2 - American Society of Regional Anesthesia and Pain Medicine

Transcription

A PUBLICATION OF THE AMERICAN SOCIETY OF REGIONAL ANESTHESIA AND PAIN MEDICINE
In This Issue
13th Annual Pain
Medicine Meeting – see page 3
Advancing the Science and Practice of Regional Anesthesia and Pain Medicine
Table of Contents
President’s Message________________________________ 2
Fall Meeting Preview________________________________ 3
Resident and Fellow Events at the
2014 Fall Annual Meeting_ ___________________________ 4
Editorial _ ________________________________________ 5
ASRA COAGS© APP REVIEW___________________________ 6
ASRA Coags© - An Electronic Decision Support Tool
for the ASRA Anticoagulation in Regional Anesthesia
Practice Advisory___________________________________ 7
Use of Digital Subtraction Angiography in
Epidural Steroid Injections: PRO_ ______________________ 9
Use of Digital Subtraction Angiography in
Epidural Steroid Injections: CON_ _____________________ 10
Outcomes in Pain Medicine: A Brief Review_ ____________ 11
Postdural Puncture Headaches:
What Works, What Doesn’t, and What Is New? ___________ 13
Beyond ACLS: Targeted Treatment for
Local Anesthetic Toxicity _ __________________________ 15
Editor
Edward R. Mariano, M.D., M.A.S.
Newsletter Committee
Steven Orebaugh, M.D. (Regional Anesthesia Lead)
Kevin Vorenkamp, M.D. (Pain Medicine Lead)
Magdalena Anitescu, M.D., Ph.D.
Melanie Donnelly, M.P.H., M.D.
Nabil Elkassabany, M.D.
Brian Harrington, M.D.
Andrea Nicol, M.D.
Maunak Rana, M.D.
Resident Section
Anish Doshi, M.D.
Foreign Corresponding
Michael Barrington, M.D.
Jose de Andres, M.D.
Officers
President: Joseph M. Neal, M.D.
President-Elect: Oscar A. De Leon Casasola, M.D.
Treasurer: Asokumar Buvanendran, M.D.
Past President: Vincent W.S. Chan, M.D.
Executive Director: Angie Stengel, MS, CAE
Board of Directors
Honorio T. Benzon, M.D.
John Butterworth, M.D.
James Hebl, M.D.
Samer Narouze, M.D.
Colin McCartney, M.B., Ch.B., F.R.C.A.,
F.C.A.R.S.C.I., F.R.C.P.C.
Santhanam Suresh, M.D., F.A.A.P.
Eugene R. Viscusi, M.D.
Founding Fathers
L. Donald Bridenbaugh, M.D.
Harold Carron, M.D. (Deceased)
Jordan Katz, M.D.
P. Prithvi Raj, M.D.
Alon P. Winnie, M.D.
Photo courtesy of Dr. Edward Mariano
American Society of Regional Anesthesia and Pain Medicine
239 Fourth Avenue, Suite 1714 • Pittsburgh PA 15222
phone toll free 855-795-ASRA • fax 412-471-7503 • www.asra.com
2
Copyright © 2012 American Society of Regional Anesthesia and Pain Medicine. All rights reserved.
Contents may not be reproduced without prior written permission of the publisher.
Article Title Message
President’s
The Cost of Doing Business
Over the past two years, the ASRA Board of Directors has been
committed to improving transparency with regard to the Society’s
inner workings. While it would be incorrect to surmise that past
ASRA leadership has consciously withheld information from the
membership, nonetheless we have not been terribly effective in
explaining organizational details – most of which even we Directors
were unaware of until we began our service on the Board. This
theme of transparency is perhaps even more apropos as part of the
2014 Year of the Member Initiative – what could be more relevant
to the member than the frequently heard question: “Why does
everything cost so much?” This quarter’s President’s Message will
attempt to bring some clarity to the two financial transactions that
most impact the individual member – meeting registration and
society dues – and conclude with an overview of what actually
happens with all of your money.
Attending an ASRA annual meeting is expensive. An ASRA member
who registers early for the upcoming fall Pain Medicine meeting
in San Francisco and attends a workshop and a problem-based
learning discussion lunch will spend about $1000. With fees like
severely limit outside support
of our meetings. Nevertheless,
exhibits and grants significantly
offset the Society’s expenses, and
we clearly could not stage our
annual meetings without industry
support. In the end, our bottom line
for ASRA’s 2012 and 2013 spring
and fall meetings varied between
a $115,000 loss and a $160,000
profit. I will explain shortly where
that profit went.
Joseph M. Neal, M.D.
ASRA President
What about dues? The Society’s
dues have remained relatively
stable over the past few years. At $225 for an active member,
ASRA’s annual dues are at the lower end of major United States
anesthesiology societies. When you toil a few hours to pay your
annual dues, are you getting value for the expenditure? We hope
so, considering the benefits – print and electronic versions of
Regional Anesthesia and Pain Medicine, the quarterly ASRA News,
substantially reduced base registration fees at the annual meetings,
“What could be more relevant to the member than the frequently heard
question: “Why does everything cost so much?”
that, ASRA must be making out like a bandit, right? Well, not exactly.
Compared to like organizations, the Society’s cost per hour of
continuing medical education (CME) credit places it in the middle
of the pack – about $28/credit hour in 2012. Since then, ASRA
has actually reduced most workshop fees twice and only slightly
increased the base registration fee. Yet these fees do not begin to
cover the meeting’s actual cost – the ~$460,000 in registration
fees that ASRA collected from the just over 1000 participants at
the recent spring meeting in Chicago covered only 60% of that
meeting’s cost. Indeed, the costs of our annual meetings are mindboggling. For instance, at the spring 2014 meeting, audiovisual
services were well in excess of $100,000 and we spent over
$15,000 for workshop models and roughly the same amount for
credit card service charges. That Diet Coke you drank at the break
– it was invoiced to ASRA at about $7.50 – a real bargain compared
to the cost of the cookie! Some members ask why industry cannot
pay for the meeting? The full answer is complicated, but suffice it
to say that budgetary cutbacks on the part of pharmaceutical and
device makers, coupled with ever-increasing scrutiny regarding
conflict of interest and expenditure-reporting to federal agencies
and weekend ultrasound/cadaver workshops, etc. Moreover, we
hope that you find value and pride in the integral role that your
membership plays in fulfilling ASRA’s mission of education and
research in our subspecialties.
The ultimate value of your membership is perhaps best judged in
light of how the Society spends your money and what happens with
our operating margin, which averaged slightly over $300,000 during
the five-year period from 2009-2013. If you were to look at ASRA
as a business, we were a $2.9 million dollar company in 2013.
Our revenues were primarily derived from member dues (25%)
and meetings (50%), with the remaining coming from a variety of
sponsorships, journal royalties, and other sources. As illustrated in
Figure 1, 38% of the Society’s expenses went toward administering
ASRA – paying our management partners and operating the
day-to-day business. The remaining 62% of your Society’s money
supported our mission of education and research. Approximately
half of total operating revenue was spent on education – about 4%
to purchase your journal subscriptions and the rest to supporting
the costs associated with the annual meetings and workshops.
Meeting expenses include that expensive glass of iced tea at the
break, but also the costs associated with tracking and awarding
2014
Continued on page 4
2
Fall Meeting Preview
I
t is with much excitement that I
am writing to you regarding the
13th Annual Pain Medicine Meeting
taking place in San Francisco
on November, 13-16, 2014. The
Scientific/Education Planning
Committee with the assistance of
the ASRA Board of Directors and
CME Committee, chaired by Dr.
Terese Horlocker, have dedicated
an extensive amount of time in
David Provenzano, M.D.
developing and executing the
Chair, ASRA Scientific/Education
scientific program. The “final”
Planning Committee
product demonstrates this effort
13th Annual Pain
with the creation of a scientific
Medicine Meeting
program that presents a platform
where knowledge and experience can be shared with worldrenowned experts.
The meeting starts off with refresher course lectures covering
crucial topics required for the advancement of pain medicine. The
first lecture by Dr.
Linda Watkins will
cover neuropathic
pain with an update
on the role of the
glial cell in the
development and
maintenance of
neuropathic pain.
Dr. Watkins has
published extensively
on the role of the glial
cell. Dr. Srinivasa Raja will discuss the updated neuropathic pain
treatment guidelines. The spine and discogenic back pain lectures
by Drs. Alexander Vaccaro and Jon Lurie will illustrate the current
understanding of the pathophysiology and treatment of degenerative
disc disease with an emphasis on the future of molecular, gene, and
cell-based therapies. Pain practitioners will also be provided with
an in-depth look at the evidence for surgery for spine conditions as
reported from the Spine Patient Outcomes Research Trial (SPORT).
An update on complex regional pain syndrome will be provided by
Drs. Timothy Lubenow and Asokumar Buvanendran. Epidural steroid
injections will be further explored in the lectures by Drs. Gary
Brenner and Steven Cohen. The field of neuromodulation is bright
and significant advancements are occurring with the development
of new technology and with our understanding of the mechanism
of action. The refresher course lectures on neuromodulation by Drs.
José De Andres (President of ESRA), Ricardo Vallejo, and Timothy
Deer (President-Elect of the International Neuromodulation Society)
will further define the anatomy and the mechanism of action of
neuromodulation. A look into the future of neuromodulation will be
provided with discussion on high-frequency, burst, and dorsal root
ganglion (DRG) stimulation. The day will conclude with a discussion
led by Drs. Sean Mackey and John Carrino on neuroimaging based
pain detection. Dr. Hank Greely, the Director of the Center for Law
and the Biosciences at Stanford University, will explore the legal
implications of neuroimaging.
On Friday, Saturday, and Sunday, parallel sessions will cover
interventional and non-interventional topics including financial
and clinical decision-making for spine care, cancer pain, the
future of education and publishing in pain medicine, implantable
pain devices, headache, neck and facial pain, and improving
interventional outcomes before-and-after placing a needle, office
based opioid and substance abuse management, and medical
marijuana for pain. The parallel sessions will be led by pain experts
including such speakers as Drs. Oscar De Leon Casasola, Juan
Francisco Asenjo, Marc Huntoon (Editor of Regional Anesthesia and
Pain Medicine), Joseph Neal (President of ASRA and previous Editor
of Regional Anesthesia and Pain Medicine) Robert Jamison, and
Nagy Mekhail. The medical marijuana session will provide insight
into the basic science, healthcare policy, and clinical evidence
for the utilization of
marijuana for pain
management. We are
fortunate to have Drs.
Mark Wallace, Marcel
Bonn-Miller and Mark
Ware. Dr. Mark Ware
from McGill University,
the Executive Director
of the Nonprofit
Canadian Consortium
for the Investigation of
Cannabinoids, will provide input on the Canadian perspective. In the
update on interventional pain care session, Dr. Samer Narouze will
present the new anticoagulation guidelines for interventional pain
management.
“The field of neuromodulation is bright and
significant advancements are occurring with the
development of new technology and with our
understanding of the mechanism of action.”
3
Three plenary sessions will occur covering “must know topics”
including musculoskeletal ultrasound, the appropriate utilization of
opioids and the FDA Safe Use Initiative Epidural Steroid Injection
Working Group Recommendations. The musculoskeletal ultrasound
interventional and diagnostic plenary session on Friday entitled
“Using Vision to Help Make Decisions” will provide insight on the
use of ultrasound for assessing and treating the musculoskeletal
system. The session will end with a live demonstration of
musculoskeletal ultrasound scanning protocols for common
joints. International experts will lead this session including Drs.
Samer Narouze, Vincent Chan, Marko Bodor, Philip Peng, and
Levon Nazarian (Editor for the Journal of Ultrasound in Medicine).
On Saturday, the plenary session entitled “The Challenges with
Opioids in Chronic Pain Management” will serve to provide a
2014
Continued on page 18
President’s Message continued...
your CME credits, paying faculty travel costs (ASRA faculty are not
paid honoraria), and hiring the audiovisual crew. Finally, our entire
operating margin (what is left over at the end of the year) was
put back into the Society. A small percentage (2% last year) was
directed to a long-term investment account, which will be tapped
this year to underwrite part of the costs of totally revamping the
ASRA website. The rest of our ‘yearly profits’ (about 11% of 2013
revenue) were donated to our research funds, which provide major
competitive funding for research grants. These two funds constitute
your Society’s largest assets – the corpus of the Koller Fund for
Regional Anesthesiology and Acute Pain Medicine research is
currently $2.8 million dollars; the newer Pain Medicine Research
Fund has $1.7 million dollars and is being funded preferentially until
it equals the Koller Fund.
On behalf of the ASRA Board of Directors, I sincerely hope that
this column has been useful to those of you who wish to better
understand the Society’s finances. The Board understands that
everything related to the ‘business of ASRA’ is expensive but works
diligently to keep these expenses reasonable while maintaining a
sufficient margin to support the mission. At our upcoming interim
board meeting in September, we plan to delve deeper into the
question of just what should be a reasonable operating margin for
a non-profit professional society like ASRA. If you have any further
questions, my fellow Directors and I welcome your inquiries.
Resident and Fellow Events at the 2014 Fall Annual Meeting
O
Anish Doshi, M.D.
Chair, ASRA Resident
Section Committee
n behalf of the ASRA Resident
Section Committee, we welcome
and encourage all residents and
fellows to attend the 13th Annual ASRA
Pain Medicine Meeting from November
13-16, 2014, in San Francisco,
California. The conference will feature
several interactive discussions and
hands-on workshops led by many of
the leading experts in the field of Pain
Medicine. It will also provide unique
networking opportunities for all those
considering fellowship training or
seeking potential career opportunities.
