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72 PART I PATIENT EVALUATION
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andsphenoidsinuses.Inrecentyears,bothENTpractitionersandoralandmaxillofacialsurgeons
havebeenusingCBCTasanefficientin-houseexaminationtool.CBCTimagesarehelpfulin
identificationofmucusretentionphenomena,antralpolyps,sinonasalpolyposis,oroantralfistula,or
displacementofanimplantintothesinus.Low-doseimagingsuchasCBCTiscrucialasinammatorysinusdiseaseisoftenrecurringandcansometimesresultinrepetitiveimagingrequests.Another
majoradvantageofCBCTisthatimageshavethesamequalityinallpossibleplanes.Onemajor
disadvantageofCBCTispoorcontrastresolution.MRIistheimagingmodalityofchoiceinpatients
withsuspectmalignancyorinpatientspresentingwithneurologicsignsand/ordeficits.MRIisuseful
asitisnotaffectedbythebeam-hardeningartifactsfromdentalamalgamordensecorticalbone.CT
isperformedininstancestoallowvisualizationoftheextentofbonedestructionandsofttissuereactionstodiseaseincludinginfiltrations.
52. What imaging modalities are used for diagnosis of inflammatory disorders of the jaw?
Mostinammatorydisordersofthejawcanbeevaluatedbyplainradiographs,butplainfilmsmay
requiresupplementationbyCT,CBCT,MRI,orradionuclidescanningtechniques.Bothinammationand
malignancycanhavesimilarradiographicfeatures,whichnecessitatecross-sectionalimagingforfurther
evaluation.Oralandmaxillofacialsurgeonsrelyonocclusalradiographstoidentifyperiostealreactionsof
thebone.However,wrongangulationorexposurefactorscanlimittheutilityofanocclusalradiograph.
WithCBCTimages,thethinlayerofperiostealbonecanbeseeninthemultiplanarslices.Inaddition,
bonysequestracanbebetteridentifiedwithcross-sectionalimaging.AlsoinevaluatingBRONJ,CBCTis
moreusefulthanpanoramicradiography.Scintigraphyorradionuclideimagingisthemostdefinitiveway
ofdemonstratingbonechangesandclinicalactivitycausedbyinammationorsuspectedosteomyelitis.
53. Which imaging techniques will reveal soft tissue infection in the head and neck
regions (Fig. 5-7)?
TheprimaryimagingmodalitiestoevaluateinfectionintheheadandneckareCTandMRI.CTand
MRIbothdifferentiateabscessfromcellulitis,indicatethepresenceofvenousthrombosisandairway
Figure 5-7. Computedtomographyscanofanabscesscollectionandgasposteriortothemandible(arrow).
CHAPTER 5 DIAGNOSTIC IMAGING FOR THE ORAL AND MAXILLOFACIAL SURGERY PATIENT 73
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compromise,andshowtheexactlocationandextentoftheinfectiousprocess.CTisbetterthanMRI
inevaluatingtheintegrityofcorticalbone,andCTtakeslesstime,costsless,andismorereadily
availablethanMRI.MRI,ontheotherhand,allowsimaginginthesagittal,coronal,andaxialplanes
withthepatientsupine,doesnotuseradiation,andisnotaffectedordegradedbyartifactsfrom
dentalamalgam.Overall,CTwithcontrastwithaveryhighdiagnosticqualityinallstagesoforaland
facialinfectionsismostcommonlyusedforthispurpose.
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II
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AnesthesiA
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LOCAL ANESTHETICS
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Ravi Agarwal, George Obeid, A. Omar Abubaker, Kenneth J. Benson
1. What is the resting membrane potential for a neuron and how does that relate to
transmission of neural impulses?
Like most cells, neurons have a resting membrane potential mostly created by the sodium-potassium
pump in which sodium is pumped extracellularly and potassium pumped intracellularly. This concentration gradient, along with other factors, leads to a relative excess of anions inside the cell leading to
a negative resting membrane potential (about −70 mV).
Neural impulses are transmitted via changes in the electrical gradient along the nerve axon
known as action potentials. To generate an action potential, there must be enough stimulation to
the voltage-gated sodium channels to depolarize the cell to exceed the threshold potential (about
−55 mV). Once reached, this allows depolarization of the cells through an influx of sodium intracellularly and propagation of the impulse along the nerve. Repolarization occurs with closure of these
sodium channels and opening of the voltage-gated potassium channels to allow more potassium to
exit the cell. The cell then returns to baseline gradient via the sodium-potassium pump (Fig. 6-1).
2. What is the mechanism of action for local anesthetics?
Local anesthetics reversibly block conduction along the nerve distal to the site of application. Once injected
into the tissue, the local anesthetic is a weak base and equilibrates into two forms: ionized and non-ionized.
