DEDICATION
I dedicate this book to Dr. Jerry Darius Vloka,
a peerless scholar whose contribution to and teaching of
regional anesthesia have provided an educational platform and
inspiration for generations of practitioners and academicians alike.
You are a beacon of light and a paragon of scholarship and virtue.
I am profoundly privileged to number you among my closest friends.
May many generations of students slake their thirst at the well of your wisdom,
and may our friendship outpace the ravages of time.
With love and respect,
Admir
“Tell me what company thou keepst, and I’ll tell thee what thou art.”
Cervantes
CONTENTS
Contributors
reface
Acknowledgments
SECTION 1
FOUNDATIONS OF PERIPHERAL NERVE BLOCKS
Essential Regional Anesthesia Anatomy
Admir Hadzic and Carlo Franco
Local Anesthetics: Clinical Pharmacology and Rational Selection
Jeff Gadsden
Equipment for Peripheral Nerve Blocks
Ali Nima Shariat, Patrick M. Horan, Kimberly Gratenstein, Colleen McCally, and Ashton P.
Frulla
Electrical Nerve Stimulators and Localization of Peripheral Nerves
Martin Simpel and Andre van Zundert
Monitoring and Documentation
Jeff Gadsden
Indications for Peripheral Nerve Blocks
Jeff Gadsden
Continuous Peripheral Nerve Blocks in Outpatients
Brian M. Ilfeld, Elizabeth M. Renehan, and F. Kayser Enneking
Regional Anesthesia in the Anticoagulated Patient
Honorio T. Benzon
Toxicity of Local Anesthetics
Steven Dewaele and Alan C. Santos
0. Neurologic Complications of Peripheral Nerve Blocks
Jeff Gadsden
SECTION 2
NERVE STIMULATOR AND SURFACE-BASED NERVE BLOCK TECHNIQUES
1. Cervical Plexus Block
2. Interscalene Brachial Plexus Block
3. Supraclavicular Brachial Plexus Block
4. Infraclavicular Brachial Plexus Block
5. Axillary Brachial Plexus Block
6. Wrist Block
7. Cutaneous Nerve Blocks of the Upper Extremity
8. Lumbar Plexus Block
9. Sciatic Block
art 1. Transgluteal Approach
art 2. Anterior Approach
0. Popliteal Sciatic Block
art 1. Intertendinous Approach
art 2. Lateral Approach
1. Femoral Nerve Block
2. Ankle Block
3. Thoracic Paravertebral Block
4. Intercostal Block
SECTION 3
INTRAVENOUS REGIONAL ANESTHESIA
5. Bier Block
SECTION 4
FOUNDATIONS OF ULTRASOUND-GUIDED NERVE BLOCKS
6. Ultrasound Physics
Daquan Xu
7. Optimizing an Ultrasound Image
Daquan Xu
SECTION 5
ULTRASOUND-GUIDED NERVE BLOCKS
8. Ultrasound-Guided Cervical Plexus Block
9. Ultrasound-Guided Interscalene Brachial Plexus Block
0. Ultrasound-Guided Supraclavicular Brachial Plexus Block
1. Ultrasound-Guided Infraclavicular Brachial Plexus Block
2. Ultrasound-Guided Axillary Brachial Plexus Block
3. Ultrasound-Guided Forearm Blocks
4. Ultrasound-Guided Wrist Block
5. Ultrasound-Guided Femoral Nerve Block
6. Ultrasound-Guided Fascia Iliaca Block
7. Ultrasound-Guided Obturator Nerve Block
8. Ultrasound-Guided Saphenous Nerve Block
9. Ultrasound-Guided Sciatic Block
art 1. Anterior Approach
art 2. Transgluteal and Subgluteal Approach
0. Ultrasound-Guided Popliteal Sciatic Block
1. Ultrasound-Guided Ankle Block
2. Common Ultrasound-Guided Truncal and Cutaneous Blocks
art 1. Transversus Abdominis Plane Block
art 2. Iliohypogastric and Ilioinguinal Nerve Blocks
art 3. Rectus Sheath Block
art 4. Lateral Femoral Cutaneous Nerve Block
SECTION 6
ULTRASOUND-GUIDED NEURAXIAL AND PERINEURAXIAL BLOCKS
3. Introduction
Manoj Karmakar and Catherine Vandepitte
4. Spinal Sonography and Considerations for Ultrasound-Guided Central Neuraxial Blockade
Wing Hong Kwok and Manoj Karmakar
5. Sonography of Thoracic Paravertebral Space and Considerations for Ultrasound-Guided Thoracic
Paravertebral Block
Catherine Vandepitte, Tatjana Stopar Pintaric, and Philippe E. Gautier
6. Ultrasound of the Lumbar Paravertebral Space and Considerations for Lumbar Plexus Block
Manoj Karmakar and Catherine Vandepitte
SECTION 7
ATLAS OF ULTRASOUND-GUIDED ANATOMY
SECTION 8
ATLAS OF SURFACE ANATOMY
Index
CONTENTS FOR DVD
5 NERVE BLOCKS FOR 95% OF INDICATIONS
Ultrasound-Guided Interscalene Block
Ultrasound-Guided Supraclavicular Block
Ultrasound-Guided Axillary Block
Ultrasound-Guided Femoral Nerve Block
Ultrasound-Guided Popliteal Block
CONTRIBUTORS
Marina Alen, MD
Fellow, Regional Anesthesia
St. Luke’s–Roosevelt Hospital Center
New York, New York
Honorio T. Benzon, MD
Professor
Department of Anesthesiology
Feinberg School of Medicine
Northwestern University
Chicago, Illinois
Rafael Blanco, MD
MBBS, F.R.C.A., D.E.A.A. & Intensive Care
Consultant Anaesthesiologist
Complexo Hospitalario Universitario A Coruña
Spain
Ana Carrera, PhD, MD
Lecturer of Human Anatomy
Faculty of Medicine
University of
Girona Girona, Spain
Lorenzo Casertano, CSCS
Physical Therapy
Columbia University, New York, New York
Junping Chen, MD
Fellow, Regional Anesthesia
St. Luke’s–Roosevelt Hospital Center
New York, New York
Thomas B. Clark, DC, RVT
Adjunct Professor of Radiology
Department of Radiology
Logan College of Chiropractic
St. Louis, Missouri
Adam B. Cohen, MD
Attending Physician
Department of Orthopedic Surgery
St. Luke’s–Roosevelt Hospital Center
New York, New York
Jose De Andrés, MD, PhD
Head of Department
Department of Anesthesia
Hospital General Universitario
Valencia. Spain
Belen De Jose Maria, MD, PhD
Senior Pediatric Anesthesiologist
Department of Pediatric Anesthesia
Hospital Sant Joan de Deu
Barcelona, Spain
Jeffrey Dermksian, MD
Assistant Clinical Professor
Department of Orthopaedic Surgery
Columbia University
New York, New York
Steven A. Dewaele, MD
Associate Consultant
Department of Anesthesiology and Intensive Care
AZ St Lucas
Ghent, Belgium
Tomás Domingo, MD
Pain Unit, Department of Anaesthesiology
Hospital Universitari de Bellvitge
Associate Professor, Human Anatomy
Universitat de Barcelona, Campus de Bellvitge
Barcelona, Spain
F. Kayser Enneking, MD
Professor and Chair
Department of Anesthesiology
University of Florida
Gainesville, Florida
Carlo D. Franco, MD
Professor
Department of Anesthesiology and Anatomy
J.H.S. Hospital Cook County
Rush University Medical Center
Chicago, Illinois
Ashton P. Frulla, BS
Research Assistant
Department of Anesthesiology
St. Luke’s–Roosevelt Hospital
New York, New York
Jeff Gadsden, MD, FRCPC, FANZCA
Assistant Professor of Clinical Anesthesiology
Department of Anesthesiology
College of Physicans and Surgeons
Columbia University
New York, New York
Philippe E. Gautier, MD
Head of Department
Department of Anaesthesia
Clinique Ste Anne-St Remi
Brussels, Belgium
Kimberly Gratenstein, MD
Regional Anesthesia Fellow
Department of Anesthesiology
St. Luke’s–Roosevelt Hospital
New York, New York
Fermin Haro-Sanz, MD
Associate Professor
Anestesiologia Reanimación Terapia del Dolor
Universidad de Navarra
Navarra, Spain
Paul Hobeika, MD
Assistant Professor of Orthopedic Surgery
Department of Orthopedics and Orthopedic Surgery
St. Luke’s–Roosevelt Hospital
College of Physicians and Surgeons Columbia University
New York, New York
Patrick Horan, MPH
Research Fellow
Department of Anesthesiology
St. Luke’s–Roosevelt Hospital
Center New York, New York
Brian M. Ilfeld, MD, MS (Clinical Investigation)
Associate Professor in Residence
Department of Anesthesiology
University of California, San Diego
San Diego, California
Manoj Kumar Karmakar, MD, FRCA, FHKCA, FHKAM
Associate Professor and Director of Paediatric Anesthesia
Department of Anaesthesia and Intensive Care
The Chinese University of Hong Kong
Prince of Wales Hospital
Shatin, New Territories
Hong Kong
Kwesi Kwofie, MD
Fellow, Regional Anesthesia
St. Luke’s–Roosevelt Hospital Center
New York, New York
Wing Hong Kwok, FANZCA
The Chinese University of Hong Kong
Prince of Wales Hospital
Shatin, New Territories
Hong Kong
Manuel Llusa, MD, PhD
Associate Professor
Department of Human Anatomy and Embryology
University of Barcelona
Barcelona, Spain
Ana M. López, MD, PhD
Senior Specialist
Department of Anesthesiology
Hospital Clínic
Barcelona, Spain
Philippe B. Macaire, MD
Senior Consultant
Department of Anesthesiology and Pain Management
Rashid Hospital
Dubai, United Arab Emirates
Thomas Maliakal, MD
Resident
Department of Anesthesiology
St. Luke’s–Roosevelt Hospital Center
New York, New York
Josep Masdeu, MD
Department of Anesthesia
Hospital Moisés Broggi
Consorci Sanitari Integral
Barcelona, Spain
Colleen E. McCally, DO
Regional Anesthesia Fellow
St. Luke’s–Roosevelt Hospital Center
New York, New York
Carlos Morros, MD, PhD
Associate Professor
Department of Anesthesia
Clínica Diagonal. Barcelona. Spain
Alberto Prats-Galino, MD, PhD
Professor
Laboratory of Surgical Neuro-Anatomy
Human Anatomy and Embryology Unit
Faculty of Medicine
University of Barcelona
Barcelona, Spain
Miguel Angel Reina, MD, PhD
Associate Professor
Department of Clinical Medical Sciences and Research
Laboratory of Histology and Imaging
Institute of Applied Molecular Medicine
CEU San Pablo University
School of Medicine
Madrid, Spain
Wojciech Reiss, MD
Fellow, Regional Anesthesia
St. Luke’s–Roosevelt Hospital Center
New York, New York
Elizabeth M. Renehan, MD, MSc, FRCPC
Department of Anesthesiology
University of Florida
Gainesville, Florida
Teresa Ribalta, MD, PhD
Professor of Pathology
Department of Anatomical Pathology
Hospital Clínic
University of Barcelona Medical School, IDIBAPS
Barcelona, Spain
Vicente Roqués, MD, PhD
Consultant Anaesthetist
Anesthesia and Intensive Care
Hospital Universitario Virgen de la Arrixaca
Murcia, Spain
Xavier Sala-Blanch, MD
Staff Anesthesiologist
Department of Anesthesia
Hospital Clinic
University of Barcelona
Barcelona, Spain
Carlos H. Salazar-Zamorano, MD
Attending Anesthesiologist
Anesthesia Resident Coordinator
Department of Anesthesiology
Hospital de Figueres
Figueres, Spain
Gerard Sanchez-Etayo, MD
Department of Anesthesiology
Hospital Clinic
Barcelona, Spain
Alan C. Santos, MD, MPH
Professor of Anesthesiology
College of Physicians and Surgeons
Columbia University
New York, New York
Chairman of Anesthesiology
St. Luke’s–Roosevelt Hospital Center
New York, New York
Luc A. Sermeus, MD
Lector, Department of Anesthesiology
University of Antwerp
Wilrijk, Belgium
Ali Nima Shariat, MD
Clinical Instructor
Department of Anesthesiology
St. Luke’s–Roosevelt Hospital Center
New York, New York
Uma Shastri, MD
Fellow, Regional Anesthesia
St. Luke’s–Roosevelt Hospital Center
New York, New York
Sanjay K. Sinha, MBBS
Director of Regional Anesthesia
Department of Anesthesiology
St. Francis Hospital and Medical Center
Hartford, Connecticut
Dr. rer. nat. Martin Sippel
Senior Vice President
Center of Excellence in Pain Control and CVC
B. Braun Melsungen AG
Melsungen, Germany
Leroy Sutherland, MD
Fellow, Regional Anesthesia
St. Luke’s–Roosevelt Hospital Center
New York, New York
Douglas B. Unis, MD
Assistant Clinical Professor
Department of Orthopaedic Surgery
College of Physicians and Surgeons
Columbia University
New York, New York
Catherine F. M. Vandepitte, MD
Consultant Anesthesiologist
Katholieke Universiteit
Leuven Leuven, Belgium
André van Zundert, MD, PhD, FRCA, EDRA
Professor of Anesthesiology
Catharina Hospital
Eindhoven, Netherlands
University Maastricht
Maastricht, Netherlands
University of Ghent
Ghent, Belgium
Chi H. Wong, MS, DO
Anesthesiology Resident
Department of Anesthesiology
Yale New Haven Hospital
New Haven, Connecticut
Daquan Xu, MD, MSc, MPH
Research Associate
Department of Anesthesiology
St. Luke’s–Roosevelt Hospital Center
New York, New York
Tatjana Stopar Pintaric, MD, PhD, DEAA
Associate Professor of Anesthesiology
University Medical Center Ljubljana
Ljubljana, Slovenia
PREFACE
Peripheral Nerve Blocks and Anatomy for Ultrasound-Guided Regional Anesthesia, second edition,
is being published at an exciting time in the development of regional anesthesia. Reflecting on the first
edition of the book,*
we believe its success was due largely to the tried-and-true nature of the
material taught. It would not be an overstatement to say that the first edition of this book influenced
professional lives of many colleagues and ultimately benefited patients worldwide. The success
helped garner the New York School of Regional Anesthesia (NYSORA) additional esteem that it
enjoys today. In line with the philosophy of the first edition, this second edition minimizes
presentation of theoretical considerations. Instead, the featured techniques and teachings are gleaned
directly from the trenches of the clinical practice of regional anesthesia.