We have planned an informative,
interactive, and educational two-day program planned specifically
for you. During the course of the program, you will learn more
about your future careers, refine your procedural dexterity, and
interact with distinguished faculty. The scheduled program will
provide you with expert opinions and valuable advice about the
fellowship application process, the transition to becoming an
attending, the selection of private vs. academic practice, the
pearls of appropriate practice management implementation, and
the management of the difficult chronic pain patient population.
Following an introductory lecture series given by world-renowned
experts, you will also participate in physician-guided procedural
workshops using flouroscopy and ultrasound guidance on live
models to practice and enhance your current skills. During the
evenings, you will be able to gather information about various
fellowship programs and meet with fellowship directors and
potential future employers at the ASRA Get Together reception and
annual career fair. Along with the Resident and Fellow Educational Program, Dr.
Provenzano and the Scientific/Education Planning Committee
have planned a remarkable conference program, which you are
all highly encouraged to attend as well. The program will provide
you with vital information that is not typically provided during
your training, and it will certainly help guide your future paths as
pain medicine physicians. For instance, at this conference, you
will have the unique opportunity to attend a presentation on the
current status of opioid therapy and diversion given directly by a
representative from the United States Drug Enforcement Agency!
We look forward to seeing you in San Francisco and ask that you
please help spread the details of our meeting and program to your
respective program’s residents and fellows.
CIVCO | GE Healthcare | Medtronic
PharMEDium Services, LLC | Purdue Pharma, LP
2014
4
Editorial
T
Edward R. Mariano, M.D., M.A.S.
Editor
Follow me on Twitter
@EMARIANOMD!
his issue of ASRA News
features the upcoming Fall Pain
Medicine annual meeting chaired
by Dr. David Provenzano. Drs.
Provenzano and Doshi provide us
with an overview of the meeting’s
highlights and resident/fellow
events that will be sure to appeal
to trainees and pain medicine
practitioners of all experience
levels. In addition to the amazing
educational offerings, this year’s
Fall Pain Medicine meeting also
happens to be in my “neck of the
woods”—one of the greatest cities
in the world—San Francisco, California. Here are a few things
you may or may not have known about San Francisco.
San Francisco is the biggest little city. At just under 47 square
miles and with more than 200,000 inhabitants, San Francisco
is second only to New York City in terms of population density.
Despite its relatively small size, “the City” (as we suburbanites
refer to it) consists of many small neighborhoods, each with its
own charm and character: Union Square, the Financial District,
Pacific Heights, the Marina, Haight-Ashbury, Chinatown (Figure
1), Little Italy, Nob Hill, Russian Hill, SoMa (South of Market), the
Fillmore, Japantown, Mission District, Noe Valley, Twin Peaks,
Castro, Sunset, Tenderloin, and others. For this reason, San
Francisco may arguably be the only option for die-hard New
Yorkers who wish to relocate away from snow.
“San Francisco
is the biggest
little city”
Figure 2
Figure 1
Figure 3
5
2014
ASRA COAGS© APP REVIEW
Even though it doesn’t snow, San Francisco weather is incredibly
unpredictable, even when going from one side of the city to the
other. “The coldest winter I ever spent was a summer in San
Francisco,” a quote often mistakenly attributed to Mark Twain
(no one really knows who actually said it), is nevertheless often
true. Here in the San Francisco Bay Area, our local meteorologists
provide daily forecasts for each of the region’s microclimates.
The western side of the City along California’s coast is regularly
plagued with fog while the eastern side of the City tends to be
sunny most days of the year. It’s always a good idea to check
the microclimate forecast before heading over to see the Golden
Gate Bridge just in case it happens to be shrouded in fog. Also,
average July temperatures in the City range in the 50s-60s
Fahrenheit (no different than average November temperatures), so
summer tourists often contribute to the local economy by buying
“SF” logo sweatshirts for their walk across the City’s most famous
bridge.
San Francisco is very family-friendly. If you’re debating whether
or not to make a family trip out of the Fall Pain Meeting, my advice
is to do it. Right around the conference hotel, the Hyatt Regency
San Francisco, there are a number of attractions and events worth
checking out. Every Saturday there is a huge farmers market at
the Ferry Building across the street from the hotel (Figure 2). As
you probably figured out, from the Ferry Building you can also
take a ferry ride to a number of other destinations in the Bay
Area (I recommend Sausalito, a short trip that takes you past
Alcatraz). For kids, there are 3 parks within walking distance,
the San Francisco Railway Museum, Exploratorium, and the cable
car turnabout at Powell and Market Street; trips to Fisherman’s
Wharf or the aquarium are a short taxi or cable car ride away. In
addition, runners will love running up and down the Embarcadero
which gives you a view of the Bay Bridge (Figure 3) and takes
you past the City’s many piers; shoppers will be in heaven; and
foodies have an impossible decision to make when choosing the
location for every meal (try Slanted Door at the Ferry Building at
least once).
Enough about San Francisco—you’ll have to see it for yourself. In
addition to the Fall Pain Medicine meeting previews, this issue of
ASRA News also includes fantastic original content covering the
topics of digital subtraction angiography, pain outcomes, ASRA’s
first entry into the app market, and much more. Enjoy!
ERRATUM
With regard to the article “Opioids for Chronic Pain: Damned If
You Do, Damned If You Don’t” by Dr. Silverman published in the
May 2014 issue of ASRA News, with reference to the case of Vasa
v. Compass Medical, the employee killed was Dr. Mark Vasa (not
Michael Vasa) who was employed by the hospital as a radiation
oncologist.
A
s an anesthesiology resident
at the largest public hospital
in America, I cannot emphasize
enough the time and energy the
ASRA COAGS© app has saved me
and my busy co-residents.
Christina Le, M.D.
Anesthesiology Chief Resident,
PGY-4
Department of Anesthesiology,
Perioperative Medicine and
Pain Management
Jackson Memorial Hospital/
University of Miami Miller School
of Medicine
There have been many occasions
in which I have found myself
discussing the proper timing
of anticoagulation and regional
anesthesia with residents
and attendings, especially for
patients on less commonly used
medications. And every time,
we revert to doing an internet
search for the most recent ASRA
Guidelines.
While the risk of a bleeding
complication is relatively low, the
neurologic consequences can be
profound and life-changing. And for this reason, we want to make
educated, evidence-based decisions concerning anticoagulation
and interventional procedures. In light of this effort, ASRA has
provided easily accessible guidelines in order to assist anesthesia
providers to take all possible precautions for prevention.
The ASRA COAGS© app offers
a user-friendly, aestheticallyappealing platform to
quickly reference the current
recommended guidelines for
placement of blocks in patients
receiving anticoagulation.
We can focus our
time and efforts
on caring for our
patients, instead
of searching for
information.
The app allows you to choose
from three different scenarios
in which you may find yourself:
neuraxial block, deep plexus/
peripheral block, or superficial
peripheral block. Once you choose your specific scenario, the
app will give you the medication’s mechanism of action and
management advice for placing a block, restarting anticoagulation
and catheter removal. Not only that, the app also gives the user
easy access to the full 2010 ASRA practice advisory.
For only $3.99, this easy resource can be used by even the
most technologically-challenged practitioner and can make all
the difference for our patients. With it, we anesthesiologists
can reliably make evidence-based decisions about invasive
procedures based on our patient’s coagulation status. And finally,
we can focus our time and efforts on caring for our patients,
instead of searching for information.
2014
63
ASRA Coags© - An Electronic Decision Support Tool for the ASRA
A
SRA has published the gold standard in recommendations on
the use of regional anesthesia in patients on anticoagulation and
antithrombolytic medications with the most recent practice advisory
being published in 2010 (Regional Anesthesia in the Patient Receiving
Antithrombotic or Thrombolytic Therapy - American Society of
Regional Anesthesia and Pain Medicine Evidence-Based Guidelines Third Edition). This is the most viewed document on ASRA’s website,
and it impacts providers on a regular basis. However, since the
publication is nearly 40 pages long, utilizing the content in real-time
can be difficult in the clinical environment.
Rajnish Gupta, M.D.
Assistant Professor, Department
of Anesthesiology
Associate Director,
Comprehensive Pain Service
Matthew McEvoy, M.D.
Associate Professor, Department
of Anesthesiology
Vice-Chair, Educational Affairs
Director, Residency Program
Vanderbilt University Medical Center, Nashville, Tennessee
Many clinicians often create tables or note cards that consolidate the
information into a usable format, but this is often created ad hoc by
the clinician or the institution; several published forms that can be
found on the internet contain errors. Therefore, we ventured to create
an electronic application (app), one that was validated by the authors
of the Practice Advisory committee and could be readily updated with
push technology when new information was available. The goal was
to make an interactive searchable experience for the clinician that
Figure 1: ASRA Coags© iOS app icon.
Figure 2: User interface within ASRA Coags© app, including
27
American Society of Regional Anesthesia
and Pain
search
field, Medicine
recommendation, and full text recommendations.
2014
Anticoagulation in Regional Anesthesia Practice Advisory
provides a consolidated version of the Practice Advisory and one that
could be utilized quickly and accurately. This app, ASRA Coags©, is
now available on the Apple iTunes Store for iOS devices (Figure 1).
Within the app user interface (Figure 2), the clinician is presented
with a search box and list of the medications discussed in the 2010
guidelines, including the ability to search for both United States
trade names and generic names of medications. Once a medication
is selected, the user is presented with the option to choose either
neuraxial procedure, deep peripheral nerve block, or superficial nerve
block. The next option presents the stage of the procedure the clinician
is asking about: before placement of a block, restarting the medication
while a catheter is in place, stopping a medication before pulling a
catheter, or when to restart a medication after the catheter is pulled.
Each option presents the proper recommendation based on the 2010
Practice Advisory.
In addition, to facilitate clinicians’ using their own clinical judgment and
interpretation, we have embedded either the full text of the Practice
Advisory Executive Summary for the selected medication’s relevant
section and even the entire PDF of the full Practice Advisory.
By taking advantage of the collaboration between academic
Regional Anesthesiologists at Vanderbilt, the authors of the ASRA
Practice Advisory, and programming skills of Mustard Seed Software
(Charleston, SC) (Figure 3), we have been able to create an accessible
and easy-to-use electronic decision support tool for a challenging and
clinically-important situation that arises frequently. Also, a multiinstitutional trial investigating the effects of this app on adherence
to the ASRA guidelines has recently been completed. Results are
promising and will be forthcoming in published form later this year.
The most exciting future plans for this app are to incorporate the
upcoming Fourth Edition Practice Advisory information directly into the
app and to develop an Android version to extend the availability of this
app to more users. We’re excited to make this available to the medical
community and hope it provides a tool for better clinical care and
patient safety.
Figure 3: ASRA Coags© contributors.
2014
38
PRO
Use of Digital Subtraction Angiography
in Epidural Steroid Injections
CNS INJURIES AFTER EPIDURAL
STEROID INJECTIONS
A retrospective review showed the
overall safety of epidural steroid
injections (ESIs). A 2.4% minor
complication rate including pain
and numbness was noted with
interlaminar (IL) injections (6%) vs.
the transforaminal approach (2.1%)
in 103 of 4265 ESIs.1 Complications
after cervical IL injections included
Honorio T. Benzon, M.D.
vasovagal episodes, facial flushing,
Professor of Anesthesiology and
headache, dural
Pain Medicine
puncture, and
Northwestern University
paraplegia from
Feinberg School of Medicine
Chicago, Illinois
spinal hematoma.2
In the latest Closed
Section Editor:
Claims
study, central
Maunak Rana, M.D.
nervous system (CNS)
injuries after cervical IL ESIs included trauma to the
spinal cord or nerve root, cord infarction or stroke after intraarterial
injection, dural puncture, hematoma, and infection.3 It was noted
that fluoroscopic guidance was used in 67% and contrast in 57%
of the claims. After a careful review of the cases, Rathmell and
colleagues concluded that the appropriate use of radiographic
guidance would have prevented injury in 49% of the claims of
spinal cord injury after cervical procedures.3
anastomose with the vertebral artery and the anterior spinal artery
through segmental medullary arteries;7 c) artery of Adamkiewicz
through its variable and aberrant origins;8,9 and d) sacral radicular
arteries which follow each root of the cauda equina and connect
with the ansa communications at the conus which in turn
connects with the anterior spinal artery.9 The last set of arterial
communications explains the occurrence of CNS injuries with S1
TF ESIs. For IL ESIs, the route of the embolus can be through the
radiculomedullary artery in the lateral or midline posterior epidural
space.10 The radiculomedullary arteries have been noted to enter
the neuroforamina then travel superiorly and laterally in the lateral
epidural space joining the anterior spinal artery.11,12 Indeed, a
cadaver study showed the presence of a posterior branch of the
“A negative aspiration does not preclude
intravascular injection.”
Paraplegia after TF ESIs has been attributed to embolism caused by
particulate steroid.4-6 The possible route of embolization includes
the following arteries: a) segmental radicular artery accompanying
the nerve root;4 b) ascending cervical and deep cervical arteries
which are close to the cervical intervertebral foramina and also
radiculomedullary artery supplying the dorsal aspect of the cauda
equina.13
INCIDENCE OF INTRAVASCULAR INJECTION AFTER EPIDURAL
INJECTIONS
Prospective studies showed the incidence of intravascular injection
to be 1.9% after lumbar IL injection, 10.8-15.5% after lumbar TF
injections, and 10.9% after caudal injections.14-16 In one study, the
authors noted the failure of blood aspiration in 74% of cases that
proved to be intravascular.14 The sensitivity and specificity of the
presence of blood, either spontaneously or after aspiration, was
44.7% and 97.9%, respectively.15 The incidence of intravascular
Figure 1: Serial images showing angiogram after contrast injection (A). The radicular artery is barely visible after contrast injection under live
fluoroscopy (B) but is clear with DSA (C). From Rathmell JP, Aprill C, Bogduk N. Cervical transforaminal injection of steroids. Anesthesiology
2004;100:1595-1600 (reprinted with permission).
