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Flashcards in Local Anesthetics Deck (69):
1

Development of Local Anesthetics

1800's Cocaine isolated & used for variety of ailments leading to it's use as a local anesthetic in ophthalmology
1905 The first synthetic local anesthetic was the ester derivative procaine
1943 Lidocaine was synthesized as an amide local anesthetic and is the standard to which all other anesthetics are compared.

2

Local Anesthetics

*are drugs that reversibly block the conduction of electrical impulses along nerve fibers.
*produce a transient and reversible loss of sensation (analgesia) in a circumscribed region of the body without loss of consciousness.
*Their ability to perform this function depends on nerves being blocked and the chemical structure & properties of the local anesthetic.
*consist of a lipophilic & a hydrophilic portion separated by a connecting hydrocarbon chain.

3

Molecular Structure of Local Anesthetics

The hydrophilic group is usually a tertiary amine, such as diethylamine, whereas the lipophilic portion is usually an unsaturated aromatic ring, such as para-aminobenzoic acid.
The lipophilic portion is essential for anesthetic activity

4

Lipophilic or hydrophilic

The hydrophilic group is usually a tertiary amine, such as diethylamine
The lipophilic portion is usually an unsaturated benzene ring, such as para-aminobenzoic acid. The lipophilic portion is essential for anesthetic activity (aromatic ring).

5

The Axon

The axon is the functional unit of peripheral nerves: where the LA works!
Each peripheral nerve axon possesses its own cell membrane—the axolemma.
A cell membrane (axolemma), and intracellular contents (axoplasm): are the major components of the axon.
Schwann cells surround each axon

6

Nodes of Ranvier

Between Schwann cells are periodic segments of nerve that do not contain myelin: Nodes of Ranvier
Voltage-gated sodium channels are located in these nonmyelinated segments and are the primary site at which local anesthetics exert their action.
Action potentials jump from node to node, and this phenomenon is known as saltatory conduction
Conduction block occurs when the ionized form of the LA binds to the voltage gated sodium channel inside the cell

7

Structure-Activity Relationship

Modifying the chemical structure of a local anesthetic alters its pharmacologic effects.
Substituting a butyl group for the amine group on the benzene ring of procaine results in tetracaine.
Compared with procaine, tetracaine is more lipid soluble, is 10 times more potent, and has a longer duration of action corresponding to a 4- to 5-fold decrease in the rate of metabolism.

8

Mechanism of Action

Local anesthetics bind to specific sites in voltage-gated Na+ channels.
Local anesthetics block initiation and propagation of action potential.
They block Na+ current, thereby reducing excitability of neuronal, cardiac or central nervous system tissue.
Local anesthetics prevent transmission of nerve impulses (conduction blockade) by inhibiting passage of sodium ions through ion-selective sodium channels in nerve membranes.
The sodium channel itself is a specific receptor for local anesthetic molecules.
Failure of sodium ion channel permeability to increase slows the rate of depolarization such that threshold potential is not reached and thus an action potential is not propagated
Local anesthetics do not alter the resting transmembrane potential or threshold potential.

9

(Na+) Sodium Channels

Local anesthetics slow the rate of depolarization of the nerve action potential such that the threshold potential is not reached. As a result, an action potential cannot be propagated in the presence of local anesthetic and conduction blockade results.

10

Local anesthetics gain access to the inner axonal membrane by

traversing sodium channels while they are more often in an open configuration

passage directly through the plasma membrane

11

Electrophysiology

*A resting peripheral nerve demonstrates a negative membrane potential of −70 to −90 mV.
*This voltage difference across the neuronal membrane at steady state is called the resting membrane potential
*Sodium-potassium pump (Na+-K+/ATPase) located in the axolemma (energy driven)

12

Action Potential

The action potential is a wave of depolarization that is propagated along the axon by continuous coupling between excited and nonexcited regions of membrane. Ionic current (the action current) enters the axon in the excited, depolarized region and then flows down the axoplasm and exits through the surrounding membrane, thereby passively depolarizing this adjacent region (see Fig. 36-3). Although this local circuit current spreads away from the excited zone in both directions, the region behind the impulse, having just been depolarized, is absolutely refractory, and propagation of impulses is thus unidirectional.

