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Contributors
vii
Preface
The sixth edition of Handbook of Local Anesthesia! switch) to increase patient comfort during injection, decrease
As happened with previous editions, I truly find it hard to onset time of anesthesia, and, perhaps, increase the depth
comprehend how many years have transpired since the 1st of anesthesia; phentolamine mesylate (the local anesthetic
edition was published in 1978. It has been 8 years since the "OFF" switch) giving the doctor the opportunity to signifi
fifth edition and in this time there have been a significant cantly minimize the duration of a patients residual soft tissue
number of changes, many of them advances, in the art and anesthesia, thereby minimizing the risk of self-inflicted soft
science of pain control in dentistry. tissue injury.
Though the drugs remain the same---articaine HCl, bupi I have asked Dr. Mark Hochman to rewrite the discussions
vacaine HCl, lidocaine HCl, mepivacaine HCl, and prilocaine in this edition on C-CLAD devices (Chapter 5-The Syringe)
HCl-the years since the fifth edition have seen the introduc and the local anesthetic techniques associated with it (Chapter
tion and refinement of drugs and devices which work to help IS-Supplemental Injections and Chapter 20---Future Con
the dental profession come ever closer to the twin goals of siderations). Dr. Hochman has been intimately involved with
truly pain free dentistry and truly pain free local anesthetic the development of C-CLAD since the mid-1990s and is
injections. the author of a number of refereed papers on the subject
As I have stated repeatedly in previous editions, "Local including two injection techniques---AMSA (anterior middle
anesthetics are the safest and the most effective drugs avail superior alveolar nerve block) and P-ASA (palatal-anterior
able in all of medicine for the prevention and the management superior alvelar nerve block) that were developed as a result
of pain. Indeed, there are no other drugs that truly prevent of his research into computer delivery of local anesthetics.
pain; no other drugs which actually prevent a propagated A DVD accompanied the fifth edition of Local Anesthesia.
nociceptive nerve impulse from reaching the patient's brain, It followed the structure of the textbook, providing clinical
where it would be interpreted as pain. Deposit a local anes demonstrations of the techniques and concepts presented in
thetic drug in close proximity to a sensory nerve and clinically the text. The DVD has proven to be a highly effective teaching
adequate pain control will result in essentially all clinical device and is used, both legally and (sadly) illegally, by stu
situations." dents, dentists and dental hygienists throughout the world.
Find the nerve with a local anesthetic drug and pain control A supplemental disk has been incuded with the original
is virtually assured. Yet in certain clinical situations "finding 2-disk set which accompanies this sixth edition. The disk pres
the nerve" remains a vexing problem. This is especially so in ents clinical updates on a number of the newer additions to
the mandible, primarily permanent mandibular molars. Over the local anesthetic armamentarium. It is my feeling, as an
my 39 years as a teacher of anesthesia in dentistry I and my educator that the combination of the written text plus the
dentist anesthesiologist colleagues have worked at "fixing" this visual impact of the DVD provides a more optimal learning
problem. experience for all who come to study this critically important
Have we succeeded? Not yet. subject.
Are we getting close to a solution? Yes. Feedback from readers of this textbook is always appreci
This sixth edition of Local Anesthesia includes new and/ or ated. Should errors be noted, or suggestions for improvement
expanded discussions of the periodontal ligament (PDL) be made, contact me at malamed@usc.edu.
injection-including the use of computer-controlled local
anesthetic delivery (C-CLAD) systems for PDL (and other Stanley F. Malamed
injections); the administration of the local anesthetic articaine
HCl by mandibular infiltration in the adult mandible; buffer October 2011
ing of local anesthetic solutions (the local anesthetic "ON" Los Angeles, California, USA
ix
Acknowledgments
The people involved with the video production of the new supplemental DVD cannot receive
enough thanks: Dr. Joseph Massad and his excellent team at Millennium Productions.
Thanks, too, to the manufacturers of local anesthetic drugs and devices in North America,
including Beutlich Pharmaceuticals; Dentsply; Kodak (Cook-Waite); Midwest; Milestone Scientific;
Novocol; Septodont, Inc; and Sultan Safety, LLC, for their assistance in supplying photographs and
graphics for use in this edition.
I also want to thank Brian S. Loehr, Senior Content Development Specialist; Rachel E. McMullen,
Senior Project Manager; and John J. Dolan, Executive Content Strategist, from Mosby (an affiliate
of Elsevier) who had the unenviable task of dealing with a frequently lazy, usually hard-to-reach
author. Their perseverance-once again-has paid off with this sixth edition.
Finally, I wish to thank the many members of our profession, the dentists and dental hygienists,
who have provided me with written and verbal input regarding prior editions of this textbook.
Many of their suggestions for additions, deletions, and corrections have been incorporated into this
new text. Thanks to you all!
Stanley F. Malamed
December 2011
Los Angeles, California
xi
Contents
xiii
New to this Edition
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www.ShayanNemoodar.com
PART
The Drugs
In the first section of this book, the pharmacologicand clinicalproperties of the classesof drugs known
as local anesthetics (Chapter 2) and vasoconstrictors (Chapter 3) are discussed Knowledgeof both the
pharmacologic and clinicalproperties of these drugs, by all persons permitted to administer them, is
absolutelyessentialfor their safeuse and for a better understanding of those potentiallylife-threatening
systemic reactions associated with their administration. Emphasis is placed on local anesthetic drug
combinations currently used in anesthesia in dentistry in North America (Chapter 4).
Chapter 1provides a background for understanding how local anestheticswork to transiently block
nerve conduction, thus preventing pain from being experienced. The anatomy and physiology of
normal neurons and nerve conduction are reviewed as a background for the discussion, which, in
subsequent chapters, takes up the pharmacology and clinical actions of various specificagents.
www.ShayanNemoodar.com
T
Neurophysiology
' I •I
www.ShayanNemoodar.com
CHAPTER1 Neurophysiology 3
OWlll
•
Figure 1-1. The fuse is lit and the flame reaches the dynamite;
Figure 1-2. Localanesthetic is placed at some point between the
pain stimulus and the brain (dynamite). The nerve impulse travels
up to the point oflocal anesthetic application and then "dies,"never
an explosion occurs, and the patient experiencespain. reaching the brain, and pain does not occur.
www.ShayanNemoodar.com
4 PART I The Drugs
CNS
Synapse with
I
Skeletal muscle cell
another neuron
A
Cell body
p
E
R
I
p
CNS H
E
Axon or Dendrite or R
y
central process peripheral process
B
Figure 1-3. A, Multipolar motor neuron. B, Unipolar sensory neuron. (From Liebgott B:Anatomical basis of dentistry, ed 2, St Louis,
2001,Mosby.)
endings respond to stimulation produced in the tissues in terminal (or bouton). Axon terminals synapse with muscle
which they lie, provoking an impulse that is transmitted cells (Fig. 1-3,A).
centrally along the axon. The axon is a thin cable-likestruc
ture that may be quite long (the giant squid axon has been The Axon
measured at 100to 200 cm). At its mesial (or central) end is The single nerve fiber,the axon, is a long cylinder of neural
an arborization similarto that seen in the peripheral process. cytoplasm (axoplasm) encased in a thin sheath, the nerve
However,in this case the arborization forms synapseswith membrane, or axolemma. Neurons have a cell body and a
various nuclei in the CNS to distribute incoming (sensory) nucleus, as do all other cells;however,neurons differ from
impulses to their appropriate siteswithin the CNSfor inter other cells in that they have an axonal process from which
pretation. The cell body is the third part of the neuron. In the the cell body may be at a considerable distance. The axo
sensory neuron described here, the cell body is located at a plasm, a gelatinoussubstance,is separated from extracellular
distance from the axon, the main pathway of impulse trans fluidsby a continuous nerve membrane. In some nerves,this
mission in this nerve. The cell body of the sensory nerve membrane is itself coveredby an insulating lipid-rich layer
therefore is not involvedin the processof impulse transmis ofmyelin.
sion, its primary function being to provide vital metabolic Current thinking holds that both sensory nerve excitabil
support for the entire neuron (Fig. 1-3, B). ity and conduction are attributable to changes developing
Nerve cellsthat conduct impulses from the CNS toward within the nerve membrane. The cellbody and the axoplasm
the periphery are termed motor neurons and are structurally are not essential for nerve conduction. They are important,
different from the sensory neurons just described in that however.The metabolic support of the membrane is prob
their cellbody is interposed between the axon and dendrites. ably derived from the axoplasm.
In motor neurons, the cellbody not only is an integral com The nerve (cell) membrane itself is approximately 70
ponent of the impulse transmission systembut alsoprovides to 80 A thick. (An angstrom unit is 1/10,000of a microm
metabolic support for the cell.Near its termination, the axon eter.) Figure 1-4represents a currently acceptableconfigura
branches with each branch, ending as a bulbous axon tion. All biological membranes are organized to block the
www.ShayanNemoodar.com
CHAPTER1 Neurophysiology 5
diffusion of water-soluble molecules; to be selectively per flexiblenonstretchable structure consisting of two layers of
meable to certain molecules via specialized pores or chan lipid molecules (bilipid layer of phospholipids) and associ
nels; and to transduce information through protein receptors ated proteins, lipids, and carbohydrates. The lipids are ori
responsive to chemical or physical stimulation by neu ented with their hydrophilic (polar) ends facing the outer
rotransmitters or hormones (chemical) or light, vibration, surfaceand their hydrophobic (nonpolar) ends projecting to
or pressure (physical).4 The membrane is described as a the middle of the membrane (Fig. 1-4,A). Proteins are visu
alizedas the primary organizational elementsof membranes
(Fig. 1-4, B).5 Proteins are classifiedas transport proteins
(channels, carriers, or pumps) and receptor sites. Channel
proteins are thought to be continuous pores through the
membrane, allowing some ions (Na+,K,+Ca") to flow pas
Monolayer of nonlipids
sively,whereas other channels are gated, permitting ion flow
only when the gate is open.4 The nerve membrane lies at the
Biomolecular layers of lipids
interface between extracellularfluid and axoplasm. It sepa
rates highly diverse ionic concentrations within the axon
from those outside. The resting nerve membrane has an
electrical resistance about 50 times greater than that of the
intracellular and extracellular fluids, thus preventing the
passageof sodium, potassium, and chloride ions down their
concentration gradients. However, when a nerve impulse
passes, electrical conductivity of the nerve membrane
increases approximately 100-fold.This increase in conduc
tivity permits the passage of sodium and potassium ions
A along their concentration gradients through the nerve mem
brane. It is the movement of these ions that provides an
immediate source of energy for impulse conduction along
the nerve.
Some nerve fibers are coveredby an insulating lipid layer
of myelin.In vertebrates,myelinatednerve fibers include all
but the smallest of axons (Table 1-1).6 Myelinated nerve
fibers (Fig. 1-5) are enclosed in spirally wrapped layers of
lipoprotein myelin sheaths, which are actually a specialized
form of Schwarm cell. Although primarily lipid (75%),
the myelin sheath also contains some protein (20%) and
carbohydrate (5%).7 Each myelinatednerve fiber is enclosed
B in its own myelin sheath. The outermost layer of myelin
Figure 1-4. A, Configuration of a biological membrane. B, Hetero consistsof the Schwanncellcytoplasmand its nucleus.Con
geneous lipoprotein membrane as suggested by Singer and strictions are located at regular intervals (approximately
Nicholson. (Redrawn from Covino BG,Vassalo HG: Local anesthet every 0.5 to 3 mm) along the myelinated nerve fiber.These
ics: mechanisms of action and clinical use, New York, 1976, Grune are nodes of Ranvier, and they form a gap between two
& Stratton.) adjoining Schwann cells and their myelin spirals.8 At these
TABLE 1-1
Classification of Peripheral Nerves According to Fiber Size and Physiologic Properties
Fiber Conduction
Class Subclass Myelin Diameter,µ Velocity, m/s Location Function
A alpha + 6-22 30-120 Afferent to and efferent from Motor, proprioception
muscles and joints
beta + 6-22 30-120 Afferent to and efferent from Motor, proprioception
muscles and joints
gamma + 3-6 15-35 Efferent to muscle spindles Muscle tone
delta + 1-4 5-25 Afferent sensory nerves Pain, temperature, touch
B + <3 3-15 Preganglionic sympathetic Various autonomic functions
c sC - 0.3-1.3 0.7-1.3 Postganglionic sympathetic Various autonomic functions
dgammaC - 0.4-1.2 0.1-2.0 Afferent sensory nerves Various autonomic functions; pain,
temperature, touch
From BerdeCB,StrichartzGR:Localanesthetics.In MillerRD,editor:Anesthesia,ed 5, Philadelphia,2000, ChurchillLlvingstone,pp 491-521.
www.ShayanNemoodar.com
6 PART I The Drugs
Schwanncell
Nodeof Ranvler
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CHAPTER1 Neurophysiology 7
Extracellularfluid
Na+ ++++ Nerve membrane
vzzzzzzzzj?zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzztf
i<+ ---- Normal
Resting -70 mV
Axoplaam (resting potential)
A Na+ + +++
Firing
i<+ ---- -50 to-60 mV
Step 1, A
and B (slow depolarizationto
V/lZZZ/l/lZZZ/lZZZ/l/lZZZ/lZZZ/l/lZZZ/l/77/lA threshold potential)
Figure 1-7. Top, Restingpotential. Step 1,
A and B, Slow depolarization to threshold.
Step 1, C, Rapid depolarization. Step 2,
C Na+ Repolarization.
Potential
++++
Step 1C +40
(rapid depolarization)
Repolarization
Step2 -60 to-90 mV
V/lZZZ/l/lZZZ/lZZZ/l/lZZZ/lZZZ/l/lZZZ/l/77/lA
www.ShayanNemoodar.com
8 PARTI The Drugs
concentration gradient (passive diffusion usually occurs its concentration gradient (higher ~ lower). After the
from a region of greater concentration to one of lesser con return of the membrane potential to its original level
centration), because the negative charge of the nerve mem (-70 mV), a slight excess of sodium exists within the nerve
brane restrains the positively charged ions by electrostatic cell, along with a slight excess of potassium extracellularly.
attraction. A period of metabolic activity then begins in which active
Chloride remains outside the nerve membrane instead of transfer of sodium ions out of the cell occurs via the
moving along its concentration gradient into the nerve cell, sodium pump. An expenditure of energy is necessary to
because the opposing, nearly equal, electrostatic influence move sodium ions out of the nerve cell against their con
(electrostatic gradient from inside to outside) forces outward centration gradient; this energy comes from the oxidative
migration. The net result is no diffusion of chloride through metabolism of adenosine triphosphate (ATP). The same
the membrane. pumping mechanism is thought to be responsible for
Sodium migrates inwardly because both the concentra the active transport of potassium ions into the cell against
tion (greater outside) and the electrostatic gradient (positive their concentration gradient. The process of repolarization
ion attracted by negative intracellular potential) favor such requires 0.7 msec.
migration. Only the fact that the resting nerve membrane is Immediately after a stimulus has initiated an action
relatively impermeable to sodium prevents a massive influx potential, a nerve is unable, for a time, to respond to
of this ion. another stimulus regardless of its strength. This is termed
the absolute refractory period, and it lasts for about the
duration of the main part of the action potential. The abso
Membrane Excitation lute refractory period is followed by a relative refractory
Depolarization. Excitation of a nerve segment leads to period, during which a new impulse can be initiated but
an increase in permeability of the cell membrane to sodium only by a stronger than normal stimulus. The relative refrac
ions. This is accomplished by a transient widening of trans tory period continues to decrease until the normal level of
membrane ion channels sufficient to permit the unhindered excitability returns, at which point the nerve is said to be
passage of hydrated sodium ions. The rapid influx of sodium repolarized.
ions to the interior of the nerve cell causes depolarization of During depolarization, a major proportion of ionic
the nerve membrane from its resting level to its firing thresh sodium channels are found in their open (O) state (thus
old of approximately-SO to -60 mV (see Fig. 1-7, Steps lA permitting the rapid influx of Na"), This is followed by a
and lB).12 The firing threshold is actually the magnitude of slower decline into a state of inactivation (I) of the channels
the decrease in negative transmembrane potential that is to a nonconducting state. Inactivation temporarily converts
necessary to initiate an action potential (impulse). the channels to a state from which they cannot open in
A decrease in negative transmembrane potential of 15 mV response to depolarization (absolute refractory period). This
(e.g., from -70 to -55 mV) is necessary to reach the firing inactivated state is slowly converted back, so that most chan
threshold; a voltage difference of less than 15 mV will not nels are found in their closed (C) resting form when the
initiate an impulse. In a normal nerve, the firing threshold membrane is repolarized (-70 mV). Upon depolarization,
remains constant. Exposure of the nerve to a local anesthetic the channels change configuration, first to an open ion
raises its firing threshold. Elevating the firing threshold conducting (O) state and then to an inactive nonconducting
means that more sodium must pass through the membrane (I) state. Although both C and I states correspond to non
to decrease the negative transmembrane potential to a level conducting channels, they differ in that depolarization can
where depolarization occurs. recruit channels to the conducting 0 state from C but not
When the firing threshold is reached, membrane perme from I. Figure 1-8 describes the sodium channel transition
ability to sodium increases dramatically and sodium ions stages.13
rapidly enter the a.xoplasm. At the end of depolarization (the
peak of the action potential), the electrical potential of the Membrane Channels. Discrete aqueous pores through the
nerve is actually reversed; an electrical potential of +40 mV excitable nerve membrane, called sodium (or ion) channels,
exists (see Fig. 1-7, Step IC). The entire depolarization are molecular structures that mediate its sodium permeabil
process requires approximately 0.3 msec. ity. A channel appears to be a lipoglycoprotein firmly situ
Repolarization. The action potential is terminated when ated in the membrane (see Fig. 1-4). It consists of an aqueous
the membrane repolarizes. This is caused by the extinction pore spanning the membrane that is narrow enough at least
(inactivation) of increased permeability to sodium. In many at one point to discriminate between sodium ions and
cells, permeability to potassium also increases, resulting in others; Na+passes through 12 times more easily than K+.The
the efflux of K', and leading to more rapid membrane repo channel also includes a portion that changes configuration
larization and return to its resting potential (see Fig. 1-7, in response to changes in membrane potential, thereby
Step 2). gating the passage of ions through the pore (C, 0, and I states
Movement of sodium ions into the cell during depolar are described). The presence of these channels helps explain
ization and subsequent movement of potassium ions out membrane permeability or impermeability to certain ions.
of the cell during repolarization are passive (not requiring Sodium channels have an internal diameter of approximately
the expenditure of energy), because each ion moves along 0.3 x 0.5 nm.14
www.ShayanNemoodar.com
CHAPTER1 Neurophysiology 9
++
Cytoplasmic
side
Figure 1-8. Sodium channel transition stages.Depolarization reversesresting membrane potential from interior negative (left) to interior
positive (center). The channel proteins undergo corresponding conformational changes from resting state (closed) to ion-conducting stage
(open). State changescontinue from open (center) to inactive (right), where channel configuration assumesa different,but still impermeable,
state. With repolarization, the inactivated refractory channel reverts to the initial resting configuration (left), ready for the next sequence.
(Redrawn from Siegelbaum SA, Koester F: Ion channels. In Kandel ER, editor: Principles of neural science, ed 3, Norwalk, Conn, 1991,
Appleton-Lange.)
11°1 i l l l
and chloride ions can pass through these channels. During
depolarization, sodium ions readily pass through the nerve
membrane because configurational changes that develop
within the membrane produce transient widening of these
0
transmembrane channels to a size adequate to allow the ::J :::I 0 ::J
unhindered passage of sodium ions down their concentra
tion gradient into the axoplasm (transformation from the
C to the 0 configuration). This concept can be visualized
as the opening of a gate during depolarization that is par
tially occluding the channel in the resting membrane (C)
(Fig. 1-10). Axoplasm
Evidenceindicates that channel specificityexists in that
sodium channels differfrom potassium channels.15The gates Figure 1-9. Membrane channels are partially occluded; the
on the sodium channel are located near the external surface nerve is at rest. Hydrated sodium ions (Na") are too large to pass
of the nerve membrane, whereas those on the potassium through channels, although potassium ions (K') can pass through
unimpeded.
channel are located near the internal surface of the nerve
membrane.
The stimulus disrupts the resting equilibrium of the nerve
Impulse Propagation membrane; the transmembrane potential is reversed
After initiation of an action potential by a stimulus, the momentarily, with the interior of the cell changing from
impulse must move alongthe surfaceof the axon.Energyfor negativeto positive,and the exterior changing from positive
impulse propagation is derivedfrom the nerve membrane in to negative.This new electrical equilibrium in this segment
the followingmanner. of nerve produces local currents that begin to fl.owbetween
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10 PART I The Drugs
Impulse
Extracellularfluid
@ Impulse
E:)
.I
j ! I.
l ! l
::J
j
::J Myelin_)
Figure 1-11. Saltatory propagation. Comparison of impulse
propagation in nonmyelinated (upper) and myelinated (lower)
axons. In nonmyelinated axons, the impulse moves forward by
sequential depolarization of short adjoining membrane segments.
Axoplasm Depolarization in myelinated axons, on the other hand, is discon
tinuous; the impulse leaps forward from node to node. Note how
much farther ahead the impulse is in the myelinatedaxon after four
Figure 1-1O. Membrane channels are open; depolarization
depolarization sequences.(Redrawnfrom de Jong RH: Localanes
occurs. Hydrated sodium ions (Na") now pass unimpeded through
thetics, St Louis, 1994,Mosby.)
the sodium channel.
the depolarizedsegment and the adjacent resting area. These in the density of current within a short distance of the depo
local currents flow from positive to negative, extending for larized segment.In areas immediatelyadjacent to this depo
severalmillimeters along the nerve membrane. larized segment, local current flow may be adequate to
Asa result of this current flow,the interior of the adjacent initiate depolarization in the resting membrane. Farther
area becomes less negative and its exterior less positive. away it will prove to be inadequate to achieve a firing
Transmembrane potential decreases, approaching firing threshold.
threshold for depolarization. When transmembrane poten The spread of an impulse in an unmyelinated nerve fiber
tial is decreased by 15 mV from resting potential, a firing therefore is characterized as a relatively slow forward
threshold is reached and rapid depolarization occurs. The creeping process (Fig. 1-11). The conduction rate in unmy
newlydepolarizedsegment sets up local currents in adjacent elinated C fibers is 1.2 m/sec compared with 14.8to 120ml
resting membrane, and the entire process starts anew. sec in myelinatedA-alpha and A-delta fibers.16
Conditions in the segment that has just depolarized
return to normal after the absolute and relative refractory Myelinated Nerves. Impulse spread within myelinated
periods. Because of this, the wave of depolarization can nerves differs from that in unmyelinated nerves because of
spread in only one direction. Backward (retrograde) move the layer of insulating material separating the intracellular
ment is prevented by the inexcitable,refractory segment. and extracellularcharges.The farther apart are the charges,
the smalleris the current necessaryto chargethe membrane.
Impulse Spread Localcurrents thus can travel much farther in a myelinated
The propagated impulse travels along the nerve membrane nerve than in an unmyelinated nerve before becoming inca
toward the CNS.The spread of this impulse differs depend pable of depolarizing the nerve membrane ahead of it.
ing on whether or not a nerve is myelinated. Impulse conduction in myelinated nerves occurs by
means of current leaps from node to node, a processtermed
Unmyelinated Nerves. An unmyelinatednerve fiberis basi saltatory conduction (see Fig. 1-11) (saltare is the Latin
cally a long cylinder with a high-electrical resistance cell verb "to leap"). This form of impulse conduction proves to
membrane surrounding a low-resistanceconducting core of be much fasterand more energyefficientthan that employed
axoplasm,all of which is bathed in low-resistanceextracel in unmyelinated nerves. The thickness of the myelin
lular fluid. sheath increases with increasing diameter of the axon. In
The high-resistance cell membrane and low-resistance addition, the distance between adjacent nodes of Ranvier
intracellularand extracellularmedia produce a rapid decrease increases with greater axonal diameter. Because of these
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CHAPTER 1 Neurophysiology 11
two factors, saltatory conduction is more rapid in a thicker because some of the local anesthetic moleculescarried a net
axon. positive charge, they made the electrical potential at the
Saltatory conduction usually progresses from one node to membrane surface more positive,thus decreasingthe excit
the next in a stepwise manner. However, it can be demon ability of the nerve by increasing the threshold potential.
strated that the current flow at the next node still exceeds Current evidence indicates that the resting potential of the
that necessary to reach the firing threshold of the nodal nerve membrane is unaltered by local anesthetics (they do
membrane. If conduction of an impulse is blocked at one not become hyperpolarized), and that conventional local
node, the local current skips over that node and proves ade anestheticsact within membrane channels rather than at the
quate to raise the membrane potential at the next node to its membrane surface. Also, the surface charge theory cannot
firing potential, producing depolarization. A minimum of explain the activity of uncharged anesthetic molecules in
perhaps 8 to 10 mm of nerve must be covered by anesthetic blocking nerve impulses (e.g.,benzocaine).
solution to ensure thorough blockade.17 Two other theories, membrane expansion and specific
receptor, are given credence today. Of the two, the specific
receptor theory is more widely held.
MODE AND SITE OF ACTION OF
The membrane expansion theory states that local anes
LOCAL ANESTHETICS
thetic molecules diffuse to hydrophobic regions of excitable
How and where local anesthetics alter the processes of membranes, producing a general disturbance of the bulk
impulse generation and transmission needs to be discussed. membrane structure, expanding some critical region(s) in
It is possiblefor localanestheticsto interferewith the excita the membrane, and preventing an increase in permeability
tion process in a nerve membrane in one or more of the to sodium ions.22.23 Local anesthetics that are highly lipid
followingways: soluble can easily penetrate the lipid portion of the cell
1. Altering the basic resting potential of the nerve membrane, producing a changein configuration of the lipo
membrane protein matrix of the nerve membrane. This results in a
2. Altering the threshold potential (firing level) decreaseddiameter of sodium channels,which leadsto inhi
3. Decreasingthe rate of depolarization bition of both sodium conductance and neural excitation
4. Prolonging the rate of repolarization (Fig. 1-12). The membrane expansion theory serves as a
It has been established that the primary effects of local possible explanation for the local anesthetic activity of a
anesthetics occur during the depolarization phase of the drug such as benzocaine, which does not exist in cationic
action potential.18 These effectsinclude a decreasein the rate form yet still exhibitspotent topical anesthetic activity.It has
of depolarization, particularly in the phase of slow depolar been demonstrated that nerve membranes,in fact,do expand
ization. Becauseof this, cellular depolarization is not suffi and become more fluid when exposed to local anesthetics.
cient to reduce the membrane potential of a nerve fiber to However,no direct evidencesuggeststhat nerve conduction
its firing level, and a propagated action potential does not is entirely blocked by membrane expansion per se.
develop. There is no accompanying change in the rate of The specific receptor theory, the most favored today, pro
repolarization. poses that local anesthetics act by binding to specificrecep
tors on the sodium channel (Fig. 1-13).24 The action of the
Where Do Local Anesthetics Work? drug is direct, not mediated by some change in the general
The nerve membrane is the site at which local anesthetics properties of the cellmembrane. Both biochemicaland elec
exert their pharmacologic actions. Many theories have been trophysiologicstudies have indicated that a specificreceptor
promulgated over the years to explain the mechanism of site for local anesthetics exists in the sodium channel either
action of local anesthetics, including the acetylcholine, on its external surface or on the internal axoplasmic
calcium displacement,and surface charge theories. The ace surface.25'26 Once the local anesthetic has gained accessto the
tylcholine theory stated that acetylcholine was involved in receptors,permeabilityto sodium ions is decreasedor elimi
nerve conduction, in addition to its role as a neurotransmit nated, and nerve conduction is interrupted.
ter at nerve synapses.19No evidenceindicatesthat acetylcho Local anesthetics are classifiedby their ability to react
line is involvedin neural transmission along the body of the with specificreceptor sitesin the sodium channel. It appears
neuron. The calcium displacement theory, once popular, that drugs can alter nerve conduction in at least four sites
maintained that local anesthetic nerve block was produced within the sodium channel (see Fig. 1-13):
by the displacement of calcium from some membrane site 1. Within the sodium channel (tertiary amine local
that controlled permeability to sodium.20 Evidence that anesthetics)
varying the concentration of calcium ions bathing a nerve 2. At the outer surface of the sodium channel
does not affect local anesthetic potency has diminished the (tetrodotoxin, saxitoxin)
credibility of this theory. The surface charge (repulsion) 3 and 4. At the activation or the inactivation gate (scorpion
theory proposed that local anesthetics act by binding to the venom)
nerve membrane and changingthe electricalpotential at the Table 1-3 is a biological classificationof local anesthetics
membrane surface.21 Cationic (RNW) (p. 16) drug mole based on their site of action and the active form of the
cules were aligned at the membrane-water interface, and compound. Drugs in Class C exist only in the uncharged
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12 PART I The Drugs
/
.... --- ....•.•. ,
,
/
' \
I
Benzocalne
\\ (RN) \ ,
''
'... ... _ ,' ,,
Extracellular Extracellular
Intracellular Intracellular
TABLE 1-3
Classification of LocalAnesthetic SubstancesAccording to Biological Site and Mode of Action
Classification Definition Chemical Substance
ClassA Agents acting at receptor site on external surface of nerve Biotoxins (e.g.,tetrodotoxin, saxitoxin)
membrane
ClassB Agents acting at receptor site on internal surface of nerve Quaternary ammonium analogs of lidocaine
membrane Scorpion venom
Class C Agents acting by a receptor-independent physico-chemical Benrocaine
mechanism
ClassD Agents acting by combination of receptor and receptor Most clinicallyuseful local anesthetic agents (e.g., articaine,
independent mechanisms lidocaine, mepivacaine,prilocaine)
Modified from Covino BG, Vassallo HG: Local anesthetics: mechanisms of action and clinical use, New York, 1976, Grune & Stratton. Used by permission.
form (RN), whereas Class D drugs exist in both charged only site at which molecules of local anesthetic have access
and uncharged forms. Approximately 90% of the blocking to the nerve membrane is at the nodes of Ranvier, where
effects of Class D drugs are caused by the cationic form of sodium channels are found in abundance. Ionic changes
the drug; only 10% of blocking action is produced by the that develop during impulse conduction arise only at the
base (Fig. 1-14). nodes.
Because an impulse may skip over or bypass one or two
Myelinated Nerve Fibers. One additional factor should blocked nodes and continue on its way, it is necessary for at
be considered with regard to the site of action of local least two or three nodes immediately adjacent to the anes
anesthetics in myelinated nerves. The myelin sheath insu thetic solution to be blocked to ensure effective anesthesia-a
lates the axon both electrically and pharmacologically. The length of approximately 8 to 10 mm.
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CHAPTER1 Neurophysiology 13
9•
(sodium channel)
\1 R-LA
Udocalne,
""""-... prllocalne,
"meplvacalne,
artlcalne,
buplvacaine
Axoplasm
Centruroides / "" Lelrus scorpion venom,
scorpion venom sea anemone venom
Figure 1-13. A, Tertiary amine local anesthetics inhibit the influx of sodium during nerve conduction by binding to a receptor within
the sodium channel (R-LA).This blocks the normal activation mechanism (O gate configuration, depolarization) and also promotes move
ment of the activation and inactivation gates (m and h) to a position resembling that in the inactivated state (I). B, Biotoxins (R-T) block
the influx of sodium at an outer surface receptor; various venoms do it by altering the activity of the activation and inactivation gates;and
benzocaine (R-B)does it by expanding the membrane. C, Channel in the closed configuration. (Redrawn from PallaschTJ: Dent Drug Serv
Newsletter4:25, 1983.)
Figure 1-14. Channel entry. On the left is an open channel, inward permeant to sodium ion. The center channel is in the resting closed
configuration;although impermeant to sodium ion here, the channel remains voltageresponsive.The channel on the right, although in open
configuration, is impermeant because it has local anesthetic cation bound to the gating receptor site. Note that local anesthetic enters the
channel from the axoplasmic (lower) side; the channel filter precludes direct entry via the external mouth. Local anesthetic renders the
membrane impermeant to sodium ion, hence inexcitableby local action currents. (Redrawn from de Jong RH: Local anesthetics, St Louis,
1994,Mosby.)
Sodium channel densities differ in myelinated and nerve membranes. For example, in the garfish olfactory
urunyelinated nerves. In small unmyelinated nerves, the nerve, the ratio of sodium channels to phospholipid
density of sodium channels is about 35/µm, whereas at molecules is 1:60,000, corresponding to a mean distance
the nodes of Ranvier in myelinated fibers, it may be as between channels of 0.2 µm, whereas at densely packed
high as 20,000/µm. On an averagenerve length basis, rela nodes of Ranvier, the channels are separated by only
tively few sodium channels are present in unmyelinated 70 A.21,2s
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14 PARTI The Drugs
Ra
i '
I : '
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CHAPTER 1 Neurophysiology 15
Procaine Lidocaine
Propoxycaine Etidocaine
CH3 , CH
I
I
/ 3
NHCOCH-:-N
I ; "\
~ "-------1...__
CH3 : :
Tetracaine Mepivacaine
Benzocaine Prilocaine
Dyclonine•
*Dyclonlne ls a ketone.
Figure 1-16. Chemical configuration of local anesthetics. (From Yagiela JA, Neid.le EA, Dowd FJ: Pharmacology and therapeutics for
dentistry, ed 6, St Louis, 2010, Mosby.)
It is wellknown that the pH of a local anesthetic solution manufacturer to inhibit oxidation of the vasopressor (p. 18).
(as well as the pH of the tissue into which it is injected) The pH of solutions without epinephrine is about 6.5;
greatly influencesits nerve-blockingaction. Acidificationof epinephrine-containing solutions have a pH of about 3.5.
tissue decreases local anesthetic effectiveness.Inadequate Clinically,this lower pH is more likelyto produce a burning
anesthesia results when local anesthetics are injected into sensation on injection, as well as a slightly slower onset of
inflamed or infected areas. The inflammatory process pro anesthesia.
duces acidic products: The pH of normal tissue is 7.4; the Elevating the pH (alkalinization) of a local anesthetic
pH of an inflamed area is 5 to 6. Localanestheticscontaining solution speedsits onset of action, increasesits clinicaleffec
epinephrine or other vasopressors are acidified by the tiveness,and makesits injection more comfortable.However,
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16 PART I The Drugs
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CHAPTER1 Neurophysiology 17
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18 PARTI The Drugs
presents a potential problem in all aspectsof dental practice, the drug provides more RN form, thereby increasing the
this situation is seen most often in endodontics. Possible potency of the topical anesthetic; however,the drug in this
remedies are described in Chapter 16. form is more rapidly oxidized.The effectiveshelf life of the
local anesthetic is decreased as the pH of the drug is
Clinical Implications of pH and Local increased.30
Anesthetic Activity To enhance the clinical efficacyof topical anesthetics, a
Most commercially prepared solutions of local anesthetics more concentrated form of the drug is commonly used (5%
without a vasoconstrictor have a pH between 5.5 and 7. or 10% lidocaine) than for injection (2% lidocaine).
When injected into tissue, the vast buffering capacity Although only a small percentage of the drug is availablein
of tissue fluids returns the pH at the injection site to a the base form, raising the concentration provides additional
normal 7.4. Local anesthetic solutions containing a vaso RN molecules for diffusion and dissociation to the active
pressor (e.g.,epinephrine) are acidifiedby the manufacturer cation form at free nerve endings.
through the addition of sodium (meta)bisulfite to retard Some topical anesthetics (e.g., benzocaine) are not
oxidation of the vasoconstrictor, thereby prolonging the ionized in solution; thus their anesthetic effectivenessis
period of effectivenessof the drug. (See Chapter 3 for a unaffected by pH. Because of the poor water solubility of
discussionof the appropriate use of vasoconstrictorsin local benzocaine, its absorption from the site of application is
anesthetics.) minimal, and systemic reactions (e.g., overdose) are rarely
Epinephrine may be added to a local anesthetic solution encountered.
immediately before its administration without the addition
of antioxidants;however,if the solution is not used in a short KINETICS OF LOCAL ANESTHETIC ONSET AND
time, it will oxidize,slowlyturning yellowthen brown (much DURATION OF ACTION
like a slicedapple oxidizing).
Rapid oxidation of the vasopressor may be delayed, Barriers to Diffusion of the Solution
thereby increasingthe shelf life of the product, through the A peripheral nerve is composed of hundreds to thousands
addition of antioxidants.Sodium bisulfitein a concentration of tightly packed axons. These axons are protected, sup
between 0.05% and 0.1% is commonly used. A 2% solution ported, and nourished by severallayersof fibrous and elastic
of lidocaine HCl, with a pH of 6.8, is acidifiedto 4.2 by the tissues. Nutrient blood vessels and lymphatics course
addition of sodium bisulfite. throughout the layers.
Evenin this situation, the enormous buffering capacityof Individual nerve fibers (axons) are coveredwith, and are
the tissues tends to maintain a normal tissue pH; however, separated from each other by, the endoneurium. The peri
it does require a longer time to do so after injection of a pH neurium then binds these nerve fiberstogether into bundles
4.2 solution than with a pH 6.8 solution. During this time, calledfasciculi. The radial nerve, located in the wrist, con
the local anesthetic is not ableto function at its full effective tains between 5 and 10 fasciculi. Each fasciculus contains
ness, resulting in a slower onset of clinical action for local between 500 and 1000individual nerve fibers.Fivethousand
anestheticswith vasoconstrictors compared with their plain nerve fibers occupy approximately 1 mm2 of space.
counterparts. The thickness of the perineurium varies with the
Localanestheticsare clinicallyeffectiveon both axonsand diameter of the fasciculusit surrounds. The thicker the peri
free nerve endings. Free nerve endings lying below intact neurium, the slower the rate of local anesthetic diffusion
skin may be reached only by injection of anesthetic beneath across it.37 The innermost layer of perineurium is the peri
the skin. Intact skin forms an impenetrable barrier to the lemma. It is coveredwith a smooth mesothelial membrane.
diffusion of local anesthetics. EMLA (eutectic mixture of The perilemma represents the main barrier to diffusion into
local anesthetics lidocaine and prilocaine) enables local a nerve.
anesthetics to penetrate intact skin, albeit slowly.35 Fasciculiare contained within a loose network of areolar
Mucous membranes and injured skin (e.g., burns, abra connective tissue called the epineurium. The epineurium
sions) lack the protection affordedby intact skin,permitting constitutes between 30% and 75% of the total cross-section
topicallyapplied localanestheticsto diffusethrough to reach of a nerve. Local anesthetics are readily able to diffuse
free nerve endings. Topical anesthetics can be employed through the epineurium because of its loose consistency.
effectivelywherever skin is no longer intact because of Nutrient blood vesselsand lymphatics traverse the epineu
injury, as well as on mucous membranes (e.g., cornea, rium. These vessels absorb local anesthetic molecules,
gingiva,pharynx, trachea, larynx, esophagus,rectum, vagina, removing them from the site of injection.
bladder).36 The outer layerof the epineurium surrounding the nerve
The buffering capacity of mucous membrane is poor; is denser and is thickened, forming what is termed the epi
thus topical application of a local anesthetic with a pH neural sheath or nerve sheath. The epineural sheath does not
between 5.5 and 6.5lowersthe regionalpH to below normal, constitute a barrier to diffusion of local anesthetic into a
and lesslocalanestheticbaseis formed. Diffusionof the drug nerve.
across the mucous membrane to free nerve endings is Table 1-5 summarizes the layers of a typical peripheral
limited, and nerve block is ineffective.Increasing the pH of nerve.
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CHAPTER 1 Neurophysiology 19
----- Solution
::.:.:~Corebundles
Mantle fibers
- - - - - - - - Epineuralsheath
A B
Figure 1-19. A, Composition of nerve fibers and bundles within a peripheral nerve. B, In a large peripheral nerve (containing hundreds
or thousands of axons), local anesthetic solution must diffuse inward toward the nerve core from the extraneural site of injection. Local
anesthetic molecules are removed by tissue uptake while tissue fluid mixes with the carrier solvent.This results in gradual dilution of the
local anesthetic solution as it penetrates the nerve toward the core.A concentration gradient occurs during induction so that the outer mantle
fibers are solidly blocked, whereas the inner core fibers are not yet blocked. Not only are core fibers exposed to a lower local anesthetic
concentration, but the drug arrives later. Delay depends on the tissue mass to be penetrated and the diffusivity of the local anesthetic.
(Redrawn from B, de Jong RH: Local anesthetics,St Louis, 1994,Mosby.)
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20 PARTI The Drugs
Blocking Process. After deposition of local anesthetic as to attach more securelyto the protein receptor sites and to
close to the nerve as possible, the solution diffuses in all possessa longer duration of clinical activity,"
directions according to prevailing concentration gradients. Vasoactivity affects both the anesthetic potency and the
A portion of the injected local anesthetic diffusestoward the duration of anesthesiaprovided by a drug. Injection of local
nerve and into the nerve. However,a significant portion of anesthetics,such as procaine,with greatervasodilatingprop
the injected drug also diffusesawayfrom the nerve.The fol erties increases perfusion of the local site with blood. The
lowing reactions then occur: injected local anesthetic is absorbed into the cardiovascular
1. Some of the drug is absorbed by nonneural tissues (e.g., compartment more rapidly and is carried away from the
muscle, fat). injection site and from the nerve,thus providing for a short
2. Some is diluted by interstitial fluid. ened duration of anesthesia,as well as decreasedpotency of
3. Some is removed by capillariesand lymphatics from the the drug. Table 1-7 summarizes the influence of various
injection site. factors on local anesthetic action.
4. Ester-type anesthetics are hydrolyzed.
The sum total effectof these factorsis to decreasethe local Recovery from Local Anesthetic Block
anesthetic concentration outside the nerve; however, the Emergence from a local anesthetic nerve block followsthe
concentration of local anesthetic within the nerve continues same diffusion patterns as induction; however,it does so in
to rise as diffusionprogresses.Theseprocessescontinue until the reverseorder.
an equilibrium results between intraneural and extraneural The extraneural concentration of local anesthetic is con
concentrations of anesthetic solution. tinually depleted by diffusion, dispersion, and uptake of the
drug, whereas the intraneural concentration of local anes
Induction Time. Induction time is defined as the period thetic remains relativelystable. The concentration gradient
from deposition of the anesthetic solution to complete con is reversed,the intraneural concentration exceedsthe extra
duction blockade. Severalfactors control the induction time neural concentration, and anesthetic molecules begin to
of a given drug. Those under the operator's control are the diffuse out of the nerve.
concentration of the drug and the pH of the local anesthetic Fasciculiin the mantle begin to lose the local anesthetic
solution. Factorsnot under the clinician'scontrol include the much sooner than do the core bundles. Local anesthetic
diffusion constant of the anesthetic drug and the anatomic within the core then diffusesinto the mantle, so that the first
diffusion barriers of the nerve. nerve fibers to entirely lose anesthesia are those centermost
in the nerve. Mantle fibers remain anesthetized the longest,
Physical Properties and Clinical Actions. Other physico and core fibers the shortest, time. Recoveryfrom anesthesia
chemicalfactors of a local anesthetic may influence its clini is a slower process than induction because the local anes
cal characteristics. thetic is bound to the drug receptor site in the sodium
The effectof the dissociation constant (pK,.)on the rate of channel and therefore is released more slowly than it is
onset of anesthesia has been described. Although both absorbed.
molecular forms of the anesthetic are important in neural
blockade,drugs with a lower pK,.possessa more rapid onset Readministration of Local Anesthetic
of action than those with a higher pK,..39 Occasionally a dental procedure outlasts the duration of
Lipid solubility of a local anesthetic appears to be related clinically effective pain control, and a repeat injection of
to its intrinsic potency. The estimated lipid solubilities of local anesthetic is necessary. Usually this repeat injection
various local anesthetics are presented in Table 1-6. Greater immediately results in a return of profound anesthesia. On
lipid solubilitypermits the anesthetic to penetrate the nerve someoccasions,however,the clinicianmayencounter greater
membrane (which itself is 90% lipid) more easily.This is difficultyin reestablishing adequate pain control with sub
reflectedbiologicallyin increased potency of the anesthetic. sequent injections.
Local anesthetics with greater lipid solubilityproduce more
effectiveconduction blockadeat lowerconcentrations (lower Recurrence of Immediate Profound Anesthesia. At the
percentage solutions or smaller volumes deposited) than is time of reinjection, the concentration of local anesthetic in
produced by less lipid-soluble local anesthetics. the core fibers is less than that in the mantle fibers.Partially
The degreeof protein binding of the local anesthetic mol recovered core fibers still contain some local anesthetic,
ecule is responsible for the duration of anesthetic activity. although not enough to provide complete anesthesia.After
Afterpenetration of the nerve sheath, a reequilibrium occurs deposition of a new high concentration of anesthetic near
between the base and cationic forms of the local anesthetic the nerve, the mantle fibers are once again exposed to a
according to the Henderson-Hasselbach equation. Now, in concentration gradient directed inward toward the nerve;
the sodium channel itself, RNH+ions bind at the receptor this eventually leads to an increased concentration in the
site. Proteins constitute approximately 10% of the nerve core fibers.This combination of residual local anesthetic (in
membrane, and local anesthetics (e.g., etidocaine, ropiva the nerve) and the newly deposited supply results in rapid
caine, bupivacaine) possessing a greater degree of protein onset of profound anesthesiaand administration of a smaller
binding (see Table 1-6) than others (e.g., procaine) appear volume of local anesthetic drug.
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CHAPTER 1 Neurophysiology 21
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CHAPTER 1 Neurophysiology 23
TABLE 1-7
Factors Affecting Local Anesthetic Action
Factor Action Affected Description
pK. Onset LowerpK. = More rapid onset of action, more RN moleculespresent to diffuse through
nerve sheath; thus onset time is decreased
Lipid solubility Anesthetic potency Increased lipid solubility= Increased potency (e.g.,procaine= 1; etidocaine = 140)
Etidocaine produces conduction blockade at very low concentrations, whereas procaine
poorly suppressesnerve conduction, even at higher concentrations
Protein binding Duration Increased protein binding allowsanesthetic cations (RNH') to be more firmly attached to
proteins located at receptor sites;thus duration of action is increased
Nonnervous tissue Onset Increased diffusibility= Decreasedtime of onset
diffusibility
Vasodilatoractivity Anesthetic potency Greater vasodilator activity= Increased blood flow to region = Rapid removal of anesthetic
and duration molecules from injection site; thus anesthetic potency and duration are decreased
From Cohen S, Burns RC: Pathways of the pulp, ed 6, St Louis, 1994, Mosby.
Difficulty Reachieving Profound Anesthesia. In this to increased protein binding, other factors that influence the
second situation, as in the first, the dental procedure has rate of removal of a drug from the injection site are the
outlasted the clinical effectiveness of the local anesthetic vascularity of the injection site and the presence or absence
drug, and the patient is experiencing pain. The doctor read of a vasoactive substance. Anesthetic duration is increased in
ministers a volume of local anesthetic, but unlike in the first areas of decreased vascularity (e.g., Gow-Gates mandibular
scenario, effective control of pain does not occur. nerve block vs. inferior alveolar nerve block), and the addi
Tachyphylaxis. In this second clinical situation, a process tion of a vasopressor decreases tissue perfusion to a local
known as tachyphylaxis occurs. Tachyphylaxis is defined as area, thus increasing the duration of the block.
increasing tolerance to a drug that is administered repeat
edly. It is much more likely to develop if nerve function is
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2. Bennett CR: Monheim's local anesthesia and pain control in
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24. Strichartz GR, Ritchie JM: The action of local anesthetics on 37. Noback CR, Demarest RJ: The human nervous system:
ion channels of excitabletissues.In Strichartz GR,editor: Local basic principles of neurobiology, ed 3, New York, 1981,
anesthetics,NewYork, 1987, Springer-Verlag. McGraw-Hill.
25. Butterworth JF IY, Strichartz GR: Molecular mechanisms of 38. de Jong RH: Local anesthetics, ed 2, Springfield, Ill, 1977,
local anesthesia:a review,Anesthesiology72:711-734, 1990. Charles C Thomas, pp 66--68.
26. Ritchie JM: Mechanisms of action of local anesthetic agents 39. RitchieJM,RitchieB,GreengardP: The activestructure oflocal
and biotoxins, Br J Anaesth 47:191-198, 1975. anesthetics,J Pharmacol Exp Ther 150:152, 1965.
27. RasminskyM: Conduction in normal and pathological nerve 40. TuckerGT:Plasmabinding and disposition oflocal anesthetics,
fibers.In SwashM, Kennard C, editors: Scientificbasis of clini Int AnesthesiolClin 13:33, 1975.
cal neurology,Edinburgh, 1985, Churchill Livingstone. 41. Cohen EN, LevineDA,CollissJE,Gunther RE:The role of pH
28. Ritchie JM: The distribution of sodium and potassium chan in the development of tachyphylaxisto local anesthetic agents,
nels in mammalian myelinatednerve.In RitchieJM,KeyesRD, Anesthesiology29:994--1001, 1968.
www.ShayanNemoodar.com
Pharmacology of Local
Anesthetics
Local anesthetics, when used for the management of pain, drug such as thiopental may produce arteriospasm with an
differ from most other drugs commonly used in medicine attendant decrease in tissue perfusion that if prolonged
and dentistry in one important manner. Virtually all other could lead to tissue death, gangrene,and loss of the affected
drugs, regardless of the route through which they are limb. In this situation, procaine is administered IA in an
administered, must ultimately enter into the circulatory attempt to break the arteriospasm and reestablishblood flow
systemin sufficientlyhigh concentrations (e.g.,attain thera to the affected limb. Tetracaine, chloroprocaine, and pro
peutic blood levelsin their target organ[s]) before they can poxycaine also possess vasodilating properties to varying
begin to exert a clinical action. Local anesthetics, however, degreesbut not to the degree of procaine.
when used for pain control, cease to provide a clinicaleffect Cocaine is the only local anesthetic that consistently
when they are absorbed from the site of administration into produces vasoconstriction.4 The initial action of cocaine
the circulation.One prime factor involvedin the termination is vasodilation followedby an intense and prolonged vaso
of action of local anesthetics used for pain control is their constriction. It is produced by inhibition of the uptake
redistribution from the nerve fiber into the cardiovascular of catecholamines (especially norepinephrine) into tissue
system. binding sites. This results in an excessof free norepineph
The presence of a local anesthetic in the circulatory rine, leading to a prolonged and intense state of vasocon
system means that the drug will be transported to every striction. This inhibition of the reuptake of norepinephrine
part of the body. Local anesthetics have the ability to alter has not been demonstrated with other local anesthetics,such
the functioning of some of these cells. In this chapter, the as lidocaine and bupivacaine.
actions of local anesthetics,other than their ability to block A significant clinical effect of vasodilation is an increase
conduction in nerve axonsof the peripheral nervous system, in the rate of absorption of the local anesthetic into the
are reviewed.A classificationof local anesthetics is shown in blood, thus decreasingthe duration and quality (e.g.,depth)
Box 2-1. of pain control, while increasing the anesthetic blood (or
plasma) concentration and its potential for overdose (toxic
PHARMACOKINETICS OF LOCAL ANESTHETICS reaction). The rates at which local anesthetics are absorbed
into the bloodstream and reach their peak blood level vary
Uptake according to the route of administration (Table2-2).
When injected into soft tissues,local anesthetics exert phar
macologicaction on blood vesselsin the area.Alllocal anes Oral Route. With the exceptionof cocaine,local anesthetics
thetics possess a degree of vasoactivity, most producing are absorbed poorly, if at all, from the gastrointestinal tract
dilation of the vascular bed into which they are deposited, after oral administration. In addition, most local anesthetics
although the degreeof vasodilation may vary,and some may (especiallylidocaine) undergo a significanthepatic first-pass
produce vasoconstriction.To some degree,these effectsmay effectafter oral administration. Afterabsorption of lidocaine
be concentration dependent.1 Relativevasodilatingvalues of from the gastrointestinaltract into the enterohepatic circula
amide local anesthetics are shown in Table2-1. tion, a fraction of the drug dose is carried to the liver,where
Ester local anesthetics are also potent vasodilating drugs. approximately72% of the dose is biotransformed into inac
Procaine,the most potent vasodilator among local anesthet tive metabolites.5 This has seriously hampered the use of
ics, is occasionallyinjected clinicallyto induce vasodilation lidocaine as an oral antidysrhythmic drug. In 1984,Astra
when peripheral blood flowhas been compromised because Pharmaceuticals and Merck Sharp & Dohme introduced an
of (accidental) intra-arterial (IA) injection of a drug (e.g., analog of lidocaine,tocainide hydrochloride,which is effec
thiopental)2 or injection of epinephrine or norepinephrine tive orally.6 The chemical structures of tocainide and lido
into a fingertip or toe.3 IA administration of an irritating caine are presented in Figure 2-1.
25
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26 PARTI The Drugs
Amides
Articaine
Bupivacaine
CH3
Dibucaine
Etidocaine
Lidocaine
Mepivacaine
Prilocaine
Q
B
CH3
NHCOCHCH3 • HCI
I
NH2
Ropivacaine
Figure 2-1. Tocainide. A, Represents a modification of lidocaine
(B) that is able to pass through the liver after oral administration
Quinoline with minimal hepatic first-pass effect.
Centbucridine
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CHAPTER2 Pharmacology of LocalAnesthetics 27
Fat Slow
equilibrium
space
Muscle
Elimination
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28 PARTI The Drugs
c
/~
Q fall, and spontaneous respiration resumes. Persons with
atypical pseudocholinesterase are unable to hydrolyze sue
cinylcholineat a normal rate;thereforethe duration of apnea
is prolonged. Atypical pseudocholinesterase is a hereditary
OH trait. Any familial history of difficultyduring general anes
thesia should be carefully evaluated by the doctor before
dental care commences.A confirmed or strongly suspected
Plasma history, in the patient or biological family,of atypical pseu
PsChE docholinesterase represents a relative contraindication to
administration of ester-type local anesthetics.
There are absolute and relative contraindications to
OH
the administration of drugs. An absolute contraindication
I implies that under no circumstance should the drug in
CH2 question be administered to this patient because the possi
I bility of potentially toxic or lethal reactions is increased,
CH2
I whereas a relative contraindication means that the drug in
/N"\. question may be administered to the patient after careful
C2Hs C2Hs weighing of the risk associatedwith use of the drug versus
Figure 2-3. Metabolic hydrolysis of procaine. PsChE, Pseudo the potential benefit to be gained, and if an acceptable
cholinesterase. (From Tucker GT: Biotransformation and toxicity alternative drug is not available. However, the smallest
of local anesthetics, Acta Anaesthesiol Belg 26[Suppl]: 123, 1975.) clinically effectivedose alwaysshould be used because the
likelihood of adverse reaction to this drug is increased in
this patient.
the blood through the processes of tissue uptake and
metabolism. Amide Local Anesthetics. The biotransformation of amide
local anesthetics is more complex than that of the esters.
Ester Local Anesthetics. Ester local anesthetics are hydro The primary site of biotransformation of amide local anes
lyzed in the plasma by the enzyme pseudocholinesterase." thetics is the liver. Virtually the entire metabolic process
The rate at which hydrolysisof different esters occurs varies occurs in the liver for lidocaine, mepivacaine, etidocaine,
considerably (Table 2-5). and bupivacaine.Prilocaine undergoes primary metabolism
The rate of hydrolysis has an impact on the potential in the liver, with some also possibly occurring in the
toxicity* of a local anesthetic. Chloroprocaine, the most lung.12·13Articaine, a hybrid molecule containing both ester
rapidly hydrolyzed, is the least toxic, whereas tetracaine, and amide components, undergoes metabolism in both the
hydrolyzed 16 times more slowlythan chloroprocaine, has blood and the liver.14
the greatestpotential toxicity.Procaine undergoes hydrolysis The rates ofbiotransformation oflidocaine, mepivacaine,
to para-aminobenzoic acid (PABA), which is excreted etidocaine,and bupivacaineare similar.Thereforeliverfunc
unchanged in the urine, and to diethylamine alcohol,which tion and hepatic perfusion significantlyinfluence the rate of
undergoes further biotransformation before excretion (Fig. biotransformation of an amide local anesthetic. Approxi
2-3). Allergicreactions that occur in response to ester local mately 70% of a dose of injected lidocaine undergoes bio
anesthetics usually are not related to the parent compound transformation in patients with normal liver function.5
(e.g.,procaine) but rather to PABA,which is a major meta Patients with lower than usual hepatic blood flow (hypo
bolic product of many ester local anesthetics. tension, congestive heart failure) or poor liver function
(cirrhosis) are unable to biotransform amide local anes
*All chemicals (drugs) have the potential to be poisons, also called toxins.
thetics at a normal rate.15•16 This slower than normal bio
When the resulting blood level is too high, drugs exert negative actions, transformation rate results in higher anesthetic blood levels
which we call a toxic reaction or overdose. and increased risk of toxicity. Significant liver dysfunction
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CHAPTER 2 Pharmacology of LocalAnesthetics 29
AMIDES
t t t t t t t t t
dibucaine lidocaine mepivacaine prilocainebupivacaineetidocaine articaine ropivacainelevobupivacaine
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30 PARTI The Drugs
Conjugates
HO t .CH3
/C2H5
NH• CO• CH2N
3-Hydroxy-lidocaine (1.1)
Lidocaine
Monoethylglycinexylidide (3.7)
~ CH,~ \CH,
Conjugates_. _
~NH, ~NHCO•CH,NH,
CH3 CH3
2.6-Xylidide(1.0) Glycinexylidide(2.3)
Cooj- ~ HO~NH,
J, ~r ~NH,
CH~ 1
CH3 COOH
4-Hydroxy-2,6-dimethylaniline 2-Amino-3-methylbenzoicacid
(72.6)
Figure 2-4. Metabolic pathways of lidocaine. Percentages of dose found in urine are indicated in parentheses. (From Kennaghan JB,
BoyesRN: The tissue distribution, metabolism, and excretion of lidocaine in rats, guinea pigs, dogs and man, J Pharmacol Exp Ther Feb
180(2):454-463, 1972.)
Local anesthetics are absorbed from their site of admin existsa spectrum of other clinicalsigns and symptoms. (See
istration into the circulatorysystem,which effectivelydilutes Box 2-2, "Preconvulsive Signs and Symptoms of Central
them and carries them to all cellsof the body. The ensuing Nervous Toxicity.")
blood level of the local anesthetic depends on its rate of
uptake from the site of administration into the circulatory Anticonvulsant Properties. Some local anesthetics (e.g.,
system (increasingthe blood level),and on the rates of dis procaine, lidocaine, mepivacaine, prilocaine, even cocaine)
tribution in tissue and biotransformation (in the liver),pro have demonstrated anticonvulsant properties.P'" These
cessesthat remove the drug from the blood (decreasingthe occur at a blood level considerablybelow that at which the
blood level) (see Fig.2-2). same drugs produce seizure activity.Valuesfor anticonvul
siveblood levelsoflidocaine are shown in Table2-7.25
Procaine, mepivacaine, and lidocaine have been used
Central Nervous System intravenouslyto terminate or decreasethe duration of both
Localanestheticsreadilycrossthe blood-brain barrier. Their grand mal and petit mal seizures.23'26 The anticonvulsant
pharmacologic action on the CNS is seen as depression.At blood level of lidocaine (about 0.5 to 4 µg/mL) is very
low (therapeutic, nontoxic) blood levels,no CNS effectsof close to its cardiotherapeutic range (see following). It has
any clinical significancehave been noted. At higher (toxic, been demonstrated to be effectivein temporarily arresting
overdose)levels,the primary clinicalmanifestation is a gen seizure activity in a majority of human epileptic patients.27
eralizedtonic-clonic convulsion.Betweenthesetwo extremes It was especiallyeffectivein interrupting status epilepticus
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CHAPTER2 Pharmacology of LocalAnesthetics 31
TABLE 2-7
Anticonvulsive Blood Levels of Lidocaine
Lidocaine Blood
Clinical Situation Level, µg/ml
Prilocaine (0.16)
Anticonvulsivelevel 0.5-4
Preseizuresigns and symptoms 4.5-7
Tonic-clonic seizure >7.5
CH3
at therapeutic doses of 2 to 3 mg/kg when given at a rate of
@- NH2 + HOOC • CH • N
I
/C3H7
CH3
"-H
40 to 50 mg/min.
Mechanism of Anticonvulsant Properties. Epileptic
patients possess hyperexcitable cortical neurons at a site
o-Toluidine n-Propylalanine within the brain where the convulsive episode originates
(0.69) (called the epileptic focus). Local anesthetics, by virtue of
t their depressant actions on the CNS,raisethe seizurethresh
[@:~~l
old by decreasing the excitabilityof these neurons, thereby
preventing or terminating seizures.
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32 PART I The Drugs
the U.S. Air Force and the U.S. Navy ground airplane pilots
TABLE 2-8
for 24 hours after receipt of a local anesthetic."
Sedation may develop in place of the excitatory signs. If
Effects of pC02 on the Convulsive Threshold {CD100) of
excitation or sedation is observed during the first 5 to 10
Various Local Anesthetics in Cats
minutes after intraoral administration of a local anesthetic, CD100. mg/kg Percent
it should serve as a warning to the clinician of a rising local pC02 pC02 Change
anesthetic blood level and the possibility (if the blood level Agent (25-40 torr) (6581 torr) in CD,oo
continues to rise) of a more serious reaction, including a Procaine 35 17 51
generalized convulsive episode. Mepivacaine 18 10 44
Prilocaine 22 12 45
Convulsive Phase. Further elevation of the local anesthetic Lidocaine 15 7 53
blood level leads to signs and symptoms consistent with a Bupivacaine 5 2.5 50
generalized tonic-donic convulsive episode. The duration of Data from EnglessonS, Grevsten S, Olin A: Some numerical methods
seizure activity is related to the local anesthetic blood level of estimating acid-basevariables in normal human blood with a
and is inversely related to the arterial partial pressure of haemoglobin concentration of 5 g/100 cm', Scand J Lab Clin Invest
carbon dioxide (pC02) level.31 At a normal pC02, a lidocaine 32:289-295, 1973.
blood level between 7.5 and 10 µg/mL usually results in a
convulsive episode. When carbon dioxide (C02) levels are
increased, the blood level of local anesthetic necessary for TABLE 2-9
seizures decreases while the duration of the seizure increases. 31 Convulsant Dose {CD100) and Acid-Base Status*
Seizure activity generally is self-limiting, because cardiovas pH 7.10 pH 7.20 pH 7.30 pH 7.40
cular activity usually is not significantly impaired, and redis
pC02 30 27.5 26.6
tribution and biotransformation of the local anesthetic
pC0240 20.6 21.4 22.0
continue throughout the episode. This results in a decrease
pC02 60 13.1 15.4 17.5
in anesthetic blood level and termination of seizure activity, 11.3 14.3
pC02 80
usually within I minute.
However, several other mechanisms also at work unfor From EnglessonS:The influence of acid-base changes on central nervous
toxicity of local anaesthetic agents,ActaAnaesthesiolScand 18:88-103,
tunately act to prolong the convulsive episode. Both cerebral 1974.
blood flow and cerebral metabolism are increased during *Intravenouslidocaine 5 mg/kg/min, cats; doses in mg/kg.
local anesthetic-induced convulsions. Increased blood flow
to the brain leads to an increase in the volume of local
anesthetic being delivered to the brain, tending to prolong convulsions) through selective blockade of inhibitory path
the seizure. Increased cerebral metabolism leads to a pro ways in the cerebral cortex.32-35 de Jong states that "inhibition
gressive metabolic acidosis as the seizure continues, and of inhibition thus is a presynaptic event that follows local
this tends to prolong the seizure activity (by lowering the anesthetic blockade of impulses traveling along inhibitory
blood level of anesthetic necessary to provoke a seizure), pathways."36
even in the presence of a declining local anesthetic level in The cerebral cortex has pathways of neurons that are
the blood. As noted in Tables 2-8 and 2-9, the dose of local essentially inhibitory and others that are facilitatory (excit
anesthetic necessary to induce seizures is markedly dimin atory). A state of balance normally is maintained between
ished in the presence of hypercarbia (see Table 2-8) or the degrees of effect exerted by these neuronal paths (Fig.
acidosis (see Table 2-9).31'32 2-6). At preconvulsant local anesthetic blood levels, observed
Further increases in local anesthetic blood level result clinical signs and symptoms are produced because the local
in cessation of seizure activity as electroencephalographic anesthetic selectively depresses the action of inhibitory
(EEG) tracings become flattened, indicative of a generalized neurons (Fig. 2-7). Balance then is tipped slightly in favor of
CNS depression. Respiratory depression occurs at this time, excessive facilitatory (excitatory) input, leading to symptoms
eventually leading to respiratory arrest if anesthetic blood of tremor and slight agitation.
levels continue to rise. Respiratory effects are a result of the At higher (convulsive) blood levels, inhibitory neuron
depressant action of the local anesthetic drug on the CNS. function is completely depressed, allowing unopposed func
Mechanism of Preconvulsant and Convulsant Actions. tion of facilitatory neurons (Fig. 2-8). Pure facilitatory input
It is known that local anesthetics exert a depressant action without inhibition produces the tonic-clonic activity
on excitable membranes, yet the primary clinical manifesta observed at these levels.
tion associated with high local anesthetic blood levels is Further increases in anesthetic blood level lead to depres
related to varying degrees of stimulation. How can a drug sion of the facilitatory and inhibitory pathways, producing
that depresses the CNS be responsible for the production of generalized CNS depression (Fig. 2-9). The precise site of
varying degrees of stimulation, including tonic-clonic action of the local anesthetic within the CNS is not known
seizure activity? It is thought that local anesthetics produce but is thought to be at the inhibitory cortical synapses or
clinical signs and symptoms of CNS excitation (including directly on the inhibitory cortical neurons.
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CHAPTER2 Pharmacology of LocalAnesthetics 33
Figure 2-6. Balancebetween inhibitory and facilitatoryimpulses Figure 2-8. In the convulsivestageoflocal anesthetic action, the
in a normal cerebral cortex. inhibitory impulse is totally depressed,permitting unopposed facil
itatory impulse activity.
~
I
x
I ''
Figure 2- 7. In the preconvulsivestage oflocal anesthetic action, Figure 2-9. In the final stage of local anesthetic action, both
the inhibitory impulse is more profoundly depressed than the inhibitory and facilitatory impulses are totally depressed,produc
facilitatory impulse. ing generalizedcentral nervous system depression.
Analgesia. Localanestheticspossessa second action in rela despite documentation of both catastrophic events (mood
tion to the CNS.Administered intravenously,they increase elevation) and lack of effect (rejuvenation).
the pain reaction threshold and also produce a degree of Cocainehas long been used for its euphoria-inducing and
analgesia. fatigue-lesseningactions, dating back to the chewingof coca
In the 1940sand 1950s,procaine was administered intra leavesby Incas and other South American natives.38.39 Unfor
venouslyfor the management of chronic pain and arthritis.37 tunately, as is well documented today, prolonged use of
The "procaine unit" was commonly used for this purpose; it cocaineleadsto habituation. William StewartHalsted (1852-
consisted of 4 mg/kg of body weight administered over 20 1922), the father of American surgery, cocaine researcher,
minutes. The technique was ineffective for acute pain. and the first person to administer a local anestheticby injec
Becauseof the relativelynarrow safety margin between the tion, sufferedgreatlybecause of an addiction to cocaine." In
analgesicactions of procaine and the occurrence of signsand more recent times, the sudden, unexpected deaths of several
symptoms of overdose, this technique is no longer in use prominent professional athletes caused by cocaine and the
today. addiction of many others clearly demonstrate the dangers
involvedin the casual use of potent drugs.41•42
Mood Elevation. The use of local anesthetic drugs for More benign, but totally unsubstantiated, is the use
mood elevationand rejuvenation has persistedfor centuries, of procaine (Novocain) as a rejuvenating drug. Clinics
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34 PARTI The Drugs
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CHAPTER 2 Pharmacology of LocalAnesthetics 35
TABLE 2-11
Peak Plasma Levels Following Local Anesthetic Administration With and Without Vasopressor
Injection Site Anesthetic Dose, mg Epinephrine Dilution Peak Level, µg/mL
Infiltration Lidocaine 400 None 2.0
Infiltration Lidocaine 400 1:200,000 1.0
Intercostal Lidocaine 400 None 6.5
Intercostal Lidocaine 400 1:200,000 5.3
Intercostal Lidocaine 400 1:80,000 4.9
Infiltration Mepivacaine 5mg/kg None 1.2
Infiltration Mepivacaine 5mg/kg 1:200,000 0.7
Data from Kopacz DJ, Carpenter RL, Mackay DL: Effect of ropivacaine on cutaneous capillary flow in pigs, Anesthesiology 71:69, 1989; Scott DB, et al:
Factors affecting plasma levels of lignocaine and prilocaine, Br J Anaesth 44:1040-1049, 1972; Duhner KG, et al: Blood levels of mepivacaine after regional
anaesthesia, Br J Anaesth 37:746-752, 1965.
blood levels are reached. The usual sequence of local 4. At lethal levels,cardiovascularcollapseis noted. This is
anesthetic-induced actions on the cardiovascular system is caused by massiveperipheral vasodilation and decreased
as follows: myocardial contractility and heart rate (sinus
1. At nonoverdose levels,a slight increase or no change in bradycardia).
blood pressure occurs because of increased cardiac 5. Certain local anesthetics such as bupivacaine (and
output and heart rate as a result of enhanced to a lesser degree ropivacaineand etidocaine) may
sympathetic activity; direct vasoconstriction of certain precipitate potentially fatal ventricular fibrillation.62•63
peripheral vascular beds is also noted.
2. At levelsapproaching yet still below overdose,a mild Local Tissue Toxicity
degree of hypotension is noted; this is produced by a Skeletal muscle appears to be more sensitive than other
direct relaxant action on the vascular smooth muscle. tissues to the local irritant properties of local anesthetics.
3. At overdoselevels,profound hypotension is caused by Intramuscular and intraoral injection of articaine,lidocaine,
decreasedmyocardial contractility,cardiac output, and mepivacaine, prilocaine, bupivacaine, and etidocaine can
peripheral resistance. produce skeletal muscle alterations.v'"" It appears that
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36 PARTI The Drugs
longer-acting local anesthetics cause more localized skeletal be absolutely contraindicated in MR-susceptible patients. 68
muscle damage than shorter-acting drugs. The changes that The Malignant Hyperthermia Association of the United
occur in skeletal muscle are reversible, with muscle regenera States (MHAUS), after evaluating recent clinical research,
tion being complete within 2 weeks after local anesthetic concluded that in fact no documented cases in the
administration. These muscle changes have not been associ medical or dental literature (over the past 30 years) support
ated with any overt clinical signs of local irritation. the concept of amide anesthetics triggering malignant
hyperthermia. 69-73
Respiratory System MHAUS maintains a Website with information for both
Local anesthetics exert a dual effect on respiration. At non health care providers and patients: www.mhaus.org.
overdose levels, they have a direct relaxant action on bron
chial smooth muscle, whereas at overdose levels, they may References
produce respiratory arrest as a result of generalized CNS 1. Aps C, ReynoldsF: The effectof concentration in vasoactivity
depression. In general, respiratory function is unaffected by of bupivacaine and lignocaine, Br J Anaesth 48:1171-1174,
local anesthetics until near-overdose levels are achieved. 1976.
2. Covino BG: Pharmacology of local anaesthetic agents, Br J
Miscellaneous Actions Anaesth 58:701-716, 1986.
Neuromuscular Blockade. Many local anesthetics have 3. U.S.Food and Drug Administration: Center for Drug Evalua
tion and Research:Approvalletter for phentolamine mesylate,
been demonstrated to block neuromuscular transmission in
1998.Availableat: www.fda.gov/cder/foi/anda/98/40235ap.pdf.
humans. This is a result of the inhibition of sodium diffusion
AccessedNovember 6, 2007.
through a blockade of sodium channels in the cell mem 4. BenowitzNL:Clinicalpharmacologyand toxicologyof cocaine,
brane. This action normally is slight and usually is clinically Pharmacol Toxicol72:1-12, 1993.
insignificant. On occasion, however, it can be additive to that 5. Arthur GR:Pharmacokineticsoflocal anesthetics.In Strichartz
produced by both depolarizing (e.g., succinylcholine) and GR,editor: Localanesthetics:handbook of experimentalphar
nondepolarizing (e.g., atracurium, vecuronium) muscle macology,vol 81, Berlin, 1987,Springer-Verlag.
relaxants; this may lead to abnormally prolonged periods of 6. Hohnloser SH, Lange HW, Raeder E, et al: Short- and long
muscle paralysis. Such actions are unlikely to occur in the term therapy with tocainide for malignant ventricular tachyar
dental outpatient. rhythmias, Circulation 73:143-149, 1986.
