Editors: Chelly, Jacques E.
Title: Peripheral Nerve Blocks: A Color Atlas, 3rd Edition
Copyright ©2009 Lippincott Williams & Wilkins
> Table of Contents > Section I – General Concepts > 3 – Local Anesthetic Solutions
3
Local Anesthetic Solutions
Andrea Casati
A. Local Anesthetics
General Overview
Local anesthetics block the generation and conduction of
nerve impulses at the level of the cell membrane. They bind directly
within the intracellular portion of voltage-gated sodium channels in
their ionized form when the channels are open. The penetration of local
anesthetics through the channels depends on the ionized form and
therefore their relative hydrophilicity. On the other hand, the local
anesthetic diffusion across membrane depends on the molecular weight
and the liposolubility of the molecule. Because all local anesthetics
have almost the same molecular weight, the diffusibility of the local
anesthetic molecules from the injection site depends on their
hydrophilicity. The hydrophilic and nonionized form of the molecule is
more lipid soluble than the ionized one and can therefore cross the
cell membrane more easily but diffuses less easily. Thus, local
anesthetics with a higher pKa are more likely to be ionized at
physiologic pH than drugs with a lower pKa; therefore, they are
typically more potent at the neuronal sites but are also more likely to
be absorbed before reaching the neuronal tissue. Moderate
hydrophobicity is required for passing through the neuronal sheath.
nerve impulses at the level of the cell membrane. They bind directly
within the intracellular portion of voltage-gated sodium channels in
their ionized form when the channels are open. The penetration of local
anesthetics through the channels depends on the ionized form and
therefore their relative hydrophilicity. On the other hand, the local
anesthetic diffusion across membrane depends on the molecular weight
and the liposolubility of the molecule. Because all local anesthetics
have almost the same molecular weight, the diffusibility of the local
anesthetic molecules from the injection site depends on their
hydrophilicity. The hydrophilic and nonionized form of the molecule is
more lipid soluble than the ionized one and can therefore cross the
cell membrane more easily but diffuses less easily. Thus, local
anesthetics with a higher pKa are more likely to be ionized at
physiologic pH than drugs with a lower pKa; therefore, they are
typically more potent at the neuronal sites but are also more likely to
be absorbed before reaching the neuronal tissue. Moderate
hydrophobicity is required for passing through the neuronal sheath.
The choice for a local anesthetic solution is based on
the expected onset time, the desired duration of the block, the need to
produce a preferential sensory, and the relative toxicity of the
mixture. These characteristics are primarily determined by their
physicochemical properties, described as follows:
the expected onset time, the desired duration of the block, the need to
produce a preferential sensory, and the relative toxicity of the
mixture. These characteristics are primarily determined by their
physicochemical properties, described as follows:
-
The potency of local anesthetic is
primary determined by its lipid solubility (expressed as lipid/water
partition coefficient). Unfortunately, the potential for toxicity also
depends on lipid solubility; accordingly, more lipophilic agents are
more potent but also have a more pronounced potential for systemic
toxicity. -
The onset time of local anesthetics is
influenced by the molecule’s pKa (the higher the pKa, the slower the
onset time of the nerve block in a physiologic environment) and
diffusibility. -
The degree of protein binding affects the duration of action.
-
The age of the patient has also been
demonstrated to affect the duration of a block: duration of action is
shorter in young patients compared with older patients.
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Table 3-1. Amide and Ester-type Local Anesthetics Used for Peripheral Nerve Blocks
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In general, small nerve fibers are more sensitive to
local anesthetics than are large nerve fibers. However, myelinated
fibers are blocked before nonmyelinated fibers of the same diameter.
Autonomic fibers, small unmyelinated C fibers, and small myelinated A-δ
fibers are blocked before larger myelinated A-γ, A-β, or A-α fibers.
Clinically, the loss of nerve function typically progresses as do loss
of pain, temperature, touch, proprioception, and skeletal muscle tone.
local anesthetics than are large nerve fibers. However, myelinated
fibers are blocked before nonmyelinated fibers of the same diameter.
Autonomic fibers, small unmyelinated C fibers, and small myelinated A-δ
fibers are blocked before larger myelinated A-γ, A-β, or A-α fibers.