13

Sodium, Chloride & Potassium & Local Anesthetic

Outside of Axon / Cell
Sodium (Na+) has a + charge
Chloride (Clˉ) has a – charge
Inside the Axon / Cell
Potassium (K+) has a + charge
The differences in charge of Na, K & Cl keep the neuron in dynamic equilibrium & ready for an action potential while at rest.

14

Mechanism of action of LA

*Local anesthetics block sodium channel:
Stops influx of Na by blocking NA channels
in a nerve
*Local anesthestics bind to the alpha subunit of the sodium channel in the active and inactive states
*Sodium channels have three functional states: resting (closed), open, and inactive.
*The resting state exists when the membrane is at its resting potential.
*An inactive state (impermeable to Na) follows the open state (activated).
*The activated state, which prevents initiation of an action potential, lasts until the restoration of the resting membrane potential (-70 to -90 RMP).

15

Resting Membrane Potential

When a neuron is not sending a signal, it is "at rest." When a neuron is at rest, the inside of the neuron is negative relative to the outside. Although the concentrations of the different ions attempt to balance out on both sides of the membrane, they cannot because the cell membrane allows only some ions to pass through channels (ion channels). At rest, potassium ions (K+) can cross through the membrane easily. Also at rest, chloride ions (Cl-)and sodium ions (Na+) have a more difficult time crossing. The negatively charged protein molecules (A-) inside the neuron cannot cross the membrane. In addition to these selective ion channels, there is a pump that uses energy to move three sodium ions out of the neuron for every two potassium ions it puts in. Finally, when all these forces balance out, and the difference in the voltage between the inside and outside of the neuron is measured, you have the resting potential. The resting membrane potential of a neuron is about -70 to -90 mV (mV=millivolt) - this means that the inside of the neuron is 70 to 90 mV less than the outside. At rest, there are relatively more sodium ions outside the neuron and more potassium ions inside that neuron

16

Pharmacokinetics

Local anesthetics are weak bases that have pK values somewhat above physiologic pH. As a result, <50% of the local anesthetic exists in a lipid-soluble nonionized form at physiologic pH. For example, at pH 7.4, only 5% of tetracaine exists in a nonionized form. Acidosis in the environment into which the local anesthetic is injected (as is present with tissue infection) further increases the ionized fraction of drug. This is consistent with the poor quality of local anesthesia that often results when a local anesthetic is injected into an acidic infected area. Local anesthetics with pKs nearest to physiologic pH have the most rapid onset of action, reflecting the presence of an optimal ratio of ionized to nonionized drug fraction

17

Important Pearls of Local Anesthetics

For myelinated axons, 2-3 nodes of Ranvier must be blocked to stop the conduction
The greater the frequency of action potentials, the faster the nerve is blocked by the LA. The LA must attache to the NA channel it’s inactivated state; the faster the nerve is firing, the more opportunities the LA will have to catch the sodium channel in the inactivated state.
Both unionized and ionized forms of the LA are required for a conduction block: the unionized form diffused across the lipid bilayer into the axon, the ionized form attaches to the inside of sodium channel and locks it shut in the inactivated state
Voltage gated sodium channels are found only in the nerve’s axon

18

Afferent & Efferent nerves

Afferent nerve: Carries nerve impulses from sensory receptors or sense organs toward the central nervous system.
Efferent nerve: Nerves that conduct signals from the central nervous system along motor neurons to their target muscles and glands.

AS:ME

19

Peripheral Nerve Fibers

Peripheral nerve fibers are grouped based on the diameter, signal conduction velocity, and myelination state of the axons. These classifications apply to both sensory and motor fibers. Fibers of the A group have a large diameter, high conduction velocity, and are myelinated.

20

A alpha Nerve Fibers

Heavy myelinated
Skeletal muscle--Motor
Proprioception

21

A beta Nerve Fibers

Heavy myelinated
Touch
Pressure

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A gamma Nerve Fibers

Medium myelinated
Skeletal muscle--tone

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A delta Nerve Fibers

Medium myelinated
Fast pain
Temperature
Touch

24

B Nerve Fibers

Light myelination
Preganglionic ANS fibers

25

C Nerve Fibers

Sympathetic:
0 myelination
Postganglionic ANS fibers

Dorsal Root:
0 myelination
Slow pain
Temperature
Touch

26

Sequence of clinical anesthesia

Sympathetic block (vasodilatation)
Loss of pain and temperature sensation
Loss of proprioception
Loss of touch and pressure sensation
Loss of motor function