92
2014
CON
in Epidural Steroid Injections
DSA SHOULD NOT BE USED ROUTINELY
Neuraxial delivery of corticosteroid or local anesthetic is generally
well tolerated with a low incidence of serious complications. Still,
adverse outcomes of irreversible paraplegia, stroke, and death
have been reported from these interventions. Digital subtraction
angiography (DSA) has been touted as an adjunct to interventional
procedures to identify peri-injection vascular compromise.
DSA has emerged as a supportive measure and has demonstrated
greater accuracy in detecting intravascular injections compared
to aspiration and live fluoroscopy.1-3 DSA is commonly used
as a safety measure in high-risk procedures such as cervical
transforaminal epidural steroid injection (TFESI), or may be useful
“DSA cannot reliably prevent adverse
outcomes in neuraxial procedures”
George C. Chang Chien, D.O.
Fellow, Pain Medicine
Anesthesiology Institute, Section
of Pain Medicine
Cleveland Clinic
Cleveland, Ohio
Kenneth D. Candido, M.D.
Professor of Clinical
Anesthesiology
University of Illinois College of
Medicine Chairman, Department of
Anesthesiology Advocate
Illinois Masonic Medical
Center, Chicago, Illinois
in clarifying an abnormal or unexpected flow pattern observed on
live fluoroscopy (Figure 1). In a study of 134 patients, Mclean et
al compared real-time fluoroscopy vs. DSA during 177 cervical
TFESI. Intravascular injection was detected in 18% of real-time
fluoroscopy cervical TFESIs vs. 32.8% when DSA was used (P
= 0.0471).1 All of the vascular angiograms identified by both
live fluoroscopy and by DSA were venous in origin.1 In one
prospective study of vascular flow detection rate in lumbosacral
TFESI, Lee et al performed 60 lumbar and 20 S1 TFESI and
found 20 cases of intravascular injection (11 at S1, and 9 in the
lumbar spine) utilizing DSA vs. real-time fluoroscopic guidance,
predicting 12 of the 20 instances.2 These authors did not
distinguish between arterial and venous uptake but conceded
that “the majority of these vascular injections were venous”
with a statistically-significant higher rate at S1.2 In a recent
study by El Abd et al, these authors also evaluated the rate of
detection of vascular uptake observed by DSA that is missed with
traditional safety precautions, including live fluoroscopy. Of the
150 consecutive patients undergoing 222 TFESI in the cervical,
lumbar, and sacral levels, 46 had evidence of intravascular flow
patterns with live fluoroscopy with contrast, and DSA identified
an additional 5 vascular venograms not identified on live
fluoroscopy.3 DSA may detect inadvertent venous injection at a
higher rate than live fluoroscopy, but there is less robust evidence
that DSA enhances recognition of arterial flow.
DSA cannot reliably prevent adverse outcomes in neuraxial
procedures (Table 1). DSA is limited by motion artifact with
recognition subject to human interpretation. Any motion between
the scout film and subsequent images will impair the subtraction
process, causing degradation of image quality. Utilization of this
technology does not negate the potential for human error. The
Figure 1: Anterior-posterior view of a C6-7 cervical
transforaminal epidural steroid injection: (A) conventional
fluoroscopic exposure; (B) digital subtraction view.21
2014
10
3
Outcomes in Pain Medicine: A Brief Review
Sean Mackey, M.D., Ph.D.
Chief, Division of Pain Medicine
and Redlich Professor
Peter Schmidt, M.D.
Chief Fellow, Division of Pain
Medicine
Department of Anesthesiology, Perioperative and Pain Medicine
Stanford University School of Medicine, Stanford, California
Section Editor: Kevin Vorenkamp, M.D.
P
ain is a subjective experience;1 therefore, unlike other chronic
diseases, there is no single objective measurement to best
characterize the extent of the problem or to evaluate treatment
outcomes. Measuring a patient’s pain must correlate objective data
with the patient’s subjective reporting to provide a comprehensive
outcome representing the pain state. Complicating the measurement
of pain is that there is often wide variability in how much pain a given
stimulus or injury will cause. This variability is influenced by genetics,
mood, beliefs, early life experiences with pain, sex, ethnicity, and
other factors.2
Chronic pain is often associated with an overall reduction in the
patient’s quality of life, encompassing domains such as depression,
anxiety, impaired social and physical function, and sleep disturbance.
Moreover, there appears to be relative independence between
pain and these co-existing stressors. Therefore, to capture the
pain experience, it is necessary to also define and characterize
these related domains. Recognizing that pain is challenging to
accurately measure, why then must we strive to better evaluate
outcomes in pain medicine? Current practice relies on evidencebased medicine to support clinical decision-making and to convince
colleagues, patients, and payers of the most efficacious treatments.
Standardization of outcome reporting will therefore allow for
comparison and systematic review of the studies that do exist to help
to answer the most pressing questions in the field of pain.
CONSIDERATIONS IN SELECTING AN OUTCOME MEASURE
Any tool used to measure pain should be appropriate for the provider
and patient needs. It is of little use to have a patient fill out multiple
forms if the provider lacks the staff or infrastructure to utilize the
data. In defining a standard set of outcome measures, the Initiative
on Methods, Measurement, and Pain Assessment in Clinical Trials
(IMMPACT) consortium granted most weight to the following criteria:3
11
2
A)Reliability—The instrument should demonstrate test-retest,
inter-rater and internal reliability.
B)Validity—The scale should measure what it is intended to
measure.
C)Responsiveness—The scale must display the ability to
detect changes over time and to distinguish between
treatments.
D)Appropriateness—The scale’s content should be in keeping
with the measured outcome and relevant to the patient
population being studied.
E)Burden—The scale should be easy to administer, complete,
and score.
UNIVARIABLE MEASURES
Unidimensional scales measure pain as a single quality varying only
in intensity. These methods are most effectively used in clinics and
acute settings. Examples include:
Verbal Rating Scale (VRS). VRS consists of a series of categorical
descriptors ordered in increasing intensity (i.e., none, mild, moderate,
severe). The advantages of the VRS are that it is easy to administer
and report, particularly for elderly patients.4 Disadvantages are
that it has fewer response choices, and the categorical options
limit statistical analysis. It has demonstrated ability to distinguish
treatment effect, test-retest reliability, and convergent validity.5
Visual Analog Scale (VAS). VAS is typically a 10 cm line anchored
by “no pain” at one end and “worst pain” at the other. The patient
marks a point on the line, and the clinician measures the length of the
line on a 101-point scale.6 The advantages of the VAS are that there
is good evidence for responsiveness, validity, test-retest reliability,
and scores can be treated as ratio data.7 The limitations are that it
can be more time-consuming, and elderly people may have difficulty
using the scale.8
Numerical Rating Scale (NRS). NRS is the most frequently used
univariable instrument. It consists of a rating scale from 0 to 10 (or 0
to 100 in some versions). Patients may respond verbally or by circling
the appropriate number. It demonstrates sensitivity to change,
test-retest reliability, and correlates well with other measures of pain
intensity.5 The NRS is recommended by IMMPACT as a core domain
measure for future chronic pain clinical trials.9
Patient Global Impression of Change (PGIC). PGIC represents an
attempt to capture pain improvement more broadly using a single
item measure. The patient is asked to rate his/her current status
compared to a prior time point (i.e., very much improved). This
scale is applicable to many conditions and treatments but lacks
sensitivity.10 It is recommended by IMMPACT as a core domain
measure and can be particularly helpful in gauging the clinical
importance of changes.11
2014
EMOTION MEASURES
Clearly, there is a relationship between pain and emotional distress;
there is also evidence of relative independence. Measurements of
depression include the Patient-Reported Outcomes Measurement
Information System (PROMIS) — Depression Item Bank,12 Beck
Depression Inventory (BDI),13 Zung Self-Rating Depression Scale,14
and Hamilton Rating Scale for Depression.15 Anxiety and fear
measures include the PROMIS — Anxiety Item Bank [12], Pain
Anxiety Symptoms Scale,16 State-Trait Anxiety Inventory,17 and FearAvoidance Beliefs Questionnaire (FABQ).18
MULTIDIMENSIONAL MEASURES
Chronic pain requires a more comprehensive assessment than a
univariable or single domain measure can provide. Multidimensional
measures often combine several dimensions of pain, disability,
emotional affect, and effect on quality of life into a single instrument.
Commonly used scales include:
Brief Pain Inventory (BPI). BPI was developed to measure both
intensity of pain and interference in the patient’s life.19 It consists of a
17-item scale that typically takes under 15 minutes to complete. The
BPI Interference Scale, in particular, has been validated as a measure
of physical functioning in multiple domains and is recommended by
IMMPACT as a core HRQoL measure.9
McGill Pain Questionnaire (MPQ). MPQ was developed to specify
the qualities of pain.20 Pain is scaled in three dimensions (sensory,
affective, and evaluative) with 20 sets of words for each dimension.
Multiple studies have supported the reliability and validity of the
MPQ for specific pain syndromes.21 The Short-Form McGill Pain
Questionnaire (SF-MPQ) was developed for research purposes and
consists of 15 words from the sensory and affective categories with a
four-point rating scale for each, a pain intensity VAS score, and overall
assessment of pain VRS score.22
West Haven-Yale Multidimensional Pain Inventory (WHYMPI).
WHYMPI best assesses adaptation to chronic pain.23 It can yield
clinically useful information regarding pain coping styles. It is
composed of 52 items with 12 subscales. Patients respond to
the questions on a seven-point scale. The WHYMPI interference
scale correlates with physical functioning and is recommended by
IMMPACT as an alternative to the BPI.9
Medical Outcome Study 36-Item Short-Form (SF-36) Health Survey
and Treatment Outcomes of Pain Survey. SF-36 is a frequently
used measure of function and quality of life.24 It consists of eight
subscales; while widely used, it features only two questions related
to pain, and there are concerns about insensitivity to change when
measuring an individual patient. The Treatment Outcomes of Pain
Survey (TOPS) is an extension of the SF-36 specifically designed for
patients with chronic pain.25,26 It consists of 120 items with a 61-item
follow-up. It has been found to be sensitive to change and have good
validity.
OBJECTIVE MEASURES
Several physiologic variables have been suggested as surrogates for
pain, including autonomic activity29,30 or biomarkers of pain intensity.31
Caution with interpreting these peripheral measures is urged as they
can be influenced by arousal other than pain and can be modulated
by medications. Physical function tests, such as range of motion and
strength, have been used as proxies for pain;32-34 however, these only
modestly predict self-reported pain scores. More recently, attempts
to objectively measure pain have focused on using neuroimaging.
Indeed, recent studies suggest that brain imaging can be used to
objectively distinguish evoked painful stimuli35 and the presence of
chronic low back pain.36 Despite these promising early reports, there
is still much research to be done to validate its use. Furthermore,
given the expense and time involved, it is more likely that
neuroimaging will primarily be used to help guide further research
and understanding of brain mechanisms involved in pain. All of these
data reinforce the complexity of pain and as such, it is unlikely that an
objective measure for pain will soon emerge.
CLINICAL TRIALS AND OUTCOMES DATA
In addition to the clinical need to provide and document appropriate
care for pain, there is clearly an impetus to provide the evidence
necessary to guide and justify appropriate treatments. This has
resulted in efforts to define and standardize outcome measures for
pain and similar related disease states. IMMPACT has defined six core
outcome domains that should be considered when designing clinical
trials.37 Further, IMMPACT defines specific validated measures for
each of the core outcome domains in IMMPACT-II.3
THE FUTURE OF PATIENT REPORTED OUTCOMES AND CLINICAL
REGISTRIES
The National Institutes of Health recently funded PROMIS with
the goal of developing modern, valid, reliable, and standardized
questionnaires to measure patient-reported outcomes (PROs) that
are free to use for the academic community. These assessment
instruments were developed to yield item banks measuring domains
such as pain, pain interference, fatigue, physical function, depression,
anxiety, and social function calibrated against the U.S. Census 2000
population. These banks can be used to produce short forms or
computerized adaptive tests for research and clinical use.12 The
ongoing second phase of PROMIS focuses on the development of
new tools to measure PROs, validation of the current item banks, and
updating the calibration against Census 2010 population.
The Institute of Medicine report, Relieving Pain in America, proposed
a need for greater development and use of patient outcome registries
that can support point-of-care treatment decision making, as well as
for aggregation of large numbers of patients to enable assessment
of safety and effectiveness of therapies. These registries can help
create “learning systems” that will provide clinicians with information
about treatment success or failure on an ongoing basis, along with
probability “filters” for information that may be particularly useful in
the care of an individual patient.
2014
12
3
What Works, What Doesn’t, and What Is New?
D
Kristopher Schroeder, M.D.
Assistant Professor, Department
of Anesthesiology
University of Wisconsin School
of Medicine and Public Health
Madison, Wisconsin
espite being described for
well over one-hundred years,
Postdural Puncture Headache
(PDPH) remains a common and
debilitating problem.1 The typical
patient is young and healthy,
caring for young children, and can
be debilitated to the point where
work or carrying out the activities
of daily living is impossible. While
an interventional procedure may
not always be the appropriate
therapeutic modality, regional
anesthesiologists and pain
specialists are frequently called upon
to care for these patients.
