CONTINUING EDUCATION
Local Anesthetic Systemic
Toxicity 1.5 www.aornjournal.org/content/cme
DIANA L. WADLUND, MSN, ACNP-BC, FNP-C, CRNFA
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Purpose/Goal
To provide the learner with knowledge of best practices related
to recognizing and treating local anesthetic systemic toxicity
(LAST).
Objectives
1. Discuss how local anesthetics work.
2. Describe local anesthetic composition.
3. Discuss LAST.
Accreditation
AORN is accredited with distinction as a provider of
continuing nursing education by the American Nurses
Credentialing Center’s Commission on Accreditation.
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This program meets criteria for CNOR and CRNFA recerti-
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Conflict-of-Interest Disclosures
Diana L. Wadlund, MSN, ACNP-BC, FNP-C, CRNFA, has
no declared affiliation that could be perceived as posing a
potential conflict of interest in the publication of this article.
The behavioral objectives for this program were created by
Helen Starbuck Pashley, MA, BSN, CNOR, clinical editor,
with consultation from Susan Bakewell, MS, RN-BC, direc-
tor, Perioperative Education. Ms Starbuck Pashley and
Ms Bakewell have no declared affiliations that could be
perceived as posing potential conflicts of interest in the
publication of this article.
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article.
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AORN Journal j 367
Local Anesthetic Systemic
Toxicity 1.5 www.aornjournal.org/content/cme

DIANA L. WADLUND, MSN, ACNP-BC, FNP-C, CRNFA

ABSTRACT
Local anesthetics are commonly used in the perioperative environment to facilitate surgical
procedures or to provide postoperative pain management for patients. The use of local anesthetics,
however, introduces the risk of complications resulting from local anesthetic systemic toxicity and
the risks of increased morbidity and mortality for the surgical patient. Systemic toxicity from the
injection or overdose of local anesthetics is a rare but potentially fatal complication that occurs in
less than 1 in 1,000 patients. This article provides the perioperative nurse with information about
local anesthetics, the signs and symptoms of local anesthetic systemic toxicity, and the information
needed to manage a patient experiencing this complication. AORN J 106 (November 2017) 367-377.
ª AORN, Inc, 2017. http://dx.doi.org/10.1016/j.aorn.2017.08.015
Key words: local anesthetic, anesthetic complications, local anesthetic systemic toxicity, amino amides,
amino esters.