In recent years, the field of regional anesthesia, and in particular peripheral nerve blockade, has
entered an unprecedented renaissance. This renaissance is due primarily to the widespread
introduction of ultrasound-guided regional anesthesia. The ability to visualize the anatomy of interest,
the needle–nerve relationship, and the spread of the local anesthetic has resulted in significant growth
of interest in and use of peripheral nerve blocks. Regardless, many aspects of ultrasound-guided
regional anesthesia still require clarification and standardization. Examples include dilemmas
regarding the ideal placement of the needle for successful and safe blockade, the number of injections
required for individual techniques, the volume of local anesthetic for successful blockade, the
integration of additional monitoring tools such as nerve stimulation and injection pressure monitoring
and many others. For these reasons, we decided to defer publication of the second edition and opted
to wait for clarification from clinical trials or collective experience to provide more solid
recommendations. As a result, just as with the first edition, the second book features only tried-andtrue descriptions of peripheral nerve block techniques with wide clinical applicability rather than a
plethora of techniques and modifications that have mere theoretical considerations. Where the
collective experience has not reached the necessary level to recommend teaching a certain technique
(e.g., neuraxial blocks), we opted to feature anatomic considerations rather than vague or
inadequately developed technique recommendations, which may lead to disappointments, or possibly
complications, if they are adopted without careful consideration.
The second edition is organized as a collection of practical introductory chapters, followed by
detailed and unambiguous descriptions of common regional anesthesia block procedures rather than
an exhaustive theoretical compendium of the literature. Although ultrasound guidance eventually may
become the most prevalent method of nerve blockade globally, most procedures world-wide are still
performed using the methods of peripheral nerve stimulation and/or surface landmarks, particularly in
the developing world. Because this book has been one of the main teaching sources internationally,
we decided to retain the section on the traditional techniques of nerve blockade in addition to the new
section on ultrasound-guided regional anesthesia. Since knowledge of surface anatomy is essential for
practice of both traditional and ultrasound regional anesthesia procedures, we decided to also add an
Atlas of Surface Anatomy (Section 8).
The book is organized in eight sections that progress from the foundations of peripheral nerve
blocks and regional anesthesia to their applications in clinical practice. Ultrasound-guided regional
anesthesia is a field in evolution, and many of its aspects still lack standardization and clear guidance.
For this reason, we decided to produce this new edition as an international collaborative effort. This
collaboration resulted in teaching that is based not only on our experience at NYSORA but also is
endorsed by a number of opinion leaders in the field from around the globe. I would like to thank themfor the contributions, enthusiasm, and passion that they invested in creating the second edition of
Peripheral Nerve Blocks. This book also would not be what it is without the large extended family of
educators and trainees, who took part in the numerous NYSORA educational programs, including our
educational outreach program in developing countries in Asia. I thank you immensely for your input,
which inspired us to deliver this updated edition, and for your multiple contributions through e-mails,
suggestions, and discussion on the NYSORA.com website.
There are no standards of care related to peripheral nerve blocks, despite their widespread use.
With this edition, we have tried to standardize the techniques and the monitoring approach during
local anesthetic delivery, for both greater consistency and greater safety of peripheral nerve blocks.
Different institutions naturally may have different approaches to techniques that they customize for
their own needs. The material we present in this volume however, comes from the trenches of clinical
practice, so to speak. Most procedures described are accompanied by carefully developed flowcharts
to facilitate decision making in clinical practice that the authors themselves use on an everyday basis.
The successful practice of ultrasound-guided regional anesthesia and pain medicine procedures
depends greatly on the ability to obtain accurate ultrasound images and the ability to recognize the
relevant structures. For these reasons, we decided to add an atlas of ultrasound anatomy for regional
anesthesia and pain medicine (Section 7) procedures to this volume. The anatomy examples consist of
a pictorial guide with images of the transducer position needed to obtain the corresponding ultrasound
image and the cross-sectional gross anatomy of the area being imaged. Once the practitioner absorbs
this material, he or she can extrapolate the knowledge of the practical techniques presented to
practice virtually any additional regional anesthesia technique. We have expended painstaking efforts
to provide cross-sectional anatomy examples where possible. Perfecting the matching of ultrasound
and anatomy sections is not always possible because the sonograms and cross-sectional anatomy
views are obtained from volunteers and fresh cadavers, respectively. The reader should keep in mind
that the ultrasound images are obtained from videos during dynamic scanning. For this reason, the
labeled ultrasound images are accurate to the best of our abilities and within the limitations of the
ultrasound equipment even when they do not perfectly match the available paired cross-sectional
anatomy.
Due to popular demand, we decided to include a DVD containing videos of the most common
ultrasound-guided nerve block procedures. Assuming that videos are the most beneficial method for
novices and trainees, we decided to include videos of well-established ultrasound-guided nerve
blocks that should cover most indications for peripheral nerve blocks. Once trainees have mastered
these techniques, they typically require only knowledge about the specific anatomy of the block(s) to
be performed to apply the principles learned in the videos to any other nerve block procedure. This is
another example of how the atlas of ultrasound anatomy (Section 7) included in the book will be
useful. With the wealth of information presented in a systematic fashion, we believe that the Atlas
also will be of value to anyone interested in the ultrasound anatomy of peripheral nerve and
musculoskeletal systems, including radiologists, sonographers, neurologists, and others.
With this edition of Peripheral Nerve Blocks and Anatomy for Ultrasound-Guided Regional
Anesthesia, we have tried to provide a wealth of practical information about the modern practice of
peripheral nerve blocks and the use of ultrasound in regional anesthesia and to present multiple
pathways to troubleshoot common clinical problems. We hope this book will continue to serve as one
of the standard teaching texts in anesthesiology, and we thank the readership of previous edition their
support and encouragement.
Sincerely,Admir Hadzic, MD
ACKNOWLEDGMENTS
This book would not be possible without the contributions and support from a number of remarkable
people and top professionals in their respective fields.
Most notably, special thanks to Professor Alan Santos, MD, the chair of the Department of
Anesthesiology at St. Luke’s–Roosevelt Hospitals, where a significant part of the clinical teaching
and research of the New York School of Regional Anesthesia (NYSORA) has taken place over the
years. Alan’s commitment to education and academics, and his leadership have created a unique
milieu where faculty and staff drawn to academics can excel and pursue their academic goals with a
remarkable departmental support.
Hats off to our current and past fellows in regional anesthesia. You have been immeasurably
helpful and a continuing source of inspiration for many projects and NYSORA endeavors, and you
have been so much fun to work with as well. In particular, thanks and love go to “NYSORA Angels”
Drs. Kim Gratenstein and Colleen Mitgang for the all-around help and positive vibe. I also extend
gratitude to our residents who have helped create teaching ideas and a multitude of didactic
algorithms through our daily interactions in clinical practice.
Many thanks to my numerous U.S. and international collaborators, whose support, relentless
challenges, and innovative didactic material have made a palpable contribution to this project. A bow
to you, my colleagues at St. Luke’s–Roosevelt Hospital, New York, and our site director, Dr. Kurian
Thomas, whose daily organizational skills and clinical leadership made many of our endeavors
possible—often magically so—in these times of increasing financial and manpower strain.
Many thanks to my family: foremost, my son Alen Hadžić, my parents Junuz and Safeta Hadžić, my
sister Admira, and the entire family for allowing me to work on this book project while depriving
them of my presence.
Special thanks to the illustrator, Lejla Hadžić. Her artistic vision and talent adorns this book with
a plethora of detailed illustrations. Lejla has been spearheading multiple projects in her own primary
area of expertise, restoration of war- and weather-ravaged cultural monuments with a Swedish-based
organization, Cultural Heritage Without Borders (CHWB), for which she has received much
international acclaim. Many thanks also to Emma Spahic for lending her artistic eye and Photoshop
skills to the project.
This book owes a great deal to a number of gifted clinicians, academicians, and regional
anesthesia teams from around the globe. Many thanks to Dr. Catherine Vandepitte, who has spent
countless hours editing and collating the material. Daquan Xu, MD, has contributed his unmatched
organizational skills and knowledge of anatomy and ultrasonography. At the peak of our efforts to
produce this book, Daquan actually moved in with me in my apartment on the Hudson River in
Lincoln Harbor, across from the Midtown section of Manhattan. While enduring 16- to 18-hour days
working on the book in the winter of 2011, Daquan would take five-minute breaks on the balcony to
gaze over the skyline of New York. We would stop working only when Daquan became so tired that
he could not see the Empire State Building any more. This sign became known as “The Daquan Sign
to Quit Working”. Boundless appreciation to Dr. Sala-Blanch and his team, Miguel Reina, Ana
Carrera, Ana Lopez, and many others, for their support, contribution in vision, and, in particular,
original anatomic material. Thank you to Dr. Manoj Karmakar and his team for their cutting-edge
contributions to various sections of the atlas of ultrasound anatomy. Thank you to Thomas Clark, who
used his unmatched skills in musculoskeletal imaging to muster some great ultrasound anatomy in the
Atlas section of the book. Many thanks to Dr. Jeff Gadsden for his contribution and best wishes for
success as he takes over the leadership of the Division of Regional Anesthesia at St. Luke’s–
Roosevelt Hospital, a position I have held for the past 15 years. As he continues to build the division
and the regional anesthesia fellowship, I have moved on to multiple other teaching and publishing
endeavors. In particular, I will focus on keeping our two textbooks on regional anesthesia current in
years to come.
Special thanks to a truly inspiring video team, the Ceho Brothers of Film Productions Division of
Stone Tone Records, Inc. Aziz and Mirza Ceho are award-winning documentary filmmakers who
have contributed their immense artistic talent to the accompanying DVD, 5 Nerve Blocks for 95% of
Indications. Making a good instructional DVD has proved to be an incredibly time-consuming task.
However, we believe our efforts have been justified and we have created a uniquely detailed and
true-to-life educational tool. This DVD should be particularly helpful to clinicians who need to adopt
a few, uniquely effective nerve block techniques that can be used to provide regional anesthesia to a
wide variety of patients.
Many thanks to Brian Belval, senior editor at McGraw-Hill Medical. Brian is one of the most
inspirational and insightful managing editors I have ever worked with. I will admit without
reservation that this book would not be what it is without his vision and personal touch. Likewise, the
unmatchable attention to detail of Robert Pancotti, senior project development editor, has much to do
with the quality of this project.
Special thanks to Lorenzo Casertano for loaning his ripped fencing body for the Atlas of Surface
Anatomy that adorns Section 8 at the end of the book. Likewise, thank you to Alecia Yufa and Alen
Hadž;ić for modeling for the Atlas and the techniques.
Finally, a word of gratitude to my bandmates from Big Apple Blues Band
(www.bigappleblues.com), who contributed the original music on all tracks on the 5 Nerve Blocks
for 95% of Indications DVD. Barry Harrison, Anthony Kane, Hugh Pool, Zach Zunis, Rich Cohen,
Tom Papadatos, and Bruce Tylor are some of the very top cats in the NYC music scene. Their talent
and passion have been an important source of inspiration for me on the band stage, in the studio, and
in life in general.
Disclosure
I have served as an industry advisor over the course of my career and have received consulting
honoraria and research grants in the past from GE, Baxter, Glaxo Smith-Kline Industries SkyPharma,
Cadence, LifeTech, and others. I hold an equity position at Macosta Medical USA. Macosta Medical
USA owns intellectual property related to injection pressure monitoring and several other patents
related to the field of anesthesiology. Finally, I have invested a lifetime’s worth of energy and love
into building NYSORA over the past 15 years. My passion for regional anesthesia and undying
commitment to these multiple endeavors undoubtedly has created biases that may have influenced the
teaching in this book; I take full responsibility and stand by all of them.
SECTION 1
Foundations of Peripheral Nerve Blocks
Chapter 1 Essential Regional Anesthesia Anatomy
Chapter 2 Local Anesthetics: Clinical Pharmacology and Rational Selection
Chapter 3 Equipment for Peripheral Nerve Blocks
Chapter 4 Electrical Nerve Stimulators and Localization of Peripheral Nerves
Chapter 5 Monitoring and Documentation
Chapter 6 Indications for Peripheral Nerve Blocks
Chapter 7 Continuous Peripheral Nerve Blocks in Outpatients
Chapter 8 Regional Anesthesia in the Anticoagulated Patient
Chapter 9 Toxicity of Local Anesthetics
Chapter 10 Neurologic Complications of Peripheral Nerve Blocks
1
Essential Regional Anesthesia Anatomy
Admir Hadzic and Carlo Franco
A good practical knowledge of anatomy is important for the successful and safe practice of regional
anesthesia. In fact, just as surgical disciplines rely on surgical anatomy, regional anesthesiologists
need to have a working knowledge of the anatomy of nerves and associated structures that does not
include unnecessary details. In this chapter, the basics of regional anesthesia anatomy necessary for
successful implementation of various techniques described later in the book are outlined.
Anatomy of Peripheral Nerves
All peripheral nerves are similar in structure. The neuron is the basic functional unit responsible for
the conduction of nerve impulses (Figure 1-1). Neurons are the longest cells in the body, many
reaching a meter in length. Most neurons are incapable of dividing under normal circumstances, and
they have a very limited ability to repair themselves after injury. A typical neuron consists of a cell
body (soma) that contains a large nucleus. The cell body is attached to several branching processes,
called dendrites, and a single axon. Dendrites receive incoming messages; axons conduct outgoing
messages. Axons vary in length, and there is only one per neuron. In peripheral nerves, axons are very
long and slender. They are also called nerve fibers.
FIGURE 1-1. Organization of the peripheral nerve.
Connective Tissue
The individual nerve fibers that make up a nerve, like individual wires in an electric cable, are
bundled together by connective tissue. The connective tissue of a peripheral nerve is an important part
of the nerve. According to its position in the nerve architecture, the connective tissue is called the
epineurium, perineurium, or endoneurium (Figure 1-2). The epineurium surrounds the entire nerve
and holds it loosely to the connective tissue through which it runs. Each group of axons that bundles
together within a nerve forms a fascicle, which is surrounded by perineurium. It is at this level that the
nerve–blood barrier is located and constitutes the last protective barrier of the nerve tissue. The
endoneurium is the fine connective tissue within a fascicle that surrounds every individual nerve
fiber or axon.
FIGURE 1-2. Histology of the peripheral nerve and connective tissues. White arrows: External
epineurium (epineural sheath), 1 = Internal epineurium, 2 = fascicles, Blue arrows: Perineurium, Red
arrow: Nerve vasculature Green arrow: Fascicular bundle.