27

Adverse Effects of local anesthetics

CNS
Ringing in ears
Circumoral numbness
Excitation – anxiety, agitation, restlessness, twitching
Convulsions

Reduced myocardial contractility

Vasodilatation

Cardiovascular collapse

28

Determinants of Potency: LIPID SOLUBILITY

There is a strong relationship between the lipid solubility of local anesthetics and their potency.
Lipid-soluble drugs pass more readily through the nerve membrane.
Larger, more lipid-soluble local anesthetics are relatively water insoluble, highly protein bound, and less readily washed out from nerves and surrounding tissues.
THE MORE LIPID SOLUBLE THE LOCAL ANESTHETIC, THE GREATER ITS POTENCY

29

Duration of Action: PROTEIN BINDING AND LIPID SOLUBILITY

The duration of action of local anesthetics demonstrates a relationship to protein binding and lipid solubility.
The degree of protein binding is the MORE important factor determining DOA GREATER THE PROTEIN BINDING: THE LONGER THE DOA
Unbound anesthetic diffuses from the injection site, some of the protein bound anesthetic is released and becomes available to diffuse to nerve axons.

30

Primary Variable: Onset of Action

pKa Value

31

Primary Variable: Potency

Lipid Solubility

32

Primary Variable: Duration of Action

Protein Binding

33

Absorption of Local Anesthetics: Many Variables

How does epinephrine affect LA?

The same local anesthetic dose and concentration injected in different areas of the body, with or without added epinephrine, can result in vastly different durations of action.

Absorption also influences toxicity.
The slower absorbed…less CNS or cardiac toxicity
Drug metabolism and elimination can “keep up” with slow absorption preventing toxicity.
SLOW ABSORPTION=PREVENTION OF TOXICITY

34

Factors Affecting Absorption

Vascularity and blood flow of the injection area
Lipid and protein binding
Vasoconstrictors
Duration Of Action

35

Tissues from highest to lowest Blood Flow

IV
Tracheal
Intercostal
Caudal
Paracervical
Epidural
Brachial Plexus
Subarachnoid, sciatic, femoral
Subcutaneous

I TICPEBSS

36

Determinants of Blood Flow

Presence of a vasoconstrictor (epinephrine) in the solution containing LA: epi constricts arterioles which decreases the rate of absorption from the injection site and prolongs DOA
EPI may increase the duration of a spinal by 75-100%
High blood flow to tissue where anesthetic is injected: the greater the blood flow, the faster the agent is absorbed into the circulation
Tissues with higher blood flows, the duration of action is reduced.
The likelihood of toxicity is increased when a local anesthetic is injected at sites with higher blood flows: The greater the tissue blood flow, the greater the rate of absorption of LA from the site of injection

37

Esters

Procaine
Chlorprocaine
Tetracaine
Cocaine
Benzocaine

38

Amides

Lidocaine
Mepivacaine
Prilocaine
Bupivacaine
Ropivacaine
Articaine

39

Metabolism of Amides

Lidocaine, Prilocaine, Mepivicaine, Bupivacaine, Ropivacaine, Dibucaine, Etidocaine
Amides are metabolized by the LIVER : LONGER Duration Of Action which leads to more toxicity
Prilocaine undergoes the most rapid metabolism; lidocaine and mepivacaine are intermediate; and etidocaine, bupivacaine, and ropivacaine undergo the slowest metabolism among the amide local anesthetics.
PLEASE ALWAYS LET ME BE REALLY EARLY (Prilocaine Amide Lidocaine Mepivicaine, Bupivacaine, Ropivacaine, Etidocaine)
Amides have 2 i’s

40

Prilocaine

Prilocaine is an amide local anesthetic that is metabolized to orthotoluidine.
Orthotoluidine converts hemoglobin to its oxidized form, methemoglobin, resulting in a potentially life-threatening complication, methemoglobinemia
When the dose of prilocaine is >600 mg, with enough methemoglobin present (3 to 5 g/dL) to cause the patient to appear cyanotic, and oxygen-carrying capacity is decreased.

41

Methemoglobinemia

Methemoglobinemia is a rare but potentially life-threatening complication (decreased oxygen-carrying capacity) that cause oxidation of hemoglobin to methemoglobin
Known oxidant substances include topical local anesthetics (prilocaine, benzocaine, and lidocaine), nitroglycerin, phenytoin, and sulfonamides.
Methemoglobinemia is readily reversed by the administration of methylene blue, 1 to 2 mg/kg intravenously, over 5 minutes (total dose should not exceed 7 to 8 mg/kg).