To effectively manage patients
presenting with a PDPH, the
anesthesiologist must first
understand the physiology related to headache manifestation.
The life-blood of the brain and spinal cord is, in fact, not blood
at all. Cerebrospinal fluid (CSF) maintains an idyllic ion and
glucose environment that is maintained by a
blood-brain barrier and blood-CSF barrier. In
addition to providing the nutrients essential for
optimal cerebral function, CSF forms a cushion
to protect the neuraxis in the event of trauma.
The total volume of CSF is 100-150 ml, and it is
formed at a rate of 0.3-0.4 ml/hour in the choroid
plexus of the cerebral ventricles. Ultimately,
CSF flows from the cisterna magna into the
cerebral and spinal subarachnoid space until it is
reabsorbed by villi in the arachnoid membrane.2
PDPH symptoms likely result from downward
traction on pain-sensitive intracranial structures or may occur via
compensatory intracranial venodilation.3-4
Section Editor:
Steven Orebaugh, MD
represents the best opportunity to decrease the incidence of
PDPH. Aligning the spinal needle with the fibers of the dura (in
the event a cutting needle is utilized), replacing the spinal needle
stylet following injection/CSF withdrawal, and performing loss
of resistance epidural access techniques with normal saline
instead of air all may reduce the incidence of PDPH.5 Decreasing
anesthesia trainee experience with epidural analgesia may be
related to an apparent increase in the rate of inadvertent dural
puncture in some locations.6 Decreased patient age (except
for children, who are generally thought to be at low risk), low
body mass index, history of previous PDPH, and female gender
represent unalterable risks for development of PDPH.3 However,
recent evidence suggests that cigarette smokers may be at lower
risk for the development of PDPH symptoms.7
Fortunately, an overwhelming majority of cases of PDPH
spontaneously resolve. In fact, 72% of headaches spontaneously
resolve within seven days, and 87% resolve within six months.8
A multidisciplinary approach including psychological therapy
may be of particular usefulness to young patients with refractory
symptoms, as they may require assistance understanding reasons
for, and appreciating outcomes of, PDPH symptoms. Conservative
treatment options of historical interest include bed rest, supine
“Symptoms likely result from downward
traction on pain-sensitive intracranial structures
or may occur via compensatory intracranial
venodilation.”
PDPH typically presents within seven days of dural puncture
(although evidence also describes positional headaches with
spontaneous dural leaks and intracranial hypotension). The
headache worsens with assumption of an upright position and
improves when supine, is predominately located in the frontal
or occipital areas, and may involve the neck or shoulders.
Accompanying symptoms may include nausea/vomiting, visual
and auditory perturbations, vertigo or backache.3-4 Importantly,
seizures, intracranial subdural hematomas, cerebral herniation
and death have been described as catastrophic outcomes
following dural puncture, and the lack of a postural component to
the headache should prompt consideration of alternate etiologies.4
Predisposing or causative factors for the development of PDPH
are numerous, and the avoidance of large, cutting needles likely
13
2
or prone posture and abdominal binders. Unfortunately, none
of these has proven to be of any real benefit. Caffeine also
appears to have little role in the treatment of PDPH as any effects
are temporary, and the doses of caffeine required can be the
equivalanet of 20 cups of coffee or 30 sodas daily.4,9,10 Fluid
administration, while likely innocuous, has little data to support
its routine application at the current time. Analgesics (nonsteroidal anti-inflammatory drugs, acetaminophen and opioids)
and antiemetics may have a role in the immediate symptomatic
management of PDPH patients but have no role in hastening
headache termination.3 A wide array of alternative pharmacologic
therapies have been considered in an effort to reduce the need for
more invasive therapies (Table 1). Unfortunately, negative results
are rarely reported and randomized trials are often lacking.
Epidural blood patch (EBP) is the currently the “gold standard”
for treatment of PDPH and results in headache resolution in
2014
more than 90% of cases. The ideal volume of blood required for
Table 1: Therapeutic agents with reported benefit for PDPH.
successful EBP is not well established, but 16-20 ml is commonly
Treatment
Dosing Regimen Duration of
Reported
Reference
used by anesthesiologists in the United States.27 The epidural
Agent
Therapy
Success
blood patch is postulated to work via one of two mechanisms:
11
ACTH
1 mg IM
Can repeat 24
hours later
Unclearly
defined
Collier et al
ACTH
1.5 units/kg
30 minutes
2/2
Kshatri et
al12
ACTH
60 units IM,
repeated x1
after 24 hours
PRN
Single injection
in 40/48
patients, 44%
of pts with relief
within 6 hours
48/48
Gupta et al13
ACTH
80 mg IM q12
hours
2 days (author
describes
typical symptom
resolution with
single dose)
1/1
Ghai et al14
Cosyntropin
0.5 mg infusion
8 hours
1/1
Carter et al15
Ergotamine/
Caffeine
1 mg
ergotamine/
100 mg caffeine
PO TID
4 days
VAS reduced
67% on day 3
Erol 201116
Gabapentin
300 mg PO TID
4 days
(gabapentin
found to be
superior to
ergotamine
for symptom
resolution)
VAS reduced
99% on day 3
Erol 201116
Epidural saline, dextran, opioids, or fibrin glue administration
have all been described as remedies for PDPH, but mainstream
application is limited by lack of data to support their use, potential
for adverse outcomes, and/or lack of training.4 Sphenopalatine
ganglion block, acupuncture and occipital nerve blockade
may represent other potential methods for PDPH symptom
alleviation, but evidence is currently lacking to support these
interventions.32-34 Surgical therapy may ultimately be required
should other measures prove ineffective, and one should not
hesitate to refer a patient to a neurosurgeon should repeated EBP
fail to result in headache resolution.5
Gabapentin
300 mg PO TID
4 days
Significant
reduction in
PDPH symptoms
Erol 200617
Hydrocortisone 200 mg IV x1,
then 100 mg
IV TID
2 days
Headache
intensity
reduced from
9.2 to 0.63 on
day 2
Ashraf et al18
Methergine
0.25 mg PO TID
3 days
24/25
Hakim et al19
Mirtazapine
30 mg PO QHS
4 days
1/1
Sheen et al20
Pregabalin
50 mg TID
3 days (BID
2/2
dosing continued
until day 5)
Zencirci21
Eradication of PDPH is likely not possible. However, a number
of interventions can be attempted to minimize the incidence
of this bothersome complication. The initial recommendation
of prolonged bedrest now seems unwarranted and potentially
dangerous in postsurgical patients. Threading an intrathecal
catheter when attempted epidural anesthesia results in an
inadvertent dural puncture may hold some promise in decreasing
the incidence of PDPH, but great care needs to be exercised in
communicating the presence of such a catheter to all healthcare
providers (not an acceptable option in thoracic cases).35 In the
event of an inadvertent dural puncture with attempted epidural
analgesia, minimizing CSF loss also makes intuitive sense
(though data definitively linking CSF loss to PDPH presentation
are lacking). Paramount to PDPH prevention is education
and appropriate needle selection. Other physicians are often
Sumatriptan
6 mg SQ
Sumatriptan
4/6
therapy repeated
PRN in two
patients
Carp et al22
Sumatriptan
6 mg SQ
Patients
assessed at
one hour for
headache
resolution
1/10
Connelly et
al23
Theophylline
200 mg IV x1,
Infusion over 40
repeated 4 hours minutes
later PRN
VAS score
reduced 59.1%
relative to
control group
Ergün et al24
Tramadol
50 mg PO q6
hours
7 days
1/1
Stephenson
et al25
Tramadol
50-100 mg PO
q6 hours
7 days
6/6
Barodka26
1. Formation of a clot or patch at the site of dural puncture and
thereby halting the continued leakage of CSF.
2. Hydrostatic mechanism where blood injected into the
epidural space causes thecal sac compression and cephalad
CSF translocation.
Interestingly, an increased duration of PDPH symptoms (over
24 hours) has been associated with an increased success rate
of EBP.3 However, significant prolongation of symptoms may
be particularly harmful in the immediate post-partum period
when it may impact the maternal bonding process.28 While the
complications of EBP are typically mild (backache, paresthesias,
EBP failure, and inadvertent dural puncture), a variety of
rare but catastrophic outcomes have been reported.29 These
include subdural hematoma, arachnoiditis, infected EBP, facial
nerve paralysis, and permanent spastic paraparesis.29 True
contraindications to EBP typically include those that apply to
epidural or spinal anesthesia. Data regarding EBP in patients with
HIV or malignancy is limited and predominately discussed in case
reports.30-31
2014
14
3
Beyond ACLS: Targeted Treatment for Local Anesthetic Toxicity
avoiding vasopressin, limiting epinephrine dose, and administering
intravenous lipid emulsion (ILE).1 We present here the logical basis
for these distinctions and other relevant treatment differences,
noting that recommendations are likely to evolve further as new
evidence emerges.
Adrian Pichurko, M.D.
Anesthesiology Resident
University of Illinois Hospital
and Health System
Chicago, Illinois
Guy Weinberg, M.D.
Professor of Anesthesiology
University of Illinois Hospital
and Health System
Jesse Brown Veterans Affairs Hospital
Chicago, Illinois
Section Editor: Steven Orebaugh, MD
L
ocal anesthetic systemic toxicity (LAST) is an unpredictable
event that can turn a routine nerve block into a life-altering
experience for both patient and physician. Fortunately, we are
now learning to better manage these occurrences, improving the
safety of regional anesthesia along the way. The ASRA Working
Group on LAST published several papers and a practice advisory
in 2010 summarizing the history, clinical presentation, prevention,
models and treatment of LAST, based on expert opinion and
laboratory findings.1-3 These papers emphasize that LAST has a
unique pathophysiology, distinct from those addressed by ACLS
guidelines. We review here aspects of LAST physiology and
treatment that distinguish it from other forms of circulatory shock.
CARDIOVASCULAR INSTABILITY
Much of LAST management focuses on cardiovascular symptoms.
Early signs include hypertension and tachycardia which
reflect CNS excitation, followed by contractile depression and
arrhythmias, which can progress to cardiac arrest that typically
resists ACLS measures.4 Recent evidence shows that local
anesthetics, particularly bupivacaine, cause a multimodal form
of toxicity via inhibition of ionotropic signaling (e.g., voltagegated sodium channels, potassium channels, calcium channels),
metabotropic signaling (e.g., beta-adrenergic receptor), and
mitochondrial metabolism (e.g., oxidative phosphorylation).5-8
“High quality BLS and ACLS are the
cornerstone of resuscitation for all
causes of cardiac arrest”
EPINEPHRINE
Animal models show mixed results for the efficacy of epinephrine
in LAST but generally demonstrate that it restores blood pressure
rapidly, although not always in a sustained manner. These trials
also demonstrate that epinephrine is highly arrhythmogenic,
worsens arterial pH and may impair the efficacy of lipid infusion
(Figure 1).10-13 Because these undesirable effects are dosedependent, we currently advise that if epinephrine is used, it
should be administered in incremental doses of <1 mcg/kg each.
Notably, the standard 1 mg bolus dose of epinephrine (~15 mcg/
kg) has not been shown to improve survival to outcome following
out-of-hospital cardiac arrest.14
Figure 1: Rate-pressure product (RPP, a surrogate for cardiac
output) versus epinephrine dose in a rat model of bupivacaine
toxicity, at the 15-minute time point. At 15 minutes, epinephrinetreated animals that received 10 mcg/kg or more of epinephrine
showed decreased RPP.
High quality BLS and ACLS are the cornerstone of resuscitation for
all causes of cardiac arrest to sustain cardiac output and tissue
oxygenation during low-flow states. However, the pathophysiology
of local anesthetic overdose requires additional, distinct treatment
measures.9 While the aim in treating myocardial ischemia is to
restore coronary perfusion, the goal in treating LAST is to reverse
the underlying toxicity and avoid treatments that worsen it. From
a practical standpoint, this translates to these recommendations:
15
2
2014
VASOPRESSIN
ACLS guidelines allow a single dose of vasopressin (40 units) as
a potential substitute for one dose of epinephrine.15 However,
this is unlikely to be efficacious in LAST since intense systemic
vasoconstriction will decrease cardiac output in the setting of
a poorly contracting (i.e., poisoned) heart. A negative effect
on outcome was confirmed in an animal model of LAST where
vasopressin reproducibly caused pulmonary edema and severely
impeded cardiovascular recovery from bupivacaine overdose (Figure
2).16 This drug is therefore not recommended to treat LAST.
ARRHYTHMIA
Alleviating the underlying toxicity is likely the best means
of addressing arrhythmias during LAST.1 Defibrillation and
cardioversion should still be performed according to ACLS
guidelines, but by themselves may not be sufficient.17 Choices
of anti-arrhythmic agents after countershock are limited; local
anesthetics such as lidocaine and procainamide would clearly
exacerbate LAST and cardio-depressant agents such as beta
blockers and calcium channel blockers should also be avoided.1
Amiodarone can also induce hypotension and, while not optimal, it
is an acceptable choice if tolerated in terms of blood pressure.18
CARDIOPULMONARY BYPASS
It is advisable to notify the nearest cardiopulmonary bypass
facility once a diagnosis of LAST is established and the patient
exhibits signs of cardiovascular toxicity. This is prudent since
patient, physician, and systems factors can hinder successful
Figure 2: Blood pressure tracings in rat models of bupivacaine toxicity treated with lipid, epinephrine, and vasopressin (ADH), respectively;
along with oxygen and chest compressions (labeled). ILE demonstrates slow but sustained return of perfusion; epinephrine shows rapid but
non-sustained improvement; and vasopressin does not demonstrate return to baseline at any point. Time course of experiment, approximately
10 minutes. Courtesy, Weinberg lab.