Nerves receive blood from the adjacent blood vessels running along their course. These feeding
branches to larger nerves are macroscopic and irregularly arranged, forming anastomoses to become
longitudinally running vessel(s) that supply the nerve and give off subsidiary branches.
Organization of the Spinal Nerves
The nervous system consists of central and peripheral parts. The central nervous system includes the
brain and spinal cord. The peripheral nervous system consists of the spinal, cranial, and autonomic
nerves, and their associated ganglia. Nerves are bundles of nerve fibers that lie outside the central
nervous system and serve to conduct electrical impulses from one region of the body to another. The
nerves that make their exit through the skull are known as cranial nerves, and there are 12 pairs of
them. The nerves that exit below the skull and between the vertebrae are called spinal nerves, and
there are 31 pairs of them. Every spinal nerve has its regional number and can be identified by its
association with the adjacent vertebrae (Figure 1-3). In the cervical region, the first pair of spinal
nerves, C1, exits between the skull and the first cervical vertebra. For this reason, a cervical spinal
nerve takes its name from the vertebra below it. In other words, cervical nerve C2 precedes vertebra
C2, and the same system is used for the rest of the cervical series. The transition from this
identification method occurs between the last cervical and first thoracic vertebra. The spinal nerve
lying between these two vertebrae has been designated C8. Thus there are seven cervical vertebrae
but eight cervical nerves. Spinal nerves caudal to the first thoracic vertebra take their names from the
vertebra immediately preceding them. For instance, the spinal nerve T1 emerges immediately caudal
to vertebra T1, spinal nerve T2 passes under vertebra T2 and so on.
FIGURE 1-3. Organization of the spinal nerve.
Origin and Peripheral Distribution of Spinal Nerves
Each spinal nerve is formed by a dorsal and a ventral root that come together at the level of the
intervertebral foramen (Figure 1-3). In the thoracic and lumbar levels, the first branch of the spinal
nerve carries visceral motor fibers to a nearby autonomic ganglion. Because preganglionic fibers are
myelinated, they have a light color and are known as white rami (Figure 1-4). Two groups of
unmyelinated postganglionic fibers leave the ganglion. Those fibers innervating glands and smooth
muscle in the body wall or limbs form the gray ramus that rejoins the spinal nerve. The gray and white
rami are collectively called the rami communicantes. Preganglionic or postganglionic fibers that
innervate internal organs do not rejoin the spinal nerves. Instead, they form a series of separate
autonomic nerves and serve to regulate the activities of organs in the abdominal and pelvic cavities.
FIGURE 1-4. Organization and function of the segmental (spinal nerve).
The dorsal ramus of each spinal nerve carries sensory innervation from, and motor innervation to,
a specific segment of the skin and muscles of the back. The region innervated resembles a horizontal
band that begins at the origin of the spinal nerve. The relatively larger ventral ramus supplies the
ventrolateral body surface, structures in the body wall, and the limbs. Each spinal nerve supplies a
specific segment of the body surface, known as a dermatome.
Dermatomes
A dermatome is an area of the skin supplied by the dorsal (sensory) root of the spinal nerve (Figures
1-5 and 1-6). In the head and trunk, each segment is horizontally disposed, except C1, which does not
have a sensory component.
FIGURE 1-5. Dermatomes and corresponding peripheral nerves: front.
FIGURE 1-6. Dermatomes and corresponding peripheral nerves: back.
The dermatomes of the limbs from the fifth cervical to the first thoracic nerve, and from the third
lumbar to the second sacral vertebrae, form a more complicated arrangement due to rotation and
growth during embryologic life. There is considerable overlapping of adjacent dermatomes; that is,
each segmental nerve overlaps the territories of its neighbors. This pattern is variable among
individuals, and it is more of a guide than a fixed map.
Myotomes
A myotome is the segmental innervation of skeletal muscle by a ventral root of a specific spinal nerve
(Figure 1-7).
FIGURE 1-7. Motor innervation of the major muscle groups. (A) Medial and lateral rotation of
shoulder and hip. Abduction and adduction of shoulder and hip. (B) Flexion and extension of elbow
and wrist. (C) Pronation and supination of forearm. (D) Flexion and extension of shoulder, hip, and
knee. Dorsiflexion and plantar flexion of ankle, lateral views.
TIPS
Although the differences between dermatomal, myotomal, and osteotomal innervation are often
emphasized in regional anesthesiology textbooks, it is usually impractical to think in those terms when
planning a regional block.
Instead, it is more practical to think in terms of areas of the body that can be blocked by a specific
technique.
Osteotomes
The innervation of the bones follows its own pattern and does not coincide with the innervation of
more superficial structures (Figure 1-8).
FIGURE 1-8. Osteotomes.
Nerve Plexuses
Although the dermatomal innervation of the trunk is simple, the innervation of the extremities, part of
the neck, and pelvis is highly complex. In these areas, the ventral rami of the spinal nerves form an
intricate neural network; nerve fibers coming from similar spinal segments easily reach different
terminal nerves. The four major nerve plexuses are the cervical plexus, brachial plexus, lumbar
plexus, and sacral plexus.
The Cervical Plexus
The cervical plexus originates from the ventral rami of C1-C5, which form three loops (Figures 1-9
and 1-10). Branches from the cervical plexus provide sensory innervation of part of the scalp, neck,
and upper shoulder and motor innervation to some of the muscles of the neck, the thoracic cavity, and
the skin (Table 1-1). The phrenic nerve, one of the larger branches of the plexus, innervates the
diaphragm.
TABLE 1-1 Organization and Distribution of the Cervical Plexus
FIGURE 1-9. Organization of the cervical plexus.
FIGURE 1-10. Superficial cervical plexus branches. ct, transverse cervical; ga, greater auricular; lo,
lesser occipital; sc, supraclavicular. Also shown is the spinal accessory nerve (SA).
The Brachial Plexus
The brachial plexus is both larger and more complex than the cervical plexus (Figures 1-11, 1-12, 1-
13, 1-14A,B, 1-15A,B, and 1-16). It innervates the pectoral girdle and upper limb. The plexus is
formed by five roots that originate from the ventral rami of spinal nerves C5-T1. The roots converge
to form the superior (C5-C6), middle (C7), and inferior (C8-T1) trunks (Table 1-2). The trunks give
off three anterior and three posterior divisions as they approach the clavicle. The divisions rearrange
their fibers to form the lateral, medial, and posterior cords. The cords give off the terminal branches.
The lateral cord gives off the musculocutaneous nerve, and the lateral root of the median nerve. The
medial cord gives off the medial root of the median nerve and the ulnar nerve. The posterior cord
gives off the axillary and radial nerves.
TABLE 1-2 Organization and Distribution of the Brachial Plexus
FIGURE 1-11. Organization of the brachial plexus.
FIGURE 1-12. View of the posterior triangle of the neck, located above the clavicle between the
sternocleidomastoid (SCM) in front and the trapezius (trap) behind. It is crossed by the omohyoid
muscle (OH) and the brachial plexus (BP).
FIGURE 1-13. The brachial plexus (in yellow) at the level of the trunks (U, M, and L) occupies the
smallest surface area in its entire trajectory. Also shown are the dome of the pleura (PL) in blue, the
subclavian artery (SA) and the vertebral artery, both in red. The phrenic nerve, in yellow, is seen
traveling anterior to the anterior scalene muscle (AS).
FIGURE 1-14. (A) A thick fascia layer (sheath) covers the brachial plexus in the posterior triangle.
Also seen is part of the sternocleidomastoid muscle (SCM), the cervical transverse vessels (CT), and
the omohyoid muscle (OH). (B) Once the sheath is removed, the brachial plexus can be seen between
the anterior scalene (AS) and middle scalene (MS) muscles. (Part A reproduced with permission
from Franco CD, Rahman A, Voronov G, et al. Gross anatomy of the brachial plexus sheath in human
cadavers. Reg Anesth Pain Med. 2008;33(1):64-69. Part B reproduced from Franco CD, Clark L.
Applied anatomy of the upper extremity. Tech Reg Anesth Pain Mgmt. 2008;12(3):134-139, with
permission from Elsevier.)
FIGURE 1-15. (A) In the axilla the brachial plexus is also surrounded by a thick fibrous fascia that
here is shown partially open with a metal probe inside. The musculocutaneous nerve can be seen
exiting the sheath and entering the coracobrachialis muscle. (B) The sheath has been open. Pectoralis
minor (pec minor) has been partially resected. The takeoff of the musculocutaneous nerve from the
lateral cord (LC) inside the sheath is clearly visible. (Reproduced with permission from Franco CD,
Rahman A, Voronov G, et al. Gross anatomy of the brachial plexus sheath in human cadavers. Reg
Anesth Pain Med. 2008;33(1):64-69.)
FIGURE 1-16. Intercostobrachial nerve (T2) is the lateral branch of the second intercostal nerve that
supplies sensory innervation to the axilla and upper medial side of the arm.
The Lumbar Plexus
The lumbar plexus is formed by the ventral rami of spinal nerves L1-L3 and the superior branch of L4
(Figures 1-17, 1-18A,B, and 1-19). In about 50% of the cases, there is a contribution from T12. The
inferior branch of L4, along with the entire ventral rami of L5, forms the lumbosacral trunk that
contributes to the sacral plexus.
FIGURE 1-17. Organization of the lumbar plexus.
FIGURE 1-18. (A) Posterior view of the back to show the thoracolumbar fascia (TLF), whose
posterior layer has been open as a small window through which part of the erector spinae muscles has
been resected to show the anterior layer of the thoracolumbar fascia. (B) One step further in the
dissection shows part of the quadratus lumborum muscle.
FIGURE 1-19. Two branches of the lumbar plexus, the femoral nerve and obturator, are seen
between the quadratus lumborum and psoas muscles in the right retroperitoneal space.
Because the branches of both the lumbar and sacral plexuses are distributed to the lower limb, they
are often collectively referred to as the lumbosacral plexus. The main branches of the lumbar plexus
are the iliohypogastric, ilioinguinal, genitofemoral, lateral femoral cutaneous, obturator, and femoral
nerves (Figures 1-19, 1-20A,B; Table 1-3).
TABLE 1-3 Organization and Distribution of the Lumbar Plexus
FIGURE 1-20. (A) Frontal view of the upper anterior thigh showing the inguinal ligament and some
branches of the lumbar plexus: FN, femoral nerve; GF, femoral branch of genitofemoral nerve; LF,
lateral femoral cutaneous nerve; OB, obturator nerve. The femoral vein (V) and artery (A) are also
shown. (B) The same nerves of (A) are shown from the lateral side.
The Sacral Plexus
The sacral plexus arises from the lumbosacral trunk (L4-L5) plus the ventral rami of S1-S4 (Figures
1-21,1- 22A,B, 1-23, and 1-24). The main nerves of the sacral plexus are the sciatic nerve and the
pudendal nerve (Table 1-4). The sciatic nerve leaves the pelvis through the greater sciatic foramen to
enter the gluteal area where it travels between the greater trochanter and ischial tuberosity. In the
proximal thigh it lies behind the lesser trochanter of the femur covered superficially by the long head
of the biceps femoris muscle. As it approaches the popliteal fossa, the two components of the sciatic
nerve diverge into two recognizable nerves: the common peroneal and the tibial nerve (Figures 1-25
and 1-26).
TABLE 1-4 Organization and Distribution of the Sacral Plexus
FIGURE 1-21. Organization of the sacral plexus.
FIGURE 1-22. (A) The back and paraspinal muscles have been removed to show the transverse
processes of the last lumbar vertebra, the psoas muscle, and the femoral nerve. (B) Same as (A)
showing that the lateral edge of the psoas muscle at the iliac crest is between 4 and 5 cm from the
midline. fem, femoral.
FIGURE 1-23. Dissection of the right gluteal area demonstrates that the inferior border of the gluteus
maximus does not correspond superficially with the subgluteal fold; instead both cross each other
diagonally. (Reproduced from Franco CD. Applied anatomy of the lower extremity. Tech Reg Anesth
Pain Mgmt. 2008;12(3):140-145, with permission from Elsevier.)
FIGURE 1-24. The sciatic nerve (SN) from the gluteal area to the subgluteal fold is located about 10
cm from the midline in adults. This distance is not affected by gender or body habitus. (Reproduced
with permission from Franco CD, Choksi N, Rahman A, Voronov G, Almachnouk MH. A subgluteal
approach to the sciatic nerve in adults at 10 cm from the midline. Reg Anesth Pain Med.
2006;31(3):215-220.)
FIGURE 1-25. Both components of the sciatic nerve, common peroneal (CP) and tibial (T) nerves
diverge from each other at the popliteal fossa. Lateral and medial gastrocnemius muscles (GN) are
also shown.
FIGURE 1-26. The sural nerve is shown behind the lateral malleolus.
Thoracic and Abdominal Wall
Thoracic Wall
The intercostal nerves originate from the ventral rami of the first 11 thoracic spinal nerves. Each
intercostal nerve becomes part of the neurovascular bundle of the rib and provides sensory and motor
innervations (Figure 1-27). Except for the first, each intercostal nerve gives off a lateral cutaneous
branch that pierces the overlying muscle near the midaxillary line. This cutaneous nerve divides into
anterior and posterior branches, which supply the adjacent skin. The intercostal nerves of the second
to the sixth spaces reach the anterior thoracic wall and pierce the superficial fascia near the lateral
border of the sternum and divide into medial and lateral cutaneous branches. Most of the fibers of the
anterior ramus of the first thoracic spinal nerve join the brachial plexus for distribution to the upper
limb. The small first intercostal nerve is in itself the lateral branch and supplies only the muscles of
the intercostal space, not the overlying skin. The lower five intercostal nerves abandon the intercostal
space at the costal margin to supply the muscles and skin of the abdominal wall.
FIGURE 1-27. Organization of the segmental spinal nerve, intercostal nerve, and innervations of the
chest wall.
Anterior Abdominal Wall
The skin, muscles and parietal peritoneum, or the anterior abdominal wall, are innervated by the
lower six thoracic nerves and the first lumbar nerve. At the costal margin, the seventh to eleventh
thoracic nerves leave their intercostal spaces and enter the abdominal wall in a fascial plane between
the transversus abdominis and internal oblique muscles. The seventh and eighth intercostal nerves
slope upward following the contour of the costal margin, the ninth runs horizontally, and the tenth and
eleventh have a somewhat downward trajectory. Anteriorly, the nerves pierce the rectus abdominis
muscle and the anterior layer of the rectus sheath to emerge as anterior cutaneous branches that supply
the overlying skin.