A pproximately 70 million surgeries are performed

annually in the United States; nearly 53 million of
these are performed on an outpatient basis.1,2
Today, clinicians use local and general anesthesia extensively
to eliminate pain from surgery. For example, dentists in the
United States use approximately 100 million carpules of local
anesthetic per day.1 Although the widespread use of local
anesthetics makes painless surgical procedures possible, the use
of such anesthetics carries the risk for local anesthetic systemic
toxicity (LAST).3 To manage and prevent LAST in patients
undergoing operative and other invasive procedures, periop-
erative nurses should be aware of the range of local anesthetics
available and the signs of, symptoms of, and treatments for this
potentially fatal complication.
HISTORY OF LOCAL ANESTHETICS
Less than 200 years ago, elective surgery was virtually
nonexistent. When surgery was performed, it was undertaken
without the benefit of anesthesia and was considered a last-
resort attempt to save a life.4 The earliest form of anesthesia
has been described as a sharp blow to the jaw that rendered the
patient unconscious.4 Over time, clinicians began using
368 j AORN Journal
various plant-based alternative therapies (eg, marijuana,
belladonna) in an attempt to dull sensation and make surgical
procedures less painful. Mesmerism, hypnosis, and distraction
also were attempted to improve the patient’s surgical
experience.4
The use of injectable local anesthetics began more than 100
years ago when surgeons started injecting cocaine, the first
local anesthetic, into the oral cavity for wisdom tooth extrac-
tion. Dr William Halsted used cocaine as a peripheral nerve
block in 1884 when he injected it into a patient’s surgically
exposed brachial plexus.5 During the same decade, Dr Carl
Koller used cocaine as a topical anesthetic during ophthalmic
surgery.6 The euphoria, potential for addiction, and mortality
associated with the use of cocaine, however, pointed to a need
for a less toxic local anesthetic. In 1904, procaine, the first
synthetic derivative of cocaine, became available; it dominated
the local anesthetic market for nearly 40 years.6
Lidocaine was created in 1943.7 Lidocaine is nonaddictive and
is generally well tolerated by most patients. For these reasons,
lidocaine quickly became the standard by which we currently
compare all anesthetic medications.7 By the mid-1960s,
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mepivacaine, prilocaine, and bupivacaine were also available.
These new medications expanded the options available for
local anesthetic use. Articaine was first synthesized in the late
1960s.6 Although articaine is not commonly used in the
United Sates because of its potency and safety profile, it is now
the most commonly used local anesthetic in Europe for dental
procedures.6
Today, local anesthetics have become a valuable part of a
multimodal postoperative pain management plan. Local
anesthetics are commonly used for topical anesthesia, skin and
soft tissue infiltration, peripheral nerve blocks, epidural or
spinal anesthesia, and IV regional anesthesia. Although local
anesthetics provide the necessary block for surgical interven-
tion and act as an adjunct for postoperative pain management,
their use is not without potential risks. Although LAST is a
rare event that occurs in approximately 1 of every 1,000
patients, the consequences are potentially life threatening.8 It
is crucial that perioperative nurses have the knowledge
necessary to understand how local anesthetics work and the
risks associated with their use and that they are able to
recognize the signs and symptoms of LAST and institute
appropriate, timely treatment.1,9
OVERVIEW OF LOCAL ANESTHETICS
Two anesthetic modalities aid in rendering the surgical expe-
rience painless for the patient: general and local anesthesia.
General anesthetics are systemic medications that render the
central nervous system (CNS) incapable of processing surgical
stimuli. Local anesthetics prevent the surgical stimuli from
reaching the CNS by binding to receptor sites on the sodium
channels in the nerve cell membrane and creating a reversible
block of the transmission of nerve impulses. This block
prevents a wave of depolarization from effectively moving
through the nerve, thereby eliminating the transmission of the
pain impulse.8
Local Anesthetic Composition
Local anesthetics are made up of three chemical components:
an aromatic ring, an intermediate chain, and a terminal
amine.10 The first component, the aromatic ring, determines
the lipid solubility of the local anesthetic. Local anesthetics
are classified as amino amides (eg, lidocaine, mepivacaine,
bupivacaine) or amino esters (eg, cocaine, procaine, tetra-
caine).7,8,11 The characteristics and differences between these
two types of local anesthetics are listed in Table 1.
Amino amides have a long duration of effect and are metab-
olized by the liver. These characteristics contribute to the
increased risk for systemic toxicity associated with their use.
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Local Anesthetic Systemic Toxicity
The onset of action of amino amides is moderate to fast. The
normal pH of amino amides ranges from 7.6 to 8.1. Allergic
reactions are rare with amino amides.7,10
Amino esters can be short, moderate, or long acting. They are
metabolized by plasma esterase in the skin and blood. When
an ester-type anesthetic is metabolized, para-aminobenzoic
acid is formed and is the main cause of the allergic reactions
commonly associated with ester anesthetics. Amino esters’
onset of action is slow and their pH is between 8.5 and 8.9.7,8
The body considers all compounds that enter it foreign and
will try to rid itself of them. The process by which the body
eliminates these medications from itself is biotransformation.
The second component of a local anesthetic, the intermediate
chain or linkage, is the basis for local anesthetic classification
and determines the pattern of this biotransformation.7,10
Amino esters are hydrolyzed by plasma esterase in the skin and
blood, whereas amino amides are biotransformed in the liver.
The differences in how the body metabolizes the medications
allow amino amides to be more effective, longer lasting, and
less likely to cause allergic reactions than amino esters.10
Another benefit of amino amides is that they dramatically
decrease or eliminate byproducts that are formed when they
are broken down in the bloodstream. The elimination of these
byproducts can decrease the potential for allergic reactions.10
The third component of local anesthetics, the terminal amine,
exists in either a tertiary (ie, three-band) or quaternary
(ie, four-band) form. The tertiary form is lipid-soluble,
whereas the quaternary form is positively charged, rendering
the molecule water-soluble. Although the aromatic ring
determines the actual degree of lipid solubility, the terminal
amine acts as an on/off switch allowing the local anesthetic to
exist in the lipid-soluble or water-soluble formation.10 The
time of onset for a local anesthetic is predicted based on its
existence in tertiary or quaternary form.7,10
Lipid Solubility
Lipid solubility allows for local anesthetic diffusion through
the nerve and cell membrane. Ninety percent of the nerve cell
membrane is composed of lipids, and the potency of the local
anesthetic is related to its lipid solubility. Local anesthetics
with a higher lipid solubility penetrate the nerve faster and
provide a more rapid block of the sodium channel. Greater
lipid solubility enhances diffusion across the nerve sheath and
through the neural membrane of individual axons. The higher
the lipid solubility of an anesthetic, the lower the concentra-
tion necessary for nerve block. This allows for a lower dose of
anesthesia and reduces the risk of LAST.10
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1-4
Table 1. Properties of Amino Ester and Amino Amide Local Anesthetics