2014
16
3
Outcomes in Pain Medicine: A Brief Review continued...
In response to this recommendation Stanford University and one of
the authors (SM) entered into a partnership with the NIH to develop,
implement and expand an open source, open standard and free
health and treatment registry platform: Health Electronic Registry
of Outcomes (HERO). HERO is a platform that is used to collect
outcomes data on large numbers of patients suffering from chronic
pain. The platform can eventually be expanded to include other
health conditions. The platform supports: clinical decision support at
the point-of-care, comparative-effectiveness research, longitudinal
outcomes research, and large simple trial designs. The NIH PROMIS
computer adaptive testing domains are integrated into HERO,
providing a fast and efficient means of capturing patient reported
outcomes. More information can be found at http://snapl.stanford.
edu/hero/.
3. Dworkin RH, Turk DC, Farrar JT, et al. Core outcome measures for chronic pain
clinical trials: IMMPACT recommendations. Pain. 2005;113:9–19.
4. Gagliese L, Melzack R. Chronic pain in elderly people. Pain. 1997;70:3–14.
5. Gilron I, Jensen MP. Clinical trial methodology of pain treatment studies:
selection and measurement of self-report primary outcomes for efficacy. Reg
Anesth Pain Med. 2011;36:374–81.
6. Miller MD, Ferris DG. Measurement of subjective phenomena in primary care
research: the Visual Analogue Scale. Fam Pract Res J. 1993;13:15–24.
7. Price DD, McGrath PA, Rafii A, Buckingham B. The validation of visual analogue
scales as ratio scale measures for chronic and experimental pain. Pain.
1983;17:45–56.
8. Revill SI, Robinson JO, Rosen M, Hogg MI. The reliability of a linear analogue for
evaluating pain. Anaesthesia. 1976;31:1191–8.
9. Dworkin RH, Turk DC, Wyrwich KW, et al. Interpreting the clinical importance of
treatment outcomes in chronic pain clinical trials: IMMPACT recommendations. J
Pain. 2008;9:105–21.
10. Younger J, McCue R, Mackey S. Pain outcomes: a brief review of instruments
and techniques. Curr Pain Headache Rep. 2009;13:39–43.
CONCLUSIONS
11.
Farrar JT, Young JP Jr, LaMoreaux L, Werth JL, Poole RM. Clinical importance
The assessment of pain remains a challenge, but the landscape
of changes in chronic pain intensity measured on an 11-point numerical pain
is improving in development and adoption of appropriate outcome
rating scale. Pain. 2001;94:149–58.
measures. Most clinicians and researchers recognize that chronic
12. Gershon RC, Rothrock N, Hanrahan R, Bass M, Cella D. The use of PROMIS and
pain is a multidimensional experience requiring appropriate attention
assessment center to deliver patient-reported outcome measures in clinical
research. J Appl Meas. 2010;11:304–14.
to sensory, emotional, functional, and cognitive aspects in addition
13.
B
eck AT, Ward CH, Mendelson M, Mock J, Erbaugh J. An inventory for
to the univariable pain intensity scores. Given the multitude of
measuring depression. Arch Gen Psychiatry. 1961;4:561–71.
instruments available to assess pain outcomes, deciding upon
14. Zung WW. A self-rating depression scale. Arch Gen Psychiatry. 1965;12:63–70.
a specific tool for any given situation can be difficult. Indeed, a
15. Hamilton M. A rating scale for depression. J Neurol Neurosurg Psychiatr.
recent systematic review of pain outcomes in chronic low back pain
1960;23:56–62.
demonstrated 75 different outcome measures cited to evaluate
16.
M
cCracken LM, Zayfert C, Gross RT. The Pain Anxiety Symptoms Scale:
38
Local
in Lower
Arthroplasty
therapy.Infiltration
RegardlessAnalgesia
of the measures
chosen, Limb
each scale
represents continued...
development and validation of a scale to measure fear of pain. Pain.
1992;50:67–73.
a compromise between factors of sensitivity and specificity,
17. Spielberger CD. State-Trait Anxiety Inventory. The Corsini Encyclopedia of
comprehensiveness and burden. The key to choosing an instrument is
Psychology. John Wiley & Sons, Inc.; 2010 [cited 2012 Jul 5]. Available at:
to be sure that it measures the appropriate domain of interest and to
http://onlinelibrary.wiley.com/doi/10.1002/9780470479216.corpsy0943/
balance the quality and quantity of information.
abstract.
The results of IMMPACT and PROMIS have suggested core
outcome domains, validated measures, and item banks that can
be easily accessed by researchers and clinicians alike. In addition,
specific pain conditions may require tailored measurements for
that population and outcome. Use of standardized outcomes and
measurements, and making these readily accessible to providers and
patients, holds significant promise to ensure the best delivery of care
and the advancement of pain medicine.
18. Waddell G, Newton M, Henderson I, Somerville D, Main CJ. A Fear-Avoidance
Beliefs Questionnaire (FABQ) and the role of fear-avoidance beliefs in chronic
low back pain and disability. Pain. 1993;52:157–68.
ACKNOWLEDGMENTS
Dr Mackey was funded by NIH K24DA029262. Dr Mackey is the
guarantor for this article,– and takes responsibility for the integrity of
the work as a whole.
23. Kerns RD, Turk DC, Rudy TE. The West Haven-Yale Multidimensional Pain
Inventory (WHYMPI). Pain. 1985;23:345–56.
REFERENCES
1. Merskey H, Bogduk N. Classification of Chronic Pain. 2nd edition. Seattle,
Washington: IASP Press; 1984.
2. Kim H, Neubert JK, San Miguel A, et al. Genetic influence on variability in
human acute experimental pain sensitivity associated with gender, ethnicity and
psychological temperament. Pain. 2004;109:488–96.
17
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19. Cleeland CS, Ryan KM. Pain assessment: global use of the Brief Pain Inventory.
Ann Acad Med Singap. 1994;23:129–38.
20. Melzack R, Torgerson WS. On the language of pain. Anesthesiology.
1971;34:50–9.
21. Chapman CR, Casey KL, Dubner R, Foley KM, Gracely RH, Reading AE. Pain
measurement: an overview. Pain. 1985;22:1–31.
22. Melzack R. The short-form McGill Pain Questionnaire. Pain. 1987;30:191–7.
24. McHorney CA, Ware JE Jr, Raczek AE. The MOS 36-Item Short-Form Health
Survey (SF-36): II. Psychometric and clinical tests of validity in measuring
physical and mental health constructs. Med Care. 1993;31:247–63.
25. Rogers WH, Wittink H, Wagner A, Cynn D, Carr DB. Assessing individual
outcomes during outpatient multidisciplinary chronic pain treatment by means
of an augmented SF-36. Pain Med. 2000;1:44–54.
26. Rogers WH, Wittink HM, Ashburn MA, Cynn D, Carr DB. Using the “TOPS,” an
outcomes instrument for multidisciplinary outpatient pain treatment. Pain Med.
2000;1:55–67.
27. Hummel P, van Dijk M. Pain assessment: current status and challenges. Semin
Fetal Neonatal Med. 2006;11:237–45.
2014
Fall Meeting Preview continued...
detailed landscape of the issues surrounding opioid management
through lectures by Drs. Robert Jamison, Asokumar Buvanendran,
and Eugene Viscusi. In addition, we are very fortunate to have
Joseph Rannazzisi, the Deputy Director of the United States Drug
Enforcement Agency, speak on the current state of opioids in the
United States. Dr. Richard Rosenquist will moderate the session.
The FDA’s Safe Use Initiative Epidural Steroid Injection Working
Group Recommendations session will be led by two of the authors
of the upcoming recommendations, Dr. Honorio Benzon and Dr.
James Rathmell. Drs. Jeffrey Petershon and Dr. Kenneth Candido
will provide an overview of the usefulness of digital subtraction
angiography in preventing vascular complications.
Currently, in the field of pain medicine we are facing many
challenges. In order to meet
the challenges head on and to
allow for successful navigation
of the new healthcare
landscape, the program will
also be providing education
through the special halfday session, “Advanced Practice Management,” led by Dr. Kevin
Vorenkamp. Topics covered will including CPT coding, navigating
local coverage determinations, ICD-10, compliance, economic
indicators for the pain practice, effective organization for the clinical
care team, insurance contracting, and shared risk agreements. In
addition, parallel sessions will include lectures on economic topics
covering spine care, value base purchasing, hospital/physician
practice relationships and agreements and current procedural
terminology creation for new treatments.
challenging cases and complication management that will allow
you interact with experts and to develop management strategies for
difficult cases.
Significant efforts have also gone into the development of the
Resident Fellow Education Program developed by the Resident
Section Committee and Drs. Ellen Rosenquist and Anish Doshi
(Chair of the Resident Section Committee). The program includes
a dedicated didactic session, job fair offering opportunity, and
personalized workshop experience (see accompanying article by Dr.
Doshi).
We are also pleased to offer again the comprehensive Physician
Assistant and Nurse Practitioner educational program on Saturday
and Sunday which is being led
by Dr. Bridget Calhoun, Chair of
the Physician Assistant Program
at Duquesne University. The
course will cover key knowledge
requirements needed for all
Physician Assistants and Nurse
Practitioners caring for individuals suffering from chronic pain.
For physicians that work in a coordinated care model, we strongly
encourage you to invite Nurse Practitioners and Physician Assistants
that are part of the team.
Currently, in the field of pain medicine
we are facing many challenges.
The treatment of pain often involves a multidisciplinary effort
with the coordination of multiple specialties. Recognizing the
importance of coordinated care, we have brought in experts from
other specialties including chiropractic medicine, physical therapy,
psychiatry, radiology, neurology, and spine surgery. Two radiologists,
Dr. John Carrino and Dr. Levon Nazarian, will be teaching at the
meeting. Drs. Lurie and Vaccaro both investigators on the Spine
Patient Outcomes Research Trials (SPORT) will provide significant
input on the treatment of spine pain. We will also have education
from both a physical therapist (Dr. Gregory Marchetti) and a
chiropractor (Dr. Kevin Pursel). Dr. Robert Jamison (psychology)
will also be speaking at the meeting. He has published extensively
on opioids and substance abuse management. Dr. Charles Brock
(neurology) will moderate a session on head, neck and facial pain.
In addition to the great didactics that will be available at this
meeting, we will also have an extensive workshop program
organized by Dr. Carlos Pino. The offered workshops will cover highend interventional techniques including radiofrequency, spinal cord
stimulation, botulinum toxin, visceral and sympathetic blocks, joint
injections, spine injections, ultrasound-guided procedures, and head
and neck blocks. There will also be a 2-hour interactive session on
The program will include 27 PBLDS that will allow participants to
meet with experts and discuss interesting and challenging topics
including pulsed radiofrequency, intrathecal drug guidelines,
medical cannabis, interpretation of EMG and nerve conduction
studies, coding and billing, and pediatric pain management.
We also encourage scientists to submit their research to the
meeting which will be reviewed by the ASRA Research Committee
led by Drs. Colin McCartney and Gary Brenner. Best of meeting
abstracts and resident/fellow scientific abstracts will be selected.
The ASRA Pain Medicine Meeting is a great place to present your
research in front of leaders in the field of pain management.
For the first time, ASRA will also be partnering with the North
American Spine Society to allow select individuals to participate in
both meetings. The North American Spine Society Annual Meeting
will also be held in San Francisco at the same time. Details will be
forthcoming.
We look forward to welcoming you to the beautiful city of San
Francisco. In addition to the excellent educational opportunities
being offered at this meeting, we will also be developing a social
event program that will allow for interaction among participants
and faculty and for the continuation of the “family” environment
seen at ASRA events. We anticipate the Pain Medicine Meeting will
be a memorable experience for all of you. Additional information on
the meeting can be found at www.asrameetings.com/13th-annualpain-medicine-meeting/.
2014
18
3
PRO
in Epidural Steroid Injections continued...
injection after cervical TF injections was noted to be 19.4%.17 The
authors concluded that detecting blood in the needle hub, either
spontaneously or after aspiration, to predict intravascular injection
was 97% sensitive but only 45.9% specific. Two studies noted
that simultaneous epidural and intravascular injection was more
common than intravascular injection alone: 12.7% vs. 2.8% in
one study16 and 8.2% vs. 4.2% in another study.18
al.19 Conventional fluoroscopy was not conclusive of intravascular
injection even after contrast; subsequent injection with DSA
showed the contrast medium filling a tiny vessel traveling directly
to the spinal cord. The procedure was aborted with no ill effects.
Rathmell et al demonstrated the ability of DSA to convincingly
show intraarterial injection when contrast injection with live
fluoroscopy was equivocal (Figure 1).4
The spontaneous presence of blood in the hub of the needle, in
the absence of intravascular cannulation, is secondary to tissue
trauma or penetration of a blood vessel during advancement of
the needle. A negative aspiration does not preclude intravascular
injection.19,20 Aspiration failed to produce a flashback of blood in
74% of cases that turned out to be intravascular.14 Although 9798% specific,15,17 the sensitivity of the presence of flash or blood
on aspiration to predict intravascular injection ranged from 25%21
to 45%.15,17 The inability of aspiration to predict intravascular
injection has been partly attributed to collapse of the blood vessel
during aspiration.