The subcostal nerve (T12) takes the line of the twelfth rib across the posterior abdominal wall. It
continues around the flank and terminates in a similar manner to the lower intercostal nerves. The
seventh to twelfth thoracic nerves give off lateral cutaneous nerves that further divide into anterior
and posterior branches. The anterior branches supply the skin as far forward as the lateral edge of
rectus abdominis. The posterior branches supply the skin overlying the latissimus dorsi. The lateral
cutaneous branch of the subcostal nerve is distributed to the skin on the side of the buttock.
The inferior part of the abdominal wall is supplied by the iliohypogastric and ilioinguinal nerves,
both branches of L1.The iliohypogastric nerve divides, runs above the iliac crest, and splits into two
terminal branches. The lateral cutaneous branch supplies the side of the buttock; the anterior
cutaneous branch supplies the suprapubic region.
The ilioinguinal nerve leaves the intermuscular plane by piercing the internal oblique muscle
above the iliac crest. It continues between the two oblique muscles eventually to enter the inguinal
canal through the spermatic cord. Emerging from the superficial inguinal ring, it gives cutaneous
branches to the skin on the medial side of the root of the thigh, the proximal part of the penis, and the
front of the scrotum in males and the mons pubis and the anterior part of the labium majus in females.
Nerve Supply to the Peritoneum
The parietal peritoneum of the abdominal wall is innervated by the lower thoracic and first lumbar
nerves. The lower thoracic nerves also innervate the peritoneum that covers the periphery of the
diaphragm. Inflammation of the peritoneum gives rise to pain in the lower thoracic wall and
abdominal wall. By contrast, the peritoneum on the central part of the diaphragm receives sensory
branches from the phrenic nerves (C3, C4, and C5), and irritation in this area may produce pain
referred to region of the shoulder (the fourth cervical dermatome).
Innervation of the Major Joints
Because much of the practice of peripheral nerve blocks involves orthopedic surgery, it is important
to review the innervation of the major joints to have a better understanding of the nerves involved for
a more rational approach to regional anesthesia.
Shoulder Joint
Innervation to the shoulder joints originates mostly from the axillary and suprascapular nerves, both
of which can be blocked by an interscalene block (Figure 1-28).
FIGURE 1-28. Innervation of the shoulder joint.
Elbow Joint
Nerve supply to the elbow joint includes branches of all major nerves of the brachial plexus:
musculocutaneous, radial, median, and ulnar nerves.
Hip Joint
Nerves to the hip joint include the nerve to the rectus femoris from the femoral nerve, branches from
the anterior division of the obturator nerve, and the nerve to the quadratus femoris from the sacral
plexus (Figure 1-29).
FIGURE 1-29. Innervation of the hip joint.
Knee Joint
The knee joint is innervated anteriorly by branches from the femoral nerve. On its medial side it
receives branches from the posterior division of the obturator nerve while both divisions of the
sciatic nerve supply its posterior side (Figure 1-30).
FIGURE 1-30. Innervation of the knee joint.
Ankle Joint
The innervation of the ankle joint is complex and involves the terminal branches of the common
peroneal (deep and superficial peroneal nerves), tibial (posterior tibial nerve), and femoral nerves
(saphenous nerve). A more simplistic view is that the entire innervation of the ankle joint stems from
the sciatic nerve, with the exception of the skin on the medial aspect around the medial malleolus
(saphenous nerve, a branch of the femoral nerve) (Figure 1-31).
FIGURE 1-31. Innervation of the ankle joint and foot.
Wrist Joint
The wrist joint and joints in the hand are innervated by most of the terminal branches of the brachial
plexus including the radial, median, and ulnar nerves (Figure 1-32).
FIGURE 1-32. Innervation of the wrist and hand.
SUGGESTED READINGS
Clemente CD. Anatomy: A Regional Atlas of the Human Body. 4th ed. Philadelphia, PA: Lippincott;
1997.
Dean D, Herbener TE. Cross-Sectional Human Anatomy. Philadelphia, PA: Lippincott; 2000.
Gosling JA, Harris PF, Whitmore I, Willan PLT. Human Anatomy: Color Atlas and Text. 5th ed.
London, UK: Mosby; 2008.
Grey H. Anatomy, Descriptive and Surgical. Pick TP, Howden R, eds. New York, NY: Portland
House; 1977.
Hahn MB, McQuillan PM, Sheplock GJ. Regional Anesthesia: An Atlas of Anatomy and Techniques.
St. Louis, MO: Mosby; 1996.
Martini FH, Timmons MJ, Tallitsch RB. Human Anatomy. 7th ed. Upper Saddle River, NJ: Prentice
Hall; 2011.
Netter FH. Atlas of Human Anatomy. Summit, NJ: Ciba-Geigy; 1989.
Pernkopf E. Atlas of Topographical and Applied Human Anatomy. 2nd ed. Munich, Germany:
Saunders; 1980. Head and Neck; vol 1.
Pernkopf E. Atlas of Topographical and Applied Human Anatomy. 2nd ed. Munich, Germany:
Saunders; 1980. Thorax, Abdomen and Extremities; vol 2.
Rohen JW, Yokochi C, Lütjen-Drecoll E. Color Atlas of Anatomy. 4th ed. Baltimore, MD: Williams
and Wilkins; 1998.
Rosse C, Gaddum-Rosse P. Hillinshead’s Textbook of Anatomy. 5th ed. Philadelphia, PA: LippincottRaven; 1997.
Vloka JD, Hadžić A, April EW, Geatz H, Thys DM. Division of the sciatic nerve in the popliteal fossa
and its possible implications in the popliteal nerve blockade. Anesth Analg. 2001;92:215-217.
Vloka JD, Hadžić A, Kitain E, et al. Anatomic considerations for sciatic nerve block in the popliteal
fossa through the lateral approach. Reg Anesth. 1996;21:414-418.
Vloka JD, Hadžić A, Lesser JB, et al. A common epineural sheath for the nerves in the popliteal fossa
and its possible implications for sciatic nerve block. Anesth Analg. 1997;84:387-390.
2
Local Anesthetics: Clinical Pharmacology and Rational Selection
Jeff Gadsden
Local anesthetics (LAs) prevent or relieve pain by interrupting nerve conduction. They bind to
specific receptor sites on the sodium (Na+
) channels in nerves and block the movement of ions
through these pores. Both the chemical and pharmacologic properties of individual LA drugs
determine their clinical properties. This chapter discusses the basics of the mechanism of action of
LAs, their clinical use, and systemic toxicity prevention and treatment.
Nerve Conduction
Nerve conduction involves the propagation of an electrical signal generated by the rapid movement of
small amounts of several ions (Na+
and potassium K+
) across a nerve cell membrane. The ionic
gradient for Na+
(high extracellularly and low intracellularly) and K+
(high intracellularly and low
extracellularly) is maintained by a Na+
-K+
pump mechanism within the nerve. In the resting state, the
nerve membrane is more permeable to K+
ions than to Na+
ions, resulting in the continuous leakage of
K+
ions out of the interior of the nerve cell. This leakage of cations, in turn, creates a negatively
charged interior relative to the exterior, resulting in an electric potential of 60–70 mV across the
nerve membrane.
Receptors at the distal ends of sensory nerves serve as sensors and transducers of various
mechanical, chemical, or thermal stimuli. Such stimuli are converted into minuscule electric currents.
For example, chemical mediators released with a surgical incision react with these receptors and
generate small electric currents. As a result, the electric potential across a nerve membrane near the
receptor is altered, making it less negative. If the threshold potential is achieved, an action potential
results, with a sudden increase in the permeability of the nerve membrane to Na+
ions and a resultant
rapid influx of positively charged Na+
ions. This causes a transient reversal of charge, or
depolarization. Depolarization generates a current that sequentially depolarizes the adjacent segment
of the nerve, thus “activating” the nerve and sending a wave of sequential polarization down the nerve
membrane.
Repolarization takes place when sodium permeability decreases and K+
permeability increases,
resulting in an efflux of K+
from within the cell and restoration of the electrical balance.
Subsequently, both ions are restored to their initial intracellular and extracellular concentrations by
the Na+
-K+
-adenosine triphosphate pump mechanism. Because the rapid influx of Na+
ions occurs in
response to a change in the transmembrane potential, Na+
channels in the nerve are characterized as
“voltage gated”. These channels are protein structures with three subunits that penetrate the full depth
of the membrane bilayer and are in communication with both the extracellular surface of the nerve
membrane and the axoplasm (interior) of the nerve. LAs prevent the generation and conduction of
nerve impulses by binding to the α subunit of the Na+
channel and preventing the influx of Na+
into the
cell, halting the transmission of the advancing wave of depolarization down the length of the nerve.
A resting nerve is less sensitive to a LA than a nerve that is repeatedly stimulated. A higher
frequency of stimulation and a more positive membrane potential cause a greater degree of
transmission block. These frequency- and voltage- dependent effects of LAs occur because repeated
depolarization increases the chance that a LA molecule will encounter a Na+
channel that is in the
activated, or open, form—as opposed to the resting form—which has a much greater affinity for LA.
In general, the rate of dissociation from the receptor site in the pore of the Na+
channel is critical for
the frequency dependence of LA action.
Structure–Activity Relationship of Local Anesthetics
The typical structure of a LA consists of hydrophilic and hydrophobic domains separated by an
intermediate ester or amide linkage. The hydrophilic group is usually a tertiary amine, and the
hydrophobic domain is an aromatic moiety. The nature of the linking group determines the
pharmacologic properties of LA agents. The physicochemical properties of these agents largely
influence their potency and duration of action. For instance, greater lipid solubility increases both the
potency and duration of their action. This is due to a greater affinity of the drug to lipid membranes
and therefore greater proximity to its sites of action. The longer the drug remains in the vicinity of the
membrane, rather than being replaced by the blood, the more likely the drug will be to effect its action
on the Na+
channel in the membrane. Unfortunately, greater lipid solubility also increases toxicity,
decreasing the therapeutic index for more hydrophobic drugs.
TIP
A common misconception is that block duration is related to protein binding. In fact, dissociation
times of local anesthetics from Na+ channels are measured in seconds and do not have a bearing on
the speed of recovery from the block. More important is the extent to which local anesthetic remains
in the vicinity of the nerve. This is determined largely by three factors: lipid solubility; the degree of
vascularity of the tissue; and the presence of vasoconstrictors that prevent vascular uptake.
The pKa
(the pH at which 50% of the drug is ionized and 50% is present as base) of the LA is
related to pH and the concentrations of the cationic and base forms by the Henderson-Hasselbalch
equation: .
The pKa
generally correlates with the speed of onset of action of most amide LA drugs; the closer
the pKa
to the body pH, the faster the onset. The coexistence of the two forms of the drug—the
charged cation and the uncharged base—is important because drug penetration of the nerve membrane
by the LA requires the base (unionized) form to pass through the nerve lipid membrane; once in the
axoplasm of the nerve, the base form can accept a hydrogen ion and equilibrate into the cationic form.
The cationic form is predominant and produces a blockade of the Na+
channel. The amount of base
form that can be in solution is limited by its aqueous solubility.
An ester or an amide linkage is present between the lipophilic end (benzene ring) and the
hydrophilic end (amino group) of the molecule. The type of linkage determines the site of metabolic
degradation of the drug. Ester-linked LAs are metabolized in plasma by pseudocholinesterase,
whereas amide-linked drugs undergo metabolism in the liver.
The Onset and Duration of Blockade
Local Anesthetic Diffusion
A mixed peripheral nerve or nerve trunk consists of individual nerves surrounded by an investing
epineurium. When a LA is deposited in proximity to a peripheral nerve, it diffuses from the outer
surface toward the core along a concentration gradient. Consequently, nerves located in the outer
mantle of the mixed nerve are blocked first. These fibers are usually distributed to more proximal
anatomic structures than those situated near the core of the mixed nerve and often are motor fibers.
When the volume and concentration of LA solution deposited in the vicinity of the nerve are adequate,
the LA eventually diffuses inward to block the more centrally located fibers. In this way, the block
evolves from proximal structures to distal structures. Smaller amounts and concentrations of a drug
only block the nerves in the mantle and smaller and more sensitive central fibers.
Onset of Blockade
In general, LAs are deposited as close to the nerve as possible, preferably into the tissue sheaths
(e.g., brachial plexus, lumbar plexus) or epineurial sheaths of the nerves (e.g., femoral, sciatic). The
actual site of local anesthetic injection and its relationship to the nerve structures is much better
understood since the advent of the use of ultrasound guidance during nerve blockade. Intraneural or
sub-epineural injections reportedly occur relatively frequently with some peripheral nerve blocks.
The available data indicate that such injections result in faster onset of blockade, most likely due to
the intimate proximity of LA to the nerve tissue. This is hardly surprising because the LA must diffuse
from the site of injection to the nerve, the site of action. However, intraneural injections should not be
recommended as a safe practice despite limited reports suggesting that intraneural injections do not
inevitably lead to nerve injury. These data must be interpreted with caution because the term
intraneural injection is often used loosely to denote injections within epineurium or even tissue
sheaths that envelop the peripheral nerves or plexi. However, neurologic injury is much more likely
to occur should an intraneural injection occur intrafascicularly.
The rate of diffusion across the nerve sheath is determined by the concentration of the drug, its
degree of ionization (ionized LA diffuses more slowly), its hydrophobicity, and the physical
characteristics of the tissue surrounding the nerve.
TIP
The relationship between concentration and block onset is logarithmic, not linear; in other words,
doubling the concentration of LA will only marginally speed up the onset of the block (although it will
block the fibers more effectively and prolong the duration).
Duration of Blockade
The duration of nerve block anesthesia depends on the physical characteristics of the LA and the
presence or absence of vasoconstrictors. The most important physical characteristic is lipid
solubility. In general, LAs can be divided into three categories: short acting (e.g., 2-chloroprocaine,
45–90 minutes), intermediate duration (e.g., lidocaine, mepivacaine, 90–180 minutes), and long
acting (e.g., bupivacaine, levobupivacaine, ropivacaine, 4–18 hours). The degree of block
prolongation with the addition of a vasoconstrictor appears to be related to the intrinsic vasodilatory
properties of the LA; the more intrinsic vasodilatory action the LA has, the more prolongation is
achieved with addition of a vasoconstrictor.
Although this discussion is in line with current clinical teaching, it is really more theoretical than
of significant clinical relevance. For instance, dense blocks of the brachial plexus with 2-
chloroprocaine are likely to outlast weak poor quality blocks with bupivacaine. In addition, classical
teaching does not take into account the nerve to be anesthetized. As an example, a sciatic nerve block
with bupivacaine lasts almost twice as long as an interscalene or lumbar plexus block with the same
drug dose and concentration. These differences must be kept in mind to time and predict the resolution
of blockade properly.