42

Lidocaine

The principal metabolic pathway of lidocaine is oxidative dealkylation in the liver followed by hydrolysis.
Hepatic disease or decreases in hepatic blood flow can decrease the rate of metabolism of lidocaine.
For example, the elimination half-time of lidocaine is increased more than fivefold in patients with liver dysfunction compared with normal patients.

43

Bupivacaine

Pathways for metabolism of bupivacaine include aromatic hydroxylation, N-dealkylation, amide hydrolysis, and conjugation.
α1-Acid glycoprotein is the most important plasma protein-binding site of bupivacaine
Marcaine, Sensorcaine, Bupivacaine
Cardiotoxic: highly lipid soluble, slow dissociation from sodium channels

44

Ropivacaine

Ropivacaine is metabolized by hepatic cytochrome P450 enzymes.
A very small fraction of ropivacaine is excreted unchanged in the urine (about 1%) when the liver is functioning normally
No dosage adjustments needed based on renal function is necessary.
Ropivacaine is highly bound to α1-acid glycoprotein.

45

Metabolism of Ester LA

Procaine, Chloroprocaine, Tetracaine (PETER CAN TALK) and cocaine/benzocaine
ONLY HAS 1 i
Ester local anesthetics undergo hydrolysis by cholinesterase enzyme: GOES AWAY QUICKLY
Rapid to Slow: chloroprocaine > procaine >tetracaine
The exception to hydrolysis of ester local anesthetics in the plasma is COCAINE, which undergoes significant metabolism in the liver.
Ester LA do not accumulate in the blood because they are metabolized by pseudocholinesterase (aka plasma cholinesterase or butyrocholinesterase)

46

Esters

Absorption in the blood stream.
Plasma cholinesterase and ester hydrolysis are not present in CSF

Plasma cholinesterase activity and the hydrolysis rate of ester local anesthetics are slowed in the presence of liver disease or an increased blood urea nitrogen concentration.
Plasma cholinesterase activity may be decreased in parturients and in patients being treated with certain chemotherapeutic drugs.
Patients with atypical plasma cholinesterase may be at increased risk for developing excess systemic concentrations of an ester local anesthetic due to absent or limited plasma hydrolysis.
Chronic therapy with acetylcholinesterase inhibitors (edrophonium, physostigmine, echothiophate) prolongs the action of ester LA because these agents depress pseudocholionesterast function (Myasthenia Gravis)

47

PABA: Para-aminobenzoic acid

True allergic reactions rare (<1%)
most commonly due to anxiety, panic attacks, intravascular injection, vasovagal responses, or epinephrine.
Ester local anesthetics > Amide Local Anesthetics Esters are derivatives of PABA
The parabens are additives in many cosmetics, lotions, and foods, and patients who are sensitized may exhibit cross-reactivity with the local anesthetics.

48

Allergy to Esters

Exposure to locals usually begins with the dentist: all add EPI…….palpitations, (from epi)
Most dentists use amides: allergies usually occur 99% of time to the ester
Esters: Para-amino Benzoic Acid: PABA (cosmetics)
If you are going to have an allergy, there is a cross allergy to all the esters NOT an AMIDE
If you are allergic to an amide: you are just allergic to that amide not the other amides
NO CROSS ALLERGIES BETWEEN CLASSES

49

Procaine

Procaine is hydrolyzed to paraaminobenzoic acid, which is excreted unchanged in urine
Increased plasma concentrations of paraaminobenzoic acid do not produce symptoms of systemic toxicity.
Primarily used to reduce the pain of IM injection of PCN or dentistry
Novocain

50

Chloroprocaine

Addition of a chlorine atom to the benzene ring of procaine to form chloroprocaine increases by 3.5 times the rate of hydrolysis of the local anesthetic by plasma cholinesterase, as compared with procaine.
Maternal and neonatal plasma cholinesterase activity may be decreased up to 40% at term
QUICK used for STAT C-SECTIONS

51

Benzocaine

Benzocaine is unique because it is a weak acid (pKa 3.5), It exists predominantly in the nonionized form at physiologic pH.
Topical anesthesia of mucous membranes prior to tracheal intubation, endoscopy, transesophageal echocardiography, and bronchoscopy.
Onset of topical anesthesia is rapid and lasts 30 to 60 minutes.
A brief spray of 20% benzocaine delivers the recommended dose of 200 to 300 mg. Systemic absorption of topical benzocaine is enhanced by defects in the skin and mucosa as well as from the gastrointestinal tract should any of the local anesthetic be swallowed.