7. Soliman IE, Broadman LM, Hannallah RS,McGillWA:Com
parison of the analgesiceffectsof EMLA(eutectic mixture of
Drug Interactions. In general, CNS depressants (e.g.,
local anesthetics) to intradermal lidocaine infiltration prior to
opioids, antianxiety drugs, phenothiazines, barbiturates),
venous cannulation in unpremedicated children, Anesthesiol
when administered in conjunction with local anesthetics, ogy 68:804--806,1988.
lead to potentiation of the CNS-depressant actions of the 8. American Heart Association:ACLSprovider manual, Dallas,
local anesthetic. The conjoint use of local anesthetics and Tex,2001,American Heart Association,pp 83-84.
drugs that share a common metabolic pathway can produce 9. Haugh KH:Antidysrhythmic agents at the turn of the twenty
adverse reactions. Both ester local anesthetics and the depo first century: a current review,Crit Care Nursing Clin North
larizing muscle relaxant succinylcholine require plasma Am 14:13-69,2002.
pseudocholinesterase for hydrolysis. Prolonged apnea may 10. KalowW: Hydrolysisof local anestheticsby human serum cho
result from concomitant use of these drugs. linesterase,J Pharmacol Exp Ther 104:122-134,1952.
Drugs that induce the production of hepatic microsomal 11. Watson CB: Respiratory complications associated with anes
thesia, Anesth Clin North Am 20:375--399,2002.
enzymes (e.g., barbiturates) may alter the rate at which
12. Harris WH, Cole DW, Mital M, Laver MB: Methemoglobin
amide local anesthetics are metabolized. Increased hepatic
formation and oxygentransport followingintravenous regional
microsomal enzyme induction increases the rate of metabo anesthesia using prilocaine, Anesthesiology29:65, 1968.
lism of the local anesthetic. 13. Arthur GR: Distribution and elimination of local anesthetic
Specific drug-drug interactions related to the administra agents: the role of the lung, liver, and kidneys, PhD thesis,
tion oflocal anesthetics are reviewed in Chapter 10. Edinburgh, 1981,Universityof Edinburgh.
14. Oertel R, Berndt A. Kirch W: Saturable in vitro metabolism
Malignant Hyperthermia. Malignant hyperthermia (MH; of articaine by serum esterases:does it contribute to the resis
hyperpyrexia) is a pharmacogenic disorder in which a genetic tance of the local anesthetic effect? Reg Anesth 21:576-581,
variant in an individual alters that person's response to 1996.
certain drugs. Acute clinical manifestations of MH include 15. Nation RL,TriggsEJ:Lidocainekineticsin cardiacpatients and
aged subjects,Br J Clin Pharmacol 4:439--448,1977.
tachycardia, tachypnea, unstable blood pressure, cyanosis,
16. Thomson PD, Melmon KL, Richardson JA. et al: Lidocaine
respiratory and metabolic acidosis, fever (as high as 42° C
pharmacokinetics in advanced heart failure, liver disease,and
[108° F] or more), muscle rigidity, and death. Mortality renal failure in humans, Ann Intern Med 78:499-508, 1973.
ranges from 63% to 73%. Many commonly used anesthetic 17. Oertel R, Rahn R, KirchW: Clinicalpharmacokinetics of artic
drugs can trigger MH in certain individuals. aine, Clin Pharmacokinet 33:617--625,1997.
Until recently, the amide local anesthetics were thought 18. Prilocaine-induced methemoglobinemia-Wisconsin, 1993,
to be capable of provoking MH and were considered to MMWR Morb Mortal Wkly Rep 43:3555-3557,1994.
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CHAPTER 2 Pharmacologyof LocalAnesthetics 37
19. Wilburn-Goo D, Lloyd LM: When patients become cyanotic: 42. Harriston K, Jenkins S: Maryland basketball star Len Bias is
acquired methemoglobinemia, J Am Dent Assoc 130:626--631, dead at 22. Washington Post, 20 June 1986.
1999. 43. de Jong RH: Local anesthetics, ed 2, Springfield, Ill, 1977,
20. Strong JM, Parker M, Atkinson AJ Jr: Identification of glycinex Charles C Thomas, p 89.
ylidide in patients treated with intravenous lidocaine, Clin 44. Scott DB: Toxicity caused by local anaesthetic drugs, Br J
Pharmacol Ther 14:67-72, 1973. Anaesth 53:553-554, 1981.
21. Gupta PP, Tangri AN, Saxena RC, Dhawan BN: Clinical phar 45. Pinter A, Dorian P: Intravenous anti.arrhythmic agents, Curr
macology studies on 4-N-butylamino-1,2,3,4,-tetrahydroacri Opin Cardiol 16:17-22, 2001.
dine hydrochloride (Centbucridine), a new local anaesthetic 46. Sugi K: Pharmacological restoration and maintenance of sinus
agent, Indian J Exp Biol 20:344-346, 1982. rhythm by antiarrhythmic agents, J Cardiol 33(Suppl 1):59--64,
22. Vacharajani GN, Parikh N, Paul T, Satoskar RS: A comparative 1999.
study of Centbucridine and lidocaine in dental extraction, Int 47. Alexander JH, Granger CB, Sadowski Z, et al: Prophylactic
J Clin Pharmacol Res 3:251-255, 1983. lidocaine use in acute myocardial infarction: incidence and
23. Bernhard CG, Bohm E: Local anaesthetics as anticonvulsants: outcomes from two international trials. The GUSTO-I and
a study on experimental and clinical epilepsy, Stockholm, 1965, GUSTO-lib Investigators, Am Heart J 137:599-805, 1999.
Almqvist & Wiksell. 48. Cannom DS, Prystowsky EN: Management of ventricular
24. Bernhard CG, Bohm E, Wiesel T: On the evaluation of the arrhythmias: detection, drugs, and devices, JAMA 281:272-
anti.convulsive effect of different local anesthetics, Arch Int 279, 1999.
Pharmacodyn Ther 108:392-407, 1956. 49. Tan HL, Lie KI: Prophylactic lidocaine use in acute myocardial
25. Julien RM: Lldocaine in experimental epilepsy: correlation of infarction revisited in the thrombolytic era, Am Heart J
anticonvulsant effect with blood concentrations, Electroen 137:570-573, 1999.
cephalogr Clin Neurophysiol 34:639--645, 1973. 50. Kowey PR: An overview of antiarrhythmic drug management
26. Berry CA, Sanner JH, Keasling HH: A comparison of the anti of electrical storm, Can J Cardiol 12(Suppl B):3B-8B; discus
convulsant activity of mepivacaine and lidocaine, J Pharmacol sion 27B-28B, 1996.
Exp Ther 133:357-363, 1961. 51. Slavik RS, Tisdale JE, Borzak S: Pharmacologic conversion of
27. Walker IA, Slovis CM: Lidocaine in the treatment of status atrial fibrillation: a systematic review of available evidence,
epilepticus, Acad Emerg Med 4:918--922, 1997. Prog Cardiovasc Dis 44:221-252, 2001.
28. Chen AH: Toxicity and allergy to local anesthesia, J Calif Dent 52. Lalka D, Meyer MB, Duce BR, Elvin AT: Kinetics of the oral
Assoc 26:983--992, 1998. antiarrhythmic lidocaine congener, tocainide, Clin Pharmacol
29. Katz J, Feldman MA, Bass EB, et al: Injectable versus topical Ther 19:757-766, 1976.
anesthesia for cataract surgery: patient perceptions of pain and 53. Perlow GM, Jain BP, Pauker SC, et al: Tocainide-associated
side effects: the Study of Medical Testing for Cataract Surgery interstitial pneumonitis, Ann Intern Med 94(4 Pt 1):489-490,
Study Team, Ophthalmology 107:2054-2060, 2000. 1981.
30. Bureau of Medicine and Surgery. Available at: http:// 54. Volosin K, Greenberg RM, Greenspon AJ: Tocainide associated
navymedicine.med.navy.mil/. Accessed October 28, 2011. agranulocytosis, Am Heart J 109:1392, 1985.
31. Englesson S: The influence of acid-base changes on central 55. Bronheim D, Thys DM: Cardiovascular drugs. In Longnecker
nervous system toxicity of local anesthetic agents. I. An experi DE, Tinker JH, Morgan GE Jr, editors: Principles and practice
mental study in cats, Acta Anaesthesiol Scand 18:79, 1974. of anesthesiology, ed 2, St Louis, 1998, Mosby.
32. Englesson S, Grevsten S, Olin A; Some numerical methods of 56. Kudenchuk PJ: Advanced cardiac life support antiarrhythmic
estimating acid-base variables in normal human blood with a drugs, Cardiol Clin 20:19-87, 2002.
haemoglobin concentration of 5 g-100 cm3, Scand J Lab Clin 57. American Heart Association: Guidelines 2000 for cardiopul
Invest 32:289-295, 1973. monary resuscitation and emergency cardiovascular care,
33. de Jong RH, Robles R, Corbin RW: Central actions oflidocaine Circulation 102:8--149, 2000.
synaptic transmission, Anesthesiology 30:19, 1969. 58. Kopacz DJ, Carpenter RL, MacKay DL: Effect of ropivacaine
34. Huffman RD, Yun GKW: Effects of diphenylaminoethanol and on cutaneous capillary flow in pigs, Anesthesiology 71:69,
lidocaine on central inhibition, Int J Neuropharmacol 8:217, 1989.
1969. 59. Scott DB, Jebson PJR, Braid DP, et al: Factors affecting plasma
35. Tanaka K, Yamasaki M: Blocking of cortical inhibitory synapses levels oflignocaine and prilocaine, Br J Anaesth 44:1040-1049,
by intravenous lidocaine, Nature 209:207, 1966. 1972.
36. de Jong RH: Local anesthetics, St Louis, 1994, Mosby. 60. Duhner KG, Harthon JGL, Hebring BG, Lie T: Blood levels of
37. Graubard DJ, Peterson MC: Clinical uses of intravenous pro mepivacaine after regional anaesthesia, Br J Anaesth 37:746-
caine, Springfield, Ill, 1950, Charles C Thomas. 752, 1965.
38. Garcilasso de la Vega: Commentarios reales de los Incas (1609- 61. Kimmey JR, Steinhaus JE: Cardiovascular effects of procaine
1617). In Freud S, editor: Uber coca, Wien, 1884, Verlag von and lidocaine (Xylocaine) during general anesthesia, Acta
Moritz Perles. Anaesthesiol Scand 3:9-15, 1959.
39. Disertacion sobre el aspecto, cultivo, comercio y virtudes de la 62. de Jong RH, Ronfeld R, DeRosa R: Cardiovascular effects of
famosa planta del Peru nombrado coca: Lima, 1794. In Freud convulsant and supraconvulsant doses of amide local anesthet
S, editor: Uber coca, Wien, 1884, Verlag von Moritz Perles. ics, Anesth Analg 61:3, 1982.
40. Olch PD, William S: Halsted and local anesthesia: contribu 63. Feldman HS, Arthur GR, Covino BG: Comparative systemic
tions and complications, Anesthesiology 42:479-486, 1975. toxicity of convulsant and supraconvulsant doses of intrave
41. Preboth M: Cocaine abuse among athletes, Am Fam Physician nous ropivacaine, bupivacaine and lidocaine in the conscious
62:1850-2000, 1915. dog, Anesth Analg 69:794, 1989.
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38 PARTI The Drugs
64. Zink W, Graf BM, Sinner B, et al: Differential effects of 69. Gielen M, Viering W: 3-in-1 lumbar plexus block for muscle
bupivacaine on intracellular ea2+ regulation: potential mecha biopsy in malignant hyperthermia patients: amide local anaes
nisms of its myotoxicity,Anesthesiology97:710-716,2002. thetics maybe used safely,ActaAnaesthesiolScand30:581-583,
65. Irwin W,Fontaine E,AgnolucciL,et al: Bupivacainemyotoxic 1986.
ity ismediated by mitochondria, J BiolChem 277:12221-12227, 70. Ording H: Incidence of malignant hyperthermia in Denmark,
2002. Anesth Analg 64:700-704, 1985.
66. Benoit PW, YagielaJA, Fort NF: Pharmacologic correlation 71. Paasuke PT, Brownell AKW: Amine local anaesthetics and
between local anesthetic-induced myotoxicity and distur malignant hyperthermia (editorial),Can AnaesthSocJ 33:126-
bances of intracellularcalciumdistribution, ToxicolAppl Phar 129, 1986.
macol 52:187-198, 1980. 72. JastakJT,YagielaJA,Donaldson D: Localanesthesia of the oral
67. Hinton RJ, Dechow PC, Carlson DS: Recoveryof jaw muscle cavity,Philadelphia, 1995,WB Saunders,pp 141-142.
function following injection of a myotoxic agent (lidocaine 73. Malignant Hyperthermia Association of the United States.
epinephrine), Oral Surg Oral Med Oral Pathol 59:247-251, Availableat: www.mhaus.org.AccessedOctober 28, 2011.
1986.
68. Denborough MA, Forster JF, Lovell RR, et al: Anaesthetic
deaths in a family,Br J Anaesth 34:395-396, 1962.
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T
Pharmacology
of Vasoconstrictors
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40 PARTI The Drugs
TABLE 3-2
Adrenergic Receptor Activity of Vasoconstrictors
Vasoconstrictorsthat do not possess OH groups in the Drug a, ai p,
third and fourth positions of the aromatic molecule are not
Epinephrine +++ +++ +++ +++
catechols but are amines because they have an NH2 group
Norepinephrine ++ ++ ++ +
attached to the aliphatic side chain.
Levonordefrin + ++ ++ +
Catecholamines Noncatecholamines Relative potency of drugs is indicated as follows: +++, high, ++,
Epinephrine Amphetamine intermediate, and +, low.
From Jastak JT,Yagiela JA, Donaldson D: Local anesthesia of the oral
Norepinephrine Methamphetamine cavity, Philadelphia, 1995, WB Saunders.
Levonordefrin Ephedrine
Isoproterenol Mephentermine
Dopamine Hydroxyamphetamine
Metaraminol have since been subcategorized. Whereas a.1 receptors
Methoxamine are excitatory-postsynaptic, a.i receptors are inhibitory
Phenylephrine postsynaptic.8
Activation of P receptors produces smooth muscle relax
Felypressin,a synthetic analog of the polypeptide vaso ation (vasodilationand bronchodilation) and cardiac stimu
pressin (antidiuretic hormone), is availablein many coun lation (increased heart rate and strength of contraction).
tries as a vasoconstrictor. As of the time of this writing Beta receptors are further divided into Pt> and P2:P1
(November 2011), felypressinis not availablein the United are found in the heart and small intestines and are respon
States. sible for cardiac stimulation and lipolysis; p2, found in the
bronchi, vascularbeds, and uterus, produce bronchodilation
and vasodilation.9
MODES OF ACTION Table 3-2 illustrates the differences in varying degrees
Three categories of sympathomimetic amines are known: of a. and p receptor activity of three commonly used
direct-acting drugs, which exert their action directly on vasoconstrictors.
adrenergic receptors; indirect-acting drugs, which act by Table 3-3 lists the systemic effects, based on a. and P
releasing norepinephrine from adrenergic nerve terminals; receptor activity,of epinephrine and norepinephrine.
and mixed-acting drugs, with both direct and indirect
actions (Box3-1).1-3 Release of Catecholamines
Other sympathomimetic drugs, such as tyramine and
Adrenergic Receptors amphetamine, act indirectly by causing the release of the
Adrenergic receptors are found in most tissues of the body. catecholamine norepinephrine from storage sites in adren
The concept of adrenergic receptors was proposed by ergic nerve terminals. In addition, these drugs may exert
Ahlquist in 1948and is well acceptedtoday.7 Ahlquist recog direct action on a. and P receptors.
nized two types of adrenergicreceptor,termed alpha (a.) and The clinical actions of this group of drugs therefore are
beta (p), based on inhibitory or excitatory actions of cate quite similar to the actions of norepinephrine. Successively
cholamines on smooth muscle. repeated doses of these drugs will prove to be less effective
Activation of a. receptors by a sympathomimetic drug than those given previouslybecause of depletion of norepi
usually produces a response that includes contraction of nephrine from storage sites. This phenomenon is termed
smooth muscle in blood vessels (vasoconstriction). Based tachyphylaxis and is not seen with drugs that act directly on
on differences in their function and location, a. receptors adrenergic receptors.
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CHAPTER 3 Pharmacology of Vasoconstrictors 41
TABLE 3-4
Concentrations of Clinically Used Vasoconstrictors
Concentration Milligrams per Micrograms per µg per Cartridge
(Dilution) Milliliter (mg/ml) Milliliter (µ.g/mL) (1.8 ml) Therapeutic Use
1:1000 1.0 1000 Epinephrine-Emergency medicine
(IM/SC anaphylaxis)
1:2500 0.4 400 Phenylephrine
1:10,000 0.1 100 Epinephrine-Emergency medicine
(IV/ET cardiac arrest)
1:20,000 0.05 50 90 Levonordefrin-Local anesthetic
1:30,000 0.033 33.3 73 (2.2-mL cartridge) Norepinephrine-Local anesthetic
1:50,000 0.02 20 36 Epinephrine-Local anesthetic
1:80,000 0.0125 12.5 27.5 (2.2-mL cartridge) Epinephrine-Local anesthetic
(United Kingdom)
1:100,000 O.ol 10 18 Epinephrine-Local anesthetic
1:200,000 0.005 5 9 Epinephrine-Local anesthetic
1:400,000 0.0025 2.5 4.5 Epinephrine-Local anesthetic
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42 PARTI The Drugs
ideal drug. The benefits to be gained from adding epineph phenylephrine 1:20,000 (lidocaineblood level= 2.4 µg/mL)
rine (or any vasoconstrictor, for that matter) to a local than with epinephrine 1:200,000 (1.4 µg/mL).23 The cardio
anesthetic solution must be weighed against any risks that vascular effects of levonordefrin most closely resemble
might be present. Epinephrine is absorbed from the site those of norepinephrine.24 Felypressin was shown to be
of injection, just as is the local anesthetic. Measurable epi about as effective as epinephrine in reducing cutaneous
nephrine blood levelsare obtained, and these influence the blood flow.5
heart and blood vessels.Resting plasma epinephrine levels Epinephrine remains the most effective and the most
(39 pg/mL) are doubled after administration of one car used vasoconstrictor in medicine and dentistry.
tridge of lidocaine with 1: 100,000 epinephrine." Elevation
of epinephrine plasma levelsis linearly dose dependent and
persists from severalminutes to a half-hour.12 Contrary to a
PHARMACOLOGY OF SPECIFIC AGENTS
previously held position that intraoral administration of The pharmacologic properties of the sympathomimetic
usual volumes of epinephrine produced no cardiovascular amines commonlyused asvasoconstrictorsin local anesthet
response, and that patients were more at risk from ics are reviewed.Epinephrine is the most useful and repre
endogenously released epinephrine than they were from sents the best example of a drug mimicking the activity of
exogenouslyadministered epinephrine,13'14 recent evidence sympathetic discharge. Its clinical actions are reviewed in
demonstrates that epinephrine plasma levels equivalent to depth. The actions of other drugs are compared with those
those achievedduring moderate to heavyexercisemay occur of epinephrine.
after intraoral lnjection.":" These are associatedwith mod
erate increasesin cardiac output and stroke volume (seethe
following section). Blood pressure and heart rate, however, Epinephrine
are minimally affectedat these dosages.17 Proprietary Name. Adrenalin.
In patients with preexisting cardiovascular or thyroid
disease, the side effects of absorbed epinephrine must be Chemical Structure. Epinephrine as the acid salt is highly
weighed against those of elevated local anesthetic blood soluble in water. Slightlyacid solutions are relativelystable
levels.It is currently thought that the cardiovasculareffects if they are protected from air. Deterioration (through oxida
of conventional epinephrine doses are of little practical tion) is hastened by heat and the presence of heavy metal
concern, evenin patients with heart disease.12 However,even ions. Sodium bisulfite is commonly added to epinephrine
followingusual precautions (e.g.,aspiration, slowinjection), solutions to delaythis deterioration. The shelf life of a local
sufficientepinephrine can be absorbed to cause sympatho anesthetic cartridge containing a vasoconstrictor is some
mimetic reactions such as apprehension, tachycardia,sweat what shorter (18 months) than that of a cartridge containing
ing, and pounding in the chest (palpitation)-the so-called no vasoconstrictor (36 months).
epinephrine reaction.18
Intravascular administration of vasoconstrictors and
NC
OHH
their administration to sensitive individuals (hyperre I I /H
sponders), or the occurrence of unanticipated drug-drug -C-N
interactions, can howeverproduce significantclinicalmani H ~ ~ ~Ha
festations. Intravenous administration of 0.015 mg of epi OH
nephrine with lidocaine results in an increase in the heart
rate ranging from 25 to 70 beats per minute, with elevations
in systolic blood from 20 to 70 mm Hg.12•19.2° Occasional Source. Epinephrine is available as a synthetic and is also
rhythm disturbances may be observed, and premature ven obtained from the adrenal medulla of animals (epinephrine
tricular contractions (PVCs)are most often noted. constitutes approximately 80% of adrenal medullary secre
Other vasoconstrictors used in medicine and dentistry tions). It exists in both levorotatory and dextrorotatory
include norepinephrine, phenylephrine, levonordefrin, and forms; the levorotatory form is approximately 15 times as
felypressin.Norepinephrine, lacking significant p2 actions, potent as the dextrorotatory form.
produces intense peripheral vasoconstriction with possible
dramatic elevation of blood pressure, and is associatedwith Mode of Action. Epinephrine acts directly on both ex-and
a side effect ratio nine times higher than that of epineph P-adrenergic receptors; P effectspredominate.
rine." Although it is currently availablein some countries in
local anesthetic solutions, the use of norepinephrine as a Systemic Actions
vasopressor in dentistry is diminishing and cannot be rec Myocardium. Epinephrine stimulates p1 receptors of the
ommended. The use of a mixture of epinephrine and nor myocardium. There is a positiveinotropic (forceof contrac
epinephrine is to be absolutely avoided.22 Phenylephrine, a tion) and a positivechronotropic (rate of contraction) effect.
pure cx-adrenergicagonist, theoretically possesses advan Both cardiac output and heart rate are increased.
tages over other vasoconstrictors.However,in clinicaltrials, Pacemaker Cells. Epinephrine stimulates p1 receptors
peak blood levels of lidocaine were actually higher with and increases the irritability of pacemaker cells,leading to
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CHAPTER3 Pharmacology of Vasoconstrictors 43
an increased incidence of dysrhythmias. Ventricular tachy Respiratory System. Epinephrine is a potent dilator (p2
cardia (VT) and premature ventricular contractions (PVCs) effect)of bronchiole smooth muscle.It is an important drug
are common. for management of more refractory episodes of broncho
Coronary Arteries. Epinephrine produces dilation of spasm (e.g., status asthmaticus).
the coronary arteries, increasingcoronary artery blood flow. Central Nervous System. In usual therapeutic dosages,
Blood Pressure. Systolic blood pressure is increased. epinephrine is not a potent central nervous system (CNS)
Diastolicpressure is decreasedwhen small doses are admin stimulant. Its CNS-stimulating actions become prominent
istered because of the greater sensitivity to epinephrine when an excessivedose is administered.
of p2 receptors compared with a. receptors in vessels Metabolism. Epinephrine increases oxygen consump
supplyingthe skeletalmuscles.Diastolicpressure is increased tion in all tissues. Through p action, it stimulates glycoge
with larger epinephrine doses because of constriction of nolysis in the liver and skeletal muscle, elevating blood
blood vessels supplying the skeletal muscles caused by a. sugar levelsat plasma epinephrine concentrations of 150to
receptor stimulation. 200 pg/mL.25 The equivalent of four dental local anesthetic
Cardiovascular Dynamics. The overall action of epi cartridges of 1: 100,000epinephrine must be administered
nephrine on the heart and cardiovascular system is direct to elicit this response.27
stimulation: Termination of Action and Elimination. The action of
• Increased systolicand diastolicpressures epinephrine is terminated primarily by its reuptake by
• Increased cardiac output adrenergic nerves. Epinephrine that escapes reuptake is
• Increased stroke volume rapidly inactivated in the blood by the enzymes catechol-
• Increased heart rate 0-methyltransferase (COMT) and monoamine oxidase
• Increased strength of contraction (MAO),both of which are present in the liver.28 Only small
• Increased myocardial oxygenconsumption amounts {approximately 1%) of epinephrine are excreted
These actions lead to an overall decrease in cardiac unchanged in the urine.
efficiency. Side Effects and Overdose. The clinical manifestations
The cardiovascularresponses of increased systolicblood of epinephrine overdose relate to CNS stimulation and
pressure and increasedheart rate developwith the adminis include increasing fear and anxiety, tension, restlessness,
tration of one to two dental cartridges of a 1: 100,000epi throbbing headache, tremor, weakness, dizziness, pallor,
nephrine dilution.25 Administration of four cartridges of respiratory difficulty,and palpitation.
1: 100,000epinephrine will bring about a slight decrease in With increasing levels of epinephrine in the blood,
diastolicblood pressure. cardiac dysrhythmias (especiallyventricular) become more
Vasculature. The primary action of epinephrine is on common; ventricular fibrillation is a rare but possible con
smaller arterioles and precapillary sphincters. Blood vessels sequence.Dramatic increasesin both systolic{>300mm Hg)
supplying the skin, mucous membranes, and kidneys pri and diastolic (>200 mm Hg) pressures may be noted and
marily contain a. receptors. Epinephrine produces constric have led to cerebral hemorrhage.29 Anginal episodes may be
tion in these vessels.Vesselssupplying the skeletal muscles precipitated in patients with coronary artery insufficiency.
contain both a. and p2 receptors, with p2 predominating. Becauseof the rapid inactivation of epinephrine, the stimu
Smalldoses of epinephrine produce dilation of these vessels latory phase of the overdose (toxic) reaction usuallyis brief.
as a result of p2 actions. p2 receptors are more sensitive to Vasoconstrictor overdose is discussed in greater depth in
epinephrine than are a. receptors. Larger doses produce Chapter 18.
vasoconstriction because a. receptors are stimulated.
Hemostasis. Clinically, epinephrine is used frequently
as a vasoconstrictor for hemostasis during surgical proce Clinical Applications
dures. Injection of epinephrine directly into surgical sites • Management of acute allergicreactions
rapidly produces high tissue concentrations, predominant • Management of refractory bronchospasm (status
a. receptor stimulation, and hemostasis. As epinephrine asthmaticus)
tissue levelsdecreaseover time, its primary action on blood • Management of cardiac arrest
vesselsreverts to vasodilation because p2 actions predomi • As a vasoconstrictor,for hemostasis
nate; therefore it is common for some bleeding to be • As a vasoconstrictor in local anesthetics,to decrease
noted at about 6 hours after a surgical procedure. In a absorption into the cardiovascularsystem
clinicaltrial involvingextraction of third molars, postsurgi • As a vasoconstrictor in local anesthetics,to increase
calbleeding occurred in 13of16 patients receivingepineph depth of anesthesia
rine with their local anesthetic for hemostasis,whereas 0 of • As a vasoconstrictor in local anesthetics,to increase
16 patients receivinglocal anesthetic without vasoconstric duration of anesthesia
tor (mepivacaineplain) had bleeding 6 hours post surgery.26 • To produce mydriasis
Additional findings of increased postsurgical pain and Availability in Dentistry. Epinephrine is the most potent
delayed wound healing were noted in the epinephrine and widely used vasoconstrictor in dentistry. It is available
receivinggroup.26 in the followingdilutions and drugs:
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44 PART I The Drugs
Epinephrine Dilution Local Anesthetic (generic) York Heart Association recommended that maximal epi
nephrine doses be limited to 0.2 mg per appointment.33In
1:50,000 Lldocaine
the followingyears,the American Heart Associationrecom
1:80,000 Lldocaine (lignocaine)
(United Kingdom)
mended the restriction of epinephrine in local anesthetics
1:100,000 Articaine when administered to patients with ischemicheart disease.34
Lidocaine More recently, the Agency for Healthcare Research and
1:200,000 Articaine Quality (AHRQ) reviewed the published literature on the
Bupivacaine subject of the effectsof epinephrine in dental patients with
Etidocainet high blood pressure.35The report reviewed six studies that
Lidocaine evaluated the effects of dental treatment (extraction of
Mepivacaine* teeth) in hypertensive patients when they received local
Prilocaine anesthetics with and without epinephrine. Results suggest
1:300,000 Lldocaine* that hypertensivesubjects undergoing an extraction experi
1:400,000 Articaine*
ence small increases in systolic blood pressure and heart
*Not availablein the United States (August2011). rate associatedwith the use of a local anesthetic containing
tNo longer marketed in the United State (2002). epinephrine. These increases associated with the use of
epinephrine occur in addition to increases in systolic and
diastolic blood pressures and heart rate associated with
Maximum Doses. The least concentrated solution that undergoing the procedure without epinephrine that are
produces effectivepain control should be used. Lidocaineis larger for hypertensive than for normotensive patients. No
availablewith two dilutions of epinephrine-I :50,000 and adverse outcomes were reported among any of the subjects
I : 100,000---in the United States and Canada, and with in the studies included in the review,and only one report of
I :80,000,I :200,000,and I :300,000dilutions in other coun an adverse event associated with the use of epinephrine in
tries. The duration of effectivepulpal and soft tissue anes local anesthetic in a hypertensive patient was identified in
thesia is equivalent with all forms. Therefore it is the literature (Table3-6).35
recommended (in North America) that the I : 100,000epi In cardiovascularly compromised patients, it seems
nephrine concentration be used with lidocaine when prudent to limit or avoid exposure to vasoconstrictors, if
extended pain control is necessary. Where I :200,000 or possible.These include poorly controlled American Society
I :300,000epinephrine is availablewith lidocaine,these con of Anesthesiologists Physical Status classification system
centrations are preferred for pain control.3° (ASA) 3 and all ASA 4 and greater cardiovascular risk
The dosagesin Table 3-5 represent recommended maxi patients. However,as stated, the risk of epinephrine admin
mums as suggested by this author and others.31They are istration must be weighed against the benefits to be gained
conservativefiguresbut still provide the dental practitioner
with adequatevolumesto produce clinicallyacceptableanes
thesia. The American Heart Association as far back as 1964
stated that "the typical concentrations of vasoconstrictors TABLE 3-6
contained in local anesthetics are not contraindicated in Means of Maximum Changes from Baseline for Blood
patients with cardiovascular disease so long as preliminary Pressure and Heart Rate*
aspiration is practiced, the agent is injected slowly,and the
max A max A max A
smallest effectivedose is administered."32In 1954 the New SBP,mm DBP,mm HR, bpm
Hypertensives
Anesthesia with 15.3 2.3 9.3
epinephrine
TABLE 3-5
Anesthesia without 11.7 3.3 4.7
Recommended Maximum Dosages of Epinephrine epinephrine
CARTRIDGES (ROUNDED OFF) Normotensives
Normal, Patient With Clinically Anesthesia with 5.0 -0.7 6.3
Epinephrine Healthy Significant epinephrine
Concentration Patient Cardiovascular Disease Anesthesia without 5.0 4.0 0.7
(µg/Cartridge) (ASA I)* (ASA Ill or IV)t epinephrine*
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CHAPTER3 Pharmacology of Vasoconstrictors 45
from its inclusion in the local anesthetic solution. Can Mode of Action. The actions of norepinephrine are almost
clinically adequate pain control be provided for this patient exclusivelyon a. receptors (90%). It also stimulates P actions
without a vasoconstrictor in the solution? What is the in the heart (10%). Norepinephrine is one fourth as potent
potential negative effect of poor anesthesia on endogenous as epinephrine.
release of catecholamines in response to sudden, unexpected
pain? Systemic Actions
The use of vasoconstrictors for cardiovascularly compro Myocardium. Norepinephrine has a positive inotropic
mised patients is reviewed in greater depth in Chapter 20. action on the myocardium through p1 stimulation.
Hemostasis. Epinephrine-containing local anesthetic Pacemaker Cells. Norepinephrine stimulates pacemaker
solutions are used, via infiltration into the surgical site, to cellsand increasestheir irritability,leading to a greater inci
prevent or to minimize hemorrhage during surgical and dence of cardiac dysrhythmias CP1 action).
other procedures. The 1:50,000 dilution of epinephrine is Coronary Arteries. Norepinephrine produces an increase
more effectivein this regardthan lessconcentrated 1: 100,000 in coronary artery blood flowthrough a vasodilatory effect.
or 1:200,000solutions.36 Epinephrine dilutions of 1:50,000 Heart Rate. Norepinephrine produces a decrease in
and 1: 100,000are considerablymore effectivein restricting heart rate caused by reflexactions of the carotid and aortic
surgical blood loss than are local anesthetics without vaso baroreceptors and the vagusnerve after a marked increasein
constrictor additives.26 both systolicand diastolicpressures.
Clinical experience has shown that effectivehemostasis Blood Pressure. Both systolicand diastolicpressures are
can be obtained with concentrations of 1: 100,000epineph increased,systolicto a greater extent. This effectis produced
rine. Although the small volume of 1:50,000 epinephrine through the a-stimulating actions of norepinephrine, which
required for hemostasis does not increase a patient's risk, lead to peripheral vasoconstriction and a concomitant
consideration alwaysshould be givento use of the 1: 100,000 increase in peripheral vascular resistance.
dilution, especiallyin patients known to be more sensitiveto Cardiovascular Dynamics. The overallaction of norepi
catecholamines.These include hyperresponders on the Bell nephrine on the heart and cardiovascular system is as
shaped curve, as well as ASA 3 or 4 risk cardiovascularly follows:
compromised individuals and geriatric patients. • Increased systolicpressure
• Increased diastolic pressure
• Decreasedheart rate
Norepinephrine (Levarterenol) • Unchanged or slightlydecreased cardiac output
Proprietary Names. Levophed, Noradrenalin; levarterenol • Increased stroke volume
is the officialname of norepinephrine. • Increased total peripheral resistance
Vasculature. Norepinephrine, through a. stimulation,
Chemical Structure. Norepinephrine (as the bitartrate) in produces constriction of cutaneous blood vessels.This leads
dental cartridgesis relativelystablein acid solutions, deterio to increasedtotal peripheral resistanceand increasedsystolic
rating on exposure to light and air. The shelf life of a car and diastolicblood pressures.
tridge containing norepinephrine bitartrate is 18 months. The degree and duration of ischemia noted after norepi
Acetone-sodium bisulfite is added to the cartridge to retard nephrine infiltration into the palate have led to soft tissue
deterioration. necrosis (Fig.3-1).
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46 PART I The Drugs
Respiratory System. Norepinephrine does not relax norepinephrine be eliminated as a vasoconstrictor in dental
bronchial smooth muscle, as does epinephrine. It does, local anesthetics,a statement with which this author whole
however,produce a-induced constriction of lung arterioles, heartedly agrees.30
which reduces airway resistance to a small degree. Norepi Normal healthy patient: 0.34 mg per appointment; 10 mL
nephrine is not clinically effectivein the management of of a 1:30,000solution
bronchospasm. Patient with clinically significant cardiovascular disease (ASA
Central Nervous System. Similar to epinephrine, nor 3 or 4): 0.14 mg per appointment; approximately4 mL
epinephrine does not exhibit CNS-stimulating actions at of a 1:30,000solution
usual therapeutic doses; its CNS-stimulating properties are
most prominent after overdose. Clinical manifestations are
similar to those of epinephrine overdose (p. 43) but are less Levonordefrin
frequent and usually are not as severe. Proprietary Name. Neo-Cobefrin.
Metabolism. Norepinephrine increases the basal meta
bolic rate. Tissue oxygen consumption is also increased in Chemical Structure. Levonordefrinis freelysolublein dilute
the area of injection. Norepinephrine produces an elevation acidic solutions. Sodium bisulfiteis added to the solution to
in the blood sugar levelin the same manner as epinephrine, delayits deterioration. The shelflifeof a cartridge containing
but to a lesser degree. levonordefrin-sodium bisulfite is 18 months.
Termination of Action and Elimination. The action of
norepinephrine is terminated through its reuptake at adren Source. Levonordefrin, a synthetic vasoconstrictor, is pre
ergic nerve terminals and its oxidation by MAO.Exogenous pared by the resolution of nordefrin into its optically
norepinephrine is inactivated by COMT. active isomers. The dextrorotatory form of nordefrin is
Side Effects and Overdose. Clinical manifestations of virtually inert.
norepinephrine overdose are similar to but less frequent
and less severe than those of epinephrine. They normally
involveCNS stimulation. Excessivelevelsof norepinephrine HXf9H
~ CH3H
I H-CH-NH
I I
in the blood produce markedlyelevatedsystolicand diastolic
pressures with increased risk of hemorrhagic stroke, head H ::::::,...
ache, angina! episodes in susceptible patients, and cardiac
dysrhythmias.
Extravascular injection of norepinephrine into tissues Mode of Action. It appears to act through direct a. receptor
may produce necrosis and sloughing because of intense stimulation (75%)with some 13 activity(25%), but to a lesser
a. stimulation. In the oral cavity, the most likely site degree than epinephrine. Levonordefrin is 15% as potent a
to encounter this phenomenon is the hard palate (see vasopressor as epinephrine.
Fig. 3-1). Norepinephrine should be avoided for vaso
constricting purposes (e.g., hemostasis), especially on the Systemic Actions. Levonordefrinproduces less cardiac and
palate.An increasingnumber of authorities have stated that CNS stimulation than is produced by epinephrine.
norepinephrine should not be used at all with local Myocardium. The same action as epinephrine is seen,
anesthetics.30•37 but to a lesser degree.
Clinical Applications. Norepinephrine is used as a vaso Pacemaker Cells. The same action as epinephrine is
constrictor in local anesthetics and for the management of seen, but to a lesser degree.
hypotension. Coronary Arteries. The same action as epinephrine is
Availability in Dentistry. In the United States, norepi seen, but to a lesser degree.
nephrine is no longer availablein local anesthetic solutions Heart Rate. The same action as epinephrine is seen, but
used in dentistry. In the past, it was included with the local to a lesser degree.
anesthetics propoxycaine and procaine in a 1:30,000 con Vasculature. The same action as epinephrine is seen,but
centration. In other countries, norepinephrine is included to a lesser degree.
withlidocaine (Germany) andmepivacaine (Germany) or as Respiratory System. Some bronchodilation occurs, but
the combination of norepinephrine and epinephrine with to a much smaller degree than with epinephrine.
lidocaine (Germany) or tolycaine (Japan).21 Central Nervous System. The same action as epineph
Maximum Doses. When given, norepinephrine should rine is seen, but to a lesser degree.
be used for pain control only,there being no justification for Metabolism. The same action as epinephrine is seen,but
its use in obtaining hemostasis. It is approximately 25% as to a lesser degree.
potent a vasopressor as epinephrine and therefore is used Termination of Action and Elimination. Levonordefrin
clinicallyas a 1:30,000dilution. is eliminated through the actions of COMT and MAO.
Recommendations of the International Federation of Side Effects and Overdose. These are the same as with
Dental Anesthesiology Societies (IFDAS) suggest that epinephrine, but to a lesser extent. With higher doses,
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CHAPTER3 Pharmacology of Vasoconstrictors 47
additional side effects include hypertension, ventricular dysrhythmias are rarely noted, even after large doses of
tachycardia, and anginal episodes in patients with coronary phenylephrine.
artery insufficiency. Cardiovascular Dynamics. Overall, the cardiovascular
Clinical Applications. Levonordefrin is used as a vaso actions of phenylephrine are as follows:
constrictor in local anesthetics. • Increased systolicand diastolic pressures
Availability in Dentistry. It can be obtained with mepi • Reflexbradycardia
vacaine in a 1:20,000dilution. • Slightlydecreased cardiac output (resulting from
Maximum Doses. Levonordefrinis considered one sixth increased blood pressure and bradycardia)
(15%) as effectivea vasopressor as epinephrine; therefore it • Powerfulvasoconstriction (most vascular beds
is used in a higher concentration (1 :20,000). constricted, peripheral resistanceincreased significantly)
For all patients, the maximum dose should be 1 mg per but without marked venous congestion
appointment; 20 mL of a 1:20,000 dilution (11 • Rarelyassociatedwith provoking cardiac dysrhythmias
cartridges).* Respiratory System. Bronchi are dilated but to a lesser
In the concentration at which it is available,levonordefrin degreethan with epinephrine. Phenylephrine is not effective
has the same effect on the clinical activity of local anes in treating bronchospasm.
thetics as does epinephrine in 1:50,000 or 1: 100,000 Central Nervous System. A minimum effect on CNS
concentration. activity is noted.
Metabolism. Some increase in the metabolic rate is
noted. Other actions (e.g., glycogenolysis)are similar to
Phenylephrine Hydrochloride those produced by epinephrine.
Proprietary Name. Neo-Synephrine. Termination of Action and Elimination. Phenylephrine
undergoes hydroxylation to epinephrine, then oxidation to
Chemical Structure. Phenylephrineis quite solublein water. metanephrine, after which it is eliminated in the same
It isthe most stableand the weakestvasoconstrictoremployed manner as epinephrine.
in dentistry. Side Effects and Overdose. CNS effects are minimal
with phenylephrine.Headacheand ventricular dysrhythmias
have been noted after overdose. Tachyphylaxisis observed
with long-term use.
Clinical Applications. Phenylephrine is used as a vaso
constrictor in localanesthetics,for the management of hypo
tension, as a nasal decongestant,and in ophthalmic solutions
to produce mydriasis.
Availability in Dentistry. Phenylephrine was used with
Source. Phenylephrine is a synthetic sympathomimetic 4% procaine in a 1:2500 dilution (no longer available in
amine. dental cartridges).
Maximum Doses. Phenylephrine is considered only one
Mode of Action. Direct a receptor stimulation occurs twentieth as potent as epinephrine, hence its use in a 1:2500
(95%). Although the effect is less than with epinephrine, dilution (equivalent to a 1:50,000 epinephrine concentra
duration is longer.Phenylephrine exertslittle or no p action tion). It is an excellentvasoconstrictor,with few significant
on the heart. Only a smallportion of its activityresults from side effects.
its ability to release norepinephrine. Phenylephrine is only Normal healthy patient: 4 mg per appointment; 10 mL of a
5% as potent as epinephrine. 1:2500 solution
Patient with clinically significant cardiovascular impairment
Systemic Actions (ASA 3 or 4): 1.6 mg per appointment, equivalent to
Myocardium. It has little chronotropic or inotropic 4 mL of a 1:2500 solution
effecton the heart.
Pacemaker Cells. Little effectis noted.
Coronary Arteries. Increased blood flow occurs as the Felypressin
result of dilation. Proprietary Name. Octapressin.
Blood Pressure. a action produces increasesin both sys
tolic and diastolic pressures. Chemical Structure
Heart Rate. Bradycardiais produced by reflexactions of
the carotid-aortic baroreceptorsand the vagusnerve.Cardiac
*Maximum volume for administration may be limited by the dose of the Cys-Phe-Phe-Gly-Asn-Cys-Pro-Lys-GlyNH2
local anesthetic.
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48 PARTI The Drugs
Source. Felypressinis a synthetic analog of the antidiuretic for postoperative pain control, and the medical status of the
hormone vasopressin. It is a nonsympathomimetic amine, patient.
categorizedas a vasoconstrictor.
Length of the Dental Procedure
Mode of Action. Felypressin acts as a direct stimulant The addition of any vasoactive drug to a local anesthetic
of vascular smooth muscle. Its actions appear to be prolongs the duration (and depth) of pulpal and soft tissue
more pronounced on the venous than on the arteriolar anesthesiaof most localanesthetics.For example,pulpal and
microcirculation.38 hard tissue anesthesiawith 2% lidocaine lasts approximately
10 minutes; the addition of 1:50,000, 1:80,000, 1: 100,000,
Systemic Actions or 1:200,000epinephrine increasesthis to approximately60
Myocardium. No direct effectsare noted. minutes. The addition of a vasoconstrictor to prilocaine, on
Pacemaker Cells. Felypressinis nondysrhythmogenic,in the other hand, does not significantlyincrease the duration
contrast to the sympathomimetic amines (e.g.,epinephrine, of clinicallyeffectivepain control. Prilocaine 4%, after nerve
norepinephrine). block injection, provides pulpal anesthesiaof about 40 to 60
Coronary Arteries. When administered in high doses minutes' duration. (Infiltration injection with prilocaine 4%
(greaterthan therapeutic), it may impair blood flowthrough provides approximately 10to 15 minutes of pulpal anesthe
the coronary arteries. sia.) The addition of a 1:200,000epinephrine concentration
Vasculature. In high doses (greater than therapeutic), to prilocaine increases this slightly (to about 60 to 90
felypressin-inducedconstriction of cutaneous blood vessels minutes).41
may produce facialpallor. Averagedurations of pulpal and hard tissue anesthesia
Central Nervous System. Felypressinhas no effect on expected from commonly used local anesthetics with and
adrenergic nerve transmission; thus it may be safelyadmin without vasoconstrictors are shown in Table3-7.
istered to hyperthyroid patients and to anyone receiving The typical dental patient is scheduled for a I-hour
MAO inhibitors or tricyclicantidepressants. appointment. The duration of actual treatment (and the
Uterus. It has both antidiuretic and oxytocicactions, the desirable duration of profound pulpal anesthesia) is 47.9
latter contraindicating its use in pregnant patients. minutes (standard deviation [SD] 14.7minutes) in a general
Side Effects and Overdose. Laboratory and clinical dentistry office,whereas in the officesof dental specialists,
studies with felypressinin animals and humans have dem treatment time is 39.1 minutes (SD 19.4minutes).42
onstrated a widemargin of safety.39 The drug iswelltolerated For routine restorativeprocedures, it might be estimated
by the tissues into which it is deposited,with little irritation that pulpal anesthesiawill be required for approximately40
developing.The incidence of systemicreactions to felypres to 50 minutes. As can be seen in Table 3-7, it is difficult to
sin is minimal. achieveconsistentlyreliablepulpal anesthesiawithout inclu
Clinical Applications. Felypressinis used as a vasocon sion of a vasoconstrictor (seeminutes marked with asterisks
strictor in local anesthetics to decreasetheir absorption and in Table3-7).
increase their duration of action.
Availability in Dentistry. Felypressinis employed in a
dilution of 0.03 IU/mL (International Units) with 3% prilo TABLE 3-7
caine in Japan, Germany,and other countries. It is not avail Average Durations of Pulpal and Hard
able as a vasoconstrictor in local anesthetics in North Tissue Anesthesia
America.
Infiltration. Nerve Block,
Maximum Doses. Felypressin-containing solutions are
Local Anesthetic minutes minutes
not recommended for use where hemostasis is necessary
because of its predominant effecton the venous rather than Lidocaine HCL
2%- no vasoconstrictor 5-10* =10-20*
the arterial circulation.40
For patients with clinically significant cardiovascular
2% +epinephrine 1:50,000 "'60 zso
2% + epinephrine 1: 100,000 =60 :?:60
impairment (ASA 3 or 4), the maximum recommended
2% +epinephrine 1:200,000 "'60 ~60
dose is 0.27 IU; 9 mL of 0.03 IU/mL. Mepivacaine HCL
3% - no vasoconstrictor 5-10* 20-40*
2% + levonordefrin 1:20,000 ~60 zso
SELECTION OF A VASOCONSTRICTOR 2% + epinephrine 1: 100,000 ~60 ~60
Prilocaine HCL
Two vasoconstrictors are availablein local anesthetic solu 4% - no vasoconstrictor 10-15* 40-60*
tions in North America: epinephrine and levonordefrin. 4% + epinephrine 1:200,000 ~o 60-90
In the selection of an appropriate vasoconstrictor,if any, Articaine HCL
for use with a local anesthetic, severalfactors must be con 4% + epinephrine 1: 100,000 ~60 :?:60
sidered: the length of the dental procedure, the need for *Indicatesduration of pulpal anesthesia usually inadequate to provide
hemostasis during and after the procedure, the requirement pain control for a typical 48-minute procedure.
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CHAPTER 3 Pharmacology of Vasoconstrictors 49
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50 PARTI The Drugs
Patients being treated with MAO inhibitors may receive 6. Myers RR,Heckman HM: Effectsof local anesthesia on nerve
vasoconstrictors within the usual dental dosage parameters blood flow:studies using lidocainewith and without epineph
without increasedrisk.47'48 Patients receivingtricyclicantide rine, Anesthesiology71:757-762, 1989.
pressants are at greater risk for the developmentof dysrhyth 7. Ahlquist RP: A study of adrenotropic receptors,Am J Physiol
153:586-600,1948.
mias with epinephrine administration. It is recommended
8. Hieble JP: Adrenoceptor subclassification: an approach to
that when epinephrine is administered to these patients, its
improved cardiovasculartherapeutics, Pharmaceut ActaHelvet
dose be minimal. Administration of levonordefrin or nor 74:63-71, 2000.
epinephrine is absolutelycontraindicated in patients receiv 9. SmileyRM, KwatraMM, Schwinn DA:New developments in
ing tricyclicantidepressants.49 Largedosesof vasoconstrictor cardiovascular adrenergic receptor pharmacology: molecular
may induce severe (exaggerated)responses. mechanisms and clinicalrelevance,J Cardiothorac VaseAnesth
Local anesthetic formulations with vasoconstrictors also 12:10-95, 1998.
contain an antioxidant (to delay oxidation of the vasocon 10. Braun H: Uber den Einfluss der Vitalitat der Gewebe auf die
strictor). Sodium bisulfite is the most frequently used anti ortlichen und allgemeinenGiftwirkungenlocalabaesthesieren
oxidant in dental cartridges. It prolongs the shelf life of the der Mittel, und uber die Bedeutung des Adrerenalins fur die
anesthetic solution with vasoconstrictorto approximately18 Lokalanasthesie,Arch Klin Chir 69:541-591, 1903.
11. Tolas AG, Pflug AE, Halter JB: Arterial plasma epinephrine
months. However,sodium bisulfite renders the local anes
concentrations and hemodynarnicresponsesafter dental injec
thetic considerably more acidic than the same solution
tion of local anesthetic with epinephrine, J Am Dent Assoc
without a vasoconstrictor.Acidicsolutions oflocal anesthet 104:41--43,1982.
ics contain a greater proportion of charged cation molecules 12. JastakJT,YagielaJA,Donaldson D, editors: Localanesthesia of
(RNH+)than of uncharged base molecules (RN). Becauseof the oral cavity,Philadelphia, 1995,WB Saunders.
this, diffusion of the local anesthetic solution into the axo 13. Holroyd SV,Requa-Clark B: Local anesthetics. In Holroyd SV,
plasm is slower,resulting in (slightly)delayedonset of anes Wynn RL, editors: Clinical pharmacology in dental practice,
thesia when local anesthetics containing sodium bisulfite ed 3, St Louis, 1983,Mosby.
(and vasoconstrictors) are injected. 14. Malamed SF: Handbook of local anesthesia, ed 5, St Louis,
Vasoconstrictors are important additions to local anes 2004,Mosby.
thetic solutions. Numerous studies have demonstrated 15. Cryer PE:Physiologyand pathophysiologyof the human sym
pathoadrenal neuroendocrine system,N Engl J Med 303:436--
conclusively that epinephrine, when added to short- or
444, 1980.
medium-duration local anesthetic solutions, slowsthe rate
16. YagielaJA: Epinephrine and the compromised heart, Orofac
of absorption, lowersthe systemicblood level,delayscresting Pain Manage 1:5-8, 1991.
of the peak blood level,prolongs the duration of anesthesia, 17. KanekoY,Ichinohe T, Sakurai M, et al: Relationship between
intensifiesthe depth of anesthesia,and reducesthe incidence changesin circulation due to epinephrine oral injection and its
of systemicreactions.18 In modern dentistry, adequate pain plasma concentration, Anesth Prog 36:188-190, 1989.
control of sufficient clinical duration and depth is difficult 18. de Jong RH: Uptake, distribution, and elimination. In de Jong
to achievewithout inclusion of vasoconstrictors in the local RH, editor: Local anesthetics,St Louis, 1994,Mosby.
anesthetic solution. Unless specificallycontraindicated by a 19. Huang KC:Effectof intravenous epinephrine on heart rate as
patient's medical status (ASA4 or above) or by the required monitored with a computerized tachometer, Anesthesiology
duration of treatment (short), inclusion of a vasoconstrictor 73:A762,1990.
20. Narchi P,Mazoit J-X,Cohen S,SamiiK:Heart rate response to
should be considered routinely.When these drugs are used,
an IV test dose of adrenaline and lignocaine with and without
however, care always must be taken to avoid unintended
atropine pretreatment, Br J Anaesth 66:583-586, 1991.
intravascular administration of the vasoconstrictor (as well 21. Malamed SF,SykesP,KubotaY,et al:Localanesthesia:a review,
as the local anesthetic) through multiple aspirations and Anesth Pain Control Dent 1:11-24, 1992.
slowadministration of minimum concentrations of both the 22. Lipp M, Dick W, Daublander M: Examination of the central
vasoconstrictor and the local anesthetic. venous epinephrine level during local dental infiltration and
block anesthesiausing tritium marked epinephrine as vasocon
References strictor, Anesthesiology69:371,1988.
1. Moore PA, Hersh EV: Local anesthetics: pharmacology and 23. Stanton-Hicks M, BergesPU, Bonica JJ: Circulatory effectsof
toxicity,Dent Clin North Am 54:587-599,2010. peridural block. IV.Comparison of the effectsof epinephrine
2. Finder RL,Moore PA:Adversedrug reactions to local anesthe and phenylephrine,Anesthesiology39:308-314, 1973.
sia, Dent Clin North Am 46:447--457,2002. 24. Robertson VJ, Taylor SE, Gage TW: Quantitative and qualita
3. Brown G: The influenceof adrenaline,noradrenaline vasocon tive analysisof the pressor effectsof levonordefrin,J Cardiovasc
strictors on the efficacyof lidocaine, J Oral Ther Pharmacol Pharmacol 6:529-935, 1984.
4:398--405,1968. 25. Clutter WE, Bier DM, Shah SD,Cryer PE:Epinephrine plasma
4. Cowan A: Further clinical evaluation of prilocaine (Citanest), metabolic clearancerates and physiologicthresholds for meta
with and without epinephrine, Oral SurgOral Med Oral Pathol bolic and hemodynarnic actions in man, J Clin Invest 66:94-
26:304-311, 1968. 101, 1980.
5. Carpenter RL, Kopacz DJ, Mackey DC: Accuracy of Doppler 26. Sveen K: Effect of the addition of a vasoconstrictor to local
capillary flow measurements for predicting blood loss from anesthetic solution on operative and postoperative bleeding,
skin incisions in pigs,Anesth Analg 68:308-311, 1989. analgesia,and wound healing,Int J Oral Surg 8:301-306, 1979.
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CHAPTER 3 Pharmacology of Vasoconstrictors 51
27. Meechan JG: The effects of dental local anaesthetics on blood 38. Altura BM, Hershey SG, ZweifachBW:Effects of a synthetic
glucose concentration in healthy volunteers and in patients analogue of vasopressin on vascular smooth muscle, Proc Soc
having third molar surgery, Br Dent J 170:373-376, 1991. Exp BiolMed 119:258-261,1965.
28. Lefkowitz RJ, Hoffman BB, Taylor P: Neurohumoral transmis 39. Sunada K, Nakamura K, Yamashiro M, et al: Clinically safe
sion: the autonomic and somatic motor nervous system. dosage of felypressinfor patients with essential hypertension,
In Brunton LL, Lazo JS, Parker KL editors: Goodman and Anesth Prog 43:408--415,1996.
Gilman's the pharmacological basis of therapeutics, ed 11, 40. Newcomb GM, Waite IM: The effectivenessof local analgesic
New York, 2006, McGraw-Hill Companies. preparations in reducing haemorrhage during periodontal
29. Campbell RL: Cardiovascular effects of epinephrine overdose: surgery,J Dent 1:37-42, 1972.
case report, Anesth Prog 24:190-193, 1977. 41. Epstein S: Clinical study of prilocaine with varying con
30. Jakob W: Local anaesthesia and vasoconstrictive additional centrations of epinephrine, J Am Dent Assoc 78:85-90,
components, Newslett Int Fed Dent Anesthesiol Soc 2:1, 1989. 1969.
31. Bennett CR: Monheim's local anesthesia and pain control in 42. American Dental Association:2009 survey of dental practice,
dental practice, ed 7, St Louis, 1983, Mosby. Chicago,February 2010,American Dental Association.
32. Management of dental problems in patients with cardiovascu 43. van der Bijl P, Victor AM: Adverse reactions associated with
lar disease: report of a working conference jointly sponsored norepinephrine in dental local anesthesia,Anesth Prog 39:37-
by the American Dental Association and American Heart Asso 89, 1992.
ciation, J Am Dent Assoc 68:333-342, 1964. 44. Hirota Y,Hori T, Kay K, Matsuura H: Effectsof epinephrine
33. Use of epinephrine in connection with procaine in dental pro and norepinephrine contained in 2% lidocaine on hemody
cedures: report of the Special Committee of the New York namics of the carotid and cerebral circulation in older and
Heart Association, Inc., on the use of epinephrine in connec younger adults, Anesth Pain Control Dent 1:343-351,1992.
tion with procaine in dental procedures, J Am Dent Assoc 45. Goulet JP,Perusse R, Turcotte JY:Contraindications to vaso
50:108, 1955. constrictors in dentistry. Part I. Cardiovascular diseases,Oral
34. Kaplan EL, editor: Cardiovascular disease in dental practice, Surg Oral Med Oral Pathol 74:579--686,1992.
Dallas, 1986, American Heart Association. 46. Goulet JP, Perusse R, Turcotte JY: Contraindications to
35. Cardiovascular effects of epinephrine in hypertensive dental vasoconstrictors in dentistry. Part II. Hyperthyroidism, dia
patients: summary, evidence report/technology assessment betes, sulfite sensitivity,cortico-dependent asthma, and pheo
number 48. AHRQ Publication Number 02-E005, March 2002, chromocytoma, Oral Surg Oral Med Oral Pathol 74:587--691,
Agency for Healthcare Research and Quality, Rockville, Md. 1992.
Availableat:http://www.ahrq.gov/clinidepcsums/ephypsum.htm 47. Goulet JP,Perusse R, Turcotte JY:Contraindications to vaso
36. Buckley JA, Ciancio SG, McMullen JA: Efficacy of epinephrine constrictors in dentistry. Part III. Pharmacologic interactions,
concentration in local anesthesia during periodontal surgery, Oral Surg Oral Med Oral Pathol 74:592--697,1992.
J Periodontol 55:653-657, 1984. 48. VerrillPJ:Adversereactions to local anaestheticsand vasocon
37. Kaufman E, Garfunkel A, Findler M, et al: Emergencies evolv strictor drugs, Practitioner 214:380-387, 1975.
ing from local anesthesia, Refuat Hapeh Vehashinayim 19:13- 49. JastakJT,YagielaJA,Donaldson D, editors: Localanesthesia of
18, 98, 2002. the oral cavity,Philadelphia, 1995,WB Saunders.
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T
Clinical Action
of Specific Agents
' I •I
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CHAPTER4 ClinicalAction of SpecificAgents 53
TABLE 4-2
Contraindications for Local Anesthetics
Type of
Medical Problem Drugs to Avoid Contraindication Alternative Drug
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54 PART I The Drugs
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CHAPTER4 ClinicalAction of SpecificAgents 55
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56 PARTI The Drugs
BOX 4-2 Calculation of Maximum Dosage and BOX 4-3 Calculation of Maximum Dosage and
Number of Cartridges (Single Drug) Number of Cartridges (Multiple Drugs)
Patient: 22 Years Old, Healthy, Female, 50 kg Patient: 45-kg Female, Healthy
Local Anesthetic: Lidocaine HCI + Epinephrine 1: 100,000 Local Anesthetic: Mepivacaine 2% + Levonordefrin
Lidocaine2% = 36 mg/cartridge 1:20,000
Lidocaine:7.0 mg/kg= 350 mg (MRD) Mepivacaine2% = 36 mg/cartridge
Number of cartridges: 350/36 = =9% Mepivacaine:6.6 mg/kg= 297 mg (MRD)
Patient receives2 cartridges = 72 mg, but anesthesia is
Patient: 40 Years Old, Healthy, Male, 90 kg inadequate.
Local Anesthetic: Articaine HCI +Epinephrine 1:200,000 Doctor wishes to change to articaine 4% + epinephrine
Articaine 4% = 72 mg/cartridge 1: 100,000.
Articaine: 7.0 mg/kg= 630 mg (MRD)
Number of cartridges: 630/72 = =9.0 How Much Articaine Can This Patient Receive?
Articaine 2% = 72 mg/cartridge
Patient: 6 Years Old, Healthy, Male, 20 kg Articaine: 7.0 mg/kg= 315 mg (MRD)
Local Anesthetic: Mepivacaine HCl, No Vasoconstridor Total dose of BOTH local anesthetics should not exceed
Mepivacaine3% = 54 mg/cartridge the lower of the two calculated doses, or 297 mg.
Mepivacaine:6.6 mg/kg= 132mg (MRD) Patient has received72 mg (lidocaine), thus can still
Number of cartridges: 130/54= =2.5 receive225 mg of articaine.
MRD, Maximum recommended dose.
Therefore,225 mg/72 mg per cartridge = =3.0
cartridges of articaine 4% + epinephrine 1: 100,000.
MRD, Maximum recommended dose.
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CHAPTER 4 ClinicalAction of SpecificAgents 57
anatomic variation and faulty technique. (However, blaming clinicallyused localanesthetics.Thus a clean (e.g.,bloodless)
failure to obtain adequate pain control on the local anes surgical field is more difficult to maintain with procaine
thetic drug serves to soothe the doctor's ego.) because of increased bleeding.
The concept of maximum recommended dose is dis Procaine is of importance in the immediate manage
cussed more fully in Chapter 18. ment of inadvertent intra-arterial (IA) injection of a drug;
Clinically available local anesthetics (the amides: artic its vasodilating properties are used to aid in breaking
aine, bupivacaine, lidocaine, mepivacaine, and prilocaine) arteriospasm.7
are discussed in detail here. Esters (procaine and propoxy Although not extremelycommon, the incidenceof allergy
caine) are mentioned in passing, more as a matter of histori to both procaine and other ester local anesthetics is signifi
cal interest than of necessity. Agents available for topical cantly greater than to amide local anesthetics.8
application (topical anesthetics) also are discussed. Metabolized in the blood by plasma cholinesterase,pro
caine does not exhibit increased toxicity in patients with
ESTER-TYPE LOCAL ANESTHETICS hepatic dysfunction.
The maximum recommended dose of procaine, used for
Procaine HCI peripheral nerve blocks, is 1000mg.9
Pertinent Information With a dissociation constant (pl<.)of 9.1, procaine has a
Classification. Ester. slowclinicalonset of anesthesia (6 to 10minutes)-a reason
Chemical Fonnula. 2-Diethylaminoethyl4-aminobenwate for inclusion of propoxycainein the anesthetic cartridge.
hydrochloride.
Propoxycaine HCI
Pertinent Information
Classification. Ester.
Chemical 2-Diethylaminoethyl-4-amino-2-
Formula.
propoxybenzoate hydrochloride.
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58 PARTI The Drugs
inclusion in a dentist's armamentarium of local anesthetics. Metabolism. In the liver, by the microsomal fixed
It was useful when the amides were absolutely contra function oxidases, to monoethylglyceine and xylidide;
indicated (e.g., because of documented allergy [although xylidide is a local anesthetic that is potentially toxic" (see
this is an extremely unlikely occurrence]), or when several Fig.2-3).
amide local anesthetics failed to provide clinicallyadequate Excretion. Via the kidneys; less than 10% unchanged,
anesthesia. Until its removal from the U.S. market in more than 80% various metabolites.
January 1996, the combination of procaine and propoxy Vasodilating Properties. Considerably less than those
caine was the only ester local anesthetic availablein dental of procaine; however, greater than those of prilocaine or
cartridge form. mepivacaine.
A dose of 0.4% propoxycaine/2%procaine with 1:20,000 pKa. 7.9.
levonordefrin (United States) or with 1:30,000norepineph pH of Plain Solution. 6.5.
rine (Canada) provided approximately40 minutes of pulpal pH of Vasoconstrictor-Containing Solution. =3.5.
anesthesiaand 2 to 3 hours of soft tissue anesthesia.The use Onset of Action. Rapid (3 to 5 minutes).
of norepinephrine in local anesthetic solutions is no longer Effective Dental Concentration. 2%.
recommended, especiallyin areaswhere prolonged ischemia Anesthetic Half-Life. 1.6hours (=90 minutes).
can lead to tissue necrosis. In the oral cavity,this is most Topical Anesthetic Action. Yes(in clinicallyacceptable
likelyto be seen in the palate. concentrations [5%]).
Pregnancy Classification. B.
Maximum Recommended The manufacturer's maxi
Dose. Safety During Lactation. S.
mum recommended dose was 3.0 mg/lb or 6.6 mg/kg of
body weight for the adult patient." For children, a dose Maximum Recommended Dose. The maximum recom
of 3.0 mg/lb was recommended up to a maximum of five mended dose by the FDAof lidocaine with or without epi
cartridges. nephrine is 3.2 mg/lb or 7.0 mg/kg of body weight for the
adult and pediatric patient, not to exceed a an absolute
AMIDE-TYPE LOCAL ANESTHETICS maximum dose of 500 mg12 (Table4-5).
TABLE 4-5
Lidocaine Hydrochloride
DURATION
Proprietary % LA Vasoconstrictor Pulpal Soft Tissue MRD
Lidocaine HCl
2 Epinephrine 1: 50,000 60 180-300 7.0 mg/kg
3.6 mg/lb 500 mg absolute maximum
2 Epinephrine 1: 100,000 60 180-300 7.0 mg/kg
3.6 mg/lb 500 mg absolute maximum
MRD, Maximum recommended dose.
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CHAPTER 4 Clinical Action of Specific Agents 59
....• -~.•......•
---~2'
(l..lDOCAJNEHYDROCHLORIDE
ANO EPINEPHRINEIN.JfCTlai, USP)
~t:SOOQO~
=..
81
C1
Figure 4-2. A, Lidocaine 2%. B, Lidocaine 2% with epinephrine 1: 50,000.C, Lidocaine with epinephrine 1: 100,000.(A, Courtesy Dent
sply, York, Pa. B and C, Courtesy Eastman Kodak, New York, NY, and Septodont, New Castle, Del.)
Lldocaine HCl is available in North America in two minutes). This vasodilatory effectleads to (1) higher blood
formulations: 2% with epinephrine 1:50,000,and 2% with levelsof lidocaine, with an attendant increase in the risk of
epinephrine 1: 100,000(Fig.4-2). A 2% lidocaine with epi adversereactions, along with (2) increased perfusion in the
nephrine 1:300,000formulation is availablein some coun area of drug deposition. Few clinical indications are known
tries (although not in North Americaas of August2011).2% for the use of 2% lidocaine without a vasoconstrictor in the
lidocaine without epinephrine (2% "plain") is no longer typical dental practice. As of August 2011, 2% lidocaine
availablein dental cartridges in North America. without epinephrine (2% "plain") was no longer availablein
1\ilroPercent Lidocaine HCI Without a Vasoconstrictor dental cartridges in North America.
(Lidocaine Plain). Its vasodilating properties severelylimit 1\ilro Percent Lidocaine With Epinephrine f:50,000.
the duration and the depth of pulpal anesthesia (5 to 10 (Table4-6)
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60 PARTI The Drugs
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CHAPTER 4 Clinical Action of Specific Agents 61
TABLE 4-8
Mepivacaine Hydrochloride
DURATION
Proprietary % LA Vasoconstrictor PuIpal Soft Tissue MRD
MepivacaineHCI 3 None 20-infiltration 120-180 6.6 mg/kg
40-nerve block 3.0 mg/lb
400 mg absolute maximum
MepivacaineHCI 2 Levonordefrin 60 180-300 6.6 mg/kg
3.0 mg/lb
400 mg absolute maximum
MRD, Maximum recommended dose.
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62 PARTI The Drugs
-
c:
~
=
~ c:a...!l0 ,1,•..
Figure 4-3. A through C, Mepivacaine 3%. D, Mepivacaine 2% with levonordefrin 1 :20,000. (A, Courtesy Dentsply, York, Pa. B, Courtesy
Eastman Kodak, New York, NY. D, Courtesy Septodont, New Castle, Del.)
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CHAPTER 4 ClinicalAction of SpecificAgents 63
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64 PART I The Drugs
TABLE 4-11
Prilocaine Hydrochloride
DURATION
Proprietary % LA Vasoconstrictor Pulpal Soft Tissue MRD
Prilocaine HCl 4 None 10-15infiltration 90-120 infiltration 8.0 mg/kg
40-60 nerve block 120-240nerve block 3.6 mg/lb
600 mg absolute maximum
Prilocaine HCl 4 Epinephrine 60-90 180-480 8.0 mg/kg
1:200,000 3.6 mg/lb
600 mg absolute maximum
MRD, Maximum recommended dose.
---
•111: •••••
-------
~---~ ~--------~-~----
A~ ,_Ml\llVI
4"::__':ioq.ooo
wilh apiiephrint
(prilocoine and epinephrine
Injection. USP)
40,..Jri
A c
B D
Figure 4-4. A and B, Prilocaine 4%. C and D, Prilocaine 4% with epinephrine 1:200,000.(Courtesy Dentsply,York,Pa.)
Comments. Clinical actions of prilocaine plain (Fig. 4-4) Clinicalactions of prilocaine with 1:200,000epinephrine
vary significantlywith the type of injection technique used are not as dependent on anesthetic technique. Prilocaine
Although true for all anesthetics, the variation between with epinephrine provides lengthy anesthesiawhile offering
supraperiosteal infiltration and nerve block is more pro a less concentrated epinephrine dilution: 1:200,000.Pulpal
nounced with prilocaine plain (and mepivacaine plain). anesthesiaof 60 to 90 minutes' duration and soft tissue anes
Infiltration provides short durations of pulpal {10 to 15 thesia of 3 to 8 hours are common. The cartridge contains
minutes) and soft tissue {l,Vi to 2 hours) anesthesia,whereas 9 µg of epinephrine; therefore epinephrine-sensitive indi
regional nerve block (e.g.,inferior alveolarnerve block) pro viduals, such as the A5A 3 cardiovascular disease patient,
vides pulpal anesthesiafor up to 60 minutes (commonly 40 may receiveup to four cartridges (36 µg) of prilocaine with
to 60 minutes) and soft tissue anesthesia for 2 to 4 hours.32 epinephrine.
Thus prilocaine plain frequentlyis ableto provide anesthesia In epinephrine-sensitive patients requiring prolonged
that is equal in duration to that attained with lidocaine or pulpal anesthesia {~60 minutes), prilocaine plain or with
mepivacainewith a vasoconstrictor. 1:200,000epinephrine is stronglyrecommended.It israpidly
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CHAPTER 4 Clinical Action of Specific Agents 65
D
TABLE 4-12 COOCH3
Prilocaine 4% With and Without Vasoconstrictor*t • HCI
CONCENTRATION: 4% CARTRIDGE CONTAINS: 72 mg
MRD: 8.0 mg/kg MRD: 3.6 mg/lb NHCOCHNHCH2CH2CH3
H3C I
Weight. Weight.
CH3
kg mg Cartridges:!: lb mg Cartridges:!:
10 80 1.0 20 72 1.0 Prepared by. H. Rusching et al, 1969.
20 160 2.0 40 144 2.0 FDA Approved. April 2000 (United States).
30 240 3.0 60 218 3.0 Introduced. 1976 in Germany and Switzerland, 1983 in
40 320 4.5 80 290 4.0 Canada, 2000 in the United States.
50 400 5.5 100 362 5.0 Potency. 1.5 times that of lidocaine; 1.9 times that of
60 480 6.5 120 434 6.0 procaine.
70 560 7.5 140 506 7.0
Toxicity. Similar to lidocaine and procaine.
