Toxicity, Local Anesthetics

Author: Raffi Kapitanyan, MD, Assistant Professor, Assistant Professor of Emergency Medicine, Emergency
Medicine, Robert Wood Johnson University Hospital/UMDNJ
Coauthor(s): Mark Su, MD, FACEP, FACMT, Consulting Staff and Director of Fellowship in Medical Toxicology,
Department of Emergency Medicine, North Shore University Hospital; Consulting Staff, North Shore University
Hospital
Contributor Information and Disclosures
Updated: *ba 0, 0

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Introduction

The need to perform painful procedures in the emergency department (ED) makes the use of local and
infiltration anesthesia necessary components of patient care. While generally safe, anesthetic agents can be
toxic if used in inappropriate doses or route. Even when properly administered, patients may experience
unintended reactions to local anesthetics. The manifestations of toxicity associated with local anesthetic agents
used in the ED and treatment strategies are discussed in this article.

Physiochemical variables

Local anesthetics can be divided into 2 groups: the esters and the amides. Onset of action, potency, and
duration of action are determined by the specific local anesthetic’s pKa, lipid solubility, protein binding, tissue
pH, and vasodilatory effects. Increasing the dose by administering a high concentration shortens onset, while
increasing potency and duration of action, as well as increasing possibility for the adverse/toxic reactions.
Other factors that affect onset, potency, and duration are described below.

 Onset of action
o pKa is the primary factor that determines onset of action.
o Lower pKa increases tissue penetration and shortens onset of action; this is due to increased
lipid solubility of nonionized (uncharged) particles.
o pKa that is closer to pH optimizes penetration.
o Inflammation in the extracellular space may decrease pH and may slow onset of action.
o Site of administration influences onset (ie, prolonged in areas with increased tissue or nerve
sheath size).
 Potency
o Local anesthetics with high partition coefficients that increase lipophilic properties easily pass
into the lipid nerve membrane.
 o Degree of vasodilation promotes vascular absorption, thereby reducing locally available drug
and decreases potency.
o Addition of epinephrine or sodium bicarbonate increases pH, thereby increasing nonionized
particles, which are more lipid soluble.
o Generally, local anesthetic solutions that contain premixed epinephrine contain preservatives;
in these solutions, the pH is adjusted lower to maintain the stability of epinephrine and
antioxidants.
 Duration of action
o Addition of epinephrine to some local anesthetic solutions prolongs duration of action by
causing vasoconstriction and decreasing systemic absorption.
o Degree of protein binding primarily determines duration of action; high protein binding
increases duration.
o Increasing pH (addition of epinephrine or sodium bicarbonate) also prolongs duration of
action.

Table 1. Local Anesthetic Agents Used Commonly for Infiltrative Injection

Open table in new window

Agent Duration of Action Maximum Dosage Guidelines (Total

Cumulative Infiltrative Injection Dose
per Procedure*)

Esters

Procaine (Novocain) Short (15-60 min) 7 mg/kg; not to exceed 350-600 mg

Chloroprocaine Short (15-30 min) Without epinephrine: 11 mg/kg; not to

(Nesacaine) exceed 800 mg total dose
With epinephrine: 14 mg/kg; not to
exceed 1000 mg

Amides

Lidocaine (Xylocaine) Medium (30-60 min) Without epinephrine: 4.5 mg/kg; not to
exceed 300 mg

Lidocaine with Long (120-360 min) With epinephrine: 7 mg/kg

epinephrine

Mepivacaine Medium (45-90 min) Long 7 mg/kg; not to exceed 400 mg

(Polocaine, (120-360 min with
Carbocaine) epinephrine)

Bupivacaine Long (120-240 min) Without epinephrine: 2.5 mg/kg; not to

(Marcaine) exceed 175 mg total dose

Bupivacaine with Long (180-420 min) With epinephrine: Not to exceed 225 mg
epinephrine total dose