52

Cocaine

Cocaine is metabolized by plasma cholinesterase and the liver.
About 1 % excreted in the urine.
Plasma cholinesterase activity is decreased in parturients, neonates, the elderly, and patients with severe underlying hepatic disease.
Cocaine may be present in urine for 24 to 36 hours, depending on the route of administration and cholinesterase activity.
Cocaine differs from the other LA in that it is a vasoconstrictor and it is naturally occurring

53

Clearance of Local Anesthetics

ESTERShydrolysis via cholinesterase


AMIDESmetabolism via hepatic enzymes

54

Absorption & Distribution

Influenced by:
Site of injection (ex. Blood flow, etc.)
Dose
Use of epinephrine
Pharmacologic characteristics of drug
Plasma concentration determined by rate of tissue distribution & clearance
Eliminated from plasma by metabolism & excretion.
Patient factors for absorption & plasma concentration:
Age, cardiovascular status, hepatic function
Protein binding will influence distribution & excretion
After systemic absorption, amide local anesthetics are more widely distributed in tissues than ester local anesthetics.

55

Mixture of Local Anesthetics

Able to compensate for short and long duration of action
Offer rapid onset infrequent systemic toxicity
DO NOT USE MAXIMUM DOSE OF TWO LOCAL ANESTHETICS IN COMBINATION. THE TOXICITIES ARE NOT INDEPENDENT BUT SHOULD BE PRESUMED TO BE ADDITIVE.

56

Ion Trapping

The pH of the fetus is lower than the pH of the mom.
The un-ionized form of circulating local anesthetic crosses the placental barrier.
Once in the fetus, equilibrium between ionized and un-ionized drug is re-established.
Because the pH is lower than mom’s, a greater amount of drug is ionized.
The ionized form of local anesthetic cannot cross the placental barrier: ionized local anesthetic is trapped in the fetus.
The lower the fetal pH, the greater the amount of local anesthetic in ionized form in the fetus: the greater the ion trapping.
Maternal alkalosis and fetal acidosis facilitates accumulation of LA by the fetus.

57

Allergic Reactions to Local Anesthetics

rare estimated that less than 1% of all adverse reactions to local anesthetics are due to an allergic mechanism.
 Instead, the overwhelming majority of adverse responses that are often attributed to an allergic reaction are instead manifestations of excess plasma concentrations of the local anesthetic.
Esters of local anesthetics that produce metabolites related to paraaminobenzoic acid are more likely than amide local anesthetics, which are not metabolized to paraaminobenzoic acid, to evoke an allergic reaction. An allergic reaction after the use of a local anesthetic may be due to methylparaben or similar substances used as preservatives in commercial preparations of ester and amide local anesthetics. These preservatives are structurally similar to paraaminobenzoic acid. As a result, an allergic reaction may reflect prior stimulation of antibody production by the preservative and not a reaction to the local anesthetic.

58

Cross-sensitivity

Cross-sensitivity between local anesthetics reflects the common metabolite paraaminobenzoic acid. A similar cross-sensitivity, however, does not exist between classes of local anesthetics. Therefore, a patient with a known allergy to an ester local anesthetic can receive an amide local anesthetic without an increased risk of an allergic reaction. Likewise, an ester local anesthetic can be administered to a patient with a known allergy to an amide local anesthetic. It is important that the “safe” local anesthetic be preservative-free.

59

Local Anesthetic Systemic Toxicity (LAST)

Serious but rare consequence of regional anesthesia/use of local drugs.
It most commonly results from an inadvertent vascular injection or absorption of large amounts of drug from certain nerve blocks requiring large volume injections.
It can also occasionally result from continuous infusion and accumulation of drug and metabolites over many days.
High systemic blood levels lead to LAST.
Accidental direct intravascular injection of local anesthetic solutions during performance of peripheral nerve block anesthesia or epidural anesthesia is the most common mechanism for production of excess plasma concentrations of local anesthetics.