Property Esther Amide

Agents  Benzocaine  Articaine
 Chloroprocaine  Bupivacaine
 Cocaine  Dibucaine
 Procaine  Etidocaine
 Proparacaine  Levobupivacaine
 Tetracaine  Lidocaine
 Mepivacaine
 Prilocaine
 Ropivacaine
Metabolism Rapid; plasma pseudocholinesterase Slow; hepatic
Systemic toxicity Less likely More likely
Allergic reactions Possible; PABA derivative Very rare
Stability Breaks down in ampules, heat, and sun Chemically stable
Onset of action Slow Moderate to fast
pH 8.5-8.9 7.6-8.1
PABA ¼ para-aminobenzoic acid.
References
1. McLeod IK. Local anesthetics: introduction and history. Medscape. http://emedicine.medscape.com/article/873879-overview. Updated July
23, 2017. Accessed July 25, 2017.
2. Noble KA. Local anesthesia toxicity and lipid rescue. J Perianesth Nurs. 2015;30(4):321-335.
3. Becker DE, Reed KL. Local anesthetics: review of pharmacological considerations. Anesth Prog. 2012;59(2):90-102.
4. McLeod IK. Local anesthetics: chemical structure. Medscape. http://emedicine.medscape.com/article/873879-overview#a3. Updated July 23,
2017. Accessed July 25, 2017.

Dissociation Constant reduces bleeding at the site of injection. Another benefit

The dissociation constant (Kd) identifies the portion of an
administered local anesthetic dose that exists in the lipid-
soluble state at a given pH. Agents with a lower dissociation
constant have a more rapid anesthetic onset. For example,
lidocaine (Kd ¼ 7.7) has a more rapid onset than bupivacaine
(Kd ¼ 8.1).10
attributed to the addition of epinephrine to a local anesthetic is
the decreased entry of the local anesthetic into plasma, which
allows for safe administration of higher doses of the chosen
local anesthetic.12 Containing the local anesthetic at the in-
jection site by vasoconstriction also increases the duration of
the nerve block.12 There are some patients in which the use of
epinephrine is contraindicated, including those with

Protein Binding  systolic blood pressure readings greater than 200 mm Hg

Local anesthetics bind with circulating plasma proteins. The
degree to which the local anesthetic binds with proteins in the
sodium channel predicts the duration of the nerve block. For
example, bupivacaine is 95% protein binding and lidocaine is
65% protein binding; therefore, bupivacaine has the greater
percentage of protein binding and is longer acting than
lidocaine.10
Local Anesthetic Additives
Other medications may be added to a local anesthetic to affect
how it works. Two common additives are epinephrine and
sodium bicarbonate. Epinephrine causes vasoconstriction,
which slows systemic absorption of the local anesthetic and
and diastolic blood pressure readings greater than 115 mm
Hg;
 uncontrolled hypertension;
 severe cardiac disease;
 a history of myocardial infarct or cerebrovascular accident in
the previous six months;
 angina;
 cardiac dysrhythmia; or
 concomitant use of medications such as beta-blockers,
monoamine oxidase inhibitors, or tricyclic antidepressants.7
Adding sodium bicarbonate to a local anesthetic speeds the
onset of nerve block by increasing the pH and tertiary state.
Although sodium bicarbonate significantly increases the speed

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1
Table 2. Maximum Doses and Durations of Various Local Anesthetics

Agent Onset Maximum Dose, mg/kg Duration, min

Without Epinephrine With Epinephrine Without Epinephrine With Epinephrine
Bupivacaine Slow 8 10 240 480
Lidocaine Rapid 4.5 7 120 240
Mepivacaine Rapid 5 7 180 360
Prilocaine Medium 5 7.5 90 360
Procaine Slow 8 10 45 90
Tetracaine Slow 1.5 2.5 180 60
Reference
1. McLeod IK. Local anesthetics: introduction and history. Medscape. http://emedicine.medscape.com/article/873879-overview. Updated July
23, 2017. Accessed July 25, 2017.

