasation or
spread ventrally or dorsally. (Used with permission from Kenneth D. Candido, M.D.)
Relevant Anatomy
Individuals with sympathetically-mediated pain occasionally fail to derive benefit from repeated local
anesthetic nerve blocks of the sympathetic ganglia. The ganglia, which are paired, may number from 3 to 4
and may be as long as 1.5 cm.
When patients have transient responses to local anesthetic blocks and wish not to undergo trial spinal
cord stimulation, they may occasionally be considered candidates for lumbar sympathetic neurolysis. An
informed consent must include discussion of the risks of psoas muscle injection, hematoma, femoral nerve
neuropathy with quadriceps weakness, and vascular injury. Male patients should be advised that they may
also develop retrograde ejaculation after procedure as genitofemoral neuralgia may occur up to 25% of
the time.
Contraindications
• Patient who is taking irreversible inhibitors of platelet aggregation
• Patient who has history of allergy to iodine-based contrast agents
• Patient who has an infection at the injection site
• Patient who is unable to remain motionless during the procedure which may cause unexpected injury
Fluoroscopic Views
• While ultrasound may be used, due to the severe potential consequences of a misplaced agent, it is
likely that fluoroscopy or CT imaging provide a more detailed assessment of the anatomical confines
required for successful blockade.
• A scout anteroposterior (AP) film of the lumbar spine will be obtained, and then the 20-degree oblique
orientation fluoroscope view will be taken.
• Prone position; alternative is lateral decubitus or modified Sims positioning
Selection of Needles, Medications, and Equipments
• A fine-gauge hypodermic needle and 1% lidocaine, 2 to 5 mL will be used for raising a skin wheal.
• A 22- or 25-gauge Whitacre-type subarachnoid needle with a curve at the distal tip and 5 to 15 mL of
5% to 7% phenol in glycerin is used for neurolytic block.

• The patient is placed in the prone position; lateral decubitus; or modified Sims position.
• An intravenous cannula is placed and standard ASA monitors are applied.
• A full surgical sterile skin preparation is undertaken.
likely that fluoroscopy provides a more detailed assessment of the anatomical confines required for
successful blockade.
• A scout anteroposterior (AP) film of the lumbar spine is obtained (Figure 77-10), and then the
fluoroscope is placed in the 20 degree oblique orientation (Figure 77-11).
• Blocks may be performed at L2, L3, or L4, with the most traditional level being selected as L2.
• After raising a skin wheal using a fine-gauge hypodermic needle and 1% lidocaine, 2 to 5 mL, a 22- or
25-gauge Whitacre-type subarachnoid needle with a curve at the distal tip is advanced from posterior
to anterior and medially until the tip sits at the anterior-lateral margin of the L2 vertebral body,
juxtaposed at the ventral one-third of the vertebral body.
• At this point, water-soluble, iodine-based contrast is injected.
• If the contrast does not adhere to the ventral surface of the vertebral column in a tight, linear array, the
needle should be positioned until such a result is attained.
• Once needle placement is considered successful, 5 to 15 mL of 5% to 7% phenol in glycerin is
incrementally injected, the final volume being determined to mimic the volume which was used to
create the observed pattern of x-ray contrast spread.
• The needle is then flushed with 1 mL of air and is withdrawn.
• Upon completion of the procedure, the patient is observed in a monitored setting for a minimum of 1
hour and is cautioned to arise slowly from a supine position to minimize the likelihood of developing
orthostatic hypotension, a common finding following even unilateral LSNB neurolysis.
Monitoring of Potential Complications8

• The most common complication is neuralgia, which occurs due to unexpected spread of the neurolytic
agents over the genitofemoral nerve
• Postdural puncture headache
• Bleeding at the injection site or localized pain
• Epidural, subdural, or subarachnoid injection
• Vascular complication such as hypotensive collapse
• Intra-aortic or intra-vena caval injection
• Thrombosis, embolization, infarction
• Paralysis
• Bladder, bowel, or sexual dysfunction
• Death
CELIAC PLEXUS NEUROLYSIS (FIGURE 77-14)

Figure 77-14. Axial CT-scan image of contrast spread following 20-mL injection; neurolytic CPB (refer
to chapter on Celiac Plexus Block for additional details and images). (Used with permission from
Kenneth D. Candido, M.D.)
Celiac plexus blocks, including neurolytic CPB, have been detailed in the chapter dedicated to that
procedure. CPB neurolysis may be used for both malignant as well as for benign conditions, most
commonly chronic pancreatitis. Fluoroscopy, CT-scan imaging, or endoscopic ultrasound use may be
employed as adjuncts to the block. Each of these modalities has been well described.
GANGLION IMPAR NEUROLYSIS (FIGURES 77-15 TO 77-17)

Figure 77-15. Ganglion impar neurolytic block using fluoroscopic guidance; needle approaches
sacrococcygeal junction; contrast injected outside junction. (Used with permission from Kenneth D.
Candido, M.D.)
Figure 77-16. Ganglion impar neurolytic block after needle has passed through sacrococcygeal junction;
additional contrast injected outlining ventral sacral margin; rectal gas pattern undisturbed by needle tip.
(Used with permission from Kenneth D. Candido, M.D.)
Figure 77-17. Ganglion impar neurolytic block; anteroposterior fluoroscopic view. (Used with
Occasionally pelvic pain may prove resistant to conventional attempts to reduce its intensity and severity.
Under these circumstances, or in the case of a malignant process, such as rectal, bladder, or cervical
cancer causing the pain, a neurolytic procedure may be considered. Visceral or SMP in the perineal area
associated with malignancies of the pelvic area produces vague, burning, localized perineal pain; and
often urgency of urination or defecation.
Relevant Anatomy
The Ganglion of Walther is the solitary terminal ganglion of the sympathetic chain located anterior to the
sacrococcygeal junction.
When one or a series of local anesthetic diagnostic blocks prove successful in reducing the pain, albeit
temporarily, neurolysis may be considered. An informed consent must include discussion of the risks of
rectal perforation, infection, bleeding and hematoma formation, and neural injury.
Contraindications
Fluoroscopic Views
• The most commonly used technique for ganglion impar neurolysis is the trans-sacrococcygeal approach
with fluoroscopy by introducing the needle through the sacrococcygeal joint (SCJ).
• Ultrasound guidance is not widely used as it cannot accurately identify the depth of needle penetration
because of some sacral and coccygeal bony artifacts. In addition, impacted stool or gas in the rectum is
possible to make it difficult to recognize the SCJ in the anteroposterior fluoroscopy view. However,
there is literature support recommending using the lateral fluoroscopy view to identify the depth of
needle and the spread of the neurolytic agents.
• Jack-knife position
• A fine-gauge hypodermic needle and 3 to 5 mL of 1% lidocaine with epinephrine 1:200,000 (5 μg/mL)
will be used to raise a skin wheal.
• A 22-gauge, 3.5-in (8.89-cm) Quincke-type subarachnoid needle and 3 to 5 mL of 5% to 7% phenol in
glycerin will be used for neurolytic blocks.

• The procedure is performed with the patient prone, preferably in the jack-knife position.
• As the anatomical boundaries are an extension of those required to perform caudal epidural injections,
most interventionalists ought to be able to identify the sacrococcygeal junction. This is situated distal
to the sacrococcygeal ligament, along the same cephalad-caudal axis.
• Due to the proximity to the perineum, a comprehensive skin cleansing needs to be undertaken, using
chlorhexidine.
• A skin wheal is raised after first identifying the anatomical boundaries of the sacrum, using a fine-
gauge hypodermic needle and 3-5 mL of 1% Lidocaine with epinephrine 1:200,000 (5 μg/mL).
• Using a 22-gauge, 3.5 inch (8.89 cm) Quincke type subarachnoid needle, the sacrococcygeal junction is
penetrated, taking care to not penetrate the rectum.
• Alternatively, a double-curved needle may be used to enter the skin more distally and advance through
the anococcygeal ligament (between the anus and tip of the coccyx) toward the ventral surface of the
sacrum, under continuous fluoroscopic guidance.
• Once the needle is appropriately situated, 3 to 5 mL of contrast may be injected.
• If the contrast spread adheres tightly to the ventral surface of the sacrum, an equivalent volume of 5%
to 7% phenol in glycerin may then be incrementally injected.
• The needle is then flushed with 1 mL of air and is withdrawn.
• The patient should be observed for 30 to 60 minutes in a monitored setting following the completion of
the procedure to be certain that there have been no adverse effects from the neurolytic agent.
• Even though there was no definitive literature description of the serious complication in patients who
received the ganglion impar neurolytic block, as with most procedures, there is the theoretical risk of
pain at the injection site, localized bleeding, infection, nerve injury, puncture of internal vessels or
organs, paralysis, and death.
SUPERIOR HYPOGASTRIC PLEXUS NEUROLYSIS (FIGURES

77-18 TO 77-21)
Figure 77-18. Superior hypogastric plexus neurolytic block; right-sided: Needle seen on lateral view.
(Used with permission from Kenneth D. Candido, M.D.)
Figure 77-19. Superior hypogastric plexus neurolytic block; right-sided: Needle seen on AP view. (Used
with permission from Kenneth D. Candido, M.D.)
Figure 77-20. Superior hypogastric plexus Neurolytic block; right-sided: Needle seen on lateral view
after injection of 5 mL of contrast. (Used with permission from Kenneth D. Candido, M.D.)
Figure 77-21. Superior hypogastric plexus neurolytic block; right-sided: Needle seen on AP view after
injection of 5 mL of contrast. (Used with permission from Kenneth D. Candido, M.D.)
Pain arising from pathologic processes of the large colon and occasionally from other pelvic viscera is
modulated by the superior hypogastric plexus. Blockade of the plexus using neurolytic agents is
occasionally effective for visceral and sympathetically-mediated pain in the pelvis where local anesthetic
diagnostic blocks have proved temporarily effective. The performance of the block is not dissimilar to
performing provocation discography at L5-S1 and requires an appreciation of the relevant anatomy
needed to perform this as well as perhaps an L5-S1 transforaminal injection. Unlike the situation noted
above for ganglion impar block, the superior hypogastric plexus is a bilateral, paired structure, and so if
the pain is diffuse and not unilateral, bilateral blocks will need to be performed to successfully modulate
this type of sympathetic or visceral pain.
Relevant Anatomy
The superior hypogastric plexus is a bilateral, paired structure and sits in the retroperitoneum at the lower
third of the fifth lumbar vertebra, at times extending down as low as the upper one-third of the first sacral
level.
rectal perforation; infection; bleeding and hematoma formation; and neural injury.
Contraindications
Fluoroscopic Views
• It is likely that fluoroscopy use is superior to ultrasound in terms of identifying the boundaries of the
vertebral body and the intradiscal space.
• A scout film of the lower lumbar spine and a lateral oblique view is employed to identify the
intradiscal space at L5-S1.
• Prone position
• A 5- or 6-in (12.7- or 15.4-cm) 22- or 25-gauge Whitacre- or Quincke-type subarachnoid needle,
curved along its mid-shaft, and 3 to 7 mL of 5% to 7% phenol in glycerin per side is used for
neurolytic block.

• The patient is placed prone, as for lumbar provocation discography.
• The usual precautions are taken in terms of ASA monitoring, intravenous access, and sterile skin
preparation.
• Ultrasound or fluoroscopy may be used as adjuncts to identifying the relevant anatomy. However, it is
likely that fluoroscopy use is superior to ultrasound in terms of identifying the boundaries of the
vertebral body and the intradiscal space.
• A scout film of the lower lumbar spine is obtained, and a lateral oblique view is then employed to
identify the intradiscal space at L5-S1.
• A 5- or 6-in (12.7- or 15.4-cm) 22- or 25-gauge Whitacre- or Quincke-type subarachnoid needle,
curved along its mid-shaft, is advanced with caution taken to avoid striking the iliac crest or placing
the needle tip into the intervertebral disc itself.
• Switching to a lateral view is then undertaken to ensure needle tip is immediately ventral to the
anterior margin of the L5 vertebral body, at the level of the disc space.
• 3 to 7 mL of water-soluble, iodine-based contrast is next injection.
• If there is no vascular uptake or intradiscal spread, an equivalent volume of 5% to 7% phenol in
glycerin per side is incrementally injected with frequent aspiration performed every 1 to 2 mL.
• The needle is flushed with 1 mL of air and is withdrawn.
• Digital subtraction angiography (DSA) may help identify vascular spread and should be considered, if
available.
• Possible risks that might occur following the procedure is urinary and bowel problems due to neural
damage.9
• In addition, as with most procedures, there is the theoretical risk of pain at the injection site, localized
bleeding, infection, never injury, puncture of internal vessels or organs, distal ischemia (if the iliac
artery is penetrated and the needle dislodges an atherosclerotic plague).10
SACROILIAC JOINT NEUROLYSIS (FIGURES 77-22 TO 77-24)

Figure 77-22. Sacroiliac joint neurolysis using phenol: CT-guided; axial image demonstrating advancing
needle tip. (Used with permission from Kenneth D. Candido, M.D.)
Figure 77-23. Sacroiliac joint neurolysis using phenol: CT-guided; axial image demonstrating advancing
needle tip now situated into center of SIJ. (Used with permission from Kenneth D. Candido, M.D.)
Figure 77-24. Sacroiliac joint neurolysis using phenol: CT-guided; axial image demonstrating contrast
injected in anticipation of phenol injection into center of SIJ. (Used with permission from Kenneth D.
Candido, M.D.)
There are occasions when neurolysis may be considered for peripheral pain issues, such as pain arising
from the SI Joint which has proven to be responsive in the short-term to local anesthetic blocks, but for
which analgesia has not been sustained. Although in contemporary practice, interventionists are
increasingly turning towards radiofrequency procedures for these scenarios, there remains a small, but
finite role for chemical neurolysis of the joint in selected cases.
Relevant Anatomy
As a true synovial joint, the SI joint is a pain-sensitive structure richly invested by unmyelinated free
nerve endings in conjunction with the posterior primary rami of L2-S3. Blockade using dilute phenol may
represent an option in cases where radiofrequency ablative techniques have either failed, or have
provided non-sustained analgesia in an otherwise uncomplicated clinical situation.
rectal perforation, infection, bleeding and hematoma formation, and neural injury.
Contraindications
Fluoroscopic Views
The use of CT-scan imaging is preferred over fluoroscopy or ultrasound to be able to make an
unequivocal determination of proper needle placement.
• Prone position
• A fine-gauge hypodermic needle and 3 to 5 mL of 1% lidocaine with epinephrine, 1:200,000 (5 μg/mL)
is used for raising the skin wheal.
• A 22-gauge, 3.5-in (8.89-cm) Quincke-type subarachnoid needle and 2 to 3 mL of 3% to 5% phenol in
glycerin is used for neurolysis block.
• Additionally, it is probably prudent to use a lower concentration of phenol (3%-5%) than that used for
spinal neurolysis (5%-7%) as the risk of spillover onto the S2-S4 nerve roots (the pudendal nerve)
needs to be accounted for and the appropriate precautions taken.

• The usual monitoring, intravenous access, and sterility precautions are undertaken.
• The skin is infiltrated near the anatomical midline using a fine-gauge hypodermic needle and 3 to 5 mL
of 1% Lidocaine with epinephrine, 1:200,000 (5 μg/mL).
• A 22-gauge, 3.5-in (8.89-cm) Quincke-type subarachnoid needle is advanced through the skin in a
slightly lateral direction until it is submerged 2 to 3 cm.
• Then, the patient is scanned to determine if the angle of entry and advancement is likely to be
successful in placing the needle tip into the SI joint.
• Intermittent advancement and scanning is undertaken until the needle reaches the mid-point of the joint.
• Then, 2 to 3 mL of dense, water-soluble, iodine-based contrast is injected.
• If there is no demonstrated spillover of contrast towards the sacral neural foramina, an equivalent
volume of 3% to 5% phenol in glycerin is incrementally injected.
• The needle is flushed with air and is withdrawn.
the procedure to be assessed for perineal numbness or urinary incontinence.
• Even though there was no definitive literature describing serious complications in patients who
received Sacroiliac Joint Injection,11 as with most procedures, there is the theoretical risk of pain at
the injection site, localized bleeding, infection, never injury, puncture of internal vessels or organs.
SPINAL AND EPIDURAL (INCLUDING TRANSFORAMINAL)

NEUROLYSIS (FIGURES 77-25 TO 77-32 AND TABLE 77-1)
Figure 77-25. Dermatome chart. (Reprinted from K. Candido, R. Stevens Best Practice & Research
Clinical Anaesthesiology, 17:3, 407-428, 2003, with permission from Elsevier.)
Figure 77-26. Sclerotome chart. (Reprinted from K. Candido, R. Stevens Best Practice & Research
Clinical Anaesthesiology, 17:3, 407-428, 2003, with permission from Elsevier.)
Figure 77-27. Spinal nerve root sites of exit from the spinal cord. (Used with permission from Kenneth
D. Candido, MD.)
Figure 77-28. Patient positioning for hypobaric alcohol subarachnoid block. (Reprinted from K.
Candido, R. Stevens Best Practice & Research Clinical Anaesthesiology, 17:3, 407-428, 2003, with
permission from Elsevier.)
Figure 77-29. Hypobaric alcohol subarachnoid block: Bathing the fila radicularia. (Reprinted from K.
Candido, R. Stevens Best Practice & Research Clinical Anaesthesiology, 17:3, 407-428, 2003, with
permission from Elsevier.)
Figure 77-30. Hyperbaric phenol subarachnoid block: patient positioning. (Reprinted from K. Candido,
R. Stevens Best Practice & Research Clinical Anaesthesiology, 17:3, 407-428, 2003, with permission
from Elsevier.)
Figure 77-31. Neurolytic transforaminal phenol injection in a patient with prior decompression
laminectomies and tumor growth prohibiting assuming lateral decubitus position as if for neurolytic
subarachnoid block. Anteroposterior fluoroscopic view with arrow pointing to needle. (Used with
Figure 77-32. Neurolytic transforaminal phenol injection in a patient with prior decompression
laminectomies and tumor growth prohibiting assuming lateral decubitus position as if for neurolytic
subarachnoid block. Lateral fluoroscopic view. (Used with permission from Kenneth D. Candido, M.D.)
TABLE 77-1. Agents Used for Subarachnoid Neurolysis

Unfamiliarity with the details of this technique has been a major obstacle to its use, and since proper
execution of the technique determines its success and safety, the focus of the present discussion is on
technical aspects of subarachnoid neurolysis.
• First, because of the “permanence” of the complications of this technique, subarachnoid neurolysis
should be attempted only after careful review of a dermatome chart to determine precisely which nerve
or nerves are subserving the patient’s pain.
• If the patient’s pain is due to one or more metastases to bone, it may be useful to refer to a sclerotome
chart because the innervation of some parts of the skeleton differs from that of the overlying soft
tissues.
• Because a neurolytic subarachnoid block must be carried out at the level where the dorsal root to be
blocked leaves the spinal cord (to spare motor function), it is essential to determine which interlaminar
foramen affords access to that root.
• Although the cervical nerves exit at a level higher than their respective vertebral bodies, all of the
other nerves exit at a level below their respective vertebral bodies.12
• Finally, a choice must be made before the procedure is undertaken to determine whether a hyperbaric
(phenol in glycerin) or hypobaric (absolute alcohol) technique is more appropriate.
• No controlled clinical trials have compared the outcomes with subarachnoid alcohol and phenol, but in
our experience hypobaric alcohol has been the technique of choice in most cases because most patients
with severe, intractable pain cannot lie on the painful side, a requirement when using hyperbaric
phenol.
• Although at one time clinicians believed that phenol might exert a preferential effect on the small fibers
subserving pain, it has been determined that neither alcohol nor phenol is a selective neurolytic agent,
eliminating this as a rationale for choosing phenol over alcohol.13-15
Relevant Anatomy
• Spinal cord is continuous with the brainstem through the foramen magnum and terminates distally in the
conus medullaris.
• The distal termination varies from L3 in infants to the lower border of L1 in adults.
• Surrounding of spinal cord in the bony vertebral column are three membranes (from within to the
periphery): the pia mater, arachnoid mater, and dura mater.
• The pia mater is a highly vascular membrane that closely invests the spinal cord and brain.
• The arachnoid mater is a delicate and nonvascular membrane. It is closely attached to the dura (the
outermost layer).
• Subarachnoid space contains the CSF, spinal nerves, a trabecular network, and blood vessels that
supply the spinal cord and lateral extensions of the pia mater and dentate ligaments, which provide
lateral support from the spinal cord to the dura mater. Although the spinal cord ends at the lower
border of L1 in adults, the subarachnoid space continues to S2.
• The epidural pain is the area surrounding the dura mater anteriorly, laterally, and more usefully,
posteriorly. The spinal epidural space extends from the foramen magnum to the sacral hiatus.
rectal perforation; infection; bleeding and hematoma formation; and neural injury.
Contraindications
Fluoroscopic Views
likely that fluoroscopy provides a more detailed assessment of the anatomical confines required for
successful blockade.
• Lateral Decubitus (“bad side” up for alcohol injection and “bad side” down for phenol injection)
• A 22-gauge Whitacre- or Quincke-type subarachnoid needle
• 100% alcohol or 3% to 12% phenol
SUBARACHNOID NEUROLYSIS WITH ALCOHOL