Etidocaine (Duranest) Long (120-180 min) Without epinephrine: 0.4 mg/kg; not to
No longer available in exceed 300 mg total dose
United States With epinephrine: 8 mg/kg

Prilocaine (Citanest) Medium (30-90 min) Body weight <70 kg: 8 mg/kg; not to
exceed 500 mg
Body weight >70 kg: 600 mg

Ropivacaine (Naropin) Long (120-360 min) 5 mg; not to exceed 200 mg for minor
nerve block

Agent Duration of Action Maximum Dosage Guidelines (Total

Cumulative Infiltrative Injection Dose
per Procedure*)

Esters

Procaine (Novocain) Short (15-60 min) 7 mg/kg; not to exceed 350-600 mg

Chloroprocaine Short (15-30 min) Without epinephrine: 11 mg/kg; not to

(Nesacaine) exceed 800 mg total dose
With epinephrine: 14 mg/kg; not to
exceed 1000 mg

Amides

Lidocaine (Xylocaine) Medium (30-60 min) Without epinephrine: 4.5 mg/kg; not to
exceed 300 mg

Lidocaine with Long (120-360 min) With epinephrine: 7 mg/kg

epinephrine

Mepivacaine Medium (45-90 min) Long 7 mg/kg; not to exceed 400 mg

(Polocaine, (120-360 min with
Carbocaine) epinephrine)

Bupivacaine Long (120-240 min) Without epinephrine: 2.5 mg/kg; not to

(Marcaine) exceed 175 mg total dose

Bupivacaine with Long (180-420 min) With epinephrine: Not to exceed 225 mg
epinephrine total dose
Etidocaine (Duranest) Long (120-180 min) Without epinephrine: 0.4 mg/kg; not to
No longer available in exceed 300 mg total dose
United States With epinephrine: 8 mg/kg

Prilocaine (Citanest) Medium (30-90 min) Body weight <70 kg: 8 mg/kg; not to
exceed 500 mg
Body weight >70 kg: 600 mg

Ropivacaine (Naropin) Long (120-360 min) 5 mg; not to exceed 200 mg for minor
nerve block

*Nondental use, administer by small incremental doses; administer the smallest dose and concentration
required to achieve desired effect; avoid rapid injection.

The search for less toxic long-acting local anesthetics was prompted after the occurrence of numerous fatalities
associated with the cardiovascular toxicity of bupivacaine. The 50:50 racemic mixture of bupivacaine consists
of the dextrorotatory R-(+)-enantiomer and the levorotatory S-(-)-enantiomer, in which the S-(-)-form is less
toxic. The less toxic S-(-)enantiomer, known as levobupivacaine, has been involved in numerous clinical
studies, which have demonstrated either, in vitro or in vivo, that this new long-acting amide has less potential
for CNS and cardiovascular toxicity. In particular, the intravascular dose required to cause lethality is almost
78% greater for levobupivacaine compared with the R-(+) enantiomer.

Further clinical trials in the 1990s led to the introduction in 1996 of ropivacaine, a pure S-(-)
enantiomer. Ropivacaine, like bupivacaine, has the capacity to produce differential blockade but has a better
sensorimotor dissociation at lower doses. This long-acting amide is the first local anesthetic drug developed
with initial extensive toxicological studies before its clinical release. Although ropivacaine may be associated
with acute CNS and cardiovascular toxicity, the incidence appears to be rare.

Dosage guidelines

Lower concentrations of local anesthetics are typically used for infiltration anesthesia.

Variation in local anesthetic dose is dependent on the procedure, the degree of anesthesia required, and
individual patient circumstances.

Reduced dosage is indicated in debilitated or acutely ill patients; in very young children or geriatric patients;
and in patients with liver disease, arteriosclerosis, or occlusive arterial disease.