60

Therapeutic to Toxic Effects of Local Anesthetic Agents

Therapeutic: Lightheadedness, circumoral & tongue numbness, tinnitis
(Lido plasma conc: 0-5mcg/mL)
Toxic: Visual disturbances, muscle twitching, convulsions, unconsciousness, coma, respiratory arrest, cardiovascular depression
(Lido plasma conc: 5-25mcg/mL)

61

Diagnose & Treat LAST

Prompt recognition and treatment are essential to minimizing adverse outcomes of LAST.
Airway management remains the primary intervention because preventing hypoxia and acidosis are essential first steps.
Seizure suppression is essential to facilitate immediate airway control and prevent or reduce metabolic acidosis.
Benzodiazepines are considered the drugs of choice because they are anticonvulsant without causing significant cardiac depression.

62

Toxic Doses

The maximum Dose to be used:
Lidocaine 4 mg/kg
Lidocaine with epi 7 mg/kg

Bupivacaine 2 mg/kg
Bupivacaine with epi 3 mg/kg

Doses exceeding these ranges lead to higher plasma levels and toxicity.

63

Lipid Emulsion Therapy for LAST

The exact mechanisms for the beneficial effects is not clear.
The mechanisms of action of lipid infusion can be broadly separated into intracellular (metabolic, signaling), intravascular (partitioning, sink), and membrane (channel) effects.
Use of lipid emulsion is recommended at the earliest sign of toxicity after airway management.
Initial bolus of 1.5 mL/kg 20% lipid emulsion followed by 0.25 mL/kg per minute of infusion, continued for at least 10 minutes after circulatory stability is attained is recommended.
Nonresponse to treatment should prompt institution of cardiopulmonary bypass (CPB), whenever this modality is available. Prompt institution of CPB, with support of circulation while drug clearance proceeds, has been associated with full recovery from LAST in a number of case reports.

64

Variety of Local Anesthetic Uses

Surface Anesthesia
Local Infiltration
Nebulized Local
Peripheral Nerve Block
Intravenous Regional Anesthesia (Bier Block)
Regional Anesthesia
Epidural Anesthesia
Spinal (subarachnoid) Anesthesia

65

Laryngeal Tracheal Anesthesia (LTA)

4mL of 4% Lidocaine carpuject with attached spray tube.
Local anesthetics are absorbed into the systemic circulation after topical application to mucous membranes.
Plasma lidocaine concentrations 15 minutes after laryngotracheal spray of the local anesthetic are similar to those concentrations present at the same time after an IV injection of a similar dose of lidocaine.
This systemic absorption reflects the high vascularity of the tracheobronchial tree and the injection of the local anesthetic as a spray that spreads the solution over a wide surface area.

66

Epinephrine Cautions

The duration of infiltration anesthesia can be approximately doubled by adding 1:200,000 epinephrine to the local anesthetic solution.
Epinephrine-containing solutions should never be injected intra-cutaneously or into tissues supplied by end arteries (fingers, toes, penis, ears, and nose) because resulting vasoconstriction can produce ischemia and may result in tissue necrosis.

67

Tumescent liposuction Solution

The “tumescent” technique for liposuction is carried out via the subcutaneous infiltration of large volumes (5 or more liters) of solution containing highly diluted lidocaine (0.05% to 0.10%) with epinephrine (1:100,000).
The taut stretching of overlying blanched skin by the large volume of solution and epinephrine-induced vasoconstriction is the origin of the term tumescent technique.
The result is sufficient local anesthesia for the liposuction, virtually bloodless aspirates, and prolonged postoperative analgesia. Slow and sustained release of lidocaine into the circulation is associated with plasma concentrations <1.5 µg/mL that peak 12 to 14 hours after injection and then decline gradually over the next 6 to 14 hours

68

Peak serum levels of local anesthetics from the tumescent solution are most commonly seen when?

Tumescent liposuction is commonly done with large volumes of tumescent solution consisting of normal saline with 1:1,000,000 epinephrine and .025% to .1% lidocaine. Peak serum levels of lidocaine occur 12 to 14 hours after injection and decline over the next 6 to 14 hours.

69

Liposuction

Tumescent technique uses large volumes of infiltrate solution to emulsify and remove fat.
EBL is 1% of recovered aspirate
Most common cause of mortality is pulmonary embolus 23%
Overall mortality .02%