(INTRAOPERATIVE TECHNICAL STEPS)
• Because absolute alcohol is extremely hypobaric, when this agent is used, the patient is first placed in
the lateral decubitus position with the painful site uppermost and is then rolled anteriorly
approximately 45 degrees to place the dorsal (sensory) root uppermost.
• After the patient has been positioned properly, a 22-gauge Whitacre- or Quincke-type subarachnoid
needle is inserted and advanced through the interlaminar space at the level of the dorsal root to be
blocked.
• If the procedure is being carried out at a thoracic level, because of the long, caudally sloping spinous
processes, a paravertebral approach is usually easier than a midline approach; whatever the approach,
the needle tip should penetrate the dura in the midline.
• Needles smaller than 22-gauge should not be selected for this technique because the free flow of CSF
is essential, and because postdural puncture headache is extremely rare after subarachnoid alcohol
neurolysis.
• A prognostic block with local anesthetic should already have been carried out to determine whether the
pain can be relieved by the technique, and, equally important, whether the patient can tolerate the
attendant numbness.
• A test dose of local anesthetic should not be given when the needle is in place for a neurolytic block.
The reason is that none of the available local anesthetics can be made as hypobaric as absolute
alcohol.
• A local anesthetic should not be administered before the injection of the alcohol because the pain
produced by the injection of the alcohol is an essential corroborating indicator that enhances the
accuracy and effectiveness of the procedure.
• The physician must tell the patient to expect severe, localized, burning pain, but only for a fraction of a
second after each injection, and to focus attention on whether that burning occurs at, above, or below
the level of the pain.
• The patient also is instructed to report any other sensations, such as tingling, warmth, or numbness.
• Subarachnoid alcohol neurolysis is a precise procedure, and to ensure efficacy and safety, the alcohol
should be injected in 0.1-mL aliquots using a tuberculin syringe.
• The syringe containing the alcohol should not be attached to the needle until the free flow of CSF
indicates that the needle is definitely in the subarachnoid space.
• When the syringe has been attached to the needle, aspiration should not be carried out to verify proper
needle placement because alcohol causes the CSF to form a white coagulum within the syringe.
• When the syringe has been attached to the needle, the subjective experience of each injection and the
importance of the brief burning sensation to the success of the technique are reiterated one more time,
after which sequential injection of 0.1-mL increments of alcohol begins.
• The first one or two increments of alcohol usually do not produce the expected burning pain simply
because this volume is just enough to fill the hub and shaft of the spinal needle. The third or fourth 0.1-
mL increment invariably produces the expected burning, however.
• When a nerve subserving a patient’s pain has been identified and blocked by this process, and a total of
0.7 mL of alcohol has been injected, the process is repeated above or below (or above and below) the
level of the initial full injection to abolish the pain completely.
• No more than three or four nerves should ever be blocked at one session, but as indicated in the
selection criteria, this procedure is best reserved for patients with pain limited to two or three
dermatomes.
• In contrast to subarachnoid injections of local anesthetics for surgical anesthesia, the injection of
alcohol for subarachnoid neurolysis must be made through a separate needle to block each nerve root.
• The reason that alcohol cannot be “floated” to a higher or lower level through a single needle, as is
done when performing a hypobaric spinal for surgery, is that alcohol “fixes” too quickly and would not
float far enough to block the adjacent dermatomes.
• Upon completion of the injection, 0.2 to 0.3 mL of air should be injected to clear the shaft and hub of
alcohol to minimize the possibility that alcohol trickling from the needle as it is withdrawn from dura
to skin will form a fistula.
SUBARACHNOID NEUROLYSIS WITH PHENOL

Intrathecal phenol in glycerin may be used as an alternative to alcohol for subarachnoid neurolysis. The
technique is similar to that described earlier except that the patient must be positioned with the painful
side down because phenol in glycerin is a hyperbaric solution.
• The patient must be tilted posteriorly with the back as close to the edge of the bed as possible.
• For this technique, a 22-gauge (or even better, a 20-gauge) spinal needle should be used because of the
viscosity of the phenol-glycerin mixture.
• In a manner essentially opposite to the technique of subarachnoid alcohol neurolysis, the bevel of the
spinal needle should be directed inferiorly (laterally toward the table).
• Because of the viscosity of phenol in glycerin, it takes significant pressure applied to the plunger of the
syringe to force the phenol into the subarachnoid space, so the injection must be done slowly and
carefully to prevent the escape of phenol from the syringe and onto the skin of the patient or the
practitioner.
• Warming the phenol lessens its viscosity and makes it easier to inject.
• Because phenol has local anesthetic properties, its injection into the subarachnoid space is not
accompanied by the burning pain produced by alcohol, although the patient may feel warmth, tingling,
or even mild dysesthesia in the distribution of the nerve being injected.
• As with alcohol, after the subarachnoid injection of phenol in glycerin, 0.1 to 0.3 mL of air is injected
to flush the lytic solution from each needle before it is removed.
EPIDURAL AND TRANSFORAMINAL NEUROLYSIS

• Occasionally, patients cannot lie on either side, due to abject misery from their underlying disease
states.
• In such cases, epidural or transforaminal injections might prove useful.
• Under these circumstances, 5% phenol in glycerin has been demonstrated to be a superior agent
compared to alcohol use, and small doses titrated to effect may provide significant analgesia in cases
of intractable pain which has been demonstrated to be responsive to local anesthetic diagnostic
blocks.16
From the point of view of complications, neurolytic subarachnoid blocks may be safest when undertaken
in the midthoracic region because this region is relatively distant from the fibers that subserve limb,
bowel, and bladder function, so any motor loss would be of little consequence. Conversely, in the
lumbosacral region, owing to the proximity of sensory and motor fibers to each other (because of the
decreasing size of the conus medullaris, the dorsal and ventral roots are very close together) and to the
proximity of both to the autonomic fibers subserving bowel and bladder function, lumbar subarachnoid
neurolysis usually is reserved strictly for select individuals in whom the risk-to-benefit ratio has been
clearly delineated. For patients who already have compromised sphincter function, lumbosacral
subarachnoid phenol neurolysis has been advocated for rectal and pelvic malignancies because of the
tendency of phenol to spare motor function.
Complications of central neuraxial blocks include the following:
• Paralysis/paraplegia
• Bladder dysfunction
• Bowel dysfunction
• Sexual dysfunction
• Anesthesia dolorosa

• Neurolysis is a technique best reserved for individuals in severe pain who are not perceived to be
candidates for neuromodulation, surgery, or pharmacological pain management without prohibitive
side effects.
• Central neuraxial neurolysis is most commonly used, but techniques for blocking somatic, sympathetic,
and visceral pain processes have been reported and should be part of the armamentarium of advanced
interventional pain physicians.
• Because of the physical separation of the sensory and motor nerve roots in the spinal canal, intrathecal
chemical dorsal rhizotomy is the only neurolytic procedure that allows sensory block without
concomitant motor block. For this reason, subarachnoid neurolysis is a unique, effective modality for
the management of cancer pain in certain patients.
• If the patients are carefully selected, and the technique is carefully carried out, pain relief can be
provided in most cases without an excessive rate of complications.
References
1. Dogliotti AM. Traitement des syndromes doloreaux de la peripherie par l’alcoholisation
subarachnoidienne des racines posterieures a leur émergence de la moelle epineri. Presse Med.
1931;39:1249.
2. Suvansa S. Treatment of tetanus by intrathecal injection of carbolic acid. Lancet. 1931;1:1075.
3. Maher RM. Relief of pain in incurable cancer. Lancet. 1955;1:18.
4. Maher RM. Neurone selection in relief of pain: Further experiences with intrathecal injections.
Lancet. 1957;1:16.
5. Katz J. Current role of neurolytic agents. Adv Neurol. 1974;4:471.
6. Hollis PH, Malis LI, Zappulla RA. Neurological deterioration after lumbar puncture below complete
spinal subarachnoid block. J Neurosurg. 1986;64:253.
7. Day M. Neurolysis of the trigeminal and sphenopalatine ganglions. Pain Pract. 2001;1:171-182.
8. Middleton WJ, Chan VWS. Lumbar sympathetic block: a review of complications. Tech Reg Anesth
Pain Manag. 1998;2:137-146.
9. Chan WS, Peh WC, Ng KF, Tsui SL, Yang JC. Computed tomography scan-guided neurolytic superior
hypogastric block complicated by somatic nerve damage in a severely kyphoscoliotic patient.
10. De Leon-Casasola O, Molloy RE, Lema M. Neurolytic visceral sympathetic blocks. In: Benzon HT,
Raja S, Molloy RE, et al, eds. Essentials of Pain Medicine and Regional Anesthesia. 2nd ed. New
York, NY: Elsevier-Churchill Livingston; 2005:542-549.
11. Cheng J, Abdi S. Complications of Joint, Tendon, and Muscle Injections. Tech Reg Anesth Pain
Manag. 2007;11:141-147.
12. Haymaker W, Woodhall B. Peripheral nerve injuries. Philadelphia, PA: WB Saunders; 1945.
13. Nathan PW, Sears TA. Effects of phenol on nervous tissue. J Physiol. 1960;150:565.
14. Nathan PW, Sears TA, Smith MC. Effects of phenol solutions on the nerve roots of the cat: An
electrophysiological and histological study. J Neurol Sci. 1965;2:7.
15. Patt R, Jain S. Management of a patient with osteoradionecrosis of the mandible with nerve blocks. J
Pain Symptom Manage. 1990;5:59.
16. Candido K, Philip C, Ghaly R, Knezevic N. Transforaminal 5% phenol neurolysis for the treatment of
intractable cancer pain. Anes Analg. 2010;110:216-219.
CHAPTER 78
Chemical Neurolysis
Michael M. Bottros and Michael A. Erdek
INDICATIONS
Neurolytic techniques have long been used in the treatment of pain. The underlying principle for
neurolytic blocks is prolonged relief of intractable pain, most often in patients with malignancies. Pain
associated with cancer may be visceral, somatic, and/or neuropathic in origin. Many cancer patients have
a combination of these pain types at the time of their diagnosis. Pain is often reported when visceral
structures are compressed, invaded, or distended. Visceral pain is often described as vague, dull, deep,
constricting, crampy, or colicky in nature. Empirical data suggests that visceral sympathetically-mediated
pain responds more favorably to neurolytic therapy than neuropathic pain.1
Neurolysis, or destruction of neural tissue, was once performed surgically under direct visualization.
As advancements in imaging and ablative techniques continued to progress, these procedures can now be
done percutaneously2 chemically, thermally with radiofrequency, or by freezing via cryoneurolysis.
The indications for chemical neurolysis include3:
• Severe, intractable pain that persists after less invasive treatments
• Intolerable side effects of analgesic therapy
• Intrathecal catheter, with or without a pump, is not a viable option
• Advanced or terminal malignancy
• Pain well localized:
Unilateral pain, localized to the trunk
Involves only a few dermatomes or one peripheral nerve
• Primary somatic pain mechanism
• Absence of intraspinal tumor spread
• Pain relieved with prognostic local anesthetic block
• No undesirable effects after local anesthetic block
• Realistic expectations by patient and family
• Informed consent clearly explains potential complications
Risks and benefits should always be weighed prior to undergoing any intervention. Extensive
communication with the patient is necessary before proceeding.
Some concerns include:
• Potential risk for infection in immunocompromised patients
• Metastatic cancer spread to the region
• Thrombocytopenia secondary to chemotherapy
• Difficulty in positioning due to tumor and pain location
Absolute contraindications for injection include:
• Infection, systemic or localized to injection site
• Coagulopathy
• Patient refusal
Relative contraindications include:
• Autonomic nervous system no longer the main transmission of the pain source for visceral pain (eg,
carcinoma of the pancreas that has begun to invade the body wall)
• Distorted or complicated anatomy (eg, large aortic aneurysm)
RELEVANT ANATOMY
Visceral neurolytic blocks are particularly effective for cancer-related pain. The paravertebral
sympathetic chain consists of sympathetic neural tissue from several sympathetic plexuses that run along
the paravertebral region of the body (Figure 78-1). There are several sites for neurolytic blockade of the
sympathetic nervous system for the treatment of cancer pain (Table 78-1).1 These axial sympathetic chains
include the cervical, thoracic, and lumbar sympathetic ganglia.
Figure 78-1. Sympathetic nervous system sites for neurolysis.
TABLE 78-1. Sympathetic Nervous System with Corresponding Anatomic Structures

The sympathetic system receives afferent nociceptive impulses from:
• Visceral fibers of the head and neck and upper extremities (stellate ganglion), cardiothoracic viscera
(thoracic sympathetic ganglia)
• The abdominal viscera (celiac plexus) (Figure 78-2)
Figure 78-2. CT Image of antecrural celiac plexus block. The arrows indicate the antecrural
radiocontrast dye spread of the celiac plexus neurolytic block. A, aorta.
• The urogenital system and lower extremities (lumbar sympathetic ganglia)

• The pelvic viscera (superior hypogastric plexus and ganglion impar)4
With ideal treatment, visceral neurolytic blocks produce satisfying analgesia without motor weakness
or somatic sensory loss.
• Anticoagulation.5,6 This is less of a concern than for an epidural injection but a concern nonetheless as
there is inherent disruption of tissue from the introduction of a needle.
• Patient must be able to lie in the intended position for the length of the procedure.
• Intravenous access for IV fluid and medications for sedation or hypotension secondary to sympathetic
block or if the patient experiences vasovagal reaction.
• Evaluation for contrast allergy. Utilization of contrast allows for precise needle placement.
Selection of Medications
The neurolytic agents [E1]most commonly used are ethyl alcohol (50%-100%) (Figure 78-3) and phenol
(5%-10%) (Figure 78-4) (Table 78-2). Alcohol was first used for neurolysis in 1902 in order to treat
trigeminal neuralgia. Phenol was introduced in the 1950s and gained widespread popularity, in part
because of its analgesic as well as neurolytic properties. These agents disrupt transmission of pain
signals by causing Wallerian degeneration distal to the lesion.7 They usually produce a block that lasts 3
to 6 months.
Figure 78-3. Ethyl alcohol. (Used with permission from Michael M. Bottros, MD.)
Figure 78-4. Phenol. (Used with permission from Michael M. Bottros, MD.)
TABLE 78-2. Common Chemical Neurolytic Agents

Alcohol:
• Damages nerves by denaturing proteins and fatty substance extraction and may be associated with
neuritis.
• The injection is painful.
• It is hypobaric in comparison to CSF.
• Denser block with longer duration.
Phenol:
• Diffuses into the axon and denatures the proteins causing Wallerian denaturation
• Has some local anesthetic properties
• Unlike alcohol, it is not painful on injection
• It is less water soluble and hyperbaric in comparison to cerebrospinal fluid (CSF).
• The intensity and [E2]duration of block with phenol are less than with alcohol and phenol carries a
lower risk of neuritis.7
The patient should be followed up by telephone the next day for the potential complications and
immediate pain relief secondary to local anesthetic. The chemical neurolysis may not be apparent for up
to 1 week. The patient should be advised to call the physician for any procedure-related complications
and/or any unexpected neurologic deficit. Patient should be monitored closely for following:
• Weakness
• Urinary or bowel incontinence
• Fever
• Bleeding
• Numbness

• Skin and other nontarget tissue necrosis and sloughing. Secondary to damage of the vascular supply
to the skin, causing ischemia and chronic trauma to denervated tissue. Necrosis of muscles, blood
vessels, and other soft tissues has also been reported.
• Neuritis. The reported incidence of neuritis is up to 10%.8 It is caused by partial destruction of
somatic nerve and subsequent regeneration. Neuritis occurs only if the nerve cell body is not
destroyed. It is less likely to occur with a subarachnoid or ganglion neurolytic block. It is clinically
manifested as hyperesthesia and dysesthesia that may be worse than the original pain problem. It is one
of the limiting factors in the use of chemical neurolysis.
• Anesthesia dolorosa. This is a poorly understood manifestation whereby the patient complains of
distressing numbness caused by an imbalance in afferent input. It is caused by long-term loss of afferent
input and resultant central nervous system changes. A local anesthetic block done a few hours prior to
the performance of the neurolytic block seems to prevent the development of this complication.8
Management of this problem is pharmacotherapy with the use of tricyclic antidepressants and
anticonvulsants.
• Prolonged motor paralysis. This can be a major complication and is greatly feared by physicians,
patients, and family. It occurs infrequently and may be temporary.
• Perineal and sexual dysfunction. This is another complication that can occur temporarily, specifically
with ganglion impar blocks. About 1.4% and 0.2% of patients will have bowel or bladder dysfunction
at 1 week and 1 month, respectively.9
• Systemic complications. These include hypotension secondary to sympathetic block and systemic toxic
reactions, heart rate and rhythm disturbances, blood pressure changes, and CNS excitation and
depression.
• The goal of performing a neurolytic block of the sympathetic axis is maximizing analgesia and possibly
reducing the dosage of these opioids to alleviate unwanted side effects.
• Opioids may have to be carefully titrated as there is the potential for respiratory depression and
narcotic withdrawal syndrome after sudden cessation of pain.
• Needle position should always confirmed with radiologic imaging prior to the injection of a neurolytic
agent, as the needle’s tip may be intravascular, in the peritoneal cavity, or in a viscus.
• A complete and careful neurologic examination, especially the extent and duration of any sensory or
motor deficits, must be documented both prior to and after the procedure. Should any complications
occur, these deficits may resolve over time. Reassure the patient and provide adequate analgesia in
such cases.
References
1. Christo PJ, Mazloomdoost D. Interventional Treatments for Cancer Pain. Ann N Y Acad Sci.
2008;1138:299-328.
2. Shah RV. Sternal kyphoplasty for metastatic lung cancer: image guided palliative care. Pain Med. 2012
Feb;13(2):198-203.
3. Malloy RE, Benzon HT. Neurolytic blocking agents: uses and complications. In: Benzon HT, Rathmell
JP, Wu CL, et al, eds. Raj’s Practical Management of Pain. 4th ed. Philadelphia, PA: Mosby Elsevier;
2008:839-850.
4. Krames E. Interventional pain management appropriate when less invasive therapies fail to provide
adequate analgesia. Med Clin N Am. 1999;83(3):787-808.
5. Raj PP, Shah RV, Kaye AD, Denaro S, Hoover JM. Bleeding risk in interventional pain practice:
6. Shah RV, Kaye AD. Bleeding risk and interventional pain management. Curr Opin Anaesthesiol. 2008
Aug;21(4):433-438.
7. Koyyalagunta D, Burton AW. The role of chemical neurolysis in cancer pain. Curr Pain Headache
Rep. 2010;14:261-267.
8. Jackson TP, Gaeta R. Neurolytic blocks revisited. Curr Pain Headache Rep. 2008;12(1):7-13.
9. Gehdoo RP. Cancer pain management. Indian J Anaesth. 2006;50(5):375-390.
CHAPTER 79
Cryoneuroablation
David Irwin and Andrea Trescot
INTRODUCTION
Cryoneuroablation is an interventional technique aimed at temporary destruction of the nerve providing
relief of the pain. The origin of this technique lies in the ancient time but modern cryoanalgesia traces its
roots to Cooper et al.1 In 1962, they developed a device that used liquid nitrogen circulating through a
hollow tube, insulated except at the tip, to achieve a tip temperature of –196,°C. Amoils,2 an ophthalmic
surgeon, developed a simpler handheld device in 1967, which used high-pressure carbon dioxide or
nitrous oxide and could achieve temperatures of –70°C. Lloyd et al3 coined the term “cryoanalgesia” for
its use in pain management. They proposed that this technique was superior to other methods of peripheral
nerve destruction, for example, alcohol, phenol, or surgical lesions, because it is not followed by neuritis
or neuralgia. The cryoneuroablation unit:
• The cryoneuroablation relies on the ability of specially constructed probe to freeze tissue around it.
• The cryoprobe consists of a hollow tube with a smaller inner tube.
• Pressurized gas (usually N2O or CO2) at 600 to 800 psi travels down the inner tube and is released
into the larger outer tube (which is at a low pressure of 10-15 psi) through a very fine aperture (0.002
mm), which allows the gas to rapidly expand into the distal tip (Figure 79-1).
Figure 79-1. Cryoneuroablation probe physics. (Reproduced with permission from Epimed, Farmers
Branch, TX.)
• The heat is extracted from the tip of the probe, resulting in temperatures as cold as –89°C at the tip
itself (Joule-Thompson effect), forming an ice ball with temperatures in the range of –70°C (Figure 79-
2).
Figure 79-2. Cryoneuroablation ice ball. (Reproduced with permission from Epimed, Farmers Branch,
TX.)
• The gas is then vented back to the machine itself through the outer tube and is scavenged through a
ventilated outlet.
• The “closed system” construction of the probe and machine ensures that no gas escapes into the
patient’s tissues.
• Precise gas flows are necessary for safe and effective cryoneuroablation; inadequate gas flows will
not produce an ice ball, while excessive flows can cause freezing proximally up the probe, which may
increase the risk of skin burns.
• The probe includes a built-in nerve stimulator with sensory and motor capabilities, which allows
precise localization of the target nerve (Figure 79-3).
Figure 79-3. Cryoneuroablation machine. (Used with permission from Andrea Trescot, MD.)
The mechanism of cryoneurolysis:

• Thermal injury interrupts the neuronal pathway and provides pain relief. More specifically, the
application of cold to tissues creates a conduction block, similar to the effect of local anesthetics.
• At 10°C, larger myelinated fibers stop conducting, but all nerve fibers stop conducting at –20°C.
• The extent and duration of the effect is therefore a function of the degree of cold obtained and the length
of time of exposure.
• Long-term pain relief from nerve freezing occurs because ice crystals create vascular damage to the
vasa nervorum, which produces severe endoneural edema. This creates a Wallerian degeneration but
leaves the myelin sheath and endoneurium intact (Figure 79-4).
Figure 79-4. Histology after cryoneuroablation. (Reproduced with permission from Myoscience,
Redwood City, CA.)
• The Schwann cell basal lamina is spared and ultimately provides the structure for regeneration (Figure
79-5)
Figure 79-5. Regeneration after cryoneuroablation. (Reproduced with permission from Myoscience,
Redwood City, CA.)
• Although demyelination and degeneration of the axon occurs, Sir Sydney Sunderland4 in 1968
demonstrated that when the endoneurium remains intact, neuroma formation does not occur, and the
nerve is typically able to regenerate at a rate of 1 to 1.5 mm/wk.5
• The intensity and duration of analgesia is dependent on the degree of nerve damage from the ice ball.
• Autoimmune phenomena are also implicated in the long-term effects of cryoneuroablation. There is a
release of sequestered proteins that may trigger an autoimmune response to the targeted lesioned
tissues, which might explain the prolonged effect.
The extent of the freezing (and subsequent nerve damage) is a function of:
• The proximity of the probe to the nerve
• The size of the cryoprobe
• The size of the ice ball formed
• The completeness of the freezing (rate and duration)
• The temperature of the tissues in proximity to the probe, which is affected by local heat sinks (such as
CSF/blood flow)
The nerve is expected to regrow and there is no evidence of permanent neurologic damage as a result of
multiple cryoneuroablation procedures. Consequently, it is critical that the period of pain relief after the
cryoneuroablation be used to regenerate as normal an environment as possible so that as the nerve
regenerates the original pathology (entrapment) does not recur. Cryoneuroablation may address the issue
of “wind up” (the continued stimulation of a nerve causing increased sympathetic outflow and thus more
stimulation), resulting in a period of reduced sympathetic stimulation that may allow aggressive
rehabilitation. When working around motor nerves, it makes sense to test for motor function during the
first freeze cycle. For instance, when treating the superior gluteal nerve, asking the patient to flex the knee
during the first minute of freezing would identify possible unintended motor paresis before full cooling
has occurred.
INDICATIONS
Cryoneuroablation is indicated for the treatment of nerve pain (neuralgia). The application of cold to
tissue creates a conduction block, similar to the effect of local anesthetics, however much longer lasting.
Success of cryoanalgesia is directly related to patient selection, accurate probe placement, and the
postprocedure rehabilitation process.
CONTRAINDICATIONS
Absolute contraindications to cryoneuroablation include lack of consent from patient, infection at the
insertion site, any allergy or sensitivity to the anesthetic agent, and distortion of anatomical landmarks.
GENERALIZED REMARKS
The cryoneurolysis technique is solely dependent on the appropriate and reliable diagnosis. It is critical
that a precise diagnosis be made prior to an attempt to freeze any nerve. These diagnostic steps include:
• Identify the clinical pattern of pain; perform a meticulous diagnostic block.
• Use small volumes of local anesthetic no greater than the volume of the freeze that would be created by
the ice ball (0.5-1 mL).
• Utilize a nerve stimulator as well as fluoroscopic guidance, ultrasound localization, direct exposure, or
absolute anatomic location.
Success of cryoanalgesia is directly related to:
• Patient selection
• Accurate diagnosis
• Accurate probe placement
• The postprocedure rehabilitation process
The recommended technique(s) encompasses the following: meticulous localization of the nerve, the
use of the largest probe appropriate, and the use of adequate freeze and defrost cycles. It is also critical
that the cryoprobe be withdrawn only after the ice ball has thawed since trying to withdraw the probe
with the ice ball present could tear the attached tissues and avulse a nerve segment.
COMMON TECHNICAL STEPS

• The skin is anesthetized using very small amounts of local anesthetic with special care not to
anesthetize the nerve.
• Next, the subcutaneous tissues around the nerve are infiltrated with 1 to 2 mL of 0.9% preservative-
free normal saline with 1:200,000 epinephrine (5 μg epinephrine per mL normal saline).
• This provides constriction of the surrounding blood vessels and will decrease bruising from the cryo
probe.
• The introducer (usually an IV catheter) is gently advanced into the tissues to the target area, and tiny
doses of local anesthetic added if needed to provide analgesia (taking care to avoid anesthetizing the
target nerve).
• The probe is then advanced through the introducer until it lies over the nerve.
• The sensory function of the probe is used to place the probe as close as possible to the nerve, using a
technique of “successive approximations”; the sensory stimulator is turned up to 1 mV and slowly
moved until the patient feels the paresthesia (a tingle or burning sensation) and then immediately turned
off.
• After a few seconds, the stimulator is turned back up to 1 mV; if the patient does not feel stimulation,
then it was a false paresthesia.
• If the patient feels the paresthesia before 1 mV is reached, the stimulator is turned up only to 0.5 mV
and the probe moved until the patient feels the paresthesia and then turned off, and the process repeated
until the stimulation is felt at 0.3 mV, each time getting closer and closer to the nerve.
• The motor function is then used to confirm the lack of motor stimulation at 2 mV.
• Two or three, 2-minute freeze cycles are usually sufficient for clinical relief. Special care must be
taken to make certain that a superficial “frostbite” burn of the dermis and epidermis is not occurring.
COMMON SIDE EFFECTS AND COMPLICATIONS

• Cryoneurolysis is a procedure with certain risks and potential problems.
• Every patient should be warned about possibility of bleeding with subsequent hematoma formation.
• Allergic or systemic reactions to an anesthetic agent do happen as well as unintentional injection into
artery or vein.
• Infection is always possible but it can be minimized by application of judicial aseptic techniques.
• Also, the nerve can be damaged, resulting in neuralgia and exacerbation of the pain.
• The other risks for cryoneurolysis include the risk of depigmentation, hyperpigmentation, or tissue
necrosis at the cryolesion site. This is sometimes compounded by alopecia.
• A separate complication is inadequate pain relief, most likely due to inadequate localization of the
nerve.
Additionally, each site has potential for specific complications that will be described below.
SUPRAORBITAL NERVE
Indications
• Commonly confused with migraines and frontal sinusitis, the pain of supraorbital neuralgia most
typically manifests itself as a frontal headache, often associated with blurred vision, nausea, and
photophobia.
• Vulnerable to blunt trauma, this nerve can be injured by deceleration against an automobile windshield
or through blows to the face.
• This neuralgia tends to worsen with time following the trauma as the injured tissue slowly develops a
cicatrix, which eventually envelops the nerve.
• Spasm of the orbicularis oculi (such as with frowning or squinting) exacerbates the entrapment. This
etiology is supported by the efficacy of botulinum toxin in the forehead region in the treatment of
“migraines.”
• However, the botulinum relief is only expected to last 2 to 3 months, where the cryoneuroablation
relief can be for up to a year or longer.
• Less commonly, the nerve can be injured as the result of acute herpetic infection (eg, shingles), Paget
disease, and neoplasm.
• Patients will often experience an increase in headache intensity and frequency with menstruation
(associated with fluid retention), salt intake, stress, and bright light or vision changes (which causes
squinting).
Relevant Anatomy
The supraorbital nerve is the termination of the first division of the trigeminal nerve. Irritation of the
nerve occurs primarily at the supraorbital notch (Figure 79-6).
Figure 79-6. Supraorbital anatomy. A, supraorbital, nerve B, supratrochlear nerve. (Used with
permission from Andrea Trescot, MD.)
• A small ligament completes the inferior border of a foramen through which the nerve passes prior to
passage through the orbicularis oculi.
• Relevant anatomy includes the supraorbital notch and supratrochlear groove.
• The supratrochlear nerve is located at the medial aspect of the orbit. Considering the cosmetic aspect,
a small probe should be used and the nerve should be approached from the inferior aspect.
Adequate preparation of the patient in respect of complications should be done, including the risk of
alopecia and depigmentation or hyperpigmentation.
Fluoroscopic Views
This procedure does not usually require fluoroscopy.
The patient can be in place sitting or in the supine position. The supine position is favorable in case the
patient has a vagal episode.

• Cryoneuroablation of the supraorbital nerve can be accomplished via an open operative technique
involving dissection under local anesthesia. The nerve can then be frozen under direct vision.
• Alternatively, the closed technique involves using the 1.4-mm probe, passed via a 14-gauge
intravenous catheter introducer.
• The approach is usually inferior to the supraorbital notch.
• The probe trajectory ideally runs parallel to the nerve.
• Special care must be taken to make certain that a superficial burn of the dermis and epidermis is not
occurring.
• Close observation of the skin during the entire freeze cycle is imperative (Figure 79-7).
Figure 79-7. Cryoneuroablation supraorbital nerve. (Used with permission from Andrea Trescot, MD.)
Changes in skin color can be expected, but generally resolve in a matter of days to months; however, the
patient must be counseled appropriately.
Monitoring for Potential Complications
Swelling and bruising of the eyelid or entire eye can occur.

Entry of the catheter and probe should be below the eyebrow line. This avoids damage to the brow
follicles, with subsequent alopecia.
INFRAORBITAL BLOCK
Indications
• The infraorbital nerve is the termination of the second division of the trigeminal nerve. Irritation
peripheral neuropathy occurs principally at the infraorbital foramen.
• Also vulnerable to blunt trauma, this nerve is often injured by pugilistic blows. This neuralgia tends to
worsen with time following the trauma as the injured tissues slowly develop cicatrix that entraps the
nerve.
• This nerve can also be injured as the result of fracture of the zygoma, with entrapment of the nerve from
the formation of bony callus.
• Commonly confused with maxillary sinusitis, the pain of infraorbital neuralgia typically presents as
maxillary pain worsened by smiling and laughter (which puts tension on the zygomaticus musculatures).
• Because of referred pain to the teeth, patients often undergo futile dental procedures prior to their
presentation.
• As with the aforementioned entrapments, these patients will often experience an increase in headache
intensity and frequency with menstruation, salt intake, stress, and bright light.
Relevant Anatomy
The infraorbital nerve is the termination of the second division of the trigeminal nerve. As second
division of the trigeminal nerve enters the infraorbital foramen, it is commonly called infraorbital nerve.
This nerve innervates the lower eyelid, upper lip, and part of the nasal vestibule and exits the infraorbital
foramen of the maxilla (Figure 79-8).
Figure 79-8. Infraorbital anatomy. (Used with permission from Andrea Trescot, MD.)
Fluoroscopic Views
The patient can be in place sitting or in the supine position. The supine position is favorable in case the
patient has vagal episode.
• Cryoneuroablation of the infraorbital nerve can be accomplished via an open operative technique
involving dissection under local anesthesia, and the nerve can be thereby frozen under direct
visualization.
• The closed technique involves using the 1.4-mm probe, passed via a 14-gauge introducer, as close as
possible to the foremen.
• This can be accomplished by a direct percutaneous approach but this area is also cosmetically
important, so to minimize cosmetic damage, the intraoral approach can be employed
• With the intraoral approach, a 12-gauge introducer and 2.0-mm probe are inserted intraorally through
the superior buccal-labial fold (Figure 79-9).
Figure 79-9. Cryoneuroablation infraorbital nerve, intraoral approach. (Used with permission from
• If performed percutaneously, close observation of the skin during the entire freeze cycle is imperative.
Changes in skin color can be expected, but generally resolve in a matter of days to months; however, the
patient must be counseled appropriately.
Swelling of the cheek up to the inferior eyelid can occur. Bleeding, infection, or hematoma formation
should also be discussed as a potential risk.
OCCIPITAL BLOCK
Indications
Occipital neuralgia presents as unilateral or bilateral occipital nerve pain and headache, radiating to
retro-orbital area. It is related to entrapment by the trapezius, splenius, and levator scapulae muscles and
flexion/extension injuries or may be related to pathology of cervical facets.
Relevant Anatomy
The greater occipital nerve originates from dorsal ramus of C2 and C3, travels cephalad, and pierces
nuchal fascia at base of skull (Figure 79-10). The fibers of C2 ganglion relay at the level of the medulla
with the caudate portion of the trigeminal ganglion, and therefore refer sensations to the face and posterior
eye area. It also picks up fibers from the lesser occipital nerve (from cervical plexus) and third occipital
nerve (posterior ramus C3).
Figure 79-10. Occipital anatomy. (Reproduced with permission from Epimed, Farmers Branch, TX.)
Fluoroscopic Views
The patient is placed in the prone position with support under the chest on the OR table and the patient’s
head flexed in a comfortable position.

• Cryoneuroablation of the greater occipital nerve can be accomplished via an open operative technique
involving dissection under local anesthesia, and the nerve can be thereby frozen under direct
visualization.
• The closed technique involves using a 12-gauge introducer and 2.0-mm probe, which is inserted
approximately 3 cm below the occipital protuberance and 1.5 cm lateral to the midline (Figure 79-11).
Figure 79-11. Cryoneuroablation occipital nerve (fluoroscopy). (Used with permission from Andrea
Trescot, MD.)
• The probe is then advanced until it lies over the greater occipital nerve on the periosteum, which is
identified by sensory stimulation.
• The probe can also be introduced under ultrasound guidance (Figure 79-12).
Figure 79-12. Cryoneuroablation occipital nerve (ultrasound). (Used with permission from Andrea
Trescot, MD.)
Although alopecia is possible, because of the position at the back of the head, it is usually not
cosmetically a problem.
Complications may include dural puncture, spinal cord trauma, subdural injection, neural trauma,
injection into the intervertebral foramen and intervertebral arteries (all related to lack of knowledge of
anatomy); intravascular injection into veins, vertebral arteries or occipital artery; infectious
complications including epidural abscess and bacterial meningitis; and side effects related to the
administration of local anesthetics and other drugs.
INTERCOSTAL BLOCK
Indications
• Of all the postoperative indications for cryoneurolysis, lesioning of the intercostal nerve
intraoperatively has been the most extensively studied.
• The nerve is very easily identified at thoracotomy, and intraoperative cryoneuroablation can provide
significant and long lasting postoperative analgesia.
• It is somewhat more difficult to address when there is a post-thoracotomy neuroma, persistent pain
after rib fractures, or thoracic postherpetic neuralgia, but a percutaneous technique can provide
excellent analgesia.
• The technique is most effective in relieving incisional pain and provides relatively little relief of
visceral pleuritic pain or the pain of ligamentous or muscle pains.
• It provides no relief for chest tube pain.
• The multiple pain generators involved in post-thoracotomy pain make cryoneuroablation difficult to
use as a sole treatment.
Despite these limitations, studies have shown that patients have less postoperative pain and less opioid
requirement, both in the immediate postoperative period and in the weeks following the procedure. It is
the experience with post-thoracotomy pain and cryoneuroablation that led to its use in other chronic chest
wall pains. The complications of postoperative neuroma, costochondritis, postherpetic neuralgia, and rib
fractures have all been treated with cryoneuroablation.
Relevant anatomy
The intercostal nerve lies posterior and cephalad to the inferior border of the rib (Figure 79-13).
Figure 79-13. Intercostal anatomy. (Used with permission from Andrea Trescot, MD.)
Fluoroscopic Views
The fluoroscopic image needs to identify the ribs clearly (Figure 79-14).
Figure 79-14. Cryoneuroablation intercostal nerve. (Used with permission from Andrea Trescot, MD.)

Positioning is dependent on the site of the lesion and comfort of the patient. Posterior pathology is treated
from a prone position, while anterior pathology is treated in the supine position. Lateral rib pain may be
best treated in a lateral position.

• In the open technique, after the thoracotomy is complete, the cryoprobe is placed directly on the nerve
at the posterior rib angle. The nerve is easily visualized beneath the parietal pleura.
• Because each rib has an innervation contribution from the rib below and the rib above, it is advisable
to lesion the intercostal nerves above and below the incision line as well.
• Because the nerves are exposed, 1 or 2 short freeze cycles should be adequate.
• In the percutaneous approach, these authors recommend approaching the rib edge tangentially from
medial to lateral, then pushing the tip of the probe up under the edge of the rib (Figure 79-14).
• It dramatically reduces the risk of pneumothorax, and it increases the length of contact of the probe on
the nerve, increasing the effectiveness of the cryolesion.
• The 12-gauge introducer and 2.0-mm probe are favored to provide the maximal area of neurolysis.
Risk of pneumothorax and bleeding is decreased with the tangential approach, with no cases of
pneumothorax or bleeding after more than 50 intercostal cryoneuroablation procedures (AMT, personal
correspondence).
• Since these are primarily sensory nerves, no motor weakness would be expected from
cryoneuroablation.
• Meticulous use of the motor stimulation capability should identify if the probe is too close to an
unintended motor nerve.
• A postprocedure chest x-ray is critical for the evaluation for pneumothorax. Cryoanalgesia of the third
and fourth intercostals can cause ipsilateral nipple anesthesia. For that reason, it has been suggested
not to freeze nerves above the fifth intercostal nerve.
• Also, there has been one case report of a neuroma formation after the use of cryoneuroablation for
post-thoracotomy pain and several patients who have noted sensory deficits for up to 6 months.
• Loss of tone from the external and internal oblique muscles (innervated by the lower intercostal
nerves) can cause a subtle but definite subcostal bulge that resolves with the return of sensation (Figure
79-15). Patients should be made aware of that preoperatively.
Figure 79-15. Abdominal wall bulge. (Used with permission from Andrea Trescot, MD.)