The non-ionized form is able to freely cross the cell membrane. Once inside the cell, re-equilibration
occurs to the ionized form, which binds to specific sites on the voltage-gated sodium channels, impairing
depolarization (Fig. 6-2). As concentration of the anesthetic increases and more receptors are occupied,
action potentials are progressively slowed and then abolished. Although the resting membrane potential
remains unchanged, the impulses never exceed the raised threshold to allow for an action potential.
3. How does the onset and recovery of anesthesia proceed in a peripheral nerve block?
The onset and recovery of nerve blocks is determined by the organization of the nerve trunk itself.
Generally, the outer (mantle) layers innervate proximal structures, whereas the inner (core) layers
innervate distal structures. Since the local anesthetic diffuses through the nerve bundle from the outer
(mantle) layer to the center (core) layers, the effects of anesthesia are noted on proximal structures
faster than distal structures. For example, after inferior alveolar nerve block, anesthesia is noticed first
at the site of injection, then from the molars to the incisors, and finally in the lower lip. Recovery also
occurs from proximal to distal, with the lower lip being the last to recover.
4. What is differential blockage and how does that relate to the order of sensation
loss after an injection of local anesthesia?
Differential blockade refers to the ability of the local anesthetic to block noxious stimuli but still retain
motor impulses. Classically, small nerve fibers (such as pain/proprioception fibers) are blocked faster
than larger motor nerves. It is important to note, not all nerve fibers are equally affected, and the sensitivity to local anesthetics are determined by factors such as axonal diameter, frequency of impulses,
length of nerve exposed to the drug, degree of myelination, and the type of local anesthetic.
The classical order of sensation loss during local anesthesia is:
• Pain
• Cold
• Warm
• Touch
• Deeppressure
• Motor
5. How are local anesthetics classified?
Local anesthetics can be classified based on their chemical structures, rate of onset, potency, or
durationofaction.Mostcommonly,thechemicalstructuredeterminesiftheanestheticisanamideor
an ester. All local anesthetics contain an aromatic, lipophilic ring linked to a hydrophilic amide group
77
CHAPTER 6
78 PART II ANESTHESIA
BH
Local anesthetics
Transmembrane potential (mV)
Resting potential
Local anesthetic
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30
0
Normal
–30
–60
Threshold potential
–90
Figure 6-1. Local anesthetics slow the rate of depolarization of the nerve action potential such that the threshold potential
is not reached. (Modified from Stoelting RK, Miller RD: Local anesthetics. In Stoelting RK, Miller RD, editors: Basics of
anesthesia, ed 3, New York, 1994, Churchill Livingstone.)
Extracellular
+
B + H
+
Lipid bilayer
+
BH
H+ + B
Figure 6-2. Mechanismofactionoflocalanesthetics. (Modified from Kumar S: Local anesthetics. In Duke J, editor:
Anesthesia secrets, ed 3, Philadelphia, 2006, Mosby.)
BH+: Ionized form
cation
H
O soluble
2
by an intermediate chain. The intermediate chain determines the chemical classification, either as an
amide or an ester (Fig. 6-3).
In dentistry, ester local anesthetics are not available in dental cartridges due to lack of efficacy,
potential for allergic reactions, and advantages of the amides.
An easy way to identify amide local anesthetics is to remember that the drug name contains an i
plus -caine (lidocaine, mepivacaine, and bupivacaine). Esters such as Novocain, procaine, benzocaine,
and tetracaine contain no i.
+
BH
Intracellular
B: Un-ionized form
free base
lipid soluble
CHAPTER 6 LOCAL ANESTHETICS 79
CnH
n
n
group
Amine
group
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Intermediate
N
chain
CnH
Aromatic
Figure 6-3. Structure of esters and amides. (Modified from Kumar S: Local anesthetics. In Duke J, editor: Anesthesia
secrets, ed 3, Philadelphia, 2006, Mosby.)
Table 6-1. Properties of Local Anesthetics
AGENT
LIPID
SOLUBILITY
PROTEIN
BINDING DURATION PKa
ONSET
TIME
Mepivacaine 1 75 Medium 7.6 Fast
Lidocaine 4 65 Medium 7.7 Fast
Bupivacaine 28 95 Long 8.1 Moderate
Tetracaine 80 85 Long 8.6 Slow
Articaine was approved for use in the United States in April 2000, although it has been used in
other countries for some time. This local anesthetic contains both an amide and an ester link, although
it is classified as an amide.