80 600 8.0 160 578 8.0
Metabolism. Articaine is the only amide-type local anes
90 600 8.0 180 600 8.0
100 600 8.0 200 600 8.0 thetic that contains a thiophene group. Because articaine
HCl is the only widely used amide-type local anesthetic that
MRD, Maximum recommended dose.
contains an ester group, biotransformation of articaine HCl
*Aswith all local anesthetics,the dose varies, depending on the area to be
anesthetized,the vascularity of the tissues, individual tolerance, and the
occurs in both plasma (hydrolysis by plasma esterase) and
technique of anesthesia.The lowest dose needed to provide effective liver (hepatic microsomal enzymes). Degradation of artic
anesthesia should be administered. aine HCl is initiated by hydrolysis of the carboxylic acid ester
+Dosesindicated are the maximum suggestedfor normal healthy groups to obtain free carboxylic acid.37 Its primary metabo
individuals (ASA1); they should be decreasedfor debilitated or elderly lite, articainic acid, is pharmacologically inactive, undergo
patients.
:j:Roundedto the nearest half-cartridge. ing additional biotransformation to form articainic acid
glucuronide.37 Additional metabolites have been detected in
animal studies. 38 From this point, the reaction can follow
several pathways: cleavage of carboxylic acid, formation of
an acid amino group by internal cyclization, and oxidation.
biotransformed and, for this reason, is considered to be a safe Excretion. Via the kidneys; approximately 5% to 10%
local anesthetic (e.g., lower toxicity).28 unchanged, approximately 90% metabolites (M1 at 87%, M2
Prilocaine is relatively contraindicated in patients with at 2%).
idiopathic or congenital methemoglobinemia, hemoglo Vasodilating Properties. Articaine has a vasodilating
binopathies (sickle cell anemia), anemia, or cardiac or effect equal to that of lidocaine. Procaine is slightly more
respiratory failure evidenced by hypoxia, because methemo vasoactive.
globin levels are increased, decreasing oxygen-carrying pK•. 7.8.
capacity. Prilocaine administration is also relatively contra pH of Plain Solution. Not available in North America
indicated in patients receiving acetaminophen or phenace (4% articaine HCl "plain" is available in Germany).
tin, both of which produce elevations in methemoglobin pH of Vasoconstrictor-Containing Solution. 3.5 to 4.0.
levels (Table 4-12). Onset of Action. Articaine 1 :200,000, infiltration 1 to
It has been claimed that prilocaine HCl 4% solution 2 minutes, mandibular block 2 to 3 minutes; articaine
(with or without vasopressor) is associated with a higher risk 1: 100,000, infiltration 1 to 2 minutes, mandibular block 2
of paresthesia, primarily of the lingual nerve, than other to 2,Vi minutes.
anesthetic formulations following inferior alveolar nerve Effective Dental Concentration. 4% with 1 : 100,000 or
block.34•35 Although the "evidence" remains anecdotal, it 1:200,000 epinephrine. Articaine HCl is available with epi
appears that this drug, as formulated in North America [as nephrine 1 :400,000 in Germany.
a 4% solution], might be more neurotoxic than other com Anesthetic Half-Life. 0.5 hours [27 minutes].39
monly used local anesthetic formulations.36 This question Topical Anesthetic Action. Not in clinically acceptable
will be discussed in greater detail in Chapter 17. concentrations.
Pregnancy Classification. C.
Safety During Lactation. Unknown (use with caution in
Articaine HCI females who are breast-feeding because it is not known
Pertinent Information whether articaine is excreted in milk).
Classification. Hybrid molecule. Classified as an amide;
however, it possesses both amide and ester characteristics. Maximum Recommended Dose. The FDA maximum rec
Chemical Formula. 3-N-Propylamino-proprionylamino- ommended dose is 7.0 mg/kg or 3.2 mg/lb of body weight
2-carbomethoxy-4-methylthiophene hydrochloride. for the adult patient (Tables 4-13 and 4-14).22•40
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66 PARTI The Drugs
TABLE 4-13
Articaine Hydrochloride
DURATION
Proprietary % LA Vasoconstrictor PuIpal Soft Tissue MRD
Articaine HCl 4 Epinephrine 1: 100,000 60-75 180-360 7.0mg/kg
3.2 mg/lb
No absolute maximum
Articaine HCl 4 Epinephrine 45-60 120-300 7.0mg/kg
1:200,000 3.2 mg/lb
No absolute maximum
MRD, Maximum recommended dose.
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CHAPTER 4 ClinicalAction of SpecificAgents 67
.
Septocetne 111 .-\niaim• lndrod1loritk ./".. 11i1/r
-
Epi11•·i1l1rirn· 1:100.(}()(}lni•~lirm
c::
.g
.s
~ 50~.--Ql-'.l.7rnl.
-
(/)
Figure 4-5. Articaine 4% with epinephrine 1: 100,000 and 1 :200,000. (Courtesy Septodont, New Castle, Dd.)
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68 PARTI The Drugs
Vasodilating Properties. Relatively significant: greater administration of any suitable (e.g., intermediate-duration)
than those of lidocaine, prilocaine, and mepivacaine, yet local anesthetic to manage periprocedural pain. A long
considerably less than those of procaine. duration local anesthetic (bupivacaine) is administered
pK•. 8.1. immediately before patient discharge (if deemed necessary),
pH of Plain Solution. 4.5 to 6.0. with the patient continuing to take the oral dose of NSAID
pH of Vasoconstrictor-Containing Solution. 3.0 to 4.5. every "x" hours as indicated (not "prn pain") for "y" number
Onset of Action. Slower onset time than other com- of days. The requirement for opioid agonist analgesics is
monly used local anesthetics (e.g., 6 to 10 minutes). significantly diminished with this protocol. Hargreaves dem
Effective Dental Concentration. 0.5%. onstrated that the preoperative oral dose of NSAID is not
Anesthetic Half-Life. 2.7 hours. necessary as long as the initial oral dose can be ingested
Topical Anesthetic Action. Not in clinically acceptable within 1 hour of the start of the surgical procedure. 65
concentrations. Onset of anesthesia with bupivacaine is commonly
Pregnancy Classification. C. delayed for from 6 to 10 minutes, a fact that is understand
Safety During Lactation. S? able in view of its pl<,. of 8.1. If this occurs, it may be
advisable, at subsequent appointments, to initiate proce
Maximum Recommended Dose. The FDA maximum rec dural pain control with a more rapid-acting amide (e.g.,
ommended dose ofbupivacaine is 90 mg. There is no recom articaine, mepivacaine, lidocaine, prilocaine), which pro
mended dosage for bupivacaine based on body weight in the vides clinically acceptable pain control within a few moments,
United States (Table 4-15).60 In Canada, the maximum dose allowing the procedure to commence more promptly. Follow
is based on 2.0 mg/kg (0.9 mg/lb). this with an injection of bupivacaine for long-duration
anesthesia.
Comments. Bupivacaine has been available in cartridge Bupivacaine is not recommended in younger patients
form since February 1982 in Canada and July 1983 in the or in those for whom the risk of postoperative soft tissue
United States. Bupivacaine is available as a 0.5% solution injury produced by self-mutilation is increased, such as
with 1: 200,000 epinephrine (Fig. 4-7); there are two primary physically and mentally disabled persons. Bupivacaine is
indications for its utilization in dentistry:
1. Lengthy dental procedures for which pulpal (deep)
anesthesia in excess of 90 minutes is necessary (e.g., full
mouth reconstruction, implant surgery, extensive
periodontal procedures)
2. Management of postoperative pain (e.g., endodontic,
periodontal, postimplant, surgical)
The patient's requirement for postoperative opioid anal
gesics is considerably lessened when bupivacaine is admin
istered for pain control.61 For postoperative pain control
after a short surgical procedure (<30 minutes), bupivacaine
may be administered at the start of the procedure; however,
for postoperative pain control after lengthy surgical proce
dures, it might be reasonable to administer bupivacaine at
the conclusion of the procedure, shortly before the patient's
discharge from the office.
A regimen for management of postsurgical pain has been
developed that is clinically quite effective. 62-64 It suggests
the pretreatment administration of one oral dose of a Figure 4- 7. Bupivacaine 0.5% with epinephrine 1:200,000.
nonsteroidal anti-inflammatory drug (NSAID), followed by (Courtesy Eastman Kodak,NewYork,NY.)
TABLE 4-15
Bupivacaine Hydrochloride
DURATION
Proprietary % LA Vasoconstridor Pu Ipal Soft Tissue MRD
BupivacaineHCl 0.5 Epinephrine 1:200,000 90-180 240-540 United States:no mg/kg or mg/lb listed
(reports up to 720) Canada: 2.0 mg/kg, 0.9 mg/lb,
90 mg absolute maximum
MRD, Maximum recommended dose.
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CHAPTER 4 ClinicalAction of SpecificAgents 69
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70 PART I The Drugs
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CHAPTER 4 ClinicalAction of SpecificAgents 71
NDC 0362-5001-50
A
Figure 4-9. Topical anesthetics-Lidocaine. A, Octocaine ointment. B, Dentipatch. (A, Courtesy Septodent, New Castle, DE. B, Courtesy
Noven Pharmaceuticals Inc., Miami, FL, www.noven.com.)
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72 PART I The Drugs
Tetracaine Hydrochloride
TABLE 4-17
Tetracaine hydrochloride (2-dimethylaminoethyl-4- Duration of Pulpal and Soft Tissue Anesthesia for
butylaminobenzoate hydrochloride) is a long-duration ester Available Local Anesthetics
local anesthetic that can be injected or applied topically.
DURATION
1. Highly soluble in water (APPROXIMATE MINUTES)
2. Applied topically,fiveto eight times more potent than
Drug Formulation PuIpal Soft Tissue
cocaine
3. Onset of action after topical application is slow. Mepivacaine3% (infiltration) 5-10 90-120
4. Duration of action is approximately45 minutes after Prilocaine 4% (infiltration) 10-15 60-120
Prilocaine 4% (nerve block) 40-60 120-240
topical application.
Articaine 4% + epinephrine 45-60 180-240
5. Metabolizedin plasma and the liver by plasma
1:200,000
pseudocholinesteraseat a slowerrate than procaine Lidocaine2% + epinephrine 60 180-300
6. When used by injection, availableas a 0.15% 1:50,000
concentration Lidocaine2% + epinephrine 60 180-300
7. 2% concentration is used for topical application. 1:100,000
8. Rapidly absorbed through mucous membranes. Use Mepivacaine2% + 60 180-300
should be limited to small areas to avoid rapid levonordefrin 1:20,000
absorption. Other, more slowlyor poorly absorbed Articaine 4% + epinephrine 60-75 180-300
agents should be used in lieu of tetracaine when larger 1:100,000
areas of topical anesthesia are necessary. Prilocaine 4% + epinephrine 60-90 180-480
9. Maximum recommended dose of 20 mg when used for 1:200,000
topical application. This represents 1 mL of a 2% Bupivacaine0.5% + >90 240-720
epinephrine 1:200,000
solution.
10. Caution is urged because of great potential for
systemictoxicity. (3) the need for hemostasis; and (4) whether any contrain
11. Availability(Canada): dications exist to administration of the selected local
a. Aerosol:0.7 mg/metered spray anesthetic.P" Table 4-17 lists currently availablelocal anes
1. Supracaine thetic formulations according to their expected duration of
12. Tetracainein a 3% concentration, with the pulpal and soft tissue anesthesia.Again,it must be noted that
vasoconstrictor oxymetazocine,has been shown to these numbers are approximations, and the actual duration
provide pulpal anesthesia of maxillary teeth when of clinical anesthesia may be somewhat longer or shorter
administered by aerosol spray into a patient's nares.81 than indicated.
Use of intranasal local anesthesia for dental pain A second consideration in the selection of a local anes
control in discussed in Chapter 20. thetic must be the requirement for pain control after treat
ment. A long-duration local anesthetic can be administered
when postoperative pain is thought to be a factor. Local
SELECTION OF A LOCAL ANESTHETIC
anesthetics providing a shorter duration of soft tissue anes
Becauseof the many local anesthetic combinations available thesia can be used for nontraumatic procedures.When post
for injection, it sometimes is difficultto select an ideal drug operative pain is considered likely,0.5% bupivacaine (for 8
for a given patient. Many dentists simply deal with this by to 12 hours of soft tissue anesthesia [via nerve block]) is
using one local anesthetic for all procedures, regardless of suggested.
their duration. For example,the dentist may elect to use 2% For patients in whom postoperative anesthesiarepresents
lidocainewith 1: 100,000epinephrine for procedures lasting a potential risk,a shorter-duration anesthetic should be con
5 to 10 minutes and for procedures involving90 minutes of sidered. These patients include younger children, the older
treatment time. Although the duration of pulpal anesthesia old patient, and the physically or mentally disabled, who
achievablewith this drug, in idealcircumstances,may permit might accidentally bite or chew their lips or tongue, and
pain-free treatment in both these instances,the patient who persons unable to miss a meal (e.g.,those with type 1 diabe
requires only 10 minutes of pulpal anesthesia will remain tes) because of residual soft tissue anesthesia. For these
anesthetized unnecessarily for an additional 3 to 5 hours patients, 3% mepivacaine is recommended for use in short
(soft tissues), whereas the patient requiring 90 minutes of procedures. However in situations in which these patients
pulpal anesthesiawill likelyexperiencepain toward the end require a more profound and/or longer duration of pulpal
of the procedure. anesthesia, use of a local anesthetic containing a vaso
A rational approach to selection of an appropriate local constrictor is necessary.The introduction of the local anes
anesthetic for a patient includes consideration of several thesia reversalagent, phentolamine mesylate(Oraverse),has
factors: (1) the length of time for which pain control is made it possible to significantly shorten the duration of
necessary; (2) the need for posttreatment pain control; residual soft tissue anesthesia, thereby minimizing the risk
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CHAPTER 4 Clinical Action of Specific Agents 73
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74 PARTI The Drugs
13. BrownRS,PaluvoiS,ChoksiS,et al:Evaluatinga dental patient 35 Garisto GA,GaffenAS,LawrenceHP,et al: Occurrence of par
for local anesthesia allergy,Comp Contin Educ Dent 23:225- esthesia after dental local anesthetic administration in the
228, 131-132, 134, 140,2002. United States,J Am Dent Assoc 141:836-844,2010.
14. Jackson D, Chen AH, Bennett CR: Identifying true lidocaine 36. Pogrel MA: Permanent nerve damage from inferior alveolar
allergy,J Am Dent Assoc 125:1362-1366,1994. nerve blocks-an update to include articaine, J Calif Dent
15. Sindel LJ, deShazo RD: Accidents resulting from local Assoc35:271-273,2007.
anesthetics: true or false allergy?Clin Rev Allergy9:379-395, 37. van Oss GE, Vree TB, Baars AM, et al: Pharmacokinetics,
1991. metabolism, and renal excretionof articaine and its metabolite
16. BallIA:Allergicreactions to lignocaine,Br Dent J 186:524--526, articainic acid in patients after epidural administration, Eur J
1999. Anaesthesiol6:19-56, 1989.
17. Baluga JC: Allergyto local anaesthetics in dentistry: myth or 38. van Oss GE, Vree TB, Baars AM, et al: Clinical effects and
reality?RevAlergMex 50:176-181,2003. pharmacokinetics of articainic acid in one volunteer after
18. ThyssenJP,Menne T,ElberlingJ,et al:Hypersensitivityto local intravenous administration, Pharm Weekbl (Sc) 10:284--286,
anaesthetics-update and proposal of evaluation algorithm, 1988.
Contact Dermatitis 59:69-78, 2008. 39. VreeTB,BaarsAM,van Oss GE,et al:High performance liquid
19. YoungER,Mason DR,SasoMA,et al: Some clinicalproperties chromatography and preliminary pharmacokinetics of artic
of Octocaine 200 (2 percent lidocaine with epinephrine aine and its 2-carboxy metabolite in human serum and urine,
1:200,000),J Can Dent Assoc55:987-991, 1989. J Chromatogr 424:240-444, 1988.
20. BuckleyJA,Ciancio SG,McMullenJA:Efficacyof epinephrine 40. Prescribing information: Septocaine, Louisville, Colo, 2011,
concentration in local anesthesia during periodontal surgery, Septodont Inc.
J Periodontol 55:653-657, 1984. 41. Malamed SF,Gagnon S, Leblanc D: Safetyof articaine: a new
21. DeToledo JC: Lldocaine and seizures, Ther Drug Monit amide local anesthetic, J Am Dent Assoc 132:177-185,2001.
22:320-322,2000. 42. Malamed SF,Gagnon S, LeblancD: Articaine hydrochloride in
22. Malamed SF,YagielaJ: Local anesthetics. In ADA Guide to pediatric dentistry: safety and efficacyof a new amide-type
Dental Therapeutics, Chicago, Ill, 1998, American Dental local anesthetic, Pediatr Dent 22:307-311,2000.
Association. 43. Malamed SF,Gagnon S, LeblancD: Efficacyof articaine: a new
23. GeddesIC: Metabolism oflocal anesthetic agents,Int Anesthe amide local anesthetic, J Am Dent Assoc 131:535--642,2000.
siol Clin 5:525-549, 1967. 44. Donaldson D,James-PerdokL,Craig BJ,et al:A comparison of
24. Severinghaus JW, Xu F-D, Spellman MJ: Benzocaine and Ultracaine DS (articaine HCl) and Citanest Forte (prilocaine
methernoglobin: recommended actions, Anesthesiology 74: HCl) in maxillary infiltration and mandibular nerve block,
385-386, 1991. J Can Dent Assoc53:38--42,1987.
25. Schroeder TH, Dieterich HJ, Muhlbauer B: Methemoglobin 45. Knoll-KohlerE, Rupprecht S:Articaine for local anaesthesiain
ernia after maxillary block with bupivacaine and additional dentistry: a lidocaine controlled double blind cross-overstudy,
injection of lidocaine in the operative field,Acta Anaesthesiol Eur J Pain 13:59--63,1992.
Scand 43:480-482, 1999. 46. Septodont Inc., NA: Personal communications, May 2011.
26. Wilburn-Goo D, Lloyd LM: When patients become cyanotic: 47. Schulze-Husmann M: Experimental evaluation of the new
acquired methemoglobinemia, J Am Dent Assoc 130:626-631, local anestheticUltracaine in dental practice, doctoral disserta
1999. tion, Bonn, 1974,Universityof Bonn.
27. de Jong RH: Local anesthetics,St Louis, 1994,Mosby. 48. Cliniciansguide to dental products and techniques,Septocaine.
28. Akerman B,Astrom A, RossS, et al: Studieson the absorption, CRANewsletterJune 2001.
distribution, and metabolism of labeled prilocaine and lido 49. Kanaa MD, Whitworth JM, Corbett IP, et al: Articaine buccal
caine in some animal species,Acta Pharmacol Toxicol24:389- infiltration enhances the effectiveness of lidocaine inferior
403, 1966. alveolarnerve block, Int Endod J 42:238--246,2009.
29. Foldes FF,MolloyR, McNallPG, et al: Comparison of toxicity 50. MeechanJG:Infiltration anesthesiain the mandible, Dent Clin
of intravenously given local anesthetic agents in man, JAMA North Am 54:621--629,2010.
172:1493-1498,1960. 51. Yonchak T, Reader A, Beck M, et al: Anesthetic efficacy of
30. EnglessonS, Eriksson E, Ortengren B:Differencesin tolerance infiltrations in mandibular anterior teeth, Anesth Prog 48:55-
to intravenous Xylocaine and Citanest, Acta Anaesthesiol 60, 2001.
Scand Suppl 16:141-145,1965. 52. Meechan JG, Ledvinka JI: Pulpal anaesthesia for mandibular
31. Deriksson E, Granberg PO: Studies on the renal excretion of central incisor teeth: a comparison of infiltration and intraliga
Citanest and Xylocaine,ActaAnaesthesiolScand Suppl 16:79- mentary injections, Int Endod J 35:629--634,2002.
85, 1985. 53. Kanaa MD, Whitworth JM, Corbett IP, et al: Articaine and
32. Smith DW, Peterson MR, DeBerard SC: Local anesthesia: lidocaine mandibular buccal infiltration anesthesia:a prospec
topical application, local infiltration, and fieldblock, Postgrad tive randomized double-blind cross-over study, J Endod
Med 106:27--60,64--66,1999. 32:296-298,2006.
33. Akinturk S, Eroglu A: A clinical comparison of topical piroxi 54. Robertson D,Nusstein J,ReaderA, et al:The anesthetic efficacy
cam and EMLAcream for pain reliefand inflammation in laser of articaine in buccalinfiltration of mandibular posterior teeth,
hair removal, LasersMed Sci 24:535-538,2009. J Am Dent Assoc 138:1104--1112,2007.
34. Haas DA, Lennon D: A 21 year retrospective study of 55. Haase A, Reader A, Nusstein J, et al: Comparing anesthetic
reports of paresthesia following local anesthetic admini efficacyof articaine versus lidocaine as a supplemental buccal
stration, J Can Dent Assoc 61:319-320, 323-326, 329-330, infiltration of the mandibular first molar after an inferior alve
1995. olar nerve block, J Am Dent Assoc 139:1228--1235,2008.
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CHAPTER 4 ClinicalActionof SpecificAgents 75
56. Jakobs W: Status of dental anesthesia in Germany, Anesth Prog 71. Alston TA: Antagonism of sulfonamides by benzocaine and
36:10--212, 1989. chloroprocaine,Anesthesiology76:375--476,1992.
57. Deutscher Dentalmarkt Jahresbericht (DDM) 2010 (German 72. Adriani J, Zepernick R: Clinicaleffectivenessof drugs used for
Dental Market Annual Report 2010) GfK HealthCare, Nurem topical anesthesia,JAMA188:93,1964.
berg, Germany. 73. TaddioA: Pain management for neonatal circumcision,Paedi
58. Malamed SF: Handbook of local anesthesia, ed 4, St Louis, atr Drugs 3:101-111,2001.
1997, Mosby, pp 63-64. 74. VanscheidtW,SadjadiZ, LillieborgS:EMLAanaestheticcream
59. Articaine, epinephrine: contraindications/precautions, MD for sharp leg ulcer debridement: a review of the clinical evi
Consult. Available at: http://www.mdconsult.com/php/25067 dence for analgesic efficacyand tolerability, Eur J Dermatol
9983-2/homepage. Revised April 21, 2010. Accessed May 24, 11:20--96,2001.
2011. 75. Wright VC:Vulvarbiopsy:techniques for reducing patient dis
60. Jakobs W: Actual aspects of dental anesthesia in Germany. Pre comfort, Adv Nurse Pract 9:17-60, 2001.
sented at the 10th International Dental Congress on Modern 76. EMLA,MD Consult.Availableat: http://www.mdconsult.com/
Pain Control, IFDAS, Edinburgh, Scotland, UK, June 2003. php/250679983-2/homepage.RevisedMay 12,2010.Accessed
61. Prescribing information: Bupivacaine HCl, Lake Forest, Ill, May 24, 2011.
November 2009, Hospira, Inc. 77. Bernardi M, SeccoF,BenechA:Anestheticefficacyof a eutectic
62. Moore PA: Bupivacaine: a long-lasting local anesthetic for den mixture of lidocaine and prilocaine (EMLA) on the oral
tistry, Oral Surg 58:369, 1984. mucosa: prospective double-blind study with a placebo,
63. Acute Pain Management Guideline Panel: Acute pain manage Minerva Stomatol 48:9-43, 1999.
ment: operative or medical procedures and trauma. Clinical 78. Munshi AK,Hegde AM, Latha R: Use of EMLA:is it an injec
practice guideline. AHCPR Publication Number 92-0032, tion free alternative?J Clin Pediatr Dent 25:215-219,2001.
Rockville, Md, 1992, Agency for Health Care Policy and 79. Franz-Montan M, Ranali J, RamacciatoJC, et al: Ulceration of
Research, Public Health Service, U.S. Department of Health gingivalmucosa after topical application of EMLA:report of
and Human Services. four cases,Br Dent J 204:133-134,2008.
64. Oxford League Table of Analgesics in Acute Pain: Bandolier 80. Nayak R, Sudha P: Evaluation of three topical anaesthetic
Website. Available at: http://www.medicine.ox.ac.uk/bandolier/ agents against pain: a clinicalstudy,Indian J Dent Res 17:155-
booth/painpag/acutrev/analgesicsflftab.html. Accessed May 24, 160,2006.
2011. 81. Universityof Buffalo,The State Universityof NewYork:Nasap
65. Hargreaves KM, Keiser K: Development of new pain manage spray may end dental needle injections for upper teeth repair.
ment strategies, J Dent Educ 66:113-121, 2002. Availableat: www.buffalo.edu/news/9911.AccessedFebruary
66. Malamed SF: Handbook of local anesthesia, ed 5, St Louis, 17,2009.
2003, CV Mosby, pp 74-75. 82. Moore PA, Hersh EY, Papas AS, et al: Pharmacokinetics
67. Adriani J, Campbell D: Fatalities following topical application of lidocaine with epinephrine following local anesthesia
of local anesthetics to mucous membranes, JAMA 162:1527, reversal with phentolamine mesylate,Anesth Prog 55:40--48,
1956. 2008.
68. Jeske AH, Blanton PL: Misconceptions involving dental local 83. Hersh EY,Moore PA, Papas AS, et al, Soft Tissue Anesthesia
anesthesia. Part 2. Pharmacology, Texas Dent J 119:310--314, RecoveryGroup: Reversalof soft-tissue local anesthesia with
2002. phentolamine mesylate in adolescents and adults, J Am Dent
69. Rosivack RG, Koenigsberg SR, Maxwell KC: An analysis of the Assoc 139:1080--1093,2008.
effectiveness of two topical anesthetics, Anesth Prog 37:290-- 84. TavaresM, Goodson JM,Studen-PavlovichD, et al, SoftTissue
292, 1990. Anesthesia ReversalGroup: Reversalof soft-tissue local anes
70. Patterson RP, Anderson J: Allergic reactions to drugs and bio thesia with phentolamine mesylate in pediatric patients, J Am
logic agents, JAMA 248:2637-2645, 1982. Dent Assoc 139:1095-1104,2008.
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IN THIS PART
Chapter 5 The Syringe
Chapter 6 The Needle
Chapter 7 The Cartridge
Chapter 8 Additional Armamentarium
Chapter 9 Preparation of the Armamentarium
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PART
The Armamentarium
The equipment necessary for the administration of local anesthetics is introduced and discussed in
this section. This includes the syringe, needle, and local anesthetic cartridge, as well as additional
items of equipment. In addition to providing a description of the armamentarium, each chapter
reviews the proper care and handling of the equipment and problems that may be encountered
with its use. A discussion of the proper technique for assembling and disassemblingthe equipment
follows.
The introduction of computer-controlled local anesthetic delivery (C-CLAD) systems has
enhanced the delivery of local anesthetic for many dentists and their patients. These devices have
demonstrated great utility in the painless delivery of dental local anesthetics and are described in
detail in this section.
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I
The Syringe
' I •I
The syringeis one of three essentialcomponents of the local The needle then passes into the barrel, where it penetrates
anesthetic armamentariwn (others include the needle and the diaphragm of the local anesthetic cartridge. The needle
the cartridge). It is the vehiclewhereby the contents of the adaptor (screw hub or convertible tip) is removable and
anesthetic cartridge are deliveredthrough the needle to the sometimes is discarded inadvertently along with the dispos
patient. able needle.
The aspirating syringehas a devicesuch as a sharp, hook
shaped end {oftencalledthe harpoon) attached to the piston
TYPES OF SYRINGES
that is used to penetrate the thick silicone rubber stopper
Eight types of syringes for local anesthetic administration (bung) at the opposite end of the cartridge (from the needle).
are available for use in dentistry today. They represent a Provided the needle is of adequate gauge, when negative
considerableimprovement over the local anesthetic syringes pressure is exerted on the thwnb ring by the administrator,
formerly used. These various types of syringes are listed in blood will enter into the needle and will be visible in the
Box 5-1. cartridge if the needle tip rests within the lwnen of a blood
Syringesthat do not permit aspiration (i.e.,nonaspirating vessel. Positive pressure applied to the thumb ring forces
syringes) are not discussed because their use unacceptably local anesthetic into the needle lwnen and the tissueswher
increases the risk of inadvertent intravascular drug admin everthe needle tip lies.The thumb ring and finger grips give
istration. Use of aspirating dental syringes (capable of the the administrator added control over the syringe.Almost all
aspiration of blood) represents the standard of care. syringe manufacturers provide syringeswith both "regular"
American Dental Association criteria for acceptance of and "small" thumb rings (Fig. 5-2). Most metallic, breech
local anesthetic syringesinclude the following'P; loading, aspirating syringes are constructed of chrome
1. They must be durable and able to withstand repeated plated brass and stainlesssteel.
sterilization without damage. (If the unit is disposable, Advantages and disadvantages of the metallic, breech
it should be packaged in a sterile container.) loading, aspirating syringe are listed in Box 5-2.
2. They should be capable of accepting a wide variety of
cartridges and needles of different manufacture, and Breech-Loading. Plastic, Cartridge-Type. Aspirating. A
should permit repeated use. plastic, reusable,dental aspirating syringe is availablethat is
3. They should be inexpensive,self-contained,lightweight, both autoclavable and chemically sterilizable.With proper
and simple to use with one hand. care and handling, this syringe may be used for multiple
4. They should provide for effectiveaspiration and be anesthetic administrations before it is discarded.Advantages
constructed so that blood may be easilyobserved in the and disadvantagesof the plastic, reusable,aspirating syringe
cartridge. are listed in Box 5-3.
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CHAPTER 5 The Syringe 79
BOX 5-1 Syringe Types Available in Dentistry BOX 5-2 Advantages and Disadvantages of the
Metallic., Breech-Loading, Aspirating Syringe
1. Nondisposable syringes:
a. Breech-loading, metallic, cartridge-type, Advantages Disadvantages
aspirating Visible cartridge Weight (heavier than
b. Breech-loading, plastic, cartridge-type, aspirating Aspiration with one hand plastic syringe)
c. Breech-loading, metallic, cartridge-type, Autoclavable Syringe may be too big for
self-aspirating Rust resistant small operators
d. Pressure syringe for periodontal ligament Long lasting with proper Possibility of infection
injection maintenance with improper care
e. Jet injector ("needle-less" syringe)
2. Disposable syringes
3. "Safety" syringes
4. Computer-controlled local anesthetic delivery BOX 5-3 Advantages and Disadvantages of the
systems Plastic., Reusable, Aspirating Syringe
Advantages Disadvantages
Plastic eliminates metallic, Size (may be too big for
clinical look small operators)
Lightweight: provides better Possibility of infection
Piston with
harpoon "feel" during injection with improper care
Cartridge is visible Deterioration of plastic
Aspiration with one hand with repeated
Rust resistant autoclaving
Long lasting with proper
maintenance
Lower cost
Syringe Thumb ring
barrel
TABLE 5-1
actual clinical practice, too little attention is paid to this Percentages of Dentists Who Aspirate Before Injection
procedure (Table 5-1).
INFERIORALVEOLAR MAXILLARY
With commonly used breech-loading, metallic, cartridge NERVEBLOCK INFILTRATION
type syringes, an aspiration test must be carried out pur
Frequency Percent Cumulative Percent Cumulative
posefully by the administrator before or during drug
deposition. The key word here is purposefully. However, as Always 63.2 40.2
demonstrated in Table 5-1, many dentists do not purpose Sometimes 14.7 77.9 24.1 64.3
Rarely 9.2 87.1 18.4 82.7
fully perform an aspiration test before injection of the anes
Never 12.9 17.3
thetic drug. 4
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80 PARTII The Armamentarium
Toincreasethe ease of aspiration, self-aspiratingsyringes The self-aspirating syringe was introduced into the
have been developed (Fig. 5-3). These syringes use the United States in 1981.After an initial period of enthusiasm,
elasticityof the rubber diaphragm in the anesthetic cartridge the popularity of this syringe decreased. Some dentists
to obtain the necessary negative pressure for aspiration. believed that the self-aspirating syringe did not provide
The diaphragm rests on a metal projection inside the syringe the same reliabledegree of aspiration that was possiblewith
that directs the needle into the cartridge (Fig.5-4). Pressure the harpoon-aspirating syringe. It has been demonstrated,
acting directly on the cartridge through the thumb disc however,that this syringe does in fact aspirate as reliablyas
(Fig. 5-5) or indirectly through the plunger shaft distorts the harpoon-aspirating syringe."? The notion can occur
(stretches) the rubber diaphragm, producing positive pres that aspiration may not be as reliablewith the self-aspirating
sure within the anesthetic cartridge. When that pressure is syringe because the administrator simply has to depress
released,sufficientnegativepressure developswithin the car and release the thumb ring to aspirate, rather than pulling
tridge to permit aspiration. The thumb ring produces twice back on the thumb ring. Moving the thumb off the thumb
as much negativepressure as the plunger shaft. The use of a ring and onto the thumb disc for aspiration has been
self-aspirating dental syringe permits easy performance of mentioned by many dentists as uncomfortable for them.
multiple aspirations throughout the period of local anes Although this is the preferred means of obtaining a satisfac
thetic deposition. tory aspiration test with these syringes, pressure adequate
for aspiration may be obtained by simply releasingthe pres
sure of the thumb on the thumb ring. Second-generation
self-aspiratingsyringeshave eliminated the thumb disc.
The major factor influencing ability to aspirate blood is
not the syringe,but the gauge of the needle being used.7 In
addition, most doctors using the harpoon-aspirating syringe
tend to overaspirate,that is,they retract the thumb ring back
too far and with excessiveforce (and, on occasion,disengage
the harpoon from the stopper). These doctors feel more
insecure with the self-aspirating syringe. Proper technique
of aspiration is discussed in Chapter 11. Advantages and
disadvantages of the metallic, self-aspirating syringe are
listed in Box 5-4.
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CHAPTER 5 The Syringe 81
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82 PARTII The Armamentarium
BOX 5-5 Advantages and Disadvantages of the BOX 5-6 Advantages and Disadvantages of the
Pressure Syringe Jet Injector
Advantages Disadvantages Advantages Disadvantages
Measured dose Cost Does not require use of Inadequate for pulpal
Overcomestissue resistance Easyto inject too rapidly needle (recommended anesthesia or for regional
Nonthreatening (new Threatening (original for needle phobics) block
devices) devices) Deliversvery small Some patients are
Cartridges protected volumes of local disturbed by the jolt of
anesthetic (0.01 to the injection.
0.2 mL) Cost
Used in lieu of topical May damage periodontal
anesthetics tissues
Disposable Syringes
Plastic disposable syringes are available in a variety of
sizeswith an assortment of needle gauges.Most often they
are used for intramuscular or intravenous drug admini
Figure 5-10. MadaJet.
stration, but they also may be used for intraoral injection
(Fig.5-11).
These syringes contain a Luer-Lok screw-on needle
Jet Injector. In 1947 Figge and Scherer introduced a new attachment with no aspirating tip. Aspiration can be accom
approach to parenteral injection-the jet or needle-less plished by pulling back on the plunger of the syringebefore
injection.8 This represented the first fundamental change in or during injection. Becausethere is no thumb ring, aspira
the basic principles of injection since 1853,when Alexander tion with the plastic disposable syringe requires the use of
Wood introduced the hypodermic syringe.The first report both hands. In addition, these syringesdo not accept dental
of the use of jet injections in dentistry was published in 1958 cartridges. The needle, attached to the syringe, must be
by Margetis and associates.9 Jet injection is based on the inserted into a vial or cartridge of local anesthetic drug and
principle that liquids forced through very small openings, an appropriate volume of solution withdrawn. Care must be
calledjets, at very high pressure can penetrate intact skin or taken to avoid contaminating the multi-use vial during this
mucous membrane (visualize water flowing through a procedure. Two- and 3-mL syringes with 25- or 27-gauge
garden hose that is being crimped). The most frequently needlesare recommended when the systemis used for intra
used jet injectors in dentistry are the SyriJetMark II (Mizzy oral local anesthetic administration.
Inc., Cherry Hill, NJ) (Fig. 5-9) and the MadaJet (Mada
Medical Products Incorporated, Carlstadt, NJ) (Fig. 5-10). *Mizzy Inc., 616 Hollywood Ave., Cherry Hill, NJ 08002; 1-800-663-4700;
The Syrilet holds any 1.8-mL dental cartridge of local www.keystoneind.com.
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CHAPTER5 The Syringe 83
c·-
l/rr rr/r 11rp rrqr11111
<?' .•• Col...,_
A
B
BOX 5-7 Advantages and Disadvantages of the
Figure 5-12. A. UltraSafety Plus XL aspirating syringe, ready for
Disposable Syringe
injection. B, UltraSafety Plus XL aspirating syringe; needle sheathed
Advantages Disadvantages to prevent needle-stick injury.
Disposable,single use Does not accept prefilled
Sterileuntil opened dental cartridges
Lightweight(may feel Aspiration difficult
awkwardto the first-time (requires two hands) BOX 5-8 Advantages and Disadvantages of the
user; tactile sensation Safety Syringe
better) Advantages Disadvantages
Disposable,single use Cost: more expensivethan
Sterile until opened reusable syringe
Lightweight(better tactile May feel awkwardto a
The plastic,disposable,non-cartridge-containing syringe sensation) first-time user
is not recommended for routine use. Its use should be
considered only when a traditional syringe is not available
or cannot be used. This system is also practical when
diphenhydramine HCl is used as a local anesthetic in the needle. Upon completion of the injection, the entire
cases of presumed local anesthetic allergy (see Chapter 18). syringe is discarded into the proper receptacle (e.g., sharps
Box 5-7 lists the advantages and disadvantages of the dis container).
posable syringe. Dental safety syringes are designed as single-use items,
although they permit reinjection. Reloadingthe syringewith
Safety Syringes a second anesthetic cartridge and reinjecting with the same
Recentyears have seen a move toward the development and syringe is discouraged because this obviates the important
introduction of safety syringes in both medicine and den safetyaspect of the device.
tistry. Safety syringes minimize the risk of an accidental In 2000, Cuny and associatesevaluatedfour dental safety
needle-stick injury occurring to a dental health provider syringesystems-Safe-Mate needle system (Septodont Inc.),
with a contaminated needle after administration of a local Safety Plus syringe (Septodont Inc.), UltraSafe syringe
anesthetic. These syringespossessa sheath that "locks"over (Septodont Inc.), and Hypo Safety syringe (Dentsply MPL
the needle when it is removed from the patient's tissues, Technologies,Franklin Park, lli)---over a I-year period at
preventing accidental needle-stick. a U.S. dental school." Their finding was that using these
Devicessuch as the UltraSafetyPlus XL*and the 1 Shot Food and Drug Administration (FDA)-approved devices
Safety Syringe+ were available as of January 2011. The resulted in an initial increase in needle-stick injuries. They
UltraSafety Plus XL aspirating syringe system contains a stated that hands-on training, monitoring, and follow-up
syringebody assemblyand a plunger assembly(Fig.5-12, A). reminders appeared to be effective in reducing injuries
Once the syringe is properly assembled and the injection associatedwith the changefrom traditional to safetyneedles.
administered,the syringemay be made "safe"with one hand Advantages and disadvantages of the safety syringe are
by gently moving the index and middle fingers against the listed in Box 5-8.
front collar of the guard (Fig. 5-12, B). Once "guarded:'
the now contaminated needle is "safe,"so that it is virtually Computer-Controlled Local Anesthetic
impossible for dental health providers to be injured with Delivery {C-CLAD) Systems
The standard dental syringe described previouslyis a simple
mechanicalinstrument that datesbackto 1853, when Charles
*illtraSafety Plus XL, Septodont Inc., 245C Quigley Blvd., New Castle,
DE 19720;1-800-872-8305;www.septodontinc.com.
Pravaz patented the first syringe.11The dental syringe is a
t 1 Shot SafetySyringe,Sultan Chemists, Englewood,NJ; 1-800-637-8582; drug deliverydevice requiring that the operator simultane
www.sultanintl.com. ously attempt to control the variables of drug infusion and
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84 PARTII The Armamentarium
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CHAPTER 5 The Syringe 85
A B
Figure 5·16. Anaeject computer-controlled local anesthetic delivery system.
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86 PARTII The Armamentarium
••
The STASystem instrument can perform all traditional considered a "blinded" approach to PDL injection. In con
injections, as well as several newer dental injection tech trast, using the DPS technology of the STASysteminforms
niques as previouslydescribed with The Wand and Compu the clinician of the status of needle position based on real
Dent Systeminstruments. In addition, the STASystemoffer time information. This transforms the PDL injection tech
a unique approach for performing PDL (intraligamentary) nique into a "guided" technique that can be easily and
injection using DPS technology.22 The instrument has been accurately performed. Additionally,the STAinstrument is
designedto accuratelyidentifythe preciseanatomic location capable of generating precise fluid pressures in ranges that
for the intraligamentary (PDL) injection." The STASystem are much lower in comparison with other injection devices.
audibly and visually "guides" placement of the needle tip This ability to maintain lower pressurespermits the absorp
into the anatomic entrance of the periodontal ligament tion of greater volumes of anesthetic solution safely and
space through DPS technology.Important to the successof effectivelythrough the intraligamentary tissues-another
the PDL injection is proper needle placement into its the benefit of this technology.24 Allowing a greater volume of
PDL space.Use of a traditional syringe provides little or no anesthetic to be safelyadministered results in a longer dura
information as to correct needle-tip location, so this can be tion of anesthesia produced by the STA intraligamentary
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CHAPTER 5 The Syringe 87
Figure 5-19. STAWand handpiece is lightweight (lessthan 10 grams) (A) and can easilybe shortened to aid in administration of some
injections (B}, such as the AMSAor other palatal techniques.
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88 PARTII The Armamentarium
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CHAPTER 5 The Syringe 89
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90 PARTII The Armamentarium
Figure 5-26. Note the bent harpoon of the syringeon the right.
RECOMMENDATIONS
Figure 5-24. Eccentricperforation. A, Centric perforation of the
diaphragm by a needle prevents leakage during injection. B, Off No conclusive evidence indicates that any manufacturer's
center perforation (arrow) permits leakage of anesthetic solution syringe is superior. Therefore the ultimate decision in selec
into the patient's mouth. tion of a syringe must be left to the discretion of the buyer.
It is recommended, however, that before purchasing any
syringe,the buyer placea full dental cartridge into it and pick
up the syringe as if to use it. It should be noted whether the
fingers (thumb to other fingers) are stretched maximally,
Disengagement of the Harpoon from the because to aspirate with a harpoon-type syringe, one must
Plunger During Aspiration be able to pull the thumb ring back several millimeters. If
Disengagement occurs if the harpoon is dull or if the one is not able to do so, reliable aspiration is not possible.
administrator applies too much pressure to the thumb Although all syringesavailabletoday are of roughlythe same
ring during aspiration. If this happens, the harpoon should dimensions, some variation is noted. Manufacturers market
be cleansed and sharpened or replaced with a new sharp syringeswith smaller thumb rings or shorter pistons. These
harpoon. Disengagement is most likely to occur when a modifications make aspiration easier to accomplish for
30-gauge dental needle is being used because significant persons with smaller hands.
resistance is produced within the needle lumen as aspira Followingare additional recommendations:
tion is attempted A very gentle backward motion of the 1. A safetysyringe,minimizing the risk of accidental
plunger is all that is necessary for successful aspiration. needle-stick injury, is recommended for use during all
Forceful action is not necessary. (See the discussion in local anesthetic injections.
Chapter 11.) 2. A self-aspiratingsyringe is recommended for
practitioners with small hands.
Surface Deposits 3. Any syringe system used must be capable of aspiration.
An accumulation of debris, saliva,and disinfectant solution Nonaspirating syringesshould never be used for local
interferes with syringe function and appearance. Deposits, anesthetic injections.
which can resemble rust, may be removed with a thorough 4. All reusable syringesmust be capable of being sterilized
scrubbing. illtrasonic cleaningwill not harm syringes. 5. Nonreusable syringesmust be disposed of properly.
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CHAPTER 5 The Syringe 91
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I
The Needle
' I •I
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CHAPTER 6 The Needle 93
\ I
lumen. Foldesand McNall11 reported the followingfindings
based on an unpublished study by Monheim:
Figure 6-2. Components of dental local anesthetic needle. Long
1. One hundred percent positive aspirations were achieved
needle (top);short needle (bottom).
from blood vesselswith 25-gaugeneedles.
2. Eighty-sevenpercent positive aspirations were achieved
from blood vesselswith 27-gaugeneedles.
In literally hundreds of clinical demonstrations, no 3. Twopercent positive aspirations were achievedfrom
patient was able to correctly determine the gauge of each blood vesselswith 30-gaugeneedles.
needle.The usual response has been that he or she could not Trapp and Davies15 reported that in vivo human blood
discern any difference. maybe aspirated through 23-,25-,27-,and 30-gaugeneedles
Larger-gaugeneedles (e.g.,25-gauge,27-gauge)have dis without a clinically significant difference in resistance to
tinct advantagesover smallerones (30-gauge)(Box6-1): less flow.
deflection occurs as the needle passes through tissues (see Despite this ambiguity concerning ability to aspirate
Table6-1 and Fig.6-3). This leads to greater accuracy during blood through needles of various gauges,the use of larger
needle insertion (it goesin a straighter line) and, it is hoped, needles (e.g., 25-gauge,27-gauge) is recommended for any
to increased successrates, especiallyfor techniques in which injection technique used in a highly vascular area, or when
the depth of soft tissue penetrated is significant(e.g.,inferior needle deflection through soft tissue would be a factor.
alveolar,Gow-Gatesmandibular, Akinosi-Vaziranimandib Although blood may be aspirated through all 23- through
ular, anterior superior alveolar [ASA;infraorbital] nerve 30-gauge needles, resistance to aspiration is greater when
blocks).Needle breakage, although rare today with the use of smaller-gauge needles are used, increasing the likelihood
disposable needles, is even less likely to occur with a larger that the metal harpoon will become dislodged from the
needle. Numerous authors'':" have demonstrated that aspi rubber plunger during aspiration, making the aspiration
ration of blood is easier and more reliable through a larger attempt futile.
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94 PART II The Armamentarium
------
No deflection on penetration
Inside diameter 0.008 inch; same as 27-gauge
A Outside diameter 0.014 inch
------
Angle of deflection on penetration
Inside diameter 0.008 inch
Outside diameter O.Q16 inch
B 27-gauge needle with standard point
Figure 6-4. A, The tip of a nondefl.ectingneedle is located in the center of the shaft,thereby minimizing deflectionas the needle penetrates
soft tissues.B, Conventional dental needle.The needle tip lies at the loweredgeof the needle shaft,thereby producing deflectionas the needle
passesthrough soft tissue.
TABLE 6-1
Deflection of Needles Inserted in Hydrocolloid Tubes
to Their Hubs
Maximum Tip
Length Deflection
(mm, Tip to Hub) (mm,± SD)
25-Gaugelong 35 7.1±0.81*
(conventional)
27-Gaugelong 36 8.4 ± 1.2*
(conventional)
27-Gauge short 26 4.6±0.97t
(conventional)
28-Gaugelong 31 1.1±0.82
(nondeflecting)
28-Gauge short 22 0.8 ± 0.91 Figure 6-5. Color-coding by needle gauge: 25-gauge, red;
(nondeflecting) 27-gauge,yellow;30-gauge,blue.
Data modified from JeskeAH, Boshart BF:Deflection of conventional
versus non-deflecting dental needles in vitro, Anesth Prog 32:62-64,1985.
*A statisticallysignificant differencefrom the nondeflecting long needle
(P < .01); n = 10 needles in each group.
tA statisticallysignificant differencefrom the nondeflecting short needle TABLE 6-2
(P < .01); n = 10 needles in each group. Needle Purchases, U.S. Dentistry, 2006
DATA PROVIDED BY
Sullivan-Schein Septodont
Gauge Length Inc. (2006) Inc. (2006)
BOX 6-1 Advantages of Larger-Gauge Needles Over 25 Short <1% 1% 0.6% 3%
Smaller-Gauge Needles Long 1% 2.3%
27 Short 10% 42% 13% 38%
1. Lessdeflection,as needle advancesthrough tissues
Long 32% 25%
2. Greater accuracyof injection
30 Short 50% 56% 51% 59%
3. Lesschance of needle breakage Extra short 6% 8%
4. Easier aspiration
5. No perceptual differencein patient comfort From Malamed SF,Reed KL,Poorsattar S:Needle breakage:incidence and
prevention, Dent Clin North Am 54:745-756,2010.
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CHAPTER 6 The Needle 95
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96 PART II The Armamentarium
which the bevel faces (e.g., if the bevel faces "up," the advanc syringerequires a palm-thumb grasp (seeFig.6-6) that does
ing movement causes a beveled needle to deflect "down not permit such a technique. A computer-controlled local
ward"). The longer the needle length, the more exaggerated anesthetic delivery (C-CLAD) device such as The Wand/
the bending or deflection becomes as a result of the greater CompuDent/STA (Milestone ScientificInc., Livingston,NJ;
distance traveled along the deflecting path. The smaller the discussed in Chapter 5) employs a lightweight handpiece
diameter of the needle, the more exaggerated the bending or that is held with a "penlike" or "dart" grasp that is easily
deflection, because a smaller-gauge needle is less capable of rotated
resisting the deflection or bending force on the surface of the A subsequent study by the same authors demonstrated
beveled needle tip. that the BRIToffersthe added benefit of reducing the force
When the BRIT is used during needle insertion, the per necessaryfor needle penetration and advancement through
pendicular force that causes deflection is eliminated or "neu tissues.18 This is explained as follows.With rotational inser
tralized" from the constant changing of bevel orientation as tion, all resultant forcesare directed toward the forward path
it is rotated (Fig. 6-7).17 This allows eccentricallybeveled of insertion because the deflecting or bending forces have
needles to travel in a straight path. The traditional handheld been eliminated from the rotational insertion technique, as
described earlier. This allows forward movement of the
needle to occur more efficientlyand with lesseffort (e.g.,less
force). In addition, rotation of the beveledneedle allowsthe
sharp cutting edge to contact the full circumference of the
tissue surface, contributing to the reduction in force that is
necessaryduring penetration and advancement. This is not
unlike the rotational effectthat a surgicaldrill bit has as it is
boring through tissue or bone.
The BRIT,or bi-rotational insertion technique has been
demonstrated to improve injection techniques because
the deflection of a standard needle during insertion is
minimized.19
LENGTH
Dental needles are availablein three lengths:long, short and
ultrashort. IBtrashort needles are availableonly as 30-gauge
needles.Despitethe claimfor uniformity oflength by manu
facturers, significant differencesare found (Table6-4).
The length of a short needle is between 20 and 25 mm
(measured hub to tip) with a standard of about 20 mm, and
is 30 to 35 mm for the long dental needle, with a standard
of about 32 mm (Fig.6-8).
Needlesshould not be inserted into tissues all the wayto
their hubs unless this is absolutelynecessaryfor the success
of the injection. This statement has appeared in "standard"
local anesthesia textbooks since the early to mid 1900s.20-24
One reason for this precaution is needle breakage, which,
Figure 6-7. BRIT(bi-rotationalinsertiontechnique). although rare, does occur.The weakestportion of the needle
TABLE 6-4
Needle Lengths*
25-Gauge 25-Gauge 27-Gauge 27-Gauge 30-Gauge 30-Gauge 30-Gauge
Manufacturer Long Short Long Short Long Short Ultrashort
Industrystandard 32 20 32 20
ManufacturerA 30 30 21 25 21
ManufacturerB 32± 1.5 22± 1.5 32± 1.5 22± 1.5 21±1.5 12 ± 1.0
ManufacturerC 32 21 25 21
ManufacturerD 35 35 25 25 10
ManufacturerE 32 21 19
*Allmeasurements
obtaineddirectly
fromneedlemanufacturers.
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CHAPTER6 The Needle 97
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98 PARTII The Armamentarium
A B
Figure 6-10. A, "Scoop"technique for recapping contaminated local anesthetic needle. B, Plastic needle cap holder.
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CHAPTER6 The Needle 99
ultrashort needle (95.23%). The remaining five needles were doubt about the presence of barbs, change the needle
27-gauge short," between insertions.
Needles recommended for specific injection techniques
are presented in the following "Recommendations" section. Injury to the Patient or Administrator
Penetration of, with resultant injury to, areas of the body
Pain on Withdrawal with the needle can occur unintentionally.A major cause is
Pain on withdrawal of the needle from tissue can be inattention by the administrator, although sudden unex
produced by "fishhook" barbs on the tip. Fishhook barbs pected movement by the patient is also a frequent cause.The
may be produced during the manufacturing process, but needle should remain capped until it is to be used and should
it is much more likely that they will develop when the be made safe(sheathed or recapped) immediatelyafterwith
needle tip forcefullycontacts a hard surface, such as bone. drawal from the mouth.
A needle should never be forced against resistance. If in
RECOMMENDATIONS
1. Sterile disposableneedles should be used.
2. If multiple injections are to be administered, needles
should be changed after three or four insertions in a
single patient.
3. Needlesmust never be used on more than one patient.
4. Needlesshould not be inserted into tissue to their hub
unless this is absolutelynecessaryfor successof the
injection.
5. The direction of a needle should not be changed while
it is still in tissue.
6. A needle should never be forced against resistance.
7. Needlesshould remain capped until used and should be
made safe immediatelywhen withdrawn.
8. Needlesshould be discarded and destroyed after use to
prevent injury or reuse by unauthorized persons.
9. The injection techniques presented in Table6-5 are
Figure 6-12. Remainder of retained local anesthetic needle listed with their recommended needles (for the adult of
shown in Figure 6-11. averagesize).
TABLE 6-5
Recommended Needles for Injection Techniques
Technique Needle Gauge Needle Length
Supraperiosteal (infiltration) 27 Short
Posterior superior alveolarnerve block 2'r Short*
Middle superior alveolarnerve block 27 Short
Anterior middle superior alveolar (AMSA)nerve block 27 Short
Palatal approach anterior superior alveolarnerve block (P-ASA) so' Short
Buccal (long) nerve block 27* Short:j:
Infiltration for hemostasis 27 Short
Periodontal ligament injection (PDL or intraligamentary [ILI]) 27 Short
Intraseptal injection 27 Short
Intraosseous injection 27 Short
Intrapulpal injection 27 Short
Anterior superior alveolarnerve block ("infraorbital") Long
Maxillary (V2) nerve block Long
Inferior alveolar ("mandibular") nerve block Long
Gow-Gatesmandibular nerve block Long
Vazirani-Akinosimandibular nerve block Long
*In earlier editions of this book, the 25-gaugelong needle was recommended. As a means of minimizing the risk of hematoma after the posterior superior
alveolarinjection, a short needle is now recommended. If available,a 25-gaugeshort needle should be used; where this is not available,the 27-gaugeshort
needle is recommended. (SeeChapter 13 for additional discussion.)
"The authors of the P-ASApaper recommend use of a 30-gaugeultrashort needle.1'-"
*Inmost clinicalsituations, the 25-gaugelong needle, used for the inferior alveolarnerve block (IANB),is used for the buccal nerve block, which is
administered immediately after the IANB.
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100 PARTII The Armamentarium
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The Cartridge
The dental cartridge is a glass cylinder containing the local 3. Aluminum cap
anesthetic drug, among other ingredients. In the United 4. Diaphragm
States and in many other countries, the glass cylinder itself The stopper (plunger, bung) is located at the end of the
can hold 2 mL of solution; however,as prepared today, the cartridge that receivesthe harpoon of the aspirating syringe.
dental cartridge contains approximately 1.8 mL of local The harpoon is embedded into the silicone (non-latex
anesthetic solution. Localanesthetic products manufactured containing) rubber plunger with gentle finger pressure
by Septodont (Lancaster, PA) list their volume as 1.7 mL applied to the thumb ring of the syringe.The plunger occu
(although in actuality they contain approximately 1.76mL pies a little less than 0.2 mL of the volume of the entire
of local anesthetic solution). In other countries, notably the cartridge.Until recently,the stopper was sealedwith paraffin
United Kingdom and Australia,the prefilleddental cartridge (wax) to produce an airtight seal against the glass walls of
contains approximately 2.2 mL of local anesthetic solution; the cartridge. Glycerin was added in channels around the
some countries including France and Japan have 1-mL stopper as a lubricant, permitting it to traverse the glass
dental cartridges (Fig.7-1). cylinder more easily.Today,most local anesthetic manufac
The dental cartridge is, by common usage,referred to by turers treat the stopper with silicone, eliminating both the
dental professionalsas a carpule. The term carpule is actually paraffin and the glycerin."Stickystoppers" (stoppers that do
a registeredtrade name for the dental cartridge prepared by not move smoothly down the glasscartridge) are infrequent
Cook-WaiteLaboratories,which introduced it into dentistry today. Recent years have seen a move toward the use of a
in 1920. uniform black rubber stopper in all local anesthetic drug
In recent years, local anesthetic manufacturers in some combinations.Virtuallygone are the color-codedred, green,
countries (but not as of yet in North America) have intro and blue stoppers that aided in identification of the drug.
duced a local anesthetic cartridge composed of plastic.' When black stoppers are used, a color-codingband, required
Plastic cartridges have several negative features, primarily by the American Dental Association (ADA)as of June 2003
leakage of solution during injection, the requirement for for products to receivethe ADASeal of Approval, is found
considerable force to be applied to the plunger of the around the glasscartridge (Table7-1).
syringe (e.g., periodontal ligament [PDL], nasopalatine),1 In an intact dental cartridge (Fig. 7-3), the stopper is
and the fact that the plunger does not "glide" down the slightlyindented from the lip of the glasscylinder.Cartridges
plastic cartridge as smoothly as it does down the glass car whose plungers are flush with or extruded beyond the glass
tridge, leading to sudden spurts of administration of local of the cylindershould not be used. This problem is discussed
anesthetic, which can produce pain in the patient. Another later in this chapter (see"Problems").
problem with plastic cartridges is the fact that they are per An aluminum cap is located at the opposite end of the
meable to air. Exposure to oxygenleads to more rapid deg cartridge from the rubber plunger. It fits snugly around the
radation of the vasoconstrictor in the cartridge and to a neck of the glass cartridge, holding the thin diaphragm in
shorter shelf-life.2 position. It is silvercolored on most cartridges.
The diaphragm is a semipermeable membrane through
which the needle penetrates into the cartridge. When prop
COMPONENTS erly prepared, the perforation of the needle is centrically
The prefilled 1.8-mLdental cartridge consists of four parts located and round, forming a tight seal around the needle.
(Fig. 7-2): Improper preparation of the needle and cartridge can
1. Cylindricalglasstube produce an eccentric puncture with ovoid holes leading to
2. Stopper (plunger,bung) leakage of the anesthetic solution during injection. The
101
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102 PART II The Armamentarium
TABLE 7-1
Color-Coding of Local Anesthetic Cartridges,
as per American Dental Association Council on
Scientific Affairs
LocalAnestheticSolution Colorof CartridgeBand
Articaine HCl 4% with
epinephrine 1: 100,000
Bupivacaine0.5% with
./ epinephrine 1:200,000
LidocaineHCl 2%
., LidocaineHCl 2% with
epinephrine 1:50,000
LidocaineHCl 2% with
epinephrine 1: 100,000
MepivacaineHCl 3%
MepivacaineHCI 2% with
levonordefrin 1:20,000
Prilocaine HCl 4%
Prilocaine HCl 4% with Yellow
epinephrine 1:200,000
Aluminum cap Drug ldentlfytng Figure 7-3. Siliconerubber plunger is slightlyindented from the
color-<Xlded band rim of the glass.
•
A thin Mylar plastic label applied to all cartridges (Fig.
7-4) servesto (1) protect the patient and the administrator
in the event that the glasscracks, and (2) provide specifica
tions about the enclosed drug. In addition, some manufac
B
turers include a volume indicator on their labels,making it
Figure 7-2. A and B, Components of the glassdental local anes easier for the administrator to deposit precise volumes of
thetic cartridge. anesthetic (see Fig.7-4).
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CHAPTER7 The Cartridge 103
0
septocame-
.
Lot number-.......... --Volume
,....
0
O
~
e Artlcalne HCI4% with
Epinephrine 1:100,000 Injection.
Contains sodium metabisulfite
C\l
'
Expiration date -
DIN number v
,.... SEPTOOONT
Proprietary name- 2'·Xylixaine·Df"•' France
Generlcname-- ~~~:.C~ 0)
,.._.__1.;1
:.-.•••..
""''··~·'·".__ .•••.:&.-'.
0 Lot: Exp:
!IA o..Jy .1•.
\:r,.,,. •••<:";·.· •:.-:-.;. •• -_, 1
lrot((l~i'~l •••..•••.••• """"'"
.•
f.•,. •• ,.,'r"Kt: ~
Manufacturer co m C'! ~
ci ci ,... ,...
A el I I I
Figure 7-4. Mylar plastic labd. Labd with volume indicator. (Courtesy Septodont, Lancaster,PA.)
TABLE 7-2
Composition of Local Anesthetic Solution
•Plain• Local
Anesthetic Vasopressor-Containing
Component Function Solution Local Anesthetic Solution
Local anesthetic drug (e.g.,lidocaine HCl) Blockadeof nerve conduction
Sodium chloride Isotonicity of the solution
Sterilewater Volume
Vasopressor(e.g.,epinephrine, t Depth and t duration of anesthesia;
levonordefrin) J. absorption of local anesthetic and
vasopressor
Sodium (meta)bisulfite Antioxidant
Methylparaben* Bacteriostaticagent
*Methylparabenis no longer included in single-usedental cartridges of local anesthetic; however,it is found in ALLmultidose vials of injectable drugs.
TABLE 7-3
Calculation of Milligrams per Cartridge
Percent Solution = Milligrams (mg} per Milliliter (ml) x Volume of Cartridge = Milligrams per Cartridge
0.5 = 5 x 1.8 = 9
1.0 = 10 x 1.8 = 18
2.0 = 20 x 1.8 = 36
3.0 = 30 x 1.8 = 54
4.0 = 40 x 1.8 = 72
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104 PARTII The Armamentarium
vs. 6.5). Becauseof this pH difference,plain local anesthetics cultures taken immediately on opening a container usually
have a somewhat more rapid onset of clinicalaction and are fail to produce any growth. Therefore it seems obvious that
more comfortable (less"burning'' on lnjection)."? extraordinary measures related to cartridge sterilization are
Cartridges containing vasopressorsalso contain an anti unwarranted. Indeed, the glass dental cartridge should not
oxidant, most often sodium (meta)bisulfite.Sodium bisulfite be autoclaved.The seals on the cartridge cannot withstand
prevents oxidation of the vasopressorby oxygen,which can the extreme temperatures of autoclaving,and the heat-labile
be trapped in the cartridge during manufacture or can vasopressorsare destroyed in the process. Plastic cartridges
diffusethrough the semipermeablediaphragm (or the walls cannot be autoclaved.
of a plastic cartridge) after filling. Sodium bisulfite reacts Most commonly today,local anesthetics are marketed in
with oxygen before the oxygen is able to destroy the vaso cardboard boxes of approximately50 cartridges.Within the
pressor. When oxidized, sodium bisulfite becomes sodium box are 5 sealedunits of 10 cartridges each (Fig.7-5), called
bisulfate,having an even lower pH. The clinicalrelevanceof blister packs. Kept in this container until use, cartridges
this lies in the fact that increased burning (discomfort) is remain clean and uncontaminated.
experienced by the patient on injection of an "older" car Localanesthetic cartridgesshould be stored in their origi
tridge of anesthetic with vasopressor compared with a nal container,preferablyat room temperature (e.g.,21° C to
fresher cartridge.Allergyto bisulfitesmust be considered in 22° C), and in a dark place. There is no need to "prepare" a
the medical evaluation of all patients before local anesthetic cartridge before use. The doctor or assistant should insert it
is administered'r"(see Chapter 10). into the syringe. However,many doctors feel compelled to
Sodium chloride is added to the cartridge to make the somehow"sterilize"the cartridge.When this urge strikes,the
solution isotonic with the tissues of the body. In the past, doctor should apply an alcohol wipe moistened with undi
isolated instances have been reported in which local anes luted 91% isopropyl alcohol or 70% ethyl alcohol to the
thetic solutions containing too much sodium chloride rubber diaphragm (Fig. 7-6).
(hypertonic solutions) produced tissue edema or paresthe If a clearplastic cartridge dispenser is used, 1day'ssupply
sia, sometimes lasting for severalmonths, after drug admin of cartridges should be placed with the aluminum cap and
istration." This is no longer a problem. diaphragm facing downward. Several (two or three) sterile
Distilled water is used as a diluent to provide the volume dry 2 x 2-inch gauze wipes are placed in the center of the
of solution in the cartridge. dispenser and are moistened with (not immersed in) 91%
A significant change in cartridge composition in the isopropyl alcohol or 70% ethyl alcohol. No liquid alcohol
United States and in many other countries was the removal should be present around the cartridges. Beforethe syringe
of methylparaben, a bacteriostatic agent. A ruling by the is loaded, the aluminum cap and the rubber diaphragm are
Foodand DrugAdministration (FDA)mandated the removal rubbed against the moistened gauze.
of methylparaben from dental local anesthetic cartridges Cartridges should not be permitted to soak in alcohol or
manufactured after January 1, 1984. Methylparaben pos other sterilizing solutions because the semipermeable dia
sessesbacteriostatic, fungistatic,and antioxidant properties. phragm allows diffusion of these solutions into the dental
It and related compounds (ethyl-, propyl-, and butylpara cartridge, thereby contaminating it. Therefore, it is recom
ben) are commonly used as preservatives in ointments, mended that cartridges be kept in their original container
creams,lotions, and dentifrices.In addition, paraben preser until they are to be used.
vatives are found in all multiple-dose vials of drugs. Cartridge warmers are unnecessary.Indeed, occasionally
Methylparaben is commonly used in a 0.1% concentration they may produce problems. Overheating the local anes
(1 mg/mL). Its removal from local anesthetic cartridges was thetic solution can lead to (1) discomfort for the patient
predicated on two facts. First, dental local anesthetic car during injection, and (2) the more rapid degradation of
tridges are single-use items meant to be discarded and not a heat-labile vasopressor (producing a shorter duration
reused. Therefore inclusion of a bacteriostatic agent is of anesthesia with more burning on injection). It has been
unwarranted. Second,repeated exposure to paraben has led demonstrated that after the warmed glass cartridge is
to reports of increasedallergicreactions in some persons.":" removed from the cartridge warmer and is placed in a
Responses have been limited to localized edema, pruritus, metal syringe with the solution forced through a fine metal
and urticaria. Fortunately,to date there has not been a sys needle, its temperature has decreased almost to room
temic allergicreaction to a paraben. Removalof methylpara temperature.2'5'13'14
ben has further decreasedan alreadyminimal risk of allergy Cartridge warmers, designedto maintain anesthetic solu
to local anesthetic drugs. tions at "body temperature," are not needed and cannot be
recommended. Localanestheticsin cartridges maintained at
room temperature (20°C to 22° C) do not cause the patient
CARE AND HANDLING
any discomfort on injection into tissues, nor do patients
Local anesthetics are marketed in vacuum-sealed tin con complain of the solution being too cold.14 On the other
tainers of 50 cartridges and in blister packs of (usually) 10 hand, warmed local anesthetic solutions at 27° C or above
cartridges. Although no manufacturer makes any claim of have a much greater incidence of being described as too hot
sterility about the exterior surface of the cartridge, bacterial or burning on injection.13
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CHAPTER 7 The Cartridge 105
2%Xylocaine'W•'Al
.,......,...._,.-.z~
~·Cl-...,.....
~.1.D".
b.""1y ~~.:~~~!~;·~·~
t;;:;. :-~;~~·,,
~-< ~1i.r.•1~
A B
Figure 7-5. A. Ten local anesthetic cartridges are contained in a sealed"blister pack."B, Back of blister pack contains information about
the drug.
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106 PART II The Armamentarium
WARNINGS
DENTAL PRACTITIONERS WHO EMPLOY LOCAL ANESTHETICS
IN THEIR OFFICES SHOULD BE WELL VERSED IN DIAGNOSIS
AND MANAGEMENT OF EMERGENCIES WHICH MIGHT ARISE
FROM THEIR USE. RESUSCITATIVE EQUIPMENT, OXYGEN, AND
OTHER RESUSCITATIVE DRUGS SHOULD BE AVAILABLE FOR
IMMEDIATE USE.
Reactions resulting in fatality have occurred on rare occasions with the use
of local anesthetics, even in the absence of a history of hypersensitivity.
8 1
Figure 7·7. A,Alllocal anesthetic containers have a product identificationpackageinsert, which should be read. B, Important information
is contained in all package inserts.
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CHAPTER7 The Cartridge 107
Burning on Injection
A burning sensation on injection of anesthetic solution may
be the result of one of the following:
1. Normal response to the pH of the drug
2. Cartridge containing sterilizingsolution
3. Overheated cartridge
4. Cartridge containing a vasopressor Figure 7-1 O. Local anesthetic cartridge with damaged cap. The
During the few seconds immediately after deposition of glass around the neck of the cartridge should be examined carefully
a local anesthetic solution, the patient may complain of a for cracks.
slight sensation of burning. This normal reaction is caused
by the pH of the local anesthetic solution; it lasts a second
or two, until the anesthetic takes effect,and is noted mainly
by sensitive patients when receiving local anesthetics con because the paraffin hardens on colder days. Using car
taining epinephrine or levonordefrin. tridges at room temperature minimizes this problem; using
A more intense burning on injection is usually the result silicone-coated stoppers eliminates it. Plastic cartridges are
of diffusion of disinfectingsolution into the dental cartridge associated with this problem to a greater degree than glass
and its subsequent injection into the oral mucous mem cartridges.
branes. Although burning most often is a mere annoyance,
the inclusion of disinfectingagents such as alcohol in dental Corroded Cap
cartridges can lead to more serious sequelae,such as postin The aluminum cap on a local anesthetic cartridge can be
jection paresthesia and tissue edema.15•16 corroded if immersed in disinfecting solutions that contain
Overheating of the solution in a cartridge warmer may quaternary ammonium salts,such as benzalkonium chloride
produce burning on injection. The (Christmas tree) bulb (e.g.,"cold" sterilizing solution). These salts are electrolyti
type cartridge warmer most often is at fault in this regard. cally incompatible with aluminum. Aluminum-sealed car
Unlesslocal anesthetic cartridges are unusually cold,there is tridges should be disinfected in 91% isopropyl alcohol or
little justification for use of a cartridge warmer. Local anes 70% ethyl alcohol. Cartridges with corroded caps must not
thetic solutions injected at room temperature are well toler be used. Corrosion may be easily distinguished from rust,
ated by tissues and patients. which appears as a red deposit on an intact aluminum cap.
Use of a vasopressor-containinglocal anesthetic solution
may be responsiblefor the sensation of burning on injection. Rust on the Cap
The addition of a vasopressor and an antioxidant (sodium Rustfound on a cartridge indicatesthat at least one cartridge
bisulfite)lowersthe pH of the solution to approximately3.5, in the tin container has broken or leaked.The "tin" container
making it significantlymore acidic than solutions not con (actually steel dipped in molten tin) rusts, and the deposit
taining a vasopressor (pH about 6.5).5-7'17 Patients are more comes off on the cartridges. Cartridges containing rust
likely to feel the burning sensation with these solutions. A should not be used. If any cartridge contains rust a dented
further decrease in the pH of the local anesthetic solution cap, or a visible crack (Fig. 7-10), all cartridges in the con
results as sodium bisulfite is oxidized to sodium bisulfate. tainer must be carefullycheckedbefore use.With the intro
This response can be minimized by careful checking of the duction of nonmetal packaging,rust is rarely seen.
expiration date on all cartridges before use. Conversely,
increasingthe pH of the anesthetic solution has the effectof Leakage During Injection
making local anesthetic administration more comfortable Leakageoflocal anesthetic solution into the patient's mouth
for the patient,":" during injection occurs if the cartridge and the needle are
prepared improperly and the needle puncture of the dia
phragm is ovoid and eccentric. Properly placed on the
Sticky Stopper syringe after the cartridge is inserted, the needle produces
The "sticky stopper" has become a rarity today, with the centric perforation of the diaphragm, which tightly seals
inclusion of silicone as a lubricant and the removal of itself around the needle. When pressure is applied to the
paraffin as a sealant in the cartridge. In caseswhere paraffin plunger during injection, all of the solution is directed into
is still used, difficulty in advancing the stopper may occur the lumen of the needle. If the cartridge is placed in a
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108 PARTII The Armamentarium
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CHAPTER 7 The Cartridge 109
4. Cartridges should not be used beyond their expiration 8. Seng GF,Gay BJ:Dangers of sulfitesin dental local anesthetic
date. solutions: warning and recommendations, J Am Dent Assoc
5. Cartridges should be checked carefullyfor cracks, 113:769-770, 1986.
chips, and the integrity of the stopper and cap before 9. Perusse R, Goulet JP,Turcotte JY:Contraindications to vaso
constrictors in dentistry. Part II. Hyperthyroidism, diabetes,
use.
sulfite sensitivity, cortico-dependent asthma, and pheochro
mocytoma, Oral Surg 74:5687-5691, 1992.