• With the percutaneous approach, the technique has to take into consideration the underlying lung and the
intercostal artery, which acts as a heat sink.
• Physicians are traditionally taught to perform intercostal nerve blocks by advancing needle
perpendicular to the inferior edge of rib and then “walking it off the edge of the bone,” dropping to just
before the parietal pleura.
• However, the nerve is actually up under the curve of the rib. In addition, the intercostal artery acts as a
huge “heat sink,” limiting the size of the ice ball and therefore the effectiveness of the cryolesion.
• By introducing the probe perpendicular to the nerve, the area of freezing is limited, which also limits
the effectiveness of the cryolesion.
• In addition, the temptation is to use a smaller probe because of the concern regarding advancing a 12-
gauge needle into the pleural space, causing a pneumothorax.
• The technique we recommend is somewhat different. We recommend approaching the rib edge
tangentially from medial to lateral, then pushing the tip of the probe up under the edge of the rib.
• This accomplishes several things. It dramatically reduces the risk of pneumothorax, and it increases the
length of contact of the probe on the nerve, increasing the effectiveness of the cryolesion.
• It is important to use the largest probe possible to overcome the arterial heat sink.
Similar treatments are available for nerves of the abdominal wall, pelvis, low back, and buttocks, as
well as the upper and lower extremities; cryoneuroablation treats pain problems from the head down to
the toes.
CONCLUSION
In conclusion, cryoneuroablation is an effective interventional pain management technique, providing
significant analgesia in an outpatient or office setting. The technique can be utilized literally from the head
down to the foot, and is limited only by the clinician’s ability to make the diagnosis of nerve pathology,
and only a few of the more common procedures have been described in this chapter. The effect is
routinely reversible, relatively painless, and is not associated with neuroma formation. An accurate
diagnosis with specific diagnostic injections of small volumes of local anesthetic and meticulous
localization of the nerve is critical for a successful outcome. Remember, “You cannot treat what you
cannot diagnose.”
Suggested Reading
Trescot AM. Cryoneurolysis. In: Manchikanti L, Singh V, eds. Interventional Techniques in Chronic
Non-spinal Pain. Paducah, KY: American Society of Interventional Pain Physicians Publishing; 2009:
Chapter 8.
Trescot AM. Cryoanalgesia. In: Boswell M, ed. Weiner’s Pain Management: A Practical Guide for
Clinicians. 7th ed. Boca Raton, FL: CRC Press, Taylor and Francis Group; 2006:1057-1077: chap
72.
Trescot AM. Cryoanalgesia in interventional pain management. Pain Physician. 2003 Jul;6(3):345-360.
Trescot AM, Noback CR. Cryoanalgesia in low back pain. In: Manchikanti L, Fellows B, Shipman C,
eds. Low Back Pain Diagnosis and Treatment. Paducah, KY: Amer Soc Interventional Pain
Physicians Press; 2002.
References
1. Cooper IS, Grissman F, Johnston R. A complete system for cytogenic surgery. St Barnabas Hosp Med
Bull. 1962;1:11-16.
2. Amoils SP. The Joules Thompson cryoprobe. Arch Ophthalmol. 1967;78:201-207.
3. Lloyd JW, Barnard JD, Glynn CJ. Cryoanalgesia. A new approach to pain relief. Lancet. 1976
Oct;2(7992):932-934.
4. Sunderland S. Nerves and Nerve Injuries. Edinburgh & London: Livingstone; 1968.
5. Evans PJ, Lloyd JW, Green CJ. Cryoanalgesia: the response to alterations in freeze cycle and
temperature. Br J Anaesth. 1981;53(11):1121-1127.
CHAPTER 80
Radiofrequency Neurolysis
Anand Thakur and Peter S. Staats
INTRODUCTION
A careful history and physical examination that implicates the lumbar facets/zygapophyseal joints and its
innervations via the lumbar medial branches of the posterior primary rami as the potential pain generators
must be clinically established (Figure 80-1).
Figure 80-1. Drawings of the nerve supply to the lumbar facet joints (arrows). (A) Anteroposterior view,
(B) oblique view.
Physical examination findings that finds direct tenderness on palpation of the skin overlying the lumbar
facet joints. Pain is described as deep, dull, achy, diffuse, and in a nondermatomal pattern. Pain may be
unilateral of bilateral. Pain is elicited with lumbar spine extension, lumbar spine extension and lateral
rotation. Rotational movements, twisting and turning about the axis of the lower lumbar spine causing
prevocational pain is suggestive of lumbar facet mediated pain (Figure 80-2).
Figure 80-2. Pain distribution in the facet syndrome. Referred pain patterns from facet joints reflect the
distribution of the segmental nerve supply at each level involved. Distal reference to the buttocks relates
to the caudal migration of posterior branches, whereas limb distribution mimicking root pain results from
pain reference in the anterior division of each segmental nerve.
Imaging studies including plain radiographs, computed tomography scanning, and magnetic resonance
imaging is used to visualize and demonstrate other potential causes of low back pain. CT scan is the gold
standard for visualization of the bony architecture of the facet joint, but it does not imply a specific
causative pain generator based on degenerative change, inflammation, synovial cyst or other potential
derangement.
INDICATIONS
• When a careful history and physical examination implicate the lumbar facet as a potential pain
generator and other pain sensitive structures have been excluded.
• A controlled series of 2 lumbar medial branch blocks is indicated first with a short-acting local
anesthetic (1% lidocaine), and then with a long-acting local anesthetic (0.5% bupivacaine).
• There must be a documented benefit from the first short-acting local anesthetic prior to going forward
with the long-acting local anesthetic.
• Benefit is described as greater than 70% to 80% positive outcome. This can be measured objectively
on a visual analogue or numeric pain scale given to the patient post procedure in the form of a “pain
diary.”
• This can also be measured subjectively in terms of improved functionality with physical therapy and
basic activities of daily living, range-of-motion, reduction of medication usage, return to work are a
few parameters that may be considered when demonstrating benefit.
• If the controlled series of lumbar medial branch blocks are deemed beneficial by the objective and
subjective criteria, the next reasonable step in care to provide durable pain relief for the patient is to
proceed with radiofrequency neurolysis of the lumbar medial branches of the posterior primary rami of
the lumbar facet joints (Figure 80-3).
Figure 80-3. This illustration shows that there is a possibility of 3 median nerve branches innervating the
one-facet joint. Note the ascending branch from the median nerve supplying the nerve above.
MECHANISM OF NEUROLYSIS
• Radiofrequency neurolysis is the heating of tissue greater than 45°C up to 90°C.
• Temperature generation is achieved via frictional heat that is generated by molecular movement in an
electrical field of alternating current above 250 kHz or at radio wave frequency. Hence, the name of
the procedure is radiofrequency neurolysis.
• The target tissue around the active tip of an insulated radiofrequency cannula is heated.
• The insulated radiofrequency cannula acts as a heat sink.
• The circuit is completed with a second electrode or the “grounding pad” to allow for current dispersal
(Figure 80-4).
Figure 80-4. The spread of the RF current density (jrf) in the tissue between the active and dispersive
electrodes.
CONTRAINDICATIONS
• Patient refusal.
• Localized skin infection over tissue area to be injected and/or systemic infection.
• Coagulopathy (INR >1.4) and/or bleeding diathesis (platelets <50,000/mm3).
• No controlled set (two) of diagnostic medial branch blocks with both a short-acting and long-acting
local anesthetic.
• One diagnostic medial branch block is not sufficient to go on to radiofrequency lesioning.
• Allergy to any of the injected components/medication necessary in the diagnostic blocks.
• Pregnancy.
RELEVANT ANATOMY
• The lumbar facet joints/zygapophyseal/z-joints are paired diarthrodial synovial joints located at the
posterior border of the spinal column.
• These joints consist of the articulations between the superior and inferior articular processes of the
adjacent vertebrae (Figure 80-5).
Figure 80-5. (A) Drawing of the lumbar spine in an oblique view identifying the “Scottie dog” in a
radiographic image and the relationship of inferior and superior articular processes. Note the facet joint
capsule stippling. (B) A cross section of the facet joints shows the details of the facet joint. (C) Drawing
of the oblique view of the lumbar spine that shows the lumbar nerve root and the formation of the lateral
and median branches of the posterior primary rami. Note the innervation at the facet joint by the median
branch.
• The facet joints are true synovial joints having a synovial membrane, joint fluid, and fibrous joint
capsule.
• The synovial membrane and joint capsule are richly innervated with sensory fibers including
unmyelinated c-fibers (Figure 80-5).
• The specific innervation of each facet joint is by the medial branch of the posterior primary ramus.
This small nerve passes over the transverse process and under the mamillo-accessory ligament.
• Each lumbar facet receives innervation from 2 medial branches: one from dorsal ramus above its level
and one from its own segmental level (Figure 80-5).
• Hence, when performing either a diagnostic lumbar medial branch blockade or a radiofrequency
neurolysis of lumbar medial branches, both dorsal rami must be blocked to achieve denervation of the
facet joint and pain relief (Figure 80-5).
• American Society of Anesthesiology standard monitoring of the patient: noninvasive blood pressure
cuff, ECG, pulse oximetry, and intravenous access.
• Anesthesiologist for administration of conscious sedation or local anesthetic only.
• Fluoroscopic unit C-arm with image storing/printing capability.
• Fluoroscopy or imaging table.
• Radiofrequency generator with simultaneous multilesion capability.
• Radiofrequency insulated cannulae of multiple lengths and gauges: 100, 145 mm (18 and 20 gauge).
• Radiofrequency cannulae 18 or 20 gauge.
• Sterile towels and half-sheet drape.
• Antiseptic skin solution: Betadine or chlorhexidine.
• Preservative-free local anesthetics: 1% lidocaine, 0.5% bupivacaine.
Fluoroscopic Views
• Pillow(s) are used to correct the lumbar lordosis and achieve mild lumbar flexion (Figure 80-6).
Figure 80-6. Patient positioning correction of lumbar lordosis.
• Anterior-posterior (AP) fluoroscopy views allow visualization of the superior articular process (SAP)
and the transverse process (TP) and the pedicle at the level to be blocked or lesioned (Figure 80-7).
Figure 80-7. RF Cannula placement at medial aspect of SAP and TP.
• Use of slight oblique views on the side to be blocked/lesioned (10-25 degrees) allows for better
visualization of the SAP and TP.
• Slight caudal angulation (10-25 degrees) after the appropriate oblique view also allows for better SAP
and TP visualization.
Patient Positioning
• Prone position with one or more pillows to correct for the lumbar lordosis and create mild lumbar
flexion (Figure 80-6).
• Arms placed comfortably in a flexed position toward the head with comfortable padding and support
for the elbow joints.
• Head turned to one side whichever is most comfortable.
• Pillow placement distal to the knees if needed for patient comfort.

• Multilesion capable radiofrequency generator (Figure 80-8).
Figure 80-8. RF generator.
• Sterilized RF cables, RF probes of multiple sizes 100, 145 mm (18 or 20 gauge) (Figures 80-9 and 80-
10).
Figure 80-9. RF Cannula.

Figure 80-10. RF probe 100 mm.
• Curved tip RF-insulated needles (one for each facet joint to be blocked/lesioned) with a 5- or 10-mm
active tip (Figure 80-9).
• Current return or “grounding pad.”
• 1% lidocaine-preservative free for skin wheal and localization prior to lesioning.
• 0.5% bupivacaine or ropivacaine-preservative free.
• 80 mg/mL methylprednisolone.
• Generic nerve block tray with multiple size syringes (5,10 mL) and 18-, 25-gauge needles.
• Record sheet for documentation of lesioning parameters: temperature, impedance, and lesion times.
• Pain diary or log to record subjective and objective response after RF neurolysis.
Interoperative Technical Steps

• Place patient in the prone position on the fluoroscopic table with a pillow at the umbilicus to correct
for the lumbar lordosis and create mild lumbar flexion.
• The patient is monitored with standard ASA monitors. Intravenous access is established. Anesthesia is
administered and supervised by an anesthesiologist or a supervised nurse anesthetist.
• The patient is prepped and draped in standard sterile fashion and technique with Betadine times 3 or
chlorhexidine times 1 in a wide field. Standard towel draping is applied to encompass the operative
field. A half-sheet surgical drape is placed from the buttock to cover the field to the end of the
fluoroscopic table.
• The C-arm fluoroscopic beam is started in the anterior-posterior position. Start the process with a
clear midline view of the lumbosacral spine visualizing the most common targets—the lumbar medial
branches at L3-L4, L4-L5, and L5-S1 bilaterally. Isolate the appropriate target site right or left side to
start.
• The C-arm is moved in the oblique direction (10-25 degrees) of the targeted medial branches right or
left. This allows for visualization of the superior articular process (SAP), transverse process (TP), and
pedicle at that level to be best visualized (Figure 80-11).
Figure 80-11. Parallel cannula placement for lesioning.
• Caudal angulation (10-20 degrees) of the C-arm will allow for better visualization of the TP and SAP
for radiofrequency neurolysis procedures.
• Mark the skin entry target area the inferomedial aspect of the TP as it meets the SAP.
• Create a skin wheal subcutaneous block with 1% lidocaine prior to RF needle insertion.
• Dependent on patient size choose the appropriate RF-curved needle size 100 or 150 mm and 18 or 20
gauge.
• Place the curved RF needle with an inferomedial approach and fluoroscopic guidance at the confluence
of the midpoint of the SAP and TP. Take care to place the curved RF needle parallel to the SAP to
allow for appropriate lesioning. A perpendicular placement will not allow for accurate medial branch
lesioning (Figure 80-11).
• After contact with bone at the superior-medial aspect of the TP-SAP confluence the RF probe lies
parallel to the medial branches of the primary posterior rami of the lumbar facet coursing underneath
the mamillo-accessory ligament (Figure 80-12).
Figure 80-12. Oblique view.
• AP and lateral C-arm views should demonstrate accurate needle position at the medial branch and not
near the transforaminal opening.
• Radiofrequency generator is activated and common cable connection is brought to the distal end of the
fluoroscopic table (Figure 80-13). Radiofrequency cables are brought from sterile supply and placed
on the sterile field and connected to the distal common cable outlet box by an assistant. This way the
operator remains sterile (Figure 80-14).
Figure 80-13. RF generator with probe connector.
Figure 80-14. Patient positioning with appropriate draping for lesioning.
• Sensory stimulation is carried out at 50 Hz and up to 1.0 mV to reproduce pain in a similar diffuse
distribution as typical lumbar facet medial branch mediated pain. There should be no stimulation of the
motor or spinal nerves or any radicular pattern of stimulation suggesting proximity to the motor nerve.
• Motor stimulation is carried out at 2 Hz and up to 2.5 V. No motor stimulation or contraction of
muscles in the distal extremity should occur nor any radicular stimulation. Localized multifidus muscle
stimulation will most likely occur.
• Impedance should be checked and documented. Normal impedance is between 250 and 500 Ω during
lesioning. Deep bony contact with RF probes produces high impedances and with blood produces low
impedances.
• After confirmation with both sensory and motor testing 1 cc PF 1% lidocaine is placed prior to
lesioning to decrease the pain of the lesioning process. (Please note that lidocaine application now
eliminates the ability to retest sensory and motor stimulation.)
• Lesioning is carried out at 80°C for 120 seconds to allow for a gentle 30-second ramp up time for the
RF probe to reach 80°C. The actual lesioning time is still 90 seconds.
• Direct fluoroscopic visualization is necessary during the lesioning process with spot imagery if there is
any change in sensation or untoward stimulation during the RF lesioning process. Needle position can
be checked instantaneously.
• The “medial branch” at the L5 position requires special attention. The target is actually the L5 dorsal
ramus (there is no L5 medial branch nerve), which is located at the juxtaposition of the sacral ala
superior articulating process of S1. The needle is then advanced slightly over the bone into the groove
of the sacral ala to contact the dorsal ramus of L5 (Figures 80-15 and 80-16).
Figure 80-15. Appropriate needle positioning for lesioning.

Figure 80-16. Lateral needle placement for lesioning.
• Sensory and motor testing is carried out as specified earlier and RF lesioning is carried out in the same
fashion.
• Postlesioning 1 to 2 cc of a solution of admixture of 80 mg methylprednisolone/1 cc and 0.5%
preservative-free bupivacaine/1.0 cc at each distinct lesioned site to help limit postprocedure pain.
• Dressings and/or bandages applied to injection sites.
• Standard PACU evaluation, monitoring, and care of the patient postprocedure.
• Examination of the patient in a sitting position regarding pain and response to treatment. Explain and
instruct patient on “pain diary” usage postprocedure.
• Examine and treat any postprocedure pain or spasm.
• Give postprocedure pain medications as indicated.
• Verify patient’s ability to ambulate and basic neurological functions are intact.
• Give patient emergency contact information and follow-up visit schedule and time.
• Discharge patient per PACU protocol with a responsible driver.
• No strenuous activity 24 to 48 hours postprocedure.
• Remove bandages in 24 hours. Keep clean and dry until removal.

• Pain, backache, or back spasm. Prescribe short-acting-opioids (SAO) and muscle relaxants (MR) as
needed. This is most likely attributed to RF needle insertion.
• Infection. Prescribe short course antibiotics, that patient is not allergic to.
• Muscle bruising or inflammation. Prescribe ice packs and/or NSAIDs.
• Localized bleeding. Change dressing, point pressure usually self-limited.
• Neuritis. None, usually it is self-limited but do a careful follow-up.
• Postdural puncture headache. Provide conservative care, short-acting opioids, NSAIDs and/or
muscle relaxants. Perform epidural blood patch if conservative care ineffective.