6. How are local anesthetics metabolized?
AmidelocalanestheticsaremetabolizedmainlybythemicrosomalP-450enzymesintheliver.The
rate of metabolism can be affected by decreases in liver function (e.g., cirrhosis) or liver blood flow
(e.g., congestive heart failure), potentially leading to systemic toxicity. Articaine is considered an amide
drug; however its ester side-chain does undergoes partial hydrolysis by nonspecific plasma esterases,
leading to a short half-life and lower risk for toxicity.
Ester local anesthetics are very rapidly metabolized by the plasma pseudocholinesterases. Benzocaine, a popular topical anesthetic, is metabolized to p-aminobenzoicacid(PABA),aknownallergen.
The elimination half-life for agents like lidocaine is about 90 minutes, whereas longer acting
agents like bupivacaine is over 200 minutes. Articaine, because of its degradation in plasma, has a
half-liferangingfrom20to40minutes.
7. What determines the rate of onset of a local anesthetic?
The pKa of a local anesthetic determines its speed of action. The pKa of a local anesthetic is the pH at
which equal concentrations of ionized and un-ionized forms exist. It is the un-ionized form that must
cross the axonal membrane to initiate neural blockade.
Thus,thecloserthepKaofalocalanestheticistothepHoftissue(7.4),themorerapidtheonset
due to the greater amount of un-ionized agent available for diffusion (Table 6-1).
8. Why are local anesthetics often ineffective when injected into an area of infection
or inflammation?
Local anesthetics exist in both an ionized (cation) and un-ionized (base) form. Keep in mind that
infected tissue has a more acidic pH due to inflammatory mediators, neutralizing the un-ionized (base)
form. Since there is less concentration of an un-ionized agent to diffuse across the nerve membrane,
the onset time can be delayed significantly. Inflammatory exudates also enhance nerve conduction,
making the blockage of nerve impulses more difficult.
9. What determines the potency of a local anesthetic?
The lipid solubility determines the potency of a local anesthetic. A greater lipid solubility produces a
more potent local anesthetic due to the fact that nerve membranes are mostly lipid (see Table 6-1).
80 PART II ANESTHESIA
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Bupivacaine is a more potent local anesthetic than lidocaine, for example. Therefore only a 0.5% solution is required to obtain comparable local anesthesia, instead of a 2% solution.
10. What determines the duration of a local anesthetic?
The degree of protein binding of a local anesthetic agent determines the duration of the anesthetic.
Sodium channels and receptor sites for the local anesthetic are mostly protein, thus an agent with a
greater degree of protein binding will have a longer duration of action (see Table 6-1). Also, protein
binding creates a “reservoir” of local anesthetic availability to bind to receptors as they become
unoccupied.
Because bupivacaine, tetracaine, and etidocaine are all highly protein bound, they are longacting local anesthetics. Vasoconstrictors will also determine the duration of a local anesthetic, but for
different reasons.
11. Why are vasoconstrictors added to local anesthetics?
Vasoconstrictors are added to prolong the duration of the anesthetic effect. Vasoconstrictors decrease
the rate of absorption of the local anesthetic by vasculature, limit systemic toxic side effects, and
decrease bleeding at the surgical sites. Because of the vasoconstriction, there is reduced blood flow
and decreased vascular absorption of the local anesthetic. This decreases the blood concentrations of
the local anesthetic and reduces the risk for toxicity.
The two vasoconstrictors available in dental cartridges are epinephrine and levonordefrin. Epinephrine can be found in concentrations of 1:50,000, 1:100,000, and 1:200,000. Levonordefrin is only
found mixed with 3% mepivacaine in a concentration of 1:20,000.
Although the most commonly used formulation is 1:100,000, there is little added benefit from
1:200,000 epinephrine. The 1:50,000 may aid in surgical hemostasis but no effects with regard to the
local anesthetic.
12. What are the cardiovascular influences associated with vasoconstrictors?
Vasoconstrictors have an impact on the cardiovascular system even with small amounts injected in
the submucosal tissues. Epinephrine acts on alpha, beta-1, and beta-2 receptors, thus increasing the
heart rate and myocardial contractility. The alpha effects cause vasoconstriction, but larger vessels in
the body have beta-2 receptors leading to vasodilation. Thus, the mean arterial pressure has minimal
change, although the systolic blood pressure increases and the diastolic pressure decreases.
Levonordefrin is a synthetic drug, closely resembling norepinephrine in action, hence the lack of
beta-2 activity. Effects on blood pressure include increased systolic, diastolic, and mean arterial
pressure leading to a reflex-induced slowing of the heart rate.
Generally, the hemodynamic effects of vasoconstrictors are seen within a few minutes and
subsideafter10to15minutes.Peakinuencesareusuallybetween5and10minutes.