Differential Sensitivity of Nerve Fibers to Local Anesthetics
Two general rules apply regarding susceptibility of nerve fibers to LAs: First, smaller nerve fibers
are more susceptible to the action of LAs than large fibers (Figure 2-1). Smaller fibers are
preferentially blocked because a shorter length of axon is required to be blocked to halt the
conduction completely. Second, myelinated fibers are more easily blocked than nonmyelinated fibers
because local anesthetic pools near the axonal membrane. This is why C-fibers, which have a small
diameter (but are unmyelinated), are the most resistant fibers to LA.
FIGURE 2-1. Differential rate of nerve blockade.
The sensitivity of a fiber to LAs is not determined by whether it is sensory or motor. In fact,
muscle proprioceptive afferent (A-beta) and motor efferent fibers (A-alpha) are equally sensitive.
These two types of fibers have the same diameter, which is larger than that of the A-gamma fibers that
supply the muscle spindles. It is the more rapid blockade of these smaller A-gamma fibers, rather than
of the sensory fibers, that leads to the preferential loss of muscle reflexes. Similarly, in large nerve
trunks, motor fibers are often located in the outer portion of the bundle and are more accessible to LA.
Thus motor fibers may be blocked before sensory fibers in large mixed nerves.
The differential rate of blockade exhibited by fibers of varying sizes and firing rates is of
considerable practical importance. Fortunately, the sensation of pain is usually the first modality to
disappear; it is followed by the loss of sensations of cold, warmth, touch, deep pressure, and, finally,
loss of motor function, although variation among patients and different nerves is considerable.
Local Anesthetics and pH
LA drugs, as previously described, pass through the nerve membrane in a nonionized lipid-soluble
base form; when they are within the nerve axoplasm, they must equilibrate into an ionic form to be
active within the Na+
channel. The rate-limiting step in this cascade is penetration of the LA through
the nerve membrane. LAs are unprotonated amines and as such tend to be relatively insoluble (Figure
2-2). For this reason, they are manufactured as water-soluble salts, usually hydrochlorides. Although
LAs are weak bases (typical pKa
values range from 7.5–9), their hydrochloride salts are mildly
acidic. This property increases the stability of LA esters and any accompanying vasoconstrictor
substance. However, this means that the cationic form predominates in solution.
FIGURE 2-2. Local anesthetics and pH. Local anesthetics pass through the nerve membrane in a
nonionized, lipid-soluble base form. When they are within the nerve axoplasm, they must equilibrate
into an ionic form to exert their action on the Na+ channel.
For this reason, sodium bicarbonate (NaHCO3
) is often added to LA. This increases the amount of
drug in the base form, which slightly shortens the onset time. Obviously, the limiting factor for pH
adjustment is the solubility of the base form of the drug. Unfortunately, only small changes in pH can
be achieved by the addition of bicarbonate because of the limited solubility of the base. As such, only
small decreases in onset time are realized. For instance, with the alkalinization of bupivacaine, an
increase in the amount of base in solution is limited by the minimal solubility of free base in solution.
For each LA, there is a pH at which the amount of base in solution is maximal (a saturated solution).
Further increases in pH result in precipitation of the drug and do not produce an additional shortening
of onset time.
Protein Binding
LAs are in large part bound to plasma and tissue proteins. However, they are pharmacologically
active only in the free, unbound state. The most important binding proteins for LAs in plasma are
albumin and alpha1
-acid glycoprotein (AAG). The binding to AAG is characterized as high-affinity
but low-capacity binding; hence LAs bind to AAG preferentially compared with albumin. However,
binding to AAG is easily saturated with clinically achieved blood levels of LA. Once AAG saturation
occurs, any additional binding is to albumin. Albumin can bind LA drugs in plasma in concentrations
many times greater than those clinically achieved.
TIP
Local anesthetic solutions containing epinephrine are made acidic to prevent breakdown of the
vasoconstrictor. There appears to be an onset advantage to alkalinizing these solutions due to their
low pH (e.g., lidocaine with epinephrine, pH 3.5). Alkalinizing plain lidocaine results in a slightly
faster onset but also a shortened duration. However, the clinical relevance of 1–2 minutes of onset
difference is of questionable practical relevance.
Note that the fraction of drugs bound to protein in plasma correlates with the duration of LA
activity: bupivacaine > etidocaine > ropivacaine > mepivacaine > lidocaine > procaine and 2-
chloroprocaine. However, no direct relationship exists between LA plasma protein binding and
binding to specific membrane-bound Na+
channels. Rather, there is a direct correlation between
protein binding and lipid solubility, as there is for all drugs. The more lipid soluble the drug, the
more likely it will remain in the lipid-rich environment of the axonal membrane where the Na+
channel resides.
The degree of protein binding of a particular LA is concentration dependent and influenced by the
pH of the plasma. The percentage of drug bound decreases as the pH decreases. This is important
because with the development of acidosis, as may occur with LA-induced seizures or cardiac arrest,
the amount of free drug increases. The magnitude of this phenomenon varies among LAs, and it is
much more pronounced with bupivacaine than with lidocaine. For instance, as the binding decreases
from 95% to 70% with acidosis, the amount of free bupivacaine increases from 5% to 30% (a factor
of 6), although the total drug concentration remains unchanged. Because of this increase in free drug,
acidosis renders bupivacaine markedly more toxic.
Systemic Toxicity of Local Anesthetics
In addition to interrupting peripheral nerve conduction, LAs interfere with the function of all organs in
which the conduction or transmission of nerve impulses occurs. For instance, they have important
effects on the central nervous system (CNS), the autonomic ganglia, the neuromuscular junction, and
musculature. The risk of such adverse reactions is proportional to the concentration of LA achieved in
the circulation.
Plasma Concentration of Local Anesthetics
The following factors determine the plasma concentration of LAs:
The dose of the drug administered
The rate of absorption of the drug
Site injected, vasoactivity of the drug, use of vasoconstrictors
Biotransformation and elimination of the drug from the circulation
Noted that although the peak level of a LA is directly related to the dose administered,
administration of the same dose at different sites results in marked differences in peak blood levels.
This explains why large doses of LA can be used with peripheral nerve blocks without the toxicity
that would be seen with an intramuscular or intravenous (IV) injection. It is also for this reason that
the adherence to strictly defined maximum doses of LAs is nonsensical. As an example, 150 mg of
ropivacaine at the popliteal fossa will result in a markedly different plasma level than the same dose
administered intercostally. Careful consideration of patient factors and the requirements of the block
should precede selection of LA type and dose for peripheral nerve block.
Short-acting ester local anesthetics are inherently safer with respect to systemic toxicity due to
their clearance by pseudocholinesterase. In the case of 2-chloroprocaine, peak blood levels achieved
are affected by the rate at which the LA drug undergoes biotransformation and elimination (plasma
half-life of about 45 seconds–1 minute). In contrast, peak blood levels of amide-linked LA drugs are
primarily the result of absorption.
Central Nervous System Toxicity
The symptoms of CNS toxicity associated with LAs are a function of their plasma level (Figure 2-3).
Toxicity is typically first expressed as stimulation of the CNS, producing restlessness, disorientation,
and tremor. As the plasma concentration of the LA increases, tonic-clonic seizures occur; the more
potent the LA, the more readily convulsions may be produced. With even higher levels of LA, central
stimulation is followed by depression and respiratory failure, culminating in coma.
FIGURE 2-3. Progression of local anesthetic toxicity.
The apparent stimulation and subsequent depression produced by applying LAs to the CNS
presumably are due to depression of neuronal activity. Selective depression of inhibitory neurons is
thought to account for the excitatory phase in vivo. However, rapid systemic administration of a LA
may produce death with no, or only transient, signs of CNS stimulation. Under these conditions, the
concentration of the drug probably rises so rapidly that all neurons are depressed simultaneously.
Airway control and support of respiration constitute essential treatment. Benzodiazepines or a small
dose of propofol (e.g., 0.5–1.0 mg/kg) administered IV in small doses are the drugs of choice for
aborting convulsions. The use of benzodiazepines as premedication is often recommended to elevate
the seizure threshold; however, they must be used with caution because respiratory depression with
excessive sedation may produce respiratory acidosis with a consequent higher level of free drug in
the serum.
Cardiovascular Toxicity
The primary site of action of LAs in the cardiovascular system is the myocardium, where they
decrease electrical excitability, conduction rate, and the force of myocardial contraction. Most LAs
also cause arteriolar dilatation, contributing to hypotension. Cardiovascular effects typically occur at
higher systemic concentrations than those at which effects on the CNS are produced. However, note
that it is possible for cardiovascular collapse and death to occur even in an absence of the warning
signs and symptoms of CNS toxicity. It is believed that this is probably the result of action on the
pacemaker cells or the sudden onset of ventricular fibrillation. In animal studies on LA cardiotoxicity,
all caused dose-dependent depression of the contractility of cardiac muscle. This depressant effect on
cardiac contractility parallels the anesthetic potency of the LA in blocking nerves. Therefore,
bupivacaine, which is four times more potent than lidocaine in blocking nerves, is also four times
more potent in depressing cardiac contractility. Deaths caused by a bupivacaine overdose have been
associated with progressive prolongation of ventricular conduction and widening of the QRS
complex, followed by the sudden onset of arrhythmia such as ventricular fibrillation.
Pregnancy and Local Anesthetic Toxicity
Plasma concentrations of AAG are also decreased in pregnant women and in newborns. This lowered
concentration effectively increases the free fraction of bupivacaine in plasma, and it may have been
an important contributing factor to the bupivacaine toxicity in pregnant patients and to the number of
cardiac arrests that have been reported with inadvertent overdoses of bupivacaine in pregnant
women. However, with intermediate-duration LAs (e.g., lidocaine and mepivacaine), smaller changes
in protein binding occur during pregnancy, and the use of these LAs is not associated with an
increased risk of cardiac toxicity during pregnancy.
Pharmacodynamics and Treatment of Local Anesthetic Toxicity
Blood levels of lidocaine associated with the onset of seizures appear to be in the range of 10 to 12
μg/mL. At these concentrations, inhibitory pathways in the brain are selectively disabled, and
excitatory neurons can function unopposed. As the blood levels of lidocaine are increased further,
respiratory depression becomes significant and at much higher levels (20–25 μg/mL), cardiotoxicity
is manifested. In contrast, for bupivacaine, blood levels of approximately 4 μg/mL result in seizures,
and blood levels between 4 and 6 μg/mL are associated with cardiac toxicity. This is reflective of a
much lower therapeutic index for bupivacaine compared with lidocaine in terms of cardiac toxicity.
In the setting of neurotoxicity without cardiac effects, high levels of LA in the brain rapidly dissipate
and are redistributed to other tissue compartments. However, with the onset of significant
cardiotoxicity, cardiac output diminishes, resulting in impairment in redistribution.
TIP
No current monitoring method can prevent systemic toxicity. Cases have been reported despite (1)
negative aspiration for blood, (2) the use of recommended dosages, and (3) the observation of local
anesthetic spread in a tissue plane and not intra-vascularly. This is a reminder that constant vigilance
and preparation for treatment is essential during all regional anesthetic procedures.
The long-acting LAs, such as bupivacaine and etidocaine, carry a significantly higher risk of
cardiac arrest and difficult resuscitation. Note that such complications do not always occur
immediately on injection of a LA and may be delayed up to 30 minutes. Many of these toxic effects
occur following inadvertent intravascular injection of large amounts of drugs via an epidural catheter
or from tourniquet failure during IV administration of a regional anesthetic. In patients with systemic
neurotoxicity, treatment consists of halting the seizure by administering a benzodiazepine (midazolam
0.05–0.1 mg/kg) or a small dose of propofol (0.5–1.0 mg/kg) while preventing the detrimental effects
of hypoxia and hypercarbia by ventilating with 100% oxygen. Providing that the hemodynamics are
adequate, this can be achieved through bag-mask ventilation or the use of a laryngeal mask airway:
Tracheal intubation is not always necessary (or always desirable) because these episodes are
fortunately often short lived. However, it is extremely important to oxygenate and ventilate the patient
because hypoxia, hypercarbia, and acidosis all potentiate the negative inotropic and chronotropic
effects of LA toxicity. If ventilation is inadequate with the measures just described, tracheal
intubation with the aid of a muscle relaxant is indicated.
For patients exhibiting signs of cardiotoxicity (widened QRS complex, bradycardia, hypotension,
ventricular fibrillation, and/or cardiovascular collapse), standard cardiac resuscitative measures
should apply. Of primary importance in cardiac arrest is the maintenance of some degree of
circulation and perfusion of vital organs by closed chest massage while electrical and pharmacologic
therapies are being instituted. Drugs that have little value or indeed worsen the resuscitative efforts
include bretylium, lidocaine, and calcium channel blockers. The use of lipid emulsion in LA toxicity
has been reported to result in remarkably successful resuscitation, despite the fact that its mechanism
remains obscure. Several theories exist, such as its role as a “lipid sink”, that draws the drug out of
solution, as well as its possible role in overriding the inhibition of mitochondrial carnitineacylcarnitine translocase, thereby providing the myocardium with fatty acid for fuel. Although neither
theory has been proven, the vast majority of experimental evidence suggests that lipid emulsion
therapy is a low-risk, high-yield intervention that can only benefit the otherwise moribund patient (see
Table 2-1 for directions for use).
TABLE 2-1 Choice of Local Anesthetic for Peripheral Nerve Blockade
The use of vasopressor agents, such as epinephrine and vasopressin, has long been a standard part
of the management of cardiac arrest, and at the moment, guidelines have not changed. However,
experimental evidence involving animals has shown worsened outcomes when combined with lipid
emulsion, perhaps due to increased myocardial intracellular acidosis. Further work in this area needs
to be done before any recommendation can be made, and at present, the inclusion of these agents as
standard resuscitative drugs is warranted. Finally, in cases of severe toxicity with large doses of
long-acting LAs, timely institution of cardiopulmonary bypass may prove lifesaving. The information
on local anesthetic toxicity was briefly presented here for the sake of clarity; an entire chapter is
devoted to the toxicity of local anesthetics (Chapter 10).
Types of Local Anesthetics
As previously mentioned, LA drugs are classified as esters or amides (Figure 2-4). A short overview
of various LAs with comments regarding their clinical applicability in peripheral blockade is
provided in this section.
FIGURE 2-4. Local anesthetics, their classification, chemical structure, and approximate time of
introduction.