McLean et al23 retrospectively analyzed their prospectivelycollected data. In their study, 177 cervical transforaminal ESIs
were performed in 134 patients between June 2004 and April 23,
2007. Intravascular injection was noted in 17.9% of the patients
before DSA was used and 32.8% after DSA was introduced
(Table).23 They concluded that the use of DSA nearly doubled
their detection of intravascular cannulation. This study has
obvious limitations: only one physician did all injections; other
factors such as the presence of foraminal stenosis, history of
prior surgery, or number of attempts were not noted; and it was
not clear whether contrast injection with and without DSA was
compared in the same patient. The implication of their study is
that the incidence of intravascular injection was probably the
same before they used the DSA but was not detected by contrast
injection alone, an unproven assumption.
DIGITAL SUBTRACTION ANGIOGRAPHY
Digital subtraction angiography (DSA) involves conversion of
the fluoroscopic image to digital data, image subtraction then
expansion. Subtraction involves the removal of the mask
(background) image from the succeeding contrast image, resulting
in contrast-filled structures that are free of background detail.
The final phase of DSA is expansion of the subtracted image to
enhance the image.22 Subtraction and enhancement occurs in
real-time allowing for technique adjustment.
In a prospective study, Lee et al compared DSA with aspiration
of blood to detect intravascular injection.21 In this study, two
fluoroscopic images – contrast injection under live fluoroscopy
and injection with DSA – were saved after each injection. The
overall rate of IV injection was 23% (20 of 87 injections). Of the
20 IV injections, 12 were noted with DSA compared to 5 with
The usefulness of DSA was shown in a case report by Baker et
contrast injection under live fluoroscopy. The sensitivity of DSA
was 60% compared to 25%
with aspiration (Table).
Figure 2: Fluoroscopy images showing epidural contrast pattern with no visible intravascular injection after
injection of contrast (A) and simultaneous epidural and clear intravascular pattern with DSA. From Lee MH,
Yang KS, Kim YH, Jung HD, Lim SJ, Moon DE. Accuracy of live fluoroscopy to detect intravascular injection
during lumbar transforaminal epidural injections. Korean J Pain 2010;23:18-23 (reprinted through the Creative
Commons Attribution Non-Commercial Use License (http://creativecommons.org/licenses/by-nc/3.0/) which
permits unrestricted reproduction provided the original work is properly cited).
19
2
2014
Simultaneous intravascular
and epidural injections,
as previously noted, are
more common than pure
intravascular injection.16,18
Intravascular injection in
the presence of epidural
spread of contrast is better
analyzed by DSA (Figure
2).21 Compared to live
fluoroscopy, smaller volumes
of contrast are needed with
DSA. Although respiratory
or motion artifacts often
occur, DSA provides
improved visualization of
the vessel course. The
limitations of using DSA
PRO
Table 1: Incidence of Intravascular Injection with and without Digital Subtraction Angiography
Study
McLean et al*
Number of
subjects or
injections
Number of
positive
intravascular
injections
Sensitivity Specificity
(Subjects)
Contrast injection
under real-time
fluoroscopy
67
12 (17.9%)
DSA
67
22 (32.8%)
Lee et al**
P value
6. Tiso RL, Cutler T, Catania JA, Whalen K. Adverse
central nervous system sequelae after selective
transforaminal block: The role of corticosteroids.
Spine J 2004; 4:468–74
7. Huntoon M. Anatomy of the cervical intervertebral
foramina: vulnerable arteries and ischemic injuries
after transforaminal epidural injections. Pain
2005;117:104-11
8. Houten JK, Errico TJ. Paraplegia after lumbosacral
nerve root block: Report of three cases. Spine J
2002; 2:70–5
0.0471
9. Aprill CN, Melfi RS. Paraplegia after lumbosacral
nerve root block: report of three cases (letter).
Spine J 2004;4:368-9
10. Chen B, Stitik TP, Foye PM. Safety of interlaminar
and transforaminal epidural steroid injections
(letter). Anesth Analg 2014;118:236
(Injections)
11. Kroszczynski AC, Kohan K, Kurowski M, Olson
TR, Downie SA. Intraforaminal location of
thoracolumbar anterior medullary arteries. Pain
Med 2013;14:808–12
87
Contrast injection
under real-time
fluoroscopy after
aspiration
5
25%
100%
DSA
12
60%
100%
*From McLean et al. PM R 2009;1:636-42; **From Lee et al. Korean J Pain 2010;23:18-23
include additional radiation, added expense of the equipment
($15,000-$20,000.00), and not enough studies supporting its
superiority over contrast injection under live fluoroscopy. It is
also not foolproof since paraplegia after TF ESI has occurred in
spite of a negative DSA.24
SHOULD DSA BE USED IN ALL EPIDURAL STEROID INJECTIONS?
The application of DSA does not make up for inadequate
knowledge, meticulous preparation and technique, or proper
interpretation of questionable images. The routine use of DSA
is not recommended as its superiority over aspiration has not
been definitely shown. However, if there is blood on the needle,
either spontaneously or after aspiration, the use of a DSA adds a
valuable piece of information in preventing avoiding events that
may be preventable.
References:
12. Murthy NS, Maus TP, Behrns CL. Intraforaminal
location of the great anterior radiculomedullary
artery (artery of Adamkiewicz): a retrospective
review. Pain Med 2010;11:1756–64
13. Rodriguez-Baeza A, Muset-Lara A, RodriguezPazos M, Domenech-Mateu JM. The arterial
supply of the human spinal cord: a new approach
to the arteria radicularis magna of Adamkiewicz.
Acta Neurochir (Wien) 1991;109:57–62
14. Sullivan WJ, Willick SE, Chira-Adisai W, Zuhosky J, Tyburski M, Dreyfuss P,
Prather H, Press JM. Incidence of intravascular uptake in lumbar spinal injection
procedures. Spine 2000;25:481-6
15. Furman M, O’Brien E, Zglszewski T. Incidence of intravascular penetration in
transforaminal lumbosacral epidural steroid injections. Spine 2000;25:2628-32
16. Hong JH, Kim SY, Huh B, Shin HH. Analysis of inadvertent intradiscal and
intravascular injectrion during lumbar transforaminal epidural injections. A
prospective study. Reg Anesth Pain Med 2013;38:520-5
17. Furman MB, Giovanniello MT, O’Brien EM. Incidence of intravascular penetration in
transforaminal cervical epidural steroid injections. Spine 2003;28:21-25
18. Smuck M, Fuller BJ, Yoder B, Huerta J. Incidence of simultaneous epidural and
vascular injection during lumbosacral transforaminal epidural injections. Spine J
2007;7:79-82
19. Baker R, Dreyfuss P, Mercer S, Bogduk N. Cervical transforaminal injection of
corticosteroids into a radicular artery: A possible mechanism for spinal cord injury.
Pain 2003; 103:211–5
1. M
cgrath JM, Schaefer MP, Malkamaki DM. Incidence and characteristics of
complications from epidural steroid injections. Pain Med 2011;12:726-31
20. Renfrew DL, Moore TE, Kathol MH, el-Khoury GY, Lemke JH, Walker CW. Correct
placement of epidural steroid injections: Fluoroscopic guidance and contrast
administration. AJNR Am J Neuroradiol 1991;12:1003-7
2. Abbasi A, Malhotra G, Malanga G, Elovic EP, Kahn S. Complications of interlaminar
cervical epidural steroid injections: A review of the literature. Spine (Phila Pa 1976)
2007;32:2144-51
21. Lee MH, Yang KS, Kim YH, Jung HD, Lim SJ, Moon DE. Accuracy of live
fluoroscopy to detect intravascular injection during lumbar transforaminal epidural
injections. Korean J Pain 2010; 23:18-23
3. R
athmell JP, Michna E, Fitzgibbon DR, Stephens LS, Posner KL, Domino KB. Injury
and liability associated with cervical procedures for chronic pain. Anesthesiology
2011;918-26
22. Harrington DP, Boxt LM, Murray PD. Digital subtraction angiography: Overview of
technical principles. AJR Am J Roentgenol 1982;139:781-786
4. R
athmell JP, April C, Bogduk N. Cervical transforaminal injection of steroids.
Anesthesiology 2004; 100:1595–1600
23. McLean JP, Sigler JD, Plastaras CT, Garvan CW, Rittenberg JD. The rate of detection
of intravascular injection in cervical transforaminal epidural steroid injections with
and without digital subtraction angiography. PM R 2009; 1:636-642
5. B
enzon HT, Chew TL, McCarthy R, Benzon HA, Walega DR. Comparison of the
particle sizes of the different steroids and the effect of dilution: A review of the
relative neurotoxicities of the steroids. Anesthesiology 2007;106:331-338
24. Chang Chien GC, Candido KD, Knezevic NN. Digital subtraction angiography does
not reliably prevent paraplegia associated with lumbar transforaminal epidural
steroid injection. Pain Physician 2012;15:515-2
2014
20
3
CON
false negative rate of live fluoroscopy is unknown but has been
observed in one study to be 0.75%, with a calculated sensitivity
of 99.25%, and specificity of 100% to detect inadvertent vascular
injections.4 DSA may provide greater sensitivity and specificity
but the exact limits of detection are unclear along with an
unvalidated safety profile.
DSA exposes the patient and
medical staff to significantly
more radiation than traditional
fluoroscopy. Extrapolation
from the interventional
vascular studies suggests
that DSA may increase
exposure to ionizing radiation
at a rate of 3-5 times the
exposure of CT angiography
(CTA).5 The routine use of
DSA may have a poor risk/benefit ratio due to escalated radiation
exposure and rates of preventing rare catastrophic outcomes that
may be averted by other safety measures during interventional
procedures.
from TFESI, all were performed utilizing particulate steroid
medications.9
Many authors have suggested that the introduction of particulate
steroid medication into a radiculo-medullary artery as the
primary cause of spinal cord infarction. Depot steroids such
as methylprednisolone and
triamcinolone aggregate into
clusters ranging from 1 to greater
than 100 μm, potentially leading
to occlusion of the medullary
arterioles measuring 10-15
μm in diameter.10-11 While pain
interventionalists have long
maintained that particulate steroid
medications are superior to nonparticulate agents, supporting
research is less definitive.12-16 Some
authors have maintained that steroids may not provide added
benefit.17
“DSA exposes the patient and
medical staff to significantly more
radiation than traditional fluoroscopy.”
DSA may also lead to increase healthcare costs without
justification of benefit. Adding digital subtraction capabilities
to an existing fluoroscopic C-arm will vary depending on
manufacturer make and model; some estimates range from
$15,000-18,000 USD.6
ALTERNATE SAFETY MECHANISMS
Several methods have been proposed to reduce the risk of
intravascular injection, including needle selection, procedural
approach, lidocaine challenge, imaging, and medication
selection.4,7,9 Despite utilizing all of these methodologies,
morbidity and mortality have occurred with the exception that
spinal cord infarction has never been reported in association with
non-particulate steroid injectate (dexamethasone). Steroid choice
is a crucial safety consideration during neuraxial interventions.
Indeed, of the 18 known reported cases of spinal cord infarction
Table 1: Disadvantages of DSA
Table 2: Techniques used to
increase safety
Increased radiation
Blunt needle
Increased cost
Live fluoroscopy
Subject to motion artifact
Non-particulate steroid
Unclear resolution
Lidocaine test dose
Not validated margin of safety
Extension tubing
Subject to interpretation error
21
2
To date, one reported case of paraplegia exists following right
side L5-S1 TFESI, utilizing 40 mg of triamcinolone, despite DSA
and lidocaine test dose being negative for signs of intravascular
uptake.7
NEW TECHNOLOGIES
New imaging technologies are currently available, improving
image quality, contrast, with little or no additional radiation.
Dynamic range management (DRM) utilizes algorithms to optimize
fluoroscopic imaging. Rather than processing the entire image
at once, anatomical sub-images are processed separately for
optimum brightness, contrast and enhancement levels and
then re-combined to create the final image. Utilizing these
algorithms, reduction in the black to white variation in the image
can be obtained without reducing vessel contrast. DRM has been
employed in other medical contexts and found to reduce ionizing
radiation dose as compared to DSA without compromising clinical
image quality.18-20
CONCLUSION
The routine use of DSA is not warranted based on the
current medical evidence. This modality exposes patients,
practitioners and ancillary staff to additional radiation;
yet the current literature does not demonstrate additional
detection of arterial flow beyond traditional fluoroscopy.
Other measures, including the use of dexamethasone vs.
particulate steroids in transforaminal epidural steroid
injections, should instead be utilized first to decrease
the risk of catastrophic complications related to vascular
injection (Table 2).
2014
CON
References:
1. McLean JP, Sigler JD, Plastaras CT, Garvan CW, Rittenberg JD. The rate of
detection of intravascular injection in cervical transforaminal epidural steroid
injections with and without digital subtraction angiography. PM R 2009; 1:636642.
2. Lee MH, Yang KS, Kim YH, Jung HD, Lim SJ, Moon DE, Accuracy of live
fluoroscopy to detect intravascular injection during lumbar transforaminal
epidural injections. Korean J Pain. 2010 Mar;23(1):18-23.
3. El Abd O, Amadera JE, Pimentel DC, Pimentel TS. Intravascular flow detection
during transforaminal epidural injections: a prospective assessment. Pain
Physician. 2014 Jan-Feb;17(1):21-7.