Administrative techniques

Infiltration anesthesia is accomplished by administering the local anesthetic solution intradermally (ID),
subcutaneously (SC), or submucosally across the nerve path supplying the area of the body requiring
anesthesia. See Local Anesthetic Agents, Infiltrative Administration.
A common administrative technique is to subcutaneously inject the local anesthetic in a circular pattern around
the operative site; this circular patterned administration is often referred to as field block technique.

Deciphering Anesthetic Concentration and Dilution

Concentration

Drug concentration is expressed as a percentage (eg, bupivacaine 0.25%, lidocaine 1%).

 Percentage is measured in grams per 100 mL (ie, 1% is 1 g/100 mL [1000 mg/100 mL], or 10 mg per
mL).
 Calculate the mg/mL concentration quickly from the percentage by moving the decimal point 1 place to
the right (see examples below).
o Bupivacaine 0.25% = 2.5 mg/mL
o Lidocaine 1% = 10 mg/mL

Dilution

When epinephrine is combined in an anesthetic solution, the result is expressed as a dilution (eg, 1:100,000).

 1:1000 means 1 mg per 1 mL (ie, 0.1%)

 1:10,000 means 1 mg per 10 mL (ie, 0.01%)
 1:2000 means 1 mg per 2 mL (ie, 0.05%)
 1:20,000 means 1 mg per 20 mL (ie, 0.005%)
 0.1 mL of 1:1000 epinephrine added to 10 mL of anesthetic solution = 1:100,000 dilution or 0.01
mg/mL

Table 2. Epinephrine Content Examples

Open table in new window

Solution Volume 1:100,000 (1 mg/100 mL) 1:200,000 (1 mg/200 mL)

1 mL 0.01 mg 0.005 mg

5 mL 0.05 mg 0.025 mg

10 mL 0.1 mg 0.05 mg

20 mL 0.2 mg 0.1 mg

Solution Volume 1:100,000 (1 mg/100 mL) 1:200,000 (1 mg/200 mL)

1 mL 0.01 mg 0.005 mg
5 mL 0.05 mg 0.025 mg

10 mL 0.1 mg 0.05 mg

20 mL 0.2 mg 0.1 mg

Example: 50 mL of 1% lidocaine with epinephrine 1:100,000 contains lidocaine 500 mg and epinephrine 0.5
mg.

Adverse effects

Adverse effects are usually caused by high plasma concentrations of local anesthetic drug that result from
inadvertent intravascular injection, excessive dose or rate of injection, delayed drug clearance, or
administration into vascular tissue.
Pathophysiology

The toxicity of local and infiltration anesthetics can be classified by local and systemic levels of manifestations.
The local adverse effects of anesthetic agents include neurovascular manifestations such as prolonged
anesthesia and paresthesias, which may become irreversible.

Systemic toxicity of anesthetics involves the central nervous system (CNS), the cardiovascular system, and the
immune system. In relatively rare instances (<1%), the effects on the immune system can produce
immunoglobulin E (IgE)–mediated allergic reaction. Most cases are associated with the use of amino
esters. Some anesthetics, particularly benzocaine, are associated with hematologic effects, namely
methemoglobinemia. Cardiovascular effects are primarily those of direct myocardial depression and
bradycardia, which may lead to cardiovascular collapse.

Note that toxicity of anesthetics may be potentiated in patients with renal or hepatic compromise, respiratory
acidosis, preexisting heart block, or heart conditions. Toxicity may be potentiated during pregnancy, at the
extremes of age, or in those with hypoxia. However, inadvertent intravascular injection is the most common
cause of local anesthetic toxicity even if anesthetic was administered within the recommended dose range.

In the following table, the minimum doses of anesthetics in which adverse reactions have occurred are listed.