13. What is the mechanism of degradation of epinephrine?
Epinephrine is rapidly metabolized and inactivated in the blood primarily by the enzyme catechol-O-
methyltransferase(COMT)andmonoamineoxidase(MAO).Thereisalsorapidneuronalreuptakeof
epinephrine by adrenergic nerves.
Oneoftheendbreakdownproductsisvanillylmandelicacid(VMA).Onlyasmallpercentage(1%)
of epinephrine is excreted unchanged in the urine.
The elimination half-life of epinephrine is rapid, typically in 1 to 3 minutes.
14. What are potential drug interactions associated with vasoconstrictor use?
Drug interactions associated with vasoconstrictors include tricyclic antidepressants (TCAs), mono-
amineoxidaseinhibitors(MAOIs),digoxin,nonselectivebetablockers,thyroidhormone,andanyof
the sympathomimetics such as drugs for weight control, attention deficit disorders, and/or cocaine.
Vasopressors are not contraindicated in these patients, but they should be administered with caution.
TCAs (e.g., amitriptyline) increase the availability of endogenous norepinephrine, which could
create an exaggerated heart rate or blood pressure response with the use of levonordefrin and to a
lessereffectwithepinephrine.PatientsonTCAsorMAOIscanhavesomedegreeofcardiacexcitement from the medications. Caution is advised when using vasoconstrictors, especially levonordefrin.
Nonselective beta blockers block both beta-1 and beta-2 receptors, influencing vasopressors
to have a more pronounced alpha agonist response leading to elevated diastolic and mean arterial
pressures. The elevated blood pressures can be significant, creating a reflex slowing of the heart rate.
It is therefore prudent to limit the amount of vasoconstrictors used in these patients and to aspirate to
prevent any intravascular injections.
CHAPTER 6 LOCAL ANESTHETICS 81
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Cocaine potentiates the effects of adrenergic vasoconstrictors. The dysrhythmic results of this
interaction can be life threatening. Unfortunately, obtaining a factual health history from a cocaine
user may be difficult. All suspected drug users should be made aware of these lethal side effects,
especially if cocaine has been used recently.
15. What is the maximum amount of 2% lidocaine with 1:100,000 epinephrine (in
milligrams) that can be administered to a healthy 150-lb man?
477mg.Themaximumdoseof2%lidocainewith1:100,000epinephrinefortheadultpatientis7mg/kg
(Table 6-2). You first must convert pounds to kilograms by dividing the weight (in lbs) by 2.2.
150 lb ÷ 2.2 lb/kg = 68 kg
68kg×7mg/kg=477mg
16. How do you calculate the amount, in milligrams, of any anesthetic and
vasoconstrictor in a given solution?
For local anesthetics, for every 1% solution there is 10 mg/mL. Therefore:
Total milligrams = % of the solution × 10 × total milliliters
For vasoconstriction, for every 1:100,000 there is 0.01 mg/mL. Therefore:
Total milligrams = ratio × total milliliters
For example, a 1.8-mL dental cartridge of 2% lidocaine with 1:100,000 epinephrine has 20 mg/mL of
lidocaine and 0.01 mg/mL of epinephrine. This totals to 36 mg of lidocaine and 0.018 mg of epinephrine.
17. What is the maximum number of dental cartridges of 2% lidocaine with 1:100,000
that can be given to this 150-lb individual?
13 cartridges. A standard dental cartridge (1.8 mL) contains 36 mg of lidocaine.
477mg÷36mg/cartridge=13.25cartridges.
18. How many dental cartridges of lidocaine or mepivacaine can be administered to a
30-lb child?
Maximumdrugdosagesareoftenunknownforthepediatricpopulation.Inaddition,pharmaceutical
manufacturers are reluctant to recommend maximum pediatric dosages of a drug because of variations in age and weight.
Table 6-2. Commonly Used Local Anesthetics in Dentistry
CARTRIDGE
AGENT
SIZE (MG) (MG/KG) (MG/LB)
2% Lidocaine with
1:100,000 epinephrine
3%Mepivacaine 54 6.6 3.0 400
2%Mepivacainewith
1:20,000 levonordefrin
4%Prilocaine 72 8 3.6 600
4%Prilocainewith
1:200,000 epinephrine
0.5% Bupivacaine with
1:200,000 epinephrine
4%Articaine* with
1:100,000 epinephrine
*Articaine (Septocaine) dosages are based on a cartridge volume of 1.7 mL/cartridge.
Maximum recommended dosages are based on an adult weight of 150lb or 70 Kg following manufacturers recommendation.
Table is adapted from Malamed S: Handbook of local anesthesia, ed 6.
Maximum Dose
MAXIMUM
DOSE
36 7 3.2 500
36 6.6 3.0 400
72 8 3.6 600
9 2.0 0.9 90
72 7 3.2 500
(suggested)
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