Ester-Linked Local Anesthetics
Ester-linked LAs are hydrolyzed at the ester linkage in plasma by pseudocholinesterase. The rate of
hydrolysis of ester-linked LAs depends on the type and location of the substitution in the aromatic
ring. For example, 2-chloroprocaine is hydrolyzed about four times faster than procaine, which in turn
is hydrolyzed about four times faster than tetracaine. However, the rate of hydrolysis of all esterlinked LAs is markedly decreased in patients with atypical plasma pseudocholinesterase, and a
prolonged epidural block in a patient with abnormal pseudocholinesterase has been reported. Another
hallmark of metabolism of ester-linked LAs is that their hydrolysis leads to the formation of paraaminobenzoic acid (PABA). PABA and its derivatives carry a small risk potential for allergic
reactions. A history of an allergic reaction to a LA should immediately suggest that a current reaction
is due to the presence of PABA derived from an ester-linked LA. However, although exceedingly
rare, allergic reactions can also develop from the use of multiple-dose vials of amide-linked LAs that
contain PABA as a preservative.
Cocaine
Cocaine occurs naturally in the leaves of the coca shrub and is an ester of benzoic acid. The clinically
desired actions of cocaine are blockade of nerve impulses and local vasoconstriction secondary to
inhibition of local norepinephrine reuptake. However, its toxicity and the potential for abuse have
precluded wider clinical use of cocaine in modern practice. Its euphoric properties are due primarily
to inhibition of catecholamine uptake, particularly dopamine, at CNS synapses. Other LAs do not
block the uptake of norepinephrine and do not produce the sensitization to catecholamines,
vasoconstriction, or mydriasis characteristics of cocaine. Currently, cocaine is used primarily to
provide topical anesthesia of the upper respiratory tract, where its combined vasoconstrictor and LA
properties provide anesthesia and shrinking of the mucosa with a single agent.
Procaine
Procaine, an amino ester, was the first synthetic LA. Procaine is characterized by low potency, slow
onset, and short duration of action. Consequently, although once widely used, its use now is largely
confined to infiltration anesthesia and perhaps diagnostic nerve blocks.
2-Chloroprocaine
An ester LA introduced in 1952, 2-chloroprocaine is a chlorinated derivative of procaine.
Chloroprocaine is the most rapidly metabolized LA used currently. Because of its rapid breakdown in
plasma (<1 minute), it has a very low potential for systemic toxicity. Enthusiasm for its use in spinal
anesthesia was tempered by reports of neurologic deficits during the 1980s. Such toxicity appeared to
have been a consequence of low pH and the use of sodium meta-bisulfite as a preservative in earlier
formulations. A newer 2-chloroprocaine commercial preparation from which the preservatives have
been removed has been released, and the initial studies appear to be promising, with no reports of
toxicity. This drug has largely replaced lidocaine in our practice for short-acting spinal anesthetics
for procedures lasting less than 1 hour.
A 3% 2-chloroprocaine solution is also our LA of choice for surgical anesthesia of short duration
that results in relatively minor tissue trauma and postoperative pain (e.g., carpal tunnel syndrome,
knee arthroscopy, muscle biopsy). Its characteristics in peripheral nerve blockade include fast onset
and short duration of action (1.5–2 hours). The duration of blockade can be extended (up to 2 hours)
by the addition of epinephrine (1:400,000).
Tetracaine
Tetracaine was introduced in 1932, and it is a long-acting amino ester. It is significantly more potent
and has a longer duration of action than procaine or 2-chloroprocaine. Tetracaine is more slowly
metabolized than the other commonly used ester LAs, and it is considerably more toxic. Currently, it
is used in spinal anesthesia when a drug of long duration is needed, as well as in various topical
anesthetic preparations. Because of its slow onset and potential for toxicity, tetracaine is used rarely
for peripheral nerve blocks in our practice. Some centers, however, have used tetracaine in
combination with other local anesthetics, commonly lidocaine, with success. The combination is often
known by the nickname “supercaine”. The prevalence of the use of supercaine in modern regional
anesthesia is not known.
Amide-Linked Local Anesthetics
As opposed to ester-linked drugs, amide-linked LAs are metabolized in the liver by a dealkalization
reaction in which an ethyl group is cleaved from the tertiary amine. The hepatic blood flow and liver
function determine the hepatic clearance of these anesthetics. Consequently, factors that decrease
hepatic blood flow or hepatic drug extraction both result in an increased elimination half-life. Renal
clearance of unchanged LAs is a minor route of elimination, accounting for only 3% to 5% of the total
drug administered.
Lidocaine
Lidocaine was introduced in 1948 by the Swedish drug manufacturer Astra, and it remains one of the
most versatile and widely used LAs. It is the prototype of the amide class of LAs. Lidocaine is
absorbed rapidly after parenteral administration and from the gastrointestinal and respiratory tracts.
Lidocaine can be used in almost any peripheral nerve block in which a LA of intermediate duration is
needed. A concentration of 1.5% or 2% with or without the addition of epinephrine is most commonly
used for surgical anesthesia. More diluted concentrations are suitable in pain management,
particularly for diagnostic blocks.
Mepivacaine
Mepivacaine, introduced in 1957, is an intermediate-duration amino amide LA. Its pharmacologic
properties are similar to those of lidocaine. Although it was suggested that mepivacaine is more toxic
to neonates (and as such is not used in obstetric anesthesia), it appears to have a slightly higher
therapeutic index in adults than lidocaine. Its onset of action is similar to that of lidocaine, but it
enjoys a slightly longer duration of action than lidocaine. Our first choice in any peripheral nerve
block technique is 1.5% mepivacaine when an intermediate-duration blockade is desired (3–6 hours,
depending on the type of nerve block and addition of a vasoconstrictor).
Prilocaine
Prilocaine is an intermediate-duration amino amide LA with a pharmacologic profile similar to that
of lidocaine. The primary differences are a lack of vasodilatation and an increased volume of
distribution, which reduces its CNS toxicity. However, it is unique among amide LAs for its
propensity to cause methemoglobinemia, an effect of metabolism of the aromatic ring to o-toluidine.
The development of methemoglobinemia depends on the total dose administered (usually requires 8
mg/kg) and does not have significant consequences in healthy patients. If necessary, it is treated by IV
administration of methylene blue (1–2 mg/kg). Prilocaine is used infrequently in peripheral nerve
blockade.
Etidocaine
Etidocaine is a long-acting amino amide introduced in 1972. Its neuronal blocking properties are
characterized by an onset of action similar to that of lidocaine and a duration of action comparable
with that of bupivacaine. Etidocaine is structurally similar to lidocaine, with alkyl substitution on the
aliphatic connecting group between the hydrophilic amine and the amide linkage. This feature
increases the lipid solubility of the drug and results in a drug more potent than lidocaine that has a
very rapid onset of action and a prolonged duration of anesthesia. A major disadvantage of etidocaine
is its profound motor blockade over a wide range of clinical concentrations, which often outlasts
sensory blockade. For these reasons, etidocaine is not used for peripheral nerve blockade.
Bupivacaine
Since its introduction in 1963, bupivacaine has been one of the most commonly used LAs in regional
and infiltration anesthesia. Its structure is similar to that of lidocaine, except that the amine-containing
group is a butylpiperidine. Bupivacaine is a long-acting agent capable of producing prolonged
anesthesia and analgesia that can be prolonged even further by the addition of epinephrine. It is
substantially more cardiotoxic than lidocaine. The cardiotoxicity of bupivacaine is cumulative and
substantially greater than would be predicted by its LA potency. At least part of the cardiotoxicity of
bupivacaine may be mediated centrally because direct injection of small quantities of bupivacaine
into the medulla can produce malignant ventricular arrhythmias. Bupivacaine-induced cardiotoxicity
can be difficult to treat.
Bupivacaine is widely used both in neuraxial and peripheral nerve blockade. The blocking
property is characterized by a slower onset and a long, somewhat unpredictable duration of blockade.
Because of its toxicity profile, large doses of bupivacaine should be avoided.
Ropivacaine
The cardiotoxicity of bupivacaine stimulated interest in developing a less toxic, long-lasting LA. The
development of ropivacaine, the S-enantiomer of 1-propyl-2′, 6′-pipecolocylidide, is the result of that
search. The S-enantiomer, like most LAs with a chiral center, was chosen because it has a lower
toxicity than the R-enantiomer. This is presumably because of slower uptake, resulting in lower blood
levels for a given dose. Ropivacaine undergoes extensive hepatic metabolism after IV administration,
with only 1% of the drug eliminated unchanged in the urine. Ropivacaine is slightly less potent than
bupivacaine in producing anesthesia when used in lower concentrations. However, in concentrations
of 0.5% and higher, it produces dense blockade with a slightly shorter duration than that of
bupivacaine. In concentrations of 0.75%, the onset of blockade is almost as fast as that of 1.5%
mepivacaine or 3% 2-chloroprocaine, with reduced CNS toxicity and cardiotoxic potential and a
lower propensity for motor blockade than bupivacaine. For these reasons, ropivacaine has become
one of the most commonly used long-acting LAs in peripheral nerve blockade.
TIP
Bupivacaine has fallen out of favor in many centers due both to its potential for serious toxicity, as
well as the availability of ropivacaine, a LA characterized by a slightly decreased duration of action
than bupivacaine but an improved safety profile. However, the advent of ultrasonography has allowed
for a dramatic reduction in the volumes of LA necessary to achieve many nerve blocks. Consequently,
some practitioners have begun to use bupivacaine again, albeit in smaller doses, to maximize the
duration of blockade.
Levobupivacaine
Levobupivacaine contains a single enantiomer of bupivacaine hydrochloride, and is less cardiotoxic
than bupivacaine. It is extensively metabolized with no unchanged drug detected in the urine or feces.
The properties of levobupivacaine in peripheral nerve blockade are less well studied than those of
ropivacaine, however, research results suggest that they seem to parallel those of bupivacaine.
Therefore, levobupivacaine is a suitable, less toxic alternative to bupivacaine.
Additives to Local Anesthetics
Vasoconstrictors
The addition of a vasoconstrictor to a LA delays its vascular absorption, increasing the duration of
drug contact with nerve tissues. The net effect is prolongation of the blockade by as much as 50% and
a decrease in the systemic absorption of LA. These effects vary significantly among different types of
LAs and individual nerve blocks. For example, because lidocaine is a natural vasodilator, the effect
is pronounced for those blocks compared with blocks using ropivacaine, which has its own slight
vasoconstricting effect. Epinephrine is the most commonly used vasoconstrictor in peripheral nerve
blockade. A decrease in nerve blood supply has been associated with epinephrine when combined
with local anesthetics. However, this effect was not seen when concentrations of epinephrine were
maintained at 1:400,000 (2.5 μg/mL). As such, this is the recommended concentration when used as
an adjuvant.
TIP
Epinephrine also serves as a marker of intravenous injection of local anesthetic. An increase in heart
rate of 20 bpm or greater and/or an increase in systolic blood pressure of 15 mmHg or greater after a
dose of 15 μg of epinephrine is should raise a suspicion of intravascular injection.
Opioids
The injection of opioids into the epidural or subarachnoid space to manage acute or chronic pain is
based on the knowledge that opioid receptors are present in the substantia gelatinosa of the spinal
cord. Thus combinations of a LA and an opiate are often successfully used in neuraxial blockade to
both enhance the blockade and prolong analgesia. However, in peripheral nerves, similar receptors
are absent or the effects of opiates are negligibly weak. For this reason, opiates do not have a
significant clinical role in peripheral nerve blockade.
Clonidine
Clonidine is a centrally acting selective partial α2
-adrenergic agonist. Because of its ability to reduce
sympathetic nervous system output from the CNS, clonidine acts as an antihypertensive drug.
Preservative-free clonidine, administered into the epidural or subarachnoid space (150–450 μg),
produces dose-dependent analgesia and, unlike opioids, does not produce depression of ventilation,
pruritus, nausea, or vomiting. Clonidine produces analgesia by activating postsynaptic α2 receptors in
the substantia gelatinosa of the spinal cord. Much less research has been done on the effects of
clonidine in peripheral nerve blockade. A recent meta-analysis showed that clonidine prolongs the
duration of both the sensory and motor block by approximately 1.5 to 2 hours. Of note, there appears
to be no benefit to using clonidine in continuous perineural infusions. In addition, side effects, notably
sedation, orthostatic hypotension, and fainting, should be considered when using clonidine. The latter
two effects, in particular, can interfere with mobilization postoperatively. Although life-threatening
hypotension or bradycardia has not been reported when clonidine is used with peripheral nerve
blocks, its circulatory effects may complicate resuscitation in a setting of LA toxicity.
Selecting Local Anesthetics for Peripheral Nerve Blocks
With a variety of LAs to choose from, it is useful to keep the following points in mind when selecting
an agent for nerve blockade. In general, the onset and duration of a LA are similar in nature. For
example, 2-chloroprocaine has a short onset but also a relatively brief duration (Table 2-1). In
contrast, bupivacaine and ropivacaine have longer durations of action but take somewhat longer to
exert their effect.
The LA should be tailored to the duration of the surgical procedure and the anticipated degree of
pain. For example, creation of an arteriovenous fistula is a relatively short operation with minimal
postoperative pain. Therefore, selection of a short-acting agent (e.g., mepivacaine) provides excellent
intraoperative conditions, without the burden of an insensate limb for 10 to 18 hours postoperatively.
A rotator cuff repair involves a greater degree of postoperative pain, and therefore selection of a
long-acting LA (e.g., ropivacaine) is appropriate.
Onset and duration for a given LA varies according to the nerve or plexus blocked. For example,
at the brachial plexus, 0.5% ropivacaine may be expected to provide 10 to 12 hours of analgesia; the
same concentration at the sciatic nerve may provide up to 24 hours of analgesia. This is likely due to
differences in the local vascularity, which influences the uptake of LA.
Blocks for postoperative analgesia (often in concert with general anesthesia) do not require a high
concentration of LA. Ropivacaine 0.2% is usually sufficient to provide excellent sensory analgesia
but spare any motor blockade.
The toxicity of the agent should be considered. Bupivacaine provides the longest duration of the
commonly used LAs but also has the worst cardiotoxic profile. However, a reduction in the dose
used, seen more and more frequently with ultrasound-guided nerve blocks, may provide an equivalent
or greater safety profile than a larger dose of ropivacaine, the drug to which it is often compared.
Ambulatory patients who are undergoing lower limb surgery should be administered long-acting
LAs with caution and with proper education regarding ambulation with assistance. Short procedures
with minimal postoperative pain (most ambulatory procedures) only require a short- to intermediateacting agent, and evidence of block resolution is often a requirement before discharge home.