of onset associated with sensory and motor nerve blocks, it
does not affect the duration of the block.3 The practice of
alkalinizing local anesthetics using sodium bicarbonate is of
uncertain benefit because this effect has not been demon-
strated to be constant across all types of nerve block.12
decrease the amount of discomfort experienced by the patient.
Another important technique to employ when injecting local
anesthetics is to frequently aspirate to check for inadvertent IV
access. Checking for inadvertent IV access will decrease the
risk for LAST.7

LOCAL ANESTHETIC SYSTEMIC

Type and Dose
TOXICITY The type of anesthetic and the dose of anesthetic injected
Local anesthetic systemic toxicity usually involves the CNS or
contribute to the potential for LAST. Individual local anes-
the cardiovascular system.13 Certain factors contribute to this
thetics should be administered using the appropriate dose for
toxicity, including the site of the injection, the injection
the individual patient.6,14 Table 2 lists the maximum dose and
technique, the type of anesthetic and dose injected, and the
duration of various local anesthetics.
individual receiving the local anesthesia.14

Site of Injection Patient Characteristics

The site of the local anesthetic injection determines the rate of
absorption. Certain sites of injection have a higher rate of IV
absorption, which correlates with a higher propensity for
toxicity. Listed in order of lowest to highest absorption rates,
these injection sites include subcutaneous tissue and brachial
plexus, epidural, caudal, and intercostal blocks. For example,
injection for pain management into the subcutaneous tissue of
the abdomen is less likely to result in toxicity than an injection
into the brachial plexus, which is an area of the body that is
more highly vascular.14
Injection Technique
The size of the needle used to inject the local anesthetic will
determine how rapidly the local anesthetic is injected. For
example, local anesthetics injected with an 18-gauge needle
will be injected more rapidly that those injected using a
25-gauge needle. A slower speed of injection, which can be
achieved by using a smaller gauge needle, will subsequently
Certain patient characteristics affect the potential for LAST.
These characteristics include the patient’s weight, comorbid-
ities, use of other medications, genetics, allergies, and other
physiologic limitations. Patients with comorbidities such as
severe renal failure or liver disease will have a decreased
clearance rate of local anesthetics. Patients who have cardiac
failure will have an increased risk for local anestheticeinduced
myocardial depression and arrhythmias. Older adult patients
are at a higher risk for LAST because they have physiologically
decreased systemic blood flow and liver function, leading to
decreased local anesthetic clearance.14
Manifestations of LAST
The manifestations of LAST may appear 30 seconds to
60 minutes after injection, but they typically appear within 1 to
5 minutes. The manifestations vary widely but are usually con-
sistent with CNS excitement (eg, oral numbness, metallic taste,
dizziness or lightheadedness, drowsiness or disorientation,