Clinically, the loss of nerve function typically progresses as do loss
of pain, temperature, touch, proprioception, and skeletal muscle tone.
There are two classes of local anesthetics: amides and esters (Table 3-1).
The primary differences between the two classes are in their relative
metabolism (amides have primarily a hepatic metabolism, whereas esters
are metabolized by plasma cholinesterases) and their potential for
allergic reactions (esters have a greater potential than do amides).
The primary differences between the two classes are in their relative
metabolism (amides have primarily a hepatic metabolism, whereas esters
are metabolized by plasma cholinesterases) and their potential for
allergic reactions (esters have a greater potential than do amides).
Important differences can be found among local
anesthetics within the same class, primarily regarding their onset,
duration of action, and potential for toxicity. Clinical
characteristics of local anesthetics, onset time, duration of the
block, and even toxicity vary significantly according to the type of
block, the approach, the concentration of the local anesthetic
solution, and the volume administered. Table 3-2 describes the onset time and duration of different nerve blocks with a number of local anesthetic solutions.
anesthetics within the same class, primarily regarding their onset,
duration of action, and potential for toxicity. Clinical
characteristics of local anesthetics, onset time, duration of the
block, and even toxicity vary significantly according to the type of
block, the approach, the concentration of the local anesthetic
solution, and the volume administered. Table 3-2 describes the onset time and duration of different nerve blocks with a number of local anesthetic solutions.
Treatment of Local Anesthetic Toxicity
To treat adverse reactions and toxicity:
-
Stop the administration of local anesthetic.
-
Maintain a patent airway.
-
Assist or control ventilation with oxygen.
-
Intralipid administration (intralipid 20%
1.5 mg/kg over 1 minute, followed immediately with an infusion at a
rate of 0.25 mg/kg/min. Continue chest compression in case of cardiac
arrest. Repeat bolus every 3–5 min up to 3 mL/kg total dose until
circulation is restored. Continue infusion until hemodynamic stability
is restored. Increase the rate to 0.5 mL/kg/min. The maximum total dose
of 8 mL/kg is recommended). www.lipidrescue.org -
Treat signs of central nervous system
toxicity with either intravenous benzodiazepines (e.g., diazepam 0.1 to
0.2 mg/kg, midazolam 2 to 5 mg) or thiopental 1 to 2 mg/kg. -
Treat with succinylcholine (1 mg/kg) to terminate a state of generalized convulsions.
-
Treat hypotension with intravenous fluids or vasopressors.
-
Treat circulatory collapse with positive
inotropic effects such as amiodarone. Avoid ephedrine or epinephrine
with peripheral vasoconstrictor effects at the same time. -
Institute cardiopulmonary resuscitation (CPR).
-
Consider cardiopulmonary bypass if the aforementioned measures are unsuccessful.
Toxicity of Local Anesthetics
Though rare, administration of local anesthetic can
produce allergic reactions. These reactions are mostly related to
aminoester drugs. The allergic reaction is related to the preservative,
the para-aminobenzoic acid. Nonetheless, risk for allergic reactions is
present also with aminoamide anesthetic, especially when using
formulations containing preservatives or antibacterial additives, like
those in multidose preparations.
produce allergic reactions. These reactions are mostly related to
aminoester drugs. The allergic reaction is related to the preservative,
the para-aminobenzoic acid. Nonetheless, risk for allergic reactions is
present also with aminoamide anesthetic, especially when using
formulations containing preservatives or antibacterial additives, like
those in multidose preparations.
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Systemic absorption of local anesthetics can produce
central nervous system and cardiovascular toxicity. The rate and extent
of absorption mainly depend on site of injection, total dose of local
anesthetic, chemical properties of the local anesthetic, and addition
of epinephrine. In general, body areas rich in vascular supply have
more rapid and complete uptake, regardless of the type of local
anesthetic. The rate of absorption is maximal for intercostals and
decreases in the following order: intercostal, caudal, epidural,
brachial plexus, sciatic, lumbar plexus, and femoral.
central nervous system and cardiovascular toxicity. The rate and extent
of absorption mainly depend on site of injection, total dose of local
anesthetic, chemical properties of the local anesthetic, and addition
of epinephrine. In general, body areas rich in vascular supply have
more rapid and complete uptake, regardless of the type of local
anesthetic. The rate of absorption is maximal for intercostals and
decreases in the following order: intercostal, caudal, epidural,
brachial plexus, sciatic, lumbar plexus, and femoral.