4. Smuck M, Fuller BJ, Chiodo A, Benny B, Singaracharlu B, Tong H, Ho S. Accuracy
of intermittent fluoroscopy to detect intravascular injection during transforaminal
epidural injections. Spine (Phila Pa1976) 2008; 33:E205-210.
5. Manninen AL, Isokangas JM, Karttunen A, Siniluoto T, Nieminen MT.
A comparison of radiation exposure between diagnostic CTA and DSA
examinations of cerebral and cervicocerebral vessels. AJNR Am J Neuroradiol.
2012 Dec;33(11):2038-42.
6. Jasper JF. Role of digital subtraction fluoroscopic imaging in detecting
intravascular injections. Pain Physician. 2003 Jul;6(3):369-72.
12. Lee JW, Park KW, Chung SK, Yeom JS, Kim KJ, Kim HJ, Kang HS. Cervical
transforaminal epidural steroid injection for the management of cervical
radiculopathy: a comparative study of particulate versus non-particulate
steroids. Skeletal Radiol. 2009 Nov;38(11):1077-82.
13. Kim D, Brown J. Efficacy and safety of lumbar epidural dexamethasone versus
methylprednisolone in the treatment of lumbar radiculopathy: A comparison of
soluble versus particulate steroids. Clin J Pain 2011; 27:518-522.
14. Dreyfuss P, Baker R, Bogduk N. Comparative effectiveness of cervical
transforaminal injections with particulate and nonparticulate corticosteroid
preparations for cervical radicular pain. Pain Med 2006; 7:237-242.
15. Kennedy DJ, Plastaras C, Casey E, Visco CJ, Rittenberg JD, Conrad B, Sigler
J, Dreyfuss P. Comparative Effectiveness of Lumbar Transforaminal Epidural
Steroid Injections with Particulate Versus Nonparticulate Corticosteroids for
Lumbar Radicular Pain due to Intervertebral Disc Herniation: A Prospective,
Randomized, Double-Blind Trial. Pain Med. 2014 Jan 2.
16. El-Yahchouchi C, Geske JR, Carter RE, Diehn FE, Wald JT, Murthy NS,
Kaufmann TJ, Thielen KR, Morris JM, Amrami KK, Maus TP.The noninferiority
of the nonparticulate steroid dexamethasone vs the particulate steroids
betamethasone and triamcinolone in lumbar transforaminal epidural steroid
injections. Pain Med. 2013 Nov;14(11):1650-7.
7. Chang Chien, GC, Candido, K. D., and Knezevic, N. N. Digital subtraction
angiography does not reliably prevent paraplegia associated with lumbar
transforaminal epidural steroid injection. Pain Physician 2012; 15:515-523.
17. Manchikanti L, Singh V, Cash KA, Pampati V, Falco FJ. The role of fluoroscopic
interlaminar epidural injections in managing chronic pain of lumbar disc
herniation or radiculitis: a randomized, double-blind trial. Pain Pract. 2013
Sep;13(7):547-58.
8. Okubadejo GO, Talcott MR, Schmidt RE, et al. Perils of intravascular
methylprednisolone injection into the vertebral artery an animal study. J Bone
Joint Surg 2008;90:1932-1938.
18. Belanger B, Boudry J. Management of pediatric radiation dose using GE
fluoroscopic equipment. Pediatr Radiol. 2006 Sep;36 Suppl 2:204-11.
9. Atluri S, Glaser SE, Shah RV, Sudarshan G. Needle position analysis in cases
of paralysis from transforaminal epidurals:Consider alternative approaches to
traditional technique. Pain Physician 2013;16:321-334.
10. Tiso RL, Cutler T, Catania JA, Whalen K. Adverse central nervous system
sequelae after selective transforaminal block:The role of corticosteroids. Spine
J 2004;4:468-474.
11. Benzon HT, Chew T-L, McCarthy RJ, Benzon HA, Walega DR. Comparison of the
particle sizes of different steroids and the effect of dilution: A review of the
relative neurotoxicities of the steroids. Anesthesiology 2007;106:331-338.
19. Philipp Bernhardt, Markus Lendl, Frank Deinzer New technologies to reduce
pediatric radiation doses Pediatr Radiol. 2006 September; 36(Suppl 2):
212–215.
20. http://www3.gehealthcare.com/en/Products/Categories/Surgical_Imaging/Carms_for_Urology/~/media/Downloads/us/Product/Product-Categories/
Surgical-Imaging/OEC_9900_Elite_c-arm_DRM.pdf
21. Baker R, Dreyfuss P, Mercer S, Bogduk N. Cervical transforaminal injection of
corticosteroids into a radicular artery: A possible mechanism for spinal cord
injury. Pain 2003; 103:211-215.
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28. Li D, Puntillo K, Miaskowski C. A review of objective pain measures for use with
critical care adult patients unable to self-report. J Pain. 2008;9:2–10.
29. Storm H. Skin conductance and the stress response from heel stick in preterm
infants. Arch Dis Child Fetal Neonatal Ed. 2000;83:F143–7.
30. Tousignant-Laflamme Y, Marchand S. Autonomic reactivity to pain throughout
the menstrual cycle in healthy women. Clin Auton Res. 2009;19:167–73.
31. Okuse K. Pain signalling pathways: from cytokines to ion channels. Int J
Biochem Cell Biol. 2007;39:490–6.
32. Stratford PW, Kennedy DM, Woodhouse LJ. Performance measures provide
assessments of pain and function in people with advanced osteoarthritis of the
hip or knee. Phys Ther. 2006;86:1489–96.
35. Brown JE, Chatterjee N, Younger J, Mackey S. Towards a physiology-based
measure of pain: patterns of human brain activity distinguish painful from nonpainful thermal stimulation. PLoS ONE. 2011;6:e24124.
36. Ung H, Mackey S. Multivariate Classification of Structural MRI Data Detects
Chronic Low Back Pain, Cerebral Cortex. In press. 2012.
37. Turk DC, Dworkin RH, Allen RR, et al. Core outcome domains for chronic pain
clinical trials: IMMPACT recommendations. Pain. 2003;106:337–45.
38. Chapman JR, Norvell DC, Hermsmeyer JT, et al. Evaluating common outcomes
for measuring treatment success for chronic low back pain. Spine (Phila Pa
1976). 2011;36(Suppl):S54–68.
33. Smeets RJ, Hijdra HJ, Kester AD, Hitters MW, Knottnerus JA. The usability of six
physical performance tasks in a rehabilitation population with chronic low back
pain. Clin Rehabil. 2006;20:989–97.
34. Goodson A, McGregor AH, Douglas J, Taylor P. Direct, quantitative clinical
assessment of hand function: usefulness and reproducibility. Man Ther.
2007;12:144–52.
2014
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What Works, What Doesn’t, and What Is New? continued...
unaware of the adverse outcomes associated with large-gauge
cutting needles used for dural puncture.36 Communication and
education between anesthesiology and neurology and emergency
medicine teams may help to prevent a large number of PDPHs.4,10
19. Hakim S, Khan RM, Maroof M, Usmani H, Huda W, Jafri F. Methylergonovine
maleate (methergine) relieves postdural puncture headache in obstetric
patients. Acta Obstet Gynecol Scand 2005;84:100-100.
We now have a number of different treatment options for PDPH
patients, but many unanswered questions remain. Hopefully,
we as regional anesthesiologists can lead the effort to further
investigate new methods of treatment and how to individualize
those treatments to particular patients.
21. Zencirci B. Postdural puncture headache and pregabalin. J Pain Res
2010;3:11-14.
References:
1. Zundert AV, Goerig M. August Bier 1861-1949. A Tribute to a Great Surgeon
Who Contributed Much to the Develoment of Modern Anesthesia. On the 50th
Anniversary of His Death. Reg Anesth Pain Med 2000;25:26-33.
2. Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. Philadelphia: Lippincott
Williams & Wilkins, 2006. Print.
3. Gaiser R. Postdural puncture headache. Curr Opin Anaesthesiol 2006;19:249253.
4. Turnbull DK, Shepherd DB. Post-dural puncture headache: pathogenesis,
prevention and treatment. Br J Anaesth 2003;91:718-729.
5. Bezov D, Ashina S, Lipton R. Post-dural puncture headache: Part II – prevention,
management and prognosis. Headache 2010;50:1482-1498
6. Gupta S, Collis RE, Harries SE. Increasing dural tap rate: is this a national trend?
Int J Obstet Anesth 2007;16:S17.
7. Dodge HS, Ekhator NN, Jefferson-Wilson L, Fischer M, Jansen I, Horn PS, Hurford
WE, Geracioti TD. Cigarette smokers have reduced risk for post-dural puncture
headache. Pain Physician 2013;16:E25-30.
8. Vandam LD, Dripps RD. Long-term follow up of patients who received 10098
spinal anesthetics. JAMA 1956;161:586-591.
9. Ona XB, Tuma SMU, Garcia LM, Sola I, Cosp XB. Drug therapy for preventing
post-dural puncture headache. Cochrane Database Syst Rev 2013, Issue 2. Art.
No.: CD001792. DOI 10.1002/14651858.CD001792.
10. Halker RB, Demaerschalk BM, Wellik KE, Wingerchuk DM, Rubin DI, Crum BA,
Dodick DW. Caffeine for the prevention and treatment of postdural puncture
headache: debunking the myth. The Neurologist 2007;13:323-327.
11. Collier BB. Treatment for post dural puncture headache. Br J Anaesth.
1994;72:366-371.
12. Kshatri AM, Foster PA. Adrenocorticotropic hormone infusion as a novel
treatment for postdural puncture headache. Reg Anesth 1997;22:432-434.
20. Sheen MJ, Ho ST. Mirtazapine relieves postdural puncture headache. Anesth
Analg 2008;107:346-346.
22. Carp H, Singh PJ, Vadhera R, Jayaram A. Effects of the serotonin-receptor
agonist sumatriptan on postdural puncture headache: report of six cases.
Anesth Analg 1994;79:180-182.
23. Connelly NR, Parker RK, Rahimi A, Gibson CS. Sumatriptan in patients with
postdural puncture headache. Headache 2000;40:316-319.
24. Ergün U, Say B, Ozer G, Tune T, Sen M, Tüfekcioglu S, Akin U, Ilhan MN, Inan
L Intravenous theophylline decreases post-dural puncture headaches. J Clin
Neurosci 2008;15:1102-1104.
25. Stephenson LL, Varness DC, Schroeder KM, Ford MP. Tramadol for postdural
puncture headache treatment in a pediatric patient following failed blood
patch. J Clin Anesth 2012;24:171-172.
26. Barodka V, Huffnagle S, Huffnagle S. Tramadol as a novel treatment for
postdural puncture headache. Reg Anesth Pain Med 2007;32:A-60.
27. Harrington BE, Schmitt AM. Meningeal (postdural) puncture headache,
unintentional dural puncture, and the epidural blood patch. A national survey
of United States practice. Reg Anesth Pain Med 2009;34:430-437.
28. Malhotra S. All Patients with a PDPH should receive an epidural blood patch.
Int J Obstet Anesth 2014; doi:http://dx.doi.org/10.1016/j.ijoa.2014.01.001.
29. Rucklidge MWM. All patients with a postdural puncture headache should
receive an epidural blood patch. Int J Obstet Anesth 2014; doi:http://dx.doi.
org/10.1016/j.ijoa.2013.07.005l.
30. Bucklin BA, Tinker JH, Smith CV. Clinical dilemma: a patient with postdural
puncture headache and acute leukemia. Anesth Analg 1999;88:166-167.
31. Cassara C, Donnelly M, Schroeder K. Epidural blood patch of post-dural
puncture headache in the HIV positive patient (abstract). Reg Anesth Pain Med
Spring 2012;A-101.
32. Sakr A, Rah K, Cohen S, Faloba K, Ramos D, Chiricolo A, Kudupudi A, Mohiuddin
A, Chhokra R. Hunter CW. Can we offer sphenopalatine ganglion block for our
obstetric patient following accidental dural puncture? (abstract) Reg Anesth
Pain Med Fall 2013;A-162.
33. Dietzel J, Witstruck T, Adler S, Usichenko TI. Acupuncture for treatment of
therapy-resistant post-dural puncture headache: a retrospective case series.
Br J Anaesth 2013;111:847-849.
13. Gupta S, Agrawal A. Postdural puncture headache and ACTH. J Clin Anesth
1997;9:258-258.
34. Naja Z, Al-Tannir M, El-Rajab M, Ziade F, Baraka A. Nerve stimulator-guided
occipital nerve blockade for postdural puncture headache. Pain Pract
2009;9:51-58.
14. Ghai A, Wadhera R. Adrenocorticotrophic hormone – is a single dose sufficient
for post-dural puncture headache? Acta Anaesthesiol Scand 2007;51(2):266266.
35. Heesen M, Klöhr S, Rossaint R, Walters M, Straube S, van d Velde A. Insertion
of an intrathecal catheter following accidental dural puncture: a meta-analysis.
Int J Obstet Anesth 2013;22:26-30.
15. Carter BL, Pasupuleti R. Use of intravenous Cosyntropin in the treatment of
postdural puncture headache. Anesthesiology 2000;92:272-274.
36. Lavi R, Rowe JM, Avivi I. Lumbar puncture: it is time to change the needle. Eur
Neurol 2010:64:108-113.
16. Erol DD. The effect of oral gabapentin on postdural puncture headache. Acute
Pain 2006;8:169.
17. Erol DD. The analgesic and antiemetic efficacy of gabapentin or ergotamine/
caffeine for the treatment of postdural puncture headache. Adv Med Sci
2011;56:25-29.