In the carefully selected patient who has undergone a successful controlled lumbar medial branch trial
with a greater than 70% to 80% relief, radiofrequency neurolysis provide a durable form of pain relief.
If a patient is a bilateral RF neurolysis candidate and is markedly obese with a difficult airway, it may
be beneficial to perform RF neurolysis unilaterally then repeat on the contralateral side in an appropriate
time interval for both patient comfort and safety.
Suggested Reading
Bogduk N, Dreyfuss P, Govid J. A narrative review of lumbar medial branch neurotomy for the treatment
of back pain. Pain Med. 2009 Nov 6;10:1035-1045.
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Index
Please note that index links point to page beginnings from the print edition. Locations are
approximate in e-readers, and you may need to page down one or more times after clicking a link to
get to the indexed material.
Numbers followed by “f” and “t” denote figures and tables, respectively.
A
Acromioclavicular joint intra-articular
injection
anatomy in, 462, 462f
blind
intraoperative steps in, 462
landmarks for, 462f
patient positioning for, 462
postoperative considerations, 462
fluoroscopy-guided
anatomy, 463
contrast for arthrogram confirmation, 463, 464f
imaging, 463
joint location, 463, 463f
indication for, 461
ultrasound-guided
intraoperative steps in, 464–465
ultrasound guidance, 464, 464f, 465
ultrasound localization for injection, 464
Adhesive capsulitis/rotator cuff disease
suprascapular nerve block for, 537
Alcohol, for neurolysis and neurolytic blocks, 369, 508, 666, 682, 688, 689, 689f
Amide prototypic local anesthetic, 52f
absorption and distribution rate versus ester, 58
Anchor(s) in spinal cord stimulation device, 587
Boston Scientific Clik, 587, 587f
Medtronic, 587
St. Jude Medical Cinch™, 587
St. Jude Swift-Lock, 587
Anesthesia dolorosa (numbness), from chemical neurolysis, 690
Angina pectoris, spinal cord stimulation for, 595
Antibiotics, allergy to, 85
Anticoagulation guidelines
for antiplatelet agents
aspirin, 81–82
clopidrogrel (Plavix), 82
ticlopidine (Ticlid), 82
interventional physician scenarios with, 78
for low molecular weight heparin, 80–81
for pentasaccharide agents (fondaparinux [Arixtra]), 81
for platelet GP IIb/IIIa receptor antagonists, 82
problems with chronic anticoagulation therapy, 78
deep vein thrombosis, 79
hypercoagulable syndromes, 79
significant bleeding, 78
spinal hematoma, 78–79
sedation and, 84–85
for thrombin inhibitors
dabigatran (Pradaxa), 80
heparin (unfractionated), 80
for warfarin (Coumadin), 79–80
Anticonvulsants, for trigeminal neuralgia, 657
Antidepressants, for trigeminal neuralgia, 657
Arixtra (fondaparinux), anticoagulation guidelines for, 81
Artery of Adamkiewicz, 321, 322f, 323–324
Arthrocentesis of knee, 469
Aspirin, anticoagulation guidelines for, 81–82
Atlanto-axial joint
anatomy of, 109–110
AP drawing of, 105f
CT reconstruction image of, 110f
greater, lesser, and occipital nerve path, 109, 110f
innervation of, 110
lateral view, 105f, 109f
tortuous vertebral artery, 106f
vertebral artery and relationship to injection sites, 105f, 110, 110f
innervation of, 106
Atlanto-axial joint injections
for cervicogenic headaches, 109
contraindications to, 109
fluoroscopic views, 111, 111f
indications for, 109
intraoperative steps
advancement of needle, 112, 112f
contrast injection, 112, 113f
local anesthetic and steroid injection, 112
needle placement on interior AA joint, 112, 112f, 113f
monitoring for complications
epidural extravasation, 113–114
intravascular injection into artery, 113
for occipital headaches, 109
preoperative considerations
positioning of patient, 111
safety, 110–111, 111f
selection of needles and medications, 112
Atlanto-occipital joint
anatomy in, 104–106
AP drawing of, 105f, 110f
innervation of, 110
lateral view, 105f, 109f
tortuous vertebral artery, 106f
vertebral artery and relationship to injection sites, 105f, 110, 110f
characterization of, 104
innervation of, 106
referred pain patterns from, 104, 104f
Atlanto-occipital joint injection
complications of
epidural extravasation, 108
intravascular injection, 108
equipment for
C-arm fluoroscope, 107
medications, 107, 108, 108f
needles, 107, 108, 108f
fluoroscopic view in
open mouth, 106, 106f
intraoperative steps in
anesthetic or steroid injection, 107
needle placement in, 107, 107f
Stealth needle in, 108, 108f
postprocedure considerations, 108
preoperative considerations, 106
B
Baclofen intrathecal pump
equipment for, 566, 567f
considerations for single shot, 573
needle placement technique for
paramedian, 563–564, 573
for painful spasticity, 566
trialing for spasticity, 573
catheter tunneling technique, 574
placement of intrathecal catheter for continuous infusion, 574
post-trial considerations, 574
single-shot delivery trial, 574
Benzocaine, metabolism and unique properties of, 61
Betamethasone, depot, adrenal suppression with, 45t
Bicipital tendon injection, 480, 480f, 481f
Bicipital tendonitis/tendonosis, bicipital tendon injection for, 476, 477f
Botulinum toxin(s)
onabotulinum toxin A for chronic migraine, 66
complications of, 68
dosing using PREEMPT injection paradigm, 67t
FDA-approved dose for, 68
general considerations, 68t
postprocedure follow-up, 68
technical considerations, 67–68
type A (Botox; Dysport; Xeomin), 66
type B (Myobloc), 66
Bullet tip needle, 37, 37f
Bupivacaine
metabolism and unique properties of, 61
non-FDA-approved for intrathecal use, 566
Bursitis
suprascapular nerve block for, 537
tendon injection for, 476
C
Cardioverter defibrillators and spinal cord stimulation system, 593
C-arm fluoroscope
components of, 6f
collimator, 4
fluoroscopy table and pad materials, 5
image intensifier, 4
optical coupling in, 4
digital image conversion technology and, 4–5
x-ray generator, 4
x-ray tube, 4, 6f
function of, 4
Catheter(s)
DuPen®, 41
Racz, 40, 41f
stimulating, 40–41
Caudal interlaminar epidural steroid injections. See also Interlaminar epidural steroid injection
AP view, 160f
needle at S3 level
lateral view with needle through sacral hiatus, 158
postlaminectomy, 158
technique, 158
Celiac plexus block (CPB)–CT guidance
anatomy in
of celiac plexus, 358, 359f
clinician knowledge of specific, 366
anterior para-aortic approach
advantages and disadvantages of, 364, 366
contrast adherence to abdominal aorta, 362f
contrast spread, 362f
CT imaging in, 361f, 362f
needle advancement, 362f
complications of, severe and grave, 365–366
endoscopic techniques in pancreatic cancer, 365
needles, medications, and equipment for, 359
neurolytic, 358
posterior para-aortic approach
injection of contrast, 360f
left-sided approaching needle, 360f
patient preparation for, 359–360
spread of contrast, 360f, 361f
posterior trans-aortic approach, 363f, 364
postprocedure considerations in, 365
preoperative considerations in
intravenous access, 359
preoperative somatic blocks and, 358
technique in
angle of insertion, 363
contrast injection, 359f, 364
contrast volume, 361f, 362f, 363f, 364
needle advancement, 361
needle direction, 361
passage through psoas fascia, 359f, 363–364
transaortic approach
contrast injection, 362f, 363f
contrast spread, 362f, 363f
Celiac plexus block (CPB)–fluoroscopic guidance
anatomy in
important vertebrae, 368
splanchnic nerves, 368
celiac plexus, characterization of, 368
complications of, 371–372
fluoroscopic views
anterior-posterior, 369
lateral, 369, 370f
postprocedure symptoms and causes, 371, 371t
aid of anesthesiologist, 369
with alcohol for neurolysis, 369
medications, 369
needles, syringes, and tubing, 369
retrocrural approach, two-needle
AP image of left-sided needle placement, 370–371, 371f
lateral image, 370, 370f
technique, 370
Celiac plexus neurolysis, 673, 673f
Cellular phones, spinal cord stimulation systems and, 594
Cervical and thoracic muscles, trigger point injections for, 428
Cervical discogram. See also Provocative discogram
anatomy of cervical disc and, 234
technique
disc “squared” in, 237
injection of contrast in, 237
note volume of contrast injected, 237
Cervical discs
anatomy in
outer annulus in, 234
posterior longitudinal ligament in, 234
sensory innervation from sympathetic chain, 234, 234f
sinovertebral nerves, 234
Cervical DRG block
at C2
fluoroscopic view, 194, 194f
lateral fluoroscopic view, 195, 195f
patient position for, 194, 194f
preferred technique, 195
at C3-C8
fluoroscopic views, 195–196, 196f
preferred technique
AP image, 196, 196f
pulsed-mode low-temperature RF in, 197
sensory and motor stimulation in, 196
Cervical interlaminar epidural steroid injection. See also Interlaminar epidural steroid injection
anatomy in, 156
midline injection, 156, 158f
positioning for, 156
technique, 156, 158, 158f
Cervical nerve root blocks
cervical foramen, 115–116
epidural space, 115
ligamentum flavum, 115
ventral and dorsal nerve roots, 115
for cervical radicular pain, 115
cervical transforaminal epidural steroid injections
safety issue and, 117
preoperative considerations in, 118
technique
anterior approach, 120f
injectate solutions, 120, 121t
posterior interlaminar approach, 119–120, 120f
transforaminal approach, 119
vascular anatomy in
anterior spinal artery, 116, 117f
cervical radicular arteries, 116, 117f
circle of Wills and, 117, 118f
radicular medullary arteries, 117
segmental nerve relationship to vertebral artery, 117, 117f
vascular neuroforamina of cervical spine, 117f
vertebral artery, 116, 117f
Cervical spinal cord, blood supply to, 329–330, 329f
Cervical spine interventions
anatomy of cervical intervertebral foramina and, 329f
transforaminal epidural steroid injection in, 327
cervical spinal infarction following, 328f
fluoroscopic views of selective nerve root block, 330, 331f
vascular complications of, 328–329, 328f, 329f
vascular complications of, 319–320, 327–329
mechanism of injury leading to, 329
vertebral artery in
course to cranium, 328f, 329–329
passage through foramen transversum, 328, 328f
Chargers for implantable pulse generators, 591
Chemical neurolysis
anatomy in
celiac plexus, 688, 688f
pelvic viscera, 688
sympathetic nervous system and corresponding structures, 688t
urogenital system, 688
complications of
anesthesia dolorosa, 690
neuritis, 690
cancer-related pain, 686
medication selection for, 688
alcohol, 688–689, 689f
phenol, 688, 689, 689f
sympathetic nervous system sites for, 687f
Chemical rhizotomy for trigeminal ganglion block, 126
Choloroprocaine, metabolism and unique properties of, 61
Clonidine, non-FDA-approved for intrathecal use, 566
Clopidogrel (Plavix), anticoagulation guidelines for, 82
Clostridium botulinum, botulinum toxins from, 66
Cluster headache
radiofrequency ablation of sphenopalatine ganglion for, 134–135
sphenopalatine ganglion block for, 134–135
Coagulase test, 71
Cocaine, metabolism and unique properties of, 62
Colon perforation
with genitofemoral nerve block, 516
with ilioinguinal/iliohypogastric block, 509
Complex regional pain syndrome
lumbar epidural sympathetic block for, 380
lumbar sympathetic nerve block for, 373, 374f
Computed tomography guidance
in acetabuloplasty for metastasis, 12f
advantages of
anatomical detail, 11–12
in facet joint injection, 11f
description of, 15
disadvantages of, 12
CT fluoroscopy in, 15–17
definitive needle placement, 15, 16f
infiltration of local anesthetic, 15
during localization of local anesthetic needle, 15, 16f
laser light in CT gantry, 17
modes of
continuous, 17
quick, 17
in needle placement, 12
for obese patients, 17
oblique axial imaging in, 17
operator protection in, 15
angled gantry approach, 14f
needle entry and trajectory planning, 14–15, 15f
oblique prone positioning, 13–14, 13f
patient positioning for needle trajectory, 12–13, 14f
radiation dose in
similar to conventional fluoroscopy in selected procedures, 16
typical, 16
radiation reduction in, 17, 18
Connecting extensions in spinal cord stimulation device, 587
Conscious sedation, 84
Contrast solutions, allergy to, 85
Corticosteroids
commercially available preparations, 45
duration of action of, 45–46, 45t
preservatives in, 46
solubility of, 45
complications from, 45, 160
adrenal insufficiency, 45, 45t
neural injury, 46
contraindications to, 42, 42t
epidural, 42
indications for
common, 42
diseases, 42
microscopic appearance of, 47f
particulate size, 46, 47t
particulate versus nonparticulate, 46–47
pharmacology of
action in neuralgic, inflammatory, and paresthetic pain, 44
action of, 43
analogues of, 43
defined, 43
locus of action, 44
role in interrupting inflammatory pathway, 43–44, 44f
physiology of cortisol, 43
spinal cord infarction from lumbar transforaminal epidural steroids, 46
Crawford needle, 38
Cryoanalgesia, of iliohypogastric/ilioinguinal nerve, 508, 509
Cryoneuroablation
common side effects and complications of, 694
common technical steps in, 694
cryoneuroablation ice ball, 691f
cryoneuroablation probe physics, 691f
cryoneuroablation unit, 691, 692f
diagnostic steps for, 693–694
freezing in, factors in, 692
histology after, 693f
for infraorbital block, 696–697
for intercostal block, 698
mechanism of, 692
for occipital block, 697–698
regeneration following, 693f
side effects and complications of, 694
success of, factors in, 694
of supraorbital nerve, 694–696
technical steps in, 694
D
Dabigatran (Pradaxa), anticoagulation guidelines for, 80
Day needle, 37, 37f
Dekompressor. See also Percutaneous disc decompression (PDD)
animation, 246f
aspiration procedure, 246
described, 243f, 244
at distal end of disc, AP view, 245f
endpoint, 246
introduced into nucleus, 245
in lateral view, 245f
at midpoint of disc, 245f
probe advanced to decompress disc material with rotating action, 245
removal of probe and introducer as 1 unit, 246
Discectomy
endoscopic, 280–286
percutaneous radiofrequency, 257–260
Disc herniation
causes of, 279
defined, 279
nerve root compression in, 280
pathology of, 280
types of
contained, 279, 280
noncontained, migration of disc fragment, 279
vascular ischemia in, 280
Discogenic pain
intradiscal electrothermal therapy for, 264–268
low back pain from, 262
lumbar, 270
intradiscal biacuplasty (annuloplasty) for, 270–278
Documentation
coding policies in, 98–99
add-on codes, 99
family of codes, 99–100
incorrect coding, 100
medically unlikely edits, 100
modifiers, 99
standards of medical/surgical practice, 99, 99t
unlisted services or procedures, 100
diagnostic
Current Procedural Terminology, 96
ICD-10, 96
International Classification of Diseases (ICD-9-CM), 96
electronic, 98
of interventional procedures, 98
medical necessity and
American Medical Association, 97
Centers for Medicare and Medicaid Services, 97
medical record, 97–98, 97t
procedural
Current Procedural Terminology, 96
Healthcare Common Procedure Coding System, 96
Medicare Relative Value Scale, 96
process in, 98
types of, 98
Dorsal root ganglion (DRG) block(s).
See also specific, e.g., Cervical DRG block
cervical
at C2, 194–195, 194f
at C3-C8, 195–197, 196f
contraindications to injection, 193
diagnostic, 193
equipment for
needles and syringes, 194
radiofrequency cannulae, 194
level-specific issues, 194–199
lumbar, 198, 198f
preoperative considerations, 193–194
RF blockade risks, 193
thoracic, 197–198, 198f
Dorsal root ganglion (DRG) stimulation
anatomy in, 626, 626f, 627f
vascular structure, 627
clinical targeting in
radiofrequency, 627–628
surgical, 627
neuroaugmentation of
lead and delivery system for, 628–629, 628f
limitations of, 630
patient selection for, 630, 630t
placement of leads, 629f
physiology of, 627
sensory pathways in
normal and altered, 627, 628f
Dural puncture
with lumbar transforaminal epidural steroid injection, 168
in spinal cord stimulation trialing procedures, 599
E
Electrocautery, spinal cord stimulation system and, 593
Electrode migration, in spinal cord stimulation trialing procedures, 599
Electromyography (EMG)
anatomy in
dermatome map, 88f
lower extremity schematic, 88, 89f
upper extremity schematic, 88f
clinical benefits of, 93
contraindications to, 87–88
defined, 87
design of, 92–93
electrophysiological parameters and normal values, 94t
EMG/NCS machine, 90f
indications for, 87
lower extremity example, 92, 94t
muscles
extensor carpi radialis, 92, 93f
tibialis anterior, 92, 93f
procedure, 91–92
technical considerations, 88
upper extremity example, 92, 94t
Electrothermal therapy. See Intradiscal electrothermal therapy (IDET)
Endoscopic discectomy
anesthesia for, 286
basic concerns in
calcified annulus fibrosus, 280
furcal nerves, 280
obese patient, 280
osteophytes, 280
small “safe triangle,” 280
biportal technique in, 286
considerations in, 280
for disc herniation
contained, 279, 280
noncontained, migration of disc fragment, 279
discitis following, 285
potential nerve issues, 286
fluoroscopic views
anterior-posterior, 281
lateral, 281
oblique, 281
goal of, 279
posterolateral intradiscal approach
Disc-FX kit with accessories for, 281f
equipment for, 282
posterolateral transdiscal approach
annulotomy in, 283, 283f
cannula and dilator insertion over guidewire, 283, 283f
discogram in, confirmatory contrast, 283
endoscopic visualization of nucleotomy and annulotomy, 284, 284f
guidewire insertion through needle, 283, 283f
insertion of needle into disc, 282, 282f
nucleotomy in, 284, 284f
radiofrequency ablation in, 284, 284f
trephine or annulotome insertion over guidewire, 283f
postprocedure follow-up in, 285
preoperative considerations in, 280–281
transforaminal approach
annular fenestration in, 285
annulotomy in, 285
dissection of annulus in, 285
equipment for, 282
medications for, 282
Enthesopathy, tendon injection for, 476
Epicondyle injection, lateral, 481–482, 482f
Epicondylosis/epicondylitis, epicondyle injection for, lateral, 477, 478f
Epidural and transforaminal neurolysis, 683–684
Epidural lysis of adhesions (Racz procedure)
anatomy in
epidural space, 315
interlaminar space, 315
sacral hiatus, 315
fluoroscopic views in, 316
catheter introduction, 317
contrast instillation under real-time fluoroscopy, 317
epidurogram, 317
evaluate for intravascular spread, 317
fluoroscopy, 316
interspinous access, 317
medication delivery, 317–318
patient positioning, 316
sacral hiatus access, 316–317
sedation, 316
patient selection for, 316
preoperative preparation, 316
technique, 2-handed, 318
Epidural steroid injection(s)
interlaminar. See Interlaminar epidural steroid injections
transforaminal. See Lumbar transforaminal epidural steroid injections
Epidurogram
in epidural lysis of adhesions, 317
in lumbar facet cyst, 191f
in minimally invasive lumbar decompression, 289, 290, 295, 296f
Equipment
anatomical considerations in, 36
cryoablation, 39–40
fluoroscopy, 38–39
needles
epidural placement, 37–38, 37f, 38f
nonepidural placement, 36–37, 36f, 37f
radiofrequency generators
conventional, 39
cooled, 39
lesions and, 39
pulsed, 39
specialized catheters
DuPen®, 41
Racz catheter, 40, 41f
stimulating, 40–41
specialized syringes
discography dual needle sets, 40, 40f
pressure monitoring manometric for controlled injection rate, 40, 40f
Ester prototypic local anesthetic, 52f
absorption and distribution rate versus amide, 58
Etidocaine, metabolism and unique properties of, 60
Extensor carpi radialis brevis (ECRB) muscle and common extensor tendon injections
needles, medication, and equipment for, 415–416
ultrasound-guided injection, 415–416, 418, 418f
ultrasound views, 416, 416f
F
Facet fusion. See Percutaneous facet fusion (PFF)
Facet joint intervention(s)
cervical spine
facet joints in, 173–174, 174f
innervation of, 171f, 174
intra-articular injections, 181–183, 182f
medial branch blocks, 183–184, 183f
radiofrequency ablation of medial branches, 185–186, 185f
nerve root damage, 186
lumbar spine
facet joints in, 170, 170f
fluoroscopy, 175
innervation of, 170, 171f, 172
intra-articular injections, 175
ligaments in, 170
procedural steps, 175–177, 176f
radiofrequency ablation of medial branches, 178–179, 178f
side effects of steroids, 186
thoracic spine
facet joints in, 172–173, 172f
innervation of, 171f, 173
intra-articular injections, 179–180, 179f
radiofrequency ablation of medial branches, 181
Facial weakness, with microvascular decompression of trigeminal nerve, 659
Failed back surgery syndrome
epidural lysis of adhesions for, 315, 316
Fasciitis, tendon injection for, 476
Fentanyl, non-FDA-approved for intrathecal use, 566
Fluoroscopy
basic concerns and contraindications, 30
history of, 2
Fluoroscopy equipment
C-arm, 38
digital technology in, 38
image storage and transport, 39
low dose setting, 38
monitors, flat LCD, 39
pulsed mode, 38
Fondaparinux (Arixtra), anticoagulation guidelines for, 81
G
Ganglion impar block
anatomy in
with relation to nearby anatomical structures, 392, 393f
structures for locating, 392
variable locations of, 393f
complications of, 399, 399f
contraindications to, 393–394, 394f
equipment for, 394
fluoroscopic views
anterior-posterior, 394, 395f
lateral, 394, 395f
postprocedure follow-up, 398–399
preferred technique
AP fluoroscopic image for, 395f, 396, 397f
lateral image contrast injection, 397–398, 398f
lateral image for, 395–396, 395f
needle advancement in, 397, 397f
needle-inside-needle, 398, 399f
technique
anococcygeal, 394–395, 395f
approaches, 394
curved needle, 396, 396f
transsacroccygeal, 396
Ganglion impar neurolysis
anatomy in
ganglion of Walther, 674
sacrococcygeal junction in, 674
fluoroscopic views
anterior-posterior, 674f
trans-sacrococcygeal approach, 674
contrast injection, 673f, 675
needle approaches to sacrococcygeal junction, 673f, 675
phenol in glycerin injected incrementally, 675
skin preparation and local anesthesia, 674
patient position for, 674
Genitofemoral nerve block
concerns in
injury to genitofemoral nerve, 511
diagnostic injection
anterior blind approach, 514
anterior fluoroscopic approach, 513f, 514
transforaminal approach, 512, 514–515, 514f
transpsoas approach, blind or image-guided, 514
equipment for
needles, sensory nerve stimulator, 512–513
for psoas injection, 513
for transforaminal injection, 513–514
fluoroscopic views of, 512
psoas muscle shadow, 512, 513f
transforaminal approach, 512, 514f
neuroablation, 515, 515f
Glenohumeral joint injection, image-guided
anterior approach, 405, 405f
brachial plexus and, 405
posterior approach, 405, 405f
fluoroscopy-guided techniques
anterior approach, 409
posterior approach, 408–409, 409f
image-guided, 404–410
needles and medication for, 406
ultrasound examination for, 406
ultrasound-guided techniques
anterior approach, 408
Glenohumeral joint injection, intra-articular
anterior-superior approach
superior approach to anterior glenohumeral joint, 453, 453f
blind, anterior Schneider technique, 451–452, 451f
anterior shoulder injection in, 451, 452f
intra-operative steps in, 454
patient prone for, 451, 451f
patient sitting for, 451–452, 452f
risk with, 454
skin marking at lateral acromion, 454, 454f
blind posterior approach, 455–456, 455f
injection site in, 455f
shoulder needle position in, 455, 455f
fluoroscopy-guided
adhesiolysis in lateral approach, 459, 459f
anterior approach, 456–457, 457f
anterior interval approach, 457
arthrogram
lateral shoulder, 458f
posterior approach, 460f
fluoroscopic landmarks for, 456f
lateral approach, 457–458
needles and medications for, 456
positioning for, 456f
rotator cuff interval approach, 452–453, 452f
anatomy in, 453
ultrasound-guided
anterior approach, 460–461, 460f, 461f
posterior approach, 461, 461f
Granuloma, with implantable drug delivery systems, 554
H
Headache(s)
cervicogenic, atlanto-axial joint injections for, 109
chronic migraine, botulinum injection for, 66–68, 67t, 68t
cluster, 134–135
occipital, atlanto-axial joint injections for, 109
postdural puncture, 672, 709
in supraorbital neuralgia, 694–695
Hearing loss, with microvascular decompression of trigeminal nerve, 658
Heparin (unfractionated), anticoagulation guidelines for, 80
Hip injection, image-guided
proximity to neurovascular bundle, 410f
relation to nearby structures, 411f
fluoroscopy-guided, 414–415
filling of capsule with contrast media, 414f, 415
posterior approach, 414f
image-guided
hip capsule attachments and, 411, 412f
needles, medication, and equipment for, 411–412
techniques
anterior, 412
lateral, 412
ultrasound-guided
Hip injection, intra-articular
blind
anatomy, 465
positioning needle in, 466, 466f
fluoroscopy-guided
anatomy, 466, 466f
lateral approach, 467, 467f
ultrasound-guided
anatomy, 468–469, 468f
intraoperative steps in, 469, 469f
transducer in, 468f
Huber needle, 37, 37f
Hustead needle, 38
Hyaluronate, for intra-articular injection of knee, 419t
Hydrodiscectomy
illustration of, 252f, 253f
insertion of cannula, 251, 252f
insertion of dilator, 251f, 252f
insertion of microresector, 251, 252f
lateral view of guide needle, 251, 252f
oblique with superior articular process over disc, 251f, 252f
removal of guide needle and dilator, 251, 252f
graphic illustration of, 254f
Kambin’s triangle in, 251
monitoring of potential complications, 253
MRI preprocedure, 250, 254
procedure
cannula advanced, 253, 254f
dilator advanced, 253, 254
fluoroscopic images of, 252f
graphic illustration of, 253, 254f
guide needle introduction, 253, 254f
positioning in, 253
SpineJet PercResector replaces dilator, 253, 254f
Hydromorphone, non-FDA-approved for intrathecal use, 566
Hydrosurgery of disc. See Hydrodiscectomy
Hypogastric plexus block(s)
documentation for off-label indications, 383–384
inferior hypogastric plexus, 388–390, 389f
anatomy and location of, 382
paresthesia risk with, 383
superior hypogastric plexus
anatomy and location of, 382
anterior approach, 386–388
lateral approach, 384–385, 384f, 385f, 386f
skin entry points for, 390f
transdiscal approach, 385–386, 387f, 388f
I
Iliohypogastric nerve block
ablation by phenol or absolute alcohol, 508
ablation by pulsed mode radiofrequency, 508
anatomy of iliohypogastric nerve, 504, 505f
entrapment at rectus border, 504, 506f
proximal entrapment, 504, 507f
cryoanalgesia in, 508
diagnostic
for proximal injections, 506–507, 507f
for rectus entrapments, 506, 507f, 508f
equipment for
needle, tubing, stimulator, 505–506
radiofrequency or cryoanalgesia machine, 506
palpation at rectus border, 507f
preemptive analgesia or surgical block, 508
Ilioinguinal nerve block
diagnostic
for proximal injections, 506–507, 507f
for rectus entrapments, 506, 507f, 508f
equipment for
needle, tubing, stimulator, 505–506
radiofrequency or cryoablation machine, 506
ultrasound guidance for, 507, 507f
Iliolumbar ligament
anatomy of, 479, 479f
injection of, 483, 484f
Iliopsoas injection
anatomy in, 439
equipment and medications for, 439
fluoroscopy-guided
infiltration with local anesthetic, 440
local anesthetic/steroid injection, 440
patient position, 440
psoas muscle contrast injection, 440, 440f
physical examination for, 438
postprocedure follow-up of, 442
provocative tests for, 438–439
ultrasound-guided technique
in-plane posterolateral psoas compartment block technique, 441, 441f
lateral approach to, 441–442, 441f
needle position in, 441, 441f
posterior approach to, 442
Image-guided peripheral joint injection
of extensor carpi radialis brevis muscle and common extensor tendon, 415–418
ultrasonography, tissue properties and, 403
Image-guided peripheral joint injection. See also under specific, e.g., Glenohumeral joint, image-guided
advantages of, 402
basic concerns, 402
of corticosteroid, 402
of glenohumeral joint, 404–410
of hip, 410–415
postprocedure follow-up, 403–404
Implantable drug delivery systems (IDDS)
complications related to pump and catheter system, 554