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Wadlund
visual or auditory disturbances).13 There are five categories of
LAST manifestation: CNS, cardiovascular, hematologic, aller-
gic, and local tissue responses.13
 Early CNS manifestations often will begin with symptoms
of confusion. Patients may complain of a metallic taste in
their mouth or tinnitus. If intervention does not take place
during these early manifestations, the patient may complain
of dizziness and experience muscle twitching, seizures, loss of
consciousness, coma, respiratory depression, or cardiovas-
cular collapse, which may progress to death.13
 Cardiovascular manifestations of LAST are usually, but not
always, preceded by CNS manifestations. These manifesta-
tions include hypertension, tachycardia, bradycardia, cardiac
arrhythmias, and asystole.13 Patients with underlying con-
duction abnormalities or patients who receive lipophilic
anesthetics (eg, bupivacaine) are at an increased risk for
cardiovascular manifestations of LAST.13
 Hematologic manifestations of LAST include methemoglo-
binemia, which is more commonly associated with the use of
prilocaine, articaine, and benzocaine. These local anesthetics
are metabolized by the liver, where ortho-toluidine is formed.
ortho-Toluidine is a potent oxidizer that converts hemoglo-
bin to methemoglobin. When blood levels of methemo-
globin are low, the patient will be asymptomatic. Higher
levels of methemoglobin result in cyanosis (ie, a gray
cutaneous discoloration), tachypnea, exercise intolerance,
fatigue, dizziness, syncope, and weakness.13
 Allergic reactions to local anesthetics are more common with
the para-aminobenzoic acideassociated ester anesthetics.13
These manifestations include urticaria, rash, and in rare
instances, anaphylaxis.
 Local tissue responses commonly include numbness and
paresthesia, which at high doses can quickly become
irreversible.13
Diagnosis and Treatment
The ability to recognize LAST is crucial. While caring for any
patient receiving local anesthesia, the surgical team should
constantly assess him or her for altered mental status, agita-
tion, loss of consciousness, seizures, and cardiac collapse.
Constant assessment is vital because early recognition and
intervention can be lifesaving.14
Immediate management of a LAST crisis is critical to the
patient’s survival. The surgeon must stop the local anesthetic
injection immediately. The RN circulator should call for help
and maintain the patient’s airway while administering 100%
oxygen and confirming IV access. He or she should constantly
assess the patient’s cardiovascular status and monitor for
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November 2017, Vol. 106, No. 5
seizure activity, which, if it occurs, should be controlled with
benzodiazepines.15
Supporting the patient’s cardiac status and maintaining an
airway are a constant priority with LAST. If the patient is not
experiencing cardiac arrest, then conventional methods
(ie, medication) should be used to treat hypertension, hypo-
tension, bradycardia, and tachycardia. Lidocaine should never
be used as an antiarrhythmic during LAST, because it can
worsen the crisis. If the patient is in cardiac arrest, the surgical
team should immediately institute advanced cardiac life
support and cardiopulmonary resuscitation. The anesthesia
professional or surgeon may need to consider the use of car-
diopulmonary bypass.
Research suggests that IV infusion of lipid emulsions (ie, an
emulsion of soybean oil, egg phospholipids, and glycerin) can
reverse the effects of LAST on the heart and CNS. If
administered when the first signs of arrhythmia in patients
with suspected LAST are recognized, lipid emulsion may
prevent sequelae such as prolonged seizure activity or rapid
progression of toxic manifestations.16 Although when to
institute lipid emulsion therapy remains controversial, it is
generally believed that administration of lipid emulsion should
be considered sooner rather than later because studies have
shown dramatic improvement in patient condition and
outcomes when lipid emulsion therapy is initiated early.14,15,17
Initially, Bartlett recommended lipid emulsion therapy for
LAST as a last-resort treatment after standard resuscitation
failed. Reports of successful resuscitation with lipid infusion
suggest that earlier use might prevent progression to cardiac
arrest.18,19 In fact, IV lipids have successfully reversed life-
threatening cardiac toxicity in situations where advanced car-
diac life support was unsuccessful.18 Lipid emulsion therapy is
now an accepted treatment for severe, LAST-associated cardiac
toxicity. Intravenous lipid emulsion therapy has been found to
be safe, available, easy to administer, and very effective.19
While the anesthesia professional begins lipid emulsion ther-
apy, the surgical team should continue cardiopulmonary
resuscitation, because lipid emulsion therapy can take up to
one hour to work.17 Lipid emulsion should be immediately
available; creating a lipid rescue kit that contains 500 mL of
20% lipid emulsion, IV tubing for delivery of the emulsion,
two 60-mL syringes, and needles is helpful. The shelf life of
lipid emulsion may vary between manufacturers, though
generally it is one year.13-15,17
There are some adverse effects associated with lipid emulsion