Central Nervous System Toxicity
Local anesthetics can cross the blood–brain barrier
readily; toxic effects are related to the plasma level of the specific
agent. The initial signs are usually excitatory, and include numbness
of the tongue, lightheadedness, dizziness, visual disturbances,
tinnitus, and disorientation. If unchecked, these symptoms progress to
tonic–clonic convulsions and eventually to generalized central nervous
system depression, respiratory depression, and respiratory arrest.
readily; toxic effects are related to the plasma level of the specific
agent. The initial signs are usually excitatory, and include numbness
of the tongue, lightheadedness, dizziness, visual disturbances,
tinnitus, and disorientation. If unchecked, these symptoms progress to
tonic–clonic convulsions and eventually to generalized central nervous
system depression, respiratory depression, and respiratory arrest.
Cardiovascular System Toxicity
Initially, there is an increase in blood pressure and
heart rate. With higher levels of local anesthetics, hypotension
(direct vasodilatory effects on peripheral arterioles and negative
inotropic action) and arrhythmias ensue, resulting in cardiac arrest.
heart rate. With higher levels of local anesthetics, hypotension
(direct vasodilatory effects on peripheral arterioles and negative
inotropic action) and arrhythmias ensue, resulting in cardiac arrest.
Suggested Readings
Erlacher
W, Schuschnig C, Koinig H, et al. Clonidine as adjuvant for
mepivacaine, ropivacaine and bupivacaine in axillary, perivascular
brachial plexus block. Can J Anaesth 2001;48:522–555.
W, Schuschnig C, Koinig H, et al. Clonidine as adjuvant for
mepivacaine, ropivacaine and bupivacaine in axillary, perivascular
brachial plexus block. Can J Anaesth 2001;48:522–555.
Klein
SM, Pietrobon R, Nielsen KC, et al. Peripheral nerve blockade with
long-acting local anesthetics: a survey of the Society for Ambulatory
Anesthesia. Anesth Analg 2002;94:71–76.
SM, Pietrobon R, Nielsen KC, et al. Peripheral nerve blockade with
long-acting local anesthetics: a survey of the Society for Ambulatory
Anesthesia. Anesth Analg 2002;94:71–76.
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ropivacaine-induced asystole after axillary plexus block using lipid
infusion. Aneasthesia 2006;61:800–801.
RJ, Popp M, Stehr SN, Koch T. Successful resuscitation of a
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infusion. Aneasthesia 2006;61:800–801.
Mather LE, Chang DH. Cardiotoxicity with modern local anaesthetics: is there a safer choice? Drugs 2001;61:333–342.
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20% lipid emulsion to resuscitate a patient after a presumed
bupivacaine-related cardiac arrest. Anesthesiology 2006;105:217–218.
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20% lipid emulsion to resuscitate a patient after a presumed
bupivacaine-related cardiac arrest. Anesthesiology 2006;105:217–218.
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B. Drugs Added to Local Anesthetics
Aims of Coadministration
Various additives can be added to local anesthetics to
accelerate the onset time, reduce the systemic absorption (thus the
risk for LA-related toxicity), and prolong the duration of nerve block
or pain relief.
accelerate the onset time, reduce the systemic absorption (thus the
risk for LA-related toxicity), and prolong the duration of nerve block
or pain relief.
The most commonly used additives for peripheral nerve
blocks are vasoactive agents like epinephrine, clonidine, and opioids.
Other additives are used for particular blocks, like hyaluronidase,
which is typically used for ophthalmic blocks. Unfortunately, few
properly designed and conducted studies have evaluated the usefulness
of each additive, and we are still lacking definitive data to recommend
or exclude additives for peripheral nerve blocks
blocks are vasoactive agents like epinephrine, clonidine, and opioids.
Other additives are used for particular blocks, like hyaluronidase,
which is typically used for ophthalmic blocks. Unfortunately, few
properly designed and conducted studies have evaluated the usefulness
of each additive, and we are still lacking definitive data to recommend
or exclude additives for peripheral nerve blocks
Epinephrine
Site of Action: Local.