Table 3. Minimum Intravenous Toxic Dose of Local Anesthetic in Humans 1

Open table in new window

Agent Minimum Toxic Dose (mg/kg)

Procaine 19.2
Tetracaine 2.5

Chloroprocaine 22.8

Lidocaine 6.4

Mepivacaine 9.8

Bupivacaine 1.6

Etidocaine 3.4

Agent Minimum Toxic Dose (mg/kg)

Procaine 19.2

Tetracaine 2.5

Chloroprocaine 22.8

Lidocaine 6.4

Mepivacaine 9.8

Bupivacaine 1.6

Etidocaine 3.4

Clinical Evaluation

After the use of local anesthetic agents, consider new signs or symptoms as a possible sign of toxicity when
evaluating patients in the ED. The manifestation of toxicity depends on the organ system or systems that are
affected. Below is a list of toxicity manifestations organized by the affected organ system.

Central nervous system signs

 Initial symptoms
o Lightheadedness
o Dizziness
o Visual and auditory disturbances (difficulty focusing and tinnitus)
o Disorientation
o Drowsiness
 Higher-dose symptoms
o Often occur after an initial CNS excitation followed by a rapid CNS depression
 o Muscle twitching
o Convulsions
o Unconsciousness
o Coma
o Respiratory depression and arrest
o Cardiovascular depression and collapse

Cardiovascular signs

 Direct cardiac effects

o Toxic doses of local anesthetic agents can cause myocardial depression (tetracaine,
etidocaine, bupivacaine), cardiac dysrhythmias (bupivacaine), and cardiotoxicity in pregnancy.
o Several anesthetics also have negative inotropic effects on cardiac muscle that lead to
hypotension. Bupivacaine is especially cardiotoxic.
 Peripheral effects
o Vasoconstriction at low doses
o Vasodilatation at higher doses (hypotension)
 The range of signs and symptoms of cardiovascular toxicity include the following:
o Chest pain
o Shortness of breath
o Palpitations
o Lightheadedness
o Diaphoresis
o Hypotension
o Syncope

Hematological signs

Methemoglobinemia has been frequently reported in association with benzocaine use; however, lidocaine
and prilocaine have also been implicated. O-toluidine, the liver metabolite of prilocaine, is a potent oxidizer of
hemoglobin to methemoglobin. At low levels (1-3%), methemoglobinemia can be asymptomatic, but higher
levels (10-40%) may be accompanied by any of the following complaints:

 Cyanosis
 Cutaneous discoloration (gray)
 Tachypnea
 Dyspnea
 Exercise intolerance
 Fatigue
 Dizziness and syncope
 Weakness

Allergic manifestations
Amino esters are derivatives of para -aminobenzoic acid (PABA), which have been associated with acute
allergic reactions. Previous studies indicate a 30% rate of allergic reactions to procaine, tetracaine, and
chloroprocaine. Amino amides are not associated with PABA and do not produce allergic reactions with the
same frequency. However, preparations of amide anesthetics may sometimes contain methylparaben, which is
structurally similar to PABA and, thus, may result in allergic reactions.

Allergic manifestations of local anesthetics include rash and urticaria. Anaphylaxis due to local anesthetics is
very rare but should be considered if the patient is wheezing or in respiratory distress following
administration. Patients who report an allergy to lidocaine are likely allergic to the methylparaben
preservative. Preservative-free lidocaine can be obtained from individual ampules of lidocaine or from
preservative-free lidocaine used by cardiologists and anesthesiologists.

Local tissue manifestations

In addition to numbness and paresthesias, which is expected in the normal range of local anesthetic
application, very high doses of local anesthetics can produce irreversible conduction block within 5 minutes.
Peripheral neurotoxicity, such as prolonged sensory and motor deficits, has also been documented. It is
hypothesized that a combination of low pH and sodium bisulfite in the mixture can be partially responsible for
these changes. Reversible skeletal muscle damage has also been reported.

Topical application

A variety of anesthetics are available for topical or mucosal application (eg, tetracaine, benzocaine, lidocaine),
and adverse effects are usually caused by high plasma concentrations of the local anesthetic resulting from
excessive exposure. Typically, this is caused by application to abraded or torn skin. The following adverse
effects may occur:

 Local burning or stinging may occur.