therapy, including pancreatitis, lung injury, acute renal failure,
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November 2017, Vol. 106, No. 5
Sidebar 1. Example of Maximum Local
Anesthetic Dose Calculation
There are two pieces of information that remain constant
when the maximum dose of a given local anesthetic
agent is calculated: the maximum dose of the local anes-
thetic (reflected in milligrams per kilogram [mg/kg]) and
the concentration of the local anesthetic (reflected in
milligrams per milliliter [mg/mL]). This information is a
necessary component of the calculation of the patient-
specific maximum local anesthetic dose.
The maximum dose of a local anesthetic is based on
patient weight. The first piece of information the
perioperative nurse must know is the patient’s weight in
kilograms. To determine the patient’s weight in
kilograms, multiply the patient’s weight in pounds by
0.45. For example, for a patient weighing 154 lb,
154 lb  0:45 kg=lb ¼ 69:3 kg;
which can be rounded up to 70 kg. The patient’s
weight in kilograms is then multiplied by the maximum
dose of local anesthetic in milligrams per kilogram. For
example, the maximum dose of lidocaine 1% is
4.5 mg/kg, so
70 kg  4:5 mg=kg ¼ 315 mg;
which is the maximum safe dose of lidocaine 1%.
Finally, convert the milligram dose into the number of
milliliters that can be safely administered. A 1% dose
of lidocaine contains 10 mg of lidocaine per milliliter of
medication. Therefore,
315 mg lidocaine 1%O10 mg=mL ¼ 31:5 mL;
which indicates that 31.5 mL can be safely administered
to a patient who weighs 70 kg.
deep vein thrombosis, recurrent and delayed signs and
symptoms of LAST, and digital amputation. The benefits of
using lipid emulsion therapy must outweigh the risks to the
patient.14,19 Care providers should not use propofol, which is
formulated in a 10% lipid solution, as a substitute for lipid
emulsion therapy, because an overdose of propofol would be
necessary to provide the effective treatment.17
Perioperative Considerations
AORN’s “Guideline for care of the patient receiving local
anesthesia”20 recommends that the perioperative nurse have
knowledge of local anesthetic medications, including indications
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Local Anesthetic Systemic Toxicity
for use, contraindications, desired effects, and adverse effects.
This knowledge will facilitate early detection and treatment
of LAST.20
The guideline also recommends that the perioperative nurse
verify the correct dosing parameters and the patient-specific
maximum dose before administering the local anesthetic.
The nurse should consult with a pharmacist or physician,
consult the health care organization’s medication formulary,
or review other published reference material to verify
these doses.20
Using a few critical pieces of information, the perioperative
nurse can calculate the maximum dose of local anesthetic for a
given patient; an example of this traditional calculation
method is given in Sidebar 1.21 Although this method of
calculating maximum doses of local anesthetics has been found
to be very accurate, it is cumbersome and time-consuming.22
Use of a nomogram is a simple, low-cost method of calculating
correct doses of local anesthetics and can assist the perioper-
ative nurse in identifying a safe maximum dose. The nomo-
gram for local anesthetic doses has been tested against other
methods of calculation.8,9,14,22 Studies have found that when
used correctly, the traditional method of calculation is more
accurate than the nomogram; however, these studies also
identified that traditional method errors produced a mean dose
overestimation of 130.5 mL compared with nomogram errors,
which overestimated the maximum permissible dose by only
0.2 mL or less.22
The AORN “Guideline for care of the patient receiving local
anesthesia”20 also discusses documentation best practices. The
perioperative nurse should document the following pieces of
information regarding the local anesthetic used during an
operative or other invasive procedure:
 type of medication,
 concentration,
 total amount administered,
 route of administration,
 time administered,
 lot number and expiration date,
 the patient’s response, and
 any adverse reactions that may have occurred.20
Additional methods to prevent LAST include using the lowest
dose of local anesthetic possible to achieve the desired result;
using a slow, careful injection technique and frequent aspira-
tion (ie, approximately every 3 mL) to determine whether
there is blood return into the syringe; and if possible, main-
taining verbal contact with the patient to identify whether
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there are any concerning signs or symptoms.8,14,15 Evidence
supports that early recognition of the signs and symptoms of
LAST is critical to its successful treatment.8,14,15
CONCLUSION
Local anesthetic systemic toxicity is a rare but potentially fatal
complication of local anesthetic use. Perioperative nurses who
recognize the symptoms of CNS toxicity will assist in
providing early treatment and preventing cardiac toxicity or
other more advanced symptoms that increase the risk of
negative outcomes, including death.21 The entire surgical team
should be aware of the potential for LAST, the signs and