Mechanisms: Slowed blood absorption of the local anesthetic by epinephrine-induced vasoconstriction.
Main Effects: Prolonged
duration of the block. Duration may be increased from 30% to 50%,
depending on the potency of local anesthetics and the vasculature at
the site of injection. The best effects are obtained with lidocaine and
during intrapleural anesthesia. No effects were observed with
ropivacaine.
duration of the block. Duration may be increased from 30% to 50%,
depending on the potency of local anesthetics and the vasculature at
the site of injection. The best effects are obtained with lidocaine and
during intrapleural anesthesia. No effects were observed with
ropivacaine.
Other Effects: Reduction of the inherent toxicity of local anesthetics. Peak plasma concentration may be reduced up to 50%.
Adverse Effects: Hemodynamic
effects if massive blood absorption or intravascular injection.
Tachycardia or arrhythmia indicates an inadvertent intravascular
placement of the needle or catheter and necessitates the immediate
cessation of local anesthetic injection.
effects if massive blood absorption or intravascular injection.
Tachycardia or arrhythmia indicates an inadvertent intravascular
placement of the needle or catheter and necessitates the immediate
cessation of local anesthetic injection.
Dose: 5 µg/mL (1/200,000).
Use: All peripheral blocks
except those in the vicinity of extremities because of terminal
arterial blood flow. For example, epinephrine is contraindicated in a
penis block. It must be considered that because vasoconstrictors reduce
the perfusion of vasa nervorum, they might potentially increase the
risk for an ischemic nerve injury. For this reason the extensive use of
vasoconstrictors is not recommended for continuous infusion, especially
when using a continuous infusion rather than an intermittent bolus
technique.
except those in the vicinity of extremities because of terminal
arterial blood flow. For example, epinephrine is contraindicated in a
penis block. It must be considered that because vasoconstrictors reduce
the perfusion of vasa nervorum, they might potentially increase the
risk for an ischemic nerve injury. For this reason the extensive use of
vasoconstrictors is not recommended for continuous infusion, especially
when using a continuous infusion rather than an intermittent bolus
technique.
Clonidine
Clonidine is the only α2-agonist used in combination with local anesthetics. Its use is well documented.
Site of Action: Local, but also central after blood absorption from the nerve sheath.
Mechanisms: Weak local
anesthetic action of the α2-agonist itself but possibility of
synergistic interaction with local anesthetics. Effects may be due in
part to a local pharmacokinetic mechanism.
anesthetic action of the α2-agonist itself but possibility of
synergistic interaction with local anesthetics. Effects may be due in
part to a local pharmacokinetic mechanism.
Main Effects: Prolonged
duration of anesthesia and analgesia that follows neural blockade,
depending on the potency of local anesthetics, lesser effects being
observed when added to ropivacaine and bupivacaine. Anesthesia may be
prolonged by 30% to 50% with mepivacaine supplemented with 150 mg
clonidine. Analgesia may be prolonged by 40% to 400% when clonidine is
added.
duration of anesthesia and analgesia that follows neural blockade,
depending on the potency of local anesthetics, lesser effects being
observed when added to ropivacaine and bupivacaine. Anesthesia may be
prolonged by 30% to 50% with mepivacaine supplemented with 150 mg
clonidine. Analgesia may be prolonged by 40% to 400% when clonidine is
added.
Other Effects: Clonidine can extend the sensory block and improve its quality at the time of surgery.
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Adverse Effects: Sedation is
the main, and often the sole, adverse effect. This must be taken into
consideration in a premedicated patient. Other effects include
decreased blood pressure and slowed heart rate. Rarely, there is an
abnormal ventilatory pattern.
the main, and often the sole, adverse effect. This must be taken into
consideration in a premedicated patient. Other effects include
decreased blood pressure and slowed heart rate. Rarely, there is an
abnormal ventilatory pattern.
Dose: The minimum dosage,
which results in significant prolongation of anesthesia, is 0.5 µg/kg.
Increasing the dose results in a greater number of adverse effects. The
suggested dose for a single shot nerve block is 1 µg/kg. Clonidine has
been also added to local anesthetic solution for continuous peripheral
nerve blocks, with a reported reduction in the number of
self-administered bolus doses on the first two postoperative days.