 Oral viscous lidocaine may cause systemic toxicity, particularly with repeated use in infants or children.
 CNS
 High plasma concentration initially produces CNS stimulation (including seizures), followed by
CNS depression (including respiratory arrest); CNS stimulatory effects may be absent in some
patients, particularly when amides (eg, tetracaine) are administered.
 Epinephrine-containing solutions may add to the CNS stimulatory effect.
 Cardiovascular
 High plasma levels typically depress the heart and may include bradycardia, dysrhythmias,
hypotension, cardiovascular collapse, and cardiac arrest
 Epinephrine-containing local anesthetics may cause hypertension, tachycardia, and
myocardial ischemia.
 Gag-reflex suppression with oral administration
 Other adverse effects include the following:
o Transient burning sensation
o Skin discoloration
 o Swelling
o Neuritis
o Tissue necrosis and sloughing
o Methemoglobinemia with prilocaine

For more information on topical anesthetics, see Anesthesia, Topical.

Warnings regarding cocaine as a topical anesthetic

Various anesthetic mixtures containing cocaine have been used to anesthetize minor skin lacerations,
especially on the face or scalp. One such combination that is extemporaneously prepared by hospital
pharmacies includes tetracaine 0.5%, epinephrine (adrenaline) 1:2000, and cocaine 11.8% (commonly referred
to as "TAC" solution). Use results in decreased pain on application and may provide better patient tolerance of
the suturing, particularly in those unable to tolerate injections or those who have difficulty following instructions
or sitting still (eg, children, mentally challenged individuals). However, serious toxic effects (eg, seizures,
cardiac death) have been described after topical cocaine application, particularly in infants and children.
Because of this, cocaine is no longer recommended for topical anesthesia due to increased toxicity, expense,
and federal regulatory issues.

Newer compounded mixtures have replaced cocaine with lidocaine 4% (LET solutions) because of its superior
safety when applied to injured skin. Still, these solutions should not be applied to wounds with end arteriolar
blood supply.

For more information on cocaine as a topical anesthetic, see Topical Anesthetics, Cocaine.

Differential Diagnosis

Anaphylaxis

Bradydysrhythmias

Methemoglobinemia

Seizures

Tachydysrhythmias

Emergency Treatment

In the patient with suspected local anesthetic toxicity, the initial step is stabilization of potential life threats.
Impending airway compromise, significant hypotension, and treatment of dysrhythmias and seizures take
precedence. Once other possible etiologies of the patient's new symptoms have been excluded, management
of the specific symptoms can begin.
Although allergic reactions to local anesthetics are extremely rare, these are treated according to severity. Mild
cutaneous reactions may be treated with diphenhydramine (Benadryl 25-50 mg IV/PO for adult doses, 1 mg/kg
for pediatric doses); treat patients with more serious reactions with 0.3 (mL) of epinephrine SC (1:1000), and
closely monitor for further decompensation. Corticosteroids (125 mg methylprednisolone IVP, or 60 mg
prednisone PO) should be given to the patient with severe allergic reactions (eg, respiratory distress,
hypotension).

Treatment of CNS complications and toxicity is still very controversial because no single remedy exists. CNS
manifestations, such as seizures, have been treated successfully with benzodiazepines and barbiturates (eg,
phenobarbital). Recent reports indicate that 1 mg/kg of intravenous propofol (Diprivan) and 2 mg/kg of
intravenous thiopental (Pentothal) are successful in stopping local anesthetic-induced seizures and muscle
twitching. Clinicians should be aware that propofol can by itself cause significant bradycardia that can further
compromise the cardiovascular status of the patient. Avoid use of phenytoin (Dilantin) because it shares
pharmacologic properties (ie, sodium channel blockade) with lidocaine and may potentiate toxicity.