References
10. NickelAA:Paresthesiaresulting from local anesthetics, J Oral
1. MeechanJG,McCabeJF,Carrick TE: Plasticdental anaesthetic MaxillofacSurg 42:52-79, 1984.
cartridges: a laboratory investigation, Br Dent J 169:254--256, 11. Wurbach G, Schubert H, Pillipp I: Contact allergy to benzyl
1990. alcoholand benzylparaben, Contact Dermatitis 28:3187-3188,
2. Meechan JG, Donaldson D, KotlickiA: The effect of storage 1993.
temperature on the resistance to failure of dental local 12. Klein CE, Gall H: Type N allergy to amide-type anesthetics,
anesthetic cartridges, J Can Dent Assoc 61:143-144, 147-148, Contact Dermatitis 25:145-148, 1991.
1995. 13. Volk RJ, Gargiulo AV:Local anesthetic cartridge warmer-first
3. SussmanGL,BeezholdDH: Allergyto latex rubber, Ann Intern in, first out, Ill Dent J 53:292-294, 1984.
Med 122:143-146, 1995. 14. RogersKB,FieldingAF,MarkiewiczSW:The effectof warming
4. Shojaei AR, Haas DA: Local anesthetic cartridges and latex localanestheticsolutionsprior to injection,Gen Dent 37:6496-
allergy:a literature review,J Can Dent Assoc 68:10622-10626, 6499, 1989.
2002. 15. Shannon IL,WescottWB:Alcoholcontamination oflocal anes
5. JeskeAH, Blanton PL: Misconceptions involving dental local thetic cartridges, J Acad Gen Dent 22:20-21, 1974.
anesthesia. Part 2, Pharmacology.Tex Dent J 119:4310--4314, 16. OakleyJ: Personal communications, 1985.
2002. 17. Moorthy AP,Moorthy SP,O'Neil R: A study of pH of dental
6. Wahl MJ,Schmitt MM, Overton DA,Gordon MK:Injection of local anesthetic solutions, Br Dent J 157:11394--11395, 1984.
bupivacaine with epinephrine vs. prilocaine plain, J Am Dent 18. Crose VW: Pain reduction in local anesthetic administration
Assoc 133:111652-111656, 2002. through pH buffering, J Ind Dent Assoc 70:224--225, 1991.
7. Wahl MJ, Overton DA, Howell J, et al: Pain on injection of 19. Hanna MN, ElhassanA,VelosoPM, et al: Efficacyof bicarbon
prilocaine plain vs. lidocaine with epinephrine: a prospective ate in decreasing pain on intradermal injection of local anes
double-blind study, J Am Dent Assoc 132:101396-101401, thetics: a meta-analysis, Reg Anesth Pain Med 34:122-125,
2001. 2009.
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I
Additional Armamentarium
' I •I
In previous chapters, the three major components of the Application of a topical antiseptic is considered an
local anesthetic armamentarium-syringe, needle, and optional step in tissue preparation before intraoral injection.
cartridge-have been discussed.Other important items are
found in the local anesthetic armamentarium, however,
TOPICAL ANESTHETIC
including the following:
1. Topicalantiseptic Topical anesthetic preparations are discussed in depth in
2. Topicalanesthetic Chapter 4. Their use before initial needle penetration of the
3. Applicator sticks mucous membrane is strongly recommended. With proper
4. Cotton gauze (2 x 2 inches) application, initial penetration of mucous membrane any
5. Hemostat where in the oral cavity can usually be made without the
patient's awareness.
For effectiveness,it is recommended that a minimal
TOPICAL ANTISEPTIC
quantity of topical anesthetic be applied to the end of
A topical antiseptic may be used to prepare the tissues at the the applicator stick and placed directly at the site of pene
injection site before the initial needle penetration. Its func tration for approximately 1 minute. Gill and Orr have
tion is to produce a transient decreasein the bacterial popu demonstrated that when topical anesthetics are applied
lation at the injection site, thereby minimizing any risk of accordingto the manufacturer's instructions (approximately
postinjection infection. 10 to 15 seconds),their effectivenessis no greater than that
The topical antiseptic, on an applicator stick, is placed of a placebo, especially for palatal injections.4 Stern and
at the site of injection for 15 to 30 seconds. There is no Giddon showed that application of a topical anesthetic to
need to place a large quantity on the applicator stick; it mucous membrane for 2 to 3 minutes leadsto profound soft
should be sufficient just to moisten the cotton portion of tissue analgesia.5
the swab. A variety of topical anesthetic agents are available for
Availableagents include Betadine (povidone-iodine) and use today. Most contain the ester anesthetic benzocaine.
Merthiolate (thimerosal). Topical antiseptics containing The likelihood of occurrence of allergic reactions to esters,
alcohol (e.g., tincture of iodine, tincture of Merthiolate) though minimal, is greater than that to amide topical
should not be used because the alcohol produces tissue irri anesthetics; however, because benzocaine is not absorbed
tation. In addition, allergyto iodine-containing compounds systemically,allergic reactions are normally localized to
is common.P Beforeany iodine-containing topical antisep the site of application. Of the amides, only lidocaine pos
tic is applied to tissues,the patient should be questioned to sesses topical anesthetic activity in clinically acceptable
determine whether adverse reactions to iodine have previ concentrations. The risk of overdose with amide topical
ously developed. anesthetics is greater than that with the esters and increases
In a survey of local anesthetic techniques in dental prac with the area of application of the topical anesthetic.Topical
tice,3 7.9% of dentists mentioned that they always used forms of lidocaine are available as ointments, gels, pastes,
topical antiseptics before injection, 22.4% sometimes used and sprays.
them, and 69.7% never used them. EMLA(eutectic mixture of local anesthetics) is a combi
Postinjectioninfectionscan and do occur,and regularuse nation oflidocaine and prilocaine in a topical cream formu
of a topical antiseptic can virtually eliminate them. If a lation, designed to provide surface anesthesia of intact skin.
topical antiseptic is not available,a sterile gauzewipe should Its primary indications are for use before venipuncture and
be used to prepare the tissues adequatelybefore injection. in pediatric surgical procedures, such as circumcision.6•7
110
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CHAPTER8 Additional Armamentarium 111
Figure 8-1. Disposablenozzle for topical anesthetic spray. Figure 8-2. Cotton-tipped applicator sticks.
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112 PARTII The Armamentarium
unlikely event that the needle breaks off within tissues 5. Stem I, Giddon DB: Topical anesthesia for periodontal proce
(Fig. 8-5). dures, Anesth Prog 22:105--108, 1975.
6. Fetzer SJ: Reducing venipuncture and intravenous insertion
pain with eutectic mixture of local anesthetic: a meta-analysis,
References Nurs Res 51:119--124, 2002.
1. Bennasr S, Magnier S, Hassan M, et al: Anaphylacticshock and 7. TaddioA:Pain management for neonatal circumcision,Paediatr
low osmolarity contrast medium, Arch Pediatr 1:155--157, 1994. Drugs 3:101-111, 2001.
2. Palobart C, Cros J,Orsel I, et al:Anaphylacticshockto iodinated 8. Bernardi M, SeccoF,BenechA;Anesthetic efficacyof a eutectic
povidone, Ann Fr Anesth Reanim 28(2):168--170, 2009. mixture oflidocaine and prilocaine (EMLA)on the oral mucosa:
3. Malamed SF:Handbook oflocal anesthesia,ed 1, St Louis, 1980, prospectivedouble-blind study with a placebo,Minerva Stoma
Mosby. tol 48:39--43, 1999.
4. Gill CJ, Orr DL II: A double blind crossover comparison of 9. Munshi AK,HegdeAM,Latha R:Useof EMLk is it an injection
topical anesthetics,J Am Dent Assoc 98:213--214, 1979. free alternative?J Clin Pediatr Dent 25:215--219, 2001.
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Preparation of the
Armamentarium
Proper care and handling of the local anesthetic armamen harpoon in the rubber stopper-a process that can lead to
tarium can prevent or at least minimize the development broken glasscartridges or leakageof anesthetic solution into
of complications associated with the needle, syringe, and the patient's mouth during the injection. The recommended
cartridge. Many of these have been discussedin the preced sequence,as alreadydescribed,virtually eliminatesthis pos
ing chapters. Other complications and minor annoyances sibility and should alwaysbe used.
may be prevented through proper preparation of the
armamentarium. Recapping the Needle
After removal of the syringe from the patient's mouth, the
needle should be recapped immediately.Recappingis one of
BREECH-LOADING, METALLIC OR PLASTIC, the two times when health professionals are most likely to
CARTRIDGE-TYPE SYRINGE be injured (stuck) with a needle*; it is probably the most
1. Removethe sterilizedsyringe from its container dangerous time to be stuck because the needle is now con
(Fig. 9-1). taminated with blood, saliva,and debris.Although a variety
2. Retract the piston fullybefore attempting to load the of techniques and devicesfor recappinghavebeen suggested,
cartridge (Fig.9-2). the technique recommended by most state safetyand health
3. Insert the cartridge, while the piston is fully retracted, agencies is termed the scoop technique (Fig. 9-7), in which
into the syringe.Insert the rubber stopper end of the the uncapped needle is slid into the needle sheath lying on
cartridge first (Fig.9-3). the instrument tray or table. Until a better method is
4. Engagethe harpoon. While holding the syringe as if designed, the scoop technique should be used for needle
injecting, gentlypush the piston forward until the recapping.
harpoon is firmly engaged in the plunger (Fig.9-4). Safetyneedles and syringesfor use in dentistry are still in
Excessiveforce is not necessary.Do NOT hit the piston their developmental stage.Most systems currently available
in an effort to engagethe harpoon because this for dental use leavemuch to be desired.
frequently leads to cracked or shattered glasscartridges Various needle cap holders are available--commercially
(Fig. 9-5). made (Fig.9-8) or self-made (from acrylic)-that hold the
5. Attach the needle to the syringe.Removethe white or cap stationary while the needle is being inserted into it,
clear protective plastic cap from the syringe end of the making recapping somewhat easier to accomplish.
needle and screwthe needle onto the syringe (Fig.9-6).
Most metal and plastic hubbed needles are prethreaded, Unloading the Breech-Loading, Metallic or
making it easyfor them to be screwedonto the syringe; Plastic, Cartridge-Type Syringe
however,some plastic hubbed syringesare not After administration of the local anesthetic, the following
prethreaded, requiring the needle to be pushed toward sequence is suggestedfor removing the used cartridge:
the metal hub of the syringe while being turned. 1. Retract the piston and pull the cartridge awayfrom the
6. Carefullyremove the colored plastic protective cap from needle with your thumb and forefinger as you retract
the opposite end of the needle, and expel a few drops of the piston (Fig.9-9), until the harpoon disengagesfrom
solution to test for proper flow. the plunger.
7. The syringe is now ready for use.
Note: It is common practice in dentistry to attach the *The other common time for needle-stick injury is during injection, when
needle to the syringe before placing the cartridge. This a finger of the opposite hand is accidentally stuck as a result of sudden
sequence requires hitting the piston hard to engage the unexpected patient movement.
113
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114 PART II The Armamentarium
-· '..,l~f,..,,,,.,.,. -·
Figure 9-1. Localanesthetic arm
;.
' H!).t,~-.i1;•,•••• - • • t
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CHAPTER 9 Preparation of the Armamentarium 115
Figure 9-4. Engagethe harpoon in the plunger with gentle finger pressure.
Figure 9·5. Do not exert force on the plunger; the glass may crack.
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Figure 9-6. If the plastic hubbed
needle is not prethreaded, it must be
screwed onto the syringe while
simultaneously being pushed into
the metal needle adaptor of the
syringe.
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CHAPTER 9 Preparation of the Armamentarium 117
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118 PARTII The Armamentarium
Figure 9·11. When discarding the needle, check to be sure that the metal needle adaptor from the syringe is not inadvertently discarded
also (arrow).
SELF-ASPIRATING SYRINGE*
1. Insert the cartridge (as in the preceding instructions).
2. Attach the needle.
3. The syringe is now ready for use.
Becauseof the absenceof a harpoon, loading and unload
ing the self-aspiratingsyringe are simple procedures.
ULTRASAFEASPIRATING SYRINGEt
Loading the Safety Syringe
1. While gripping the barrel firmly,fully insert the
anesthetic cartridge into the open end of the injectable
system (Fig.9-13).
2. Grip the plunger handle, putting the thumb behind the
finger holder. Introduce the handle tip into the barrel
of the injectable system,behind the cartridge
(Fig.9-14).
Figure 9-12. A, A sharps container is required for storage of 3. Next, slide the sheath protecting the needle backward,
discarded contaminated needles. B, A separate sealed container is toward the handle, until it CLICKS(the click is made as
recommended for discarded local anesthetic cartridges.
*From Dentsply,www.dentsply.com.This is a portion of the instructions
that Dentsply encloseswith its syringes.
tFrom SafetySyringes,Arcadia, Calif (www.safetysyringes.com).This is a
portion of the instructions that SafetySyringesencloseswith its syringes.
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CHAPTER 9 Preparation of the Armamentarium 119
Figure 9-13. Insert the local anesthetic cartridge into the safety Figure 9-16. Remove the needle cap and discard. (Courtesy
syringe. (Courtesy Septodont, Inc., Lancaster,PA.) Septodont, Inc., Lancaster,PA.)
Figure 9-14. Introduce the handle tip into the barrel of the
injectable system,behind the cartridge. (Courtesy Septodont, Inc.,
Lancaster,PA.)
B
Figure 9-17. A. Passiveaspiration. B, Activeaspiration. (Cour
tesy Septodont, Inc., Lancaster,PA.)
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120 PARTII The Armamentarium
Figure 9·18. Move the sheath toward the needle until it reaches the 'A'
holding position (A) so that the syringe may be used again. (Courtesy
Septodont, Inc., Lancaster,PA.)
"""/
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CHAPTER 9 Preparation of the Armamentarium 121
while using the other hand, place a finger in the ring of Hold the barrel of the injectable system with one hand,
the plunger handle and pull backward until the plunger and, while using the other hand, place a finger in the ring
is fully retracted. After you have fully retracted the of the plunger handle and pull backward until the plunger
plunger, peel off the handle in one movement (Fig. is fully retracted. Now that you have fully retracted the
9-20). Now the injectable system can be disposed of plunger, peel off the handle in one movement.
safely and the handle autoclaved. 8. Take hold of the plunger handle of the injection system,
7. When inserting a second cartridge: and pull the grip handle back toward the ring. Now
Note: During procedures that require more than one insert the tip of the plunger into the empty cartridge,
cartridge, retract the sheath to the holding position (A) as which is inside the injectable system. Pull out the
a needle-stick prevention device. Should the system be cartridge attached to the plunger by the silicone tip,
inadvertently fully locked into position (B), no attempt remove the cartridge from the plunger, and dispose of
whatsoever should be made to unlock it. Use a new injection safely. You are now ready to insert a fresh cartridge and
system. proceed as from step 1.
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IN THIS PART
Chapter 10 Physical and Psychological Evaluation
Chapter 11 Basic Injection Technique
Chapter 12 Anatomic Considerations
Chapter 13 Techniques of Maxillary Anesthesia
Chapter 14 Techniques of Mandibular Anesthesia
Chapter 15 Supplemental Injection Techniques
Chapter 16 Local Anesthetic Considerations in
Dental Specialties
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PART
Techniques of Regional
Anesthesia in Dentistry
The anatomy of the head, neck, and oral cavityis presented as a prelude to detailed descriptions of the
techniques of regional anesthesia. Techniques that are commonly used in dentistry are presented.
Although many of the techniques described in these chapters also may be carried out successfullywith
an extraoral approach, the author has limited descriptions to intraoral techniques, primarily because
of the extremelylimited use of extraoral nerve blocks in contemporary dental practice. The interested
reader is referred to textbooks that describe extraoral techniques at some length.1•2
Eachinjection technique usuallyhas severalvariations. Subtledifferencesare noted when techniques
are taught to students by different persons. The reader must alwayskeep in mind that there is never
only one "correct" technique. Goals in the administration of local anesthesia are to provide clinically
adequate pain control without unnecessarily increasing risk or provoking any immediate or delayed
complicationsin the patient. Any technique that meets these two criteria is acceptable.The techniques
presented in this section are those that this author finds most acceptable.In severalsituations, alterna
tive approaches to the technique are also described.
A subject that is all too often neglected-the requirements for pain control and local anesthesia
within the dental specialties-is discussed after these basic injection techniques are described. These
requirements vary somewhat from endodontics to pediatric dentistry to periodontics to prosthodontics
to oral and maxillofacialsurgery and require special attention (Chapter 16).Administration of local
anesthetics to the geriatric patient, a significant and growing segment of the population, is also
reviewed.
The beginning of this section, Chapters 10 and 11, addressestwo important subjects related to all
injections:the physicaland psychologicalevaluation of the patient before injection and basic injection
technique (e.g., preparation of the patient and tissues for administration of any local anesthetic, the
procedure for an atraumatic [painless]injection).
References
1. Hadzic A, Vloka JD: Peripheral nerve blocks: principles and practice, New York, 2004, McGraw-Hill.
2. Chelly J: Peripheral nerve blocks: a color atlas, ed 3, Philadelphia, 2009, Lippincott Williams &: Wtlldns.
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I
Beforestarting any dental procedure, the doctor or hygienist physical examination of the patient. Adequate use of these
must determine whether the patient can tolerate the planned tools can lead to an accurate determination of a patient's
dental procedure in relativesafety.If this is not the case,the physical status and can prevent up to 90% of all life
specific treatment modifications necessary to decrease the threatening medical emergenciesin dental practice.2
risk presented by the patient must be determined. This is
especiallyimportant whenever drugs are to be administered
during treatment, such as analgesics,sedatives, inhalation
GOALS OF PHYSICAL AND
sedation (N20-02) agents, and local anesthetics. Before
PSYCHOLOGICAL EVALUATION
administering local anesthetics, the administrator must In the followingdiscussion,a comprehensivebut easy-to-use
determine the relative risk presented by the patient. This is program of physical evaluation is described.3•4Used as rec
important because local anesthetics, like all drugs, exert ommended, it allows the dental team to accurately deter
actions on many parts of the body (see Chapter 2). Actions mine any potential risk presented by the patient before the
of local anesthetics include depressant effects on excitable start of treatment. This system can be used to meet the fol
membranes (e.g., central nervous system [CNS],cardiovas lowing goals:
cular system [CVS]).Becauselocal anesthetics undergo bio 1. To determine the patient's ability to tolerate physically
transformation primarily in the liver (amides) or blood the stressesinvolvedin the planned dental treatment
(esters) the functional status of these systemsmust be deter 2. To determine the patient's ability to tolerate
mined before drug administration. Becausea small percent psychologically the stressesinvolvedin the planned
age of all injected local anesthetic is excreted in an active dental treatment
(unmetabolized) form in the kidneys,kidney function must 3. To determine whether treatment modification is
be evaluated. Other questions should be asked: Has the indicated to enable the patient to better tolerate the
patient ever receiveda local anesthetic for medical or dental stressesof dental treatment
care?If so, were any adversereactions observed? 4. To determine whether the use of psychosedation is
Most undesirable reactions to local anesthetics are pro indicated
duced not by the drugs themselvesbut as a response to the 5. To determine which technique of sedation is most
act of drug administration.1 These reactions are commonly appropriate for the patient
psychogenic and have the potential to be life threatening 6. To determine whether contraindications exist to (a) the
if not recognized and managed promptly. The two most planned dental treatment or (b) any of the drugs to be
commonly occurring psychogenic reactions are vasode used.
pressor syncope and hyperventilation. Other psychogeni The first two goalsinvolvethe patient's ability to tolerate
callyinduced reactionsnoted as a responseto localanesthetic the stress involvedin the planned dental care. Stressmay be
administration may include tonic-clonic convulsions,bron of a physiologic or psychological nature. Patients with
chospasm, and angina pectoris. underlying medical problems may be lessable to tolerate the
However,local anesthetics are not absolutely innocuous usual levelsof stress associatedwith various types of dental
drugs, nor is the act of local anesthetic administration care. These patients are more likely to experience an acute
entirely benign. The doctor must seek to uncover as much exacerbation of their underlying medical problem(s) during
information as possibleconcerningthe patient's physicaland periods of increased stress. Such disease processes include
mental status before administration of a local anesthetic. angina pectoris, seizure disorders, asthma, and sickle cell
Fortunately the means to do so exist in the form of the disease. Although most of these patients will be able to
medical history questionnaire, the dialogue history, and the tolerate the planned dental care in relative safety,it is the
124
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CHAPTER 10 Physicaland PsychologicalEvaluation 125
obligation of the dental team to determine whether a Many types of medical history questionnaires are avail
problem does exist and the severity of the problem and to able; however,most are simply modifications of two basic
decide how it might impact the proposed dental treatment types: the "short" form and the "long" form. The short form
plan. medicalhistory questionnaire providesbasic medicalhistory
Excessive stress can prove detrimental to the non information and is best suited for use by a dentist or hygien
medically compromised (i.e., "healthy") patient. Fear, ist with considerable clinical experience in physical evalua
anxiety, and acute pain produce abrupt changes in the tion. When using the short-form history, the dentist or
homeostasis of the body that may prove detrimental. Many hygienistmust have a firm grasp of the appropriate dialogue
"healthy" patients suffer from fear-related emergencies, history required to aid in determination of the relative risk
including hyperventilation and vasodepressor syncope (also presented by the patient. The dentist or the hygienistshould
known as vasovagal syncope and "fainting"). be experienced in the use of techniques of physical evalua
The third goal is to determine whether the usual treat tion and interpretation of findings. Unfortunately, most
ment regimen for a patient should be modified to enable the dentist offices use the short form or a modification of it
patient to better tolerate the stress of treatment. In some primarily as a conveniencefor their patient and themselves.
cases, a healthy patient will be psychologically unable to The long form, on the other hand, results in a more detailed
tolerate the planned treatment. Treatment may be modified database concerning the physical condition of the prospec
to minimize the stress faced by this patient. The medically tive patient. It is used most often in teaching situations and
compromised patient will also benefit from treatment modi represents a more ideal instrument for teaching physical
fication aimed at minimizing stress. The stress reduction evaluation.
protocols (SRPs) outlined in this chapter are designed to aid In recent years, computer-generated medical history
the dentist and the hygienist in minimizing treatment questionnaires have been developed.5 These questionnaires
related stress for both healthy and medically compromised permit patients to enter their responses to questions elec
patients. tronically on a computer. Whenever a positive response is
When it is believed that the patient will require some given,the computer asks additional questions related to the
assistance in coping with his or her dental treatment, the use positive response. In effect,the computer asks the questions
of psychosedation should be considered. The last three goals called for in the dialogue history.
involve determination of the need for use of psychosedation, Any medical history questionnaire can prove to be
selection of the most appropriate technique, and selection of extremelyvaluable or entirelyworthless.The ultimate value
the most appropriate drug(s) for patient management. of the questionnaire resides in the ability of the dentist or
hygienist to interpret the significanceof the answers and to
elicit additional information through physical examination
PHYSICAL EVALUATION and dialogue history.
The term physical evaluation is used to describe the steps In this sixth edition of Local Anesthesia, the prototypical
involved in fulfilling the aforementioned goals. Physical adult health history questionnaire that has been developed
evaluation in dentistry consists of the following three by the University of the Pacific {UOP) School of Dentistry
components: in conjunction with MetLifehas been included (Fig. 10-1).6
1. Medicalhistory questionnaire Figure 10-2 is an example of a pediatric medical history
2. Physicalexamination questionnaire.
3. Dialogue history This health history has been translated into 36 different
With the information (database) collected from these languages,constituting the languagesspoken by 95% of the
three steps, the dentist and the hygienist will be better able persons on this planet. The cost of the translation was sup
to (1) determine the physicaland psychologicalstatus of the ported by several organizations including the California
patient (establish a risk factor classificationfor the patient); Dental Association,but most extensivelyby MetLifeDental.
(2) seek medical consultation, if indicated; and (3) appro The health history (see Fig. 10-1),translations of the health
priately modify the planned dental treatment, if indicated. history (Fig. 10-3), the interview sheet (Fig. 10-4), the
Each of the three steps in the evaluation processis discussed medical consultation form (Fig. 10-5), and protocols for
in generalterms, with specificemphasisplaced on its impor the dental management of medically complex patients
tance in the evaluation of the patient for whom local anes may be found on the University of the PacificWebsite at
thesia is to be administered. www.dental.pacific.eduunder "Dental Professionals" and
then under "Health History Forms."Protocols for the man
Medical History Questionnaire agement of medicallycomplex patients can be found at the
The use of a written, patient-completed medical history sameWebsiteunder "PacificDental Management Protocols."
questionnaire is a moral and legal necessity in the practice Translations of the medical history form can be found at
of both medicine and dentistry.Suchquestionnaires provide www.metdental.comunder "Multilanguage Medical Health
the dentist and the hygienist with valuable information History Forms Available."
about the physicaland in some casesthe psychologicalcon
dition of the prospectivepatient. Text continued on p. 131
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126 PART III Techniques of Regional Anesthesia in Dentistry
\"I.WO:WF.'lrti 0:\1.Y:
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Dentistry, San Francisco.)
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CHAPTER 10 Physical and Psychological Evaluation 127
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hil/her bealdl or 1111/her nxdlcinCI c1nnF, I will lnfimn lbe dactar at lhe next appolnmcnt wllhlllll fai.
Parent'aSignUure: ·--
MtD.ICAL HISTORY I PH•CIU.11.XAMIHmON
_
ll\U:W
·- Dale .:::::..===-=· =
Addi don
Figure 10·2. Pediatric medical history questionnaire. (From Malamed SF: Medical emergencies in the dental office, ed 6, St Louis, 2007,
Mosby.)
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128 PART III Techniques of Regional Anesthesia in Dentistry
1 Sf l'>D o.111.
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6!. Sf ••••• 5 - .....:--.... ••• _....,_ mtiriio:>r. 61. :!I •••• •.••••••••••lbclrda i*ohdli.mr.
Lble •••.•.b"1C
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SI.wort Jar lhe bnllltkrl illd cbsa1•edull of lhe ••••••• tlslaies CGllll5him Med.J'!DemI Ccn
Figure 10-3.. Spanish health history questionnaire. (Reprinted with permission from Universityof the PacificArthur A. Dugoni School
of Dentistry, San Francisco.)
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CHAPTER 10 Physical and Psychological Evaluation 129
PallenlNama: _
Dale
n...-..~=-tr=:'=~:..~'"=-~~rmdam.C6Mna
Figure 10-4. Health history interview sheet. (Reprinted with permission from University of the Pacific Arthur A. Dugoni School of Den
tistry, San Francisco.)
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130 PART III Techniques of Regional Anesthesia in Dentistry
RE:
Phone# _
Date of Birth
Fax# _
Most patients experience the following with the above planned procedures:
bleeding: • minimal (<50ml) • significant (>50ml)
stress and anxiety: • low • medium • high
PHYSICIAN'S RESPONSE
Please provide any information regarding the above patient's need for antibiotic prophylaxis, current cardiovascular condition,
coagulation ability, and the history and status of infectious diseases. Ordinarily, local anesthesia is obtained with 2% lidocaine,
1:100,000 epinephrine. For some surgical procedures, the epinephrine concentration may be increased to 1:50,000 for
hemostasis. The epinephrine dose NEVER exceeds 0.2 mg total.
CHECKALL THATAPPLY
• OK to PROCEED with dental treatment; NO special precautions and NO prophylactic antibiotics
are needed.
• Antibiotic prophylaxis IS required for dental treatment according to the current American Heart Association
and/or American Academy of Orthopedic Surgeons guidelines.
• Other precautions are required (please list}:. _
Physiciansignature Date
PATIENT CONSENT
I agree to the release of my medical information to the University of the Pacific School of Dentistry.
This Medical Consultation form is created and maintained by the University of the Pacific School of Dentistry, San Francisco, California.
Support for the translation and dissemination of the health histories comes from MetLife Dental Care.
Figure 10-5. Medical consultation form. (Reprinted with perntlssion from University of the Pacific Arthur A. Dugoni School of Dentistry,
San Francisco.)
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CHAPTER 10 Physicaland PsychologicalEvaluation 131
The health history has been translated while keeping the 4. Are You Being Treated by a Physician Now?
same question numbering sequence. Thus a dentist who For What?
speaks English and is caring for a patient who does not can Date of last medical exam?
ask the patient to complete the health history in his or her Date of last dental exam?
own language. The dentist then compares the English health Comment: Question Nos. 2, 3, and 4 seek information
history with the patient's translated health history, scanning regarding recent changesin the patient's physicalcondition.
the translated version for YES responses. When a YES is In all instances of a positive response, an in-depth dialogue
found, the dentist is able to look at the question number and history must ensue to determine the precise nature of the
match it to the question number on the English version. For change in health status, the type of surgical procedure or
example, the dentist would know that a YES response to illness, and the names of any medications the patient may
question No. 34 on the non-English version is the same as now be taking to help manage the problem.
this response to question No. 34 on the English version,
which relates to high blood pressure (HBP). For that matter, 5. Have You Had Problems With Prior Dental
a Mandarin Chinese-speaking dentist could use the multi Treatment?
language health history with an English-speaking patient Comment: Many adults are reluctant to verbally admit
and have the same cross-referenced information. A dentist to the dentist, hygienist,or assistant their fears about treat
who speaks Spanish could use the multilanguage health ment, for fear of being labeleda "baby."This is especiallytrue
history with a patient who speaks French. With the uniform of young men in their late teens or early twenties; they
health history question sequence, these health history trans attempt to "take it like a man" or "grin and bear it" rather
lations can serve patients and dentists all around the world. than admit their fears.Becausethe most common fear men
The health history is divided into sections related to signs tioned by dental patients is fear of injection (the "shot," in
and symptoms ("Have you experienced?"), diagnosed dis their words), all too often, such macho behavior results in
eases ("Do you have or have you had?"), medical treatments an episode of vasodepressor syncope. Whereas many such
(including drugs and other physiologically active com patients will not offer verbal admissions of fear, many of
pounds), and several other questions. these same patients will volunteer this information in
Although both long- and short-form medical history writing.
questionnaires are valuable in determining a patient's physi
cal condition, one criticism of most available health history 6. Are You in Pain Now?
questionnaires is the absence of questions related to the Comment: The primary aim of this question is related to
patient's attitudes toward dentistry. It is recommended the need for immediate dental care. Its purpose is to deter
therefore that one or more questions be included that relate mine what prompted the patient to seek dental care. If pain
to this all-important subject: is present, the dentist may need to treat the patient immedi
1. Do you feel very nervous about having dental ately on an emergency basis, whereas in the more normal
treatment? situation, treatment can be delayed until future visits. This
2. Have you ever had a bad experience in the dental may affect the use of local anesthesia, in that effectivepain
office? control can be more difficult to achieve in the presence of
Question Nos. 5 and 6 on the UOP medical history ques infection and chronic, albeit, now acute, pain in the fearful
tionnaire address these points. patient.
Following is the UOP medical history questionnaire with
a discussion of the significance of each point.
II. HAVE YOU EXPERIENCED:
7. Chest Pain (Angina)?
I. CIRCLE APPROPRIATE ANSWER:
Comment: A history of angina (defined,in part, as chest
(Leave blank if you do not understand pain brought on by exertion and alleviatedby rest) usually
the question.) indicatesthe presence of coronary artery diseasewith atten
1. Is Your General Health Good? dant ischemia of the myocardium. The risk factor for the
Comment: General survey questions seek patients' gen typicalpatient with stableangina isASA3 (AmericanSociety
eral impression of their health. Studies have demonstrated of Anesthesiologists' [ASA] physical status classification
that a YES response to this question does not necessarily system).* In the presence of dental fears, sedation is abso
correlate with the patient's actual state ofhealth.7 lutely indicated in the angina! patient. Inhalation sedation
with N20-02 is preferred.Effectivepain control-local anes
2. Has There Been a Change in Your Health Within the thesia with vasoconstrictor included-is absolutely indi
Last Year? cated.Patientswith unstable or recent-onset anginarepresent
ASA4 risks.
3. Have You Been Hospitalized or Had a Serious Illness
in the Last 3 Years? *The ASA physical status classification system is discussed in detail later in
If YES, Why? this chapter.
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132 PART III Techniques of Regional Anesthesia in Dentistry
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CHAPTER10 Physicaland PsychologicalEvaluation 133
GI and systemic infections, viral and bacterial, are the myasthenia gravis, vascular disturbance, and intracranial
second most common cause of nausea and vomiting. tumor.
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134 PARTIII Techniquesof RegionalAnesthesiain Dentistry
28. Joint Pain, Stiffness'? warranted. In this situation, the dentist must consider
Comment: A history of joint pain and stiffness(arthritis) whether the patient requires supplemental 02 during treat
may be associatedwith long-term use of salicylates{aspirin) ment. Whereas most HF patients are classifiedaccording to
or other NSAIDs,some of which may alter blood clotting. the ASAphysicalstatus classificationsystem as ASA2 (mild
Arthritic patients who are receivinglong-term corticosteroid HF without disability) or ASA3 (disabilitydevelopingwith
therapy may suffer increased risk of acute adrenal insuffi exertion or stress) risks,the presence of dyspnea at rest rep
ciency,especiallythe patient who has recentlystopped taking resents an ASA4 risk. Effectivepain control is essential in
the steroid. Such patients may require a short course of the ASA2 and 3 HF patient, but care must be taken in select
steroid therapy or a modification (increase)in corticosteroid ing the appropriate drugs and technique to prevent signifi
dose during dental treatment, so that their body is better able cant increases in the cardiac workload. Local anesthetics
to respond to any additional stress that might be associated containing vasopressors are definitely indicated in these
with the treatment. patients because they are more likely to provide successful
Becauseof possible difficultiesin positioning the patient pain control for dental procedures compared with "plain"
comfortably,modifications may be necessary to accommo local anesthetics.
date the patient's physicaldisability.Most patients receiving Congenital heart lesions: An in-depth dialogue history
corticosteroids are categorized as ASA2 or 3 risk depend is required to determine the nature of the lesion and the
ing on the reason for the medication and the degree of degree of disability present. Patients can represent ASA 2,
disabilitypresent. Patientswith significantlydisablingarthri 3, or 4 risk. The dentist may recommend medical consulta
tis are ASA 3 risks. Problems secondary to arthritis may tion, especiallyfor the pediatric patient, to judge the severity
require modification in positioning during local anesthetic of the lesion. Some dental treatments require prophylactic
injection. antibiotics.
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CHAPTER 10 Physical and Psychological Evaluation 135
TABLE 10-1
Antibiotic Prophylaxis 2007*
Situation Agent Adults Children
Oral Amoxicillin 2g 50 mg/kg
Unable to take oral medication Ampicillin or 2 gIM or IVt 50 mg/kg IM or IV
Cefazolinor ceftriaxone 1 gIM or IV 50 mg/kg IM or IV
Allergicto penicillins or ampicillin Cephalexin:j:§ 2g 50 mg/kg
Oral or
Clindamycin 600mg 20 mg/kg
or
Azithromycin or clarithromycin 500mg 15 mg/kg
Allergicto penicillins or ampicillin Cefazolinor ceftriaxone§ 1 gIM or IV 50 mg/kg IM or IV
and unable to take oral or
medication Clindamycin 600 mg IM or IV 20 mg/kg IM or IV
From Wilson W, Taubert KA,Gewitz M, et al: Prevention of infectiveendocarditis: guidelinesfrom the American Heart Association:a guideline from the
American Heart AssociationRheumatic Fever,Endocarditis, and KawasakiDiseaseCommittee, Council on CardiovascularDiseasein the Young,and the
Council on Clinical Cardiology,Council on CardiovascularSurgery and Anesthesia,and the Quality of Care and Outcomes ResearchInterdisciplinary
Working Group, Circulation 116:1736--1754,2007.
*Regimen:single dose 30 to 60 minutes before procedure.
tIM, Intramuscular; N, intravenous.
:j:Orother first- or second-generation oral cephalosporin in equivalent adult or pediatric dosage.
§Cephalosporins should not be used in an individual with a history of anaphylaxis,angioedema, or urticaria with penicillins or ampicillin.
BOX 10-1 Cardiac Conditions Associated With the BOX 10-2 Dental Procedures for Which Endocarditis
Highest Risk of Adverse Outcome from Prophylaxis Is Recommended for Patients
Endocarditis for Which Prophylaxis With
All dental procedures that involvemanipulation of gingi
Dental Procedures Is Recommended
val tissue or the periapical region of teeth or perforation
• Prosthetic cardiac valve of the oral mucosa.*
• Previous infectiveendocarditis
*The followingprocedures and events do not need prophylaxis:routine
• Congenital heart disease (CHD)* anesthetic injections through noninfected tissue, taking of dental
• Unrepaired cyanotic CHD, including palliative radiographs, placement of removable prosthodontic or orthodontic
shunts and conduits appliances,adjustment of orthodontic appliances,placement of
• Completelyrepaired congenital heart defect with orthodontic brackets, shedding of deciduous teeth, and bleeding from
trauma to the lips or oral mucosa.
prosthetic material or device,whether placed by
surgery or by catheter intervention, during the first
6 mo after the proceduret
• Repaired CHD with residual defectsat the site or presence of transient cerebralischemia (TCI), a precursor to
adjacent to the site of a prosthetic patch or CVA;TCI represents an ASA3 risk. The post-CVApatient is
prosthetic device (which inhibits endothelialization) an ASA 4 risk within 6 months of the CVA,becoming an
• Cardiac transplantation recipients who develop ASA3 risk 6 or more months after the incident (if the recov
cardiac valvulopathy ery is uneventful). In rare cases,the post-CVApatient can be
an ASA2 risk.
tProphylaxisis recommended because endothelialization of prosthetic
material occurs within 6 mo after the procedure.
*Exceptfor the conditions listed previously,antibiotic prophylaxisis no 34. High Blood Pressure?
longer recommended for any form of CHD. Comment: Elevatedblood pressure (BP) measurements
are frequently encountered in the dental environment sec
ondary to the added stressthat many patients associatewith
the victim of a CVA).A patient who has suffered a CVAis a visit to the dental office.With a history of HBP,the dentist
at greater risk of suffering another CVAor a seizure should must determine the drugs the patient is taking, the potential
he or she become hypoxic. The importance of effective side effectsof those medications, and any possible interac
pain control, through administration of local anesthetic tions with other drugs that might be used during dental
solutions with vasopressors,cannot be overstated.Epineph treatment. Guidelines for clinical evaluation of risk (ASA
rine concentrations should be minimized (e.g., 1:200,000) categories) based on adult BP values are presented later in
but this agent should be included as it increases anesthetic this chapter. The SRP is a significant factor in minimizing
effectiveness.The dentist should be especiallysensitiveto the further elevation in BP during treatment.
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136 PART III Techniques of Regional Anesthesia in Dentistry
35. Asthma, Tuberculosis (TB), Emphysema, Other administration are selected for the patient with significant
Lung Disease? hepatic dysfunction. In general, local anesthetics and vaso
Comment: Determining the nature and severity of res pressors are indicated for use, with consideration of mini
piratory problems is an essential part of patient evaluation. mizing the dose in patients with severe hepatic dysfunction
Many acute problems developing in the dental environment (e.g., ASA 4).
are stress related, increasing the workload of the cardio
vascular system and the 02 requirements of many tissues 37. Stomach Problems, Ulcers?
and organs in the body. The presence of severe respiratory Comment: The presence of stomach or intestinal ulcers
disease can greatly influence the planned dental treatment may be indicative of acute or chronic anxiety and the pos
and the choice of drugs and technique if sedation is required. sible use of medications such as tranquilizers, H 1-inhibitors,
Asthma (bronchospasm) is marked by a partial obstruc and antacids. Knowledge of which drugs are taken is impor
tion of the lower airway. The dentist must determine the tant before additional drugs are administered in the dental
nature of the asthma (intrinsic [allergic] vs. extrinsic [nonal office. A number of H 1-inhibitors are now over-the-counter
lergic]), the frequency of acute episodes, causal factors, the (OTC) drugs. Because many patients do not consider OTC
method of management of acute episodes, and drugs the drugs "real" medications, the dentist must specifically ques
patient may be taking to minimize the occurrence of acute tion the patient about them. The presence of ulcers does not
episodes. Stress is a common precipitating factor in acute itself represent increased risk during treatment. In the
asthmatic episodes. The well-controlled asthmatic patient absence of additional medical problems, the patient may
represents an ASA 2 risk, whereas the well-controlled but represent an ASA 1 or 2 risk.
stress-induced asthmatic patient is an ASA 3 risk. Patients
whose acute episodes are frequent and/or difficult to termi 38. Allergies to: Drugs, Foods, Medications, Latex?
nate (requiring hospitalization [status asthmaticus]) are Comment: The dentist must evaluate a patient's allergies
ASA 3 or 4 risk. thoroughly before administering dental treatment or drugs.
With a history of tuberculosis, the dentist must first deter The importance of this question and its full evaluation
mine whether the disease is active or arrested. (Arrested cannot be overstated. A complete and vigorous dialogue
tuberculosis represents an ASA 2 risk.) Medical consultation history must be undertaken before any dental treatment is
and dental treatment modification are recommended when begun, especially when a presumed or documented history
such information is not easily determined. of drug allergy is present. Adverse drug reactions (ADRs)
Emphysema is a form of chronic obstructive pulmonary are not uncommon. Many, if not most, ADRs are labeled
disease (COPD), also called chronic obstructive lung disease as "allergy" by the patient and also on occasion by his or
(COLD). The emphysematous patient has a decreased respi her health care professional. However, despite the great fre
ratory reserve from which to draw if cells of the body require quency with which allergy is reported, true documented
additional 02, which they do during stress. Supplemental 02 and reproducible allergic drug reactions are relatively rare.
therapy during dental treatment is recommended in severe A recent review of food allergy revealed 30% self-reporting
cases of emphysema; however, the severely emphysematous of "food allergy" by the studied population, when the reality
(ASA 3 and 4) patient should not receive more than 3 L of is that true food allergy is seen in 8% of children and 5%
02 per minute.18 This flow restriction helps to ensure that of adults."
the dentist does not eliminate the hypoxic drive, which is the All ADRs must be evaluated thoroughly, especially when
emphysematous patient's primary stimulus for breathing. the dentist plans to administer or prescribe closely related
The emphysematous patient is an ASA 2, 3, or 4 risk, depend medications for the patient during dental treatment. Alleged
ing on the degree of disability. "allergy to Novocaine" is frequently reported.
The incidence of true, documented, reproducible allergy
36. Hepatitis, Other Liver Disease? to the amide local anesthetics is virtually nil. 21·22However,
Comment: Liver diseases may be transmissible (hepatitis reports of alleged allergy to local anesthetics is common.P'"
A and B) or may indicate the presence of hepatic dysfunc Thorough investigation of the alleged allergy is essential
tion. A history of blood transfusion or of past or present if the patient is not to be assigned the label of "allergic
drug addiction should alert the dentist to a probable increase to all -caine drugs:' thereby precluding dental (and surgical)
in the risk of hepatic dysfunction. (Hepatic dysfunction is care in a normal manner. Avoidance of dental care or receipt
a common finding in the parenteral drug abuse patient.) of care under general anesthesia is the alternative in these
Hepatitis C is responsible for more than 90% of cases of cases.
posttransfusion hepatitis, but only 4% of cases are attri Reports of allergy to "epinephrine" or "adrenaline" also
butable to blood transfusion; up to 50% of cases are related must be carefully evaluated. Most often, such reports prove
to N drug use. Incubation of hepatitis C averages 6 to 7 to be simply an exaggerated physiologic response by the
weeks. The clinical illness is mild, usually asymptomatic, and patient to the injected epinephrine or, more commonly, to
characterized by a high rate (>50%) of chronic hepatitis.19 endogenous catecholamine release in response to the act of
Because most drugs undergo biotransformation in the liver, receiving the injection (the "adrenal squeeze," as a colleague
care must be taken when specific drugs and techniques of called it recently).
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CHAPTER 10 Physicaland PsychologicalEvaluation 137
Two essential questions that must be asked in all instances scopolamine, and glycopyrrolate, are contraindicated in
of alleged allergy are these: (1) Describe your reaction, and patients with acute narrow angle glaucoma because these
(2) How was it managed? drugs produce an increase in intraocular pressure. Patients
The presence of allergy alone represents an ASA 2 risk. with glaucoma are usuallyASA2 risks. There is no contra
No emergency situation is as frightening to health care indication to local anestheticadministration with or without
professionals as the acute, systemic allergic reaction known vasopressors.
as anaphylaxis. Prevention of this life-threatening situation
is more gratifying than treatment of anaphylaxis once it 44. Skin Diseases?
develops. Comment: Skin represents an elastic, rugged, self
Investigation into a patient's report of "allergy to local regenerating,protective coveringfor the body. The skin also
anesthesia"is so important that it is discussed in depth in represents our primary physical presentation to the world
Chapter 18. and as such displays a myriad of clinical signs of disease
processes,including allergyand cardiac,respiratory,hepatic,
39. Family History of Diabetes. Heart Problems. and endocrine disorders.25
Tumors?
Comment: Knowledge of family history can assist in 45. Anemia?
determining the presenceof a number of disorders that have Comment: Anemia is a relativelycommon adult ailment,
some hereditary component. especially among young adult women (iron deficiency
anemia). The dentist must determine the type of anemia
40. Acquired Immunodeficiency Syndrome (AIDS}? present. The ability of the blood to carry 02 or to giveup 02
Comment: Patients who have a positive test result for to other cellsis decreased in anemic patients. This decrease
human immunodeficiencyvirus (HN) are representativeof can become significantduring procedures in which hypoxia
every area of the population. The usual barrier techniques is likely to develop. There is no contraindication to local
should be employed to minimize risk of cross-infection for anesthetic administration with or without vasopressors.
both patient and staff members. Patients who are HN posi Sickle cell anemia is seen exclusivelyin black patients.
tive are considered ASA2, 3, 4, or 5 risk depending on the Periods of unusual stress or of 02 deficiency(hypoxia) may
current status of their infection. precipitate sicklecell crisis.Administration of supplemental
Proper care and handling of the local anesthetic syringe/ 02 during treatment is strongly recommended for patients
needle must be observed, as in all situations, to avoid acci with sicklecelldisease.Personswith sicklecelltrait represent
dental needle-stick injury. ASA2 risk, whereas those with sicklecell disease are 2 or 3
risks.
41. Tumors. Cancer? In addition, congenital or idiopathic methemoglobin
Comment: The presence or prior existence of cancer emia, although rare, represents a relativecontraindication to
of the head or neck may require specific modification of administration of the amide local anesthetic prilocaine.26
dental therapy. Irradiated tissues have decreased resistance
to infection, diminished vascularity, and reduced healing 46. VD (Syphilis or Gonorrhea}?
capacity. No specific contraindication exists to admini
stration of drugs for the management of pain or anxiety in 47. Herpes?
these patients; however,techniques of local anesthetic drug Comment: When treating patients with sexually trans
administration may, on rare occasion,be contraindicated if mitted diseases (STDs), dentists and staff members are at
the tissues in the area of deposition have been irradiated. risk of infection. In the presence of oral lesions, elective
Many persons with cancer may be receiving long-term dental caremight be postponed. Standardbarrier techniques,
therapy with CNS depressants, such as antianxiety drugs, such as protective gloves, eyeglasses,and masks, provide
hypnotics, and opioids. Consultation with the patient's operators with a degree of (but not total) protection. Such
oncologistis recommended before dental treatment isbegun. patients usuallyrepresent ASA2 and 3 risks but may be 4 or
A past or current history of cancer does not necessarily 5 risks in extreme situations.
increaseASArisk status.However,patients who are cachectic
or hospitalized or are in poor physicalcondition may repre 48. Kidney. Bladder Disease?
sent ASA4 or 5 risk. Comment: The dentist should evaluate the nature of
the renal disorder. Treatment modifications including anti
42. Arthritis. Rheumatism? biotic prophylaxis may be appropriate for several chronic
Comment: See Comment for question No. 28. forms of renal disease. Functionally anephric patients are
ASA 3 or 4 risks, whereas patients with most other forms
43. Eye Disease? of renal dysfunction may be ASA 2 or 3 risks. Box 10-3
Comment: For patients with glaucoma, the need to shows a sample dental referral letter for a patient on long
administer a drug that diminishes salivarygland secretions term hemodialysistreatment as the result of chronic kidney
will haveto be addressed.Anticholinergics,such as atropine, disease.
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CHAPTER 10 Physicaland PsychologicalEvaluation 139
TABLE 10-2
Dental Drug Interactions With Local Anesthetics and Vasopressors*
Dental Drug Interacting Drug Consideration Action
Local anesthetics Cimetidine, P-adrenergicblocker Hepatic metabolism of amide LA Use LAscautiously,especially
(LAs) (propranolol) may be depressed repeat dosages
Antidysrhythmics (mexiletine,tocainide) Additive CNS,CVSdepression Use LAscautiously-keep
dose as low as possibleto
achieveanesthesia
CNS depressants:alcohol, antidepressants, Possibleadditive or supra-additive Consider limiting maximum
antihistamines, benzodiazepines, CNS,respiratory depression dose of LAs,especiallywith
antipsychotics,centrally acting opioids
antihypertensives,muscle relaxants,
other LAs,opioids
Cholinesteraseinhibitors: antimyasthenics, Antimyasthenic drug dosage may Physicianconsultation
antiglaucoma drugs require adjustment because LA
inhibits neuromuscular
transmission
Vasoconstrictors; a-Adrenergic blockers Possiblehypotensiveresponse Use vasoconstrictor
epinephrine (phenoxybenzamine,prazosin); followinglarge dose of cautiously-as low a dose as
antipsychotics (haloperidol, epinephrine possible
entacapone)
Catecholamine-0-methyltransferase May enhance systemicactions of Use vasoconstrictor
inhibitors (tolcapone, entacapone) vasoconstrictors cautiously-as low a dose as
possible
CNS stimulants (amphetamine, Effectsof stimulant or Use vasoconstrictor
methylphenidate); ergot derivatives vasoconstrictor may occur cautiously-as low a dose as
(dihydroergotamine,methysergide) possible
Cocaine Effectsof vasoconstrictors;can result Avoiduse of vasoconstrictor
in cardiac arrest in patient under influence
of cocaine
Digitalisglycosides(digoxin,digitoxin) Risk of cardiac dysrhythmias Physicianconsultation
Levodopa,thyroid hormones Largedoses of either (beyond Use vasoconstrictor
(levothyroxine,liothyronine) replacement doses) may risk cautiously-as low a dose as
cardiac toxicity possible
Tricyclicantidepressants (amitriptyline, May enhance systemiceffectsof Avoiduse of levonordefrin or
doxepin, imipramine) vasoconstrictor norepinephrine; use
epinephrine cautiously-as
low a dose as possible
NonselectiveP-blockers (propranolol, May lead to hypertensiveresponses, Monitor BP after initial LA
nadolol) especiallyto epinephrine injection
From Ciancio SG:ADA/PDRguide to dental therapeutics, ed 5, Chicago,2010,American Dental Association.
BP,Blood pressure; CNS, central nervous system;CVS, cardiovascularsystem.
*Drug-drug interactions of greater clinicalsignificanceare emboldened for emphasis.
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CHAPTER10 Physicaland PsychologicalEvaluation 141
64. Alcohol? (or the parent or guardian if the patient is a minor or is not
Comment: Chronic use of tobacco and/or alcohol over legallycompetent) and the dentist who reviewsthe history.
extended periods can lead to the development of potentially This in effectbecomesa contract obligingthe patient, parent,
life-threateningproblems including neoplasms,hepatic dys or guardian to report any changes in the patient's health or
function, and, in women, complications during pregnancy. medications. Brady and Martinoff' demonstrated that a
patient's analysisof personal health frequentlyis overlyopti
mistic, and that pertinent health matters sometimes are not
VI. WOMEN ONLY: immediately reported.
65. Are You or Could You Be Pregnant or Nursing? The medical history questionnaire should be updated on
a regular basis, approximately every 3 to 6 months or after
66. Taking Birth Control Pills? any prolonged lapse in treatment. In most instances, the
Comment: Pregnancy represents a relativecontraindica entire medical history questionnaire need not be redone.
tion to extensiveelectivedental care, particularly during the The dentist or dental hygienist need only ask the following
first trimester. Consultation with the patient's obstetrician questions:
gynecologist(OBGYN)is recommended before the start of 1. Haveyou experiencedany change in your general health
any dental treatment. Administration of local anesthetics since your last dental visit?
with or without epinephrine is acceptableduring pregnancy. 2. Are you now under the care of a physician?If so, what
Food and Drug Administration (FDA)pregnancy categories is the condition being treated?
are presented in Box 10-4, and known fetal effectsof local 3. Are you currently taking any drugs, medications, or
anesthetics and vasopressorsare presented in Table 10-4. over-the-counter products?
If any of these questions elicits a positive response, a
detailed dialogue history should follow. For example, a
VII. ALL PATIENTS: patient may answer that no change has occurred in general
67. Do You Have or Have You Had Any Other Diseases health but may want to notify the dentist of a minor change
or Medical Problems Not Listed on This Form? in condition, such as the end of a pregnancy (It's a girl!) or
Comment: The patient is encouraged to comment on a recent diagnosis of NIDDM or asthma.
specific matters not previously mentioned. Examples of In either situation, a written record of havingupdated the
severalpossiblysignificantdisorders include acute intermit history should be appended to the patient's progress notes
tent porphyria, methemoglobinemia, atypical plasma cho or on the health history form. When the patient's health
linesterase,and malignant hyperthermia. status has changed significantly since the last history was
To the best of my knowledge, I have answered every completed, the entire history should be redone (e.g., if a
question completely and accurately. I will inform my patient was recently diagnosed with cardiovascular disease
dentist of any change in my health and/or medication. and is managing it with a variety of drugs that he or she was
Comment: This final statement is important from a not previouslytaking).
medicolegalperspectivebecause although instances of pur In reality, most persons do not undergo significant
poseful lying on health histories are rare, they do occur.This changesin their health with any regularity.Thus one health
statement should be accompanied by the date on which the history questionnaire can remain current for many years.
history was completed and the signatures of both the patient Therefore the abilityto demonstrate that a patient's medical
history has been updated on a regular basis becomes all the
more important.
BOX 10-4 FDAPregnancyCategories The medical history questionnaire should be completed
in ink. Corrections and deletions are made by drawing a
A Studies have failed to demonstrate a risk to the fetus singleline through the original entry without obliterating it.
in any trimester.
B Animal reproduction studies fail to demonstrate a
risk to the fetus; no human studies available
C Only given after risks to the fetus are considered; TABLE 10-4
animal reproduction studies have shown adverse Known Fetal Effects of Drugs
effectson fetus; no human studies available Drug Effect
D Definite human fetal risks; may be given in spite of Anesthetics, local No adverse effects in dentistry
risks if needed in life-threatening conditions Articaine No adverse effects reported in dentistry
X Absolute fetal abnormalities; not to be used at any Bupivacaine Does not cross placenta readily; no adverse
time during pregnancy because risks outweigh effects in dentistry
benefits Epinephrine No adverse effects reported for dental use
Lidocaine No adverse effects reported in dentistry
From FDApregnancy risk categoriesfor local anesthetics:B---lidocaine, Mepivacaine No adverse effects reported in dentistry
prilocaine; C-articaine, bupivacaine, mepivacaine.Availableat: Prilocaine No adverse effects reported in dentistry
www.epocrates.com.AccessedOctober 28, 2010.
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142 PARTIII Techniquesof RegionalAnesthesiain Dentistry
The change is then added along with the date of the change. 1. Monitoring of vital signs
The dentist initials the change. 2. Visual inspection of the patient
A written notation should be placed in the chart when 3. Function tests, as indicated
ever a patient reveals significant information during the 4. Auscultation of heart and lungs and laboratory tests, as
dialogue history. As an example, when a patient answers indicated
affirmativelyto the question about a "heart attack",the den Minimal physical evaluation for all potential patients
tist's notation may read "2008" (the year the MI occurred). should consist of (1) measurement of vital signs and (2)
visual inspection of the patient.
The primary value of the physical examination is that it
PHYSICAL EXAMINATION
provides the dentist with important (up-to-the-minute)
The medical history questionnaire is quite important to the information concerningthe physicalcondition of the patient
overall assessment of a patient's physical and psychological immediatelybefore the start of treatment, as contrasted with
status. However,the questionnaire has limitations. For the the questionnaire, which provides historical (dated) infor
questionnaire to be valuable,the patient must (1) be aware mation. The patient should undergo a minimal physical
of the presence of any medical condition and (2) be willing evaluation at the initial visit to the office before the start
to share this information with the dentist. of any dental treatment. Readings obtained at this time,
Most patients do not knowingly deceivetheir dentist by called baseline vital signs, are recorded on the patient's
omitting important information from the medical history chart.
questionnaire, although cases in which such deception has
occurred are on record. A patient seeking treatment for an Vital Signs
acutelyinflamed tooth decidesto withhold from the dentist The six vital signs are as follows:
that he had an MI 2 months earlier because he knows that 1. Blood pressure (BP)
to tell the dentist would mean that he would likely not 2. Heart rate (pulse) and rhythm
receivethe desired treatment (e.g.,extraction). 3. Respiratory rate
The other factor,a patient's knowledgeof his or her physi 4. Temperature
cal condition, is a much more likelycauseof misinformation 5. Height
on the questionnaire. Most "healthy'' persons do not visit 6. Weight
their physicianregularlyfor routine checkups.Recentinfor Vital signs and guidelinesfor their interpretation follow.
mation has suggested that annual physical examination
should be discontinued in the younger healthy patient Blood Pressure
because it has not proved as valuable an aid in preventive Technique. The followingtechnique is recommended for
medicine, as was once thought. 32• In addition, most patients the accurate manual determination of BP.33 A stethoscope
simply do not visit their physician on a regular basis, doing and a sphygmomanometer (blood pressure cuff) are the
so instead whenever they become ill. From this premise, it required equipment. The most accurate and reliableof these
stands to reason that the true state of the patient's physical devices is the mercury-gravity manometer. The aneroid
condition may be unknown to the patient. Feeling well, manometer, probably the most frequently used, is calibrated
although usuallya good indicator of health, is not a guaran to be read in millimeters of mercury (mm Hg) and is quite
tor of good health.7 Many diseaseentities may be present for accurate if well maintained. Rough handling of the aneroid
a considerablelength of time without exhibiting overt signs manometer may lead to erroneous readings. It is recom
or symptoms that alert the patient of their presence (e.g., mended that the aneroid manometer be recalibrated at least
HBP,diabetes mellitus, cancer). When signs and symptoms annually.Useof automatic BPmonitors hasbecomecommon
are present, they are frequently mistaken for other, more because their accuracy has increased while their cost has
benign problems. Although they may answer questions on decreased,ranging from wellunder $100to severalthousand
the medical history questionnaire to the best of their knowl dollars.Likewise,their accuracyvaries.The use of automatic
edge,patients cannot give a positive response to a question monitors simplifiesthe monitoring of vital signs, but den
unless they are awarethat they have the condition. The first tists should be advisedto checkthe accuracyof these devices
few questions on most histories refer to the length of time periodically (comparing valueswith those of the more accu
sincethe patient's last physicalexamination.The value of the rate mercury or aneroid manometer).
remaining answers, dealing with specific disease processes, Although they are most accurate, the use of mercury
can be gauged from the patient's responses to these initial manometers has become increasinglyrare because they are
questions. too bulky for easycarrying and mercury spillsare potentially
Becauseof these problems, which are inherent in the use dangerous.34 Aneroid manometers are easyto use, are some
of a patient-completed medical history questionnaire, the what less accurate than mercury manometers, and are more
dentist must look for additional sources of information delicate, requiring recalibration at least annually or when
about the physicalstatus of the patient. Physicalexamination dropped or bumped."
of the patient provides much of this information. This con Automatic devices containing all equipment in one unit
sists of the following: negate the need for a separate stethoscope and manometer.
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CHAPTER 10 Physical and Psychological Evaluation 143
TABLE 10-5
Guidelines for Blood Pressure (Adult)
Blood Pressure, ASA
mm Hg. or torr Classification Dental Therapy Consideration
<140 and <90 1. Routine dental management
2. Recheckin 6 mo, unless specifictreatment dictates more frequent monitoring.
140-159and/or 2 1. RecheckBP before dental treatment for three consecutiveappointments; if all exceedthese
90-94 guidelines,medical consultation is indicated.
2. Routine dental management
3. SRP as indicated
160-199and/or 3 1. RecheckBP in 5 min.
95-114 2. If BP is still elevated,medical consultation before dental therapy is warranted.
3. Routine dental therapy
4. SRP
zoo- and/or 115+ 4 1. RecheckBP in 5 min.
2. Immediate medical consultation if still devated
3. No dental therapy, routine or emergency,*until elevatedBP is corrected
4. Referto hospital if immediate dental therapy is indicated.
ASA, American Societyof Anesthesiologists;BP, blood pressure; SRP, stress reduction protocol.
*When the BP of the patient is slightlyabove the cutoff for category 4 and anxiety is present, inhalation sedation may be employed in an effort to diminish
the BP (via the elimination of stress).
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144 PART III Techniques of Regional Anesthesia in Dentistry
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CHAPTER10 Physicaland PsychologicalEvaluation 145
Additional Evaluation Procedures 2. Does the patient represent a greater risk (of
Followingcompletion of these three steps (medical history morbidity or mortality) than normal during this
questionnaire,vital signs,and physicalexamination), it occa treatment?
sionallywillbe necessaryto followup with additional evalu 3. If the patient does represent an increased risk, what
ation for specificmedical disorders. This examination may modifications will be necessaryin the planned
include auscultation of the heart and lungs,testing for blood treatment to minimize this risk?
glucoselevels,retinal examination, function tests for cardio 4. Is the risk too great for the patient to be managed safely
respiratory status (e.g.,breath-holding test, match test), elec as an outpatient in the medical or dental office?
trocardiographic examination, and blood chemistries.Many In an effortto answerthese questions,the Herman Ostrow
of these tests are used in dental officesbut do not represent School of Dentistry of USC developeda physicalevaluation
a standard of care in dentistry. system that attempts to assist the dentist in categorizing
patients from the standpoint of risk factor orientation."
Dialogue History Its function is to assign the patient an appropriate risk
After patient information has been collected, the dentist category so that dental care can be provided to the patient
reviewswith the patient any positive responses on the ques in comfort and with increased safety.The system is based
tionnaire, seeking to determine the severity of these disor on the ASA physical status classification system, which is
ders and any potential risk that they might represent during described next.
the planned treatment. This process, the dialogue history, is
an integral part of patient evaluation. The dentist must put
PHYSICAL STATUS CLASSIFICATION SYSTEM
to use all available knowledge of the disease to assess the
degree of risk to the patient. In 1962 the American Society of Anesthesiologists (ASA)
One example of dialogue history is presented below.For adopted what is now referred to as the ASAphysical status
a more in-depth description of dialogue history for specific (ASAPS) classification system.41 This system represents a
disease states, the reader is referred to Medical Emergencies means of estimating medical risk presented by a patient
in the Dental Office, 6th edition.37 undergoing a surgical procedure. The system has been in
The followingis a dialogue history to be initiated with a continual use since 1962,virtually without change, and has
positive reply to angina pectoris: proved to be a valuablemethod of determining surgicaland
1. What precipitates your angina? anestheticrisk beforethe actual procedure.f'? The classifica
2. How frequently do you experienceanginal episodes? tion systemfollows:
3. How long do your anginal episodes last? Class 1. A healthy patient (no physiologic,physical,or
4. Describe a typical anginal episode. psychologicalabnormalities)
5. How does nitroglycerin affectthe anginal episode? Class 2. A patient with mild systemicdiseasewithout
6. How many tablets or sprays do you normally need to limitation of daily activities
terminate the episode? Class 3. A patient with severesystemicdiseasethat limits
7. Are your anginal episodes stable (similar in nature), or activitybut is not incapacitating
has there been a recent change in their frequency, Class 4. A patient with incapacitating systemicdiseasethat
intensity, radiation pattern of pain, or response to is a constant threat to life
nitroglycerin (seekingunstable or preinfarction angina)? Class 5. A moribund patient not expectedto survive 24
Dialogue history should be completed for every positive hours with or without the operation
response noted on the medicalhistory.Awritten note should Class 6. A brain-dead patient whose organs are being
be included on the questionnaire that summarizes the removed for donor purposes
patient's response to the questions. For example, "heart When this systemwas adapted for use in a typical outpa
attack" is circled.Written by the dentist next to this on the tient dental or medical setting,ASA5 and 6 were eliminated
questionnaire is the statement "June 2008,"implyingthat the and an attempt made to correlate the remaining four clas
patient stated that the heart attack occurred in June 2008. sificationswith possible treatment modifications for dental
Dialogue history related to the administration of local treatment. Figure 10-6 illustrates the USC physical evalua
anesthetic in patients with alleged allergy is presented in tion form on which a summary of the patient's physicaland
Chapter 18. psychologicalstatus is presented along with planned treat
ment modifications.
Determination of Medical Risk In the discussionof the ASAcategoriesto follow,the term
Having completed all components of the physical evalua normal or usual activity is used along with the term distress.
tion and a thorough dental examination, the dentist next Definitions of these terms follow:Normal or usual activityis
takes all of this information and answers the following defined as the ability to climb one flight of stairs or to walk
questions: two level city blocks; distress is defined as undue fatigue,
1. Is the patient capable,physicallyand psychologically,of shortness of breath, or chest pain. Figure 10-7illustrates the
tolerating in relative safetythe stressesinvolvedin the ASAclassificationsystem based on the ability to climb one
proposed treatment? flight of stairs.
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146 PARTIII Techniquesof RegionalAnesthesiain Dentistry
~I.
: ":
CURRENT MEDICAL PROBLEMS
1· 1-··
":
CURRENTMEDICATIONS
".:.
__ H_T_
MODIFICATIONS TO THERAPY:
-General- Specific
Figure 10-6. The Herman Ostrow School of Dentistry of University of Southern California (USC) physical evaluation (PE) summary
form.
ASA CLASSIFICATION
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CHAPTER 10 Physicaland PsychologicalEvaluation 147
the patient is at increased risk during treatment. The dentist be necessary.AnASA5 classificationis a red light with regard
should give serious consideration to implementing treat to dental care.
ment modifications. The ASA PS classification system is not meant to be
inflexible;rather, it is meant to function as a relative value
ASA4 systembased on a dentist's clinicaljudgment and assessment
A patient in the ASA4 category has an incapacitating sys of available relevant clinical data." When the dentist is
temic disease that is a constant threat to life. Patients with unable to determine the clinicalsignificanceof one or more
this classificationhave a medical problem or problems of diseases,consultation with the patient's physician or other
greater significancethan the planned dental treatment. The medical or dental colleaguesis recommended. In all cases,
dentist postpones elective dental care until the patient's however,the treating dentist makesthe final decisionregard
physical condition has improved to at least an ASA3 clas ing whether to treat or postpone treatment. The ultimate
sification.A patient in the ASA4 category exhibits clinical responsibilityfor the health and safetyof a patient lies solely
signs and symptoms of disease at rest. This classification with the dentist, who decidesto treat or not treat the patient.
represents a red light, a warning that the risk involved in Table 10-8summarizes the ASAphysicalstatus classifica
treating the patient is too great to permit elective care. In tion system as modified for use in dentistry.
dental emergencies,such as casesof infection or pain, clini
cians should treat patients conservativelyin the dental office
until their medical condition improves. When possible,
DRUG-DRUG INTERACTIONS
emergency treatment should be noninvasive, consisting of
AND CONTRAINDICATIONS
drugs such as analgesicsfor pain and antibiotics for infec Potential drug-drug interactions involvinglocal anesthetics
tion. When the dentist believesthat immediate intervention or vasopressors,and three relative contraindications to the
is required (e.g., incision and drainage, extraction, pulpal administration of local anesthetics-malignant hyperther
extirpation), it is suggestedthat the patient receivecare in an mia (malignant hyperpyrexia), atypical plasma cholinester
acute care facility (i.e., a hospital) whenever possible. ase, and idiopathic or congenital methemoglobinemia-are
detailed in the following discussion.A fourth-allergy (an
ASAS absolute contraindication)-is discussedin Chapter 18.
An ASA 5 classificationindicates a moribund patient not The importance of each potential interaction is listed in
expectedto survive24 hours without surgery.Patients in this its significancerating as designedby Moore and associates."
categoryalmost alwaysare hospitalized and terminally ill.In The rating system is defined in Box 10-5.
many institutions, these patients are not to be resuscitatedif
they experiencerespiratory or cardiacarrest (they are termed Drug-Drug Interactions
"DNR" ["Do Not Resuscitate"].Electivedental treatment is Amide Local Anesthetics With Inhibitors of Metabolism
contraindicated; however, emergency care in the realm of (e.g., Cimetidine, Lidocaine) (Significance Rating= 5). The
palliativetreatment (i.e.,relief of pain and/or infection) may Hi-receptor blocker cimetidine (Tagamet) modifies the
TABLE 10-8
American Society of Anesthesiologists Physical Status (ASA PS) Classification System
ASA PS Definition Example Treatment Recommendations
1 Healthy patient - No special precautions
2 Patient with mild systemic Pregnancy, well-controlled type 2 diabetes, Elective care okay; consider treatment
disease epilepsy,asthma, thyroid dysfunction, BP modification
140-159/90-94 mm
Patient with an incapacitating Unstable angina pectoris, post myocardial Elective care contraindicated; emergency
systemic ilisease that is a infarction <6 months, uncontrolled seizures, care: noninvasive (e.g., drugs) or in a
constant threat to life BP >200/>115 mm Hg controlled environment
Moribund patient not expected End-stage cancer, end-stage infectious disease, Palliative care
to survive 24 hours without end-stage cardiovascular ilisease, end-stage
operation hepatic dysfunction
Modified from Malamed SF:Knowingyour patient, J Am Dent Assoc 141:3S-7S,2010.
BP,Blood pressure; CVA, cerebrovascularaccident; mm Hg, millimeters of mercury.
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150 PARTIII Techniquesof RegionalAnesthesiain Dentistry
accidental intravascular administration of a vasopressor For a thorough review of potentially significant drug
containing local anesthetic could lead to hypotension in interactions occurring in dentistry, the reader is referred to
patients receivingphenothiazines.67 the excellentseries of papers that appeared in 1999 in the
Localanesthetics containing vasopressorsare not contra Journal of the American Dental Association. 44•43•72-74
indicated in patients receivingphenothiazines; however,it is •••
recommended that the smallest volume of vasopressor Most known drug-drug interactions involvinglocal anes
containing local anesthetic that is compatible with clinically thetics or vasopressors occur with CNS and CVS depres
adequate pain control be administered. sants.Whenevera potential drug-drug interaction is known,
Commonly prescribed phenothiazines include chlor doses of local anesthetics should be decreased.There is no
promazine (Thorazine) and promethazine (Phenergan). formula for the correct degree of reduction. Prudence dic
tates, however,that the smallest dose of local anesthetic or
Vasoconstrictor With Thyroid Hormone {e.g .• Epinephrine vasopressorthat is clinicallyeffectiveshould be used.
and Thyroxine) {Significance Rating =
4). Summation of Knowledgeof all drugs and medications, including pre
effects is possible when thyroid hormones are taken in scription and nonprescription drugs, as well as herbal rem
excess.Vasoconstrictorsshould be used with caution when edies, being taken by a patient better enables the doctor to
clinicalsigns and symptoms indicating hyperthyroidism are evaluatethe patient's overallphysicaland psychologicalwell
present.70•71 being. Drug referencessuch as Mosby's Drug Consult, Com
pendium of Pharmaceuticals and Specialties (CPS) (Canada},
Vasoconstrictor and Monoamine Oxidase Inhibitors {Sig Lexi-Comp,*and Epocrates.comt are valuable resources in
nificance Rating = 5). Monoamine oxidase inhibitors determining drug information, including the potential for
(MAOis)are prescribed in the management of major depres drug-drug interactions. Current medications should be
sion,certain phobic-anxietystates,and obsessive-compulsive listed in the dental record.
disorders (Box 10-8).67 They are capable of potentiating the
actions of vasopressors used in dental local anesthetics by
MALIGNANT HYPERTHERMIA
inhibiting their biodegradation by the enzyme monoamine
oxidase (MAO) at the presynaptic neuron level.58 Malignant hyperthermia (MH; malignant hyperpyrexia) is
Historically,the administration of local anesthetics con one of the most intense and life-threatening complications
taining vasopressorshas been absolutelycontraindicated for associatedwith the administration of general anesthesia. It
patients receiving MAOis because of the increased risk of is rare: 1: 15,000incidenceamong children receivinggeneral
hypertensive crisis. However, Yagiela and others demon anesthesiaand 1:50,000incidencein adults.75 The syndrome
strated that such an interaction among epinephrine, levo is transmitted geneticallyby an autosomallydominant gene.
nordefrin, norepinephrine, and MAO did not occur.52•67 Reduced penetrance and variable expressivityin siblings of
Such a response,hypertensivecrisis,did developwith phen familiesinheriting the syndrome are also characteristicof its
ylephrine, a vasopressor not used at present in dental local genetic transmission. MH is seen more frequently in males
anesthetic solutions. than females-a finding that increases with increasing age.