symptoms associated with it, and the treatment modalities to
help ensure patient safety.
References
1. Golembiewski J, Dasta J. Evolving role of local anesthetics in
managing postsurgical analgesia. Clin Ther. 2015;37(6):
1354-1371.
2. Hollingsworth JM, Birkmeyer JD, Ye Z, Miller DC. Specialty-spe-
cific trends in the prevalence and distribution of outpatient surgery:
implications for payment and delivery system reforms. Surg Innov.
2014;21(6):560-565.
3. Saraghi M, Moore PA, Hersh EV. Local anesthetic calculations:
avoiding trouble with pediatric patients. Gen Dent. 2015;63(1):48-52.
4. Sullivan JT. Surgery before anesthesia. Newsl Am Soc Anesthesiol.
1996;60(9):8-10.
5. Fencl JL. Local anesthetic systemic toxicity: perioperative impli-
cations. AORN J. 2015;101(6):697-700.
6. Ciechanowicz S, Patil V. Lipid emulsion for local anesthetic
systemic toxicity. Anesthesiol Res Pract. 2012;2012:131784. doi:
10.1155/2012/131784.
7. McLeod IK. Local anesthetics: introduction and history. Medscape.
http://emedicine.medscape.com/article/873879-overview. Updated
July 23, 2017. Accessed July 25, 2017.
8. Noble KA. Local anesthesia toxicity and lipid rescue. J Perianesth
Nurs. 2015;30(4):321-335.
9. Hsu DC. Subcutaneous infiltration of local anesthetics. UpToDate.
http://www.uptodate.com/contents/infiltration-of-local-anesthetics?
source¼search_result&search¼localþanesthetics&selectedTitle¼
1%7E150 [by subscription]. Updated January 3, 2017. Accessed
July 10, 2017.
10. Becker DE, Reed KL. Local anesthetics: review of pharmacological
considerations. Anesth Prog. 2012;59(2):90-102.
374 j AORN Journal
November 2017, Vol. 106, No. 5
11. McLeod IK. Local anesthetics: chemical structure. Medscape.
http://emedicine.medscape.com/article/873879-overview#a3.
Updated July 23, 2017. Accessed July 25, 2017.
12. Bailard NS, Ortiz J, Flores RA. Additives to local anesthetics for
peripheral nerve blocks: evidence, limitations, and recommenda-
tions. Am J Health Syst Pharm. 2014;71(5):373-385.
13. Kapitanyan R. Local anesthetic toxicity: practice essentials.
Medscape. http://emedicine.medscape.com/article/1844551
-overview. Updated August 17, 2017. Accessed September
13, 2017.
14. Christie LE, Picard J, Weinberg GL. Local anaesthetic systemic
toxicity. Contin Educ Anaesth Crit Care Pain. 2015;15(3):136-142.
15. Dewaele S, Santos AC. Toxicity of local anesthetics. New York
School of Regional Anesthesia (NYSORA). http://www.nysora.com/
toxicity-of-local-anesthetics. Accessed July 25, 2017.
16. Neal JM, Mulroy MF, Weinberg GL. American Society of Regional
Anesthesia and Pain Medicine checklist for managing local
anesthetic systemic toxicity: 2012 version. Reg Anesth Pain Med.
2012;37(1):16-18.
17. Kapitanyan R. Local anesthetic toxicity treatment & management.
Medscape. http://emedicine.medscape.com/article/1844551
-treatment. Updated August 17, 2017. Accessed September
13, 2017.
18. Muller SH, Diaz JH, Kaye AD. Intralipid emulsion rescue therapy:
emerging therapeutic indications in medical practice. J La State
Med Soc. 2016;168(3):101-103.
19. Bartlett D. Intravenous lipids: antidotal therapy for drug overdose
and toxic effects of local anesthetics. Crit Care Nurs. 2014;34(5):
62-66.
20. Tierney KJ, Murano T, Natal B. Lidocaine-induced cardiac arrest in
the emergency department: effectiveness of lipid therapy. J Emerg
Med. 2016;50(1):47-50.
21. Guideline for care of the patient receiving local anesthesia. In:
Guidelines for Perioperative Practice. Denver, CO: AORN, Inc;
2017:617-628.
22. Williams DJ, Walker JD. A nomogram for calculating the maximum
dose of local anesthetic. Anaesthesia. 2014;69(8):847-853.
Diana L. Wadlund, MSN, ACNP-BC, FNP-C, CRNFA,
is an ACNP/CRNFA for Surgical Specialists and an ACNP
at Paoli Hospital Trauma Service, PA. Ms Wadlund has no
declared affiliation that could be perceived as posing a
potential conflict of interest in the publication of this
article.
www.aornjournal.org
EXAMINATION