described, 554
granuloma with use, 554
intrathecal drugs for, 565, 566
side view of device, 554f
Implantable pulse generators in spinal cord stimulation device
chargers for, 591
conventional non-rechargeable, 588
Medtronic, 589
non-rechargeable, 589
rechargeable, 589–590
parameters of, 588
rechargeable, 588–589
Bion Microstimulation, Boston Scientific, 589, 589f
Precision Plus, Boston Scientific, 589, 589f
restore advanced rechargeable battery, 590
St. Jude Medical
EonC non-rechargeable, 590
external radiofrequency Renew IPG, 590–591
Genesis non-rechargeable, 590
rechargeable Eon Mini, 590
stimulation based on energy source
current-constant system, 588
independent, 588
voltage-constant system, 588
types of, 588
Infection
diagnosis of, 75
discitis, postprocedural, 76
with implantable devices
coagulase test for, 71
common organisms, 70
MRSA, 71
pathophysiology of, 71
management of
for deep neuraxial infection, 75–76
for superficial infection, 75
patient-related risk factors for, 71–72
patients at risk for, 70
prevention of
Avagard pump for antisepsis, 72, 72f
with implantable devices, 72–73
intrathecal versus epidural infection, 74–75
postoperative care, 74
prepping and draping for implant placement, 73–74, 73f, 74f
preprocedural or preoperative considerations and, 72
prophylactic antibiotics, 72–73
in provocative discography, 72
in vertebral augmentation, 72
sources of, 70
surgical site
defined, 71
impact of, 70
wound seroma, 75
Infraclavicular nerve cryoneuroablation
anatomy in, 500f
nerve stimulator approach
abduction of arm in, 500
landmarks in, 500
unacceptable and acceptable biceps twitches in, 500–501
ultrasound approach
benefits of, 501
injection and spread of local anesthetic in, 502
introduction of needle in, 502
needle path visualization throughout, 501
nerves, visualization of, 502
probe in, 501
setup of probe and needle for, 501, 501f
visualize vascular structures, 501
Infraorbital cryoneuroablation
infraorbital anatomy in, 696, 696f
closed technique, 697
intraoral approach, 697, 697f
open technique, 697
Infraorbital nerve
peripheral nerve stimulation trial, 641–642, 641f, 643f
permanent implant, 642–643
Intercostal cryoneurolysis
complications of
neuroma formation, 700
subcostal bulge, 700, 700f
fluoroscopic image to identify ribs, 699, 699f
closed, percutaneous approach, 699–700, 699f
open technique, 699–700
pneumothorax and, 700
for post-thoracotomy pain, 699
Intercostal nerve block
advantages of, 488
anatomy in, 493f
anterior cutaneous branches, 490, 490f
intercostal space, 489f
lateral cutaneous branches, 490, 490f
white and gray rami, 489
complications of, 488f
indications for, 488f
nerve root divisions in
ventral ramus, 489–490
preoperative considerations in, 489–481
at T12, 489–490
technique
anatomical landmark in, 491
fluoroscopy-guided, 491, 492f
ultrasound-guided, 492, 492f, 493f
Intercostal peripheral nerve stimulation trial, 650, 650f
Interlaminar epidural steroid injection
anatomy in
epidural space, 154
ligamentum flavum, 154
for midline approach, 154
for paramedian approach, 154
approaches to
blind, 154
fluoroscopy guided, 154
complications of
contrast dye reaction, 160
corticosteroid effects, 160
procedure related, 161
contraindications to
absolute, 155
relative, 155
fluoroscopic views
AP, 156, 157
lateral, 156, 157
midline, 157
indications for
postlaminectomy syndrome, 154
radiculopathy, 154
spondylolisthesis, 154
postoperative instructions, 159
preoperative preparations for
epidural kits, 155–156
IV access, 155
medications, 156
pain level and character, 155
positioning, 155
technique. See also specific, e.g., Caudal interlaminar epidural injection
caudal, 158, 160f
cervical, 156, 158, 158f
lumbar, 156, 157f
thoracic, 158, 159f
Internal disc disruption (IDD)
Dallas criteria for, 255f
Dallas discogram grades of annular tissues, 263f
Dallas grade IV tear, 256f
defined, 262
diagnostic criteria for, 256
discogram with manometry in
diagnostic, 264, 264t
findings amenable to intradiscal therapy, 264t
intradiscal electrothermal therapy for. See Intradiscal electrothermal therapy
percutaneous radiofrequency discectomy for. See Percutaneous radiofrequency discectomy
Intervertebral disc. See also specific disc, e.g., Cervical disc
anatomy in
inner nucleus (nucleus pulposus), 234
ligaments, 262
nerve supply, 262
outer annulus (annulus fibrosus), 233
segmental radicular arteries, 262
blood supply, segmental arteries, 234
comparison of intact and degenerated, 270f
composition of, 262
innervation of, 234, 262, 263f
Intervertebral disc herniation
contained, 256
degenerative, 255–256
internal disruption
with annular tear, 255
Dallas criteria classification, 255f, 256f
Intra-articular joint injection(s)
ultrasound-guided
probe with bio-occlusive cover in, 449f
sterile surgical lubricant in, 449f
ultrasound sterile sleeve in, 450f
Intra-articular joint injection(s). See also under named joint, i.e. Knee, intra-articular injection
of acromioclavicular joint, 461–465
anatomic landmarks in, 446
blind
anatomy for, 450, 451f
disadvantages of, 450
of glenohumeral joint, 404–410, 450–461
of hip, 451–461, 465–469
of knee, 419–426, 469–474
needles, medications and equipment for, 446
posprocedural considerations in, 448
reducing pain of injection in, 447–448
ultrasound-guided
basic principles for, 448
marker in, 448f
sterility and, 448, 450
Intradiscal biacuplasty (annuloplasty)
candidate selection for, 271
complications following, 276–277
defined, 270, 275
description of procedure, 270, 271f
disc anatomy in
innervation of, 272
nucleus pulposus and annulus fibrosus, 272
reverse innervation of, 272
structures in placement of electrodes, 272
vertebral endplates, 272
fluoroscopic views
anterior-posterior placement of introducers, 273, 274f
electrode depth, 273, 274f, 275f
oblique, 272–273, 273f, 275
functional rehabilitation after, 277
postprocedure follow-up
use of lumbar sacral orthosis, 276
written post-op instructions, 276
technique
common elctrode placement mistakes, 276f
duration and temperature of RF energy, 275–276
RF generator delivery of RF energy, 275
TransDiscal introducer advanced, 275, 275f
TransDiscal probe advanced through introducer, 274f, 275, 275f
Intradiscal electrothermal therapy (IDET)
pitfalls of, 266
technique
electrode advancement, 265f–268f
electrode heated and temperature maintained, 265–266
introducer needle insertion, 264–265, 264f
needle placement, 264
oblique lumbar spine radiograph of superior articular facet, 264f
placement of IDET catheter, 265f–268f
Intrathecal drug delivery
Codman 3000 infusion pump in, 545f
advantages of, 552
bypass for bolus injection, 545, 546f
MRI compatibility, 546
pitfalls with, 551
specifications of, 545t
comparison of SynchroMed EL to SynchroMed II, 550f, 552f
continuous infusion pumps in
advantage of, 544
design of, 544
disadvantage of, 544
programmable pumps in
commercially available, 546
fundamentals of, 546
SynchroMed EL by Medtronic in, 546–547
design of, 547
morphine and baclofen stability in, 547
pitfalls with, 551
precautions during implantation, 548
schematic drawing of, 548f
settings for drug administration, 549
side catheter access port, 547, 548f
specifications of, 545t
SynchroMed II by Medtronic in
clinical changes with, 552
design of, 549–550
initial programming of, 550–551
pitfalls with, 551–552
precautions during implantation of, 550
specifications of, 550f
Intrathecal drug delivery trialing
anatomy in, 560
for needle placement, 560
considerations for
choice of interlaminar space, 560–561
fluoroscopy, 561
hematologic, 561
immunocompromised patients, 561
of continuous epidural infusion of opiates
of continuous epidural infusion of opiates
AP image, 568f
desired location of needle, 567
needle placement procedure, 567–568, 568f
needle placement with catheter, 567, 568f
for continuous intrathecal infusion of medication
post-trial considerations, 569–570
fluoroscopic imaging in, 562–563
needle tip insertion location, 563
intrathecal baclofen pump for spasticity
catheter placement for continuous infusion, 574
catheter tunneling technique, 574
needle placement technique, 573
patient criteria for, 573
single-shot, 573, 574
intrathecal medications for pain
FDA-approved, 565–566
non-FDA-approved, 566
intrathecal pump infusion system
continuous infusion trial, 565
intrathecal pump infusion system trial, 565
objective measures in, 565
single-shot trialing, 565
paramedian technique for interlaminar needle placement, 563, 563f
advancement to intrathecal space, 564
lateral image diagram of lumbar spine anatomy for, 564f
loss of resistance for placement depth, 564f
patient categories for, 560
perioperative considerations in
anatomical, 561
dosing epidural versus intrathecal, 562
preadmission testing, 561
during the trial, 561–562
Polyanalgesic Consensus Conference trialing algorithm, 562f
single-shot trial
with ziconotide. See also Ziconotide trialing
continuous infusion versus single shot, 570
continuous intrathecal infusion, 570–573
Intrathecal drug selection
compounding of medications, 556–557
Polyanalgesic Consensus Conference recommendations, 554–556
catheter obstruction from precipitants, 558f
for compounding medications, 558
corrosion of pump components, 557f, 558
on drug admixtures, 557–558
against drugs used intrathecally, 555t
flow rates and bolusing, 558–559
for maximum daily doses and concentrations, 555t
for prevention of granuloma, 555
recommended doses of agents, 555t
therapies for neuropathic pain, 555t
therapies for nociceptive pain, 556t
trialing to consider permanent intrathecal therapy, 559
Intravascular injection
with lumbar transforaminal epidural steroid injection, 168
K
Knee, intra-articular injection
anatomy in, 420–421, 420f, 421f, 469, 470f
arthrocentesis, 469
for aspiration/steroid injection
fluoroscopic or ultrasound guidance, 422
medial suprapatellar approach, 423–424, 423f, 424f
parapatellar approach, medial or lateral, 422
suprapatellar approach, medial or lateral, 422, 423f
blind, 470
infrapatellar, 471, 471f
midpatellar approach, 470–471
suprapatellar approach, 470, 470f
fluoroscopy-guided
anatomy for, 472
intraoperative steps in anterolateral or anteromedial patella approach, 473, 473f
knee image, 472f
patent positioning for, 472, 472f
indications for
arthrocentesis, 469
viscosupplementation, 469
medial suprapatellar approach
marking of key anatomical landmarks in, 423, 423f
needle entry site marked, 423, 423f
needle placement in, 424f
patella tilt in, 424, 424f
patient positioning for, 422–423, 423f
ultrasound-guided
ultrasound positioning for, 473, 474f
of viscosupplements/steroids
anatomic landmarks for, 420–421, 420f, 421f
basic concerns with, 421
complications of, product-specific, 425
indications for, 419–420
injection site preparation, 423f, 424
manufacturer and brand names, 419t
marking with anatomical landmarks, 423f, 424
medial suprapatellar approach, 422–423, 422–424, 423f, 424f
needle directed to enter joint capsule, 424–425, 424f
needles, equipment, and medications for, 424
patella tilt for, 424f, 425
patient positioning for, 422–423, 423f
potential complications of, 425
Knee osteoarthritis
clinical criteria for diagnosis, 420
radiographic evidence of, 420
viscosupplements and steroid injections for
manufacturer and brand names, 419t
Kyphoplasty. See also Vertebroplasty
balloon insertion, deflated, and inflation, 307, 307f
cannula placement in, 307, 307f
cement extravasation in, 308f
cement placement in, 307–308
described, 298, 299
drill insertion in, 307
steps additional to vertebroplasty procedure, 306f, 307–308, 308f
L
Lateral epicondylitis, extensor carpi radialis brevis muscle injections for, 415
Lateral femoral cutaneous nerve block
anatomy in
cutaneous distribution of, 518f
lateral femoral cutaneous nerve location, 517, 518f
differential diagnoses and, 517–518
equipment for, 518–519
fanning technique in
localization and injection of nerve, 519, 519f
fluoroscopic confirmation with neurogram, 519
lateral femoral cutaneous nerve
described, 517
transinguinal technique, 519, 519f
ultrasound-guided, 519, 520f
Lead placement
antegrade positioning
directing needle to interlaminar space, 622, 622f
dual lead insertion and final placement, 622, 622f, 623f
entry point for Coude needle, 621, 622f
patient positioning for, 621, 621f
surgical drape, 621, 622f
antegrade/retrograde
equipment for, 620
Coude needles, 620, 621f
Pyles epidural needles, 620, 621f
fluoroscopic views
antegrade positioning, 620
retrograde position, 620
lead fixation
Stayfix dressing and Opsite, 624–625, 624f, 625f
pelvic innervation and, 619–620
parasympathetic, 619
somatic efferent/afferent, 619
sympathetic, 619
preoperative considerations for, 620
retrograde placement
bilateral, 624, 624f
needle insertion and placement in, 623, 624f
skin entry point in, 623, 623f
unilateral, 624, 624f
Leads in spinal cord stimulation device, 585
percutaneous, 585
configuration of, 586
octad, 585
spacing of, 585, 586f
surgical or paddle, 586
five-column, 586–587
single-column, 586
three-column, 586
two-column, 586
Levator scapula tendon injection, 481, 481f
Levobupivacaine, metabolism and unique properties of, 61
Lidocaine
intravenous, 53
IV infusion, 53
systemic via implanted osmotic pump, 53–54
Ligamentum flavum, in cervical nerve root block, 115
Ligamentum hypertrophy, in spinal stenosis, 288, 289f
Local anesthetic(s)
absorption and rate of distribution of, 58, 58f
amide versus ester, 58
cardiac output and, 58
protein binding and, 58
actions and interactions of, 50
amide (lidocaine), 51f
chemical structure of, 52f
metabolism and unique properties of, 60–61
chronology of development, 54f
clearance of, 59
comparative pharmacology of, 51, 54t
ester (procaine), 51f
chemical structure of, 52f
metabolism and unique properties of, 61–62
frequency-dependent and statedependent block, 55, 57
interaction with sodium channels to prevent threshold activation, 54f
intravenous lidocaine, 53
lidocaine infusions, 53
mechanism of action of, 51, 53
minimum concentration of
in differential conduction blockade, 57
factors influencing, 57
in preganglionic B fibers, 57
pregnancy and, 57
myotoxicity of, 59
pharmacokinetics of, 57–58
placental transfer of, 58–59
structure of
parts of molecule, 50, 52f
pipecoloxylidides, 50
systemic lidocaine via implanted osmotic pump, 53–54
toxicity of, 59
lipid emulsion therapy for, 60
methemoglobinemia, 59
seizures, 60
uses of, 50
voltage-dependent sodium channels in pain states, 55
knock-down and knock-out studies of sodium, 56t
neuron-specific, 55
nonneuronal, 55
preferential expression in peripheral neurons, 56t
voltage-gated sodium channels
activated, 54f, 55
functional states of, 54, 54f
inactivated, 54f, 55
resting closed, 54f, 55
Lower extremity
electromyography of, 88, 89f, 92, 94f
Low molecular weight heparin
anticoagulation guidelines for, 80–81
Lumbar discogram. See also Provocative discogram
anatomy of lumbar disc and, 234
posterolateral approach in, 233
technique
disc “squared” in, 236
evaluation of disc and adjacent disc spaces, 236–237
injection of contrast with syringe connected to disc pressure monitor, 236
injection of local anesthetic into disc space, 237
needle advanced to middle of disc, 236
Lumbar discs
anatomy of, 234
intradiscal pressure based on spine position, 233
Lumbar DRG block
confirmation of placement in, 199
local anesthetic for, 199
preferred technique
needle position AP fluoroscopic view, 198–199, 198f
pulsed-dose low-temperature radiofrequency, 199
sensory and motor stimulation, 199
Lumbar facet joint
classification of arthropathy in, 188
effusions, 187–188, 187f
nerve supply to, 702f
radiographic assessment for pain, 187–188, 188f
Lumbar facet joint cyst
chronic, 191
defined, 187, 188f, 189f
drainage and injection
preferred technique, 190–191, 191f
drainage and injection of
by CT scan, 191f
epidurogram in, 191f
fluoroscopic views, oblique, 190, 190f
septic arthropathy and, 189–190, 189f
surgical options, 191
techniques, 190
facet capsule effusion and, 187
sites of, 187–188, 189f
Lumbar interlaminar epidural steroid injection. See Interlaminar epidural steroid injection
Lumbar spine, trigger point injections for, 428
Lumbar sympathetic nerve block
advantages of, 373–375
alternative technique
ipsilateral oblique fluoroscopy, 379, 379f
anatomy in
landmarks in, 375
postganglionic fibers, 375
preganglionic fibers, 375
sympathetic fibers, 375
epidural in complex regional pain syndrome, 380
indications for, 373–375, 373f
needles, syringes, and medications for, 376
neurolysis for lumbar sympathectomy, 380
postprocedure considerations in
pain relief assessment, 379–380
patient evaluation for, 375–376
requirements for optimal results, 375, 376t
in regional pain syndrome continuum of care, 373, 374f
spinal cord stimulation in, advantages of, 373–374
technique
injection of contrast media in, 377f, 378
intravascular injection avoidance and detection, 378, 378f
medication injection, 379, 379f
radiographic imaging in, 377f–379f
types of, 373t
Lumbar sympathetic neurolysis
candidates for, 670, 672
fluoroscopy-guided
contrast injection in, 671f, 672
needle placement and advancement, 671, 671f
phenol in glycerin injected incrementally, 672
scout AP film for, 671
Lumbar transforaminal epidural steroid injection
concerns in, 165
equipment for
injectate, 168
needle choice, 167–168
fluoroscopic views and technique
AP view and contrast injection, 165, 167f
epidural spread of contrast, 167, 167f
lateral view, needle placement at L4-5 and L5-S1, 165, 166f
oblique angle “Scottie dog” view, 165, 166f
retrodiscal approach, 167
lumbar anatomy in
arteria radicularis magna, 163
coronal section of, 163f
intervertebral foramen, 162–164
sagittal section, 163f
segmental arteries, 163, 163f
spinal nerve root and sinuvertebral nerve, 162
superior articular process of inferior vertebra, 162, 163f
for lumbar radiculopathy, 162
safe triangle and, 164–165, 164f
spinal column anatomy, 162f
technique
“squaring” the level, 165
M
Magnetic resonance imaging (MRI)
spinal cord stimulation system and, 593
Mandibular nerve block, 128
Maxillary nerve block
infraorbital, 127
maxillary, 127
Mepivacaine
Methylprednisolone, depot
adrenal suppression with, 45t
Migraine headache
botulinum toxin injection for chronic, 66–68, 67t, 68t
peripheral facial stimulation for, 663
Minimally invasive lumbar decompression (MILD)
contrast for, 292
defined, 287
epidurogram in, 289, 290
post-mild, 295, 296f
pre-mild, 290
equipment for
epidural needle, 292
mild kit, 292, 292f
radiolucent procedure table, 292
fluoroscopic views
contralateral oblique, 290, 291f
posterior-anterior for epidural needle placement, 290
indications for, 287, 290
bony tissue decompression with Bone Sculpter Ronguer, 294, 295f
depth guide placement, 294
epidural needle placement, 292–293, 294f
fluoroscopy, 292
ligamentum flavum debulking, 295, 295f
loss of resistance technique in, 292–293
needle advancement in contralateral oblique, 293
portal stabilizer placement, 294, 294f
repeat epidurogram, 295
skin entry site and trajectory planning, 293
skin markings in, 293f
tissue access device insertion, 293
trocar positioning and removal, 294, 294f
wound dressing, 295, 296
mechanism of action for, 288
postprocedure considerations in, 295–296
IV antibiotic preoperative, 290
workup for, 290
Morphine
intrathecal for nociceptive pain, 565
single shot injection trial, 569
MRSA infection, surgical site, 71
Myofascial injection(s), 434
iliopsoas, 438–442
piriformis, 435–438
scalene muscle, 442–444
trigger point, 428, 434–435
N
Needle(s)
epidural placement of
Crawford, 38
Hustead, 38
RX coudé, 38, 38f
Touhy, 37, 38f
Touhy with flexible introducer cannula, 38, 38f
nonepidural placement of
bullet tip, 37, 37f
Chiba, 37, 37f
Day, 37, 37f
Huber, 37, 37f
pencil point, 36–37, 36f
Quincke, 36, 36f
Stealth™, 143, 144f
Nerve conduction study (NCS)
anatomy in
dermatome map, 88f
lower extremity schematic, 88, 89f
upper extremity schematic, 88f
defined, 87
described, 88–89
indications for, 87
median nerve, 89–90, 90f, 92f, 92t
motor nerve, 89–91, 92t
NCS stimulator in, 90f
peroneal motor nerve, 90–91, 91f
sensory nerve, 91, 92f
surface and needle electrodes in, 90f
technical considerations, 88
Neurolytic block(s). See also specific, e.g., Celiac plexus
agents for
alcohol, 666
phenol, 666
celiac plexus, 673
documentation for off-label indications, 667
epidural and transforaminal, 683–684
ganglion impar, 673–675
historical perspective, 666
informed consent to numbness in place of pain, 667
lumbar sympathetic neurolysis, 670, 671f, 672–673
diagnostic block, 667
sacroiliac joint, 677–679
selection criteria for, 667
spinal and epidural, 679–682
subarachnoid with alcohol, 682
subarachnoid with phenol, 683
superior hypogastric plexus, 675–677
trigeminal neurolysis, 668–670
Neuroma formation, with intercostal block, 700
Neuroma injections
equipment and supplies for, 432–433
goal of, 432
neuromas versus tender points, 432
postinjection instructions, 433
procedure, 433
Neuromas/ganglion cysts
tendon injection for, 476
Nucleoplasty. See also Percutaneous disc decompression (PDD)
animation of, 248f
coblation technology in, 246, 247
described, 246–247
Perc-D wand introduced into disc space, 247
probe entering disc space, 246f, 247f
probe in distal end of disc, lateral view, 247f
Numbness
from chemical neurolysis, 690
from neurolytic blocks, 667
O
Obturator nerve block
anatomy of obturator nerve, 531f
anterior branch, 530
posterior branch, 530
sagittal section, 530, 531f
in sensory innervation of hip, 530, 532f
complications of
laceration of corona mortis, 535
perforations, 535
contraindications to, 530, 533
equipment for, 533
neurostimulation technique, 533–534, 533f
proximal approach, 534–535
Occipital cryoneurolysis
closed technique for, 608f, 698
ultrasound guidance for probe advancement, 698, 698f
open operative technique for, 698
Occipital nerve block
cervico-trigeminal nucleus and, 137f
equipment for
for adhesiolysis, 141
for blind diagnostic or therapeutic, 141
for fluoroscopic diagnostic, 141
Stealth™ needle, 143, 144f
for ultrasound diagnostic, 141
indications for
occipital neuralgia and cervicogenic headache, 137
blind technique, 141
classic approach, 142, 142f
fluoroscopy-guided injections, 143
injection of lesser occipital nerve, 142–143
injection sites and landmarks, 142f
injection technique, 142, 143f
occipital adhesiolysis/suboccipital decompression, 143, 144f
Trescot approach, 142, 142f
ultrasound-guided injections, 143, 144f, 145f
preoperative consideration in, 140
Occipital nerve(s), 138f
connection between greater and lesser, 140f
dissection of, 139f
fluoroscopic location of, 141f
greater
and artery, 138, 138f
versus lesser occipital nerve pattern, 139f
parts of, 138, 139f
lesser, 139, 139f
infection of, 142–143, 143f
third, 140
Occipital nerve stimulation
anatomy in
anatomic landmarks in, 633
common injury sites and, 633
greater and lesser occipital nerves in, 633
assessment of results, criteria for, 634
complications of
hardware-related, 636
surgical, 636
electrode insertion, 635
landmarks for placement, 634
neurostimulation mechanisms, 632
permanent, 635–636
surgical procedure
anatomical landmarks, 634
anteroposterior fluoroscopy for electrode placement, 634
trial stimulation, 634
ultrasound probe placement, 634, 634f, 635f
ultrasound views, 634, 634f, 635f
Ophthalmic nerve block(s)
supraorbital, 127
supratrochlear, 127
Opiate trialing
continuous epidural infusion, 566–568, 567f, 568f
continuous intrathecal administration, 568–569
morphine single-shot injection, 569
Opioids, history of intrathecal use, 576
P
Pencil point needle, 36–37, 36f
Percutaneous disc decompression (PDD). See also Dekompressor; Nucleoplasty
characterization and techniques for, 241
contraindications and exclusion criteria for, 242–243
disc herniation
confirmation of contained, 241f
types of, 242f
equipment for, 243
ArthroCare Nucleopasty probe, 241, 241f
Stryker Disc Dekompressor, 241, 241f, 243
fluoroscopic views of, 243, 243f
monitored anesthesia care during, 242
patient education postprocedure, 248
patient selection criteria for, 231
potential complications of, 248
“Scottie dog” image for approach to, 241, 241f
techniques
decompression, 243, 244–246
initial steps, 244, 245f
nucleoplasty, 243, 246–248
Percutaneous facet fusion (PFF)
advantages of, 227
cortical bone allograft in, dowel shape, 228
described, 228
indications for procedure termination, 227
advance and tap cannulated facet distractor, 229, 229f
advance drill into directional cannula, 229
drill cores hole in facet joint, 229–230
fluoroscopic visualization in, 229
implant bone dowel in left and right L5-S1 facet joint, 230, 230f
Steinman pin placement, 229, 229f
lumbar facet joint
arthropathy of, 227–228
postoperative bracing with lumbosacral orthosis, 230
postprocedure monitoring
axial CT scan seated dowel at L5-S1, 231f
3D CT scan of TruFUSE implant, 231f
sagittal CT scan seated dowel at L4-5, 231f
postprocedure monitoring for potential complications, 230
cardiopulmonary safeguards, 228
intravenous access, 228
Percutaneous radiofrequency discectomy
anatomy of disc and
blood supply to, 257, 257f
nerve supply to, 257, 258f
Disk IT 11
described, 256
fluoroscopic views in, 258
for internal disc disruption-associated pain, 256
perioperative provocative manometric discopgraphy for, 257
equipment for
Disk IT 11 introducer, 260f
needles and electrodes, 259, 259f
Neurotherm NT1100 machine, 259, 259f, 260f
intraoperative technical steps
bilateral needle placement, 259f
identification of Kambin’s triangle, 258, 258f, 259f
square end plates of disc, 258
postprocedure instructions, 259–260
monitoring potential complications, 260
Periorbital nerve block(s)
anatomy in
infraorbital foramen, 147f
supraorbital notch, 147f, 151f
supratrochlear groove, 147f
supratrochlear nerve, 148, 149f
trigeminal pattern in, 147f
trigeminal terminal branches, 148f
contraindications to, 148, 148t
examination for
infraorbital, 149f
supraorbital, 149f
infraorbital, 149f, 150, 150f
intraoral approach, 150–151, 150f
infraorbital foramen and
3D reconstruction of, 151f
supraorbital, 148, 149f, 150f
supraorbital foramen and
infraorbital foramen and, 151f
supratrochlear, 150
Peripheral nerve field stimulation (PNFS), 650–651
patient selection for, 638–639
permanent implant, 652
trial of, 651–652, 652f
for chronic pancreatitis, 652f
duration of, 653
placement technique in, 651, 652f
for thigh pain, 652f
Peripheral nerve stimulation (PNS)
defined, 638
greater occipital nerve permanent implant, 646
greater occipital nerve trial
anatomy and anatomic dissection in, 643, 644f
medial, nuchal line approach, 644–645, 645f
percutaneous and paddle techniques for, 643–644, 645f
preparation for, 644
iliohypogastric/ilioinguinal, genitofemoral nerves trials, 650, 651f
imaging in
fluoroscopy, 640
ultrasound, 640
infraorbital nerve trial
lead placement in, 641–641, 643f
intercostal nerve trial, 650, 650f
lateral femoral cutaneous nerve trial, 649–650
patient selection for, 638–639
permanent implant
median, ulnar, and radial nerve, 646
peroneal nerve trial
popliteal fossa in, 648, 648f
sciatic nerve and, 648
technique in, 648–649
risk factors for infection, 640
saphenous nerve trial, 649, 649f
selection of needles, medications, and equipment for, 640–641
sites for, 639
supra- and infraorbital nerve permanent implant
introducer needle with stylet in place technique, 642
IPG placement in, 643
needle-over-stylet technique, 642
preparation for, 642
supraorbital nerve trial, 641, 641f