However, the addition of 1 µg/mL clonidine for continuous femoral nerve
block after knee joint replacement has also been demonstrated to
produce persistent motor function impairment after 48 hours of infusion
in 27% of patients compared with only 6% of cases in patients not
receiving clonidine at all or receiving it only with the initial bolus.
This potentiation of motor block effects of local anesthetics has also
been reported during continuous epidural infusion, and must be
considered if early mobilization is required to implement patient
rehabilitation.
which results in significant prolongation of anesthesia, is 0.5 µg/kg.
Increasing the dose results in a greater number of adverse effects. The
suggested dose for a single shot nerve block is 1 µg/kg. Clonidine has
been also added to local anesthetic solution for continuous peripheral
nerve blocks, with a reported reduction in the number of
self-administered bolus doses on the first two postoperative days.
However, the addition of 1 µg/mL clonidine for continuous femoral nerve
block after knee joint replacement has also been demonstrated to
produce persistent motor function impairment after 48 hours of infusion
in 27% of patients compared with only 6% of cases in patients not
receiving clonidine at all or receiving it only with the initial bolus.
This potentiation of motor block effects of local anesthetics has also
been reported during continuous epidural infusion, and must be
considered if early mobilization is required to implement patient
rehabilitation.
Use: All peripheral nerve blocks.
Opioids
Although opioid agents are known to exert their
analgesic activity at a spinal and supraspinal level, there are
biochemical and clinical evidences suggesting that opioids may also act
at the level of peripheral nerves, due to the peripheral expression of
opioid receptors activated by tissue stress and inflammation. Whether
such an effect may improve clinical neural blockade and analgesia is
debated. Inflammatory phenomena, history of chronic pain, and site of
injection might account for conflicting results. However, at the
current status of the art, there is no strong enough evidence
supporting the extensive use of peripheral opioids as additives to
local anesthetics.
analgesic activity at a spinal and supraspinal level, there are
biochemical and clinical evidences suggesting that opioids may also act
at the level of peripheral nerves, due to the peripheral expression of
opioid receptors activated by tissue stress and inflammation. Whether
such an effect may improve clinical neural blockade and analgesia is
debated. Inflammatory phenomena, history of chronic pain, and site of
injection might account for conflicting results. However, at the
current status of the art, there is no strong enough evidence
supporting the extensive use of peripheral opioids as additives to
local anesthetics.
Tramadol is a weak opioid receptor agonist; however, in
contrast to other opioid agents it also has a significant effect on the
reuptake of serotonin and norepinephrine. Moreover, it has been
demonstrated to have a local anesthetic-like effect on peripheral
nerves, potentially providing a synergistic effect when added to local
anesthetics.
contrast to other opioid agents it also has a significant effect on the
reuptake of serotonin and norepinephrine. Moreover, it has been
demonstrated to have a local anesthetic-like effect on peripheral
nerves, potentially providing a synergistic effect when added to local
anesthetics.
Site of Action: Central, but hypothesized also local.
Mechanisms: Hypothetical
effect on axonal opioid receptors. Action on spinal cord either by
diffusion or by centripetal axonal transport also has been invoked.
effect on axonal opioid receptors. Action on spinal cord either by
diffusion or by centripetal axonal transport also has been invoked.
Main Effects: Analgesia lasting several hours, unrelated to the opioid dose injected.
Other Effects: Reduction of onset time of the block with the use of highly lipid soluble drugs.
Adverse Effects: Nausea and vomiting, some cases of pruritus.
Dose: The addition of 3 to 5
mg of morphine to the local anesthetic mixture has been reported to
prolong the duration of analgesia up to 36 hours. The combination of
0.1 mg/kg of morphine and lidocaine injected locally can reduce by 50%
the total dose of morphine required for postoperative analgesia.
mg of morphine to the local anesthetic mixture has been reported to
prolong the duration of analgesia up to 36 hours. The combination of
0.1 mg/kg of morphine and lidocaine injected locally can reduce by 50%
the total dose of morphine required for postoperative analgesia.
Use: Documented only for brachial plexus blocks.
