ANESTHESIA Hadzic's Peripheral Nerve Blocks Hadzic parte 01

 

















































































































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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