lead placement in, 641, 642f
surgical or percutaneous technique, 638
upper and lower extremity
median nerve trial, 646–647, 647f
radial nerve trial, 647–648, 647f
ulnar nerve trial, 646, 646f
Peripheral vascular disease, spinal cord stimulation for, 595
Peritoneum
penetration with genitofemoral nerve block, 516
perforation with ilioinguinal/iliohypogastric block, 509
Permanent intrathecal pump implant
anatomy in
location of pump, 577f
for needle insertion, 576, 577f
anesthesia for, 579
comparison of commercially available pumps, 579t
fluoroscopic views, 578
implantation technique
accessing intrathecal space, 579–580
anchoring of catheter, 580
creating pump pocket, 580
pump placement and catheter connection, 581
tunneling the intrathecal catheter, 580–581
wound closure and dressing, 581
medications for, 576, 576t
marking of pump pocket site, 578
optimal pump position, 578, 578f
patient multidisciplinary team, 577
trial methods for, 577
Peroneal peripheral nerve stimulation trial, 648–649, 648f
Phenol
ablation of iliohypogastric/ilioinguinal nerve, 508
for neurolytic blocks, 666
Piriformis, distal
anatomy of, 478–479, 478f
injection of, 484–485, 484f
Piriformis injection
equipment and medication for, 435
fluoroscopy-guided, 436–437
piriformis muscle outlined with dye injection, 435f
for piriformis syndrome, 434–435
ultrasound-guided
alternative approach, 437
classic technique, 437, 437f
confirmation of piriformis muscle, 437, 438f
postprocedure follow-up of, 442
Platelet GP IIb/IIIa receptor antagonists anticoagulation guidelines, 82
Plavix (clopidogrel) anticoagulation guidelines, 82
Pneumothorax risk
with intercostal block, 700
with splanchnic nerve block, 356, 356f
with suprascapular nerve block, 540, 541
with thoracic ganglion block, 349
with trigger point injections, 429
Pradaxa (dabigatran) anticoagulation guidelines, 80
Prilocaine metabolism and unique properties, 60
Procaine metabolism and unique properties, 61
Programmers for spinal cord stimulation system
Boston Scientific
Bionic navigator, 592f
Precision Plus system, 92f, 592
configuration of
amplitude, 591
frequency of electrical waves, 592
pulse width, 592
stimulating electrode in, 591
Medtronic N’Vision Clinician Programmer, 592
St. Jude Medical
active balancing programming, 593
Clinician programmer, 592
dynamic multiStim technology, 593
PC-stim programming, 593
Provocative discogram. See also specific, e.g., Cervical discogram
cervical, 234, 237
diagnostic purpose of, 233, 235, 271
equipment for
controlled injection syringe, 236
graphic pressure recording, 236f
numeric pressure reading printout, 236f
for single vs. dual needle technique, 234
fluoroscopic views
of “squared” lumbar disc, 235f
for various lumbar discs, 235, 235f
lumbar, 234, 235, 235f, 237
normal and abnormal findings, 237, 238f
contrast spread patterns, 237f
leaking disc, 238f
normal disc, 237, 238f
on postdiscogram CT scan, 239f
preferred technique
disc pressure monitor, 239f
dual needle set for, 239f, 240f
manometry with syringe and Stryker Disc monitor, 238
mixing technique, 238–239
needles in, 238
thoracic, 234, 237
Pterygopalatine fossa
boundaries of, 131
foramen and connections, 130, 131t
Pudendal nerve block
anatomy in, 522f
deep dissection of gluteal region, 523f
inferior rectal nerve, 522, 523f
pudendal bundle, 522
pudendal nerve branches, 521
complications of
intraoperative, 528
postoperative, 528
leg weakness
from sciatic nerve proximity, 528, 528f
options
botulinum toxin, 526–527
cryoanalgesia, 527
peripheral stimulation, 527
radiofrequency, 527
pararectal approach using PNS, 525
posterior approach
CT-guided, 526, 526f
using PNS and fluoroscopy, 525, 525f, 526f
for pudendal neuralgia
diagnosis of, 521
pudendal pain and, 521
risks with, 527–528
transperineal approach using PNS and fluoroscopy, 525, 525f
transvaginal approach
Iowa trumpet, 524f
Kobak needle, 524f
needles, equipment, and medications for, 524, 524f
technical steps, 524–525
Q
Quincke needle, 36, 36f
R
Racz procedure. See Epidural lysis of adhesions (Racz procedure)
Radiation safety
anatomic issues in, 30
C-arm fluoroscopes in
digital enhancement of image in, 33
digital subtraction angiography, 34
flat panel monitors, 34
pulsed mode delivery, 34, 34f
technique using, 34, 34f
collimation in, 8f
concerns and contraindications, 30
dosimetry badges for, 6
effects on human tissue, 31
fluoroscopic views and radiation exposure, 32–33, 32f, 33f
image intensifier placement and radiation scatter, 30, 31f
lead aprons and thyroid shields for operator, 9
leaded gloves, 9
maximum permissible dosages, 31
minimizing radiation during interventional procedures, 32
amount of radiation, 32
barriers and lead-based protection, 32
collimation to reduce x-rays emitted by tube, 33, 34f
distance, 32, 34f
reduction of exposure time, 32
occupational exposure
basic principles, 7–8
recommendations for, 6–7
patient injury from prolonged exposure, 7–8
protection standards for, 6
terminologies in, 30–31
yearly maximum allowable dose and effects on human tissue, 31
Radicular arteries, cervical, 116, 117f
Radiculomedullary arteries, 321, 321f, 322–323, 322f
Radiofrequency ablation
of iliohypogastric/ilioinguinal nerve, 508, 509
of sacroiliac joint, 217
Radiofrequency generator(s)
conventional, 39
cooled, 39
pulsed, 39
Radiofrequency neurolysis
defined, 703
for facet syndrome
median nerve branches innervating one facet joint, 703f, 704
pain distribution in, 703f
fluoroscopic views, 704–705, 706f
fluoroscopy-guided intraoperative steps
activation of RF generator, 707, 708f
anterior-posterior position, 707
fluoroscopy-guided intraoperative steps
motor stimulation, 708
needle positioning for lesioning, 708, 708, 709f
parallel cannula placement for lesioning, 707, 707f
patient positioning, 707, 708f
sensory stimulation, 707–708, 708f
visualization of superior articular process and transverse process, 707
imaging studies, 702
of lumbar facet joint/zygapophyseal joint
in pain generation, 702, 702f
mechanism of
current dispersal in, 703, 704f
temperature generation in, 703
patient positioning for, 705, 706
selection of needles, medication, and equipment for, 706
cannula, 706f
generator, 706f
grounding pad, 706
probe, 706f
Rhizotomy
chemical, 126
preprocedure diagnostic block, 128
thermal, 126, 128
for trigeminal ganglion and nerve block, 126, 128
Ropivacaine, metabolism and unique properties, 61
Rotator cuff muscles, trigger point injections for, 428
RX coudé needle, 38, 38f
S
Sacral insufficiency fractures
Dens classification of location, 222, 222f
diagnostic imaging of
MRI, 221
SPECT, Honda sign on, 222
T2-fat suppression image, 221, 222f
open vs. percutaneous reduction of, 221
osteoporotic, 221
percutaneous sacroplasty for. See Sacroplasty
Sacroiliac joint (SIJ)
anatomy in
cooled RF lesions, 208, 210f, 211f
diarthrodial classification of, 215
dorsal ramus of L5 nerve root, 208, 209f
fibrous articulation of sacrum and ilium, 215
inter- and intrapatient variation in, 215, 215f
muscles in, 216
S1-S3 lateral branches, 208, 210f
S1 superior articular process, 208, 209f
indications for radiofrequency denervation of, 216
innervation of, 208, 209f, 210f
lateral branches from S1 to S4 sacral foramen, 201f
ligaments of, 200, 201f
neuroanatomy of
innervation of anterior, 216
posterior surface, 216
neurolytic block of, 677–679
pain pattern secondary to joint pain, 200
pathology of in chronic low back pain, 216
physical examination of
Faber Patrick test, 201, 202f
Gaeslen’s test, 202, 202f
Gillet’s test, 202, 202f
sacroiliac shear test, 202
Yeoman’s test, 202, 202f
Sacroiliac joint (SIJ) denervation
blockade of L4 and L5 dorsal ramus and lateral branches of S1-S3, 205
equipment for, 203
fluoroscopic guidance in, 202, 203f
indications for
diagnostic, 202
therapeutic and prognostic, 203
intra-articular technique, 204, 204f
periarticular technique, 203–204, 205
Epsilon for spacing between target sites, 212
equipment for, 212
radiofrequency ablation in
strip lesioning technique, 206, 207
radiofrequency lesioning of lateral branches, 206, 207
Simplicity III procedure for. See Simplicity III radiofrequency neuroablation
technique
cold radiofrequency introducer in, 212, 213, 213f
pulsed spinal frequency ablation, 212
radiofrequency electrode position in, 213f
RF energy delivery in, 214
using synergy system
contraindications to, 209, 211
criteria for, 208–209
Sacroiliac joint (SIJ) injections, periarticular versus intra-articular, 200
Sacroiliac joint (SIJ) neurolysis
CT-guided
advancement of needle in, 677f, 678f, 679
contrast injection in, 678f, 679
injection of phenol in glycerin in, 679
selection of needles, medications, and equipment for, 678
Sacroplasty
basic concerns in, 223
defined, 221
polymethylmethacrylate (PMMA) cement in, 221, 223
structures relevant to, 222–223
technique
CT guidance in, 223
fluoroscopic guidance in, 223, 224f, 225f, 226f
for H-shaped fractures, 223, 224f
insertion of vertebroplasty trocars in, 223–224, 224f
PMMA cement placement in, 224–225, 225f, 226f
Saphenous peripheral nerve stimulation trial, 649, 649f
Scalene muscle injections
preprocedure imaging for, 443
for thoracic outlet syndrome, 442
ultrasound-guided technique
identification of brachial plexus at supraclavicular area, 444
identify external landmarks, 443
out-of-place needle approach in, 444, 444f
scalene muscle identification, 444
Sedation
choice of, 84
of chronic pain patient, relevant factors, 84–85
conscious, 84
diagnostic blocks, 86
intraoperative care, 86
multiple allergies and, 85
post anesthetic care, 86
preoperative anticoagulants and, 84–85
preoperative assessment for, 84–85
propofol administration, 84
realistic expectations of patient, 85–86
types of anesthesia
conscious sedation, 84
local, 84
regional, 84
typical agents for, 86t
Selective nerve root blocks. See Transforaminal epidural steroid injections
Simplicity III radiofrequency neuroablation
described, 215
equipment for
dispersal pad, 217
needles and syringe, 217
fluoroscopic guidance
anterior-posterior view of probe, 217, 217f
lateral view, 217
medications, 217
placement of Simplicity III probe
final position in AP and lateral views, 218–219, 218f, 219f
radiofrequency lesioning protocol
L5 primary dorsal ramus, 219–220, 220f
steps in, 219, 219f
strip lesion on piece of meat, 219, 219f
Simplicity II lesioning protocol for slender patients, 220
Simplicity probe III in, 217–218, 217f
technique
anesthetization of lesion track, 218
patient position in, 218
Sphenopalatine ganglion block
anatomy of
pterygopalatine fossa, 130–130, 131t
approaches to
transnasal, 132–133
transoral, 133
infrazygomatic approaches to
anterior, 132f, 133
coronoid, 132f, 133
technique, 132f, 133
medications for, 132–133
neuroanatomy of, 130
anticoagulation, 131
AP fluoroscopic view, 131, 132f
contrast allergy, 131
lateral fluoroscopic view, 131, 132f
radiofrequency ablation technique, 133, 134, 134f
efficacy of in cluster headache, 134–135
stimulation before attempting, 134, 134t
Spinal and epidural neurolysis including transforaminal
agents used for, 681f
anatomy in
membranes surrounding spinal cord, 681–682
spinal cord in, 680f
preprocedure review
of dermatome chart, 679f
of sclerotome chart, 679f
technique, hyperbaric(phenol) or hypobaric (alcohol), 680–681, 680f
Spinal cord stimulation (SCS)
advantages of, 584
device components in. See also specific, e.g., Anchors
anchors, 587
charger, 591–593
connecting extensions, 587
implantable pulse generators or battery, 588–589
leads, 585–587
programmer, 591
external neurostimulation trialing system
benefits of, 591
components of, 591
description of, 591
implantation of multiple leads, 593
implantation of two systems, 593
indications for
off-label, 584–585
on-label, 584
warnings with, 593–594
Spinal cord stimulation (SCS) trialing procedures
appropriate patient diagnoses for, 595
off-label indications for, 595
purposes of, 595
Spinal cord stimulation (SCS) implant
anatomy in
CSF space, 604, 604f, 605f
dorsal columns, 603–604, 604f
dorsal root entry zone, 604, 605f
epidural space, 603, 603f, 605f
complications of
biological, 618
technical, 618
equipment for
anchors, 607, 607t
percutaneous leads, 607
pulse generators, 607
rechargeable pulse generators, 608t
fluoroscopic views
lateral, 612–613, 613f
lead anchoring, 613
posteroanterior for lead steering, 613
posteroanterior, 612
pulsed mode fluoroscopy, 613
intraoperative steps in percutaneous trial, 608–609
cervical lead placement, 609, 611f, 612
lateral view, 609, 610f, 611f
lead placement, 609, 610f, 611f
lead steering into epidural space, 609, 610f
mid-thoracic lead placement, 612
needle bevels turned for lead steering, 609, 610f
needle entry into epidural space, 609
lead location and paresthesia coverage
cervical, 612
thoracic, 612
mechanism of action
current research in, 602
gate theory of pain, 602
parameters of stimulation, 607–608
amplitude, 608
frequency, 608
pulse width, 608
permanent
entry into epidural space, 610f, 615, 615f
fluoroscopic anatomy and incision, 613, 614f
generator site location and preparation, 616–617, 616f, 617f
lead anchoring, 607f, 615–616
lead placement in, 614–615, 615f, 616f
marking anatomical landmarks, 610f, 613
operative field preparation for, 614f, 6113
coagulopathy, 605
informed consent for, 604
patient position, 605–606
risk of revision surgery, 604–605
statement of medical necessity in, 602
technical details of procedure
needles, medications, and equipment selection, 606
positioning of patient, 606
Spinal cord stimulation (SCS) trialing procedures
anatomy in, 596
monitoring for complications, 599
percutaneous electrode placement
amplitude range for stimulation, 597, 597f
electrode designed for chronic therapy, 598
loss of resistance confirmation of epidural space entry, 597
multiple electrode arrays for trial, 597–598
place trial connector for pulse generator, 597
Tuohy needle interlaminar puncture, 596, 596f
plate/paddle trial electrode placement, 598–599
duration of trial, 599
Spinal stenosis
adjacent segmental disease with, 289
ligamentum hypertrophy in, 288, 289f
post laminectomy, 289
lumbar
anatomy in, 288f
neurogenic claudication in, 288
pathophysiology of, 288
treatment algorithm for, 287f
Splanchnic nerve block
anatomy in
greater splanchnic nerve, 351
lesser splanchnic nerve, 351
complications of
chylothorax, 356
pneumothorax, 356
CT imaging (anterior approach)
advantages of, 355
technique, 356
fluoroscopic posterior approach
AP view T12 vertebral body “squared off,” 352, 353f
contrast injection, oblique view, 353, 354f
CT reconstruction of needle placement, 354, 354f, 355f
diagnostic blocks, 354
final needle placement, lateral view, 352, 353f
initial needle placement, oblique view, 352, 353f
injection site, oblique view, 352, 353f
neurolytic blocks, 354
radiofrequency ablation, 354
fluoroscopic transdiscal approach, 355
fluoroscopic views for, 352
failure to respond to celiac plexus block, 356
needles and syringes for, 352
postprocedure considerations in
pneumothorax risk, 356, 356f
IV access, 352
splanchnic nerve anatomy and, 351f
Stealth™ needle, 143, 144f
Stellate ganglion block
anatomy in
carotid and vertebral arteries in, 341–342
cervical sympathetic chain and, lying over longus colli muscle, 336, 338f
cervicothoracic (stellate) ganglion, 336, 337f
anterior paratracheal (classic) approach, 340, 341f
equipment for, 338
fluoroscopic views in anteroposterior
approach, 337, 339f
oblique approach, 337, 339f
needles and supplies, 337–338
oblique approach to
anteroposterior view of injectate, 340, 340f
AP view in, 339, 339f
fluoroscopic oblique view in, 339, 340f
injection of anesthetic or steroid, 340, 340f
injection of contrast in, 339–340, 340f
needle placement in, 339
patient preparation for, 338–339
posterior approach, 342
patient education in post procedural effects, 336–337
previous neck or thyroid surgery, 336
Subarachnoid neurolysis
agents used for, 680–681, 681t
with alcohol, intraoperative steps, 682–683
with phenol, intraoperative steps, 683
Sufentanil
non-FDA-approved for intrathecal use, 566
Superior hypogastric plexus neurolysis
anatomy in, 676
complications of, 677, 679
described, 675–676
anterior-posterior, 675f
lateral, 675f
advancement of needle, 677
injection of contrast, 677
injection of phenol in glycerin, 677
scout film of lumbar spine, 677
Supraclavicular nerve block
anatomy in
brachial plexus, 495–496
relationship of brachial plexus trunks to subclavian artery, 495f
relationship of subclavian artery and vein in, 496, 496f
nerve stimulator technique
landmarks for, 496, 497f
ultrasound technique
anatomy for supraclavicular brachial plexus block, 498f
probe in, 497
probe position in, 497, 498f
setup of probe and needle in, 499, 499f
Supraorbital nerve
peripheral nerve stimulation trial, 641, 641f, 642f
permanent implant, 642–643
Supraorbital nerve cryoneuroablation
anatomy in, 695
supratrochlear nerve, 695, 695f
technique, 696f
closed, 695
open operative, 695
Supraorbital neuralgia, 694–695
Suprascapular nerve block
anatomy in
important to performance of block, 538
motor nerves to supraspinatus and infraspinatus muscle, 537
sensory nerve branches, 537
suprascapular artery, 538
suprascapular nerve in relation to muscles and vasculature, 538f
suprascapular notch, 537–538
supraspinous fossa, 537
classic approach (Wertheim), 539–540, 539f, 540f
Dangoisse-modified method, 540, 540f
fluoroscopic image of, 540f
equipment for
in blind approach, 538
in fluoroscopic procedure, 539
in ultrasound block, 538
historical perspective on, 537
pneumothorax risk with, 540, 541
suprascapular nerve described, 537
ultrasound-guided, 541
Supraspinous/interspinous ligaments
anatomy of, 477–478, 478f
injection of, 482–483, 483f
Syringes, specialized, 40, 40f
T
Tendinopathy/tendonosis
tendon injection for, 476, 477f
Tendon injection(s)
anatomy in
bicipital tendonitis/tendonosis, 476, 477f
distal piriformis, 478–479, 478f
iliolumbar ligament, 479, 479f
lateral epicondylosis/epidondylitis, 477, 478f
levator scapula, 477, 477f
supraspinous/interspinous ligaments, 477–478, 478f
of bicipital tendon, 480, 480f, 481f
of distal piriformis, 484–485, 484f
equipment and medications, 480
fluoroscopic/ultrasound views, 479–480
of iliolumbar ligament, 483, 484f
of lateral epicondyle, 481–482, 482f
of levator scapula, 481, 481f
of supraspinous/interspinous ligament, 482–483, 483f
Tennis elbow
extensor carpi radialis brevis muscle and common extensor tendon injections for, 415
Tetracaine metabolism and unique properties, 61–62
Thermal rhizotomy, for trigeminal ganglion block, 126, 128
Thoracic disc anatomy, 234
Thoracic discogram. See also Provocative discogram
injection of contrast in, 237
needle advancement to middle of disc under fluoroscopic guidance, 237
patient position in, 237
Thoracic DRG block
fluoroscopic views
oblique, 197, 197f
preferred technique
digital subtraction fluoroscopy in, 197
pulsed-dose low-frequency in, 198
sensory and motor stimulation in, 198
Thoracic (T2-3) ganglion block
anatomy and
autonomic nervous system, 344
radiologic landmarks for oblique technique, 345, 345f
sympathetic trunk and, 344f
thoracic ganglia, 344–345
basic concerns
risk of pneumothorax, 345, 347
complications of
pneumothorax, 349
equipment for, 345
indications for, 343t
pain syndromes, 343
vascular insufficiency, 344
intercostal oblique approach to sympathetic ganglia
AP fluoroscopic view and, 347, 348f
“gunsight” view of needle and target in, 347, 348f
laser sighting device and, 347
needle insertion in, 347, 348f
ribs and their articulations in, 346f, 347
neurolytic procedure
phenol in, 349
radiofrequency ablation in, 349
oblique technique, 345, 345f
advantages of, 345
paraspinous approach
anatomy, 346f
needle insertion in, 346
radiofrequency lesioning in, 346–347
Thoracic interlaminar epidural steroid injections. See also Interlaminar epidural steroid injection
paramedian approach, 158, 159f
Thoracic outlet syndrome
anterior scalene muscle injection with local anesthetic for, 443
scalene muscle injections for, 442
Thoracolumbar spine interventions, vascular complications in, 319–320
Ticlid (ticlopidine), anticoagulation guidelines for, 82
Ticlopidine (Ticlid), anticoagulation guidelines for, 82
Touhy needle, 37, 38f
with flexible introducer cannula, 38, 38f
Transducers
in portable ultrasound machine
frequency ranges in, 20–21
types of, 20, 21f–22f
Transforaminal epidural steroid injection (TFESI)
advantages of, 162
cervical spine, 327–331
safe performance of, Kambin vs. “safe triangle” approach for, 324–325, 324f, 325f
technique in Kambin triangle
final needle position, 325, 326f, 327f
injection of dye following, 327f
oblique approach, 325, 325f
skin entry site, 325, 325f
thoracolumbar, 319
vascular complications of, 324–325, 324f, 325f
Triamcinolone acetonide, depot
adrenal suppression with, 45t
Trigeminal ganglion
anatomy of
external landmarks, 123
mandibular division, 122
maxillary division, 122
Meckel cavity and, 122
ophthalmic division, 122
radiographic, 122
Trigeminal ganglion nerve block
chemical rhizotomy, 126
fluoroscopic views of
AP, 123, 123f
lateral, 123, 124f
oblique, 123, 124f, 125
submental, 123, 124f
anticoagulation, 123
conscious sedation, 123
pulsed radiofrequency, 126–127
technique
advance needle through foramen ovale, 125, 125f
aspirate, 125–126
inject contrast and local anesthetic, 125
insert block needle, 125, 125f
oblique image intensifier, 125, 125f
patient preparation, 124
thermal rhizotomy
lesioning in, 126
lesioning of ophthalmic division, 128
radiofrequency needle in, 126
Trigeminal nerve division blocks
mandibular nerve block
maxillary nerve block, 127
intraorbital, 127
maxillary, 128
radiofrequency, 128
ophthalmic
for supraorbital nerve, 127
for supratrochlear nerve, 127
Trigeminal neuralgia
balloon compression for, 661
diagnosis of, 656
glycerol infusion for, 661
medical therapy for, 657
problems with, 657
microvascular decompression for, 657–658
procedure in, 658, 659f
of superior cerebellar artery, 658, 658f
motor cortex stimulation for, 662
neuromodulation therapies for, 661–662
versus other facial pain disorders, 656
pathophysiology of, 656–657
percutaneous lesioning at gasserian ganglion for, 659
anatomy in, 660f
biplane fluoroscopy in, 659, 660f
radiofrequency thermocoagulation lesioning, 659
recurrence rate with, 660
steps in, 659–660
peripheral facial stimulation
advantages of, 662
localization of electrode for, 662, 663f
nonapproved, 662
uses of, 663
stereotactic radiosurgery for, 661
surgical therapy for, 657
Trigeminal neurolysis
CT-guided
advancing needle tip in relationship to foramen ovale, 668f, 669f, 670
contrast in Meckel cave, 669f, 670
injection of absolute alcohol, 670
needle placement in, 668f
needle tip entering foramen ovale, 668f
patient position in, 668f, 670
Trigger point injections, 434
basic concerns, 434
defined, 428, 434
equipment and supplies for, 428–429, 429f
example of, 430f
goal of, 428
mark trigger points with reference zone marked, 429, 430f
postinjection instructions, 429
technique, 435
trigger points and, 434
U
Ultrasound
advantages of, 20t
basic physics of
acoustic impedance, 19
attenuation, 19
common procedures performed with, 20t
principles of
in medical imaging, 20
scattering in, 20
specular reflection in, 20
transducers in, 20
Ultrasound imaging
advances in
echogenic needles coated with nanoparticles, 28, 28f
needle optimization technology, 29, 29f
three-dimensional, 28, 28f
artifacts in
anisotropy, 28–29
comet tail, 27, 27f
enhancement, 26, 27f
mirror images, 26f, 27
reverberation, 27, 27f
ergonomics during, 27–28
limitations of, 26, 26f
recommendations for, 29
Ultrasound portable machine
image optimization during scanning, 26t
image optimization functions
depth, 22, 23f
focus, 22
gain, 22, 23f
tissue harmonic imaging, 23–24
zoom, 23
transducers in
frequency ranges in, 20–21
types of, 20, 21f–22f
troubleshooting if needle not visualized, 25–26
Ultrasound sonopathology, 26, 26f
Upper extremity
electromyography of, 88f, 92, 94f
V
Vascular complications of spinal interventions
anatomy and
artery of Adamkiewicz, 321, 322f, 323–324
radiculomedullary arteries, 321, 321f, 322–323, 322f
“safe triangle “ in, 321f
in cervical spine, 319–320, 327–329
embolism theories of vascular injury, 330
other mechanisms of, 330
intravascular uptake
technique modifications to detect, 330–331, 332f
intravascular uptake prevention
epimed blunt-tipped needle, 332f
interlaminar approach with steerable catheter, 332, 332f
technique modifications for, 330–332, 333
use of nonparticulate steroid, 331–332
radiculomedullary arteries, 322, 322f
in lumbar spine, 322
nervous system branches, 323
spinal canal branches, 323
in thoracic spine, 322
spinal cord injury
from lumbar transforaminal procedures, 320, 321f
from vascular ischemia, 320–321
sympathetic blocks or neurolytic procedures
in sympathetic blocks or neurolytic procedures, 325–326, 327f
oblique approach, 326
transdiscal approach, 326, 327f
in thoracolumbar spine, 319–320
indications for interventional procedures in, 320
procedures and procedure-related complications, 320
in transforaminal epidural steroid injections, 324–325, 324f, 325f
vascular injury, theories of, 321
vascular supply of spinal cord
artery of Adamkiewicz, 321, 322f
radiculomedullary arteries, 321f, 322, 433f
vascular uptake of dye and steroid, protective strategies against, 324
Vertebral augmentation. See also Kyphoplasty; Vertebroplasty
anatomy in, 299
historical perspective on, 298
kyphoplasty for, 306f, 307–308
for osteoporotic vertebral compression fracture, 298–299
goal of, 299
vertebroplasty for, 299–306
Vertebral compression fracture, 298, 299
Vertebroplasty. See also Kyphoplasty; Vertebral augmentation
complications of
aortic embolism, 309, 311f
cement embolization into lungs and cerebral circulation, 309
cement extravasation in, 308, 308f, 309
cement extrusion, 308
intradural leakage, 310f
nerve root severed, 309, 311f
pedicle fracture, 309, 311f
posterior leakage, 309, 310f
transient radiculopathy, 308
needle placement in
AP and lateral views for correct, 312, 312f
guide for, 312, 312f
needle trajectories, unsafe, 312, 313f
parapedicular approach
in thoracic spine above T8, 306
C-arm fluoroscopy, 301f
CT guidance, 299
fluoroscopy, 301, 302f
imaging in, 300
real-time imaging in, 299, 300
spinal needle entry into vertebral body, 300f
transpedicular approach
danger zone in, 305, 305f
injection of cement, 303, 305, 305f
safe deposit of cement in, 303
“Scottie dog” view of vertebral body in, 301, 303f
unipedicular versus bipedicular needle in, 303, 305f
views of vertebroplasty needle in pedicle, 301–302, 303f
Viscosupplement
FDA approval of, 419
intra-articular injection in knee, 423f, 424–425, 424f
injection site preparation for, 423f, 424
marking anatomical landmarks, 423f, 424
needle directed to enter joint capsule, 424–425, 424f
needles and equipment for, 424
patella tilt for, 424f, 425
positioning for, 422–423, 423f
manufacturer and brand information, 419t
W
Warfarin (Coumadin), anticoagulation guidelines for, 79–80
X
X-rays
fluoroscopic image analogous to photographic negative, 3, 3f
physics of, 2–3
plain radiography, chest, analogous to photograph, 4f
Z
Ziconotide, intrathecal for neuropathic pain, 565
Ziconotide trialing
bolus trials, single or multiple injections, 572
continuous intrathecal infusion, 570–571
equipment for needle placement, 566, 567f
procedure for, 571–572
psychosis as side effect of, 570–571
single-shot trial procedure, 572–583
limited duration trials, 571
single-shot trial procedure, 572