Anticipated pain lasting longer than 15 to 20 hours should warrant the consideration of a
perineural catheter. The appreciation that patients show for any effective block will fade quickly
when it wears off in the middle of the night, leaving them unprepared, in pain, and unable to access
alternative pain therapies.
Mixing of Local Anesthetics
Mixing of LAs (e.g., lidocaine and bupivacaine) is often done in clinical practice with the intent of
obtaining the faster onset of the shorter acting LAs and the longer duration of the longer acting LA.
Unfortunately, when LAs are mixed, their onset, duration, and potency become much less predictable,
and the end result is far from expected. For instance, work performed at our institution has shown that
combining mepivacaine 1.5% with bupivacaine 0.5%, versus either drug alone for interscalene
brachial plexus block, results in little clinical advantage. Onset times for all three solutions were
indistinguishable, and the duration of the combined solution was significantly shorter than
bupivacaine alone. Moreover, a separate experiment looking at the sequence of LAs (i.e.,
bupivacaine first, mepivacaine second versus mepivacaine first, bupivacaine second) showed no
difference in the onset and duration between groups.
Therefore, if long duration is desired, a long-acting drug alone will provide the best conditions. In
addition, mixing LAs also carries a risk of a drug error. For this reason, we rarely mix LAs; instead,
we choose drugs and concentrations of single agents to achieve the desired effects.
The vast majority of nerve block goals can be met using one short/intermediate and one long-acting
LA. At our institution, more than 90% of peripheral nerve blocks for surgical anesthesia are
performed with one of two LAs: 1.5% mepivacaine or 0.5%–0.75% ropivacaine. Of course, there are
times when other LAs are used. Chloroprocaine is used for quick knee arthroscopies, for example,
when the postoperative pain is minimal and rapid return to ambulation is required.
Table 2-1 shows the commonly used local anesthetics, with and without bicarbonate and/or
epinephrine, and their expected onset and duration of actions. As mentioned previously, these
numbers do not apply to all scenarios, all nerves, and all plexuses but can be used as a rough
comparative guide to aid in decision making.
SUGGESTED READINGS
Albright GA. Cardiac arrest following regional anesthesia with etidocaine or bupivacaine.
Anesthesiology. 1978;51:285-287.
Auroy Y, Narchi P, Messiah A, et al. Serious complications related to regional anesthesia: results of a
prospective survey in France. Anesthesiology. 1997;87:479-486.
Avery P, Redon D, Schaenzer G, et al. The influence of serum potassium on the cerebral and cardiac
toxicity of bupivacaine and lidocaine. Anesthesiology. 1985;61:134-138.
Berry JS, Heindel L. Evaluation of lidocaine and tetracaine mixture in axillary brachial plexus block.
AANA J. 1999;67:329-334.
Blanch SA, Lopez AM, Carazo J, et al. Intraneural injection during nerve stimulator-guided sciatic
nerve block at the popliteal fossa. Br J Anaesth. 2009;102:855-861.
Braid BP, Scott DB. The systemic absorption of local analgesic drugs. Br J Anaesth. 1965;37:394.
Burney RG, DiFazio CA, Foster JA. Effects of pH on protein binding of lidocaine. Anesth Analg.
1978;57:478-480.
Butterworth JF, Strichartz GR. The molecular mechanisms by which local anesthetics produce impulse
blockade: a review. Anesthesiology. 1990;72:711-734.
Carpenter RI, Mackey DC. Local anesthetics. In: Barash PG, Cullen BF, Stoelting RK, eds. Clinical
Anesthesia. 2nd ed. Philadelphia, PA: Lippincott; 1992:509-541.
Casati A, Magistris L, Fanelli G, et al. Small-dose clonidine prolongs postoperative analgesia after
sciatic-femoral nerve block with 0.75% ropivacaine for foot surgery. Anesth Analg. 2000;91:388.
Catterall WA. Cellular and molecular biology of voltage-gated sodium channels. Physiol Rev.
1992;72:S15-S48.
Clarkson CW, Hondeghem LM. Mechanism for bupivacaine depression of cardiac conduction: fast
block of sodium channels during the action potential with slow recovery from block during diastole.
Anesthesiology. 1985;62:396-405.
Courtney KR, Strichartz GR. Structural elements which determine local anesthetic activity. In:
Strichartz GR, ed. Handbook of Experimental Pharmacology. Vol 81. Berlin, Germany: SpringerVerlag; 1987:53-94.
Cousins MJ, Bridenbaugh PO, eds. Neural Blockade in Clinical Anesthesia and Management of Pain.
3rd ed. Philadelphia, PA: Lippincott; 1995.
Cousins MJ, Mather LE. Intrathecal and epidural administration of opioids. Anesthesiology.
1984;61:276-310.
Covino BG. Toxicity and systemic effects of local anesthetic agents. In: Strichartz GR, ed. Handbook of
Experimental Pharmacology. Vol 81. Berlin, Germany: Springer-Verlag; 1987:187-212.
Covino BG, Vassallo HG. Local Anesthetics: Mechanisms of Action and Clinical Use. New York,
NY: Grune & Stratton; 1976.
De Negri P, Visconti C, DeVivo P, et al. Does clonidine added to epidural infusion of 0.2%
ropivacaine enhance postoperative analgesia in adults? Reg Anesth Pain Med. 2000;25:39.
DiFazio CA, Rowlingson JC. Additives to local anesthetic solutions. In: Brown DL, ed. Regional
Anesthesia and Analgesia. Philadelphia, PA: Saunders; 1996:232-239.
Gormley WP, Murray JM, Fee JPH, Bower S. Effect of the addition of alfentanil to lignocaine during
axillary brachial plexus anaesthesia. Br J Anaesth. 1996;76:802-805.
ibuch EE, Opper SE. Back pain following epidurally administered Nesacaine MPF. Anesth Analg.
1989;69:113-115.
Gadsden J, Hadzic A, Gandhi K, et al. The effect of mixing 1.5% mepivacaine and 0.5% bupivacaine
on duration of analgesia and latency of block onset in ultrasound-guided interscalene block. Anesth
Analg. 2011;112:471-6.
Garfield JM, Gugino L. Central effects of local anesthetics. In: Strichartz GR, ed. Handbook of
Experimental Pharmacology. Vol 81. Berlin, Germany: Springer-Verlag; 1987:187-212.
Gissen AJ, Datta S, Lambert D. The chloroprocaine controversy. II. Is chloroprocaine neurotoxic? Reg
Anesth. 1984;9:135-145.
Graf BM, Martin E, Bosnjak ZJ, et al. Stereospecific effect of bupivacaine isomers on atrioventricular
conduction in the isolated perfused guinea pig heart. Anesthesiology. 1997;86:410-419.
Harwood TN, Butterworth JF, Colonna DM, et al. Plasma bupivacaine concentrations and effects of
epinephrine after superficial cervical plexus blockade in patients undergoing carotid endarterectomy.
J Cardiothorac Vasc Anesth. 1999;3:703-706.
Hilgier M. Alkalinization of bupivacaine for brachial plexus block. Reg Anesth. 1985;10:59-61.
Huang YF, Pryor ME, Mather LE, et al. Cardiovascular and central nervous system effects of
intravenous levobupivacaine and bupivacaine in sheep. Anesth Analg. 1998;86:797-804.
Kasten GW, Martin ST. Bupivacaine cardiovascular toxicity: comparison of treatment with bretylium
and lidocaine. Anesth Analg. 1985;64:911-916.
Moore DC. Administer oxygen first in the treatment of local anesthetic-induced convulsions.
Anesthesiology. 1980;53:346-347.
Nath S, Haggmark S, Johansson G, et al. Differential depressant and electrophysiologic cardiotoxicity
of local anesthetics: an experimental study with special reference to lidocaine and bupivacaine.
Anesth Analg. 1986;65:1263-1270.
Ragsdale DR, McPhee JC, Scheuer T, et al. Molecular determinants of state-dependent block of Na+
channels by local anesthetics. Science. 1994;265:1724-1728.
Raymond SA, Gissen AJ. Mechanism of differential nerve block. In: Strichartz GR, ed. Handbook of
Experimental Pharmacology. Vol 81. Berlin, Germany: Springer-Verlag; 1987:95-164.
Reiz S, Haggmark S, Johansson G, et al. Cardiotoxicity of ropivacaine—a new amide local anesthetic
agent. Acta Anaesthesiol Scand. 1989;33:93-98.
Ritchie JM, Greengard P. On the mode of action of local anesthetics. Annu Rev Pharmacol.
1966;6:405-430.
Rowlingson JC. Toxicity of local anesthetic additives. Reg Anesth. 1993;18:453-460.
age DJ, Feldman HS, Arthur GR, et al. Influence of bupivacaine and lidocaine on isolated guinea pig
atria in the presence of acidosis and hypoxia. Anesth Analg. 1984;63:1-7.
antos AC, Arthur GR, Lehning EJ, et al. Comparative pharmacokinetics of ropivacaine and
bupivacaine in nonpregnant and pregnant ewes. Anesth Analg. 1997;85:87-93.
antos AC, Arthur GR, Padderson H, et al. Systemic toxicity of ropivacaine during bovine pregnancy.
Anesthesiology. 1994;75: 137-141.
Singelyn FJ, Gouvernuer JM, Robert A. A minimum dose of clonidine added to mepivacaine prolongs
the duration of anesthesia and analgesia after axillary brachial plexus block. Anesth Analg.
1996;83:1046.
Stevens RA, Urmey WF, Urquhart BL, et al. Back pain after epidural anesthesia with chloroprocaine.
Anesthesiology. 1993;78:492-497.
Strichartz GR, Ritchie JM. The action of local anesthetics on ion channels of excitable tissues. In:
Strichartz GR, ed. Handbook of Experimental Pharmacology. Vol 81. Berlin, Germany: SpringerVerlag; 1987:21-53.
Tucker GT, Mather LE. Pharmacokinetics of local anesthetic agents. Br J Anaesth. 1975;47:213-214.
Wagman IH, Dejong RH, Prince DA. Effect of lidocaine on the central nervous system. Anesthesiology.
1967;28:155-172.
Wang BC, Hillman DE, Spiedholz NI, et al. Chronic neurologic deficits and Nesacaine-CE. An effect ofthe anesthetic, 2-chloro-procaine, or the antioxidant, sodium bisulfite. Anesth Analg. 1984;63:445-
447.
Winnie AP, Tay CH, Patel KP, et al. Pharmacokinetics of local anesthetics during plexus blocks. AnesthAnalg. 1977;56:852-861.
3
Equipment for Peripheral Nerve Blocks
Ali Nima Shariat, Patrick M. Horan and Kimberly Gratenstein and Colleen McCally and Ashton P.
Frulla
Introduction
Over the past several decades, regional anesthesia equipment has undergone substantial technological
advances. Historically, the development and consequent introduction of the portable nerve stimulator
to clinical practice in the 1970s and 1980s was a critical advance in regional anesthesia, allowing the
practitioner to better localize the targeted nerve. In recent years, however, the advent of ultrasound,
better needles, catheter systems, and monitoring has entirely rejuvenated, if not revolutionized, the
practice of regional anesthesia.
Induction and Block Room
Regional anesthesia is ideally performed in a designated area with access to all the appropriate
equipment necessary to perform blocks. Whether this area is the operating room or a separate block
room, there must be adequate space, proper lighting, and equipment to ensure successful, efficient,
and safe performance of peripheral nerve blocks (PNBs). Provision for proper monitoring, oxygen,
equipment for emergency airway management and positive-pressure ventilation, and access to
emergency drugs is of paramount importance (Figure 3-1).
FIGURE 3-1. Typical block room setup. Shown are monitoring, oxygen source, suction apparatus,
ultrasound machine, and nerve block cart with equipment.
Cardiovascular and Respiratory Monitoring During Application of Regional
Anesthesia
Patients receiving regional anesthesia should be monitored with the same degree of vigilance as
patients receiving general anesthesia. Local anesthetic toxicity due to intravascular injection or rapid
absorption into systemic circulation is a relatively uncommon but potentially life-threatening
complication of regional anesthesia. Likewise, premedication, often necessary before many regional
anesthesia procedures, may result in respiratory depression, hypoventilation, and hypoxia. For these
reasons, patients receiving PNBs should have vascular access and be appropriately monitored.
Routine cardio-respiratory monitoring should consist of pulse oximetry, noninvasive blood pressure,
and electrocardiogram. Respiratory rate and mental status should also be monitored. The risk of the
local anesthetic toxicity has a biphasic pattern and should be anticipated (1) during and immediately
after the injection and (2) 10 to 30 minutes after the injection. Signs and symptoms of toxicity
occurring during or shortly after the completion of the injection are due to an intravascular injection
or channeling of local anesthetics to the systemic circulation (1–2 minutes). In the absence of an
intravascular injection, the typical absorption rate of local anesthetics after injection peaks at
approximately 10 to 30 minutes after performance of a PNB1
; therefore patients should be
continuously and closely monitored for at least 30 minutes for signs of local anesthetic toxicity.
TIPS
• Routine monitoring during administration of nerve blocks:
Pulse oximetry
Noninvasive blood pressure
Electrocardiogram
Respiratory rate
Mental status
Regional Anesthesia Equipment Storage Cart
A regional anesthesia cart should have all drawers clearly labeled and be portable to enable transport
to the patient’s bedside. The anesthesia cart should also be well stocked with all equipment necessary
to perform PNBs effectively, safely, and efficiently. Supplies such as needles and catheters of various
sizes, local anesthetics, and emergency airway and resuscitation equipment should also be included
(Figures 3-2,3-3, and 3-4).
FIGURE 3-2. Typical nerve block cart with labels for each drawer.
FIGURE 3-3. Drawer 1, including electrocardiogram leads, 18-gauge needles, skin adhesive and
catheter securing systems, alcohol swabs, clear, occlusive dressing, tape, iodine swabs, and
lubricating gel.
FIGURE 3-4. Drawer 2, including propofol, lidocaine 2%, sterile saline, and atropine, sterile saline,
lidocaine 2% and sterile water, syringe labels, bupivacaine 0.5%, ropivacaine 1%, and spinal
needles.
Different drawers are best organized in a logical manner to ensure quick and easy access. One
drawer should be designated for emergency equipment and should include laryngoscopes with an
assortment of commonly used blades, styletted endotracheal tubes and airways of various sizes
(Figure 3-5). Emergency drugs that should be present include atropine, ephedrine, phenylephrine,
propofol, succinylcholine, and intralipid 20%. The latter can alternatively be stored in a nearby drug
cart or drug-dispensing system that is immediately available and in close proximity to the block room.