Prolonged PR, QRS, and QT intervals potentiating reentrant tachycardias with aberrant conduction may herald
cardiovascular toxicity. Expect that cardiac resuscitation of such patients may be difficult and prolonged (30-45
min) because some anesthetics are very lipid soluble and require a long time for redistribution. However, most
cases of lidocaine-induced cardiac toxicity can be successfully treated with properly conducted
cardiopulmonary resuscitation (CPR) (airway protection and chest compression) due to its relatively short
duration of action.

In the setting of anesthetic toxicity, avoiding the use of class IB antidysrhythmic agents, such as phenytoin,
mexiletine (Mexitil), and tocainide (Tonocard), is crucial because they may worsen toxicity. Bupivacaine
depresses conduction and contractility at low doses. Lidocaine has been used successfully in bupivacaine-
induced dysrhythmias, but its additive CNS toxicity is still a major concern. Even though bretylium theoretically
should not potentiate CNS toxicity (as does lidocaine), its benefits in cardiovascular resuscitation are
unclear. Evidence for use of amiodarone is also lacking at this time. A study performed in a porcine model
shows that CPR with a combination of vasopressin and epinephrine resulted in significantly better survival rates
than either drug alone.2 Human data are currently lacking. Lastly, some recent case reports have indicated that
the use of cardiac pacing and cardiopulmonary bypass may improve the outcome in the setting of prolonged
resuscitation.1

In a Korean study, combined boluses of glucose, insulin, and potassium were successful in reversing
bupivacaine-induced cardiovascular collapse.3 However, the 2 units/kg dose of insulin used in this protocol
may be challenging to use in clinical practice because of physicians' reluctance to administer such unusually
high doses of insulin. In China, shenfu, an extract of traditional Chinese herbal medicines, was shown to
reduce the CNS and cardiovascular toxicity of bupivacaine on rats.4

In cases of refractory cardiovascular collapse caused by an overwhelming overdose of local anesthetic,

Weinberg et al (1998 and 2003) demonstrated the successful application of lipid emulsion infusion in the
resuscitation of bupivacaine-induced cardiac arrest.5,6 The proposed mechanism is that lipid infusion
accelerates the decline in bupivacaine myocardial content (reduced tissue binding) by creating a lipid phase
that extracts the lipid-soluble bupivacaine molecules from the aqueous plasma phase (lipid sink hypothesis). A
beneficial energetic-metabolic effect may also occur.7

To date, 7 successful case reports have been documented in humans with the use of lipid infusion in significant
local anesthetic toxicity. Rosenblatt and colleagues (2006) were the first to report use of a 20% lipid infusion to
resuscitate a patient from prolonged cardiac arrest that followed an interscalene block with bupivacaine and
mepivacaine.8 Litz and colleagues (2006) published a case report after ropivacaine-induced asystole.9 Foxall
and colleagues (2007) successfully treated levobupivacaine-induced seizures and cardiovascular collapse.10
This case was the first one to demonstrate efficacy of lipid emulsion in a peri-arrest situation. Zimmer et al,
Warren et al, and Ludot et al have continued to demonstrate the clinical efficacy of lipid infusion therapy for
local anesthetic toxicity.11,12,13 Marwick and colleagues are the first to report a case of successful lipid rescue in
which systemic toxicity recurred after 40 minutes. Since additional lipid supply was not available, amiodarone
was used for the recurrent dysrhythmia. This case highlights the importance of the availability of a sufficient
quantity of lipid emulsion (1000 mL) when regional anesthesia is performed.14

In recent studies, Weinberg and colleagues, using an intact animal model of bupivacaine overdose, have
shown that lipid emulsion therapy provides superior hemodynamic and metabolic recovery from bupivacaine-
induced cardiac arrest than do vasopressors (epinephrine and vasopressin).15,16

Weinberg's recommended dosing regimen for use in humans

In cardiac arrest secondary to local anesthetic toxicity that is unresponsive to standard therapy, intravenous
administration of a lipid such as Intralipid 20% is recommended in the following regimen:

1. Administer 1 mL/kg over 1 minute.

2. Repeat twice more at 3– to 5-minute intervals.
3. Then (or sooner if stability is restored), convert to an infusion at a rate of 0.25 mL/kg/min, continuing
until hemodynamic stability is restored.
4. Increasing the dose beyond 8 mL/kg is unlikely to be useful.
5. In practice, resuscitate an adult weighing 70 kg as follows:
1. Use a 500-mL bag of fat emulsion (Intralipid 20%) and a 50-mL syringe.
2. Draw up 50 mL and give it stat intravenously, and then draw up and give another 20 mL.
3. Do exactly the same thing up to twice more as the epinephrine is given—if necessary or
appropriate.
4. Then, attach the fat emulsion bag to a giving set and administer it intravenously over the next
15 minutes.

Note that propofol (Diprivan) is not a component of lipid rescue. It is formulated in a 10% lipid emulsion and
therefore an overdose of propofol (gram quantities) would be necessary to provide an adequate dose of lipid
emulsion. Propofol is contraindicated when there is any evidence of cardiovascular toxicity.

Local ischemic or nerve toxicities may occur, particularly in the extremities with prolonged anesthesia or
epinephrine use. Suspected nerve damage should prompt neurologic consultation for urgent peripheral nerve
studies. If vascular compromise, such as limb ischemia, is suspected, consult a vascular surgeon immediately.
Therapy for extravasation (eg, warm compresses, phentolamine, nitroglycerin cream) should be initiated for
localized vascular toxicity.

Methemoglobinemia should initially be treated symptomatically and then guided by blood levels of
methemoglobin. Methylene blue and hyperbaric oxygen may be required in severe cases. See
Methemoglobinemia for specific treatment.

Finally, the prevention of local anesthetic toxicity should always be the primary consideration. Although all
adverse reactions cannot be anticipated, complications can be avoided by strict adherence to the guidelines of
anesthetic dosing, identification of patients at increased risk, and implementation of appropriate anesthetic
application techniques to avoid unintentional intravascular injection.
Disposition

Patients with persistent or unresolved significant reactions require admission to a monitored bed for
observation, further evaluation, and treatment. Patients who are stable and have minor or easily controlled
adverse reactions can be discharged and monitored on an outpatient basis. Advise patients with adverse
reactions to avoid the specific anesthetic agent in the future and to alert medical personnel of the reaction.

If a patient has experienced an adverse reaction to one class of anesthetic (ester or amide), risk for adverse
reactions is higher for all agents in that class.

Medical/Legal Pitfalls

The following are suggestions that may help avoid complications related to local anesthetic use in the ED:

 Consider obtaining and documenting informed consent in individuals with a prior history of anesthetic
reactions.
 Document amount and type of anesthetic used during the procedure.
 Always obtain an adequate history and physical examination to identify risk factors and allergies.
 Do not use class IB antidysrhythmics (including phenytoin) for seizures or dysrhythmias believed to be
due to cocaine toxicity.
 Consider changes in signs or symptoms as a possible manifestation of anesthetic toxicity.
 Admit patients with serious or unresolved symptoms.

Keywords

local anesthetic toxicity, anesthetic poisoning, local anesthetic exposure, local anesthetic agent, anesthetic
agents, anesthesia, ester anesthetics, amide anesthetics, procaine, chloroprocaine, lidocaine, lidocaine with
epinephrine, mepivacaine, bupivacaine, bupivacaine with epinephrine, etidocaine, prilocaine, ropivacaine, long-
acting local anesthetics, short-acting local anesthetics, infiltration anesthesia, adverse effects of local
anesthesia, procedures in the emergency department, anaphylaxis, prolonged anesthesia, paresthesias,
topical anesthetics, allergic reactions, cardiovascular toxicity, cocaine as an anesthetic
Acknowledgments
The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Roham T Zamanian, MD, Bret
Ginther, MD, and Julie K Olsson, MD, to the development and writing of this article.