18. Ashraf N, Sadeghi A, Azarbakht Z, Salehi S, Hamediseresht E. Hydrocortisone in
post-dural puncture headache. MEJ Anesth 2007;19:415-422.
23
2
2014
Local Anesthetic Toxicity continued...
resuscitation despite the use of ILE.1 If the patient remains
pulseless after lipid infusion, CPB is the best opportunity for
surviving the event.19
SEIZURE SUPPRESSION
In addition to cardiovascular instability, severe LAST can present
with signs of neurologic derangement.20 The ASRA practice advisory
prioritizes seizure suppression in addition to airway management
to avoid hypoxemia and acidosis since both worsen LAST.21-23
Benzodiazepines are recommended for treating such seizures.1
Propofol may seem an appealing alternative for this purpose
because it is handy, effective, and delivered in a lipid emulsion.
However, the potential benefits of propofol are outweighed by its
cardio-depressant effects. Moreover, effective lipid resuscitation
(see below) requires bulk administration (~100 mL of 20% lipid for
an adult), and the small volume of a seizure-suppressing propofol
dose (~5-10 mL of 10% lipid) provides no benefit in reversing
toxicity. Propofol is therefore recommended as a second line
treatment for seizure control and then only in small doses.1
LIPID INFUSION
Laboratory studies and case reports show that ILE can be an
effective antidote, reversing both cardiac and CNS signs of
LAST (Figure 2).13-24 This antidotal effect derives from several
mechanisms, including some demonstrated only recently. It has
long been known that lipophilic local anesthetics will partition
into a lipid phase both in vivo and in vitro.25-27 However, in silico
modeling casts doubt on whether the lipid ‘sink’ can by itself
exert sufficient effect to reverse LAST.28 Moreover, pharmacologic
investigations in human volunteers have shown that ILE shortens
the context-sensitive half-life of bupivacaine but does not
produce a demonstrable sink effect.29 Recent reports suggest
that inhibiting fatty acid metabolism prevents ILE reversal of
bupivacaine cardiac toxicity, supporting a metabolic mechanism
for lipid infusion.30 In addition, ILE rapidly exerts a direct inotropic
effect in normal hearts that can contribute to resuscitation from
LAST.31 ILE also improves cardiac function in recovery from an
ischemic insult by activating cell-saving signaling pathways.32
Finally, free fatty acids can also interfere with bupivacaine binding
of sodium channels on the plasma membrane.33-34 In sum, ILE
improves the pharmacokinetic disposition of local anesthetic
and exerts positive effects on diverse metabolic and signaling
pathways that in combination accelerate recovery from LAST.
PREPARATION AND PREVENTION
While it is reassuring to have a rational plan to treat LAST,
preventing it in the first place is obviously preferred.35 ASRA
recently released a nine-point safety checklist to review prior
to nerve block that includes preparedness for LAST.2 Vigilance
for clinical signs of LAST will reduce the risk of local anesthetic
toxicity (estimated to be approximately 1 in 1000 peripheral nerve
blocks).36 Risk factors should be identified in selecting patients
for regional analgesia; these include pre-existing cardiac disease,
small size, extremes of age, metabolic or mitochondrial disease,
liver disease, acidosis, and possibly, use of sodium channel
blocking medication such as phenothiazines or lamotrigine.1,37,38
The ASRA practice advisory recommends using the lowest
effective dose of local anesthetic, and some (though not all)
experts in the field also favor using epinephrine or other tracer in
the local anesthetic solution to serve as a marker of intravascular
injection.1 Ultrasound guidance reduces, but does not eliminate
the risk of LAST.39-41
The use of a checklist during resuscitation has been shown
to improve practitioner decision-making in simulated LAST.3
Simulation experience is also a sensible preparation for LAST,
and a local anesthetic resuscitation kit should be readily available
wherever regional anesthesia is performed.1 Because the severity
of LAST can vary greatly, clinicians must use their discretion
to decide at which point to use lipid emulsion; however, it is
important to note that LAST can progress to cardiovascular
collapse even after initial symptoms subside.42 The authors
encourage incidents of lipid resuscitation to be reported at www.
lipidrescue.org.
In summary, recommendations for treatment of LAST are evolving
away from the standard ACLS protocol. One may understandably
hesitate in deviating from traditional methods of resuscitation.
However, laboratory findings continue to provide support for
these specific interventions, and clinical experience indicates that
patients are increasingly surviving this often fatal event.9
References:
1. Neal, J.M., et al., ASRA practice advisory on local anesthetic systemic toxicity.
Reg Anesth Pain Med, 2010. 35(2): p. 152-61.
2. Mulroy, M. A checklist for performing regional nerve blocks. Regional Anesthesia
and Pain Medicine, 2014. 39(3): p.195-199.
3. Neal, J.M., et al., ASRA checklist improves trainee performance during a
simulated episode of local anesthetic systemic toxicity. Reg Anesth Pain Med,
2012. 37(1): p. 8-15.
4. Albright, G., Cardiac Arrest Following Regional Anesthesia with Etidocaine or
Bupivacaine. Anesthesiology. 51(4): p. 285-287.
5. Bonnet, D., et al., Arrhythmias and Conduction Defects as Presenting Symptoms
of Fatty Acid Oxidation Disorders in Children. Circulation, 1999. 100(22): p.
2248-2253.
6. Butterworth, J.F., R.L. James, and J. Grimes, Structure-Affinity Relationships
and Stereospecificity of Several Homologous Series of Local Anesthetics for the
&Adrenergic Receptor. Anesth Analg, 1997. 85: p. 336-42.
7. Hori, K., et al., The effect of lipid emulsion on intracellular bupivacaine as a
mechanism of lipid resuscitation: an electrophysiological study using voltagegated proton channels. Anesth Analg, 2013. 117(6): p. 1293-301.
8. Weinberg, G., et al., Bupivacaine Inhibits Acylcarnitine Exchange in Cardiac
Mitochondria. Anesthesiology, 2000. 92(2): p. 523-8.
9. Ozcan, M.S. and G. Weinberg, Update on the use of Lipid Emulsions in Local
Anesthetic Systemic Toxicity: A Focus on Differential Efficacy and Lipid Emulsion
as Part of Advanced Cardiac Life Support. International Anesthesiology Clinics,
2011. 49(4): p. 99-103.
2014
24
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Article Title
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th Annual Pain
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November 13-16, 2014
San Francisco, California
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PAIN MEDICINE
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May 31- June 1, 2014
Chicago, Illinois
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AND ACUTE PAIN MEDICINE
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th Annual Regional
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May 14-16, 2015
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For more information about ASRA CME meetings and courses
please visit our website at www.asrameetings.com
2014
Local Anesthetic Toxicity continued...
10. de Queiroz Siqueira, M., et al., Resuscitation with lipid, epinephrine, or both
in levobupivacaine-induced cardiac toxicity in newborn piglets. Br J Anaesth,
2014. 112(4): p. 729-34.
11. Hiller, D.B., et al., Epinephrine Impairs Lipid Resuscitation from Bupivacaine
Overdose: A Threshold Effect. Anesthesiology, 2009. 111: p. 498-505.
12. Li, B., et al., Association of sustained cardiovascular recovery with epinephrine
in the delayed lipid-based resuscitation from cardiac arrest induced by
bupivacaine overdose in rats. Br J Anaesth, 2012. 108(5): p. 857-63.
27. Weinberg, G., et al., Partitioning effect in lipid resuscitation: Further evidence
for the lipid sink. Crit Care Med, 2010. 38(11): p. 2268-9.
28. Kuo, I. and B.S. Akpa, Validity of the Lipid Sink as a Mechanism for the Reversal
of Local Anesthetic Systemic Toxicity: A Physiologically Based Pharmacokinetic
Model Study. Anesthesiology, 2013. 118(6): p. 1350-61.
29. Litonius, E., et al., Effect of intravenous lipid emulsion on bupivacaine plasma
concentration in humans. Anaesthesia, 2012. 67(6): p. 600-5.
13. Weinberg, G., et al., Resuscitation with Lipid versus Epinephrine in a Rat Model
of Bupivacaine Overdose. Anesthesiology, 2008. 108: p. 907-13.
30. Partownavid, P., et al., Fatty-acid oxidation and calcium homeostasis are
involved in the rescue of bupivacaine-induced cardiotoxicity by lipid emulsion
in rats. Crit Care Med, 2012. 40(8): p. 2431-7.
14. Krishnamoorthy, V., et al., Epinephrine for Cardiac Arrest: Are We Doing More
Harm Than Good? Anesthesiology, 2014. 120(4): p. 792-794.
31. Fettiplace, M.R., et al., Rapid cardiotonic effects of lipid emulsion infusion*. Crit
Care Med, 2013. 41(8): p. e156-62.
15. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care Science. Circulation, 2010. 122(18).
32. Rahman, S., et al., Phosphorylation of GSK-3beta mediates intralipid-induced
cardioprotection against ischemia/reperfusion injury. Anesthesiology, 2011.
115(2): p. 242-53.
16. Di Gregorio, G., et al., Lipid emulsion is superior to vasopressin in a rodent
model of resuscitation from toxin-induced cardiac arrest. Crit Care Med, 2009.
37(3): p. 993-9.
17. Groban, L., et al., Cardiac resuscitation after incremental overdosage with
lidocaine, bupivacaine, levobupivacaine, and ropivacaine in anesthetized dogs.
Anesth Analg, 2001. 92(1): p.37-43.
18. Marwick, P.C., A.I. Levin, and A.R. Coetzee, Recurrence of cardiotoxicity after
lipid rescue from bupivacaine-induced cardiac arrest. Anesth Analg, 2009.
108(4): p. 1344-6.
33. Mottram, A.R., C.R. Valdivia, and J.C. Makielski, Fatty acids antagonize
bupivacaine-induced I(Na) blockade. Clin Toxicol (Phila), 2011. 49(8): p. 72933.
34. Wagner, M., et al., Lipid Rescue Reverses the Bupivacaine-induced Block
of the Fast Na+ Current (INa) in Cardiomyocytes of the Rat Left Ventricle.
Anesthesiology, 2014. 120: p. 724-36.
35. Mercado, P. and G.L. Weinberg, Local anesthetic systemic toxicity: prevention
and treatment. Anesthesiol Clin, 2011. 29(2): p. 233-42.
19. Soltesz, E.G., F. van Pelt, and J.G. Byrne, Emergent cardiopulmonary bypass for
bupivacaine cardiotoxicity. Journal of Cardiothoracic and Vascular Anesthesia,
2003. 17(3): p. 357-358.
36. Mulroy, M., Systemic toxicity and cardiotoxicity from local anesthetics:
Incidence and preventive measures. Regional Anesthesia and Pain Medicine,
2002. 27(6): p. 556-561.
20. Di Gregorio, G., et al., Clinical Presentation of Local Anesthetic Systemic
Toxicity. Regional Anesthesia and Pain Medicine, 2010. 35(2): p. 181-187.
37. Nogar, J.N., Minns, A.B., Savaser, D.J. and Ly, B.T., Severe sodium channel
blockade and cardiovascular collapse due to a massive lamotrigine overdose.
Clin Toxicology, 2011. 49(9): p.854-7.
21. Heavner, J.E., et al., Severe Hypoxia Enhances Central Nervous System
and Cardiovascular Toxicity of Bupivacaine in Lightly Anesthetized Pigs.
Anesthesiology, 1992. 77: p. 142-147.
38. Kolecki, P.F., Curry, S.C., Poisoning by sodium channel blocking agents. Crit
Care Clin, 1997. 13(4): p.829-48.
22. Moore, D.C., R.D. Crawford, and J.E. Scurlock, Severe Hypoxia and Acidosis
Following Local Anesthetic-induced Convulsions. Anesthesiology, 1980. 53: p.
259-260.
39. Barrington, M.J. and R. Kluger, Ultrasound guidance reduces the risk of local
anesthetic systemic toxicity following peripheral nerve blockade. Reg Anesth
Pain Med, 2013. 38(4): p. 289-97.
23. Rosen, M.A., et al., Bupivacaine-Induced Cardiotoxicity in Hypoxic and Acidotic
Sheep. Anesth Analg, 1985. 64: p. 1089-96.
40. Orebaugh, S.L., et al., Adverse outcomes associated with stimulator-based
peripheral nerve blocks with versus without ultrasound visualization. Reg
Anesth Pain Med, 2009. 34(3): p. 251-5.
24. Cave, G., et al., LIPAEMIC Report: Results of Clinical Use of Intravenous Lipid
Emulsion in Drug Toxicity Reported to an Online Lipid Registry. J Med Toxicol,
2014.
25. Samuels, T.L., et al., In vitro suppression of drug-induced methaemoglobin
formation by Intralipid((R)) in whole human blood: observations relevant to the
‘lipid sink theory’. Anaesthesia, 2012. 67(1): p. 23-32.
26. Mazoit, J.X., et al., Binding of Long-lasting Local Anesthetics to Lipid
Emulsions. Anesthesiology, 2009. 110(2): p. 380-6.
41. Zetlaoui, P.J., J. Labbe, and D. Benhamou, Ultrasound Guidance for Axillary
Plexus Block Does Not Prevent Intravascular Injection. Anesthesiology, 2008.
108(4): p. 557-8.42.
42. Vadi, M.G., Patel, N., Stiegler, M.P., Local Anesthetic Systemic Toxicity after
Combines Psoas Compartment-Sciatic Nerve Block: Analysis of Decision
Factors and Diagnostic Delay. Anesthesiology, 2014. 120(4): p.987-96.
2014
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