This way, it can be prepared within minutes in case of emergency (Figures 3-6, 3-7, and 3-8).
FIGURE 3-5. Drawer 3, including laryngoscope, assorted blades, and Magill forceps, emergency
medications, stylleted endotracheal tubes, and laryngeal mask airways of assorted sizes, nasal
airways, and oral airways.
FIGURE 3-6. Drawer 4, including syringes of assorted sizes, pressure monitors, stimulating needles,
and nonstimulating catheters.
FIGURE 3-7. Drawer 5, including sterile drape, sponges, sterile gloves, oxygen masks, and sterile
transducer coverings.
FIGURE 3-8. Drawer 6, including custom nerve block tray and continuous nerve block kit with
stimulating catheters.
Suggested Emergency Drugs Required During Nerve Block
Procedures
See Table 3-1.
TABLE 3-1 Suggested Emergency Drugs Required During Nerve Block Procedures
Treatment of Severe Local Anesthetic Toxicity
A 1998 study heralded the clinical utility of intralipid therapy in the treatment of local anesthetic
toxicity. Administration of 20% intralipid solution to rats increased the lethal dose of bupivacaine by
48% when compared with untreated controls. The same study also showed increasing survival rates
when used as part of a resuscitation protocol. The results were explained by the portioning of
bupivacaine into the newly created lipid phase.2
In follow-up studies, dogs that had bupivacaineinduced cardiovascular collapse were successfully resuscitated after receiving lipid infusion,
demonstrating the utility of intralipid in a large animal model that more closely approximates human
physiology.3
In 2006, Rosenblatt et al published the first use of intralipids in a patient to reverse
bupivacaine-induced cardiotoxicity.4
Soon thereafter, additional case reports of successful
resuscitation from local anesthetic-induced toxicity with intralipid were published5–8 establishing
intralipid infusion as an important emergency intervention in the practice of regional anesthesiology.
Based on laboratory evidence and a growing body of anecdotal reports in clinical practice, it appears
prudent to keep intralipid solution 20% in close proximity to locations where regional anesthesia is
administered.9
Peripheral Nerve Block Trays
Commercially available, specialized nerve block trays are useful for time-efficient practice of PNBs.
An all-purpose tray that can be adapted to a variety of blocks may be the most practical, given the
wide array of needles and catheters that may be needed for specific procedures. Appropriate needles,
catheters, and other specialized equipment are simply opened and added to the generic nerve block
tray as needed (Figure 3-9).
FIGURE 3-9. An example of a custom nerve block tray, including lidocaine 1%, lidocaine 1% with
epinephrine, sterile saline, syringes, connector, and marker, prep sponges and iodine solution, sterile
occlusive dressing and drape, and extension tubing.
Regional Nerve Block Needles
A wide array of needles is available for performing PNBs (Figure 3-10). Choice of needle depends
on the block being performed, the size of the patient, and preference of the clinician. Needles are
typically classified according to tip design, length, gauge, and the presence or absence of electrical
insulation or other specialized treatment of the needles (e.g., etching for better ultrasound
visualization).
FIGURE 3-10. Common needle tip designs.
Needle Tip Design
Direct evidence for an association between needle tip design and the incidence of nerve injury is
scarce. In a rabbit sciatic nerves model, Selander demonstrated that the risk of fascicle injury was
lower when a short bevel needle penetrated a nerve as opposed to a long bevel needle.10 However,
another experiment by Rice and colleagues suggested that the reverse may be true.11 This disparity
might be explained by the fact that the study of Rice et al examined the effect of needle bevel design
on the severity and consequences of intrafascicular should accidental fasicular penetration occur.
Therefore, although it may be more difficult to enter a nerve fascicle with a short bevel needle as
compared with a long bevel needle, the short bevel needle may cause a more severe lesion should a
nerve be impaled by such a needle.12 Needle design can also have a direct effect on the
anesthesiologist’s ability to perceive tissue planes. Tuohy and short bevel noncutting needles provide
more resistance and thus enhance the feel of the needle traversing different tissues. Long bevel cutting
needles, by contrast, do not provide as much tactile information while traversing different tissues.
Pencil point needles may be associated with less tissue trauma than short bevel needles when bony
contact occurs during spinal anesthesia, resulting in a lower incidence of postdural puncture
headache.13 It is unclear however, whether pencil point needles have any advantage over other needle
designs in practice of PNBs.
Needle Length
The length of the needle should be selected according to the type of block being performed (Table 3-
2). A short needle may not reach its target. Long needles have a greater risk of causing injury due to
increased difficulty in their handling and possibility of being inserted too deeply. The needle lengths
recommended in this text are based on the author’s experience and are intended as a general guide.
Note that the needle length is often longer by 2 to 3 cm for ultrasound-guided blocks because needles
are inserted further from the target to visualize the course of the needle on the image. Needles should
have depth markings on their shaft to allow monitoring for the depth of placement at all times.
TABLE 3-2 Block Technique and Recommended Needle Length
Needle Gauge
The choice of the needle gauge depends on the depth of the block and whether a continuous catheter is
placed. Steinfeldt et al recently demonstrated the correlation between larger needle gauge and
increasing levels of nerve damage after intentional nerve perforation in a porcine model.14 Thus, a
small gauge needle may theoretically reduce the tissue trauma and discomfort to patients, whereas a
long gauge needle bends more easily, making it more difficult to control. The needles of smaller
caliber however, may also be more likely to penetrate the fascicles. In addition, needles of smaller
gauges have more internal resistance, making it more difficult to gauge injection resistance and
aspirate blood. Needles of very small size (25 and 26 gauge) are most commonly used for superficial
and field blocks. Larger gauge needles (20–22 gauge) may be used in deeper blocks to avoid bending
of the shaft and to maintain better control over the needle path. When placing a continuous catheter,
the needle gauge must be large enough to allow passage of the catheter. Consequently, 17-19 gauge
needles are most commonly used with an 18- gauge catheter for continuous catheters.
Echogenic Needles
Visualization of the needle tip is one of the more challenging aspects of performing an ultrasoundguided PNB. To facilitate the ease of needle visualization, specialized needle designs are being
developed that allow greater visibility of the needle when performing ultrasound-guided PNBs. One
example of such needle designs is coating with a biocompatible polymer that traps microbubbles of
air, thus creating specular reflectors of air.15 The design improves needle visibility and aids in the
performance of sonographically guided biopsies.16 Another echogenic needle design incorporates
echogenic “dimples” at the tip to improve visibility.17 Unique texturing on the needle tip also
demonstrated improvement in visibility.18 The design of echogenic needles is a continuously evolving
field.
Ultrasound Machines
Ultrasound technology allows visualization of the anatomic structures, the approaching needle, and
the spread of local anesthetic.19 Ease of use, image quality, ergonomic design, portability, and cost
are all important considerations when choosing an ultrasound machine. To curtail costs, some
institutions or practices purchase a single ultrasound machine to use for several purposes such as
obstetrics, regional anesthesia, abdominal scanning, or echocardiography.20 Recently, a number of
newer ultrasound machine models have evolved that are portable or can be mounted on the wall,
which is beneficial in a setting where there is limited space to perform a block. The ultrasound
technology is continually and rapidity evolving with an increasing focus on its application in regional
anesthesia.
Sterile Technique
Strict adherence to sterile technique is of importance in the practice of regional anesthesia. Infections
due to PNBs are uncommon, but potentially devastating, yet largely preventable complications. A
report of a fatality due to an infectious complication of a PNB underscores the importance of sterile
techniques.21 One study found that 57% of femoral catheters demonstrated bacterial colonization,
although only 3 of 208 showed signs suggestive of infection (shivering and fever) that subsided after
catheter removal.22 Another study documented 1 infectious complication of 405 axillary catheters
placed,23 reflecting the relative rarity of such events. However, several case reports reflect the
severity of infections caused by indwelling catheters. One case of psoas abscess complicating a
femoral catheter placement has been reported.24 Capdevila and colleagues reported an occurrence of
acute cellulitis and mediastinitis following placement of a continuous interscalene catheter that may
have resulted from the refilling of local anesthetic into the elastomeric pump.25 More recently, sepsis
following interscalene catheter placement was complicated by hematoma.26 These cases illustrate the
importance of adherence to aseptic technique in all phases of needle puncture, catheter insertion and
management, as well as administration of local anesthetics.
The hands of health care workers are the most common vehicles for the transfer of microorganisms
from one patient to another.27 Studies show that although soap and water may remove bacteria, only
alcohol-based antiseptics provide superior disinfection, and solutions of povidone iodine and
chlorhexidine possibly provide the most extended antimicrobial activity.28 Sterile gloves should be
used throughout in addition to all other measures discussed.29 No evidence exists to prove that
gowning decreases the incidence of nosocomial infection.30 One study showed no difference between
infection or colonization rates between gowning and not gowning in the pediatric intensive care unit
(ICU).31 Another study showed that use of gowns and gloves was no better than use of gloves alone in
preventing rectal colonization of vancomycin-resistant enterococci in the medical ICU.32 Therefore,
although gowning during the performance of PNBs is recommended by some, there is not sufficient
evidence that such practice is beneficial in decreasing the incidence of infection.30
Surgical masks have become commonplace when performing invasive procedures. In an
experiment where volunteers were asked to speak with and without surgical masks in close proximity
to agar plates, it was found that wearing a mask significantly reduced the contamination of the
plates.33 However, there is considerable debate whether their use is effective at decreasing
nosocomial infection with some arguing that they represent an essential component of sterile
practice34,35 and others maintaining there is no scientific evidence to support the practice. A postal
survey of 801 anesthesiologists in Great Britain found that only 41.3% routinely wore face masks
while performing spinal and epidural anesthesia, whereas 50.6% did not.36 The work of Schweizer
indicates that masks may increase contamination of a sterile field possibly due to the increase in
shedding skin scales.37 These results were supported by the work of Orr et al that found a significant
(p < 0.05) decrease in the amount of infections when masks were not worn during surgical
procedures.38 However, one case series reported four cases of meningitis due to viridans
streptococci following spinal anesthesia performed by the same anesthesiologist.39 The same
causative bacteria were later cultured from the anesthesiologist’s nasopharyngeal mucosa, and the
anesthesiologist was noted not to wear surgical masks when performing spinal anesthesia. Another
case report described two cases of bacterial meningitis following diagnostic lumbar puncture due to
Streptococcus salivarius. The same bacteria were cultured from the oropharyngeal mucosa of the
neurologist who performed the lumbar puncture.40 At this time there is no evidence that wearing a
mask can prevent infectious complications of PNBs, although some clinicians suggest this practice.41–
43
Transducer Covers and Gel
Sterile clear dressings or sterile ultrasound transducer covers constitute sound clinical practice and
are routinely used by most clinicians. A variety of sterile ultrasound transducer covers are available.
Some come in sets with sterile ultrasound gel and rubber bands to pull the transducer covers tightly
over the transducers to facilitate imaging.
However, the incidence of contact dermatitis due to ultrasound gel is rare considering the
frequency of its worldwide use, several case reports have emerged that have been attributed to the
bacteriostatic preservatives propylene glycol and parabens.44,45 Regardless, contact dermatitis from
ultrasound gel has also been attributed to the imidazolidinyl urea.46 Drugs such as diazepam that have
propylene glycol in their solvent solutions are known to cause myotoxicity when injected
intramuscularly.47 In the 1950s, a preparation of procaine called Efocaine was introduced for its long
duration of action. However, reports surfaced of neuritis and local irritation after perineural injection
of Efocaine. The mechanism of action of the drug was attributed to coagulation necrosis, and it is
noteworthy that the preparation of Efocaine contained 78% propylene glycol.48 Likewise, safety of
inadvertent injection of ultrasound gel during ultrasound-guided nerve blocks has been questioned. A
recent study has demonstrated that the lumen of PNB needles can carry and deposit ultrasound gel in
close proximity to nerves, suggesting that further studies are needed to ascertain whether the amounts
of gel under consideration are enough to cause toxicity.49
Injection Pressure Monitoring
Intrafascicular injections during the performance of PNBs are associated with high injection
pressures during injection of the local anesthetic.50 Such injections lead to neural damage and
neurologic deficits in animal models.51 Assessment of resistance to injection is routinely done in
clinical practice to reduce a risk of an intraneural injection and constitutes a suggested routine
documentation of PNB procedure.71 Traditionally, however, anesthesiologists have relied on a
subjective “syringe feel,” that is, the feeling of increased resistance on injection. Recent studies have
cast doubt on the ability of anesthesiologists to detect intraneural injections using this method. In fact,
studies show that anesthesiologists may often inject local anesthetic at injection pressures capable of
rupturing a fascicle.52 An inline injection pressure manometer can be placed between the syringe and
the injection tubing with the needle to objectively quantify and monitor the injection pressure (Figure
3-11). Injection pressures greater than 20 psi are associated with intraneural intrafascicular injection.
Alternatively, an air-compression test in the syringe is used to avoid injection using pressure greater
than 20 psi.72,73 In actual clinical practice, injection with pressures <15 psi establishes a wider
margin of safety in reducing the risk of an intrafascicular injection or too forceful spread of the local
anesthetics.
FIGURE 3-11. Monitoring injection pressure at the femoral nerve using an in-line injection pressure
monitor (BSmart, Concert Medical USA). A color-coded piston moves during the block performance
to indicate pressure during injection.
Continuous Nerve Catheters
Sutherland was first to introduce the stimulating catheter to improve the success rates over blindly
inserted catheters.53 This was followed closely by further reports of similar techniques.54,55 For the
performance of continuous peripheral nerve catheters, a wide range of needle and catheter types are
available. Two main types of catheters are the stimulating catheters, which can provide stimulation
through the catheter itself, and the nonstimulating catheters, which do not allow this option.
Stimulation is typically accomplished through a metal stylet or coil that conducts electricity through or
around the catheter lumen. Several designs are available on the market. Although it would appear
logical that the confirmation of the catheter placement using electrolocalization should result in a
greater consistency of catheter placement and higher success rate, the data on any advantages of the
stimulating catheters over nonstimulating catheter remain conflicting. One study in volunteers found
that although there was no statistically significant difference in block success rate between stimulating
and nonstimulating catheters, the stimulating catheters did provide an increase in depth of both
sensory and motor block.56 Another study found that using a stimulating catheter as opposed to a
nonstimulating catheter resulted in a significant lowering of the local anesthetic volume required to
block the sciatic nerve.57 Stimulating may also result in shorter onset time for sensory and motor
anesthesia hadzic's peripheral vision
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