Atlas of Pain Medicine Procedures PDF

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SECTION I: Basic Applications Mark J. Lema

SECTION II: Head and Neck Injections Sudhir Diwan

SECTION III: Spinal Interventions Vikram B. Patel

SECTION IV: Sympathetic Blocks Andrea Trescot

SECTION V: Musculoskeletal Injections Vijay Vad

SECTION VI: Peripheral Nerve Blocks Christopher Gharibo

SECTION VII: Intrathecal Drug Delivery Peter S. Staats

SECTION VIII: Neuroaugmentation Techniques Sudhir Diwan

SECTION IX: Neurolytic Procedures Rinoo V. Shah

Section III: Spinal Interventions- Vikram B. Patel, MD, FIPP, DABIPP

Section IV: Sympathetic Blocks- Andrea Trescot, MD, ABIPP, FIPP

Section V: Musculoskeletal Injections- Vijay Vad, MD

Section VI: Peripheral Nerve Blocks- Christopher Gharibo, MD

Section VIII: Neuroaugmentation Techniques- Sudhir Diwan, MD, DABIPP, FIPP

Section IX: Neurolytic Procedures- Rinoo V. Shah, MD

Nirmala R. Abraham, MD, FABPM (Chapter 10)

Gerard W. Abrahamsen, PA-C (Chapter 32)

Marina V. Abramova, MD (Chapter 74)

David B. Albert, MD (Chapter 58)

Kenneth M. Alo, MD (Chapter 74)

Robert Altman, MD (Chapter 58)

Charles E. Argoff, MD (Chapter 8)

Juan Francisco Asenjo, MD, FRCPC (Chapter 54)

Arthur Atchabahian, MD (Chapter 63)

Steve M. Aydin, DO (Chapter 64)

Sanjay Bakshi, MD, D.A.B.P.M (Chapter 32)

Robert Balch III, DO (Chapter 56)

Marshall D. Bedder, MD, FRCP (C) (Chapter 72)

Ramsin Benyamin, MD, DABIPP (Chapter 39)

Honorio T. Benzon, MD (Chapters 26 and 54)

Michael M. Bottros, MD (Chapter 78)

Lora L. Brown, MD (Chapter 38)

Michael N. Brown, MD (Chapter 55)

Allen Burton, MD (Chapter 39)

Kenneth D. Candido, MD (Chapters 17, 45, 46 and 77)

David Caraway, MD, PhD (Chapter 65)

Bridget T. Carey, MD (Chapter 12)

Ronil V. Chandra, MBBS, FRANZCR (Chapter 2)

Kenneth Chapman, MD, FIPP (Chapter 37)

Susanti Chowdhaury, MD (Chapter 62)

Harold Cordner, MD, FIPP (Chapter 29)

Sukdeb Datta, MD, MBA (Chapter 23)

Samyadev Datta, MD, FRCA (Chapter 34)

Nimish Davé, MD, MPH (Chapter 28)

Miles Day, MD, FIPP, DABIPP (Chapter 17)

Timothy R. Deer, MD (Chapters 67, 73 and 75)

Didier Demesmin, MD (Chapter 33)

Lisa Doan, MD (Chapter 58)

Raj Doshi, MD (Chapter 21)

Christine E. Draper, PhD (Chapter 73)

Richard S. Epter, MD, DABAPM, DABIPP, DABPM, FIPP (Chapter 42)

Michael A. Erdek, MD (Chapter 78)

Michael E. Frey, MD (Chapter 29)

Christopher Gharibo, MD (Chapters 6, 24 and 64)

Scott E. Glaser, MD, DABIPP (Chapter 41)

Stanley Golovac, MD (Chapter 16)

Gail Gray, ARNP (Chapter 62)

Eric J. Grigsby, MD (Chapters 73 and 75)

Karina Gritsenko, MD (Chapter 69)

Amitabh Gulati, MD, FIPP (Chapter 57)

Salim M. Hayek MD, PhD (Chapter 71)