Therefore, it seems appropriate to state, "there seems to To date, the youngest reported caseof MH occurred in a boy
be no restriction, from a theoretical basis, to use local anes aged 2 months and the oldest in a 78-year-oldman.
thetic with vasoconstrictor other than phenylephrine in Reports of MH in North America appear to be clustered
patients currently treated with MAOis."67 in three regions: Toronto (in Canada) and Wisconsin and
Nebraska (in the United States).Most persons with MH are
functionally normal, the presence of MH becoming known
only when the individual is exposed to triggering agents or
BOX 10-8 Monoamine Oxidase Inhibitors through specifictesting.
Generic Proprietary For many years, it was thought that MH could be trig
Clorygyline geredwhen susceptiblepatients were exposedto amide local
Isocarboxazid Marplan anesthetics.76Indeed, in both the first and second editions of
Moclobemide Aurorix this textbook, MH was considered an absolute contraindica
Pargyline Eutonyl tion to amide local anesthetics.However,recent findings":"
Phenelzine Nardil and publications by the Malignant Hyperthermia Associa
Selegiline Deprenyl,Eldepryl tion of the United States(MHAUS}80havedemonstrated that
Tranylcypromine Parnate amide localanestheticsare not likelyto trigger such episodes;
Brofaromine Consonar thus MH has been re-categorizedas a relativecontraindica
Iproniazid Marsilid tion in the third and subsequent editions.
Isoniazid
MDMA
Fluoxetine Prozac *Lexi-Comp (www.lexi.com).
tEpocrates.com.
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154 PARTIII Techniques of Regional Anesthesia in Dentistry
be minimized. Whenever possible, alternate local anesthetics Rosemont, lli, February 2009, Revised June 2010, American
should be used. Academyof Orthopedic Surgeons.
The maximum recommended dose of prilocaine is listed 18. National Collaborating Centre for Chronic Conditions,
by the manufacturer as 8.0 mg/kg (3.6 mg/lb). Methemoglo Chronic Obstructive Pulmonary Disease: National clinical
guideline on management of chronic obstructive pulmonary
binemia is unlikely to develop at doses below this level.
disease in adults in primary and secondary care, Thorax
59(Suppl 1):1-232, 2004.
19. YakahaneY,KojimaM, SugaiY,et al:Hepatitis C virus infection
References in spouses of patients with type C chronic liver disease,Ann
1. Daublander M, Muller R, Lipp MD: The incidence of compli Intern Med 120:748-752,1994.
cations associated with local anesthesia in dentistry, Anesth 20. Chafen JJ,Newberry SJ,Riedl MA,et al: Diagnosing and man
Prog 44:132-141, 1997. aging common food allergies: a systematic review, JAMA
2. McCarthy FM: Essentials of safe dentistry for the medically 303:1848-1856,2010.
compromised patient, Philadelphia, 1989,WB Saunders. 21. Haas DA:An update on local anesthetics in dentistry, J Can
3. McCarthy FM: Stress reduction and therapy modifications, Dent Assoc68:546-551,2002.
J Calif Dent Assoc9:41-47, 1981. 22. YagielaJA: Injectable and topical local anesthetics. In ADN
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8. JeskeAH, editor: Mosby'sdental drug reference,ed 9, St Louis, 27. Hersh EV,Moore PA,PapasAS,et al, and the SoftTissueAnes
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10. Skidmore-Roth L: Mosby's 2010 nursing drug reference, 28. Malamed SF: Reversing local anesthesia, Inside Dent 4:2-3,
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14. Shah KB,Kleinman BS,SarniH, et al: Reevaluationof periop 31a. GruenwaldJ, Brendler T,JaenickeC, editors: 2011 Physicians'
erativemyocardialinfarction in patients with prior myocardial desk referencefor herbal medicines,Oradell,NJ,2011,Medical
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71:231-235, 1990. 32. American DentalAssociation:ADNPDR guideto dental thera
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a guideline from the American Heart Association Rheumatic evaluation,primary care, Clin Off Pract 18:777-807,1991.
Fever,Endocarditis,and KawasakiDiseaseCommittee, Council 33. American Heart Association: Recommendations for human
on Cardiovascular Disease in the Young,and the Council on blood pressure determination by sphygmomanometry,Dallas,
Clinical Cardiology, Council on Cardiovascular Surgery and 1967,The Association.
Anesthesia, and the Quality of Care and Outcomes Research 34. Pickering TG, Hall JE, Appel LJ, et al: Recommendations for
Interdisciplinary Working Group, Circulation 116:1736-1754, blood pressure measurement in humans and experimental
2007. animals. Part 1. Blood pressure measurement in humans: a
16. American Dental Association,AmericanAcademyof Orthope statement for professionals from the Subcommittee of Pro
dic Surgeons:Antibiotic prophylaxis for dental patients with fessionaland Public Education of the American Heart Associa
total joint replacements, J Am Dent Assoc 134:895--898, tion Council on High Blood Pressure Research,Hypertension
2003. 45:142-161,2005.
17. Public RelationsDepartment, AmericanAcademyof Orthope 35. Mitchell PT, Parlin RW, Blackburn H: Effect of vertical dis
dic Surgeons:Information statement 1033:antibiotic prophy placement of the arm on indirect blood pressure measurement,
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36. Wonka F, Thummler M, Schoppe A: Clinical test of a blood 58. Hardman JG,Limbird LE,editors: Goodman and Gilman'sthe
pressure measurement device with a wrist cuff, Blood Press pharmacologicalbasis of therapeutics, ed 10,NewYork,2001,
Monit 1:361-366, 1996. McGraw-Hill.
37. Malamed SF. Prevention. In Malamed SF, editor: Medical 59. Hoffman BB,LefkowitzRJ, Taylor P: Neurotransmission: the
emergencies in the dental office, ed 6, St Louis, 2007, Mosby autonomic and somatic motor nervous systems.In Goodman
Elsevier. and Gilman's the pharmacological basis of therapeutics, ed 9,
38. Little JW, Palace DA, Miller CS, et al: Dental management NewYork,1996,McGraw-Hill.
of the medically compromised patient, ed 7, St Louis, 2007, 60. Benzaquen BS, Cohen V,Eisenberg MJ: Effectsof cocaine on
Mosby. the coronary arteries, Am Heart J 142:302-410,2001.
39. Seidel HM, Ball JW, Dains J, editors: Mosby's guide to physical 61. Gradman AH: Cardiac effects of cocaine: a review,Biol Med
examination, St Louis, 2006, CV Mosby. 61:137-141, 1988.
40. McCarthy FM, Malamed SF: Physical evaluation system to 62. VasicaG,Tennant CC:Cocaineuse and cardiovascularcompli
determine medical risk and indicated dental therapy modifica cations, Med J Austral 177:260--262,2002.
tions, J Am Dent Assoc 99:181-184, 1979. 63. Hahn IH, Hoffman RS: Cocaine use and acute myocardial
41. American Society of Anesthesiologists: New classification of infarction, Emerg Med Clin North Am 19:493--510,2001.
physical status, Anesthesiology 24:111, 1963. 64. MyerburgRJ:Sudden cardiac death in persons with normal (or
42. Lagasse RS: Anesthesia safety: model or myth? A review of the near normal) hearts, Am J Cardiol 79:3-9, 1997.
published literature and analysis of current original data, Anes 65. Van Dyke D, Barash PG, Jatlow P, et al: Cocaine: plasma
thesiology 97:1609-1617, 2002. concentrations after intranasal application in man, Science
43. Fleisher LA: Risk of anesthesia. In Miller RD, Fleisher LA, 191:859-861,1976.
Johns RA, editors: Miller's anesthesia, ed 6, New York, 2005, 66. Friedlander AH, Gorelick DA: Dental management of the
Churchill Livingstone. cocaine addict, Oral Surg 65:45-48, 1988.
44. Moore PA, Gage nv, Hersh EV,et al:Adversedrug interactions 67. PerusseR, Goulet J-P,Turcotte J-Y:Contraindications to vaso
in dental practice: professional and educational implications, constrictors in dentistry. Part III. Pharmacologic interactions,
J Am Dent Assoc 130:17-54, 1999. Oral Surg Oral Med Oral Pathol 74:592-697, 1992.
45. KishikawaK, Namiki A, Miyashita K, et al: Effectsof famoti 68. Debruyne FM: Alpha blockers: are all created equal? Urology
dine and cimetidine on plasma levels of epidurally adminis 56(5 Suppl 1):20--22,2000.
tered lignocaine,Anaesthesia45:719-721, 1990. 69. Emmelin N, Engstrom J: Supersensitivity of salivary glands
46. Wood M: Pharmacokinetic drug interactions in anaesthetic followingtreatment with bretylium or guanethidine, Br J Phar
practice, Clin Pharmacokinet 21:85-307, 1991. macol Chemother 16:15-319,1961.
47. Wu FL, Razzaghi A, Souney PE: Seizure after lidocaine for 70. McDevitt DG, Riddel JG, Hadden DR, et al: Catecholamine
bronchoscopy: case report and review of the use of lidocaine sensitivity in hyperthyroidism and hypothyroidism, Br J Clin
in airway anesthesia,Pharmacotherapy 13:12-78, 1993. Pharmacol 6:97-301, 1978.
48. Moore PA: Adverse drug interactions in dental practice: 71. Johnson AB, Webber J, Mansell P, et al: Cardiovascular and
interactions associated with local anesthetics, sedatives and metabolic responses to adrenaline infusion in patients with
anxiolytics.Part N of a series,J Am Dent Assoc 130:441-554, short-term hypothyroidism, Clin Endocrinol 43:647-751,
1999. 1995.
49. Wilburn-Goo D, Lloyd LM: When patients become cyanotic: 72. YagielaJA:Adversedrug interactions in dental practice: inter
acquired methemoglobinemia, J Am Dent Assoc 130:26-31, actions associated with vasoconstrictors. Part V of a series,
1999. J Am Dent Assoc 130:501-709,1999.
50. Jastak JT, YagielaJA: Vasoconstrictors and local anesthesia: 73. Hersh EV:Adversedrug interactions in dental practice:interac
a review and rational use, J Am Dent Assoc 107:623-630, tions involvingantibiotics. Part II of a series,J Am Dent Assoc
1983. 130:236-251,1999.
51. BoakesAJ,LaurenceDR, LovelKW,et al:Adversereactions to 74. Haas DA:Adversedrug interactions in dental practice:interac
local anesthetic vasoconstrictor preparations: a study of the tions associatedwith analgesics.Part III of a series.J Am Dent
cardiovascularresponses to xylestesinand hostcain with nor Assoc 130:397-407,1999.
adrenalin, Br Dent J 133:137-140,1972. 75. RosenbergH, FletcherJE:An update on the malignant hyper
52. YagielaJA,Duffin SR,Hunt LM: Drug interactions and vaso thermia syndrome, Ann Acad Med Singapore23(Suppl 6):84-
constrictors used in local anesthetic solutions, Oral Surg 97, 1994.
59:565--571,1985. 76. Carson JM,Van SickelsJE:Preoperativedetermination of sus
53. Hansbrough JF,Near A: Propranolol-epinephrine antagonism ceptibility to malignant hyperthermia, J Oral MaxillofacSurg
with hypertension and stroke, Ann Intern Med 92:717, 1980 40:432-435, 1982.
(letter). 77. Gielen M, Viering W: 3-in-1 lumbar plexus block for muscle
54. KramJ,Bourne HR,Melmon KL,et al:Propranolol,Ann Intern biopsy in malignant hyperthermia patients: amide local anaes
Med 80:282,1974 (letter). thetics maybe used safely,ActaAnaesthesiolScand30:581-583,
55. Foster CA, Aston SJ: Propranolol-epinephrine interaction: a 1986.
potential disaster,Reconstr Surg 72:74-78, 1983. 78. Paasuke RT, Brownell AKW: Amine local anaesthetics and
56. Ghoneim MM: Drug interactions in anaesthesia:a review,Can malignant hyperthermia, Can Anaesth Soc J 33:126-129, 1986
Anaesthet Soc J 18:353-375,1971. (editorial).
57. ReichleFM,Conzen PF:Halogenatedinhalational anaesthetics: 79. Ording H: Incidence of malignant hyperthermia in Denmark,
best practice and research, Clin Anaesthesiol 17:19-46,2003. Anesth Analg 64:700--704,1985.
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80. Malignant Hyperthermia Association of the United States: 89. Williams FM: Clinical significance of esterases in man, Clin
Anesthetic list for MH-susceptible patients. www.mhaus.org. Pharmacokinet 10:392-403, 1985.
AccessedSeptember 9, 2011. 90. Abernethy MH, GeorgePM, Herron JL,et al: Plasma cholines
81. Jurkat-Rott K, McCarthy T, Lehmann-Horn F: Genetics and terase phenotyping with use of visible-regionspectrophotom
pathogenesis of malignant hyperthermia, MuscleNerve 23:1- etry, Clin Chem 32(1 Pt 1):194-197, 1986.
17, 2000. 91. Prilocaine-induced methemoglobinemia-Wisconsin, 1993,
82. Steelman R, Holmes D: Outpatient dental treatment of pedi MMWR Morb Mortal Wkly Rep 43:555--657, 1994.
atric patients with malignant hyperthennia: report of three 92. BellamyMC, Hopkins PM, Hallsall PJ, et al: A study into the
cases,ASDCJ Dent Child 59:12--65, 1992. incidence of methaemoglobinaemia after "three-in-one" block
83. Amato R, Giordano A, Patrignani F, et al: Malignant hyper with prilocaine, Anaesthesia 47:1084-1085, 1992.
thermia in the course of general anesthesia in oral surgery: 93. Guertler AT, Pearce WA: A prospective evaluation of
a case report, J Int AssocDent Child 12:15-28, 1981. benzocaine-associatedmethemoglobinemia in human beings,
84. The European Malignant HyperpyrexiaGroup: A protocol for Ann Emerg Med 24:426--630, 1994.
the investigationof malignant hyperpyrexia (MH) susceptibil 94. Rodriguez LF, Smolik LM, Zbehlik AJ: Benzocaine-induced
ity, Br J Anaesth 56:1267-1269, 1984. methemoglobinemia: a report of a severereaction and review
85. Malignant Hyperthermia Association of the United States: of the literature, Ann Pharmacother 28:543--649, 1994.
MHAUS Professional Advisory Council adopts new policy 95. Eilers MA, Garrison TE: General management principles. In
statement on local anesthetics,Communicator 3:4, 1985. Marx J, Hockberger R, Walls R, editors: Rosen's emergency
86. Adragna MG: Medical protocol by habit: avoidance of medicine: concepts and clinical practice, ed 5, St Louis, 2002,
amide local anestheticsin malignant hyperthermia susceptible Mosby.
patients, Anesthesiology62:99-100, 1985 {letter). 96. Sarangi MP, Kumar B: Poisoning with writing ink, Indian
87. AdrianiJ,Sundin R:Malignanthyperthermia in dental patients, Pediatr 31:756-857, 1994.
J Am Dent Assoc 108:180-184, 1984. 97. Daly DJ, Davenport J, Newland MC: Methemoglobinemia
88. Kaus SJ, Rockoff MA: Malignant hyperthennia, Pediatr Clin following the use of prilocaine, Br J Anaesth 36:737-739,
North Am 41:121-237, 1994. 1964.
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Basic Injection Technique
Absolutelynothing that is done for patients by their dentist and those givenby a more experiencedpractitioner? All too
is of greater importance than the administration of a drug often, local anesthetic administration becomes increasingly
that prevents pain during dental treatment.1 Yet the very traumatic for the patient the longer a dentist has been out
act of administering a local anesthetic commonly induces of school. Can this discouraging situation be corrected?
great anxiety or is associated with pain in the recipient. Localanesthetic administration need not, and should not,
Patients frequentlymention that they would prefer anything be painful. Everyone of the local anesthetic techniques pre
to the injection or "shot" (to use patients' term for the local sented in the followingchapters can be done atraumatically,
anesthetic injection). Not only can the injection of local including the administration of local anesthetics on the
anesthetics produce fear and pain, it is also a factor in the palate (the most sensitive area in the oral cavity). Several
occurrence of emergencymedical situations. In a review of skills and attitudes are required of the drug administrator,
medical emergencies developing in Japanese dental offices, the most important of which is probably empathy. If the
Matsuura determined that 54.9% of emergency situations administrator truly believesthat local anesthetic injections
arose either during administration of the local anesthetic do not have to be painful, then through a conscious or sub
or in the 5 minutes immediately after its administration.2 conscious effort, it is possible to make minor changes in
Most of these emergency situations were directly related technique that will cause formerly traumatic procedures to
to increased stress associated with receipt of the anesthetic be less painful for the patient.
(the injection) and not to the drug being used. Moreover, Additionally,the abilityto buffer the pH of the local anes
in a survey on the occurrence of medical emergencies in thetic solution to a more physiologic7.35to 7.5from the pH
dental practices in North America, 4309 dentists responded of 3.5 in the cartridge has greatly aided in the process of
that a total of more than 30,000 emergency situations had atraumatic injection.4•5
developed in their offices over the previous 10 years.3 An atraumatic injection has two components: a technical
Ninety-five percent of respondents stated that they had aspect and a communicative aspect.
experienceda medical emergencyin their officein this time
period. More than half of these emergencies {15,407)were + Step 1: Use a sterilized sharp needle. Stainlesssteel dis
vasodepressor syncope (common faint), most of which posable needles currently used in dentistry are sharp and
occurred during or immediately after administration of the rarelyproduce anypain on insertion or withdrawal.However,
local anesthetic. because these needles are machine manufactured, occasion
Local anesthetics can and should be administered in a ally(rarely)a fishhook-typebarb may appear on the tip. This
nonpainful, or atraumatic, manner. Most dental students' results in atraumatic insertion of the needle followed by
first injections were given to classmate"patients:' who then painful withdrawal as the barb tears the unanesthetized
gavethe same injection to the student who had just injected tissue. This may be avoided by the use of sterile 2 x 2-inch
them. Most likely,these students went out of their way to gauze. Place the needle tip against the gauze and draw the
make their injection as painless as possible.At the Herman needle backward. If the gauze is snagged, a barb is present
Ostrow School of Dentistry of U.S.C.,these first injections and the needle should not be used. (This procedure is
usuallyare absolutelyatraumatic. Students are routinely sur optional and may be omitted if fear of needle contamination
prised by this, some having experiencedthe more usual (e.g., is great.)
painful) injection at some time in the past when they were Disposableneedles are sharp on first insertion. However,
"real" dental patients. Why should there be a difference in with each succeeding penetration, their sharpness dimin
dental injections and in the degree of pain between injec ishes. By the third or fourth penetration, the operator can
tions administered by an inexperienced beginning student feel an increase in tissue resistance to needle penetration.
157
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158 PART III Techniques of Regional Anesthesia in Dentistry
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CHAPTER11 BasicInjection Technique 159
Figure 11-2. Sterilizedgauzeis used to gentlywipe tissue at site Figure 11-4. A small quantity of topical anesthetic is placed at
of needle penetration. the site of needle penetration and is kept in place for at least 1
minute.
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A
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CHAPTER 11 Basic Injection Technique 161
Figure 11-6. A, Use of the patient's chest for stabilization of syringe during right inferior alveolar nerve block (circle). Never use the
patient's arm to stabilizea syringe.B, Use of the chin (1) as a finger rest, with the syringebarrel stabilizedby the patient's lip (2). C, When
necessary,stabilization may be increased by drawing the administrator's arm in against his or her chest (3).
Figure 11-7. A, Syringestabilizationfor a right posterior superior alveolarnerve block:syringebarrel on the patient's lip, one fingerresting
on the chin and one on the syringe barrel (arrows), upper arm kept closeto the administrator's chest to maximize stability.B, Syringesta
bilization for a nasopalatine nerve block: index finger used to stabilizethe needle, syringebarrel resting in the comer of the patient's mouth.
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162 PART III Techniques of Regional Anesthesia in Dentistry
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CHAPTER11 BasicInjection Technique 163
Figure 11-11. DentalVibe. Figure 11-13. Passing syringe from assistant to administrator
behind the patient, out of his or her line of sight.
+ Step 10: Keepthe syringe out of the patient's line of sight + Step 11B: Watch and communicate with the patient.
With the tissue prepared and the patient positioned, the During Step 1lA, the patient should be watched and com
assistant should pass the syringeto the administrator out of municated with; the patient's face should be observed for
the patient's line of sight either behind the patient's head or evidence of discomfort during needle penetration. Signs
across and in front of the patient. A right-handed practitio such as furrowing of the brow or forehead and blinking of
ner administrating a right-side injection can sit facing the the eyes may indicate discomfort (Fig. 11-15). More fre
patient (Fig. 11-13)or, if administering a left-side injection, quently, no change will be noticed in the patient's facial
facingin the same direction as the patient (Fig.11-14).In all expressionat this time (indicating a painless,or atraumatic,
cases,it is better if the syringe is not visible to the patient. needle insertion).
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164 PART III Techniques of Regional Anesthesia in Dentistry
The practitioner should communicate with the patient as + Step 14: Deposit several drops of local anesthetic before
Step 1lA is carried out. The patient should be told in a posi touching the periosteum. In techniques of regional block
tive manner, "I don't expect you to feel this:' as the needle anesthesiain which the needle touches or comes closeto the
penetrates the tissues.The words,"Thiswillnot hurt," should periosteum, several drops of solution should be deposited
be avoided;this is a negativestatement, and the patient hears just before contact. The periosteum is richly innervated,
only the word (hurt). and contact with the needle tip produces pain. Anesthetizing
the periosteum permits atraumatic contact. Regionalblock
+ Step 12: Inject several drops of local anesthetic solution injection techniques that require this are the inferior alveo
(optional). lar, Gow-Gates mandibular, and anterior superior alveolar
(infraorbital) nerve blocks.
+ Step 13: Slowly advance the needle toward the target. Knowledgeof when to deposit the local anesthetic comes
Steps 12 and 13 are carried out together. The soft tissue with experience. The depth of penetration of soft tissue
in front of the needle may be anesthetized with a few drops at any injection site varies from patient to patient; therefore
of local anesthetic solution. After 2 or 3 seconds are allowed the periosteum may be contacted inadvertently. However,
for anesthesiato develop,the needle should be advancedinto a keen tactile sense is developed with repetition, enabling
this area and a little more anesthesia deposited. The needle the needle to be used gently as a probe. This enables the
should then be advanced again. These procedures may be administrator to detect subtle changes in tissue density as
repeated until the needle reaches the desired target area. the needle nears bone. With experience and development
Use of a buffered local anesthetic will increase patient of this tactile sense,a small volume of local anesthetic solu
comfort during injection as a result of (1) the increased tion may be deposited just before gentle contact with the
pH of the anesthetic solution (7.35to 7.5) and (2) the pres periosteum.
ence of C02 in the buffered solution. C02 possesses anes
thetic properties.12 + Step 15: Aspirate.Aspiration must alwaysbe carried out
In most patients, however, injection of local anesthetic before a volume of local anesthetic is deposited at any site.
during insertion of the needle toward the target area is Aspiration dramatically minimizes the possibility of an
entirelyunnecessary.Pain is rarely encountered between the intravascular injection. The goal of aspiration is to deter
surface mucosa and the mucoperiosteum. If patients are mine where the tip of the needle tip is situated (within a
asked post injection what they felt as the needle was being blood vesselor without). To aspirate, one must create nega
advanced through soft tissue (as in an inferior alveolar or tive pressure within the dental cartridge. The self-aspirating
posterior superior alveolar nerve block), the usual reply is syringedoes this wheneverthe operator stops applyingposi
that they were aware that something was there, but that it tive pressure to the thumb ring (plunger). With the tradi
did not hurt. tional harpoon-aspirating syringe, the administrator must
On the other hand, patients who are apprehensiveabout make a conscious effort to create this negative pressure
injections of local anestheticsare likelyto react to any sensa within the cartridge.
tion as though it werepainful.Thesepatients are saidto have Adequate aspiration requires that the tip of the needle
a lowered pain reaction threshold (PRT). Apprehensive remain unmoved, neither pushed farther into nor pulled out
patients should be told, "To make you more comfortable, I of the tissues,during the aspiration test. Adequate stabiliza
will deposit a little anesthetic as I advance (the needle) tion is mandatory. Beginners have a tendency to pull the
toward the target."Minimal amounts of the local anesthetic syringe out of the tissues while attempting to aspirate.
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CHAPTER 11 BasicInjection Technique 165
Figure 11-16. A, Negative aspiration. With the needle in position at the injection site, the administrator pulls the thumb ring of the
harpoon-aspirating syringe 1 or 2 mm. The needle tip should not move. Check the cartridge at the site where the needle penetrates the
diaphragm (arrow) for a bubble or blood. B, Positiveaspiration. A slight reddish discoloration at the diaphragm end of the cartridge (arrow)
on aspiration usually indicatesvenous penetration. Repositionthe needle,reaspirate,and, if negative,deposit the solution. C, Positiveaspira
tion. Bright red blood rapidly filling the cartridge usually indicates arterial penetration. Removethe syringe from the mouth, change the
cartridge, and repeat the procedure.
A B c
Figure 11-17. A, Needle tip within blood vesselbut bevel abuts the wall of the vein. B, On aspiration vein wall is sucked into needle tip
producing a false negative aspiration test. C, Rotating syringe 45 degrees and reaspirating will provide a true "positive"aspiration in this
scenario.
When the harpoon-aspirating syringe is used, the thumb technique being employed), with the orientation of the
ring should be pulled back gently. Movement of only 1 bevel changed (rotate barrel of syringe about 45 degreesfor
or 2 mm is needed This produces negative pressure within second aspiration test) to ensure that the bevel of the needle
the cartridge that then translates to the tip of the needle. is not located inside a blood vessel but is abutting against
Whatever is lying in the soft tissues around the needle tip the wall of the vessel,providing a false-negativeaspiration
(e.g., blood, tissue [or air, if tested out of the mouth]) (Fig.11-17).Severaladditional aspiration tests are suggested
will be drawn back into the anesthetic cartridge. By observ during administration of the anesthetic drug. This serves
ing the needle end visible within the cartridge for signs two functions: (1) to slow down the rate of anesthetic
of blood return, the administrator can determine whether administration, and (2) to preclude the deposition oflarge
positiveaspiration has occurred.Any sign of blood is a posi volumes of anesthetic into the cardiovascularsystem.
tive aspiration, and local anesthetic solution should not be A major factor determining whether aspiration can be
deposited at that site (Fig.11-16).No return at all,or a small performed reliablyis the gauge of the needle. Larger-gauge
air bubble, indicatesa negativeaspiration. Aspiration should needles (e.g.,25) are recommended more often than smaller
be performed at least twice before the larger volume of gauge needles (e.g.,27, 30) whenever a greater risk of posi
local anesthetic is administered (as required by the injection tive aspiration exists.
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166 PART III Techniques of Regional Anesthesia in Dentistry
+ Step 16A: Slowly deposit the local anesthetic solution. anesthetic. Most patients are accustomed to receivingtheir
With the needle in position at the target area and aspirations local anesthetic injections rapidly. Statements such as, "I'm
completed and negative, the administrator should begin depositing the solution (or "I'm doing this") slowlyso it will
pressing gently on the plunger to start administering the be more comfortable for you, but you're not receivingany
predetermined (for the injection technique) volume of more than is usual" go far to allay a patient's apprehension
anesthetic. Slow injection is vital for two reasons: (1) of at this time. The second part of the statement is important,
utmost significanceis the safetyfactor (discussedin greater because some patients might not realizethat there is a fixed
detail in Chapter 18); and (2) slow injection prevents volume of anesthetic solution in the syringe.A reminder that
the solution from tearing the tissue into which it is they are not receivingany more than is usual is a comfort to
deposited. Rapid injection results in immediate discomfort the patient.
(for a few seconds) followed by prolonged soreness (days)
when the numbness provided by the local anesthetic dissi + Step 17: Slowly withdraw the syringe.After completion
pates later. of the injection, the syringe should be slowly withdrawn
Slowinjection is definedideallyas the deposition of 1 mL from the soft tissues and the needle made safeby capping it
of local anesthetic solution in not less than 60 seconds. immediatelywith its plastic sheath via the scoop technique.
Therefore a full 1.8mL cartridge requires approximately 2 Concerns about the possibilityof needle-stickinjury and
minutes to be deposited.Through slowdeposition, the solu the spread of infection caused by inadvertent sticking with
tion is able to diffuse along normal tissue planes without contaminated needles have led to the formulation of guide
producing discomfort during or followinginjection. lines for the recapping of needles for health care providers.14
Most local anesthetic administrators tend to administer It has been demonstrated that the time health professionals
these drugs too rapidly. In a survey of 209 dentists, 84% are most apt to be injured with needles is when recapping
stated that the averagetime spent to deposit 1.8 mL oflocal after administration of an injection.15•16 At this time, the
anesthetic solution was less than 20 seconds.13 needle is contaminated with blood, tissue, and (after intra
In actual clinical practice, it therefore seems highly oral injection) saliva.A number of deviceshave been mar
improbable to expect doctors to change their rate of injec keted to aid the health professional in recapping the needle
tion from less than 20 seconds to a safe and comfortable 2 safely.17Needle guards, placed over the needle cap before
minutes per cartridge.A more realistictime span in a clinical injection,prevent fingersfrom being stuck during recapping.
situation is 60 seconds for a full 1.8mL cartridge. This rate Although guidelines are not yet in effect,the following are
of deposition of solution does not produce tissue damage most often mentioned for preventing accidental needle
during or after anesthesia and, in the event of accidental stick: Needlesshould not be reused. After their use, needles
intravascular injection, does not produce an extremely should immediately be discarded into a sharps container.
seriousreaction.Fewinjection techniquesrequirethe admin This policy,although applicablein almost all nondental hos
istration of 1.8mL for success. pital situations in which only one injection is administered
For many years, the author has used one particular is,in many clinicalsituations,impractical in dentistry,where
method to slow the rate of injection. After two negative multiple injections are commonplace. The "scoop" tech
aspirations,he deposits a volume of solution (approximately nique (Fig. 11-18)-in which the needle cap has been placed
one fourth of the total to be deposited) and then aspirates on the instrument tray,and after injection the administrator
again.If the aspiration is negative,he depositsanother fourth simply slides the needle tip into the cap (without physically
of the solution, reaspirates,and continues this process until touching the cap), scooping up the needle cap-can be used
the total volume of solution for the giveninjection is depos for multiple injections without increased risk. The capped
ited. This enableshim to do two positivethings during injec needle is then discarded in a sharps container (Fig. 11-19).
tion: (1) to reaffirm through multiple negative aspirations An acrylic needle holder that holds the cap upright during
that the solution is in fact being deposited extravascularly, injection can be purchased or fabricated. The needle then
and (2) to stop the injection for aspiration; this automati can be reinserted into the cap without difficultyafter injec
callyslowsthe rate of deposit and thereby minimizes patient tion (Fig. 11-20).
discomfort.In the first situation, if positiveaspiration occurs
after deposition of one-fourth of a cartridge, only 9 mg of a + Step 18: Observethe patient. After completion of the
2% solution, or 13.5mg of a 3% solution, or 18 mg of a 4% injection, the doctor, hygienist, or assistant should remain
solution will have been deposited intravascularly---doses with the patient while the anesthetic begins to take effect
unlikely to provoke a drug-related adverse reaction. The (and its blood levelincreases).Most true adversedrug reac
needle tip should be repositioned, negative aspiration (X2) tions, especially those related to intraorally administered
achieved,and the injection continued. The risk of an adverse local anesthetics, develop either during the injection or
reaction secondaryto intravascularinjection is greatlymini within 5 to 10 minutes of its completion. All too often,
mized in this manner. reports are heard of situations in which a local anesthetic
was administered and the doctor left the patient alone for a
+ Step 168: Communicate with the patient. The patient few minutes only to return to find the patient seizing or
should be communicated with during deposition of the local unconscious. Matsuura reported that 54.9% of all medical
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CHAPTER 11 Basic Injection Technique 167
.
~~-'~
1 ~tt A'i'•Ut••. 111•.1..,t'Jt
Figure 11-19. Sharps container for needle. Figure 11-20. Plastic needle cap holder.
emergencies arising in Japanese dental offices developed The administrator of local anesthetics who adheres to
either during the injection of local anesthetics or in the 5 these steps developsa reputation among patients as a "pain
minutes immediately after their administration.2 Patients less dentist." It is not possible to guarantee that every injec
should not be left unattended after administration of a local tion will be absolutely atraumatic because the reactions of
anesthetic. both patients and doctors are far too variable.However,even
when they feel some discomfort, patients invariably state
+ Step 19: Recordthe injection on the patient's chart. An that the injection was better than any other they had previ
entry must be made of the local anesthetic drug used, the ouslyexperienced.This should be the goal sought with every
vasoconstrictor used (if any), the dose (in milligrams) of the local anesthetic injection.
solution(s) used, the needle(s) used, the injection(s) given, The atraumatic injection technique was developed over
and the patient's reaction. For example, in the patient's many yearsby Dr. Nathan Friedman and the Department of
dental progress notes, the following might be inscribed: Human Behavior at the University of Southern California
R-IANB,25-long,2% lido+ 1: 100,000epi, 36 mg. Tolerated School of Dentistry. These principles are incorporated into
procedure well. this section.
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168 PARTIII Techniquesof RegionalAnesthesiain Dentistry
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Anatomic Considerations
169
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Trigeminal ganglion
Trigeminal
nerve (V)
Figure 12-1. The general pathway of the trigeminal or fifth cranial nerve and its motor and sensory roots and three divisions (inset shows
the pattern of innervation for each nerve division). (From Fehrenbach MJ, Herring SW: Anatomy of the head and neck, ed 3, St Louis, 2007,
Saunders.)
TABLE 12-1
Cranial Nerves
Number Name Type Function
I Olfactory Sensory Smell
II Optic Sensory Vision
III Oculomotor Motor Supplies 4 of the 6 extraocular muscles of the eye and the muscle of the upper eyelid
N Trochlear Motor Innervates superior oblique muscle (turns eye downward and laterally)
v Trigeminal Mixed
Ophthalmic Sensory V1 Sensory from muscles of forehead; V2 Sensory from lower eyelids, zygoma and
Maxillary Sensory upper lip; V3 Sensory from lateral scalp, skin anterior to ears, lower cheeks, lower
Mandibular Sensory& lips and anterior aspect of mandible; Motor to muscles of mastication (temporalis,
motor masseter, medial and lateral pterygoids, tensor veli palatine and tensor tympani)
VI Abducens Motor Innervates lateral rectus muscle of eye
VII Facial Motor Innervates muscles of facial expression; taste sensation from anterior 2/3 of tongue,
hard and soft palates; Secretomotor innervation of salivary glands (except parotid)
and lacrimal gland
VIII Auditory Sensory Vestibular branch = equilibrium; Cochlear branch = hearing
(vestibulocochlear)
IX Glossopharyngeal Mixed Taste from posterior 1/3 of tongue; Secretomotor innervation to parotid gland;
Motor to stylopharyngeal muscle
x Vagus Mixed Motor to voluntary muscles of pharynx and larynx (except stylopharyngeal);
Parasympathetic to smooth muscle and glands of pharynx and larynx, and viscera
of thorax and abdomen; Sensory from stretch receptors of aortic arch and
chemoreceptors of aortic bodies; Controls muscles for voice and resonance and
the soft palate
XI Accessory Motor Motor to stemocleidomastoid and trapezius muscles; Innervates muscles of larynx
and pharynx
XII Hypoglossal Motor Motor to muscles of tongue and other glossal muscles
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CHAPTER 12 Anatomic Considerations 171
Trigeminal nerve M
Vestlbulocochlear
nerve (VIII)
Glossopharyngeal
nerve (IX)
A
- Hypoglossal nerve (XII)
Figure 12-2. A, Inferior view of the brain showing cranial nerves and the organs and tissues they innervate.
Continued
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172 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Cribrifonn plate
Foramen rotundum
Ophthalmic:J-nerve
Maxillary nerve Trigeminal
nerveM
Mandibular
nerve
Oculomotor nerve (111) ""'
j :.·. Trochlear nerve (IV)
Foramen ovale
& .ft ..\ Abducent nerve (VI)
• , - .· Facial nerve (VII)
Internal
acoustic meatus Vestlbulocochlear
nerve (VIII)
Jugular foramen Glossopharyngeal
nerve (IX)
Hypoglossalcanal Vagus nerve (X)
B
Figure 12-2, cont'd. B, Internal view of the base of the skull showing cranial nerves exiting or entering the skull. (From Fehrenbach MJ,
Herring SW: Anatomy of the head and neck, ed 3, St Louis, 2007, Saunders.)
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CHAPTER 12 Anatomic Considerations 173
15
ACF r-9
.if L18
'6 'Ji 35
~
.~5
.......
. .. .~
'
-- - ......... .•
''
\1',,
__
' '"', 31 32
4s- 40 / 1~;3 17'
383f 6 I
"-3 / 12
MCF
2&-
, '.?·~\. ~' ~· "'..
4,i 10
I
)24
I ,.., 19 4
25,,,/' ~28 37
, 43
,,
,, 2
,,.-' ..·p 30 21
,,
;
; \ 20
,; . '
33
PCF
36
23 23
29
22
-,
.... :..· .
.
Figure 12-3. Internal surfaceof the base of the skull (cranial fossa).ACF, Anterior cranial fossa;MCF, middle cranial fossa;PCP, posterior
cranial fossa. 1, Anterior clinoid process;2, arcuate eminence; 3, carotid groove; 4, clivus;5, cribriform plate of ethmoid bone; 6, crista galli;
7, diplot!;8, dorsurn sellae;9, foramen cecum; 10, foramen lacerurn; 11, foramen magnum; 12, foramen ovale; 13, foramen rotundurn; 14,
foramen spinosum; 15,frontal crest; 16,frontal sinus; 17,greater wing of sphenoid bone; 18,groovefor anterior ethmoidal nerve and vessels;
19, groove for inferior petrosal sinus; 20, groove for sigmoid sinus; 21, groove for superior petrosal sinus; 22, groove for superior sagittal
sinus; 23, groove for transverse sinus; 24, groovesfor middle meningeal vessels;25, hiatus and groove for greater petrosal nerve; 26, hiatus
and groove for lesser petrosal nerve; 27, hypoglossal canal; 28, internal acoustic meatus; 29, internal occipital protuberance; 30, jugular
foramen; 31, jugurn of sphenoid bone; 32, lesserwing of sphenoid bone; 33, occipitalbone; 34, optic canal; 35, orbital part of frontal bone;
36, parietal bone (posteroinferior angle only); 37, petrous part of temporal bone; 38, pituitary fossa (sella turcica); 39, posterior clinoid
process; 40, prechiasmatic groove; 41, squamous part of temporal bone; 42, superior orbital fissure; 43, tegmen tympani; 44, trigerninal
impression;45,tuberculurn sellae;46,venous foramen. (Data from Abrahams PH, Marks SCJr,Hutchings RT:McMinn'scolor atlas of human
anatomy, ed 5, St Louis,2003,Mosby.)
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174 PARTIII Techniquesof RegionalAnesthesiain Dentistry
r
.33'\- .
' 52
I
9 36
Figure 12-4. External surface of the base of the skull. 1, Apex of petrous part of temporal bone; 2, articular tubercle; 3, carotid canal; 4,
condylar canal (posterior); 5, edge of tegmen tympani; 6, external acoustic meatus; 7, external occipital crest; 8, external occipital protuber
ance; 9, foramen lacerum; 10, foramen magnum; 11, foramen ovale; 12, foramen spinosum; 13, greater palatine foramen; 14, horizontal plate
of palatine bone; 15, hypoglossal (anterior condylar) canal; 16, incisivefossa; 17, inferior nuchal line; 18, inferior orbital fissure; 19, infra
temporal crest of greater wing of sphenoid bone; 20, jugular foramen; 21, lateral pterygoid plate; 22, lesserpalatine foramina; 23, mandibular
fossa;24, mastoid foramen; 25, mastoid notch; 26, mastoid process; 27, medial pterygoid plate; 28, median palatine (intermaxillary) suture;
29, occipital condyle; 30, occipital groove; 31, palatine grooves and spines; 32, palatine process of maxilla; 33, palatinovaginal canal; 34,
petrosquamous fissure; 35, petrotympanic fissure; 36, pharyngeal tubercle; 37, posterior border of vomer; 38, posterior nasal aperture
(choana); 39, posterior nasal spine; 40, pterygoid hamulus; 41, pyramidal process of palatine bone; 42, scaphoid fossa;43, spine of sphenoid
bone; 44, squamotympanic fissure; 45, squamous part of temporal bone; 46, styloid process; 47, stylomastoid foramen; 48, superior nuchal
line; 49, transversepalatine (palatomaxillary)suture; 50, tuberosity of maxilla; 51, tympanic part of temporal bone; 52, vomerovaginalcanal;
53, zygomatic arch. (Data from Abrahams PH, Marks SC Jr, Hutchings RT:McMinn's color atlas of human anatomy, ed 5, St Louis, 2003,
Mosby.)
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CHAPTER 12 Anatomic Considerations 175
Two or three long ciliary nerves supply the iris and cornea.
The infratrochlear nerve suppliesthe skin of the lacrimal sac
and the lacrimal caruncle, the posterior ethmoidal nerve
supplies the ethmoidal and sphenoidal sinuses, and the
externalnasal nerve suppliesthe skin overthe apex (tip) and
the ala of the nose.
Frontal Nerve. The frontal nerve travels anteriorly in
the orbit, dividing into two branches: supratrochlear and
supraorbital. The frontal is the largestbranch of the ophthal
mic division. The supratrochlear nerve supplies the con
junctiva and skin of the medial aspect of the upper eyelid
and the skin over the lower and mesial aspects of the
forehead. The supraorbital nerve is sensory to the upper
eyelid, the scalp as far back as the parietal bone, and the
lambdoidal suture.
Lacrimal Nerve. The lacrimalnerveisthe smallestbranch
of the ophthalmic division. It suppliesthe lateral part of the
upper eyelidand a small adjacent area of skin.
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176 PART III Techniques of Regional Anesthesia in Dentistry
Frontal nerve
.Nasociliary nerve
External nasal
nerve
nerve
Figure 12-6. Lateral view of the cut-away orbit with the pathway of the ophthalmic nerve of the trigeminal nerve highlighted. (From
Fehrenbach MJ, Herring SW: Anatomy of the head and neck, ed 3, St Louis, 2007, Saunders.)
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CHAPTER12 Anatomic Considerations 177
The zygomatic nerve comes off the maxillary division in continues downward, reaching the floor of the nasal
the pterygopalatine fossa and travels anteriorly, entering the cavity and givingbranches to the anterior part of the
orbit through the inferior orbital fissure, where it divides nasal septum and the floor of the nose. It then enters
into the zygomaticotemporal and zygomaticofacial nerves: the incisivecanal, through which it passes into the oral
the zygomaticotemporal supplying sensory innervation to cavityvia the incisiveforamen, located in the midline of
the skin on the side of the forehead, and the zygomaticofacial the palate about 1 cm posterior to the maxillary central
supplying the skin on the prominence of the cheek. Just incisors. The right and left nasopalatine nerves emerge
before leaving the orbit, the zygomatic nerve sends a branch together through this foramen and provide sensation to
that communicates with the lacrimal nerve of the ophthal the palatal mucosa in the region of the premaxilla
mic division. This branch carries secretory fibers from the (canines through central incisors) (Fig. 12-9).
sphenopalatine ganglion to the lacrimal gland 3. The palatine branches include the greater (or anterior)
The pterygopalatine nerves are two short trunks that palatine nerve and the lesser (middle and posterior)
unite in the pterygopalatine ganglion and are then redistrib palatine nerves (Fig. 12-10).The greater (or anterior)
uted into several branches. They also serve as a communica palatine nerve descendsthrough the pterygopalatine
tion between the pterygopalatine ganglion and the maxillary canal, emerging on the hard palate through the greater
nerve (V2). Postganglionic secretomotor fibers from the palatine foramen (which is usually located about 1 cm
pterygopalatineganglionpass through these nervesand back toward the palatal midline, just distal to the second
along V2 to the zygomatic nerve, through which they are molar). Sicher and DuBrul have stated that the greater
routed to the lacrimal nerve and the lacrimal gland palatine foramen may be located 3 to 4 mm in front of
Branchesof the pterygopalatinenerves include those that the posterior border of the hard palate.1 The nerve
supply four areas: orbit, nose, palate, and pharynx. courses anteriorly between the mucoperiosteum and the
1. The orbital branches supply the periosteum of the orbit. osseous hard palate, supplying sensory innervation to
2. The nasal branches supply the mucous membranes of the palatal soft tissues and bone as far anterior as the
the superior and middle conchae, the lining of the first premolar, where it communicates with terminal
posterior ethmoidal sinuses,and the posterior portion fibers of the nasopalatine nerve (see Fig. 12-10).It also
of the nasal septum. One branch is significantin provides sensory innervation to some parts of the soft
dentistry, the nasopalatine nerve, which passes across palate. The middle palatine nerve emergesfrom the
the roof of the nasal cavity downward and forward, lesser palatine foramen, along with the posterior
where it lies between the mucous membrane and the palatine nerve. The middle palatine nerve provides
periosteum of the nasal septum. The nasopalatine nerve sensory innervation to the mucous membrane of
Sphenoldal sinus
Maxillary /
Figure 12·9. Medial view of the lateral nasal wall and the opened pterygopalatine canal highlighting the maxillary nerve and its palatine
branches. The nasal septum has been removed, thus severingthe nasopalatine nerve. (From Fehrenbach MJ, Herring SW:Anatomy of the
head and neck, ed 3, St Louis,2007,Saunders.)
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178 PART III Techniques of Regional Anesthesia in Dentistry
ARTERIES NERVES
Figure 12·10. Blood and sensory nerve supply to hard and soft palate. a, Artery; n, nerve. (Data from Liebgott B: The anatomical basis
of dentistry, ed 3, St Louis, 2010, Mosby.)
the soft palate; the tonsillar region is innervated, in part, The middle superior alveolar (MSA)nerve branches off
by the posterior palatine nerve. the main nerve trunk (V2) within the infraorbital canal to
4. The pharyngeal branch is a small nerve that leavesthe form a part of the superior dental plexus,1 composed of the
posterior part of the pterygopalatine ganglion,passes posterior, middle, and anterior superior alveolarnerves.The
through the pharyngeal canal, and is distributed to the site of origin of the MSA nerve varies, from the posterior
mucous membrane of the nasal part of the pharynx, portion of the infraorbital canal to the anterior portion, near
posterior to the auditory (eustachian) tube. the infraorbital foramen. The MSA nerve provides sensory
The posterior superior alveolar (PSA)nerve descends innervation to the two maxillarypremolars and, perhaps, to
from the main trunk of the maxillary division in the the mesiobuccal root of the first molar and periodontal
pterygopalatine fossajust before the maxillary division tissues,buccal soft tissue, and bone in the premolar region.
enters the infraorbital canal (see Fig. 12-7). Commonly Traditionallyit has been stated that the MSAnerve is absent
there are two PSAbranches, but on occasion a single in 30%2 to 54%3 of individuals.Loetscherand Walton4 found
trunk arises.Passingdownward through the the MSAnerve to be present in 72% of the specimensexam
pterygopalatine fossa,they reach the inferior temporal ined. In its absence, its usual innervations are provided by
(posterior) surface of the maxilla.When two trunks are either the PSAor the anterior superior alveolar(ASA)nerve,
present, one remains external to the bone, continuing most frequently the latter.1
downward on the posterior surface of the maxilla to The anterior superior alveolar (ASA)nerve, a relatively
provide sensory innervation to the buccal gingivain the largebranch, is givenoff the infraorbital nerve (V2) approxi
maxillary molar region and adjacent facialmucosa! mately 6 to 10 mm before the latter exits from the infraor
surfaces,whereas the other branch enters into the bital foramen. Descending within the anterior wall of the
maxilla (along with a branch of the internal maxillary maxillarysinus, it provides pulpal innervation to the central
artery) through the PSAcanal to travel down the and lateral incisors and the canine, and sensory innervation
posterior or posterolateral wall of the maxillary sinus, to the periodontal tissues, buccal bone, and mucous mem
providing sensory innervation to the mucous branes of these teeth (Fig.12-11).
membrane of the sinus. Continuing downward, this The ASAnerve communicates with the MSA nerve and
second branch of the PSAnerve provides sensory gives off a small nasal branch that innervates the anterior
innervation to the alveoli,periodontal ligaments, and part of the nasal cavity,along with branches of the pterygo
pulpal tissues of the maxillarythird, second, and first palatine nerves. In persons without an MSAnerve, the ASA
molars (with the exception [in 28% of patients] of the nerve frequentlyprovides sensoryinnervation to the premo
mesiobuccalroot of the first molar). lars and occasionally to the mesiobuccal root of the first
Branches in the Infraorbital Canal. Within the infraor molar.
bital canal,the maxillarydivision (V2) givesoff two branches The actual innervation of individual roots of all teeth,
of significancein dentistry: the middle superior and anterior bone, and periodontal structures in both the maxillaand the
superior alveolarnerves.While in the infraorbital grooveand mandible derivesfrom terminal branches of larger nerves in
canal, the maxillary division is known as the infraorbital the region. These nerve networks are termed the dental
nerve. plexus.
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CHAPTER 12 Anatomic Considerations 179
Zygomatic
•-- Pterygopalatine
ganglion
Dental plexus
l_,.,_,...' ··-
Figure 12-11. Lateral view of the skull (a portion of the lateral wall of the orbit has been removed) with the branches of the maxillary
nerve highlighted. (From Fehrenbach MJ, Herring SW:Anatomy of the head and neck, ed 3, St Louis,2007,Saunders.)
The superior dental plexus is composed of smaller nerve labial branches provide sensory innervation to the skin and
fibers from the three superior alveolar nerves (and in the mucous membranes of the upper lip.
mandible, from the inferior alveolar nerve). Three types of Although anesthesia of these nerves is not necessary for
nerves emerge from these plexuses: dental nerves, interdental adequate pain control during dental treatment, they are fre
branches, and interradicular branches. Each is accompanied quently blocked in the process of carrying out other anes
along its pathway by a corresponding artery. thetic procedures.
The dental nerves are those that enter a tooth through the Summaty. The following is a summary of the branches
apical foramen, dividing into many small branches within of the maxillary division (italicized nerves denote those of
the pulp. Pulpal innervation of all teeth is derived from special significance in dental pain control):
dental nerves. Although in most instances one easily identifi 1. Branches within the cranium
able nerve is responsible, in some cases (usually the maxillary a. Middle meningeal nerve
first molar) more than one nerve is responsible. 2. Branches within the pterygopalatine fossa
The interdental branches (also termed perforating a. Zygomatic nerve:
branches) travel through the entire height of the interradicu Zygomaticotemporal nerve
lar septum, providing sensory innervation to the periodontal Zygomaticofacial nerve
ligaments of adjacent teeth through the alveolar bone. They b. Pterygopalatine nerves
emerge at the height of the crest of the interalveolar septum Orbital branches
and enter the gingiva to innervate the interdental papillae Nasal branches
and the buccal gingiva. Nasopalatine nerve
The interradicular branches traverse the entire height of Palatine branches
the interradicular or interalveolar septum, providing sensory Greater (anterior) palatine nerve
innervation to the periodontal ligaments of adjacent roots. Lesser (middle and posterior) palatine nerves
They terminate in the periodontal ligament (PDL) at the Pharyngeal branch
root furcations. c. Posterior superior alveolar nerve
Branches on the Face. The infraorbital nerve emerges 3. Branches within the infraorbital canal
through the infraorbital foramen onto the face to divide into a. Middle superior alveolar nerve
its terminal branches: inferior palpebral, external nasal, b. Anterior superior alveolar nerve (Fig. 12-12)
and superior labial. The inferior palpebral branches supply 4. Branches on the face
the skin of the lower eyelid with sensory innervation, the a. Inferior palpebral branches
external nasal branches provide sensory innervation to the b. External nasal branches
skin on the lateral aspect of the nose, and the superior c. Superior labial branches
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180 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Tympanic
membrane
~ r.ierve to tensor veli palatini muscle
Nerve to medial pterygoid muscle
I
/
Branches to
tongue
Submandlbular
Submandlbular ganglion
duct
muscle
Figure 12-13. Medial view of the mandible with the motor and sensory branches of the mandibular nerve highlighted. (From Fehrenbach
MJ, Herring SW: Anatomy of the head and neck, ed 3, St Louis, 2007, Saunders.)
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CHAPTER 12 Anatomic Considerations 181
Auriculotemporal
nerve
c. Mandibular teeth and periodontal tissues Branches from the Anterior Division. Branches from
d. Bone of the mandible the anterior division of V3 provide motor innervation to
e. Temporomandibular joint the muscles of mastication and sensory innervation to the
f. Parotid gland mucous membrane of the cheek and the buccal mucous
2. Motor root membrane of the mandibular molars.
a. Masticatory muscles The anterior divisionis significantlysmallerthan the pos
Masseter terior. It runs forward under the lateral (external) pterygoid
Temporalis muscle for a short distance and then reaches the external
Pterygoideusmedialis surface of that muscle by passing between its two heads or,
Pterygoideuslateralis less frequently,by winding over its upper border. From this
b. Mylohyoid point, it is known as the buccal nerve. Although under the
c. Anterior belly of the digastric lateral pterygoid muscle, the buccal nerve gives off several
d. Tensor tympani branches:the deep temporal nerves (to the temporal muscle)
e. Tensorveli palatini and the masseter and lateral pterygoid nerves (providing
Branches. The third division of the trigeminal nerve motor innervation to the respectivemuscles).
givesoff branches in three areas:from the undivided nerve, The buccal nerve, also known as the buccinator nerve
and from the anterior and posterior divisions. and the long buccal nerve, usually passes between the two
Branches from the Undivided Nerve. On leaving the heads of the lateral pterygoid to reach the external surfaceof
foramen ovale,the main undivided nerve trunk givesoff two that muscle.It then followsthe inferior part of the temporal
branches during its 2- to 3-mm course.These are the nervus muscle and emerges under the anterior border of the mas
spinosus (meningeal branch of the mandibular nerve) and seter muscle,continuing in an anterolateral direction. At the
the medial pterygoid nerve. The nervus spinosus reenters levelof the occlusalplane of the mandibular third or second
the cranium through the foramen spinosum along with the molar, it crossesin front of the anterior border of the ramus
middle meningeal artery to supply the dura mater and and enters the cheekthrough the buccinator muscle.Sensory
mastoid air cells. The medial pterygoid nerve is a motor fibers are distributed to the skin of the cheek. Other fibers
nerve to the medial (internal) pterygoid muscle. It givesoff pass into the retromolar triangle, providing sensoryinnerva
smallbranches that are motor to the tensor veli palatini and tion to the buccal gingivaof the mandibular molars and the
the tensor tympani. mucobuccal fold in that region. The buccal nerve does not
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182 PART III Techniques of Regional Anesthesia in Dentistry
innervate the buccinator muscle; the facial nerve does. Nor and gustation (taste) for this region. It is the nerve that
does it provide sensory innervation to the lower lip or the supplies fibers for general sensation, whereas the chorda
corner of the mouth. This is significant because some doctors tympani (a branch of the facial nerve) supplies fibers for
do not administer the "long" buccal injection immediately taste. In addition, the lingual nerve provides sensory inner
after completing the inferior alveolar nerve block until the vation to the mucous membranes of the floor of the mouth
patient's lower lip has become numb. Their thinking is that and the gingivaon the lingual of the mandible. The lingual
the buccal nerve block will provide anesthesia to the lower nerve is the nerve most commonly associatedwith cases of
lip and therefore might lead them to believe that their infe paresthesia(prolongedor permanent sensorynervedamage).
rior alveolar nerve block has been successful, when in fact it The inferior alveolar nerve is the largest branch of the
has been missed. Such concern is unwarranted. The buccal mandibular division (see Fig. 12-14). It descends medial to
nerve block may be administered immediately after completion the lateralpterygoidmuscleand lateroposterior to the lingual
of the inferior alveolar nerve block. nerve, to the region between the sphenomandibular liga
Anesthesia of the buccal nerve is important for dental ment and the medial surface of the mandibular ramus,
procedures requiring soft tissue manipulation on the buccal where it enters the mandibular canal at the levelof the man
surface of the mandibular molars. dibular foramen. Throughout its path, it is accompanied by
Branches of the Posterior Division. The posterior divi the inferior alveolar artery (a branch of the internal maxil
sion of V, is primarily sensory with a small motor compo lary artery) and the inferior alveolarvein.The artery liesjust
nent. It descendsfor a short distance downward and medial anterior to the nerve.The nerve, artery, and vein travel ante
to the lateral pterygoid muscle, at which point it branches riorly in the mandibular canal as far forward as the mental
into the auriculotemporal, lingual, and inferior alveolar foramen, where the nerve dividesinto its terminal branches:
nerves. the incisivenerve and the mental nerve.
The auriculotemporal nerve is not profoundly significant Bifid (from the Latin meaning "cleft into two parts")
in dentistry. It traversesthe upper part of the parotid gland inferior alveolar nerves and mandibular canals have been
and then crossesthe posterior portion of the zygomaticarch. observed radiographically and categorized by Langlaisand
It givesoff a number of branches, all of which are sensory. associates.5 Among 6000 panoramic radiographs studied,
These include a communication with the facial nerve, pro bifid mandibular canals were evident in 0.95%. The bifid
viding sensory fibersto the skin over areas of innervation of mandibular canal is clinicallysignificant in that it increases
the followingmotor branches of the facialnerve: zygomatic, the difficulty of achieving adequate anesthesia in the man
buccal,and mandibular; a communication with the otic gan dible through conventional techniques. This is especiallyso
glion, providing sensory,secretory,and vasomotor fibers to in the type 4 variation (Fig. 12-15), in which two separate
the parotid gland;the anterior auricular branches, supplying mandibular foramina are present on each side of the mouth.
the skin over the helix and tragus of the ear; branches to the The mylohyoidnerve branches from the inferior alveolar
external auditory meatus, innervating the skin over the nerve before entry of the latter into the mandibular canal
meatus and the tympanic membrane; articular branches to (see Figs. 12-13and 12-14).It runs downward and forward
the posterior portion of the temporomandibular joint; and in the mylohyoidgroove on the medial surfaceof the ramus
superficial temporal branches, supplying the skin over the and along the body of the mandible to reach the mylohyoid
temporal region.!" muscle.The mylohyoidis a mixed nerve,being motor to the
The lingual nerve is the second branch of the posterior mylohyoid muscle and the anterior belly of the digastric. It
division of V3• It passes downward medial to the lateral is thought to contain sensory fibers that supply the skin on
pterygoid muscle and, as it descends, lies between the the inferior and anterior surfaces of the mental protuber
ramus and the medial pterygoid muscle in the pterygoman ance. It also may provide sensory innervation to the man
dibular space. It runs anterior and medial to the inferior dibular incisors.Evidencesuggeststhat the mylohyoidnerve
alveolar nerve, whose path it parallels. It then continues alsomay be involvedin supplyingpulpal innervation to por
downward and forward, deep to the pterygomandibular tions of the mandibular molars in some persons, usuallythe
raphe and below the attachment of the superior constrictor mesial root of the mandibular first molar.6
of the pharynx, to reach the side of the base of the tongue Once the inferior alveolar nerve enters the mandibular
slightlybelow and behind the mandibular third molar (see canal, it travels anteriorly along with the inferior alveolar
Figs. 12-13 and 12-14). Here it lies just below the mucous artery and vein. The dental plexus serves the mandibular
membrane in the lateral lingual sulcus,where it is so super posterior teeth, entering through their apices and providing
ficial in some persons that it may be seen just below the pulpal innervation. Other fibers supply sensory innervation
mucous membrane. It then proceeds anteriorly across the to the buccal periodontal tissues of these same teeth.
muscles of the tongue, looping downward and medial to The inferior alveolar nerve divides into its two terminal
the submandibular (Wharton's) duct to the deep surface of branches: the incisive nerve and the mental nerve at the
the sublingual gland, where it breaks up into its terminal mental foramen (seeFig. 12-14).The incisivenerve remains
branches. within the mandibular canal and forms a nerve plexus
The lingual nerve is the sensory tract to the anterior that innervates the pulpal tissues of the mandibular first
two thirds of the tongue. It provides both general sensation premolar, canine, and incisors via the dental branches. The
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CHAPTER12 Anatomic Considerations 183
Type I
Q G
ryp.2
u••1cnni1. Ualdenll.
lilllhldIll l'mmi mMtlngillobody
~ ~
G g
Bikdlrol. Bila'-',
,,,.. 3 lrpa .C
c-hinntinn o.sgu....,o ,_, -
Ag CJY
Figure 12-15. A, Variations in bifid mandibular canals. B and C, Radiographs of a type 4 bifid mandibular canal (B, on the patient's right;
C, outlined). (Data from Langlais RP, Broadus R, Glass BJ: Bifid mandibular canals in panoramic radiographs, J Am Dent Assoc 110:923-926,
1985.)
mental nerve exits the canal through the mental foramen forward and laterally.At its inferior borders are a series of
and dividesinto three branches that innervate the skin of the eminences that correspond to the roots of the maxillary
chin and the skin and mucous membrane of the lower lip. teeth. The most prominent usually is found over the canine
Summary. The following outline summarizes the bran tooth and is often referred to as the canine eminence. Supe
ches of the mandibular division (italicized nerves denote rior to the canine fossa (located just distal to the canine
those especiallysignificant in dental pain control): eminence) is the infraorbital foramen, through which blood
1. Undivided nerve vessels and terminal branches of the infraorbital nerve
a. Nervus spinosus emerge. Bone in the region of the maxillary teeth is com
b. Nerve to the medial pterygoid muscle monly of the more porous cancellous variety, leading to a
2. Divided nerve significantlygreater incidenceof clinicallyadequate anesthe
a. Anterior division sia than in areas where more dense cortical bone is present,
Nerve to the lateral pterygoid muscle such as in the mandible. In many areas,bone over the apices
Nerve to the masseter muscle of the maxillaryteeth is tissue-paper thin or showsevidence
Nerve to the temporal muscle of dehiscence.
Buccal nerve The inferior temporal surface of the maxilla is directed
b. Posterior division backward and laterally (Fig. 12-17). Its posterior surface is
Auriculotemporal nerve pierced by severalalveolarcanalsthat transmit the posterior
Lingual nerve superior alveolar nerves and blood vessels.The maxillary
Mylohyoid nerve tuberosity, a rounded eminence, is found on the inferior
Inferior alveolar nerve: dental branches posterior surface. On the superior surface is a groove,
Incisive branch: dental branches directed laterally and slightlysuperiorly,through which the
Mental nerve maxillary nerve passes. This groove is continuous with the
infraorbital groove.
The palatal processes of the maxilla are thick horizontal
OSTEOLOGY: MAXILLA
projections that form a largeportion of the floor of the nose
In addition to the neuroanatomy of pain control in dentistry, and the roof of the mouth. The bone here is considerably
one should be aware of the relationship of these nerves to thicker anteriorly than posteriorly. Its inferior (or palatal)
the osseous and soft tissues through which they course. surface constitutes the anterior three fourths of the hard
The maxilla (more properly, the right and left maxillae) palate (Fig. 12-18). Many foramina (passages for nutrient
is the largest bone of the face, excluding the mandible. Its blood vessels) perforate it. Along its lateral border, at the
anterior (or facial) surface (Fig. 12-16) is directed both junction with the alveolarprocess,is a groovethrough which
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184 PARTIII Techniquesof RegionalAnesthesiain Dentistry
6
2°'-.
'.518
Figure 12-16. Anterior view of the skull. 1, Anterior nasal spine; 2, body of mandible; 3, frontal bone; 4, frontal notch; 5, frontal process
of maxilla;6, glabella;7, greater wing of sphenoid bone; 8, infraorbital foramen; 9, infraorbital margin; 10, inferior nasal concha; 11, inferior
orbital fissure; 12, lacrimal bone; 13, lesser wing of sphenoid bone; 14, maxilla; 15, mental foramen; 16, mental protuberance; 17, middle
nasal concha; 18, nasal bone; 19, nasal septum; 20, nasion; 21, orbit (orbital cavity); 22, ramus of mandible; 23, superior orbital fissure;
24, supraorbital foramen; 25, supraorbital margin; 26, zygomaticbone. (Data from Abrahams PH, Marks SC Jr, Hutchings RT:McMinn's
color atlas of human anatomy, ed 5, St Louis,2003,Mosby.)
the anterior palatine nerve passes from the greater palatine palatine processby the canine teeth. The small area anterior
foramen. In the midline in the anterior region is the funnel to this suture is termed the premaxilla.
shaped opening of the incisive foramen. Four canals are The horizontal plate of the palatine bone forms the pos
located in this opening: two for the descending palatine terior fourth of the hard palate. Its anterior border articu
arteries and two for the nasopalatine nerves.In many skulls, lateswith the palatine processof the maxilla,and its posterior
especiallythose of younger persons, a fine suture line extends border servesas the attachment for the soft palate. Foramina
laterally from the incisive foramen to the border of the are present on its surface,representing the lower end of the
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CHAPTER 12 Anatomic Considerations 185
Figure 12-17. Infratemporal aspect of the maxilla. 1, Articular tubercle; 2, external acoustic meatus; 3, horizontal plate of palatine bone;
4, inferior orbital fissure; 5, infratemporal crest; 6, infratemporal (posterior) surface of maxilla; 7, infratemporal surface of greater wing of
sphenoid bone; 8, lateral pterygoid plate; 9, mandibular fossa; 10,mastoid notch; 11, mastoid process; 12,medial pterygoid plate; 13,occipital
condyle; 14, occipital groove; 15,pterygoid hamulus; 16,pterygomaxillary fissure and pterygopalatine fossa; 17,pyramidal process of palatine
bone; 18, spine of sphenoid bone; 19, styloid process and sheath; 20, third molar tooth; 21, tuberosity of maxilla; 22, vomer; 23, zygomatic
arch. (Data from Abrahams PH, Marks SC Jr, Hutchings RT: McMinn's color atlas of human anatomy, ed 5, St Louis, 2003, Mosby.)
Medan
palatine -.'!ri1
SI.lb.Jr&
~ Greater palalirie
Palatine '!'2 i-.- foramen
bones ~
~/ Les~r palatine
Spli=~ f~ foramen
Figure 12-18. Inferior view of the hard palate. (Data from Fehrenbach MJ, Herring SW: Illustrated anatomy of the head and neck, ed 2,
Philadelphia, 2002, WB Saunders.)
pterygopalatine canal, through which descending palatine anterior region (incisors) is usually less dense than that
blood vesselsand the anterior palatine nerve run. over the posterior teeth, permitting infiltration (supraperi
osteal) anesthesiato be employed with some expectation of
success.8•9In the region of the second premolar on each side,
OSTEOLOGY: MANDIBLE
midway between the upper and lower borders of the body,
The mandible is the largest and strongest bone of the face. lies the mental foramen. Phillips and associates,in an evalu
It consists of a curved horizontal portion (the body) and ation of 75 dry,adult human mandibles,determined that the
two perpendicular portions (the rami). The buccal cortical usual position of the mental foramen is below the crown of
plate of the adult mandible most often is sufficientlydense the second premolar,10 The mental nerve, artery, and vein
so as to preclude effective infiltration of anesthesia in its exit the mandibular canal here. Bone along this external
vicinity.7 surface of the mandible is commonly thick cortical bone.
The external (lateral) surfaceof the body of the mandible The lingualborder of the body of the mandible is concave
is marked in the midline by a faint ridge, an indication from side to side (Fig. 12-19,Band D). Extending upward
of the symphysis of the two pieces of bone from which and backward is the mylohyoid line, giving origin to the
the mandible is created (Fig, 12-19, A and C). The bone mylohyoid muscle, Bone along the lingual of the mandible
that forms the buccal and lingual alveolar processes in the is usually quite thick; however, in approximately 68% of
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186 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Figure 12-19. The mandible (A) from the front, (B) from behlnd and above,and (C) from the left and front, and (D) internal view from
the left. 1, Alveolarpart; 2, angle; 3, anterior border of ramus; 4, base; 5, body; 6, coronoid process; 7, digastric fossa; 8, head; 9, inferior
border of ramus; 10, lingula; 11, mandibular foramen; 12, mandibular notch; 13, mental foramen; 14, mental protuberance; 15, mental
tubercle; 16, mylohyoidgroove; 17, mylohyoidline; 18, neck; 19, oblique line; 20, posterior border of ramus; 21, pterygoid fovea;22, ramus;
23, sublingual fossa; 24, submandibular fossa; 25, superior and inferior mental spines (genial tubercles). (Data from Abrahams PH, Marks
SC Jr, Hutchings RT:McMinn's color atlas of human anatomy,ed 5, St Louis,2003,Mosby.)
mandibles, lingual foramina are located in the posterior Hetson and associates15located it 55% distal to the anterior
(molar) region." The function of these foramina is as yet ramus (range, 44.4% to 65.5%). The mandibular canal
unclear,but some may contain sensoryfibersfrom the mylo extends obliquely downward and anteriorly within the
hyoid nerve that innervate portions of mandibular molars.2 ramus. It then courses horizontally forward in the body,
In addition, bone on the lingual surface of the incisor teeth distributing small dental branches to the mandibular teeth
frequentlydemonstratesmultiple smallperforations,perhaps posterior to the mental foramen. The mandibular foramen
explainingrecent clinicaltrials in which mandibular lingual is the point of entrance through which the inferior alveolar
infiltration had significantsuccessrates in providing pulpal nerve, artery, and vein enter the mandibular canal. The
anesthesia.8 height of this foramen varies greatly, ranging from 1 to
The lateral surface of each ramus is flat, composed of 19 mm or more above the level of the occlusal plane.13 A
dense cortical bone and providing attachment for the mas prominent ridge,the lingula mandibulae, lieson the anterior
seter musclealong most of its surface(seeFig.12-19, C).The margin of the foramen. The lingula servesas an attachment
medial surface (see Fig. 12-19,D) contains the mandibular for the sphenomandibular ligament.At the lower end of the
foramen, located roughly halfwaybetween the superior and mandibular foramen, the mylohyoidgroovebegins,coursing
inferior borders and two thirds to three fourths the distance obliquely downward and anteriorly. In this groove lie the
from the anterior border of the ramus to its posterior mylohyoidnerve and vessels.
border.12 Other studies of the anteroposterior location of the Bone along the lingual surface of the mandible usually is
mandibular foramen have provided differing locations. dense (see Fig. 12-19,D). On rare occasions,bone over the
Hayward and associates13found the foramen most often in lingual aspect of the third molar roots is less dense, permit
the third quadrant from the anterior part of the ramus, ting a greater chance that supraperiosteal anesthesia will be
Monheim14 found it at the midpoint of the ramus, and successful.However,the proximity of the lingual nerve to
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CHAPTER 12 Anatomic Considerations 187
this site leads to cautions against attempting lingual infiltra 2. Heasman PA:Clinicalanatomy of the superior alveolarnerves,
tion in the area of the mandibular molars. Br J Oral MaxillofacSurg 22:439-447, 1984.