Continuing Education:
Local Anesthetic Systemic
Toxicity 1.5 www.aornjournal.org/content/cme

PURPOSE/GOAL
To provide the learner with knowledge of best practices related to recognizing and treating local
anesthetic systemic toxicity (LAST).

OBJECTIVES
1. Discuss how local anesthetics work.
2. Describe local anesthetic composition.
3. Discuss LAST.

The Examination and Learner Evaluation are printed here for your convenience. To receive
continuing education credit, you must complete the online Examination and Learner Evaluation
at http://www.aornjournal.org/content/cme.

QUESTIONS 4. Amino amides

1. Local anesthetics prevent the surgical stimuli from 1. rarely cause allergic reactions.
reaching the central nervous system by 2. increase the risk for systemic toxicity.
1. binding to receptor sites on the calcium channels in 3. have a long duration of effect.
the nerve cell membrane. 4. have a moderate to fast onset of action.
2. binding to receptor sites on the sodium channels in 5. are metabolized by the liver.
the nerve cell membrane. a. 4 and 5 b. 1, 2, and 3
3. creating an irreversible block of the transmission of c. 1, 2, 3, and 4 d. 1, 2, 3, 4, and 5
nerve impulses.
4. creating a reversible block of the transmission of nerve
5. Ester-type anesthetics
impulses.
1. form para-aminobenzoic acid when metabolized.
a. 1 and 3 b. 2 and 4
2. are metabolized by plasma esterase in the skin and
c. 1, 2, and 4 d. 1, 2, 3, and 4
blood.
2. Local anesthetics produce a block that prevents a wave of 3. increase the risk for systemic toxicity.
depolarization from effectively moving through the nerve, 4. can be short, moderate, or long acting.
thereby eliminating the transmission of the pain impulse. 5. rarely cause allergic reactions.
a. true b. false a. 4 and 5 b. 1, 2, and 3
c. 1, 2, and 4 d. 1, 2, 3, 4, and 5
3. Local anesthetics are classified as __________ or
__________.
a. amino amides; amino esters 6. Two common local anesthetic additives are epinephrine
b. amino esters; amino acids and sodium bicarbonate.
c. amino acids; amino amides a. true b. false

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Wadlund November 2017, Vol. 106, No. 5

7. Certain factors contribute to LAST, including 1. confirming IV access.

1. medications added to the local anesthetic. 2. monitoring for seizure activity.
2. the type and dose injected. 3. maintaining the patient’s airway while administering
3. the site of the injection. 100% oxygen.
4. other medications used to treat comorbidities. 4. stopping the local anesthetic injection immediately.
5. the individual. 5. constantly assessing the patient’s cardiovascular status.
6. the injection technique. 6. calling for help.
a. 1, 3, and 5 b. 1, 2, 4, and 6
a. 1, 3, and 5 b. 2, 4, and 6
c. 1, 2, 3, 5, and 6 d. 1, 2, 3, 4, 5, and 6
c. 2, 3, 5, and 6 d. 1, 2, 3, 4, 5, and 6

8. The manifestations of LAST typically appear within one 10. Additional actions the perioperative team should under-
to five minutes and may include take to treat LAST include
1. agitation. 1. determining what type of local anesthetic was used.
2. drowsiness or disorientation. 2. administering IV lipid emulsion (ie, an emulsion of
3. dizziness or lightheadedness. soybean oil, egg phospholipids, and glycerin).
4. visual or auditory disturbances. 3. administering dantrolene.
5. oral numbness. 4. instituting advanced cardiac life support and cardio-
6. changes in respiration. pulmonary resuscitation if needed.
5. using lidocaine to treat arrhythmias.
a. 2, 3, 4, and 5 b. 2, 4, and 6
6. treating hypertension, hypotension, bradycardia, and
c. 2, 3, 5, and 6 d. 1, 2, 3, 4, 5, and 6
tachycardia.
9. Immediate actions the surgical team should take to treat a. 2, 4, and 5 b. 2, 4, and 6
LAST include c. 2, 3, 5, and 6 d. 1, 2, 3, 4, 5, and 6

376 j AORN Journal www.aornjournal.org

LEARNER EVALUATION

Continuing Education:
Local Anesthetic Systemic
Toxicity 1.5 www.aornjournal.org/content/cme

T his evaluation is used to determine the extent to

which this continuing education program met
your learning needs. The evaluation is printed
here for your convenience. To receive continuing education
credit, you must complete the online Examination and
7. Will you change your practice as a result of reading this
article? (If yes, answer question #7A. If no, answer
question #7B.)

Learner Evaluation at http://www.aornjournal.org/content/cme.

Rate the items as described below. 7A. How will you change your practice? (Select all that
apply)
1. I will provide education to my team regarding why
OBJECTIVES
change is needed.
To what extent were the following objectives of this
2. I will work with management to change/implement
continuing education program achieved?
a policy and procedure.
1. Discuss how local anesthetics work. 3. I will plan an informational meeting with physicians
Low 1. 2. 3. 4. 5. High to seek their input and acceptance of the need for
change.
2. Describe local anesthetic composition. 4. I will implement change and evaluate the effect of
Low 1. 2. 3. 4. 5. High the change at regular intervals until the change is
incorporated as best practice.
3. Discuss LAST.
5. Other: __________________________________
Low 1. 2. 3. 4. 5. High

CONTENT
4. To what extent did this article increase your knowledge 7B. If you will not change your practice as a result of
of the subject matter? reading this article, why? (Select all that apply)
Low 1. 2. 3. 4. 5. High 1. The content of the article is not relevant to my
practice.
5. To what extent were your individual objectives met?
2. I do not have enough time to teach others about the
Low 1. 2. 3. 4. 5. High
purpose of the needed change.
6. Will you be able to use the information from this article 3. I do not have management support to make a
in your work setting? change.
1. Yes 2. No 4. Other: __________________________________

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