Alkalinization
All local anesthetics are weak bases, with a pKa ranging
between 7.6 and 8.9; while most local anesthetic solutions commercially
available are at low pH, ranging between 3 and 6. The addition of
sodium bicarbonate is aimed at increasing the proportion of local
anesthetic molecules not in cationic form, thus increasing the gradient
of more lipophilic state of the molecule penetrating the phospholipidic
layers of the nervous fibers membrane. This has been reported to
accelerate the onset time of nerve block.
between 7.6 and 8.9; while most local anesthetic solutions commercially
available are at low pH, ranging between 3 and 6. The addition of
sodium bicarbonate is aimed at increasing the proportion of local
anesthetic molecules not in cationic form, thus increasing the gradient
of more lipophilic state of the molecule penetrating the phospholipidic
layers of the nervous fibers membrane. This has been reported to
accelerate the onset time of nerve block.
Site of Action: Local.
Mechanisms: Local
anesthetics penetrate nerve cell membranes in their nonionized form and
act intracellularly in their ionized form. Because local anesthetics
are weak bases, addition of sodium bicarbonate increases their pH to
the physiologic range, thus decreasing the
anesthetics penetrate nerve cell membranes in their nonionized form and
act intracellularly in their ionized form. Because local anesthetics
are weak bases, addition of sodium bicarbonate increases their pH to
the physiologic range, thus decreasing the
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ionized/nonionized
ratio. This results in both an increased rate of penetration and a
greater total mass of local anesthetic in the nerve.
Main Effects: There is a 30%
to 50% reduction in onset time (i.e., approximately a 4-minute
reduction with mepivacaine, 8 minutes with lidocaine, and 14 minutes
with bupivacaine). The extent and quality of the block are improved.
to 50% reduction in onset time (i.e., approximately a 4-minute
reduction with mepivacaine, 8 minutes with lidocaine, and 14 minutes
with bupivacaine). The extent and quality of the block are improved.
Other Effects: Prolonged duration of analgesia has also been reported.
Adverse Effects: Unknown.
Dose: Theoretically, to
adjust the pH of local anesthetic solutions to the physiologic range.
This is unknown in clinical practice, which may account for many
supportive trials being negative.
adjust the pH of local anesthetic solutions to the physiologic range.
This is unknown in clinical practice, which may account for many
supportive trials being negative.
Use: All peripheral nerve blocks.
Neostigmine
Neostigmine is an acetylcholinesterase inhibitor that
has been found after systemic or spinal administration to enhance
analgesic effects of opioids or local anesthetics through activation of
intrinsic ascending and descending cerebral cholinergic pathways. It
has a possible peripheral analgesic effect after intraarticular
injection.
has been found after systemic or spinal administration to enhance
analgesic effects of opioids or local anesthetics through activation of
intrinsic ascending and descending cerebral cholinergic pathways. It
has a possible peripheral analgesic effect after intraarticular
injection.
Site of Action and Mechanisms: Hypothetical stimulation of acetylcholine receptors at the peripheral nerve level.
Main Effects: Not proved with 500 mg.
Adverse Effects: Gastrointestinal disorders with this dosage.
Verapamil
Verapamil is the only calcium blocker used in
combination with local anesthetics to potentiate the channel-blocking
activity of local anesthetic molecules.
combination with local anesthetics to potentiate the channel-blocking
activity of local anesthetic molecules.
Site of Action: Local, but also possibly central.
Mechanisms: Fast channel-blocking effects as local anesthetics.
Main Effects: 30% prolongation of sensory blockade with lidocaine with 2.5 mg verapamil.
Adverse Effects: Not reported with this dosage.
Dose: 2.5 mg.
Hyaluronidase
Site of Action: Local.
Mechanisms: Enzyme acting on
hyaluronic acid, a component of several connective tissues.
Hyaluronidase liquefies the interstitial barriers and increases the
spread of local anesthetic solutions through tissue planes.
hyaluronic acid, a component of several connective tissues.
Hyaluronidase liquefies the interstitial barriers and increases the
spread of local anesthetic solutions through tissue planes.
Main Effects: Reduction of onset time (not evaluated).
Adverse Effects: Rare cases of allergy.
Dose: Not clearly established, from 50 to 150 U.
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