The superior border of the ramus has two processes: the 3. McDanielWL:Variations in nerve distributions of the maxil
coronoid anteriorly and the condylar posteriorly. Between lary teeth, J Dent Res 35:916--921, 1956.
4. LoetscherCA,WaltonRE:Patterns of innervation of the maxil
these two processes is a deep concavity, the mandibular
lary first molar: a dissection study, Oral Surg 65:86--90, 1988.
(sigmoid) notch. The coronoid process is thinner than the
5. LanglaisRP, Broadus R, Glass BJ: Bifid mandibular canals in
condylar. Its anterior border is concave-the coronoid notch. panoramic radiographs, J Am Dent Assoc 110:923-926, 1985.
The coronoid notch represents a landmark for determining 6. Frommer J, Mele FA, Monroe CW: The possible role of the
the height of needle penetration in the inferior alveolar mylohyoid nerve in mandibular posterior tooth sensation,
nerve block technique. The condylar process is thicker than J Am Dent Assoc 85:113-117, 1972.
the coronoid. The condylar head, the thickened articular 7. Blanton PL, JeskeAH: The key to profound local anesthesia:
portion of the condyle, sits atop the constricted neck of the neuroanatomy, J Am Dent Assoc 134:753--760, 2003.
condyle. The condylar neck is flattened front to back. The 8. Yonchak T, Reader A, Beck M, et al: Anesthetic efficacy of
attachment for the external pterygoid muscle is on its ante infiltrations in mandibular anterior teeth, Anesth Prog 48:55-
rior surface. 60, 2001.
9. Meechan JG, Ledvinka JI: Pulpal anaesthesia for mandibular
When cut horizontally at the level of the mandibular
central incisor teeth: a comparison of infiltration and intraliga
foramen, the ramus of the mandible can be seen to be thicker
mentary injections, Int Endod J 35:629-634, 2002.
in its anterior region than it is posteriorly. This is of clinical 10. Phillips JL,WellerN, KulildJC: The mental foramen. Part III.
importance during the inferior alveolar nerve block. The Size and position on panoramic radiographs, J Endodont
thickness of soft tissues between needle penetration and 18:383-386, 1992.
the osseous tissues of the ramus at the level of the man 11. Shiller WR, Wiswell OB: Lingual foramina of the mandible,
dibular foramen averages about 20 to 25 mm. Because of Anat Rec 119:387-390, 1954.
increased thickness of bone in the anterior third of the 12. Bremer G: Measurementsof specialsignificancein connection
ramus, the thickness of soft tissue is decreased accordingly with anesthesiaof the inferior alveolarnerve, Oral Surg 5:966--
{approximately 10 mm). Knowing the depth of penetration 988, 1952.
of soft tissue before contacting osseous tissues can aid the 13. Hayward J, Richardson ER, Malhotra SK: The mandibular
foramen: its anteroposterior position, Oral Surg 44:837--843,
administrator in determining correct positioning of the
1977.
needle tip.
14. Monheim LM: Local anesthesia and pain control in dental
practice, ed 4, St Louis, 1969, Mosby.
References 15. Hetson G, ShareJ,Frommer J,et al:Statisticalevaluation of the
1. DuBrul EL:Sicher'soral anatomy,ed 7, St Louis, 1980, Mosby. position of the mandibular ramus, Oral Surg 65:32-34, 1988.
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I
echniques of Maxillary
Anesthesia
Severalgeneralmethods of obtaining pain control with local pulpal and soft tissues distal to the injection site are
anesthetics are available.The site of deposition of the drug anesthetized.
relativeto the area of operative intervention determines the Field block and nerve block may be distinguished by the
type of injection administered. Three major types of local extent of anesthesia achieved. In general, field blocks are
anesthetic injection can be differentiated: local infiltration, more circumscribed,involvingtissues in and around one or
field block, and nerve block. two teeth, whereasnerve blocks affecta larger area (e.g.,that
observed after inferior alveolaror anterior superior alveolar
+ Local Infiltration Smallterminal nerve endings in the nerve block).
area of the dental treatment are flooded with localanesthetic The type of injection administered for a given treatment
solution. Incision (or treatment) is then made into the same is determined by the extent of the operative area. For man
area in which the local anesthetic has been deposited (Fig. agement of small,localizedareas,as in providing hemostasis
13-1).An example oflocal infiltration is the administration for soft tissue procedures,infiltration anesthesiamay suffice.
of a localanesthetic into an interproximal papillabefore root When two or three teeth are being restored, field block is
planing. The term infiltration has been in common usage in indicated, whereas for pain control in quadrant dentistry,
dentistry to define an injection in which the local anesthetic regional block anesthesia is recommended.
solution is deposited at or above the apex of the tooth to be
treated. Although technically incorrect-this technique is a
MAXILLARY INJECTION TECHNIQUES
field block (seefollowing)-the common term will continue
to be used for this type of injection. Numerous injection techniques are availableto provide clin
ically adequate anesthesia of the teeth and soft and hard
+ Field Block Localanesthetic is deposited near the larger tissues in the maxilla. Selection of the specifictechnique to
terminal nerve branches so the anesthetized area will be be used is determined, in large part, by the nature of the
circumscribed,preventing the passageof impulses from the treatment to be provided. The following techniques are
tooth to the central nervous system (CNS). Incision (or available:
treatment) is then made into an area awayfrom the site of 1. Supraperiosteal (infiltration), recommended for
injection of the anesthetic (Fig. 13-2). Maxillary injections limited treatment protocols
administered above the apex of the tooth to be treated are 2. Periodontal ligament (PDL,intraligamentary)
properlytermedfield blocks (although common usageidenti injection, recommended as an adjunct to other
fiesthem as infiltration or supraperiosteal). techniques or for limited treatment protocols
3. Intraseptal injection, recommended primarily for
+ Nerve Block Local anesthetic is deposited close to a periodontal surgical techniques
main nerve trunk, usually at a distance from the site of 4. Intracrestal injection, recommended for singleteeth
operative intervention (Fig. 13-3). Posterior superior alveo (primarily mandibular molars) when other techniques
lar, inferior alveolar,and nasopalatine injections are exam have failed
ples of maxillary nerve blocks. 5. Intraosseous (IO) injection, recommended for single
teeth (primarily mandibular molars) when other
+ Discussion Technically,the injection commonly refer techniques have failed
red to in dentistry as a local infiltration is a field block 6. Posterior superior alveolar (PSA)nerve block,
because anesthetic solution is deposited at or above the recommended for management of severalmolar teeth
apex of the tooth to be treated. Terminal nerve branches to in one quadrant
188
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CHAPTER13 Techniquesof MaxillaryAnesthesia 189
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190 PART III Techniques of Regional Anesthesia in Dentistry
Alternatives. PDL, IO, regional nerve block. *Bevelorientations are specifiedfor all injection techniques in Chapters 13
and 14.The orientation of the needle bevel is not a significantfactor in the
Technique success or failure of an injection technique, and these recommendations
need not be rigidly adhered to; yet there will be a fuller expectation of suc
1. A 27-gaugeshort needle is recommended. cessful anesthesia if they are followed, provided all other technical and
2. Area of insertion: height of the mucobuccal fold above anatomic principles are maintained. In general,wheneverpossible,the bevel
the apex of the tooth being anesthetized of the needle is to be facing toward bone; then, in the unlikely event that
3. Targetarea: apical region of the tooth to be anesthetized the needle comes into contact with bone, the bevelwill slide over the peri
4. Landmarks: osteum, provoking minor discomfort but not tearing the periosteum. If the
bevel faces away from bone, the sharp point of the needle would contact
a. Mucobuccalfold the periosteum, tearing it and leading to a more painful (subperiosteal)
b. Crown of the tooth injection. Postinjection discomfort is considerablygreater with subperios
c. Root contour of the tooth teal than with supraperiosteal injections.
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CHAPTER13 Techniquesof MaxillaryAnesthesia 191
i. Make the needle safe. Complications. Pain on needle insertion with the needle tip
j. Wait 3 to 5 minutes before commencing the dental againstthe periosteum. Tocorrect:Withdraw the needle and
procedure. reinsert it farther from the periosteum.
TABLE 13-1
Average Tooth Length
Length of Crown, mm + Length of Root, mm = Length of Tooth
Maxillary
Central incisors 11.6 12.4 24.0
Lateral incisors 9.0-10.2 12.3-13.5 22.5
Canines 10.9 16.1 27.0
First premolars 8.7 13.0 21.7
Second premolars 7.9 13.6 21.5
First molars 7.7 13.6 21.3
Second molars 7.7 13.4 21.1
Third molars Extremely variable Extremely variable Extremely variable
Mandibular
Central incisors 9.4 12.0 21.4
Lateral incisors 9.9 13.3 23.2
Canines 11.4 14.0 25.4
First premolars 7.5-11.0 11.0-16.0 18.5-27.0
Second premolars 8.5 14.7 23.2
First molars 8.3 14.5 22.8
Second molars 8.1 14.7 22.8
Third molars Extremely variable Extremely variable Extremely variable
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192 PARTIII Techniquesof RegionalAnesthesiain Dentistry
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CHAPTER 13 Techniquesof MaxillaryAnesthesia 193
Figure 13·8. Position of the administrator for (A) right and (B) left posterior superior alveolar (PSA)nerve block.
Figure 13-9. Posterior superior alveolar (PSA) nerve block. Figure 13-10. Advance the needle upward, inward, and
Tissue retracted at the site of penetration. Note the orientation of backward.
the needle: inward, upward, backward.
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194 PARTIII Techniquesof RegionalAnesthesiain Dentistry
(2) Inward: medially toward the midline at a surface of the maxilla.When a long needle is
45-degree angle to the occlusalplane used (averagelength, 32 mm), it is inserted half
(Fig. 13-11) its length into the tissue.With a short needle
(3) Backward:posteriorly at a 45-degree angle to (averagelength, 20 mm), approximately4 mm
the long axis of the second molar should remain visible.
i. Slowlyadvance the needle through soft tissue. (2) For smaller adults and children, it is prudent to
(1) There should be no resistanceand therefore no halt the advance of the needle short of its usual
discomfort to the patient. depth of penetration to avoid a possible
(2) If resistance (bone) is felt, the angle of the hematoma caused by overpenetration.
needle in toward the midline is too great. Penetrating to a depth of 10 to 14 mm places
(a) Withdraw the needle slightly (but do not the needle tip in the target area in most
remove it entirely from the tissues) and smaller-skulledpatients.
bring the syringebarrel closer to the Note: The goal is to deposit local anesthetic close to the PSA
occlusalplane. nerves, located posterosuperior and medial to the maxillary
(b) Readvancethe needle. tuberosity.
j. Advancethe needle to the desired depth (see k. Aspirate in two planes.
Fig. 13-11). (1) Rotate the syringebarrel (needle bevel) one
(1) In an adult of normal size,penetration to a fourth tum and reaspirate.
depth of 16 mm placesthe needle tip in the 1. If both aspirations are negative:
immediate vicinity of the foramina through (1) Slowly,over 30 to 60 seconds,deposit 0.9 to
which the PSAnerves enter the posterior 1.8 mL of anesthetic solution.
(2) Aspirate severaladditional times (in one plane)
during drug administration.
(3) The PSAinjection is normally atraumatic
because of the large tissue space availableto
accommodate the anesthetic solution and the
fact that bone is not touched
m. Slowlywithdraw the syringe.
n. Make the needle safe.
o. Wait minimally 3 to 5 minutes before commencing
the dental procedure.
Safety Features
1. Slowinjection, repeated aspirations
2. No anatomic safetyfeatures to prevent overinsertion
of the needle; therefore careful observation is
necessary
Failures of Anesthesia
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CHAPTER13 Techniquesof MaxillaryAnesthesia 195
Complications
1. Hematoma:
a. This is commonly produced by inserting the needle
too far posteriorly into the pterygoid plexus of veins.
In addition, the maxillary artery may be perforated.
Use of a short needle minimizes the risk of pterygoid
plexus puncture.
b. A visibleintraoral hematoma developswithin several
minutes, usually noted in the buccal tissues of the
Greater Palatal soft
mandibular region (see Chapter 17). tissue
palatine
(1) There is no easilyaccessibleintraoral area to foramen and bone
which pressure can be applied to stop the
hemorrhage.
Figure 13-12. Area anesthetized by a middle superior alveolar
(2) Bleedingcontinues until the pressure of (MSA)nerve block.
extravascularblood is equal to or greater than
that of intravascular blood.
2. Mandibular anesthesia:
a. The mandibular division of the fifth cranial nerve
(V3) is located lateral to the PSAnerves. Deposition
of local anesthetic lateral to the desired location may
produce varying degreesof mandibular anesthesia.
Most often, when this occurs, patients mention that
their tongue and perhaps their lower lip are
anesthetized.
Contraindications Technique
1. Infection or inflammation in the area of injection or 1. A 27-gaugeshort or long needle is recommended.
needle insertion or drug deposition 2. Area of insertion: height of the mucobuccal fold above
2. Where the MSAnerve is absent, innervation is through the maxillary second premolar
the anterior superior alveolar (ASA)nerve; branches of 3. Target area: maxillarybone above the apex of the
the ASAinnervating the premolars and the mesiobuccal maxillary second premolar (Fig. 13-13)
root of the first molar can be anesthetized by means of 4. Landmark: mucobuccal fold above the maxillary second
the MSAtechnique. premolar
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196 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Figure 13·14. Position of the administrator for a (A) right and (B) left middle superior alveolar (MSA) nerve block.
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CHAPTER13 Techniquesof MaxillaryAnesthesia 197
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198 PARTIII Techniquesof RegionalAnesthesiain Dentistry
first premolar usually provides the shortest route to this administrator should sit at the 10 o'clock position,
targetarea. directly facing the patient or facing in the same
3. Targetarea: infraorbital foramen (below the infraorbital direction as the patient.
notch). b. Position the patient supine (much preferred) or
4. Landmarks: semisupine with the neck extended slightly.If the
a. Mucobuccalfold patient's neck is not extended, the patient's chest may
b. Infraorbital notch interfere with the syringe barrel.
c. Infraorbital foramen c. Prepare the tissues at the injection site (height of the
5. Orientation of the bevel:toward bone mucobuccal fold) for penetration.
6. Procedure: (1) Dry with sterile gauze.
a. Assume the correct position (Fig. 13-17).For a right (2) Applytopical antiseptic {optional).
or left infraorbital nerve block, a right-handed {3) Applytopical anesthetic for a minimum of 1
minute.
d.. Locatethe infraorbital foramen (Fig. 13-18).
(1) Feelthe infraorbital notch.
(2) Moveyour finger downward from the notch,
applying gentle pressure to the tissues.
(3) The bone immediately inferior to the notch is
convex (felt as an outward bulge). This
represents the lower border of the orbit and the
roof of the infraorbital foramen (Fig. 13-18,B).
(4) As your finger continues inferiorly,a concavityis
felt;this is the infraorbital foramen.
(5) While applying pressure, feel the outlines of the
infraorbital foramen at this site. The patient
sensesa mild sorenesswhen the foramen is
palpated as the infraorbital nerve is pressed
against bone.
e. Maintain your finger on the foramen or mark the
skin at the site (Fig. 13-19).
f. Retract the lip, pulling the tissues in the mucobuccal
fold taut and increasingvisibility.A 2 x 2-inch sterile
gauze placed beneath your glovedfinger aids in
retraction of the lip during the ASAinjection.
g. Insert the needle into the height of the mucobuccal
Figure 13-17. Position of the administrator for a right or left fold over the first premolar with the bevel facing
anterior superior alveolar (ASA)nerve block. The patient's head bone (Fig. 13-20).
should be turned slightlyto improve visibility. h. Orient the syringe toward the infraorbital foramen.
Figure 13·18. A, Palpate the infraorbital notch. B, Location of the infraorbital foramen in relation to the infraorbital notch.
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CHAPTER13 Techniquesof MaxillaryAnesthesia 199
Figure 13-19. Using a finger over the foramen, lift the lip, and
hold the tissues in the mucobuccal fold taut.
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200 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Precautions
1. For pain on insertion of the needle and tearing of the
periosteum, reinsert the needle in a more lateral (away
from bone) position, or deposit solution as the needle
advancesthrough soft tissue.
2. To prevent overinsertion of the needle, estimate the
depth of penetration before injection (review
Figure 13-22. Position of the needle tip before deposition of
procedure), and exert finger pressure over the
local anesthetic at the infraorbital foramen. infraorbital foramen.
a. Overinsertion is unlikelybecause of the rim of bone
that forms the superior rim of the infraorbital
foramen. The needle tip contacts this rim.
(providing anesthesia to the teeth and their supporting
structures), do the following: Failures of Anesthesia
o. Maintain firm pressure with your finger over the 1. Needle contacting bone below (inferior to) the
injection site both during and for at least 1 minute infraorbital foramen: Anesthesiaof the lower eyelid,
after the injection (to increase the diffusion of local lateral side of the nose, and upper lip may develop with
anesthetic solution into the infraorbital foramen). little or no dental anesthesia;a bolus of solution may be
p. Withdraw the syringe slowlyand immediately make felt beneath the skin in the area of deposition, which
the needle safe. lies at a distance from the infraorbital foramen (which
q. Maintain direct finger pressure over the injection is still palpable after the local anesthetic solution has
site for a minimum of 1 minute, preferably2 been injected). These are, by far, the most common
minutes, after injection. causes of anesthetic failure within the distribution
r. Wait a minimum of 3 to 5 minutes after completion of the ASAnerve. In essence,a failed ASAis a
of the injection before commencing the dental supraperiosteal injection over the first premolar. To
procedure. correct:
a. Keepthe needle in line with the infraorbital foramen
Signs and Symptoms during penetration. Do not direct the needle toward
1. Subjective:Tingling and numbness of the lower eyelid, bone.
side of the nose, and upper lip indicate anesthesia of b. Estimate the depth of penetration before injecting.
the infraorbital nerve, not the ASAor MSAnerve 2. Needle deviation medial or lateral to the infraorbital
(soft tissue anesthesia developsalmost instantly as foramen. To correct:
the anesthetic is being administered). a. Direct the needle toward the foramen immediately
2. Subjectiveand objective:numbness in the teeth and soft after inserting and before advancing through the
tissues along the distribution of the ASAand MSA tissue.
nerves (developingwithin 3 to 5 minutes if pressure is b. Recheckneedle placement before aspirating and
maintained over the injection site) depositing the anesthetic solution.
3. Objective:use of electricalpulp testing with no
response from tooth with maximal EPT output (80/80) Complications. Hematoma (rare) may develop across the
4. Absenceof pain during treatment lower eyelid and the tissues between it and the infraorbital
foramen. To manage, apply pressure on the soft tissue over
Safety Features the foramen for 2 to 3 minutes. Hematoma is extremely
1. Needle contact with bone at the roof of the infraorbital rare because pressure is routinely applied to the injection
foramen prevents inadvertent overinsertion and possible site both during and after administration of the ASA
puncture of the orbit. nerve block.
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CHAPTER13 Techniquesof MaxillaryAnesthesia 201
PALATAL ANESTHESIA
Anesthesia of the hard palate is necessary for dental pro
cedures involving manipulation of palatal soft or hard
tissues. For many dental patients, palatal injections prove
to be a very traumatic experience. For many dentists,
administration of palatal anesthesiais one of the most trau
matic procedures they perform in dentistry.2 Indeed, many
dentists and dental hygienistsadvisetheir patients that they
expectthem to feelpain (dental professionalsusuallyuse the
term discomfort rather than pain when describing painful
procedures) during palatal injections! Forewarning the
patient about procedural pain permits the patient to become
more prepared psychologically("psychthemselvesup") and
relieves the administrator of responsibility when the pain
occurs.When the patient acknowledgesthe existenceof pain, Figure 13-23. Note ischemia (arrows) of palatal tissues pro
the administrator can consolethe patient with a shrug of the duced by pressure from the applicator stick.
shoulders and a kind word, once again confirming to both
the patient and the administrator that palatal injections
alwayshurt. pressure (dull and tolerable, not sharp and painful) (Fig.
However,palatal anesthesia can be achieved atraumati 13-23). Pressure anesthesia should be maintained during
cally.At best, patients are unaware of the needle penetration penetration of the soft tissues with the needle and must be
of soft tissuesand deposition of the local anesthetic solution maintained throughout the time the needle remains in the
(they won't even feel it). At worst, when the followingtech palatal soft tissues.
niques are adhered to, patients state that although they still Control overthe needle is probably of greater importance
were somewhat uncomfortable, this palatal injection was the in palatal anesthesia than in other intraoral injections.
least painful they had ever received To achieve this control, the administrator must secure a
With the introduction of computer-controlled localanes firm hand rest. Severalpositions are illustrated in Chapter
thetic delivery (C-CLAD) systems (The Wand, Comfort 11. When palatal anesthesia is administered, it is possible
Control Syringe,and STA[seeChapter SJ),deliveryof atrau on occasion to stabilize the needle with both hands (Fig.
matic palatal injections has become even more simplified.l" 13-24). Perfection of this technique is attained only with
The steps in the atraumatic administration of palatal experience.
anesthesia are as follows: The 27-gauge short needle is recommended for palatal
1. Provide adequate topical anesthesia at the site of needle injection techniques because patients are unable to distin
penetration. guish the "feel"between a 27- and a 30-gaugeneedle.7
2. Use pressure anesthesia at the site both before and Slowdeposition of the local anesthetic is important in all
during needle insertion and the deposition of solution. injection techniques, not only as a safetyfeature but also as
3. Maintain control over the needle. a means of providing an atraumatic injection.Becauseof the
4. Deposit the anesthetic solution slowly. density of the palatal soft tissuesand their firm adherence to
5. Trust yourself... that you can complete the procedure underlying bone, slow deposition is of even greater impor
atraumatically. tance here. Rapid injection of the solution produces high
Adequate topical anesthesia at the injection site can be tissue pressure, which tears the palatal soft tissues and leads
provided by allowingtopical anesthetic to remain in contact to both pain on injection and localized soreness when the
with the soft tissues for at least 2 minutes. The palate is the anesthetic actions are terminated. Slowinjection of the local
one area in the mouth where the cotton swab must be held anesthetic is not uncomfortable for the patient.
in position by the administrator the entire time. Probably the most important factor in providing an
Pressure anesthesia can be produced at the site of injec atraumatic palatal injection is the beliefbythe administrator
tion by applying considerablepressure to tissues adjacent to that it can be done painlessly;from this belief,specialcare is
the injection site with a firm object,such as the cotton appli then taken to minimize discomfort to the patient; this gener
cator stick previously used to apply the topical anesthetic. ally results in a more atraumatic palatal injection.
Other objects,such as the handle of a mouth mirror, are used Fivepalatal injections are described.Three-the anterior
by some, but because these objects are metal or plastic,they (or greater) palatine nerve block,providing anesthesiaof the
are more likely to hurt the patient. The goal is to produce posterior portions of the hard palate;the nasopalatine nerve
anesthesiaof the soft tissues through use of the gate control block, producing anesthesia of the anterior hard palate; and
theory of pain.6 The applicator stickshould be pressedfirmly local infiltration of the hard palate-are used primarily to
enough to produce ischemia (blanching) of the normally achievesoft tissue anesthesia and hemostasisbefore surgical
pink tissues at the penetration site and a feeling of intense procedures. None provides any pulpal anesthesia to the
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202 PARTIII Techniquesof RegionalAnesthesiain Dentistry
mucous
membrane
Indications
1. When palatal soft tissue anesthesia is necessaryfor
restorative therapy on more than two teeth (e.g.,with
subgingivalrestorations, with insertion of matrix bands
subgingivally)
2. For pain control during periodontal or oral surgical
procedures involvingthe palatal soft and hard tissues
Contraindications
1. Inflammation or infection at the injection site
2. Smallerareas of therapy (one or two teeth)
Advantages
Figure 13-24. Stabilization of the needle for (A) greater palatine 1. Minimizes needle penetrations and volume of solution
and (B) nasopalatine nerve block. With both injections, the barrel 2. Minimizes patient discomfort
of the syringe should rest against the patient's lower lip.
Disadvantages
1. No hemostasis exceptin the immediate area of injection
2. Potentiallytraumatic
maxillary teeth. AMSAand P-ASAare recently introduced
techniques that provide extensiveareas of pulpal and palatal Positive Aspiration. Lessthan 1%.
anesthesia.5'8
Alternatives
Greater Palatine Nerve Block 1. Local infiltration into specificregions
The greater palatine nerve block is useful for dental proce 2. Maxillarynerve block
dures involving the palatal soft tissues distal to the canine.
Minimum volumesof solution (0.45to 0.6 mL) provide pro Technique
found hard and soft tissue anesthesia.Although potentially 1. A 27-gaugeshort needle is recommended.
traumatic, the greater palatine nerve block is lessso than the 2. Area of insertion: soft tissue slightlyanterior to the
nasopalatine nerve block because tissues surrounding the greater palatine foramen
greater palatine foramen are not as firmly adherent to bone 3. Target area: greater (anterior) palatine nerve as it passes
and therefore are better able to accommodate the volume of anteriorly between soft tissues and bone of the hard
solution deposited. palate (Fig. 13-26)
4. Landmarks: greater palatine foramen and junction of
Other Common Name. Anterior palatine nerve block. the maxillary alveolarprocess and palatine bone
5. Path of insertion: advancethe syringe from the opposite
Nerve Anesthetized. Greater palatine. side of the mouth at a right angle to the target area
6. Orientation of the bevel:toward the palatal soft tissues
Areas Anesthetized. The posterior portion of the hard (Seesteps g and h, p. 204.)
palate and its overlying soft tissues, anteriorly as far as the 7. Procedure:
first premolar and medially to the midline (Fig. 13-25). a. Assumethe correct position (Fig. 13-27).
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CHAPTER13 Techniquesof MaxillaryAnesthesia 203
(1) For a right greater palatine nerve block, a (1) Place a cotton swab at the junction of the
right-handed administrator should sit facing the maxillary alveolarprocess and the hard palate.
patient at the 7 or 8 o'clock position. (2) Start in the region of the maxillary first molar
(2) For a left greater palatine nerve block, a right and palpate posteriorly by pressing firmly into
handed administrator should sit facing in the the tissues with the swab.
same direction as the patient at the 11 o'clock (3) The swab"falls"into the depression created by
position. the greater palatine fora.men(Fig. 13-29).
b. Ask the patient, who is in a supine position (Fig. (4) The fora.menis most frequently located distal to
13-28, A), to do the following: the maxillary second molar, but it may be
(1) Open wide. located anterior or posterior to its usual
(2) Extend the neck. position. (See"MaxillaryNerve Block,"p. 220.)
(3) Turn the head to the left or right (for improved cl. Prepare the tissue at the injection site,just 1 to 2 mm
visibility). anterior to the greater palatine fora.men.
c. Locate the greater palatine foramen (Fig. 13-28, B, (1) Clean and dry with sterile gauze.
and Table 13-2). (2) Applytopical antiseptic (optional).
(3) Applytopical anesthetic for 2 minutes.
e. After 2 minutes of topical anesthetic application,
move the swab posteriorly so it is directly over the
greater palatine foramen.
(1) Apply considerablepressure at the area of the
foramen with the swab in the left hand (if
right-handed).
(2) Note the ischemia (whitening of the soft tissues)
at the injection site.
TABLE 13-2
Location of the Greater Palatine Foramen*
Location No. Percent
Anterior half second molar 0 0
Posterior half second molar 63 39.87
Anterior half third molar 80 50.63
Posterior half third molar 15 9.49
From Malamed SF,1HegerN: lntraoral maxillary nerve block: an
anatomical and clinicalstudy,Anesth Prog 30:44-48, 1983.
*Measurementsfrom 158 skullswith the maxillary second and third
Figure 13·26. Target area for a greater palatine nerve block. molars present.
Figure 13·27. Position of the administrator for (A) right and (B) left greater palatine nerve block.
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204 PART III Techniques of Regional Anesthesia in Dentistry
Figure 13-30. Note the angle of needle entry into the mouth.
The insertion is into ischemictissues slightlyanterior to the appli
cator stick. The barrel of the syringe is stabilizedby the comer of
the mouth and the teeth.
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CHAPTER 13 Techniques of Maxillary Anesthesia 205
Safety Features
1. Contact with bone
2. Aspiration
Failures of Anesthesia
1. The greater palatine nerve block is not a technically
difficult injection to administer. The incidence of
success is well above 95%.
2. If local anesthetic is deposited too far anterior to the
foramen, adequate soft tissue anesthesia may not occur
in the palatal tissues posterior to the site of injection
Figure 13-32. Note the spread ofischemia (arrows) as the anes (partial success).
thetic is deposited. 3. Anesthesia on the palate in the area of the maxillary
first premolar may prove inadequate because of
overlapping fibers from the nasopalatine nerve (partial
success).
a. To correct: Local infiltration may be necessary as a
supplement in the area of inadequate anesthesia.
Complications
1. Few of significance
2. Ischemia and necrosis of soft tissues when highly
concentrated vasoconstricting solution used for
hemostasis over a prolonged period
a. Norepinephrine should never be used for hemostasis
on the palatal soft tissues (norepinephrine is not
available in dental local anesthetics in the United
States or Canada).
3. Hematoma is possible but rare because of the density
and firm adherence of palatal tissues to underlying
Figure 13-33. The cotton swab is removed when the deposition bone.
of solution ceases. 4. Some patients may be uncomfortable if their soft palate
becomes anesthetized; this is a distinct possibility when
the middle palatine nerve exits near the injection site.
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206 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Alveolar
mucous
membrane
Figure 13·34. Area anesthetized by a nasopalatine nerve block. Figure 13·35. Target area for a nasopalatine nerve block.
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CHAPTER13 Techniquesof MaxillaryAnesthesia 207
(3) Turn the head to the left or right for improved f. With the bevel lying against the tissue:
visibility (Fig. 13-37). (1) Apply enough pressure to bow the needle
c. Prepare the tissue just lateral to the incisivepapilla slightly.
(Fig. 13-38). (2) Deposit a small volume of anesthetic. The
(1) Clean and dry with sterile gauze. solution will be forced against the mucous
(2) Applytopical antiseptic (optional). membrane.
(3) Applytopical anesthetic for 2 minutes. g. Straighten the needle and permit the bevel to
d. After 2 minutes of topical anesthetic application, penetrate the mucosa.
move the swab directly onto the incisivepapilla (see (1) Continue to deposit small volumes of anesthetic
Figs. 13-38and 13-39). throughout the procedure.
(1) With the swab in your left hand (if right (2) Observe ischemia spreading into adjacent tissues
handed), apply pressure to the area of the as solution is deposited.
papilla. h. Continue to apply pressure with the cotton
(2) Note ischemia at the injection site. applicator stick while injecting the anesthetic.
e. Placethe bevel against the ischemic soft tissues at the i. Slowlyadvancethe needle toward the incisiveforamen
injection site. The needle must be well stabilizedto until bone is gentlycontacted (seeFig. 13-35).
prevent accidental penetration of tissues (see Fig. (1) The depth of penetration normally is not greater
13-39). than 5 mm.
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208 PART III Techniques of Regional Anesthesia in Dentistry
(2) Deposit small volumes of anesthetic while tissues palatal to the canine and the first premolar
advancing the needle. As the tissue is entered, could be inadequate.
resistanceto the deposition of solution is b. To correct: Localinfiltration may be necessaryas a
significantlyincreased;this is normal with the supplement in the area inadequately anesthetized.
nasopalatine nerve block.
j. Withdraw the needle 1 mm (to prevent Complications
subperiosteal injection). The bevel now lies over the 1. Fewof significance
center of the incisiveforamen. 2. Hematoma is possiblebut extremelyrare because of the
k. Aspirate in two planes. density and firm adherence of palatal soft tissues to
1. If negative,slowlydeposit (IS- to 30-second bone.
minimum) not more than one fourth of a cartridge 3. Necrosis of soft tissues is possiblewhen highly
(0.45 mL). concentrated vasoconstricting solution (e.g.,
(1) In some patients, it is difficultto deposit norepinephrine) is used for hemostasis over a
0.45 mL of anesthetic solution in this injection. prolonged period (norepinephrine is not availablein
Injection of anesthetic can ceasewhen the area dental local anesthetics in the United States or Canada).
of ischemia noted at the injection site has 4. Becauseof the density of soft tissues, anesthetic solution
expanded from that produced by the application may "squirt" back out the needle puncture site during
of pressure alone. administration or after needle withdrawal. (This is of
m. Slowlywithdraw the syringe. no clinicalsignificance.However,do not let it surprise
n. Make the needle safe. you into uttering a statement such as "Whoops!"that
o. Wait 2 to 3 minutes before commencing the dental might frighten the patient.)
procedure.
Technique {Multiple Needle Penetrations}
Signs and Symptoms 1. A 27-gaugeshort needle is recommended.
1. Subjective:numbness in the anterior portion of 2. Areas of insertion:
the palate a. Labialfrenum in the midline between the maxillary
2. Objective:no pain during dental therapy central incisors (Fig. 13-40,B)
b. Interdental papilla between the maxillary central
Safety Features incisors (Fig. 13-40,C)
1. Contact with bone c. If needed, palatal soft tissues lateral to the incisive
2. Aspiration papilla (Fig. 13-40,D)
3. Target area: incisiveforamen, beneath the incisive
Precautions papilla
1. Againstpain: 4. Landmarks: central incisors and incisivepapilla
a. Do not insert directly into the incisivepapilla (quite 5. Path of insertion:
painful). a. First injection: infiltration into the labial frenum
b. Do not deposit solution too rapidly. b. Second injection: needle held at a right angle to the
c. Do not deposit too much solution. interdental papilla
2. Against infection: c. Third injection: needle held at a 45-degree angle to
a. If the needle is advanced more than 5 mm into the the incisivepapilla
incisivecanal and the floor of the nose is entered 6. Orientation of the bevel:
accidentally,infection may result. There is no reason a. First injection: bevel toward bone
for the needle to enter the incisivecanal during a b. Second injection: not relevant
nasopalatine nerve block. c. Third injection: not relevant
7. Procedure:
Failures of Anesthesia a. First injection: infiltration of 0.3 mL into the labial
1. Highly successfulinjection (>95% incidence of success) frenum (see Fig. 13-40,B)
2. Unilateral anesthesia: (1) Prepare the tissue at the injection site.
a. If solution is deposited to one side of the incisive (a) Clean and dry with sterile gauze.
canal, unilateral anesthesia may develop. (b) Apply topical antiseptic (optional).
b. To correct: Reinsert the needle into the already (c) Apply topical anesthetic for 1 minute (Fig.
anesthetized tissue and reinject solution into the 13-40,A).
unanesthetized area. (2) Retract the upper lip to stretch tissues and
3. Inadequate palatal soft tissue anesthesia in the area of improve visibility.(Be careful not to overstretch
the maxillary canine and first premolar: the frenum.)
a. If fibers from the greater palatine nerve overlap those (3) Gently insert the needle into the frenum and
of the nasopalatine nerve, anesthesia of the soft deposit 0.3 mL of anesthetic in approximately 15
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CHAPTER 13 Techniques of Maxillary Anesthesia 209
Figure 13-40. A. Topical anesthetic is applied to the mucosa of the frenum. B, First injection, into the labial frenum. C, Second injection,
into the interdental papilla between the central incisors. D, Third injection, when anesthesia of the nasopalatine area is inadequate after the
first two injections.
seconds. (The tissue may balloon as solution is (c) With the patient's head extended backward,
injected.) you can see the ischemia produced by the
(4) Anesthesiaof soft tissue developsimmediately. local anesthetic and (on occasion) can
The aim of this first injection is to anesthetize see the needle tip as it nears the palatal
the interdental papilla between the two central aspect of the incisivepapilla. Care must be
incisors. taken to avoid needle puncturing through
b. Second injection: penetration through the labial the papilla into the oral cavity on the
aspect of the papilla between the maxillary central palatal side.
incisors toward the incisivepapilla (see Fig. 13-40,C) (4) Aspirate in two planes when ischemia is noted in
(1) Retract the upper lip gentlyto increase visibility. the incisivepapilla or when the needle tip
(Do not overstretchthe labial frenum.) becomes visiblejust beneath the tissue surface.If
(2) If a right-handed administrator, sit at 11 or 12 negative,administer no more than 0.3 mL of
o'clock facing in the same direction as the anesthetic solution in approximately 15 seconds.
patient. Tilt the patient's head toward the right There is considerable resistanceto the deposition
to provide a proper angle for needle penetration. of solution but no patient discomfort.
(3) Holding the needle at a right angle to the (5) Stabilizationof the syringe in this second
interdental papilla, insert it into the papilla just injection is somewhat awkward,but critical. Use
above the levelof crestal bone. of a finger from the other hand to stabilizethe
(a) Direct it toward the incisivepapilla (on the needle is recommended (Fig. 13-41).However,
palatal side of the interdental papilla). the syringe barrel must be held such that it
(b) Soft tissues on the labial surfacehave been remains within the patient's line of sight; this is
anesthetized by the first injection, so there is potentially disconcerting to some patients.
no discomfort. However,as the needle (6) Slowlywithdraw the syringe.
penetrates toward the unanesthetized palatal (7) Make the needle safe.
side, it becomes necessaryto administer (8) Anesthesiawithin the distribution of the right
minute amounts of local anesthetic to and left nasopalatine nerves usually developsin a
prevent discomfort. minimum of 2 to 3 minutes.
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210 PARTIII Techniques of Regional Anesthesia in Dentistry
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CHAPTER13 Techniquesof MaxillaryAnesthesia 211
Indications 7. Procedure:
1. Primarily for achievinghemostasis during surgical a. If a right-handed administrator, sit at the 10 o'clock
procedures position.
2. Palatogingivalpain control when limited areas of (1) Facetoward the patient for palatal infiltration
anesthesia are necessaryfor application of a rubber dam on the right side.
clamp, packing of retraction cord in the gingivalsulcus, (2) Face in the same direction as the patient for
or operative procedures on not more than two teeth palatal infiltration on the left side.
b. Ask the patient to do the following:
Contraindications (1) Open wide.
1. Inflammation or infection at the injection site (2) Extend the neck.
2. Pain control in soft tissue areas involvingmore than (3) Turn the head to the left or right for improved
two teeth visibility.
c. Prepare the tissue at the site of injection.
Advantages (1) Clean and dry with sterile gauze.
1. Provides acceptablehemostasis when a vasoconstrictor (2) Applytopical antiseptic (optional).
is used (3) Applytopical anesthetic for 2 minutes.
2. Provides a minimum area of numbness d After 2 minutes of topical anesthetic application,
place the swab on the tissue immediately adjacent to
Disadvantage. Potentiallytraumatic injection. the injection site.
(1) With the swab in your left hand (if right
Positive Aspiration. Negligible. handed), apply pressure to the palatal soft
tissues.
Alternatives (2) Observe the ischemia at the injection site.
1. For hemostasis:none e. Place the bevel of the needle against the ischemic
2. For pain control: nasopalatine or greater palatine nerve soft tissue at the injection site. The needle must be
block,AMSA,maxillary nerve block well stabilizedto prevent accidental penetration of
tissues.
Technique f. With the bevel lying against tissue:
1. A 27-gaugeshort needle is recommended. (1) Applyenough pressure to bow the needle slightly.
2. Area of insertion: the attached gingiva 5 to 10 mm from (2) Deposit a small volume of local anesthetic. The
the free gingivalmargin (Fig. 13-43) solution is forced against the mucous
3. Targetarea: gingivaltissues 5 to 10 mm from the free membrane, forming a droplet.
gingivalmargin g. Straighten the needle and permit the bevel to
4. Landmark: gingivaltissue in the estimated center of the penetrate mucosa.
treatment area (1) Continue to deposit small volumes of local
5. Pathwayof insertion: approaching the injection site at a anesthetic throughout this procedure.
45-degree angle (2) Ischemia of the tissues spreads as additional
6. Orientation of the bevel:toward palatal soft tissues anesthetic is deposited. (When this injection is
used for hemostasis,the vasoconstrictor in the
local anesthetic produces intense ischemia of
tissues.)
h. Continue to apply pressure with the cotton
applicator stick throughout the injection.
i. Continue to advance the needle and deposit
anesthetic until bone is gently contacted Tissue
thickness is only 3 to 5 mm in most patients.
j. If hemostasis is the goal in this technique, continue
to administer solution until ischemia encompasses
the surgical site. In usual practice, 0.2 to 0.3 mL of
solution is adequate.
k. For hemostasis of larger surgical sites:
(1) Removethe needle from the first injection site.
(2) Place it in the new injection site at the
periphery of the previously anesthetized tissue
(Fig. 13-44).
Figure 13-43. Areaof insertionand target area for a palatal (3) Penetrate the tissues and deposit anesthetic as in
infiltration. Step j. Topicalanesthetic may be omitted for
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212 PARTIII Techniquesof RegionalAnesthesiain Dentistry
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CHAPTER 13 Techniques of Maxillary Anesthesia 213
Figure 13-46. Anatomy of anterior middle superior alveolar (AMSA) nerve block. A, Palatal aspect: local anesthetic injected in area of
circle. B, Buccal aspect: local anesthetic injected on palatal side in area of circle.
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214 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Disadvantages
1. Requiresa slow administration (0.5 mL/min) time Figure 13-48. Prepuncturetechnique.
2. Can cause operator fatigue with a manual syringe
because of extended injection time
3. May be uncomfortable for the patient if administered
improperly d. Use comfortable arm and finger rests to avoid
4. May need supplemental anesthesia for central and fatigue during the extended administration time.
lateral incisor teeth e. Use of a C-CLADsystem is suggestedbecause it
5. May cause excessiveischemia if administered too makes this injection easierto administer.
rapidly f. Initial orientation of bevel is "face down" toward the
6. Use of local anesthetic containing epinephrine with a epithelium, while the needle is held at approximately
concentration of 1:50,000is contraindicated. a 45-degree angle with a tangent to the palate.
g. The final target is the bevel in contact with the
Positive Aspirations. Lessthan 1%. palatal bone.
h. A prepuncture technique can be utilized.Applythe
Alternatives bevel of the needle toward the palatal tissue. Place
1. Multiple supraperiosteal or PDL injections for each a sterile cotton applicator on top of the needle tip
tooth (Fig. 13-48).Applylight pressure on the cotton
2. ASAand MSAnerve blocks applicator to create a "seal"of the needle bevel
3. Maxillarynerve block against the outer surface.Initiate deliveryof the
local anesthetic to the surface of the epithelium.
Technique The objectiveis to force the solution through the
1. A 27-gaugeshort needle is recommended. outer epithelium into the surface tissue. The cotton
2. Area of insertion: on the hard palate about halfway applicator provides stabilization of the needle
along an imaginary line connecting the midpalatal and prevents any excesslocal anesthetic solution
suture to the free gingivalmargin; the location of the from dripping into the patient's mouth. When
line is at the contact point between the first and second a C-CLADsystem is used, a slow rate of delivery
premolars (approximately0.5 mL/min) is maintained during
3. Targetarea: palatal bone at injection site the entire injection. Maintain this position and
4. Landmarks:the intersecting point midway along a line pressure on the surface of the epithelium for 8 to
from the midpalatine suture to the free gingivalmargin 10 seconds.
intersecting the contact point between the first and i. An "anesthetic pathwaytechnique" can be utilized.
second premolars Veryslowlyadvance the needle tip into the tissue.
5. Orientation of the bevel:The bevel of the needle is Rotating the needle allowsthe needle to penetrate
placed "face down" against the epithelium. The needle is the tissue more efficiently,"Advancethe needle 1 to
typicallyheld at a 45-degree angle to the palate. 2 mm every 4 to 6 seconds while administering the
6. Procedure: anesthetic solution at the recommended slow rate.
a. Sit at the 9 or 10 o'clock position facing same Attempt to not expand the tissue or advancethe
direction as the patient. needle too rapidly if performing this with a manual
b. Position the patient supine with slight syringe.Use of a C-CLADsystem makes this process
hyperextension of the head and neck so you can considerablyeasier to perform.
visualizethe nasopalatine papilla more easily. j. After initial blanching is observed (approximately30
c. Use preparatory communication to inform the seconds), pause for severalsecondsto allow for
patient that the injection may take severalminutes to onset of superficialanesthesia.
administer, and that it may produce a sensation of k. Continue the slow insertion technique into the
firm pressure in the palate. palatal tissue. Orientation of the handpiece should
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CHAPTER13 Techniquesof MaxillaryAnesthesia 215
Precautions
1. Against pain:
a. Extremelyslow insertion of needle
b. Slowadministration during insertion with
simultaneous administration of anesthetic solution
c. C-CLADdevice recommended
2. Againsttissue damage:
a. Avoidexcessiveischemiaby avoidinglocal anesthetics
containing vasoconstrictorswith a concentration of
1:50,000.
b. Avoidmultiple infiltrations of local anesthetic with
vasoconstrictor in the same area at a single
Figure 13-49. Anteriormiddlesuperioralveolar(AMSA)nerve
appointment.
block.Notesyringeangulationfromoppositesideof mouth.
Failure of Anesthesia
1. May need supplemental anesthesia for central and
be from the contralateral premolars (Fig. 13-49). lateral incisors
The needle is advanced until contact with bone a. Adequate volume of anesthetic may not reach dental
occurs. branches.
1. Ensure that needle contact is maintained with the b. To correct: Add more anesthetic or supplement in
bony surface of the palate. The bevel of the needle proximity to these teeth from the palatal approach.
should face the surface of the bone.
m. Aspirate in two planes. Complications
n. Anesthetic is deliveredat a rate of approximately 1. Palatal ulcer at injection site developing 1 to 2 days
0.5 mL per minute during the injection for a total postoperatively
dosage of approximately 1.4to 1.8mL. a. Self-limiting
o. Advisethe patient that he or she will experiencea b. Heals in 5 to 10 days
sensation of firm pressure. c. Prevention includes slow administration to avoid
excessiveischemia.
Signs and Symptoms d. Avoidexcessiveconcentrations of vasoconstrictor
1. Subjective:A sensation of firmness and numbness is (e.g., 1:50,000).
experiencedimmediately on the palatal tissues. e. Avoidmultiple infiltrations of local anesthetic with
2. Subjective:Numbness of the teeth and associatedsoft vasoconstrictor in the same area at a single
tissues extends from the central incisor to the second appointment.
premolar on the side of the injection. 2. Unexpected contact with the nasopalatine nerve
3. Objective:Blanchingof the soft tissues (if a 3. Density of tissues at injection site causing squirt-back of
vasoconstrictor is used) of the palatal and facial anesthetic and bitter taste
attached gingivais evident, extending from the central a. Aspiratewhile withdrawing syringe from tissue.
incisor to the premolar region. b. Pause 3 to 4 secondsbefore withdrawing the needle
4. Objective:Use of electricalpulp testing with no to allow pressure to dissipate.
response from teeth with maximal EPT output (80/80} c. Instruct assistant to suction any excessanesthetic
5. Objective:Absenceof pain during treatment that escapesduring administration.
6. Objective:No anesthesia of the face and upper lip
occurs. Note: In some patients, additional anesthetic may
be necessary to supplement the incisor teeth. This can be Palatal Approach-Anterior Superior Alveolar
provided from a palatal approach or as individual PDL The palatal approach-anterior superior alveolar (P-ASA)
injections. injection, as with the AMSA injection, was defined by
Friedman and Hochman in conjunction with the clinical
Safety Features use and development of a C-CLAD system in the mid-
1. Contact with bone 1990s.4,s,sThe P-ASA injection shares several common
2. Lowrisk of positive aspiration elements with the nasopalatine nerve block but differs
3. Slowinsertion of needle (1 to 2 mm every 4 to 6 sufficientlyto be considered a distinct identity. The P-ASA
seconds) uses a similar tissue point of entry (lateral aspect of the
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216 PARTIII Techniquesof RegionalAnesthesiain Dentistry
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CHAPTER13 Techniquesof MaxillaryAnesthesia 217
5. Eliminates the postoperative inconvenience of b. Position the patient supine with slight
numbness to the upper lip and muscles of facial hyperextension of the head and neck so you can
expression visualizethe nasopalatine papilla more easily.
6. Can be performed comfortably with a C-CLAD system c. Use preparatory communication to inform the
patient that the injection may take severalminutes to
Disadvantages administer and may produce a sensation of firm
1. Requiresslow administration (0.5 mL/min) pressure in the palate.
2. Operator fatigue with a manual syringe because of d. Use comfortable arm and finger rests to prevent
extended injection time fatigue during the extended administration time.
3. May be uncomfortable for the patient if administered e. Use of a C-CLADsystem makes this injection easier
improperly to administer.
4. May require supplemental anesthesia for canine teeth f. Initial orientation of bevel is "face down" against the
5. May cause excessiveischemia if administered too epithelium, while the needle is held at approximately
rapidly a 45-degree angle with a tangent to the palate.
6. Use of local anesthetic containing epinephrine with g. A prepuncture technique can be utilized. Place the
a concentration of 1:50,000is contraindicated. bevel of the needle against the palatal tissue. Place
a sterile cotton applicator on top of the needle tip
Positive Aspiration. Lessthan 1% (assumed from data on (see Fig. 13-48).Applylight pressure on the cotton
nasopalatine block). applicator to create a "seal"of the needle bevel
against the outer surface.Initiate deliveryof the
Alternatives anesthetic solution to the surface of the epithelium.
1. Supraperiostealor PDL injections for each tooth The objectiveis to force the solution through the
2. Right and left (bilateral) ASAnerve blocks outer epithelium into the tissue.Allowanesthetic
3. Right and left (bilateral) maxillary nerve blocks solution to be deliveredthrough the layer of the
outer epithelium. The cotton applicator provides
Technique stabilization of the needle and prevents any excess
1. A 27-gaugeshort needle is recommended. dripping of anesthetic solution into the patient's
2. Area of insertion: just lateral to the incisivepapilla in mouth. When a C-CLADdeviceis used, a slow rate
the papillary groove (Fig. 13-51) of delivery (approximately0.5 mL/min) is
3. Targetarea: nasopalatine foramen maintained throughout injection. Maintain this
4. Landmarks: nasopalatine papilla position and pressure on the surface of the
5. Orientation of the bevel:The bevel of the needle is epithelium for 8 to 10 seconds.
placed "face down" against the epithelium. The needle h. An anesthetic pathwaytechnique can be utilized.
is typicallyheld at a 45-degree angle to the palate. Veryslowlyadvance the needle into the tissue.
6. Procedure: Rotating the needle allowsthe needle to penetrate
a. Sit at the 9 or 10 o'clock position facing in the same the tissue more efficiently.Advancethe needle 1 to
direction as the patient. 2 mm every 4 to 6 seconds while administering
the anesthetic solution at the recommended (slow)
rate. Avoidexpanding the tissue or advancingthe
needle too rapidly if performing the P-ASAwith a
traditional syringe.It is at this step where a C-CLAD
system makes the process easier to achieve.
i. After initial blanching is observed (approximately
30 seconds), pause for severalseconds to permit
onset of superficialanesthesia.
j. Continue the slow insertion technique into the
nasopalatine canal. Orientation of the needle should
be parallel to the long axis of the central incisors.
The needle is advanced to a depth of 6 to 10 mm
(Fig. 13-52).Note: If resistance is encountered before
the final depth of penetration is reached, do not force
the needle forward. Withdraw it slightly and reorient it
to minimize the risk of penetration of the floor of the
nose.
k. Ensure that the needle is in contact with the inner
Figure 13-51. Palatal approach-anterior superior alveolar bony wall of the canal. (A well-definednasopalatine
(P-ASA)area of needle insertion. canal may not be present in some patients.)
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218 PART III Techniques of Regional Anesthesia in Dentistry
Safety Features
1. Contact with bone
2. Minimal aspiration rate
3. Slowneedle insertion (1to2 mm every 4 to 6 seconds)
4. Slowadministration (0.5 mL/min) oflocal anesthetic
5. Lessanesthetic volume than necessaryif administered
via traditional injections
Precautions
1. Against pain:
a. Extremelyslow insertion
b. Slowadministration during insertion with
simultaneous administration of anesthetic solution
(creating an anesthetic pathway)
c. Consider use of a C-CLADsystem.
2. Againsttissue damage
Figure 13·52. Palatal approach-anterior superior alveolar a. Avoidexcessiveischemiaby not using drugs
(P-ASA)orientation of syringe. containing epinephrine in a concentration of
1:50,000.
b. Avoidmultiple infiltrations of local anesthetic with
vasoconstrictor in the same area at a single
1. Aspirate in two planes within the canal space to appointment.
avoid intravascular injection.
m. Anesthetic is deliveredat a rate of approximately Failure of Anesthesia
0.5 mL during the injection to a total volume of 1. Highly successfulinjection for maxillary incisors
1.4to 1.8mL. Advisethe patient that he or she 2. May need supplemental anesthesia for canines
will experiencea sensation of firm pressure. in patients with long roots
Note: It has been reported that in a small percentage a. Adequate volume of anesthetic may not reach dental
of cases, needle insertion can stimulate the branches.
nasopalatine nerve (similar to contacting a nerve b. To correct: Add more anesthetic or supplement
during an inferior alveolar block). This may be an in proximity to the canine teeth from the palatal
unsettling surprise to the patient (and the operator) approach.
if it occurs. Reassure the patient with verbal support 3. Unilateral anesthesia
that this is not uncommon and is not a problem. a. Look for bilateral blanching.
If this should occur, reposition the needle and b. To correct: Administer additional anesthetic.
continue to administer the anesthetic before
advancing farther. Complications
1. Palatal ulcer at injection site developing 1 to 2 days
Signs and Symptoms postoperatively
1. Subjective:A sensation of firmness and anesthesia is a. Self-limiting
immediately experiencedin the anterior palate. b. Heals in 5 to 10 days
2. Subjective:Numbness of the teeth and associatedsoft c. Prevention includes slow administration to avoid
tissues extends from the right to the left canine. excessiveischemia.
3. Objective:Ischernia (blanching) of the soft tissues (if a d. Avoidexcessiveconcentrations of vasoconstrictor
vasoconstrictor is used) of the palatal and the facial (e.g., 1:50,000)
attached gingivais evident extending from the right to 2. Unexpected contact with the nasopalatine nerve
the left canine region. 3. Density of soft tissues at injection site causing squirt
4. Objective:Use of electricalpulp testing with no back of anesthetic and bitter taste
response from teeth with maximal EPT output (80/80) a. Aspiratewhile withdrawing syringe from tissue.
5. Objective:Absenceof pain during treatment b. Pause 3 to 4 secondsbefore withdrawing the needle
6. Objective:No anesthesia of the face and upper lip to allow pressure to dissipate.
occurs. Note: In patients with long canine roots, c. Instruct assistant to suction any excessanesthetic
additional local anesthetic may be needed. This can be that escapesduring administration.
provided through a palatal approach at a point that
approximates the canine root tips. Maxillary Nerve Block
a. In rare instances, a facial approach (traditional) The maxillary(seconddivisionor V2) nerveblock is an effec
supraperiosteal injection may be necessaryfor the tivemethod of achievingprofound anesthesiaof a hemimax
canine teeth. illa. It is useful in procedures involving quadrant dentistry
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CHAPTER13 Techniquesof MaxillaryAnesthesia 219
3. Uncooperativepatients
4. Inflammation or infection of tissues overlyingthe
injection site
5. When hemorrhage is risky (e.g.,in a hemophiliac)
6. In the greater palatine canal approach: inability to gain
accessto the canal;bony obstructions may be present in
5% to 15% of canals
Advantages
Greater Palatal soft
tissue
1. Atraumatic injection via the high-tuberosity approach
palatine I 11~ e
foramen and bone 2. High successrate (>95%)
3. Positiveaspiration is less than 1% {greaterpalatine
canal approach).
Figure 13-53. Areas anesthetized by a maxillary nerve block.
4. Minimizesthe number of needle penetrations necessary
for successfulanesthesia of the hemimaxilla (minimum
of four via PSA,infraorbital, greater palatine, and
and in extensive surgical procedures. Two approaches are nasopalatine)
presented here. Both are effective, and the author does 5. Minimizestotal volume of local anesthetic solution
not maintain a preference for either one. Major difficulties injected to 1.8versus 2.7 mL
with the greater palatine canal approach involve locating 6. Neither high-tuberosity nor greater palatine canal
the canal and negotiating it successfully.The major difficulty approach is usuallytraumatic.
in the high-tuberosity approach is the higher incidence of
hematoma. Disadvantages
1. Risk of hematoma, primarily with the high-tuberosity
Other Common Names. Second division block, V2 nerve approach.
block. 2. High-tuberosity approach is relativelyarbitrary.
Overinsertion is possiblebecause of the absence of bony
Nerve Anesthetized. Maxillary division of the trigeminal landmarks if proper technique is not followed.
nerve. 3. Lack of hemostasis:If necessary,this necessitates
infiltration with vasoconstrictor-containinglocal
Areas Anesthetized. (Fig. 13-53) anesthetic at the surgical site.
1. Pulpal anesthesia of the maxillary teeth on the side of 4. Pain: The greater palatine canal approach is potentially
the block (although not usually) traumatic.
2. Buccalperiodontium and bone overlyingthese teeth
3. Soft tissues and bone of the hard palate and part of the Alternatives. Toachievethe same distribution of anesthesia
soft palate, medial to midline present with a maxillary nerve block, all of the following
4. Skin of the lower eyelid,side of the nose, cheek, and must be administered:
upper lip 1. PSAnerve block
2. ASAnerve block
Indications 3. Greater palatine nerve block
1. Pain control before extensiveoral surgical,periodontal, 4. Nasopalatine nerve block
or restorative procedures requiring anesthesia of the
entire maxillary division Technique {High-Tuberosity Approach). (Fig. 13-54)
2. When tissue inflammation or infection precludes the 1. A 25-gaugelong needle is recommended. A 27-gauge
use of other regional nerve blocks (e.g.,PSA,ASA, long is acceptable.
AMSA,P-ASA)or supraperiosteal injection 2. Area of insertion: height of the mucobuccal fold above
3. Diagnostic or therapeutic procedures for neuralgias or the distal aspect of the maxillary second molar
tics of the second division of the trigeminal nerve 3. Target area:
a. Maxillarynerve as it passesthrough the
Contraindications pterygopalatine fossa
1. Inexperienced administrator b. Superior and medial to the target area of the PSA
2. Pediatric patients nerve block
a. More difficultbecause of smaller anatomic 4. Landmarks:
dimensions a. Mucobuccalfold at the distal aspect of the maxillary
b. A cooperativepatient is needed. second molar
c. Usuallyunnecessary in children because of the b. Maxillarytuberosity
high successrate of other regional block c. Zygomaticprocess of the maxilla
techniques 5. Orientation of the bevd: toward bone
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220 PART III Techniques of Regional Anesthesia in Dentistry
6. Procedure:
a. Measure the length of a long needle from the tip to
the hub (average,32 mm, but varies by
manufacturer).
b. Assume the correct position.
(1) For a left high-tuberosity injection, a right
handed administrator should sit at the 10
o'clock position facing the patient (see Figure
13-8,A).
(2) For a right high-tuberosity injection, a right
handed administrator should sit at the 8 o'clock
position facing the patient (see Figure 13-8,B). Figure 13-55. A, Maxillary nerve block, greater palatine canal
c. Position the patient supine or semisupine for the approach. Note the direction of the needle and the syringe barrel
right or left block. into the canal.B, Seconddivisionnerve block (V2), greater palatine
cl. Prepare the tissue in the height of the mucobuccal canal approach. Note the location of the needle tip in the pterygo
fold at the distal of the maxillary second molar. palatine fossa (circle).
(1) Dry with sterile gauze.
(2) Applytopical antiseptic (optional).
(3) Applytopical anesthetic.
e. Partiallyopen the patient's mouth; pull the mandible (2) If negative:
toward the side of injection. (a) Slowly(more than 60 seconds) deposit
f. Retract the cheek in the injection area with your 1.8 mL.
index finger to increase visibility. (b) Aspirate severaltimes during injection.
g. Pull the tissues taut with this finger. L Withdraw the syringe.
h. Placethe needle into the height of the mucobuccal m. Mairethe needle safe.
fold over the maxillary second molar. n. Wait a minimum of 3 to 5 minutes before
i. Advancethe needle slowlyin an upward, inward, and commencing the dental procedure.
backward direction as described for the PSAnerve
block {p. 191). Technique (Greater Palatine canal Approach). (Fig.13-55)
j. Advancethe needle to a depth of 30 mm. 1. A 25-gaugelong needle is recommended. A 27-gauge
(1) No resistanceto needle penetration should be long needle is also acceptable.
felt. If resistanceis felt, the angle of the needle in 2. Area of insertion: palatal soft tissue directly over
toward the midline is too great. the greater palatine foramen
(2) At this depth (30 mm), the needle tip should lie 3. Target area: the maxillary nerve as it passes through
in the pterygopalatine fossa in proximity to the the pterygopalatine fossa;the needle passesthrough the
maxillary division of the trigeminal nerve. greater palatine canal to reach the pterygopalatine fossa
k. Aspirate in two planes. 4. Landmark: greater palatine foramen, junction of the
(1) Rotate the syringe (needle bevel) one fourth turn maxillary alveolarprocess and the palatine bone
and reaspirate. 5. Orientation of the bevel:toward palatal soft tissues
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CHAPTER13 Techniquesof MaxillaryAnesthesia 221
6. Procedure:
a. Measure the length of a long needle from the tip to
the hub (average, 32 mm, but varies by
manufacturer).
b. Assume the correct position.
(1) For a right greater palatine canal V2 block, sit
facing toward the patient at the 7 or 8 o'clock
position.
(2) For a left greater palatine canal V2 block, sit
facing in the same direction as the patient at
the 10 or 11 o'clock position.
c. Ask the patient, who is supine, to do the following:
(1) Open wide.
(2) Extend the neck.
(3) Tum the head to the left or right (to improve Figure 13-56. Maxillary nerve block, greater palatine canal
visibility). approach.
d. Locatethe greater palatine foramen.
(1) Place a cotton swab at the junction of the
maxillary alveolarprocess and the hard palate.
(2) Start in the region of the second molar and
TABLE 13-3
palpate by pressing posteriorly into the tissues
Angle of the Greater Palatine Foramen to
with the swab.
the Hard Palate
(3) The swab "falls"into the depression created by
the greater palatine foramen. Angle, degrees n = 199 Percent
(4) The foramen is most frequently located at the 20-22.5 2 1.005
distal aspect of the maxillary second molar 25-27.5 4 2.01
(see Table 13-2). 30-32.5 18 9.045
e. Prepare the tissues directly over the greater palatine 35-37.5 28 14.07
40-42.5 25 12.56
foramen.
45-47.5 34 17.08
(1) Clean and dry with sterile gauze.
50-52.5 34 17.08
(2) Applytopical antiseptic (optional). 55-57.5 29 14.57
{3) Applytopical anesthetic for 2 minutes. 60-62.5 17 8.54
f. After 2 minutes of topical anesthetic application, 65-67.5 7 3.51
move the swab posteriorly so it lies just behind the 70 1 0.50
greater palatine foramen.
From Malamed SF,1Heger N: Intraoral maxillary nerve block: an
(1) Applypressure to the tissue with the cotton anatomical and clinical study, Anesth Prog 30:44--48, 1983.
swab,held in the left hand (if right-handed).
(2) Note ischemia at the injection site.
g. Direct the syringe into the mouth from the opposite
side with the needle approaching the injection site at k. Continue to apply pressure with the cotton
a right angle (Fig. 13-56). applicator stick during this part of the procedure.
h. Placethe bevel against the ischemic soft tissue at The greater palatine nerve block is now complete.
the injection site. The needle must be well 1. Probe gently for the greater palatine foramen.
stabilizedto prevent accidental penetration of the (1) The patient feelsno discomfort because of the
tissues. previously deposited anesthetic solution.
i. With the bevel lying against the tissue: (2) The angle of the needle and syringe may be
(1) Apply enough pressure to bow the needle changed if needed.
slightly. {3) The needle usually must be held at a 45-degree
(2) Deposit a small volume oflocal anesthetic. The angle to facilitate entry into the greater palatine
solution is forced against the mucous membrane, foramen (Table 13-3).
forming a droplet. m. After locating the foramen, very slowlyadvance the
j. Straighten the needle and permit the bevel to needle into the greater palatine canal to a depth of
penetrate the mucosa. 30 mm. Approximately5% to 15% of greater
(1) Continue to deposit small volumes of anesthetic palatine canals have bony obstructions that prevent
throughout the procedure. passageof the needle.
(2) Ischemia spreads into adjacent tissues as the (1) Never attempt to force the needle against
anesthetic is deposited. resistance.
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222 PART III Techniques of Regional Anesthesia in Dentistry
(2) If resistance is felt, withdraw the needle slightly d. The greater palatine canal approach usually is
and slowly attempt to advance it at a different successfulif the long dental needle has been
angle. advanced at least two thirds of its length into the
(3) If the needle cannot be advanced farther and canal.
the depth of penetration is almost adequate,
continue with the next steps; however, if the Complications
depth is considerably deficient, withdraw the 1. Hematoma developsrapidly if the maxillary artery is
needle and discontinue the attempt. punctured during maxillary nerve block via the high
n. Aspirate in two planes. tuberosity approach. (Referto discussion of PSAnerve
(1) Rotate the needle one fourth turn and block, complications,p. 195.)
reaspirate. 2. Penetration of the orbit may occur during a greater
(2) If negative, slowly deposit 1.8 mL of solution palatine foramen approach if the needle goes in too far;
over a minimum of 1 minute. more likelyto occur in the smaller-than-averageskull
o. Withdraw the syringe. 3. Complications produced by injection of local anesthetic
p. Make the needle safe. into the orbit include the following*:
q. Wait a minimum of 3 to 5 minutes before a. Volumedisplacement of the orbital structures,
commencing the dental procedure. producing periorbital swellingand proptosis
b. Regionalblock of the sixth cranial nerve (abducens),
Signs and Symptoms producing diplopia
1. Subjective:Pressurebehind the upper jaw on the side c. Classicretrobulbar block, producing mydriasis,
being injected; this usually subsides rapidly,progressing corneal anesthesia,and ophthalmoplegia
to tingling and numbness of the lower eyelid,side of the d. Possibleoptic nerve block with transient loss of
nose, and upper lip vision (Amaurosis)
2. Subjective:Sensation of numbness in the teeth and e. Possibleretrobulbar hemorrhage
buccal and palatal soft tissues on the side of f. To prevent intraorbital injection: Strictly adhere to
injection protocol and modify your technique for the smaller
3. Objective:Use of electricalpulp testing with no patient.
response from teeth with maximal EPT output (80/80) 4. Penetration of the nasal cavity
4. Objective:Absenceof pain during treatment a. If the needle deviates medially during insertion
through the greater palatine canal, the paper-thin
Safety Feature. Careful adherence to technique. medial wall of the pterygopalatine fossa is penetrated
and the needle enters the nasal cavity.
Precautions (1) On aspiration, large amounts of air appear in the
1. Pain on insertion of the needle, primarily with the cartridge.
greater palatine canal approach; prevent by using (2) On injection, the patient complains that local
atraumatic palatal injection protocol anesthetic solution is running down his or her
2. Overinsertion of the needle; can occur with both throat.
approaches (although much less likelywith the greater (3) To prevent: Keepthe patient's mouth wide open
palatine canal approach); prevent through careful and take care during penetration that the
adherence to protocol advancing needle staysin the correct plane.
3. Resistanceto needle insertion in the greater palatine (4) To prevent: Do not force needle if resistanceis
canal approach; never try to advance a needle against encountered.
resistance Table 13-4summarizes the indications for maxillarylocal
anesthesia.Table 13-5includes volumes of solutions recom
Failures of Anesthesia mended for maxillary injections.
1. Partial anesthesia;may result from underpenetration by
needle. To correct: Reinsert the needle to proper depth,
SUMMARY
and reinject.
2. Inability to negotiate the greater palatine canal. Providing clinically adequate anesthesia in the maxilla is
To correct: rarely a problem. The thin and porous bone of the maxilla
a. Withdraw the needle slightlyand reangulate it. permits the ready diffusion of local anesthetic to the apex of
b. Reinsert carefullyto the proper depth. the tooth to be treated. For this reason, many dentists rely
c. If unable to bypass the obstruction easily,withdraw
the needle and terminate the injection. *It has been reported that complications a, b, and c were most
(1) The high-tuberosity approach may prove more common after intraorbital injection; complications d and e were never
successfulin this situation. encountered.1•.2•
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CHAPTER13 Techniquesof MaxillaryAnesthesia 223
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15. N"u:hollcm Jw. Bmy TG, Smmmtt JB. et al: Pain pen:eption 18. PulmJama H, Yolbikawa 1\ lC'obaleH, et al: BffiaK:y of AMSA
and utility: ammparilcm of the qrinp and mmputem.ed1oc:al anesthesia Ulins a ncw injection .,mm. the Wand. Quhrt Int
injection tec:lmiqua, Gm. Dent 49:167-172, 2001. 34:537-541, 2003.
16. ffoc:hman MN, CliliuelJo D, ffodiman C, et al: Computcrir.ecl 19. Malamecl SP, 'nUpr N: Intramal maillary nerw= block:
1oc:alanesthesia w traditional qrinp tedmique: mbjectift an anatmnical and clinical stud}\ Anath Pros 30:44-48,
pain mpome, NYSDJ63:2t-29, UJ97. 1983.
17. N"u:hollcmJw. Bmy TG, Smmmtt JB. et al: Pain pen:eption 20. Poon TB, CAmey PMT: Mu:iDary nerw=block: a ueful tech
and utility: a mmparilcm of the qrinp and mmputem.ed1oc:al nique, 1OnlSmg31:74:9-755, 1973.
injection tec:lmiqua, Gm. Dent 49:167-172, 2001.
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Techniques of
Mandibular Anesthesia
Providingeffectivepain control is one of the most important the inferior alveolarneurovascularbundle or the mandibular
aspects of dental care. Indeed, patients rate a dentist "who foramen revealedthat accurate needle location did not guar
does not hurt" and one who can "givepainlessinjections" as antee successfulpain control.14The central core theory best
meeting the second and first most important criteria used in explainsthis problem.F" Nerveson the outside of the nerve
evaluatingdentists.1Unfortunately,the abilityto obtain con bundle supply the molar teeth, while nerves on the inside
sistently profound anesthesia for dental procedures in the (core fibers) supply incisor teeth. Therefore the local anes
mandible has proved extremelyelusive.This is even more of thetic solution deposited near the IANmay diffuseand block
a problem when infected teeth are involved,primarily man the outermost fibers but not those located more centrally,
dibular molars. Anesthesia of maxillary teeth on the other leading to incomplete mandibular anesthesia.
hand, although on occasion difficultto achieve,is rarely an This difficulty in achieving mandibular anesthesia has
insurmountable problem. Reasons for this include the fact over the years led to the development of alternative
that the cortical plate of bone overlying maxillary teeth is techniques to the traditional (Halsted approach) inferior
normally quite thin, thus allowingthe local anesthetic drug alveolar nerve block. These have included the Gow-Gates
to diffuse when administered by supraperiosteal injection mandibular nerve block,17 the Akinosi-Vazirani closed
(infiltration). Additionally, relatively simple nerve blocks, mouth mandibular nerve block,18the periodontal ligament
such as the posterior superior alveolar (PSA),middle supe (PDL, intraligamentary) injection,19 intraosseous anes
rior alveolar (MSA),anterior superior alveolar (ASA,infra thesia," and, most recently, buffered local anesthetics.21
orbital), and anterior middle superior alveolar(AMSA),2are Although all maintain some advantagesover the traditional
availableas alternativesto infiltration. Halsted approach, none is without its own faults and
It is commonly stated that the significantlyhigher failure contraindications.
rate for mandibular anesthesia is related to the thickness of Six nerve blocks are described in this chapter. Two of
the cortical plate of bone in the adult mandible. Indeed it is these-involving the mental and buccal nerves-provide
generallyacknowledgedthat mandibular infiltration is suc regional anesthesiato soft tissues only and have exceedingly
cessfulin cases where the patient has a full primary denti high successrates. In both instances,the nerve anesthetized
tion.3'4Once a mixed dentition develops,it is a general rule liesdirectlybeneath the softtissues,not encasedin bone. The
of teaching that the mandibular cortical plate of bone has four remaining blocks-inferior alveolar, incisive, Gow
thickened to the degree that infiltration might not be effec Gates mandibular, and Vazirani-Akinosi (closed-mouth)
tive,leadingto the recommendation that "mandibular block'' mandibular-provide regional anesthesia to the pulps of
techniques should now be employed.5 some or all of the mandibular teeth in a quadrant. Three
A second difficultywith the traditional Halsted approach other injections of importance in mandibular anesthesia
to the inferior alveolarnerve (IAN) (i.e.,"mandibular block,'' periodontal ligament, intraosseous, and intraseptal-are
or IANB) is the absence of consistent landmarks. Multiple described in Chapter 15. Although these supplemental tech
authors have described numerous approaches to this often niques can be used successfullyin the maxilla or the man
times elusivenerve.r" Indeed, reported failure rates for the dible, their greatest utility lies in the mandible, because in
IANB are commonly high, ranging from 31% and 41% in the mandible, they can provide pulpal anesthesia of a single
mandibular second and first molars to 42%, 38%, and 46% tooth without providingthe accompanyinglingualand facial
in second and first premolars and canines,respectively,9and soft tissue anesthesia that occurs with other mandibular
81 % in lateral incisors." nerve block techniques.
Not only is the inferior alveolar nerve elusive, studies The success rate of the inferior alveolar nerve block is
using ultrasound" and radiography12·13 to accurately locate considerably lower than that of most other nerve blocks.
225
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226 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Because of anatomic considerations in the mandible (pri Recentworkwith mandibular infiltration in adult patients
marily the density of bone), the administrator must accu with the local anesthetic drug articaine HCl has demon
rately deposit local anestheticsolution to within 1 mm of the strated significant rates of success in mandibular anterior
target nerve. The inferior alveolarnerve block has a signifi teeth in lieu of block injection.22-24 When articaine HCl is
cantly lower successrate because of two factors-anatomic administered by buccal infiltration in the adult mandible
variation in the height of the mandibular foramen on the following IANB, success rates are even greater.25•26 The
lingual aspect of the ramus, and the greater depth of soft concept of mandibular infiltration in adult patients will be
tissue penetration necessary-that lead to greater inaccu discussed in depth in Chapter 20.
racy.Fortunately,the incisivenerve block can provide pulpal
anesthesiato the teeth anterior to the mental foramen (e.g.,
incisors, canines, first premolars, and [in most instances]
INFERIOR ALVEOLAR NERVE BLOCK
second premolars). The incisive nerve block is a valuable The inferior alveolar nerve block (IANB), commonly (but
alternative to the inferior alveolar nerve block when treat inaccurately) referred to as the mandibular nerve block, is
ment is limited to these teeth. To achieve anesthesia of the the second most frequentlyused (after infiltration) and pos
mandibular molars, however, the inferior alveolar nerve sibly the most important injection technique in dentistry.
must be anesthetized,and this frequently entails (with all its Unfortunately,it also provesto be the most frustrating, with
attendant disadvantages) a lower incidence of successful the highest percentageof clinicalfailuresevenwhen properly
anesthesia. administered.6-10
The third injection technique that provides pulpal anes It is an especiallyuseful technique for quadrant dentistry.
thesiato mandibular teeth, the Gow-Gatesmandibular nerve A supplemental block (buccal nerve) is needed only when
block, is a true mandibular block injection, providing soft tissue anesthesiain the buccal posterior region is neces
regional anesthesia to virtually all sensory branches of V3• sary.On rare occasions,a supraperiosteal injection (infiltra
In actual fact, the Gow-Gates may be thought of as a tion) may be needed in the lower incisor region to correct
(very) high inferior alveolar nerve block. When used, two partial anesthesia caused by the overlap of sensory fibers
benefits are seen: (1) the problems associatedwith anatomic from the contralateral side. A periodontal ligament (PDL)
variations in the height of the mandibular foramen are injection might be necessarywhen isolatedportions of man
obviated, and (2) anesthesia of the other sensory branches dibular teeth (usually the mesial root of a first mandibular
of V3 (e.g., the lingual, buccal, and mylohyoid nerves) is molar) remain sensitiveafter an otherwisesuccessfulinferior
usually attained along with that of the inferior alveolar alveolarnerve block. lntraosseous anesthesia (IO) is a sup
nerve. With proper adherence to protocol (and experience plemental technique employed,usuallyon molars, when the
using this technique), a success rate in excessof 95% can IANB has proven ineffective,primarily when the tooth is
be achieved. pulpally involved.
Another V3 nerve block, the closed-mouth mandibular Administration of bilateral IANBsis rarely indicated in
nerve block,is included in this discussion,primarily because dental treatments other than bilateral mandibular surgeries.
it allowsthe doctor to achieveclinicallyadequate anesthesia They produce considerable discomfort, primarily from the
in an extremely difficult situation-one in which a patient lingual soft tissue anesthesia, which usually persists for
has limited mandibular opening as a result of infection, several hours after injection (the duration is dependent on
trauma, or postinjection trismus. It is also known as the the particular localanesthetic used). The patient feelsunable
Vazirani-Akinosi technique (after the two doctors who to swallow and, because of the absence of all sensation, is
developedit independent of each other). Somepractitioners more likelyto self-injurethe anesthetized soft tissues.Addi
use it routinely for anesthesia in the mandibular arch. The tional residual soft tissue anesthesia affects the patient's
closed-mouth technique is described mainly because with ability to speak and to swallow.When possible, it is prefer
experience it can provide a successrate of better than 80% able to treat the entire right or left side of a patient's oral
in situations (extremetrismus) in which the inferior alveolar cavity (maxillary and mandibular) at one appointment
and Gow-Gatesnerve blocks have little or no likelihood of rather than administer a bilateral IANB.Patients are much
success. more capable of handling the posttreatment discomfort
In ideal circumstances, the individual who is to admi (e.g., feeling of anesthesia) associated with bilateral maxil
nister the local anesthetic should be familiar with each of lary than with bilateral mandibular anesthesia.
these techniques. The greater the number of techniques at One situation in which bilateral mandibular anesthesiais
one's disposal with which to attain mandibular anesthesia, frequently used involvesthe patient who presents with six,
the less likely it is that a patient will be dismissed from an eight, or ten lower anterior teeth (e.g., canine to canine;
office as a result of inadequate pain control. More realisti premolar to premolar) requiring restorative or soft tissue
cally,however,the administrator should become proficient procedures. Twoexcellentalternativesto bilateral IANBsare
with at least one of these procedures and should have a bilateral incisivenerve blocks (wherelingual soft tissue anes
working knowledgeof the others to be ableto use them with thesia is not necessary)and unilateral inferior alveolarblocks
a good expectation of successshould the appropriate situa on the side that has the greater number of teeth requiring
tion arise. restoration or that requires the greater degree of lingual
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CHAPTER 14 Techniques of Mandibular Anesthesia 227
Lingual soft
tissue
and bone
intervention, combined with an incisive nerve block on the 2. Patients who are more likelyto bite their lip or tongue,
opposite side. It must be remembered that the incisive nerve for instance, a very young child or a physicallyor
block does not provide lingual soft tissue anesthesia; thus mentally handicapped adult or child
lingual infiltration may be necessary. Infiltration of articaine
HCl in the mandibular incisor region on both the buccal and Advantages. One injection provides a wide area of anes
lingual aspects of the tooth has been associated with consid thesia (useful for quadrant dentistry).
erable success in providing pulpal anesthesia. 22
In the followingdescription of the inferior alveolarnerve Disadvantages
block, the injection site is noted to be slightly higher than 1. Wide area of anesthesia (not indicated for localized
that usually depicted. procedures)
2. Rate of inadequate anesthesia (31 % to 81%)
Other Common Names. Mandibular block. 3. Intraoral landmarks not consistentlyreliable
4. Positiveaspiration (10% to 15%, highest of all intraoral
Nerves Anesthetized injection techniques)
1. Inferior alveolar,a branch of the posterior division of 5. Lingual and lower lip anesthesia,discomfitingto many
the mandibular division of the trigeminal nerve (V3) patients and possibly dangerous (self-inflictedsoft tissue
2. Incisive trauma) for certain individuals
3. Mental 6. Partial anesthesiapossible where a bifid inferior
4. Lingual (commonly) alveolarnerve and bifid mandibular canals are present;
cross-innervation in lower anterior region
Areas Anesthetized. (Fig. 14-1)
1. Mandibular teeth to the midline Positive Aspiration. 10% to 15%.
2. Body of the mandible, inferior portion of the ramus
3. Buccalmucoperiosteum, mucous membrane anterior to Alternatives
the mental foramen (mental nerve) 1. Mental nerve block, for buccal soft tissue anesthesia
4. Anterior two thirds of the tongue and floor of the oral anterior to the first molar
cavity (lingual nerve) 2. Incisivenerve block, for pulpal and buccal soft tissue
5. Lingual soft tissues and periosteum (lingual nerve) anesthesia of teeth anterior to the mental foramen
(usuallysecond premolar to central incisor)
Indications 3. Supraperiostealinjection, for pulpal anesthesia of
1. Procedures on multiple mandibular teeth in one the central and lateral incisors, and sometimes
quadrant the premolars and molars (discussedfully in
2. When buccal soft tissue anesthesia (anterior to the Chapter 20)
mental foramen) is necessary 4. Gow-Gatesmandibular nerve block
3. When lingual soft tissue anesthesia is necessary 5. Vazirani-Akinosimandibular nerve block
6. PDL injection for pulpal anesthesia of any mandibular
Contraindications tooth
1. Infection or acute inflammation in the area of injection 7. IO injection for pulpal and soft tissue anesthesia of any
(rare) mandibular tooth, but especiallymolars
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228 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Technique
1. A long dental needle is recommended for the adult
patient. A 25-gaugelong needle is preferred; a 27-gauge
long is acceptable.
2. Area of insertion: Mucous membrane on the medial
(lingual) side of the mandibular ramus, at the
intersection of two lines--one horizontal, representing
the height of needle insertion, the other vertical,
representing the anteroposterior plane of injection
3. Targetarea: Inferior alveolarnerve as it passes
downward toward the mandibular foramen but before it
enters into the foramen
4. Landmarks (Figs. 14-2 and 14-3)
a. Coronoid notch (greatest concavity on the anterior
border of the ramus) Figure 14-3. Theposteriorborderofthemandibularramuscan
b. Pterygomandibular raphe (verticalportion) beapproximatedintraorallybyusingthepterygomandibular
raphe
c. Occlusalplane of the mandibular posterior teeth as it turns superiorlytowardthe maxilla.
5. Orientation of the needle bevel: Lesscritical than with
other nerve blocks,because the needle approaches the
inferior alveolarnerve at roughly a right angle Three parameters must be consideredduring administra
6. Procedure tion of IANB:(1) the height of the injection, (2) the antero
a. Assume the correct position. posterior placement of the needle (which helps to locate a
(1) For a right IANB,a right-handed administrator preciseneedle entry point), and (3) the depth of penetration
should sit at the 8 o'clock position facing the (which determines the location of the inferior alveolar
patient (Fig. 14-4,A). nerve).
(2) For a left IANB,a right-handed administrator (1) Height of injection: Placethe index finger or the
should sit at the 10 o'clock position facing in the thumb of your left hand in the coronoid notch.
same direction as the patient (Fig. 14-4,B). (a) An imaginary line extends posteriorly from
b. Position the patient supine (recommended) or the fingertip in the coronoid notch to the
semisupine (if necessary).The mouth should be deepest part of the pterygomandibular raphe
opened wide to allow greater visibilityof, and access (as it turns verticallyupward toward the
to, the injection site. maxilla), determining the height of injection.
c. Locatethe needle penetration (injection) site. This imaginary line should be parallel to the
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CHAPTER 14 Techniques of Mandibular Anesthesia 229
Figure 14-4. Position of the administrator for a (A) right and (B) left inferior alveolar nerve block.
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230 PARTIII Techniquesof RegionalAnesthesiain Dentistry
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CHAPTER 14 Techniques of Mandibular Anesthesia 231
(i) Withdraw the needle slightly but do not d. Insert the needle. When bone is contacted, withdraw
remove it from the tissue. approximately 1 mm to prevent subperiosteal
(ii) Bring the syringe barrel more toward injection.
the front of the mouth, over the canine e. Aspirate in two planes. If negative, slowly deposit
or lateral incisor on the contralateral 1.5 mL of anesthetic over a minimum of 60 seconds.
side. (Because of the high incidence of positive aspiration
(iii) Redirect the needle until a more and the natural tendency to deposit solution too
appropriate depth of insertion is rapidly, the sequence of slow injection, reaspiration,
obtained. The needle tip is now located slow injection, reaspiration is strongly
more posteriorly in the mandibular recommended.)
sulcus. f. Slowly withdraw the syringe, and when
(f) If bone is not contacted, the needle tip approximately half its length remains within tissues,
usually is located too far posterior (medial) reaspirate. If negative, deposit a portion of the
(Fig. 14-9). To correct: remaining solution (0.2 mL) to anesthetize the
(i) Withdraw it slightly in tissue (leaving lingual nerve.
approximately one fourth its length in (1) In most patients, this deliberate injection for
tissue) and reposition the syringe barrel lingual nerve anesthesia is not necessary, because
more posteriorly (over the mandibular local anesthetic from the IANB anesthetizes the
molars). lingual nerve.
(ii) Continue needle insertion until contact g. Withdraw the syringe slowly and make the needle
with bone is made at an appropriate safe.
depth (20 to 25 mm). h. After approximately 20 seconds, return the patient to
the upright or semiupright position.
i. Wait 3 to 5 minutes before testing for pulpal
anesthesia.
Precautions
1. Do not deposit local anesthetic if bone is not
contacted. The needle tip may be resting within the
B parotid gland near the facial nerve (cranial nerve
Figure 14-9. A, Overinsertion with no contact of bone. The VII), and a transient blockade (paralysis) of the facial
needle is usually posterior (medial) to the ramus. B, To correct: nerve may develop if local anesthetic solution is
Withdraw it slightlyfrom the tissues (1) and reposition the syringe deposited.
barrel over the premolars (2); reinsert. 2. Avoid pain by not contacting bone too forcefully.
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232 PART III Techniques of Regional Anesthesia in Dentistry
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CHAPTER 14 Techniques of Mandibular Anesthesia 233
Figure 14·11. With supraperiosteal injection, the needle tip is directed toward the apical region of the tooth in question. A, On a skull.
B, In the mouth.
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234 PART III Techniques of Regional Anesthesia in Dentistry
Lingual soft
tissue
and bone
Tongue
Indication. When buccal soft tissue anesthesia is necessary (1) For a right buccal nerve block, a right-handed
for dental procedures in the mandibular molar region. operator should sit at the 8 o'clock position
directly facing the patient (Fig. 14-13,A).
Contraindication. Infection or acute inflammation in the (2) For a left buccal nerve block, a right-handed
area of injection. operator should sit at 10 o'clock facing in the
same direction as the patient (Fig. 14-13,B).
Advantages b. Position the patient supine (recommended) or
1. High successrate semisupine.
2. Technicallyeasy c. Prepare the tissues for penetration distal and buccal
to the most posterior molar. *
Disadvantages. Potential for pain if the needle contacts the (1) Dry with sterile gauze.
periosteum during injection. (2) Applytopical antiseptic (optional).
(3) Applytopical anesthetic for 1 to 2 minutes.
Positive Aspiration. 0.7%. d. With your left index finger (if right-handed), pull the
buccal soft tissues in the area of injection laterally so
Alternatives that visibilitywill be improved. Taut tissues permit
1. Buccalinfiltration an atraumatic needle penetration.
2. Gow-Gatesmandibular nerve block e. Direct the syringe toward the injection site with the
3. Vazirani-Akinosimandibular nerve block bevel facing down toward bone and the syringe
4. PDL injection aligned parallel to the occlusalplane on the side of
5. Intraosseous injection injection but buccal to the teeth (Fig. 14-14,A).
6. Intraseptal injection f. Penetrate mucous membrane at the injection
site, distal and buccal to the last molar
Technique (Fig. 14-14,B).
1. A 25- or 27-gaugelong needle is recommended. This is g. Advancethe needle slowlyuntil mucoperiosteum is
most often used because the buccal nerve block is gently contacted.
usually administered immediately after an IANB.A long (1) To prevent pain when the needle contacts
needle is recommended because of the posterior mucoperiosteum, deposit a few drops of local
deposition site, not the depth of tissue insertion (which anesthetic just before contact.
is minimal). (2) The depth of penetration is seldom more than 2
2. Area of insertion: Mucous membrane distal and buccal to 4 mm, and usually only 1 or 2 mm.
to the most distal molar tooth in the arch h. Aspirate.
3. Target area: Buccalnerve as it passes over the anterior i. If negative,slowlydeposit 0.3 mL (approximately
border of the ramus one eighth of a cartridge) over 10 seconds.
4. Landmarks: Mandibular molars, mucobuccal fold
5. Orientation of the bevel: Towardbone during the
injection *Because the buccal nerve block most often immediately follows an inferior
6. Procedure alveolar nerve block, steps (1), (2), and (3) of tissue preparation usually are
a. Assume the correct position. completed before the inferior alveolar block.
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CHAPTER 14 Techniques of Mandibular Anesthesia 235
Figure 14-13. Position of the administrator for a (A) right and (B) left buccal nerve block.
Safety Features
1. Needle contacts bone, therein preventing overinsertion.
2. Minimum positive aspiration rate
Precautions
1. Pain on insertion from contacting unanesthetized
Figure 14-14. Syringe alignment. A. Parallel to the occlusal periosteum. This can be prevented by depositing a few
plane on the side of injection but buccal to it. B, Distal and buccal drops of local anesthetic before touching the
to the last molar.
periosteum.
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236 PART III Techniques of Regional Anesthesia in Dentistry
2. Local anesthetic solution not being retained at the administrator to deposit the anesthetic drug "lower" (e.g.,in
injection site. This generally means that needle the "usual"place).Twoapproaches are suggestedfor becom
penetration is not deep enough, the bevel of the needle ing accustomed to the GGMNB.The first is to begin to use
is only partially in the tissues, and solution is escaping the technique on all patients requiring mandibular anesthe
during the injection. sia. Allow at least 1 to 2 weeks to gain clinical experience.
a. To correct: The second approach is to continue using the conventional
(1) Stop the injection. IANB,but to use the GGMNBtechnique wheneverclinically
(2) Insert the needle to a greater depth. inadequate anesthesia occurs. Reanesthetize the patient
(3) Reaspirate. using the GGMNB. Although experience is accumulated
(4) Continue the injection. more slowly with this latter approach, its effectivenessis
more dramatic because patients who were previously diffi
Failures of Anesthesia. Rare with the buccal nerve block: cult to anesthetize now may be more easilymanaged.
1. Inadequate volume of anesthetic retained in the tissues
Other Common Names. Gow-Gatestechnique, third divi
Complications sion nerve block,V3 nerve block.
1. Few of any consequence
2. Hematoma (bluish discoloration and tissue swellingat Nerves Anesthetized
the injection site). Blood may exit the needle puncture 1. Inferior alveolar
point into the buccal vestibule.To treat: Applypressure 2. Mental
with gauze directly to the area of bleeding for a 3. Incisive
minimum of 3 to 5 minutes. 4. Lingual
5. Mylohyoid
6. Auriculotemporal
MANDIBULAR NERVE BLOCK: 7. Buccal (in 75% of patients)
THE GOW-GATES TECHNIQUE
Successful anesthesia of the mandibular teeth and soft Areas Anesthetized. (Fig. 14-15)
tissues is more difficultto achievethan anesthesia of maxil 1. Mandibular teeth to the midline
lary structures. Primary factors for this failure rate are 2. Buccalmucoperiosteum and mucous membranes on
the greater anatomic variation in the mandible and the the side of injection
need for deeper soft tissue penetration. In 1973, George 3. Anterior two thirds of the tongue and floor of the oral
Albert Edwards Gow-Gates (1910-2001),33a general practi cavity
tioner of dentistry in Australia, described a new approach 4. Lingual soft tissues and periosteum
to mandibular anesthesia. He had used this technique in 5. Body of the mandible, inferior portion of the ramus
his practice for approximately30years,with an astonishingly 6. Skin over the zygoma,posterior portion of the cheek,
high success rate (approximately 99% in his experienced and temporal regions
hands).
The Gow-Gates technique is a true mandibular nerve Indications
block because it provides sensory anesthesiato virtually the 1. Multiple procedures on mandibular teeth
entire distribution ofV 3. The inferior alveolar,lingual,mylo 2. When buccal soft tissue anesthesia,from the third molar
hyoid, mental, incisive,auriculotemporal, and buccal nerves to the midline, is necessary
all are blocked in the Gow-Gatesinjection. 3. When lingual soft tissue anesthesia is necessary
Significantadvantages of the Gow-Gatestechnique over 4. When a conventional inferior alveolarnerve block is
IANB include its higher successrate, its lower incidence of unsuccessful
positive aspiration (approximately2% vs. 10% to 15%with
the IANB),33.34 and the absence of problems with accessory Contraindications
sensory innervation to the mandibular teeth. 1. Infection or acute inflammation in the area of injection
The only apparent disadvantageis a relativelyminor one: (rare)
An administrator experienced with the IANB may feel 2. Patients who might bite their lip or their tongue, such
uncomfortable while learning the Gow-Gates mandibular as young children and physicallyor mentally
nerve block (GGMNB).Indeed, the incidence of unsuccess handicapped adults
ful anesthesiawith GGMNBmay be as high as (if not higher 3. Patients who are unable to open their mouth wide (e.g.,
than) that for the IANB until the administrator gains trismus)
clinical experience with it. Followingthis "learning curve:'
successrates greater than 95% are common. A new student Advantages
of local anesthesia usually does not encounter as much dif 1. Requiresonly one injection; a buccal nerve block is
ficulty with the GGMNBas the more experienced adminis usually unnecessary (accessoryinnervation has been
trator. This is a result of the strong bias of the experienced blocked)
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CHAPTER14 Techniquesof Mandibular Anesthesia 237
Lingual soft
tissue
and bone
Tongue
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238 PART III Techniques of Regional Anesthesia in Dentistry
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CHAPTER14 Techniquesof Mandibular Anesthesia 239
g. Direct the syringe (held in your right hand) toward Gow-Gatestechnique has demonstrated that
the site of injection from the comer of the mouth on medial deflection of the needle is the most
the opposite side (as in IANB). common cause of failure to contact bone.) Move
h. Insert the needle gently into tissues at the injection the barrel of the syringe somewhat more distally,
site just distal to the maxillary second molar at the thereby angulating the needle tip anteriorly,and
height of its mesiolingual (mesiopalatal) cusp. readvancethe needle until bony contact is made.
i. Align the needle with the plane extending from the
comer of the mouth on the opposite side to the
intertragic notch on the side of injection. It should
be parallel with the angle between the ear and the
face (Fig. 14-20).
j. Direct the syringe toward the target area on the
tragus.
(1) The syringe barrel lies in the comer of the
mouth over the premolars, but its position may
vary from molars to incisors, depending on the
divergence of the ramus as assessed by the angle
of the ear to the side of the face (Fig. 14-21).
(2) The height of insertion above the mandibular
occlusal plane is considerably greater (10 to
25 mm, depending on the patient's size) than
that of the IANB.
(3) When a maxillary third molar is present in a
normal occlusion, the site of needle penetration
is just distal to that tooth.
k. Slowly advance the needle until bone is contacted.
(1) Bone contacted is the neck of the condyle.
(2) The average depth of soft tissue penetration to
bone is 25 mm, although some variation is
observed. For a given patient, the depth of soft
tissue penetration with the GGMNB
approximates that with the IANB. Figure 14-20. The barrel of the syringeand the needle are held
(3) If bone is not contacted, withdraw the needle parallel to a line connecting the comer of the mouth and the inter
slightly and redirect. (Experience with the tragic notch.
\ '
', I
1. Flat tragus
2. Mildly divergent tragus
3. Widely divergent tragus
Figure 14·21. The location of the syringebarrel depends on the divergenceof the tragus.
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240 PARTIII Techniquesof RegionalAnesthesiain Dentistry
(a) A second cause of failure to contact bone is two consecutivetests at least 2 minutes apart serves
partial closure of the patient's mouth (see as a "guarantee" of successfulpulpal anesthesia in
step 6, b[2]). Once the patient closeseven nonpulpitic teeth.24'27'28
slightly,two negativesoccur: (1) The 4. Objective: No pain is felt during dental therapy.
thickness of soft tissue increases,and
(2) the condyle moves in a distal direction. Safety Features
Both of these make it more difficultto 1. Needle contacting bone, thereby preventing
locate the condylar neck with the needle. overinsertion
(4) If bone is not contacted, do not deposit any 2. Verylow positive aspiration rate; minimizes the risk of
local anesthetic. intravascular injection (the internal maxillary artery lies
1.Withdraw the needle 1 mm. inferior to the injection site)
m. Aspirate in 2 planes.
n. If positive,withdraw the needle slightly,angle it Precautions. Do not deposit local anesthetic if bone is not
superiorly,reinsert, reaspirate, and, if now negative, contacted; the needle tip usually is distal and medial to the
deposit the solution. Positiveaspiration usually desired site:
occurs in the internal maxillary artery, which is 1. Withdraw slightly.
located inferior to the target area. The positive 2. Redirect the needle laterally.
aspiration rate with the GGMNBtechnique is 3. Reinsert the needle. Make gentle contact with bone.
approximately2%.33'34 4. Withdraw 1 mm and aspirate in two planes.
o. If negative,slowlydeposit 1.8mL of solution over 60 5. Inject if aspiration is negative.
to 90 seconds. Gow-Gatesoriginallyrecommended
that 3 mL of anesthetic be deposited.33 However, Failures of Anesthesia. Rare with the Gow-Gates mandi
experiencewith the GGMNBshows that 1.8 mL is bular block once the administrator becomes familiar with
usually adequate to provide clinicallyacceptable the technique:
anesthesia in virtually all cases.When partial 1. Too little volume. The greater diameter of the
anesthesia developsafter administration of 1.8mL, a mandibular nerve may require a larger volume of
second injection of approximately 1.2 mL is anesthetic solution. Deposit up to 1.2 mL in a second
recommended. injection if the depth of anesthesia is inadequate after
p. Withdraw the syringe and make the needle safe. the initial 1.8 mL.
q. Requestthat the patient keep his or her mouth open 2. Anatomic difficulties.Do not deposit anesthetic unless
for 1 to 2 minutes after the injection to permit bone is contacted.
diffusion of the anesthetic solution.
(1) Use of a rubber bite block may assist the patient Complications
in keeping the mouth open. 1. Hematoma (<2% incidence of positive aspiration)
r. After completion of the injection, return the patient 2. Trismus (extremelyrare)
to the upright or semiupright position. 3. Temporary paralysisof cranial nerves III, N, and VI. In
s. Wait at least 3 to 5 minutes before commencing the a case of cranial nerve paralysisafter a right Gow-Gates
dental procedure. Onset of anesthesiawith the mandibular block, diplopia, right-sided blepharoptosis,
GGMNBmay be somewhat slower,requiring 5 and complete paralysisof the right eye persisted for 20
minutes or longer for the followingreasons: minutes after the injection. This has occurred after the
(1) Greater diameter of the nerve trunk at the site accidental rapid intravenous administration of local
of injection anesthetic.35 The recommendations of Dr. Gow-Gates
(2) Distance (5 to 10 mm) from the anesthetic include placing the needle on the lateral side of the
deposition site to the nerve trunk anterior surface of the condyle,aspirating carefully,and
depositing slowly.33•34If bone is not contacted, anesthetic
Signs and Symptoms solution should not be administered.
1. Subjective: Tingling or numbness of the lower lip
indicates anesthesia of the mental nerve, a terminal
branch of the inferior alveolarnerve. It is also a good
VAZIRANl-AKINOSI CLOSED-MOUTH
indication that the inferior alveolarnerve may be
MANDIBULAR BLOCK
anesthetized. The introduction of the Gow-Gatesmandibular nerve block
2. Subjective: Tingling or numbness of the tongue indicates in 1973spurred interest in alternativemethods of achieving
anesthesia of the lingual nerve, a branch of the posterior anesthesia in the lower jaw. In 1977, Dr. Joseph Akinosi
division of the mandibular nerve. It is alwayspresent in reported on a closed-mouth approach to mandibular anes
a successfulGow-Gatesmandibular block. thesis." Although this technique can be used whenever
3. Objective: Using an electricalpulp tester (EPT) and mandibular anesthesia is desired, its primary indication
eliciting no response to maximal output (80/80) on remains those situations where limited mandibular opening
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CHAPTER 14 Techniquesof Mandibular Anesthesia 241
precludes the use of other mandibular injection techniques. mandibular blockscan be administeredthrough the sigmoid
Such situations include the presence of spasm of the muscles notch or inferiorly from the chin (Fig. 14-22).37•38Because
of mastication (trismus) on one side of the mandible the mandibular division of the trigeminal nerve provides
after numerous attempts at IANB, as might occur with motor innervation to the muscles of mastication, a third
a "hot" mandibular molar. In this instance, multiple injec division (V3) block will relievetrismus that is produced sec
tions have been necessary to provide anesthesia adequate ondary to muscle spasm (trismus may also result from other
to extirpate the pulpal tissues of the involved mandibular causes).Although dentists are permitted to administer extra
molar. When the anesthetic effect resolves hours later, the oral nerve blocks,fewin clinicalpractice actually do so. The
muscles into which the anesthetic solution was deposited Vazirani-Akinositechnique is an intraoral approach to pro
become tender, producing some discomfort on opening the viding both anesthesiaand motor blockadein casesof severe
jaw. During a period of sleep, when the muscles are not in unilateral trismus.
use, the muscles go into spasm (the same way one's leg In earlyeditions of this textbook, the technique described
muscles might go into spasm after strenuous exercise, making in the followingsectionwastermed the Akinosi closed-mouth
it difficult to stand or walk the next morning), leaving mandibular block. However, a very similar technique was
the patient with significantly reduced occlusal opening in described in 1960by Vazirani.39 The name Vazirani-Akinosi
the morning. closed-mouth mandibular block was adopted for the fourth
The management oftrismus is reviewed in Chapter 17. edition, giving recognition to both of the doctors who
If it is necessary to continue dental care in the patient devisedand publicizedthis closed-mouth approach to man
with significant trismus, the options for providing mandibu dibular anesthesia.
lar anesthesia are extremely limited. Inferior alveolar and In 1992,Wolfe described a modification of the original
Gow-Gates mandibular nerve blocks cannot be attempted Vazirani-Akinositechnique." The technique described was
when significant trismus is present. Extraoral mandibular identical to the original technique, except that the author
nerve blocks can be attempted and, indeed, possess a sig recommended bending the needle at a 45-degree angle to
nificantly high success rate in experienced hands. Extraoral enable it to remain in closeproximity to the medial (lingual)
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242 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Lingual soft
tissue
and bone
side of the mandibular ramus as the needle is advanced 3. Inability to visualizeor gain accessto the lingual aspect
through the tissues. Becausethe potential for needle break of the ramus
age is increased when it is bent, bending any needle that is
to be inserted into tissuesto any significantdepth cannot be Advantages
recommended. The Vazirani-Akinosi closed-mouth man 1. Relativelyatraumatic
dibular block can be administered successfully without 2. Patient need not be able to open the mouth.
bending the needle. 3. Fewerpostoperative complications (e.g.,trismus)
4. Loweraspiration rate {<10%)than with the inferior
Other Common Names. Akinosi technique, closed-mouth alveolarnerve block
mandibular nerve block, tuberosity technique. 5. Provides successfulanesthesiawhere a bifid inferior
alveolarnerve and bifid mandibular canals are present
Nerves Anesthetized
1. Inferior alveolar Disadvantages
2. Incisive 1. Difficultto visualizethe path of the needle and the
3. Mental depth of insertion
4. Lingual 2. No bony contact; depth of penetration somewhat
5. Mylohyoid arbitrary
3. Potentiallytraumatic if the needle is too closeto the
Areas Anesthetized. (Fig. 14-23) periosteum
1. Mandibular teeth to the midline
2. Body of the mandible and inferior portion of the ramus Alternatives. No intraoral nerve blocks are available.If a
3. Buccalmucoperiosteum and mucous membrane patient is unable to open his or her mouth becauseof trauma,
anterior to the mental foramen infection, or postinjection trismus, no other suitable intra
4. Anterior two thirds of the tongue and floor of the oral oral techniques are available. The extraoral mandibular
cavity (lingual nerve) nerve block may be used when the doctor is well versed in
5. Lingual soft tissues and periosteum (lingual nerve) the procedure.
Indications Technique
1. Limited mandibular opening 1. A 25-gaugelong needle is recommended (although a
2. Multiple procedures on mandibular teeth 27-gaugelong may be preferred in patients whose
3. Inability to visualizelandmarks for IANB (e.g.,because ramus flareslaterallymore than usual).
oflarge tongue) 2. Area of insertion: Soft tissue overlyingthe medial
(lingual) border of the mandibular ramus directly
Contraindications adjacent to the maxillary tuberosity at the height of the
1. Infection or acute inflammation in the area of injection mucogingivaljunction adjacent to the maxillary third
(rare) molar (Fig. 14-24)
2. Patients who might bite their lip or their tongue, such 3. Target area: Soft tissue on the medial (lingual) border
as young children and physicallyor mentally of the ramus in the region of the inferior alveolar,
handicapped adults lingual, and mylohyoidnerves as they run inferiorly
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CHAPTER14 Techniquesof Mandibular Anesthesia 243
A B
Figure 14-24. A, Area of needle insertion for a Vazirani-Akinosi block. B, Hold the syringe and needle at the height of the mucogingival
junction above the maxillary third molar. (Redrawn from Gustainis JF, Peterson LJ: An alternative method of mandibular nerve block, J Am
Dent Assoc 103:33-36, 1981.)
from the foramen ovaletoward the mandibular foramen f. Ask the patient to occlude gentlywith the cheeks
(the height of injection with the Vazirani-Akinosibeing and muscles of mastication relaxed.
below that of the GGMNBbut above that of the IANB) g. Reflectthe soft tissues on the medial border of the
4. Landmarks: ramus laterally.
a. Mucogingivaljunction of the maxillary third (or h. The barrel of the syringe is held parallel to the
second) molar maxillary occlusalplane, with the needle at the level
b. Maxillarytuberosity of the mucogingivaljunction of the maxillary third
c. Coronoid notch on the mandibular ramus (or second) molar (Fig. 14-24).
5. Orientation of the bevel (bevelorientation in the i. Direct the needle posteriorly and slightlylaterally,so
closed-mouth mandibular block is very important): it advancesat a tangent to the posterior maxillary
The bevel must be oriented awayfrom the bone of alveolarprocess and parallel to the maxillary
the mandibular ramus (e.g.,bevel facestoward the occlusalplane.
midline). j. Orient the bevel awayfrom the mandibular ramus;
6. Procedure: thus as the needle advancesthrough tissues,needle
a. Assume the correct position. For a right or a left deflection occurs toward the ramus and the needle
Vazirani-Akinosi,a right-handed administrator remains in close proximity to the inferior alveolar
should sit in the 8 o'clock position facingthe nerve (Fig. 14-25).
patient. k. Advancethe needle 25 mm into tissue (for an
b. Position the patient supine (recommended) or average-sizedadult). This distanceis measured from
semisupine. the maxillarytuberosity.The tip of the needle should
c. Placeyour left index finger or thumb on the lie in the midportion of the pterygomandibular
coronoid notch, reflectingthe tissues on the medial space,closeto the branches of V, (Fig.14-26).
aspect of the ramus laterally.Reflectingthe soft 1. Aspirate in two planes.
tissues aids in visualization of the injection site and m. If negative,deposit 1.5to 1.8mL of anesthetic
decreasestrauma during needle insertion. solution in approximately60 seconds.
d. Visualizelandmarks: n. Withdraw the syringe slowlyand immediately make
(1) Mucogingivaljunction of the maxillary third or the needle safe.
second molar o. After the injection, return the patient to an upright
(2) Maxillarytuberosity or semiupright position.
e. Prepare the tissues at the site of penetration: p. Motor nerve paralysisdevelopsas quicklyas or
(1) Dry with sterile gauze. more quicklythan sensory anesthesia.The patient
(2) Applytopical antiseptic (optional). with trismus begins to notice increased ability to
(3) Applytopical anesthetic for minimum of 1 open the jaws shortly after the deposition of
minute. anesthetic.
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244 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Figure 14·25. Vazirani-Akinosiclosed-mouth mandibular nerve block. Barrel of syringe is held parallel to maxillary occlusalplane with
the needle at the levelof the mucogingivaljunction of the second or third maxillary molar.
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CHAPTER 14 Techniquesof Mandibular Anesthesia 245
Lingual soft
tissue
and bone
Tongue
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246 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Figure 14·28. Position of the administrator for a (A) right and (B) left mental/incisivenerve block.
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CHAPTER 14 Techniques of Mandibular Anesthesia 247
Figure 14-30. Radiographs can assist in locating the mental foramen (arrows). (Courtesy Dr. Robert Ziehm.)
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248 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Lingual soft tissues are not anesthetized with this block. If 0.3 to 0.6 mL of local anesthetic under the lingual mucosa
lingual soft tissues in very isolated areas require anesthesia, just distal to the last tooth to be treated. This provides
local infiltration can be readily accomplishedby advancing lingual soft tissue anesthesia adequate for any dental proce
a 27-gaugeshort needle through the interdental papillae on dure in this area. The danger in this procedure is that the
both mesial and distal aspects of the tooth being treated. lingual nerve may be contacted by the needle provoking a
Becausethe buccal soft tissuesare alreadyanesthetized (inci sensation of an "electric shock" or varying degrees of
sivenerve block), the penetration is atraumatic. Localanes paresthesia.
thetic solution should be deposited as the needle is advanced It is not necessary for the needle to enter into the
through the tissue toward the lingual (Fig.14-32).This tech mental foramen for an incisivenerve block to be successful.
nique provides lingual soft tissue anesthesia adequate for The first edition of this book and other textbooks of
deep curettage, root planing, and subgingivalpreparations. local anesthesia for dentistry recommended insertion of
Where there is a significant requirement for lingual soft the needle into the foramen.38'41'42 At least two disadvan
tissue anesthesia, an inferior alveolar or mandibular nerve tages are associatedwith the needle entering into the mental
block should be administered on that side, with the incisive foramen: (1) The administration of an incisivenerve block
nerve block administered on the contralateral side. In this becomes technically more difficult, and (2) the risk of
manner, the patient does not have to endure bilateral anes traumatizing the mental or incisivenerves and their associ
thesia of the tongue, which is a verydisconcertingexperience ated blood vesselsis increased.As described in the following
for many patients. sections, for the incisive nerve block to be successful,the
Another method of obtaining lingual anesthesiaafter the anesthetic should be deposited just outside the mental
incisivenerve block is to administer a partial lingual nerve foramen and, under pressure, directed into the foramen.
block (Fig. 14-33). Using a 25-gauge long needle, deposit Indeed, the incisive nerve block may be considered the
mandibular equivalent of the anterior superior alveolar
nerve block, with the mental nerve block the equivalent
of the infraorbital nerve block. Both of the disadvantages
just mentioned are minimized by not entering into the
mental foramen.
Advantages
1. Provides pulpal and hard tissue anesthesiawithout
lingual anesthesia (which is uncomfortable and
unnecessary for many patients); useful in place of
Figure 14-33. Retract the tongue to gain accessto, and increase bilateral IANBs
the visibilityof, the lingual border of the mandible. 2. High successrate
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CHAPTER14 Techniquesof Mandibular Anesthesia 249
Tongue
r 7 Alveolar mucous
membrane
Mental
foramen
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250 PARTIII Techniquesof RegionalAnesthesiain Dentistry
TABLE 14-1
Mandibular Teeth and Available Local
Anesthetic Techniques
SOFT TISSUE
Teeth Pulpal Buccal Lingual
Incisors Incisive (Inc) IANB IANB
Inferior alveolar (IANB) GG GG
Gow-Gates (GG) VA VA
Vazirani-Akinosi (VA) Inc PDL
Periodontal ligament (PDL) IS IS
injection
Intraseptal (IS) Mental Inf
Intraosseous (IO) PDL IO
Figure 14-35. Retract the lip to improve access and permit Infiltration (buccal and Inf Inf
atraumatic needle insertion. lingual infiltration)
IO
Canines Inferior alveolar IANB IANB
g. Penetrate mucous membrane at the canine or first Gow-Gates GG GG
premolar, directing the needle toward the mental Vazirani-Akinosi VA VA
foramen. Incisive Inc PDL
h. Advancethe needle slowlyuntil the mental foramen Periodontal ligament injection PDL IS
is reached The depth of penetration is 5 to 6 mm. Intraseptal IS Inf
There is no need to enter the mental foramen for Intraosseous IO IO
the incisivenerve block to be successful. Inf
i. Aspirate in two planes. Mental
j. If negative,slowlydeposit 0.6 mL (approximately Premolars Inferior alveolar IANB IANB
one third of a cartridge) over 20 seconds. Gow-Gates GG GG
Vazirani-Akinosi VA VA
(1) During the injection, maintain gentle finger
Incisive Inc PDL
pressure directly over the injection site to
Periodontal ligament injection PDL IS
increasethe volume of solution entering into Intraseptal IS IO
the mental foramen. This may be accomplished lntraosseous IO Inf
with intraoral or extraoral pressure. Mental
(2) Tissuesat the injection site should balloon, but Inf
very slightly. Molars Inferior alveolar IANB IANB
k. Withdraw the syringe and immediately make the Gow-Gates GG GG
needle safe. Vazirani-Akinosi VA VA
1. Continue to apply pressure at the injection site for 2 Periodontal ligament injection PDL PDL
minutes. lntraseptal IS IS
m. Wait 3 to 5 minutes before commencing the dental Intra osseous IO IO
Inf Inf
procedure.
(1) Anesthesiaof the mental nerve (lower lip,
buccal soft tissues) is observedwithin seconds
of the deposition.
(2) Anesthesiaof the incisivenerve requires TABLE 14-2
additional time. Recommended Volumes of Local Anesthetic Solution
for Mandibular Injection Techniques
Signs and Symptoms
Technique Volume, ml
1. Subjective: Tingling or numbness of the lower lip
Inferior alveolar 1.5
2. Objective: Using an electricalpulp tester (EPT) and
Buccal 0.3
eliciting no response to maximal output (80/80) on two
Gow-Gates 1.8-3.0
consecutivetests at least 2 minutes apart servesas a Vazirani-Akinosi 1.5-1.8
"guarantee" of successfulpulpal anesthesia in Mental 0.6
nonpulpitic teeth.24•27.is Incisive 0.6-0.9
3. Objective: No pain is felt during dental therapy.
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CHAPTER 14 Techniquesof Mandibular Anesthesia 251
Precaution. Usually an atrawnatic injection unless the 7. Evers H, Haegerstam G: Anaesthesia of the lower jaw. In
needle contacts periostewn or solution is deposited too Evers H, Haegerstam G, editors: Introduction to dental local
rapidly. anaesthesia,Fribourg, Switzerland, 1990, MediglobeSA.
8. TriegerN: New approachesto local anesthesia.In Pain control,
ed 2, St Louis, 1994, CV Mosby.
Failures of Anesthesia
9. OnPharma Inc: Results of 38 studies on LA success rates,
1. Inadequate volwne of anesthetic solution in the mental
unpublished. Availableat: www.onpharma.com.
foramen, with subsequent lack of pulpal anesthesia.To 10. Kanaa MD, Whitworth JM, Corbett IP, et al: Articaine buccal
correct: Reinjectinto the proper region and apply infiltration enhances the effectiveness of lidocaine inferior
pressure to the injection site. alveolarnerve block, Int Endod J 42:238--246, 2009.
2. Inadequate duration of pressure after injection. It is 11. Hannan L, Reader A, Nist R, et al: The use of ultrasound for
necessaryto apply firm pressure over the injection site guiding needle placement for inferior alveolar nerve blocks,
for a minimwn of 2 minutes to force the local Oral Surg Oral Med Oral Pathol Oral Radiol Endod 87:658--
anesthetic into the mental foramen and provide 665, 1999.
anesthesia of the second premolar, which may be distal 12. Berns JM, SadoveMS: Mandibular block injection: a method
to the foramen. Failure to achieveanesthesia of the of study using an injected radiopaque material, J Am Dent
Assoc 65:736-745, 1962.
second premolar is usually caused by inadequate
13. Galbreath JC: Tracing the course of the mandibular block
application of pressure after the injection.
injection, Oral Surg Oral Med Oral Pathol 30:571-582, 1970.
14. Reader A, American Association of Endodontists: Taking the
Complications pain out of restorative dentistry and endodontics: current
1. Few of any consequence thoughts and treatment options to help patients achieve
2. Hematoma (bluish discoloration and tissue swellingat profound anesthesia, Endodontics: Colleaguesfor Excellence.
injection site). Blood may exit the needle puncture site Winter 2009.
into the buccal fold. To treat: Applypressure with gauze 15. DeJong RH: Local anesthetics, St Louis, 1994, CV Mosby,
directly to the area for 2 minutes. This is rarely a pp 110-111.
problem because proper incisivenerve block protocol 16. Strichartz G: Molecular mechanisms of nerve block by local
includes the application of pressure at the injection site anesthetics,Anesthesiology45:421-444, 1976.
17. Gow-Gates GA: Mandibular conduction anesthesia: a new
for 2 minutes.
technique using extraoral landmarks, Oral Surg Oral Med Oral
3. Paresthesiaof lip and/or chin. Contact of the needle
Pathol 36:321-328, 1973.
with the mental nerve as it exits the mental foramen 18. Akinosi JO: A new approach to the mandibular nerve block,
may lead to the sensation of an "electric shock" or to Br J Oral Surg 15:83--87, 1977.
varying degreesof paresthesia (rare). 19. Malamed SF: The periodontal ligament (PDL) injection: an
Table 14-1 swnmarizes the various injection techniques alternative to inferior alveolarnerve block, Oral Surg 53:117-
applicable for mandibular teeth. Table 14-2 swnmarizes 121, 1982.
the recommended volwnes for the various injection 20. Coggins R, Reader A, Nist R, et al: Anesthetic efficacyof the
techniques. intraosseous injection in maxillaryand mandibular teeth, Oral
Surg Oral Med Oral Pathol 81:634-641, 1996.
21. Whitcomb M, Drum M, Reader A, et al: A prospective,
References randomized, double-blind study of the anesthetic efficacyof
1. De St Georges J: How dentists are judged by patients, Dent sodium bicarbonate buffered 2% lidocaine with 1:100,000
Today 23:96, 98-99, 2004. epinephrine in inferior alveolar nerve blocks, Anesth Prog
2. Friedman MJ, Hochman MN: The AMSA injection: a new 57:59--66, 2010.
conceptforlocalanesthesiaof maxillaryteeth usinga computer 22. Meechan JG, Ledvinka JI: Pulpal anaesthesia for mandibular
controlled injection system, Quintessence Int 29:297-303, central incisor teeth: a comparison of infiltration and intraliga
1998. mentary injections, Int Endod J 35:629--634, 2002.
3. Oulis CJ, Vadiakis GP, Vasilopoulou A: The effectivenessof 23. Kanaa MD, Whitworth JM, Corbett IP, et al: Articaine and
mandibular infiltration compared to mandibular block anes lidocaine mandibular buccal infiltration anesthesia: a pro
thesia in treating primary molars in children, Pediatr Dent spective randomized double-blind cross-over study, J Endod
18:301-305, 1996. 32:296-298, 2006.
4. Sharaf AA:Evaluationof mandibular infiltration versus block 24. Robertson D, Nusstein J, Reader A, et al: The anesthetic
anesthesia in pediatric dentistry, J Dent Child 64:276-281, efficacyof articaine in buccal infiltration of mandibular post
1997. erior teeth, J Am Dent Assoc 138:1104--1112, 2007.
5. Malamed SF:Localanesthetic considerationsin dental special 25. Haase A, Reader A, Nusstein J, et al: Comparing anesthetic
ties. In Malamed SF, editor: Handbook of local anesthesia, efficacyof articaine versus lidocaine as a supplemental buccal
ed 5, St Louis, 2004, CV Mosby. infiltration of the mandibular first molar after an inferior alve
6. Bennett CR: Techniques of regional anesthesia and analgesia. olar nerve block, J Am Dent Assoc 139:1228--1235, 2008.
In Bennett CR, editor: Monheim's local anesthesia and 26. Kanaa MD, Whitworth JM, Corbett IP, et al: Articaine buccal
pain control in dental practice, ed 7, St Louis, 1984, CV infiltration enhances the effectiveness of lidocaine inferior
Mosby. alveolarnerve block, Int Endod J 42:238--246, 2009.
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27. DrevenLJ,ReaderA, BeckM, et al:An evaluation of the electric 34. Malamed SF: The Gow-Gates mandibular block: evaluation
pulp tester as a measure of analgesia in human vital teeth, after 4275 cases,Oral Surg 51:463, 1981.
J Endod 13:233-238, 1987. 35. Fish LR, Mcintire DN, Johnson L: Temporary paralysis of
28. Certosimo AJ,Archer RD: A clinical evaluation of the electric cranial nerves III, IY,and VI after a Gow-Gatesinjection, J Am
pulp tester as an indicator of local anesthesia, Oper Dent Dent Assoc 119:127-130, 1989.
21:25-30, 1996. 36. Akinosi JO: A new approach to the mandibular nerve block,
29. Wilson S,Johns Pl, FullerPM: The inferior alveolarand mylo Br J Oral Surg 15:83--87, 1977.
hyoid nerves:an anatomic study and relationship to local anes 37. Murphy TM: Somatic blockade. In Cousins MJ, Bridenbaugh
thesia of the anterior mandibular teeth, J Am Dent Assoc PO,editors:Neural blockadein clinicalanesthesiaand manage
108:350-352, 1984. ment of pain, Philadelphia, 1980, JB Lippincott.
30. Frommer J, Mele FA, Monroe CW: The possible role of the 38. Bennett CR: Monheim's local anesthesia and pain control in
mylohyoid nerve in mandibular posterior tooth sensation, dental practice, ed 6, St Louis, 1978, Mosby.
J Am Dent Assoc 85:113--117, 1972. 39. VaziraniSJ:Closedmouth mandibular nerveblock:a newtech
31. Roda RS, Blanton PL: The anatomy oflocal anesthesia,Quin nique, Dent Dig 66:10-13, 1960.
tessence Int 25:27-38, 1994. 40. WolfeSH:The Wolfenerve block: a modified high mandibular
32. MeechanJG:Infiltration anesthesiain the mandible, Dent Clin nerve block, Dent Today 11:34-37, 1992.
N Am 54:621-629, 2010. 41. Malamed SF: Handbook of local anesthesia, St Louis, 1980,
33. Gow-Gates GAE: Mandibular conduction anesthesia: a new Mosby.
technique using extraoral landmarks, Oral Surg 36:321-328, 42. JastakJT,YagielaJA,Donaldson D: Localanesthesia of the oral
1973. cavity,Philadelphia, 1995, WB Saunders.
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Supplemental Injection
Techniques
In this chapter,a number of injections are describedthat are anesthesiawith infiltration of 0.9 mL of articaine HCl (with
used in specializedclinical situations. Some may be used as epinephrine 1: 100,000) on BOTH the buccal and lingual
the soletechnique for pain control for certain types of dental aspects of the teeth.6 Some successis achievablein the pos
treatment. For example, the periodontal ligament (PDL) terior teeth as well.7-8Mandibular infiltration is reviewed
injection and intraosseous (IO) and intraseptal techniques later in this chapter.
provide effectivepulpal anesthesiafor a singletooth without An old technique has been repopularized.The PDLinjec
the need for other injections. On the other hand, use of the tion (alsoknown as the intraligamentary injection [ILI])was
intrapulpal injection is almost alwaysreservedfor situations originally described as the peridental injection in local anes
in which other injection techniques have failed or are con thesia textbooks dating from 1912to 1923.9•10
traindicated for use.The PDL,IO, and intraseptal techniques The peridental injection was not well received in those
also are frequently used to supplement failed or only par earlyyearsbecause it was claimed that the risk of producing
tially successfultraditional injection techniques. blood-borne infection and septicemia was too great to
Sincethe previous edition of this textbook was published warrant its use in patients. The technique never became
(2004), considerable interest has arisen in the effectiveness popular but was used clinicallyby many doctors, although it
of mandibular infiltration in the adult mandible with the was not referred to as the peridental technique. In clinical
local anesthetic articaine HCI. The ability to provide pulpal situations in which an inferior alveolarnerve block failed to
anesthesia in circumscribed areas of the mandible without provide adequatepulpal anesthesiato the first molar (usually
the need for nerve blocks (e.g.,inferior alveolarnerve block its mesial root), the doctor inserted a needle along the long
[IANB], Gow-Gates) is valuable when these nerve blocks axis of the mesial root as far apicallyas possible and depos
fail to provide the depth of anesthesia required for painless ited a small volume of local anesthetic solution under pres
dentistry. sure. This invariablyprovided effectivepain control.
It was not until the early 1980sthat the intraligamentary
or PDL injection regained popularity. Credit for increased
INTRAOSSEOUS ANESTHESIA
interest in this approach must go to the manufacturers of
IO anesthesia involves the deposition of local anesthetic syringe devices designed to make the injection easier to
solution into the cancellous bone that supports the teeth. administer. The original devices-the Peripress (Universal
Although not new (IO anesthesia dates back to the early Dental, Boyerstown,Pa) and the Ligmaject(IMAAssociates,
1900s),a resurgenceof interest in this technique in dentistry Largo, Fla) (Fig. 15-1)-provide a mechanical advantage
has occurred over the past 15 years.!? Three techniques are that allowsthe administrator to deposit the anesthetic more
discussed here, two of which-the PDL injection and the easily (and sometimes too easily). They appear similar to
intraseptal injection-are modifications of traditional IO the Wilcox-JewettObtunder (Fig. 15-2), which was widely
anesthesia. advertisedto the dental profession in a 1905catalog,Dental
Furniture, Instruments, and Materials, perhaps reconfirming
Periodontal Ligament Injection the adage that there is "nothing new under the sun.?"
Becauseof the thicknessof the cortical plate of bone in most Why has the PDL (nee peridental) injection enjoyed a
patients and in most areas of the mandible, it is not possible renewal of popularity? Perhaps it is because the primary
to achieveprofound pulpal anesthesia on a solitary tooth in thrust of advertising for the new syringes focused on being
the adult mandible with the techniques describedin Chapter able to "avoid the mandibular block" injection with the
14. An exception to this is the mandibular incisor region, PDL or intraligamentary technique, a concept to which the
where Certosimo demonstrated a 97%successrate for pulpal dental profession is receptive,giventhe fact that virtually all
253
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CHAPTER15 Supplemental Injection Techniques 255
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256 PART III Techniques of Regional Anesthesia in Dentistry
Advantages
1. There is no anesthesia of the lip, tongue, and other soft
tissues,thus facilitatingtreatment in multiple quadrants
during a single appointment.
2. Minimum dose of local anesthetic necessaryto achieve
anesthesia {0.2mL per root)
3. An alternative to partially successfulregional nerve
block anesthesia
4. Rapid onset of profound pulpal and soft tissue
Figure 15-4. Area anesthetized by a periodontal ligament
anesthesia (30 seconds)
injection. 5. Lesstraumatic than conventionalblock injections
6. Wellsuited for procedures in children, extractions, and
periodontal and endodontic single-tooth and multiple
enough reports to convince me that many doctors quadrant procedures
believethis to be so. Use of C-CLADsystems (e.g.,
STA-SingleTooth AnesthesiaSystem,Milestone Disadvantages
Scientific,Inc., Livingston,NJ) does enable the PDL 1. Proper needle placement is difficultto achievein some
injection to be deliveredpainlessly(e.g., 0 to 1 on a areas (e.g.,distal of the second or third molar).
visual analog scale [VAS]).The PDL technique utilizing 2. Leakageof local anesthetic solution into the patient's
a C-CLADdevice is described in detail in the section mouth produces an unpleasant taste.
immediately followingthis. 3. Excessivepressure or overlyrapid injection may break
the glasscartridge.
Other Common Names. Peridental (original name) injec 4. A special syringe may be necessary.
tion, intraligamentary injection (ILI). 5. Excessivepressure can produce focal tissue damage.
6. Postinjection discomfort may persist for severaldays.
Nerves Anesthetized. Terminalnerve endings at the site of 7. The potential for extrusion of a tooth exists if excessive
injection and at the apex of the tooth. pressure or volumes are used.
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CHAPTER 15 Supplemental Injection Techniques 259
Figure 15-6. Dynamic Pressure Sensing (DPS) on the STASingle Tooth Anesthesia C-CLAD device provides both visual and audible
feedbackregarding placement of the needle tip during the periodontal ligament (PDL) injection. Horizontal color bars indicate pressure at
the tip of the needle. A, Red-pressure is too low.B, Orange and dark yellow-increasing pressure but not yet adequate. C, Light yellow
correct pressure for PDL injection. At this point (C) the STAunit will also provide an audible clue "PDL. PDL, PDL"that the needle tip is
properly situated. STAWand handpiece is lightweight (less than 10 grams) and can easilybe shortened to aid in administration of some
injections (D), such as the AMSAor other palatal techniques.
a visual pressure-sensing scale on the front of the unit that that the pressure is rising.When the periodontal ligament is
is composed of a series of light-emitting diode (LED)lights identified, the letters "P-D-L'' are spoken, indicating that
(orange, yellow,and green) (Fig. 15-6, A-C). Orange lights correct needle position has been achieved. Maintaining a
indicate minimal pressure at the needle tip, yellowindicates consistent levelof moderate pressure throughout the injec
mild to moderate pressure, and green indicates moderate tion process is necessary for success. Audible and visual
tissue pressure indicative of the PDL space. PDL tissue feedback provides this important information. When the
may be identified at pressures of the yellow LED at high STA-PDLinjection is performed, it is not uncommon for
range as well.39 the clinician to reposition the needle to find the optimal
Through auditory feedback,the clinician becomes aware position within periodontal ligament tissues,allowinga high
of how to maintain correct needle-to-intraligamentary degree of predictability and accuracywhen this injection is
position throughout the injection. Auditory feedback con performed. This transforms the "blind" syringe approach,
sists of a series of sounds with a pressure-sensing scale described above, into an objective method of locating and
composed of ascending tones to guide the clinician.When maintaining correct needle position when performing the
the clinician hears the ascending sequence, this indicates PDL injection.
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260 PART III Techniques of Regional Anesthesia in Dentistry
Ferrari and coworkers published data on 60 patients in benefits that cannot be achieved with use of the manually
whom they compared the STA System versus two standard driven conventional syringe, the pistol-grip high-pressure
PDL hand-driven manual syringes: a high-pressure mechan syringe,or previous C-CLADinstruments.
ical syringe (Ligmaject) and a conventional dental syringe.32
Electrical pulp testing was performed on all tested teeth at Other Common Names. Peridental (original name) injec
regular intervals to determine successor failure of these dif tion, intraligamentary injection (ILI).
ferent instruments and the techniques used. In addition to
EPT results, subjective pain responses of the patient were Nerves Anesthetized. Terminalnerve endings at the site of
recorded after treatment. Ferrari reported a successrate of injection and at the apex of the tooth.
100%for the STASystem.In addition, a rapid onset of anes
thesia was observed. In this study, the PDL injection was Areas Anesthetized. Bone,softtissue,and apicaland pulpal
performed as the primary injection for restorative dental tissues in the area of the injection.
care in mandibular teeth. Investigators reported subjective
pain responsesof"minimal or no pain" in all patients receiv Indications
ing the PDL injection performed with the STAdevice. In 1. Pulpal anesthesia of one or two teeth in a quadrant
contrast, injections performed with the other two systems 2. Treatment of isolated teeth in two mandibular
(high-pressuremechanicalsyringeand conventionalsyringe) quadrants (to avoid bilateral IANB)
werefound to result in higher pain scoresthroughout testing 3. Patients for whom residual soft tissue anesthesia is
and required repeated attempts to achieve a successful undesirable
outcome. Researchers concluded the STA System device 4. Pediatric dental patient in treatment of the primary
resulted in a more predictable, more reliable, and more dentition
comfortable anesthesia technique than the high-pressure a. A recent study conclusivelyreported that using the
mechanical syringe and/or the conventional dental syringe. STASystemdoes not present the previous risk of
enamel hypoplasia that was reported with a manually
Pediatric Use. Brannstrom and associates reported on the driven syringe,and that using the STASystem
use of a high-pressure PDL injection to anesthetize 16 instrument does not adverselyaffect the developing
monkey primary teeth." Hypoplasia or hypomineralization permanent tooth when PDL injection is performed.
defects developed on 15 of the permanent teeth, but none 5. Situations in which regional block anesthesia is
in controls. The PDL injection, when deliveredby a hand contraindicated
driven mechanical syringe, produces uncontrolled high 6. As a possible aid in diagnosis of pulpal discomfort
pressures and is associatedwith damage to the periodontal 7. As an adjunctive technique after nerve block anesthesia
tissues." Other reports have also recommended avoidance if partial anesthesia is present
of the PDL injection on primary teeth when a traditional
syringe or PDL syringe is used.13 Contraindications
In 2010, Ashekenzi and coworkers published the first 1. Infection or inflammation at the site of injection
long-term, clinical controlled study using a low-pressure 2. Patients who require a "numb" sensation for
PDL injection with the STASystemwith dynamic pressure psychologicalcomfort
sensing (DPS) technology.31The study population consisted
of 78 children (ages, 4.1 to 12.8 years) who received STA Advantages
intraligamentary injections in 166 primary molar teeth. 1. The STASystemdevicewith dynamic pressure-sensing
Teeth receivingconventional dental anesthesia or that were technology provides an objectivemeans by which to
not anesthetizedby local anesthesiaserved as controls.After identify the correct target location to perform a PDL
reviewingdata collectedbetween 1999and 2007,Ashekenzi injection, improving the predictability of this injection
concluded that performing the PDL injection using a low when compared with previous techniques and
pressure C-CLADinjection instrument, specificallythe STA instruments.
Systemwith DPS,did not produce damageto the underlying 2. The STASystemdeviceuses a controlled low-pressure
developingpermanent tooth bud and was deemed safe and fluid dynamic that has been shown to reduce the risk of
effective.The same authors, in another study, demonstrated tissue injury and to minimize subjectivepain responses.
that children exhibited minimal disruptive pain-related 3. The STASystemdevice,through use of a controlled
behavior and minimal levelsof dental-related stress during low-pressurefluid dynamic, allowsa greater volume of
and immediately after STA intraligamentary anesthesia.41 anesthetic solution (0.45 mL to 0.90 mL) to be safely
These findings represent a new perspective on dental local administered, thereby increasingthe effectiveworking
anesthesiaand the treatment of primary teeth of the pediat time of this PDL injection {30to 45 minutes).
ric patient. 4. The STASystemdevicewith dynamic pressure-sensing
The PDLinjection performed with the STASystemdevice technology can detect local anesthetic solution leakage
represents a single-tooth injection technique that provides a into the patient's mouth, avoiding an unpleasant taste.
level of safety,comfort, and predictability previously unat 5. The STASystemdevicewith dynamic pressure-sensing
tainable. The system provides the clinician with multiple technology can detect excessivepressure and can
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CHAPTER 15 Supplemental Injection Techniques 261
safeguard patient and operator from glass cartridge of two longer "beeps,"indicating that proper
breakage. pressure is being maintained, and that you have
identified the correct needle tip position for the
Disadvantages PDL injection.
1. Requiresthe use of a specializedC-CLADinstrument 10. It is important to note that a successfulPDL may
and associatedcosts of purchase and use occur when the LEDlights are in green or high yellow
2. Requiresadditional training zones. It is necessaryto maintain the LEDlight
indicators throughout the injection processto achieve
Positive Aspiration. 0%. success.Note that you will not hear the audible spoken
word "PDL''in the yellowzone.
Technique 11. Deposit 0.45 mL to 0.90 mL of local anesthetic
1. A STA-Wandbonded handpiece with a 30-gauge Yi per root.
inch needle
2. Set the STAinstrument to the STAmode. Signs and Symptoms
3. Area of insertion: 1. Indicators of success:
a. The needle should be placed at a 45-degree angle to Subjective: There are no signs that absolutelyassure
the long axis of the tooth. adequate anesthesia;the anesthetized area is quite
b. When a PDL injection is performed on a single circumscribed.When the followingsign is present, there
rooted tooth, only a single site is necessary. is an excellentchance that profound anesthesia is
c. When a PDL injection is performed on a present:
multirooted tooth, it is recommended that two sites Subjective: Ischemia of soft tissues at the injection site
be used: one on the distal root and a second on the Subjective: Maintenance of high yellowand green LED
mesial root. zones on the front of the STAdrive unit throughout the
d. Start with the distal aspect of the tooth. injection process
e. The injection can be performed anywherefrom the 2. Objective: Use of electricalpulp testing (EPT) with no
lingual line angle to the interproximal contact for response from the tooth with maximal EPT output
each root. (80/80)
4. To improve accessibilityin difficult areas,shorten the
STAhandpiece by breaking off a section of the handle. Safety Feature. The STASysteminstrument DPS technol
This will allow easier access(Fig. 15-6,D). ogy precisely regulates and monitors fluid exit-pressures
5. Place the needle very slowlyinto the gingivalsulcus as within the tissues, thereby preventing buildup of excessive
if it was a periodontal probe, while simultaneously pressure and ensuring a safe and effectivecontrolled flow
initiating the ControlFlo (0.005 mL/sec) flow rate. rate of local anesthetic solution.
Advancethe needle slowlyinto the sulcus,moving it
gently down into the sulcus until you encounter Precautions
resistance. 1. Maintain direct vision of the needle as it enters the
6. The ControlFlo rate can be initiated by pressing on sulcus of the tooth.
the foot control; after three audible beeps, you will 2. Keepthe needle at a 45-degree angle to the long axis of
hear the unit announce "Cruise."Once you hear the tooth to ensure that the needle is inserted into the
the word "Cruise,"you may remove your foot. The entrance to the PDL space at the level of the crest of
STAsystemwill continue the flow of anesthetic bone.
solution. 3. Do not inject directly into infected or highly inflamed
7. Once you feel you are at the base of the sulcus,you tissues.
need to minimize movement for 10 to 15 seconds as
the dynamic pressure-sensingtechnology analyzesthe Failures of Anesthesia
location of the needle tip. 1. Infected or inflamed tissues.The pH and vascularity
8. As the STAsystem DPS sensespressure building, you changes at the apex of, and periodontal tissues
will see a sequential illumination of LEDlights on the surrounding, infected teeth minimize the effectiveness
front of the unit. The visual pressure sensing scale of the local anesthetic.
consists of a series of orange, yellow,and green LED 2. Inability to generate STASystemin the high yellowor
lights. If after 20 to 30 seconds,pressure does not green LEDzone. In this case,remove and reenter at a
build, you will need to relocate the needle. The STA different site(s) until the STASystemcan generate and
Systemalso provides audible pressure feedback,with a maintain the proper DPS outcome.
series of three ascending tones indicating that the
system is detecting pressure at the needle tip. Complications
9. After 20 to 30 seconds with the needle tip in the 1. Pain during insertion of the needle
correct location, the STASystemwill announce Cause:The needle is inserted into the sulcus too rapidly.
"P-D-L,P- D-L."This will be followedby a series To correct: Enter and move the needle very slowly
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262 PART III Techniques of Regional Anesthesia in Dentistry
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CHAPTER15 Supplemental Injection Techniques 263
Advantages
1. Laclcof lip and tongue anesthesia (appreciated by most
patients)
2. Minimum volumes of local anesthetic necessary
3. Minimized bleeding during the surgical procedure
4. Atraumatic
5. Immediate (<30 second) onset of action
Figure 15-9. Orientation of the needle for an intraseptal
6. Fewpostoperative complications
injection.
7. Usefulon periodontally involvedteeth (avoidsinfected
poclcets)
Disadvantages 6. Procedure:
1. Multiple tissue punctures may be necessary. a. Assumethe correct position, which varies
2. Bitter taste of the anesthetic drug (if leakageoccurs) significantlyfrom tooth to tooth. The administrator
3. Short duration of pulpal anesthesia;limited area of soft should be comfortable, have adequate visibilityof
tissue anesthesia (may necessitatereinjection) the injection site, and maintain control over the
4. Clinical experiencenecessaryfor success needle.
b. Position the patient supine or semisupine with the
Positive Aspiration. 0%. head turned to maximize accessand visibility.
c. Prepare tissue at the site of penetration.
Alternatives (1) Dry with sterile gauze.
1. PDL injection in the absence of infection or severe (2) Applytopical antiseptic (optional).
periodontal involvement (3) Applytopical anesthetic for minimum of
2. IO anesthesia 1 minute.
3. Regionalnerve bloclcwith local infiltration for d. Stabilizethe syringe and orient the needle correctly
hemostasis (Fig. 15-9).
(1) Frontal plane: 45 degreesto the long axis of the
Technique tooth
1. A 27-gaugeshort needle is recommended. (2) Sagittalplane: At right angle to the soft tissue
2. Area of insertion: Center of the interdental papilla (3) Bevelfacing the apex of the tooth
adjacent to the tooth to be treated (Fig. 15-8) e. Slowlyinject a few drops of local anesthetic as the
3. Target area: Same needle enters soft tissue, and advance the needle
4. Landmarks: Papillarytriangle, about 2 mm below the until contact with bone is made.
tip, equidistant from adjacent teeth f. While applying pressure to the syringe,push the
5. Orientation of the bevel: Not significant,although needle slightlydeeper (1 to 2 mm) into the
Saadoun and Malamed recommend toward the apex42 interdental septum.
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264 PARTIII Techniquesof RegionalAnesthesiain Dentistry
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CHAPTER 15 Supplemental Injection Techniques 265
Figure 15-12. Alternative Stabident System. Guide sleeve Other Common Names. None.
remains in hole in bone, permitting easyaccessfor needle.
Nerves Anesthetized. Terminalnerve endings at the site of
injection and in adjacent soft and hard tissues.
needle, which is recommended by the manufacturer for
injection of local anesthetic into the cancellous bone. The Areas Anesthetized. Bone,soft tissue,and root structure in
Alternative Stabident System introduced shortly thereafter the area of injection (Fig. 15-14).
eliminated the problem of locating the "hole" by inserting a
conical-shaped "guide sleeve"into the hole. The 27-gauge Indication. Pain control for dental treatment on single or
short needle could then be easily placed into the hole multiple teeth in a quadrant.
(Fig. 15-12).
The IntraFlow HTP Anesthesia Delivery System,which Contraindication. Infection or severe inflammation at the
was recently introduced, combines the two steps previously injection site.
described into one (Fig. 15-13).3The IntraFlowhandpiece is
attached to a standard four-hole air hose on a treatment Advantages
room deliveryunit and is controlled by a foot rheostat. The 1. Lack of lip and tongue anesthesia (appreciated by most
lntraFlow is a speciallymodified slow-speedhandpiece that patients)
consists of four main parts: 2. Atraumatic
1. A needle or drill that makes the perforation through the 3. Immediate (<30 seconds) onset of action
bone and deliversthe local anesthetic 4. Fewpostoperative complications
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266 PART III Techniques of Regional Anesthesia in Dentistry
A
Gear set
Transfuser
Hypodennic tubing
t Drug cartridge t
t t
I t
.!Latch head
B T Clutch I Pneumatic motor Gearbox
Needle dull Dental handplece
Figure 15·13. Intraosseous anesthesia-IntraFlow HTP Anesthesia Delivery System. Components: A. Disassembled. B, Assembled.
......,,,..
-t--m- Lingual soft Alternatives
tissue 1. PDL injection, in the absence of infection or severe
and bone
periodontal involvement
Tongue 2. Intraseptal injection
3. Supraperiostealinjection
4. Regionalnerve block
Mental
foramen
Technique*
1. Selectionof site for injection
a. Lateral perforation
(1) At a point 2 mm apical to the intersection of
lines drawn horizontally along the gingival
Figure 15-14. Area anesthetized by intraosseus injection. margins of the teeth and a vertical line through
the interdental papilla
(2) The site should be located distal to the tooth to
be treated, if possible,although this technique
Disadvantages provides anesthesia in most caseswhen injected
1. Requiresa specialsyringe (e.g.,Stabident System,X-Tip, anterior to the tooth being treated.
IntraFlow) (3) Avoidinjecting in the mental foramen area
2. Bitter taste of the anesthetic drug (if leakageoccurs) (increased risk of nerve damage).
3. Occasional (rare) difficultyin placing anesthetic needle b. Verticalperforation (for edentulous areas)
into predrilled hole (primarily in mandibular second (1) Perforate at a point on the alveolarcrest mesial
and third molar regions) or distal to the treatment area (also called the
4. High occurrence of palpitations when vasopressor crestal anesthesia techniq_ue).
containing local anesthetic is used
*From the instruction manual, CE-Magic, 1-877-478-9748; www.CE-Magic.
Positive Aspiration. 0%. com.
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CHAPTER 15 Supplemental Injection Techniques 267
Figure 15-15. Drillholeusinga gentle"pecking"motion. Figure 15-16. Hold the guide sleevein place as the drill is
withdrawn.
2. Technique
a. Removethe X-Tip from its sterile vial.
(1) Hold the protective cover as you insert the X-Tip
onto the slow speed handpiece (20,000rpm).
b. Prepare soft tissues at perforation site:
(1) Prepare tissue at the injection site with 2 x 2
inch sterile gauze.
(2) Applytopical anesthetic to the injection site for
minimum of 1 minute.
(3) Placebevel of needle against gingiva,injecting a
small volume of local anesthetic until blanching
occurs.
(4) Check soft tissue anesthesia using a cotton pliers.
(a) Cotton pliers leavea slight dimple marking
of the perforation site.
(5) Inject a few drops oflocal anesthetic into the Figure 15-17. Insert needleinto guidesleeveand injectlocal
dimple. anestheticsolution.
c. Perforation of the cortical plate
(1) While holding the perforator perpendicular to
the cortical plate, gently push the perforator e. X-Tip doses: Recommended dosagesfor the X-Tip
through the attached gingivauntil its tip rests are the same for each local anesthetic solution as is
against bone (without activatingthe handpiece). recommended for other injections.
(2) Activatethe handpiece, using a gentle "pecking" f. Stabident doses (Table 15-1)
motion on the perforator until a sudden loss of g. Recommended technique for the lntraFlow IO
resistanceis felt. Cortical bone will be perforated syringe system is presented in Box 15-2.
within 2 seconds (Fig. 15-15).
(3) Hold the guide sleevein place as the drill is Signs and Symptoms
withdrawn (Fig. 15-16).Withdraw the perforator 1. Subjective:Ischemia of soft tissues at the injection site
and dispose of it safely(sharps container). 2. Objective:Use of electricalpulp testing with no
(a) The guide sleeveremains in place until you response from tooth with maximal EPT output (80/80)
are certain you have adequate anesthesia.
d. Injection into cancellousbone: Safety Feature. Intravascularinjection is extremelyunlikely,
(1) It is easyto insert the needle into the hole when although the area injected into is quite vascular.Slowinjec
a short needle is used (Fig. 15-17). tion of the recommended volume of solution is important
(2) Press the tapered needle gently against the guide to keeping IO anesthesia safe.
sleeveto minimize local anesthetic leakage.
(a) Compress a cotton roll or 2 x 2 sterile gauze Precautions
against the mucosa to absorb any excess 1. Do not inject into infected tissue.
local anesthetic. 2. Do not inject rapidly.
(3) Slowlyand gently inject the local anesthetic 3. Do not inject too much solution. (Seerecommended
solution. dosagesin Table 15-1.)
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268 PARTIII Techniquesof RegionalAnesthesiain Dentistry
TABLE 15-1
Stabident Dosages*
STABIDENT MANDIBULAR DOSAGES
Dose (number of
To Anesthetize Injection Site 1.8 ml cartridges}
One tooth Immediately distal OR immediately mesial .Xto y,
Twoadjacent teeth Betweenthe two teeth OR immediately distal to the more distal tooth Y, to Yi
Three adjacent teeth Immediately distal to the middle tooth Yi
Six front teeth plus the first premolars Givetwo injections, one on each side,between the canine and the first Yi on each side (total
(i.e.,total of eight teeth) premolar of 1)
STABIDENTMAXILLARY DOSAGES
Dose (number of
To Anesthetize Injection Site 1.8 ml cartridges}
One tooth Immediately distal OR immediately mesial
Twoadjacent teeth Betweenthe two teeth
Four adjacent teeth (e.g., 1, 2, 3, and 4) Midway (e.g.,two teeth distal and two teeth mesial to the injection site)
Up to eight teeth on one side Midway (e.g.,four teeth distal and four teeth mesial to the injection site)
*From www.stabident.com/manualall.htm.
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CHAPTER 15 Supplemental Injection Techniques 269
Figure 15-19. For the intrapulpal injection, a 25-gauge 1 or 1Ys inch needle is inserted into the pulp chamber or a specificroot canal.
Bending the needle may be necessaryto gain access.(From Cohen S, Bums RC:Pathwaysof the pulp, ed 8, St Louis,2001,Mosby.)
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270 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Precautions
1. Do not inject into infected tissue.
2. Do not inject rapidly (not less than 20 seconds).
3. Do not inject too much solution (0.2 to 0.3 mL).
Failures of Anesthesia
1. Infected or inflamed tissues. Changes in tissue pH
minimize the effectivenessof the anesthetic. However,
intrapulpal anesthesia invariablyworks to provide
effectivepain control.
2. Solution not retained in tissue.To correct:Tryto
advancethe needle farther into the pulp chamber or root
canal,and readminister 0.2 to 0.3 mL of anesthetic drug.
Figure 15-20. The needle may have to be bent to gain access to
a canal. (Modified from Cohen S, Bums RC: Pathways of the pulp,
ed 8, St Louis, 2001, Mosby.) Complication. Discomfort during the injection of anes
thetic. The patient may experiencea brief period of intense
discomfort as the injection of the anesthetic drug is started.
Within a second (literally),the tissue is anesthetized and the
discomfort ceases.The use of inhalation sedation (nitrous
a. Occasionally,the needle does not fit snugly into oxide or oxygen) can help to minimize or alter the feeling
the canal. In this situation, the anesthetic can be experienced.
deposited in the chamber or canal.Anesthesiain
this case is produced only by the pharmacologic Duration of Expected Anesthesia. The duration of anes
action of the local;there is no pressure thesiaisvariableafterintrapulpal injection.In most instances,
anesthesia. the duration is adequate to permit atraumatic extirpation of
3. Deposit anesthetic solution under pressure. the pulpal tissues.
a. A small volume of anesthetic (0.2 to 0.3 mL) is
necessaryfor successfulintrapulpal anesthesia,if the
anesthetic stayswithin the tooth. In many situations,
MANDIBULAR INFILTRATION IN ADULTS
the anesthetic simply flowsback out of the tooth
into the aspirator (vacuum) tip. Providingeffectivepain control is one of the most important
4. Resistanceto injection of the drug should be felt. aspects of dental care. Indeed, patients rate a dentist "who
5. Bend the needle, if necessary,to gain accessto the pulp does not hurt" and one who can "givepainlessinjections" as
chamber (Fig. 15-20). meeting the second and first most important criteria used in
a. Although there is a greater risk of breakagewith a evaluatingdentists." Unfortunately,the abilityto attain con
bent needle, this is not a problem during intrapulpal sistently profound anesthesia for dental procedures in the
anesthesia,because the needle is inserted into the mandible of adult patients has proved extremelyelusive.This
tooth itself,not into soft tissues.Retrievalis relatively is even more of a problem when infected teeth are involved,
simple if the needle breaks. primarily mandibular molars. Anesthesia of maxillary teeth
6. When the intrapulpal injection is performed properly, on the other hand, although on occasion difficultto achieve,
a brief period of sensitivity (ranging from mild to very is rarely an insurmountable problem. Reasons for this, as
painful) usually accompaniesthe injection. Pain relief discussed in Chapter 12, include the fact that the cortical
usually occurs immediatelythereafter, permitting plate of bone overlyingthe maxillary teeth is normally thin,
instrumentation to proceed atraumatically. thus allowing the local anesthetic drug to diffuse when
7. Instrumentation may begin approximately30 seconds administered by supraperiosteal injection (infiltration).
after the injection is given. Additionally,relativelysimple nerve blocks,such as the PSA,
MSA,ASA(infraorbital), and AMSA,are availableas alterna
Signs and Symptoms tives to infiltration. Maxillaryanesthesia technique was dis
1. As with PDL, intraseptal, and IO injections, no cussed in Chapter 13.
subjectivesymptoms ensure adequate anesthesia.The It is commonly stated that the significantlyhigher failure
area is too circumscribed. rate for mandibular anesthesia is related to the thickness of
2. Objective:The endodontically involvedtooth may be the cortical plate of bone in the adult mandible. Indeed it is
treated painlessly. generallyacknowledgedthat mandibular infiltration is suc
cessful where the patient has a full primary dentition (see
Safety Features discussion of pediatric local anesthesia in Chapter 16).45•46
1. Intravascular injection is extremelyunlikelyto occur. Once a mixed dentition develops,it is a generalrule of teach
2. Smallvolumes of anesthetic are administered. ing that the mandibular cortical plate of bone has thickened
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CHAPTER15 Supplemental Injection Techniques 271
to the degree that infiltration might not be effective, leading with lingual infiltrations of the same solution for lateral inci
to the recommendation that "mandibular block" techniques sors, and 63% and 47% for central incisors on labial and
should now be employed.47 lingual infiltration.62
A second difficultywith the traditional Halsted approach Meechan and Ledvinkafound similar successrates (50%)
to the inferior alveolar nerve (e.g., IANB, "mandibular on central incisorteeth followinglabialor lingual infiltration
block") is the absence of consistent landmarks. Multiple of 1.0 mL oflidocaine 2% with 1:80,000 epinephrine.63
authors have described numerous approaches to this often In 1990, Haas and coworkers compared mandibular
times elusivenerve.48-50Reported failure rates for the IANB buccal infiltrations for canines with prilocaine HCl versus
are commonly high, ranging from 31% and 41% in man articaine HCl and found no significantdifferences." Success
dibular second and first molars to 42%, 38%, and 46% in rates were 50% for prilocaine and 65% for articaine (both
second and first premolars and canines, respectively,51and 4% with epinephrine 1:200,000). A second study noted a
81o/o in lateral incisors.52 63% successrate on mandibular second molars with artic
Not only is the inferior alveolar nerve elusive, studies aine and 53% with prilocaine (both 4% with epinephrine
using ultrasound53and radiography54•55 to accurately locate 1:200,000).65
the inferior alveolar neurovascular bundle or the mandi Since the introduction of articaine HCl 4% with epi
bular foramen revealed that accurate needle location did nephrine 1: 100,000 into the U.S. dental market in June
not guarantee successful pain control." The central core 2000, numerous anecdotal reports have been receivedfrom
theory best explains this problem.F'" Nerves on the out doctors who claimed that they no longer needed to admin
side of the nerve bundle supply the molar teeth, while ister the IANB to work painlessly in the adult mandible.
nerves on the inside (core fibers) supply the incisor teeth. They claimed that mandibular infiltration with articaine
Therefore the local anesthetic solution deposited near the HCl was uniformly successful.These claims were initially
IAN may diffuse and block the outermost fibers but not met with skepticism.In the past 5 years,four well-designed
those located more centrally, leading to incomplete man clinical trials have been reported comparing infiltration in
dibular anesthesia. the adult mandible of articaine HCl 4% with epinephrine
This difficulty in achieving mandibular anesthesia has 1: 100,000versus lidocaine 2% with epinephrine 1: 100,000
led to the development of alternative techniques to the tra or 1:80,000.7'8'52'66
ditional (Halsted approach) inferior alveolar nerve block. Followingis a summary of these papers.
These have included the Gow-Gates mandibular nerve
block, the Akinosi-Vaziraniclosed-mouth nerve block, the Kanaa MD, Whitworth JM, Corbett IP,Meechan JG:Artic
periodontal ligament (PDL, intraligamentary) injection, aine and lidocaine mandibular buccal infiltration anes
intraosseous anesthesia, and, most recently, buffered local thesia: a prospective randomized double-blind cross-over
anesthetics.59Although all maintain some advantages over study, J Endod 32: 296-298, 2oofi8
the traditional Halsted approach, none is without its own
faults and contraindications. Design. Infiltrations were administered to 31 subjects in
The ability to provide localized areas of anesthesia by the buccal fold adjacent to the mandibular first molar. A
infiltration injection without the need for nerve block injec dose of 1.8mL was administered at a rate of 0.9 mL per 15
tions has a number of benefits. Meechan" has enumerated seconds.The order of drug administration was randomized,
them as follows:(1) technicallysimple, (2) more comfortable with the second injection administered at least 1 week after
for patients, (3) can provide hemostasiswhen needed, (4) in the first. The same investigator administered all injections.
many cases obviate the presence of collateral innervation, Electricalpulp testing (EPT) was used to determine pulpal
(5) avoid the risk of potential damage to nerve trunks, sensitivity.Baseline readings were obtained, and EPT was
(6) lesser risk of intravascular injection, (7) safer in patients repeated once every2 minutes after injection for 30 minutes.
with clotting disorders, (8) reduce risk of needle-stickinjury, If no response (to maximal EPT stimulation of 80 µA)
and (9) preinjection application of topical anesthetic masks occurred, the number of episodesof no response at maximal
needle penetration discomfort. stimulation was recorded. The criterion for successfulanes
Attempts at mandibular infiltration in adult patients have thesia was no volunteer response to maximal stimulation on
been made in the past. In a 1976studyof331 subjectsreceiv two or more consecutiveepisodes of testing. (This had been
ing IANBwith lidocaineHCl 2% with epinephrine 1:80,000, established as the criterion for success in many previous
23.7% had unsuccessfulanesthesia.61Supplemental infiltra clinicaltrials.)
tion of 1.0mL of the same drug on the buccal aspect of the
mandible proved successfulin 70 of the 79 failures. Of the Results. The total number of episodes of no sensation on
remaining 9, 7weresuccessfullyanesthetizedfollowingaddi maximal stimulation in first molars over the period of the
tional infiltration of 1.0mL on the lingual aspect of the trial (32 minutes) was greater for articaine (236 episodes)
mandible. than for lidocaine (129) (P < .001).Twenty(64.5%) subjects
Yonchakand colleaguesinvestigatedinfiltration on inci experienced anesthetic successfollowing articaine, whereas
sors, reporting 45% success following labial infiltration 12 (38.7%)did so with lidocaine (P< .08).The design of the
(lidocaine2% with 1: 100,000epinephrine) and 50% success trial allowed for a maximal possible duration of anesthesia
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272 PART III Techniques of Regional Anesthesia in Dentistry
of 28 minutes. Six subjects receiving articaine achieved 28 Results. Articaine was significantly better than lidocaine
minutes of anesthesia compared with two for lidocaine. in achieving pulpal anesthesia in each of the four teeth
(P < .0001 for all four teeth). Table 15-2 summarizes these
Discussion. The difference between articaine and lidocaine findings.
was most obvious toward the end of the study period. The The onset of successful anesthesia was significantly
percentage of patients showing no response at maximal faster for articaine than for lidocaine for all four teeth tested
stimulation was reduced at all reference points after 22 (Table 15-3).
minutes with lidocaine. With articaine, however, the greatest
percentage of nonresponders was noted at the end of the trial Discussion. The exact mechanism of the increased efficacy
(32 minutes). of articaine is not known. One theory relates to the 4%
concentration of articaine versus the 2% lidocaine solution.
Conclusion. It was noted that 4% articaine with epineph However, Potocnik and associates found that 4% and 2%
rine was more effective than 2% lidocaine with epinephrine articaine were superior to 2% lidocaine in blocking nerve
in producing pulpal anesthesia in lower molars following conduction.67 A second theory is that the thiophene ring of
buccal infiltration. articaine enables it to diffuse more effectively than the
benzene ring found in other local anesthetics.
Robertson D, Nusstein ], Reader A, Beck M, McCartney M: Regarding onset of anesthesia, previous studies with
The anesthetic efficacy of articaine in buccal infiltration onset oflidocaine following IANB found onset times ranging
of mandibular posterior teeth, J Am Dent Assoc 138:1104- from 8 to 11 minutes for the first molar and from 8 to 12
1112,2007.7 minutes for the first premolar. 68-73 Articaine provided a more
rapid onset of pulpal anesthesia for all tested teeth than was
Design. Sixty blinded subjects randomly received buccal provided by IANB. However, pulpal anesthesia declined
infiltration injections of 1.8 mL of 2% lidocaine with epi steadily over the 60 minute test period. Therefore, if pro
nephrine 1 : 100,000 and 4% articaine with epinephrine found pulpal anesthesia is required for 60 minutes, buccal
1: 100,000 at two separate appointments at least 1 week infiltration of 4% articaine with epinephrine 1 : 100,000 will
apart. Each subject served as his or her own control. Sixty not provide the duration needed because of declining pulpal
infiltrations were administered on the right side and 60 on anesthesia.
the left side. For the second infiltration in each subject, the
investigator used the same side randomly chosen for the first Conclusion. Buccal infiltration of the first mandibular
infiltration. The teeth chosen for evaluation were the first molar with 1.8 mL of 4% articaine with epinephrine
and second molars and the first and second premolars. The 1: 100,000 is significantly better than similar infiltration of
same investigator administered all injections. Before injec 2% lidocaine with epinephrine 1: 100,000 in achieving
tions were administered, baseline values were determined on pulpal anesthesia in mandibular posterior teeth. Clinicians
the experimental teeth with EPT. A single infiltration was should keep in mind that pulpal anesthesia will likely decline
administered buccal to the first mandibular molar, bisecting slowly over 60 minutes.
the approximate location of the mesial and distal roots. The
1.8 mL was deposited over a period of 1 minute. One minute
TABLE 15-2
after injection, the first and second molars were pulp tested.
Summary of Articaine vs. Lidocaine Success
At 2 minutes, the premolars were tested. At 3 minutes, the
control canine (contralateral side) was tested. This testing Articaine % Lidocaine %
cycle was repeated every 3 minutes for 60 minutes. Complete Tooth Success Success
absence of sensation to maximal EPT stimulation on two or Second molar 75 45
more consecutive readings was the criterion for successful First molar 87 57
anesthesia. Onset of anesthesia was defined as the time at Second premolar 92 67
which the first of two consecutive no responses to EPT of 80 First premolar 86 61
1
occurred. P < .0001for all teeth tested.
TABLE 15-3
Results of the Onset of Successful Anesthesia, Articaine vs. Lidocaine
Articaine Onset (min) ± Lidocaine Onset (min) ±
Tooth Standard Deviation Standard Deviation PValue
Second molar 4.6 ±4.0 11.1±9.5 .0001
First molar 4.2 ± 3.1 7.7 ± 4.3 .0002
Secondpremolar 4.3 ± 2.3 6.9 ± 6.6 .0014
First premolar 4.7 ± 2.4 6.3 ± 3.1 .0137
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CHAPTER15 Supplemental Injection Techniques 273
Haase A, Reader A, Nusstein J, Beck M, Drum M: Compar treatments. The 2% lidocaine demonstrated a decline after
ing anesthetic efficacy of articaine versus lidocaine as a the 60th minute.
supplemental buccal infiltration of the mandibular first
molar after an inferior alveolar nerve block, J Am Dent Conclusion. Buccalinfiltration of the first molar with a car
Assoc 139:1228-1235,2008.66 tridge of 4% articaine with epinephrine 1: 100,000resulted
in a significantlyhigher successrate (88%) than was attained
Design. Seventy-three subjects participated in a prospec with buccal infiltration of a cartridge of 2% lidocaine with
tive, randomized, double-blinded, crossover study compar epinephrine 1: 100,000(71%) after an IANBwith 4% artic
ing the degree of pulpal anesthesia achievedby means of a aine with epinephrine 1: 100,000.
mandibular buccal infiltration of two anesthetic solutions:
4% articaine with epinephrine 1: 100,000,and 2% lidocaine Kanaa MD, Whitworth JM, Corbett IP, Meechan JG:
with epinephrine 1: 100,000,following an IANB with 4% Articaine buccal infiltration enhances the effectiveness of
articaine with epinephrine 1: 100,000.The subject served as lidocaine inferior alveolar nerve block,Int Endod J 42:238-
his/her own control. The side chosen for the first infiltration 246, 2009.52
was used again for the second infiltration. Injections were
administered at least 1 week apart. The same investigator Design. The goal of this study was to compare mandibular
administered all injections.An EPTwas used to test the first tooth anesthesiafollowinglidocaine IANBwith and without
molar for anesthesia in 3 minute cyclesfor 60 minutes. The supplementary articaine buccal infiltration. In this prospec
IANB was administered over 60 seconds. Fifteen minutes tive randomized, double-blind, crossover study, 36 subjects
after completion of the IANB,the infiltration was adminis receivedtwo IANBinjections with 2.2 mL lidocaine 2% with
tered buccal to the first mandibular molar, bisecting the epinephrine 1:80,000overtwo visits.At one visit,an infiltra
approximate location of the mesial and distal roots. The tion of 2.2 mL of articaine 4% with epinephrine 1: 100,000
1.8mL was deposited over a period of 1 minute. Sixteen was administered in the mucobuccalfold opposite the man
minutes after completion of the IANB (1 minute following dibular first molar.At the other visit,a dummy injection was
the infiltration), EPT testing of the first molar was per performed. At least 1 week separated the two visits. Pulpal
formed. At 3 minutes, the contralateral canine was tested. anesthesia of first molar, first premolar, and lateral incisor
This cycle was repeated every 3 minutes for 60 minutes. teeth was assessedwith an EPT every2 minutes for the first
Anesthesiawas considered successfulwhen two consecutive 10 minutes, and then at 5 minute intervals for 45 minutes
EPT readings of 80 were obtained within 10 minutes of the post injection. Successful anesthesia was defined as the
IANB and infiltration injection, and the 80 reading was absence of sensation on two or more consecutivemaximal
maintained continuously through the 60th minute. EPT stimulations. The number of episodes of no response
to maximal EPT stimulation was also recorded. Onset of
Results. The articaine formulation was significantlybetter pulpal anesthesia was considered the first episode of no
than the lidocaine formulation with regard to anesthetic responseto maximal stimulation (two consecutivereadings),
success:88% versus 71% for lidocaine (P < .01), with anes whereas duration of anesthesia was taken as the time from
thesia developingwithin 10 minutes after IANBand buccal the first of at least two consecutivemaximal readings with
infiltration, sustaining the 80 reading on the EPT continu no response until the onset of more than two responses at
ously for the 60 minute testing period. less than maximal stimulation or the end of the 45 minute
test period, whicheverwas sooner.
Discussion. Anesthetic successwas significantlybetter with
the 4% articaine formulation than the 2% lidocaine formu Results. IANBwith supplemental articaine infiltration pro
lation. Both anesthetic formulations demonstrated a gradual duced greater successthan IANBalone in first molars (33 vs.
increase in pulpal anesthesia. This is likely a result of the 20 subjects, respectively; P < .001), premolars {32 vs. 24;
effect of the infiltrations' overcoming failure or the slow P = .021), and lateral incisors (28 vs. 7; P < .001).Addition
onset of anesthesia following IANB. Therefore, for a ally,IANBwith articaine supplemental infiltration produced
maximum effect with 4% articaine infiltration, a waiting significantlymore episodesof no response than IANBalone
time is required before onset of pulpal anesthesiais achieved. for first molars (339 vs. 162 cases, respectively;P < .001),
It may be prudent to wait for signs of lip numbness before premolars {333vs. 197; P < .001), and lateral incisors (227
administering the infiltration. Without an effectiveIANB, vs. 63; P < .001) (Table 15-4).
buccal infiltration of articaine alone has a relativelyshort
duration (seeprevious two citations). A fairlyhigh percent Discussion. Onset of pulpal anesthesia: In this study, the
ageof patients receivingthe articaine infiltration maintained anesthetic effect for mandibular first molars peaked 25
pulpal anesthesia through the 50th minute. Articaine infil minutes post injection with the dummy injection versus 6
tration demonstrated a decline in the incidence of pulpal minutes followingarticaine infiltration. For first premolars,
anesthesia after the 52nd minute. Becausemost dental pro peak anesthetic effectoccurred at 30 minutes post injection
cedures require less than 50 minutes for completion, this versus 8 minutes following articaine infiltration, and for
injection protocol should prove successfulfor most dental lateral incisors,peak anesthetic effectoccurred at 40 minutes
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274 PART III Techniques of Regional Anesthesia in Dentistry
TABLE 15-4
Successof IANB with Supplemental Articaine Infiltration vs. IANB Alone
First Molar First Premolar Lateral Incisor
Success IANB + dummy 55.6% 66.7% 19.4%
Success IANB + infiltration 91.7% 88.9% 77.8%
(P< .001) =
(P .021) (P < .001)
Onset (mean) IANB + dummy (minutes) 6.8 8.9 10.9
Onset (mean) IANB + infiltration(minutes) 4.5 4.2 6.9
(P< .06) (P< .002) (P= .40)
Duration of pulpal anesthesia (mean) IANB + dummy (minutes) 29.0 31.3 29.1
Duration of pulpal anesthesia (mean) IANB + infiltration (minutes) 38.8 37.8 30.0
(P< .001) (P= .013) (P= .90)
IANB, Inferior alveolarnerve block.
post injection versus 20 minutes followingarticaine infiltra Jaber A, Al-Baqshi B, Whitworth B, et al: The efficacy
tion in the first molar region. of infiltration anesthesia for adult mandibular incisors,
J Dent Res 88:SpecialIssue A (Abstract 702), 2009.74
Duration of Pulpal Anesthesia. The maximum duration of Jaber and colleaguesused a split dose (0.9 mL per site) of
anesthesiapossiblein this trial was 43 minutes. The duration 2% lidocaine with 1: 100,000 epinephrine to confirm this
of pulpal anesthesiawas significantlylonger for first molars finding."
and first premolars but not for lateral incisors (see previous For buccal infiltration of 1.8mL alone, successfulanes
chart). thesia of the central incisor was 77% vs. 97% for the split
buccal/lingual dose. Investigators also compared articaine
Conclusions. IANB injection supplemented with articaine 4% with epinephrine 1: 100,000versus lidocaine 2% with
by buccal infiltration was more successful than IANB epinephrine 1: 100,000as an anesthetic for infiltration in the
alone for pulpal anesthesia in mandibular teeth. Articaine anterior mandible and found that articaine was superior to
infiltration increased the duration of pulpal anesthesia in lidocainein obtaining pulpal anesthesiaof the central incisor
premolar and molar teeth when given in combination with when infiltrated adjacent to the tooth buccallyalone (94%)
a lidocaine IANB and produced a more rapid onset for or with split buccalJlingualinjections {97%).
premolars. The increased success rate for infiltration in the adult
These four clinical trials clearly demonstrate that arti mandibular incisor region is thought to be due to the fact
caine given by mandibular buccal infiltration in the muco that the cortical plate of bone, both buccal and lingual, is
buccal fold by the first mandibular molar can provide more thin and might provide little resistanceto infiltration.
successfulanesthesiaof longer duration to mandibular teeth
when administered alone or as a supplement to IANB.
One thing to consider is that in each of these trials, buccal
SUMMARY AND CONCLUSIONS
infiltration of articaine was administered adjacent to the Failure rates for profound pulpal anesthesia following the
first mandibular molar. These trials demonstrated the effec traditional inferior alveolar nerve block (IANB) on non
tivenessof articaine in improving pulpal anesthesia success pulpally involved teeth are quite high. This has led to the
rates in molars and premolars. However,success rates and development of severalalternativetechniques, including the
duration of anesthesiawere not improved as significantlyin Gow-Gates mandibular nerve block, the Akinosi-Vazirani
lateral incisors-teeth at a distance from the site of local closed-mouth mandibular nerve block, periodontal liga
anesthetic deposition. ment injection, and intraosseous anesthesia. The introduc
tion of articaine HCl spurred interest in its use by infiltration
Meechan JG, Ledvinka JI: Pulpal anaesthesia for man in the adult mandible.
dibular central incisor teeth: a comparison of infiltration Initial studies infiltrating articaine in the buccalfold adja
and intraligamentary injections, Int Endod J 35:629-634, cent to the first mandibular molar showed significantly
2002.63 greater successrates compared with lidocaine2% infiltration
In 2002,Meechanand Ledvinkastudied the effectof infil (all with epinephrine). Additional studies using articaine
trating 1.0 mL of 2% lidocaine with 1:80,000 epinephrine mandibular infiltration (by the first molar) as a supplement
buccallyor linguallyto the mandibular central incisor.63 to IANB (with lidocaine or articaine) demonstrated the
A success rate of 50% was achieved with the buccal or same significant increases. In each of these studies, a full
lingual injection site. However,when the injection dose was cartridge of local anesthetic was administered (1.8mL
split (0.5 mL per site) between buccal AND lingual, the [USA]or 2.2 mL [UK]).Further researchis needed to deter
successrate increased to a statisticallysignificant92%. mine the minimal volume of LAsolution needed to produce
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CHAPTER15 Supplemental Injection Techniques 275
the best clinical result. At this time, the recommendation is 14. Council on Dental Materials, Instruments, and Equipment:
to administer a full cartridge of articaine 4% with epineph Status report: the periodontal ligament injection, J Am Dent
rine 1: 100,000 (or 1 :200,000) in the mucobuccal fold adja Assoc 106:222-224, 1983.
cent to the mandibular first molar when treating molars or 15. Walton RE, Garnick JJ: The periodontal ligament injection:
histologiceffectson the periodontium in monkeys,J Endodod
premolars in the adult mandible.
8:22-26, 1982.
When treating mandibular incisors, the recommendation
16. Nelson PW: Injection system,J Am Dent Assoc 103:692, 1981
is to administer a split dose of articaine 0.9 mL in the buccal (letter).
fold adjacent to the tooth being treated and 0.9 mL on the 17. Shepherd PA, Eleazer PD, Clark SJ, et al: Measurement of
lingual aspect of the same tooth. Splitting of the LA dose is intraosseous pressures generated by the Wand, high-pressure
not effectivein the mandibular molar region. periodontal ligament syringe, and the Stabident system,
The articaine mandibular infiltration injection can be J Endodont 27:381-384, 2001.
repeated later in the dental procedure if pulpal anesthesia 18. MeechanJG:Supplementary routes to local anaesthesia,Intern
begins to resolveand the patient starts to become sensitive. Endod J 35:885--896, 2002.
An electricalpulp tester (EPT) can be used effectivelydo 19. Wong JK: Adjuncts to local anesthesia: separating fact from
assesspulpal anesthesia before invasivedental treatment is fiction, Can Dent Assoc 67:391-397, 2001.
20. Quinn CL: Injection techniques to anesthetize the difficult
begun.7 Studies have demonstrated that the absence of
tooth, J Calif Dent Assoc 26:665--667, 1998.
patient response to an 80 reading was an assurance of pulpal
21. Hochman M, Chiarello D, Hochman C, et al: Computerized
anesthesia in vital asymptomatic teeth.6'75 Two consecutive local anesthesia vs. traditional syringe technique: subjective
EPT readings at maximal output (80 µA) 2 or 3 minutes pain response, NY State Dent J 63:24--29, 1997.
apart is almost always indicative of profound anesthesia. 22. Cassamani C: Une NouvelleTechniqued'AnesthesiaIntraliga
Certosimo and Archer demonstrated that patients who had mentarire [PhD thesis], Paris, 1924.
EPT readings ofless than 80 experiencedpain during opera 23. Fischer G: Local anesthesia in dentistry, ed 4, Philadelphia,
tive procedures in asymptomatic teeth.6 1933, Lea & Febiger.
24. Hoffmann-Axtheim W: History of dentistry, Chicago, 1981,
Quintessence.
25. Dreyer WP, van Heerden JD, de V Joubert JJ: The route of
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control in dental practice, ed 7, St Louis, 1984,CV Mosby. prilocaine with 1:200,000 epinephrine and 2% mepivacaine
49. EversH, Haegerstam G:Anaesthesiaof the lowerjaw.In Evers with 1:20,000levonordefrin compared with 2% lidocainewith
H, Haegerstam G, editors: Introduction to dental local anaes 1:100,000epinephrine for inferior alveolarnerveblock,Anesth
thesia, Fribourg, Switzerland,1990,MediglobeSA. Prog 38:84-89, 1991.
50. TriegerN: New approachesto local anesthesia.In Pain control, 70. Chaney MA, Kerby R, Reader A, et al: An evaluation of lido
ed 2, St Louis, 1994,CV Mosby. caine hydrocarbonate compared with lidocaine hydrochloride
51. OnPharma Inc.: Results of 38 studies on LA success rates, for inferior alveolar nerve block, Anesth Prog 38:212-216,
unpublished. Available at: www.onpharma.com. Accessed 1991.
September 22, 2011. 71. McClean C, Reader A, Beck M, et al: An evaluation of 4%
52. Kanaa MD, Whitworth JM, Corbett IP, et al: Articaine buccal prilocaine and 3% mepivacaine compared with 2% lidocaine
infiltration enhances the effectiveness of lidocaine inferior (1: 100,000 epinephrine) for inferior alveolar nerve block,
alveolarnerve block, Int Endod J 42:238-246,2009. J Endod 19:146--150,1993.
53. Hannan L, Reader A, Nist R, et al: The use of ultrasound for 72. Ridenour S, Reader A, Beck M, et al: Anesthetic efficacyof a
guiding needle placement for inferior alveolar nerve blocks, combination of hyaluronidase and lidocaine with epinephrine
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 87:658- in inferior alveolarnerve blocks,Anesth Prog 48:9-15, 2001.
665, 1999. 73. Steinkruger G, Nusstein J, Reader A, et al: The significanceof
54. Berns JM, SadoveMS: Mandibular block injection: a method needle bevelorientation in achievinga successfulinferior alve
of study using an injected radiopaque material, J Am Dent olar nerve block, J Am Dent Assoc 137:1685--1691,2006.
Assoc65:736--745,1962. 74. Jaber A, Al-BaqshiB,Whitworth C, et al: The efficacyof infil
55. Galbreath JC: 'fracing the course of the mandibular block tration anesthesia for adult mandibular incisors, J Dent Res
injection, Oral Surg Oral Med Oral Pathol 30:571-582, 1970. 88(SpecialIssue A):Abstract702,2009.
56. Reader A, American Association of Endodontists: Taking the 75. DrevenLJ,ReaderA,BeckM, et al:An evaluation of the electric
pain out of restorative dentistry and endodontics: current pulp tester as a measure of analgesia in human vital teeth,
thoughts and treatment options to help patients achieve J Endod 13:233-238,1987.
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Anesthetic Considerations
in Dental Specialties
The techniques of local anesthesia described previously in Once injected,the pH of the anesthetic solution is slowly
this section are valuable to doctors in virtually all areas of increased toward the body's normal pH of approximately
dental practice. However,specific needs and problems are 7.4 by tissue fluid buffers.As this conversion occurs, RNH+
associatedwith pain control in particular areas of dentistry. ions loseW,becoming un-ionized RN ions (accordingto the
This chapter discussesthe dental specialtieslisted below and Henderson-Hasselbalch equation; see Chapter 1), which
their peculiar needs in the area of pain control: now are able to diffuse across the nerve membrane to the
• Endodontics interior of the nerve.
• Pediatric dentistry Pulpal and periapical inflammation or infection can
• Periodontics cause significant alterations in tissue pH in the affected
• Oral and maxillofacialsurgery region, including decreasedpH (e.g.,pus has a pH of 5.5 to
• Fixed prosthodontics 5.6) and increased vascularity.Increased acidity has several
• Long-duration anesthesia {postsurgicalpain control) negative aspects.1 It severely limits the formation of RN,
• Dental hygiene increasingthe formation of RNH+.RNs that do diffuse into
the nerve find a normal tissue pH of 7.4 within the nerve
and re-equilibrate into both RN and RNH+ forms. These
ENDODONTICS RNH+forms are then able to enter into and block sodium
channels, blocking nerve conduction. But with fewer total
Effects of Inflammation on Local Anesthesia anesthetic molecules (RN's and RNH+'s)diffusing into the
Inflammation and infection lower tissue pH, altering the nerve,there is a greaterlikelihoodthat incompleteanesthesia
ability of a local anesthetic to provide clinically adequate will develop.The overalleffectof ion entrapment is to delay
pain control. As a review,local anesthetics are weak bases the onset of anesthesia and possibly interfere with nerve
(pKa, 7.5 to 9.5) and are not water-soluble compounds. blockade.2 Ion entrapment changesthe products of inflam
Combined with hydrochloric acid (HCl), local anesthetics mation, so they inhibit anesthesia by directly affecting the
are injected in their acid-salt form (e.g., lidocaine HCl), nerve. Brown demonstrated that inflammatory exudates
improving their water solubility and stability. The pH of enhance nerve conduction by loweringthe response thresh
a "plain" local anesthetic is approximately 6.5, and the pH old of the nerve,1 which may inhibit local anesthesia. This
of one containing a vasoconstrictor is approximately 3.5. causesblood vesselsin the region of inflammation to become
In an acidic solution, hydrogen ions (H+) are "floating unusually dilated, allowingmore rapid removal of the anes
around." If we abbreviate the anesthetic drug as RN (the thetic from the site of injection. This leads to an increased
un-ionized form of the local anesthetic), then some of these possibilitythat resultant local anesthetic blood levelswill be
RNs will attach to an H+,forming the cationic form of the elevated (from those seen in normal tissue).2
local anesthetic (RNH+). The more acidic the anesthetic Although there are no magic bullets for attaining pro
solution, the greater the number of W ions available,and found pain control in teeth requiring pulpal extirpation,
the greater the percentage of RNH+found in the solution. severalmethods may increasethe likelihood of success.First,
Because only the RN ionic form is lipid soluble and is administer the local anesthetic at a site distant from the
able to cross the lipid-rich nerve membrane, the lower the area of inflammation. It is undesirable to inject anesthetic
pH of the anesthetic solution and the tissue into which it solutions into infected tissue because this may cause the
is injected, the lower is the percentage of RN ions, the infection to spread to uninvolved regions.3•4 Administration
slower is the onset, and the less profound is the resultant of local anesthetic solution into a site distant from the
anesthesia. involved tooth is more likely to provide adequate pain
277
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278 PARTIII Techniquesof RegionalAnesthesiain Dentistry
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CHAPTER 16 Anesthetic Considerations in Dental Specialties 279
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CHAPTER 16 Anesthetic Considerations in Dental Specialties 281
TABLE 16-2
Local Anesthetic Administration by Dentists Who Treat Children (n = 117)
Patient
Age Weight. kg Mean Dose. mg/kg Mean. mg/kg Range. mg Range. mg/kg Recommended (MRD). mg/kg
2 13 69.9 5.4 12-252 0.9-19.3 Lidocaine 4.4-7.0
Mepivacaine 4.4-6.0
5 20 96.5 4.8 18-252 0.9-12.6
10 35 135 3.8 36-252 1.0-7.2
Modified from Cheatham BD,Primosch RE,Courts FJ:A survey oflocal anesthetic usage in pediatric patients by Florida dentists, J Dent Child 59:401-407,
1992.
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282 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Figure 16-4. Lip trauma caused by biting while the area was anesthetized.
TABLE 16-4
Relative Durations of Pulpal and Soft Tissue Anesthesia
Approximate Approximate
Pulpal Anesthesia, Soft Tissue
Drug min Anesthesia, hr
Mepivacaineplain 20-40 3-4
Prilocaine plain (infiltration) 10 lY,:-2
Lidocaineplain 5-10 1-lY,:
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CHAPTER 16 Anesthetic Considerations in Dental Specialties 283
complete diffusion of the anesthetic solution. Also, children bone in the mandible in younger children.The rate of success
are smaller; thus standard injection techniques usually can of mandibular infiltration anesthesia decreases somewhat
be completed with decreased depth of needle penetration. for primary mandibular molars as the child increasesin age.
The technique of supraperiostealinfiltration in the mandible
Maxillary Anesthesia. All primary teeth and permanent is the same as in the maxilla.The tip of the needle is directed
molars can be anesthetized by supraperiosteal infiltration toward the apex of the tooth, in the mucobuccal fold, and
in the mucobuccal fold. The posterior superior alveolar approximatelyone fourth to one third {0.45to 0.6 mL) car
(PSA) nerve block is rarely necessary because of the effec tridge is slowlydeposited.
tiveness of infiltration in children. However,in some indi The IANB has a greater successrate in children than in
viduals, the morphology of the bone surrounding the apex adults because of the location of the mandibular foramen.
of the permanent first molar does not permit effectiveinfil The mandibular foramen in children lies distal and more
tration of local anesthetic, because the zygomatic process inferior to the occlusalplane. Benham37 demonstrated that
lies closer to the alveolar bone in children. A PSA nerve the mandibular foramen lies at the height of the occlusal
block may be warranted in this clinicalsituation. A 27-gauge plane in children and extends an averageof 7.4 mm above
short dental needle should be used and the depth of needle the occlusalplane in adults. He also found that there is no
penetration modified to meet the smaller dimensions of age-related difference as to the anteroposterior position of
the pediatric patient, to minimize the risk of overinsertion the foramen on the ramus.
leading to hematoma. As an alternative to the PSA,Rood32 The technique for an IANB is essentially identical for
has suggestedusing buccal infiltrations on both the mesial adults and children.The syringebarrel is placed in the comer
and the distal of the maxillary first molar to avoid a pro of the mouth on the opposite side. The average depth of
minent zygomatic process. The anterior superior alveolar penetration to bone is approximately 15 mm, although this
(ASA)nerve block also can be used in children, as long as may vary significantlywith the size of the mandible and the
it is realized that the depth of penetration is probably just age of the patient. As with the adult, bone should be con
slightlygreaterthan with a supraperiostealinjection (because tacted before any solution is deposited. In general,the more
of the lower height of the maxillae in children). Generally, inferior location of the mandibular foramen in children pro
there are few indications for the PSA or ASA nerve block vides a greater opportunity for successfulanesthesia. "Too
in children. low" injections are more likely to be successful.In clinical
Occasionally,a maxillary tooth remains sensitive after a situations, the successrate for well-behavedchildren usually
supraperiosteal injection because of accessory innervation exceeds90% to 95%.
from the palatal nerves33 or widelyflaredpalatalroots. Palatal Becauseof the decreasedthicknessof soft tissue overlying
anesthesiacan be attained in children through the nasopala the inferior alveolarnerve (about 15 mm), a 25- or 27-gauge
tine and greater (anterior) palatine nerve blocks. The tech short needle may be recommended for the IANBin younger,
nique for a nasopalatine nerve block proceeds exactly as smaller patients. This should be changed to a long needle
described in Chapter 13. That for a greater palatine nerve once the patient is of sufficientsizethat a short needle does
block is as follows:The administrator visualizesa line from not reach the injection site without entering tissue almost to
the gingival border of the most posterior molar that has its hub.
erupted to the midline. The needle is inserted from the The buccal nerve may be anesthetized if anesthesiaof the
opposite side of the mouth, distal to the last molar,bisecting buccal tissues in the permanent molar region is necessary.
this line. If the child has only primary dentition, the needle The needle tip is placed distal and buccal to the most poste
is inserted approximately 10 mm posterior to the distal rior tooth in the arch. Approximately0.3 mL of solution is
surfaceof the secondprimary molar,bisectingthe line drawn deposited.
toward the midline. The Vazirani-Akinosiand Gow-Gatesmandibular nerve
An intrapapillary injection also can be used to achieve blocks also can be used in children. Akinosi38 advocatesthe
palatal anesthesiain young children. Once buccal anesthesia use of short needleswith this technique in children.He states
is effective,the needle {27-gaugeshort) is inserted horizon that the technique appears lessreliablein children, which he
tallyinto the buccalpapillajust abovethe interdental septum. relates to the difficultyof judging the depth of penetration
Localanesthetic is injected as the needle is advanced toward necessary in a growing child. The Gow-Gates mandibular
the palatal side. This should cause ischemia of the soft block can be used successfullyin children.39 However,these
tissue.34 injections are rarely necessaryin pediatric dentistry because
of the effectivenessof mandibular infiltration {when the
Mandibular Anesthesia. Supraperiostealinfiltrationusually dentition is composed entirely of primary teeth) and the
is effectivein providing pain control in mandibular primary relative ease with which one can achieve inferior alveolar
teeth.35•36 Sharaf reported that buccal infiltration in the man and incisivenerve block anesthesia.
dible in 80 children (ages 3 to 9 years) was as effectiveas The incisivenerve block provides pulpal anesthesiato the
inferior alveolarnerve block (IANB)anesthesia in all situa fiveprimary mandibular teeth in a quadrant. Deposition of
tions, exceptwhen pulpotomywas performed on the primary anesthetic solution outside the mental foramen with appli
second molar.35 This was the result of decreased density of cation of finger pressure for 2 minutes provides a very high
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284 PART III Techniques of Regional Anesthesia in Dentistry
degree of success. The mental foramen usually is located recommended for use in hemostasis.w" Epinephrine is most
between the two primary mandibular molars. A volume of commonly used for hemostasis in a concentration of
0.45 mL (X of a cartridge) is suggested. 1:50,000(0.2 mg/mL).Generally,smallvolumes(not exceed
The PDL injection has been well accepted in pediatric ing 0.1 mL) are deposited when used for hemostasis. Epi
dentistry and can be used as an alternativeto supraperiosteal nephrine alsoprovidesexcellenthemostasisin aconcentration
injection. It provides the doctor with the means to achieve of 1: 100,000,although surgicalbleeding is inverselypropor
anesthesia of proper depth and duration on one tooth, tional to the concentration of vasopressor administered.
without unwanted residual soft tissue anesthesia. The PDL When plain local anesthetic is infiltrated (e.g., 3% mepiva
is also useful when a child has discrete carious lesions in caine) during periodontal surgery,blood loss is two to three
multiple quadrants. See Chapter 15 for a complete discus times that noted when 2% lidocaine with 1: 100,000 epi
sion of technique for the PDL injection. It is recommended nephrine is administered." Buckleyand associatesdemon
that the described technique be scrupulously adhered to, to strated that use of a 1:50,000 epinephrine concentration
avoid physiologic(pain) and psychological(fear) trauma to produced a 50% decrease in bleeding during periodontal
the patient. The PDL injection is not recommended for use surgeryfrom that seenwith a 1: 100,000concentration (with
on primary teeth because of the possibilityof enamel hypo 2% lidocaine).45 However,epinephrine is not a drug without
plasia occurring in the developingpermanent tooth." systemic effectsand some undesirable local effects.Studies
have shown that eventhe smallvolumesof epinephrine used
in dentistry can significantlyincrease the concentrations of
PERIODONTICS plasma catecholamine and can alter cardiac function."
Specialrequirements for localanesthesiain periodontal pro Therefore,it is prudent to administer the smallestvolume of
cedures center on the use of vasopressorsto provide hemo the least concentrated form of epinephrine that provides
stasis and the use of long-duration local anesthetics for clinicallyeffectivehemostasis.
postoperative pain control. Postsurgical pain management, As tissue levelsof epinephrine decreaseafter its injection
including the use of long-duration anesthesia, is discussed for hemostasis,a rebound vasodilationdevelops.Sveendem
as a separate subject later in this chapter. onstrated that postsurgicalbleeding (at 6 hours) occurred in
Soft tissue manipulation and surgical procedures are 13of16 (81.25%)patients receiving2% lidocaine with epi
associated with hemorrhage, especially when the tissues nephrine for surgical removal of a third molar, whereas 0 of
involvedare not healthy.Administration of local anesthetics 16 patients who underwent surgery with 3% mepivacaine
without vasopressorsprovesto be counterproductivebecause bled at 6 hours post surgery," Bleedinginterfered with post
the vasodilating property of the local anesthetic increases operativehealingin 9of16 (56.25%)patients receivinglido
bleeding in the region of the injection.41 Vasopressorsare caine with epinephrine, compared with 25% of patients
added to counteract this undesirable property of local receivingno epinephrine. Evidencealso suggeststhat the use
anesthetics. of epinephrine in local anesthetics during surgery may
The pharmacology of vasopressors is more completely produce an increase in postoperative pain.47
discussed in Chapter 3. As a review,vasopressors produce Many doctors use a 30-gauge short needle to deposit
arterial smooth muscle contraction through direct stimula anestheticsfor hemostasis.Their rationale is that the thinner
tion of a. receptors located in the wall of the blood vessel. needle produces a smaller defect {puncture) in the tissue.
Consequently,it followsthat localanestheticswith vasopres If a small puncture is important, then the 30-gauge needle
sors used for hemostasis must be injected directly into the should be used, but only for this purpose (hemostasis).
region where the bleeding is to occur. The 30-gauge short needle should not be used if there is
Pain control for periodontal procedures should be the possibility of positive aspiration of blood, or if any
achieved through nerve block techniques, including poste depth of soft tissue must be penetrated. Aspiration of blood
rior superior alveolar, inferior alveolar, and infraorbital through a 30-gauge needle is difficult (although possible).
nerve blocks.Saadoun18 has shown that the intraseptal tech A 27-gauge needle can be used for local infiltration to
nique is very effectivefor periodontal flap surgical proce achievehemostasis when vascularityis a problem, or in any
dures.It decreasesthe total volumeof administeredanesthetic other area of the oral cavity without an increase in patient
and the volume of blood lost during the procedure. Local discomfort.
anesthetic solutions used for nerve blocks should include a
vasopressor in a concentration not greater than 1: 100,000
epinephrine or 1:20,000levonordefrin.An epinephrine con
ORAL AND MAXILLOFACIAL SURGERY
centration of 1:50,000is not recommended for pain control Pain control during surgicalprocedures is achievedthrough
because depth, duration, and success rates are no greater administration oflocal anesthetics,givenalone or in combi
than those seen with anesthetics containing 1: 100,000 or nation with inhalation sedation, intravenous sedation, or
1:200,000epinephrine. general anesthesia.As is the case with periodontal surgery,
Epinephrine is the drug of choice for local hemostasis. long-duration local anesthetics play an important role in
Norepinephrine (which is not available in North America postoperative pain control and are discussedseparately.
in dental local anesthetics) can produce marked tissue isch Local anesthetic techniques used in oral surgery do not
emia, which can lead to necrosis and sloughing and is not differ from those employed in nonsurgical procedures.
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CHAPTER 16 Anesthetic Considerations in Dental Specialties 285
Therefore it should be expected that instances of partial or Chapter 14 provide only partial anesthesia in this situation.
incomplete anesthesia will occur. Oral and maxillofacial sur The PDL injection usually corrects the lack of pain control
geons frequently treat patients who have received intrave in this circumstance.
nous sedation or general anesthesia before the start of
surgery. These techniques act to modify the patient's reaction
to pain, leading to a decrease in the number of reported
FIXED PROSTHODONTICS
instances of inadequate local anesthesia. When preparing a tooth for full coverage(crown or bridge),
Local anesthesia is administered almost routinely to it is necessary to place a provisional restoration over the
patients for third molar extractions under general anesthe prepared tooth. Although achievingpain control might not
sia. The reasons for this are as follows: be difficultat the initial visit,it maybe difficultat subsequent
1. General anesthesia does not prevent pain. General visits to adequately anesthetize the prepared tooth. The
anesthesia prevents the patient from responding reason for this is probablythe provisionalrestoration. Overly
outwardly to painful stimulation. Blood pressure (BP), high restorations produce traumatic occlusion, which can
heart rate (HR), and respiratory rate (RR) do respond lead to considerable sensitivity after about a day. Poorly
to surgical stimulation (increases in BP, HR, and RR). adapted gingivalmargins developmicroleakage,alsocausing
2. Pain control through local anesthetic administration sensitivity.Preparation of the tooth itself can cause sensitiv
during surgery permits lessened exposure to general ity, through desiccation of tooth structure, possible pulpal
anesthetic agents, allowing for a faster postanesthetic involvement, and periodontal irritation. The longer these
recovery period and minimizing drug-related sources of irritation are present, the greater the trauma to
complications. the tooth is likelyto be, and the more difficultit is to achieve
3. Hemostasis is possible if a vasopressor is included. adequate anesthesia.Usuallya regional nerve block is effec
4. Residual local anesthesia in the postoperative period tive. Supraperiosteal injections generally do not provide
aids in postsurgical pain control. adequate pain control in these situations (depth may be
The volume of drug and the rate at which it is adminis adequate, but duration is considerably shorter than that
tered are important in all areas of dental practice, but prob usually expectedfrom the drug).
ably are most important during extraction of teeth from
multiple quadrants. When four third molars are extracted, LONG-DURATION LOCAL ANESTHESIA
effective pain control must be obtained in all four quadrants.
This requires multiple injections of local anesthetics, which Prolonged Dental or Surgical Procedures
usually occur within a relatively short time. Four cartridges Severalspecialtyareas of dental practice require longer than
or more of local anesthetic are frequently used.* The rate at usual pulpal or soft tissue anesthesia. They include fixed
which these local anesthetics are administered must be prosthodontics, oral surgery, and periodontics. During
closely monitored to lessen the occurrence of complications. longer procedures (2 or more hours), an adequate duration
Complications arising from rapid administration of local of pulpal anesthesia may be difficult to achievewith more
anesthetic include any of the following: commonly used anesthetics such as articaine, lidocaine,
1. Pain during injection mepivacaine, and prilocaine. Bupivacaine is a long-acting
2. Greater possibility of a serious overdose reaction, if the local anesthetic that can then be used. It is discussed more
local anesthetic is administered intravascularly (the completelyin Chapter 4.
speed of N drug administration significantlyaffectsthe Bupivacaine,a homolog of mepivacaine,has a long dura
clinicalmanifestations of toxicity) tion of clinical effectivenesswhen used for regional nerve
3. Postanestheticpain caused by tissue trauma during the block. Its duration of action when administered by supra
injection periosteal injection, although still long, is somewhat shorter
These complications and their prevention, recognition, (shorter even than that of lidocaine with epinephrine).48 Its
and management are discussedin greater detail in Chapters postoperative analgesicperiod lasts an averageof 8 hours in
17 and 18. the mandible and 5 hours in the maxilla.
It should be noted that in some persons, the inferoposte Bupivacaine is available with a vasopressor (1:200,000
rior border of the mandible is not innervated by the trigemi epinephrine). It is interesting to note that the addition of
nal nerve.Any of the mandibular nerve blocks described in vasopressorto bupivacaine does not prolong its duration of
action.49
*Typical local anesthetic injections for extraction of four third molars Postsurgical Management of Pain
include the following:
1. Right and left inferior alveolarnerve blocks, 1.8 mL each (3.6 mL) Frequently, after extensive surgical procedures, patients
2. Right and left posterior superior alveolarnerve blocksor supraperiosteal experienceintense pain when the local anesthetic effectdis
infiltration over each third molar, 1.3to 1.8 mL each (2.6 to 3.6 mL) sipates. It was, and still is in many cases,common practice
3. Right and left palatal infiltration over the maxillary third molars, to treat postoperative pain through the use of opioid anal
0.45 mL each,or right and left greaterpalatine nerveblock, 0.45 mL each
(0.09 mL)
gesics.However,opioids havea high incidenceof undesirable
Total volume of local anesthetic: 8.1 mL or 162mg or a 2% solution, side effectssuch as nausea, vomiting, constipation, respira
243 mg of a 3%, or 324 mg of a 4%. tory depression, and postural hypotension, especially in
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286 PARTIII Techniquesof RegionalAnesthesiain Dentistry
Protocol for Perioperative and Postoperative Pain Control number needed to treat (NNT), the number of patients
in Surgical Patients. Postoperative pain associated with who need to receive the active drug for one to achieve at
most uncomplicated dental surgical procedures is mild and least 50% relief of pain compared with placebo over a
is well managed by oral administration of nonsteroidal 4- to 6-hour treatment period," The most effectiveanalge
anti-inflammatory drugs (NSAIDs) such as aspirin and sics have an NNT of just over 2 (Table 16-5). Effective
ibuprofen." Preoperativeadministration of NSAIDsappears pain relief for dental surgery normally can be achievedwith
to delay the onset of postoperative pain and to lessen its oral nonopioid, nonsteroidal anti-inflammatory drugs,
severity.s2•54 When a patient is unable to tolerate aspirin coxibs,and combinations of acetaminophen (paracetamol)
or other NSAIDs, acetaminophen can provide acceptable and codeine."
analgesia. As noted in Table 16-5, few,if any, analgesicsare better
Other dental surgicalprocedures,such as removalof bony than NSAIDsfor acute pain. AllNSAIDson the Leaguetable
impactions and osseous periodontal or endodontic surgery, have NNTs of 1.6 to 3.0. Alternative analgesics, such as
are more traumatic and typically are associatedwith more codeine 60 mg and tramadol 50 mg, have NNTsof 16and 8,
intense and prolonged postoperativepain. The onset of such respectively.Parenteral morphine 10 mg and meperidine
pain can be delayed by presurgical administration of an 100mg haveNNTsof2.9.si,s6Acetaminophen (paracetamol),
NSAID followed by administration of a long-acting local administered orally at a dose of 1000mg, has an NNT of
anesthetic (bupivacaine) at the completion of surgery.'" almost 4. When combined with codeine 60 mg, its NNT
The Oxford League Table of AnalgesicEfficacypresents improves to 2.2. Ibuprofen 400 mg at 2.4 and diclofenac
a meta-analysis of randomized, double-blind, single-dose, 50 mg and rofecoxib50 mg at about 2.3 are better. NSAIDs
placebo-controlled studies in patients with moderate to generallydo well with lower (better) NNTs.s1
severe postoperative dental, orthopedic, gynecologic, and For effective postsurgical pain management (i.e., no
general surgical pain." Analgesic efficacy is expressed as breakthrough pain), it is important to maintain a therapeutic
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CHAPTER 16 Anesthetic Considerations in Dental Specialties 287
TABLE 16-6
Nonsteroidal Anti-Inflammatory Drugs
Generic Proprietary Availabiity, mg Dosage Regimen
Ibuprofen Advil,Caldolor, 100,200, 400, 600, 800 Adults: 400 mg PO every 4-6 hours as needed
Motrin, and others
Ketorolac Toradol 10 10 mg PO q4-6h; max 40 mg/day
Start 20 mg PO if <65 yo and >50 kg
Note: PO only for patients who have receivedparenteral treatment;
duration of combined PO/IM/IV treatment not to exceed5 days
Diclofenac Cambia, Zipsor 50 50 mg POtid
potassium Start 100mg PO; 200 mg/day first 24 hours only, 150mg/day thereafter
Piroxicam Feldene 10,20 Adults: 20 mg PO once daily.Adjust dose, as needed. Daily dose may be
divided into two doses,if desired.
Celecoxib Celebrex 50, 100,200,400 Start 400 mg PO, then 200 mg PO bid
Naproxen Naprosyn 250,375,500 250-500mg PO q12h. Max: 1250mg/day
Tramadol Ultram, Ryzolt 50, 100,200 ER 50-100 mg PO q4-6h; Max: 400 mg/day
Data from Mosby'sdental drug reference,St Louis,2012,Mosby.
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288 PART III Techniques of Regional Anesthesia in Dentistry
planing without discomfort requires pulpal anesthesia, along irreversible pulpitis, Oral Surg Oral Med Oral Pathol Oral
with soft tissue and osseous anesthesia. 60 More than 70% of Radiol Endodont 84:676-682, 1997.
respondents to a survey on dental hygiene patients' need for 9. Leonard M: The efficacyof an intraosseous injection system
pain control reported that their patients needed anesthesia of delivering local anesthetic, J Am Dent Assoc 126:11-86,
but did not receive it.61 1995.
10. Coury KA:Achievingprofound anesthesiausing the intraosse
Feedback from dentists whose hygienists administer local
ous technique, TexDent J 114:34-39, 1997.
anesthesia has been uniformly positive; negative comments
11. Nusstein J, Reader A, Nist R, et al: Anesthetic efficacyof the
have been extremely rare.62 Dental patients themselves are supplemental intraosseous injection of 2% lidocaine with
aware of the difference between local anesthesia adminis 1:100,000 epinephrine in irreversible pulpitis, J Endodont
tered by the dental hygienist and that administered by 24:478-491, 1998.
the dentist. They frequently comment on the lack of dis 12. Quinn CL: Injection techniques to anesthetize the difficult
comfort when the hygienist injects the local anesthetic. Be tooth, J Calif Dent Assoc 26:665--667, 1998.
it a slower rate of administration, greater attention to the 13. Parente SA,Anderson RW,Herman WW, et al:Anesthetic effi
details of atraumatic injection technique, or greater empathy, cacy of the supplemental intraosseous injection for teeth with
it works. irreversiblepulpitis, J Endodont 24:826-828, 1998.
14. Brown R: Intraosseous anesthesia:a review,J Calif Dent Assoc
27:785-792, 1999.
References 15. WeathersA Jr: Takingthe mystery out of endodontics. Part 6.
1. Brown RD:The failure oflocal anaesthesiain acute inflamma Painlessanesthesia for the "hot" tooth, Dent Today 18:90-93,
tion, Br Dent J 151:47-51, 1981. 1999.
2. Vandermeulen E: Pain perception, mechanisms of action of 16. Stabile P, Reader A, Gallatin E, et al: Anesthetic efficacyand
local anesthetics and possible causes of failure, Rev Belge heart rate effectsof the intraosseous injection of 1.5% etido
Medecine Dent 55:19-40, 2000. caine (1:200,000 epinephrine) after an inferior alveolar nerve
3. KitayD, Ferraro N, Sonis ST:Lateralpharyngeal space abscess block, Oral Surg Oral Med Oral Pathol Oral Radiol Endodont
as a consequence of regional anesthesia, J Am Dent Assoc 89:407-411, 2000.
122:56-59, 1991. 17. ReplogleK, Reader A, Nist R, et al: Cardiovascular effects of
4. Connor JP,Edelson JG: Needle tract infection: a case report, intraosseous injections of 2% lidocaine with 1:100,000 epi
Oral Surg 65:401-403, 1988. nephrine and 3% mepivacaine,J Am Dent Assoc 130:549--657,
5. Malamed SF: Buffering local aesthetics in dentistry, ADSA 1999.
Pulse. In press. 18. SaadounAP,MalamedSF:Intraseptal anesthesiain periodontal
6. Personal communication, Onpharma Inc., February 2011. surgery,J Am Dent Assoc 111:249-256, 1985.
7. Coggins R, Reader A, Nist R, et al: Anesthetic efficacyof the 19. Goodsen JM,Moore PA:Life-threateningreactions after pedo
intraosseous injection in maxillaryand mandibular teeth, Oral dontic sedation: an assessment of narcotic, local anesthetic,
Surg Oral Med Oral Pathol Oral Radiol Endodont 81:634-641, and antiemetic drug interaction, J Am Dent Assoc 107:239-
1996. 245, 1983.
8. Reisman D, Reader A, Nist R, et al: Anesthetic efficacyof the 20. Moore PA: Preventing local anesthesia toxicity, J Am Dent
supplemental intraosseous injection of 3% mepivacaine in Assoc 123:60-64, 1992.
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CHAPTER 16 Anesthetic Considerations in Dental Specialties 289
21. Berquist HC: The danger of mepivacaine 3% toxicity in analgesia and wound healing, Int J Oral Surg 8:301-306,
children, Can Dent AssocJ 3:13, 1975. 1979.
22. Malamed SF:Morbidity, mortality and local anesthesia, Prim 45. BuckleyJA,Ciancio SG,McMullenJA:Efficacyof epinephrine
Dent Care 6:11-15, 1999. concentration in local anesthesia during periodontal surgery,
23. AmericanAcademyon Pediatric Dentistry Council on Clinical J Periodontol 55:653--657,1984.
Affairs: Guideline on appropriate use of local anesthesia for 46. Jastak JT, YagielaJA: Vasoconstrictors and local anesthesia;
pediatric dental patients, Pediatr Dent 30(Suppl 7):134-139, a review and rationale for use, J Am Dent Assoc 107:623--630,
2008-2009. 1983.
24. MeechanJG,Rood JP:Adverseeffectsof dental local anaesthe 47. Skoglund LA,Jorkjend L: Postoperative pain experience after
sia, Dent Update 24:315-318, 1997. gingivectomies using different combinations of local anaes
25. DavisMJ,VogelLD:Localanestheticsafetyin pediatric patients, thetic agents and periodontal dressings, J Clin Periodontol
NY State Dent J 62:22-35, 1996. 18:204-209,1991.
26. Cheatham BD,Primosch RE,Courts FJ:A surveyof local anes 48. Danielsson K, EversH, Nordenram A: Long-actinglocal anes
thetic usage in pediatric patients by Florida dentists, J Dent thetics in oral surgery: an experimental evaluation of bupiva
Child 59:401-407, 1992. caine and etidocaine for oral infiltration anesthesia, Anesth
27. YagielaJA:Regionalanesthesiafor dental procedures,Int Anes Prog 32:65--68,1985.
thesiol C1in27:28-82, 1989. 49. Danielsson K, EversH, Holmlund A, et al: Long-acting local
28. Malamed SF:Allergicand toxic reactions to local anesthetics, anaestheticsin oral surgery,Int J Oral MaxillofacSurg 15:119--
Dent Today22:114-121,April 2003. 126, 1986.
29. CollegeC, FeigalR,WanderaA, et al: Bilateralversusunilateral 50. Hardman JG, Limbird LE, editors: Goodman & Gilman's the
mandibular block anesthesiain a pediatric population, Pediatr pharmacologicalbasis of therapeutics, ed 10,NewYork,2001,
Dent 22:453-457,2000. McGraw-Hill.
30. FDAapprovesOraVerse.Availableat:www.drugs.com.Accessed 51. The Oxford LeagueTableof Analgesicsin Acute Pain, Bando
February 7, 2011. lier Website,2007.Availableat: http://www.medicine.ox.ac.uk/
31. Tavares M, Goodson JM, Studen-Pavlovich D, et al, and bandolier/booth/painpag/ Acutrev/Analgesics/Leagtab.html.
The Local Anesthetic ReversalGroup: Reversalof soft tissue AccessedOctober 6, 2011.
anesthesia with phentolamine mesylate in pediatric patients, 52. Jackson DL, Moore PA, Hargreaves KM: Pre-operative non
J Am Dent Assoc 139:1095-1104,2008. steroidal anti-inflammatory medication for the prevention
32. Rood JP: Notes on local analgesiafor the child patient, Dent of postoperative dental pain, J Am Dent Assoc 119:641--647,
Update 8:377-381, 1981. 1989.
33. Kaufman L, Sowray JH, Rood JP: General anaesthesia, local 53. Linden ET, Abrams H, Matheny J, et al: A comparison of
analgesia,and sedation in dentistry, Oxford, UK, 1982,Black postoperative pain experience following periodontal surgery
well Scientific. using two local anesthetic agents, J Periodontol 57:637--642,
34. O'Sullivan VR, Holland T, O'Mullane DM, et al: A review of 1986.
current local anaesthetic techniques in dentistry for children, 54. Acute Pain Management Guideline Panel:Acute pain manage
J Irish Dent Assoc32:17-27, 1986. ment: operative or medical procedures and trauma. Clinical
35. Sharaf AA:Evaluationof mandibular infiltration versus block practice guideline, AHCPR Pub. No. 92-0032,Rockville,Md,
anesthesia in pediatric dentistry, ASDC J Dent Child 64:276- 1992, Agency for Health Care Policy and Research, Public
281, 1997. Health Service, U.S. Department of Health and Human
36. Oulis CJ, Vadiakis GP, Vasilopoulou A: The effectivenessof Services.
mandibular infiltration compared to mandibular block anes 55. Cook RJ, Sackett DL: The number needed to treat: a
thesia in treating primary molars in children, Pediatr Dent clinicallyusefulmeasure of treatment effect,BMJ310:452-454,
18:301-305,1996. 1995.
37. Benham NR: The cephalometric position of the mandibular 56. Ong CKS,Lirk P,Tan CH, et al: An evidence-basedupdate on
foramen with age,J Dent Child 43:233-237, 1976. nonsteroidal anti-inflammatory drugs, Clin Med Res 5:19-34,
38. Akinosi JO: A new approach to the mandibular nerve block, 2007.
Br J Oral Surg 15:83--87,1977. 57. Ibuprofen monograph. Indications-Dosage. Available at:
39. Yamada A, Jastak JT: Clinical evaluation of the Gow-Gates www.mdconsult.com. Updated August 16, 2010. Accessed
block in children, Anesth Prog 28:106-109, 1981. October 6, 2011.
40. Brannstrom M, LindskogS,NordenvallKJ:Enamel hypoplasia 58. Malamed SF: Local anesthetics: dentistry's most important
in permanent teeth induced by periodontal ligament anes drugs, J Am Dent Assoc 125:1571-1576,1994.
thesia of primary teeth, J Am Dent Assoc 109:535-736, 1984. 59. American Dental Hygienists Association: Availableat: www.
41. Davenport RE, Porcelli RJ, Iacono VJ, et al: Effects of anes adha.org, January 2011.AccessedOctober 6, 2011.
thetics containing epinephrine on catecholaminelevelsduring 60. Sisty-LePeauN, BoyerEM, Lutjen D: Dental hygienelicensure
periodontal surgery,J Periodontol 61:553--558,1990. specificationson pain control procedures, J Dent Hyg 64:179--
42. van der Bijl P, Victor AM: Adverse reactions associated with 185, 1990.
norepinephrine in dental local anesthesia,Anesth Prog 39:37- 61. Sisty-LePeauN, Nielson-Thompson N, Lutjen D: Use, need
89, 1992. and desire for pain control procedures by Iowa hygienists,
43. Jakob W: Local anaesthesia and vasoconstrictive additional J Dent Hyg 66:137-146, 1992.
components, NewslettInt Fed Dent AnesthesiolSoc 2:1, 1989. 62. DeAngelis S, Goral V: Utilization of local anesthesia by
44. Sveen K: Effect of the addition of a vasoconstrictor to local Arkansasdental hygienists,and dentists' delegation/satisfaction
anesthetic solution on operative and postoperative bleeding, relativeto this function, J Dent Hyg 74:196-204,2000.
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IN THIS PART
Chapter 17 Local Complications
Chapter 18 Systemic Complications
Chapter 19 Legal Considerations
Chapter 20 Recent and Future Trends in Pain Control
Chapter 21 Questions
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PA T
Complications, Legal
Considerations, Questions,
and Future
In spite of careful patient evaluation, proper tissue preparation, and meticulous technique of admin
istration, local and systemic complications associated with dental anesthesia occasionally develop.
These problems are addressed in Chapters 17 and 18.Emphasis is placed on prevention, recognition,
and management of the complications.
Dr. Daniel Orr II discusseslegalconsiderations associatedwith the administration oflocal anesthet
ics in Chapter 19.
Chapter 20,"Future Trends in Pain Control,"first appeared in the third edition and is updated here.
Starting in the late 1990s,there has been a renewalof interest in the field of local anesthesia... a renais
sance of sorts... beginning with the introduction of computer-controlled local anesthetic delivery
(C-CLAD),and in 2000,the introduction of articaine HCl in the United States.Most recently,the local
anesthesiareversalagentphentolamine mesylate(2008)and bufferedlocalanesthetics (2011)havebeen
introduced. As for the future, research is now being conducted into providing maxillary pulpal anes
thesia without the need for injection of local anesthetics.
Chapter 21 presents a series of questions related to local anesthesia and pain control in dentistry.
These frequently asked questions (FAQs)come from doctors who have had peculiar situations arise in
connection with local anesthetic administration. The more common questions are presented here as a
matter of interest and in the hope that the answersto specificquestions or problems might be included.
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I
Local Complications
' I •I
A number of potential complications are associated with do appear. A MedLine search for broken dental needles
the administration of local anesthetics. For purposes of from 1951through February 2010 uncovered 26 published
convenience, these complications may be separated into reports of broken dental needles, including their cause and
those that occur locally in the region of the injection and management.P:" Reviewof 20 of these reports, for which
those that are systemic. Systemiccomplications associated information regarding needle gauge and length and tech
with the administration of local anesthesia are discussed in nique of anesthesia employed is available, reveals that 15
Chapter 18,and include overdosage(toxicreaction), allergy, were inferior alveolar nerve block (IANB) and 5 were
and psychogenicreactions. The followinglocalizedcompli posterior superior alveolar (PSA) nerve block. All 5 PSA
cations are described in this chapter: reports described adult patients, whereas 9 of the 15broken
• Needle breakage needle reports followingIANBoccurred in children. Needle
• Prolonged anesthesia or paresthesia gauge and/or length was presented in 11 papers. Ten of the
• Facialnerve paralysis 11needles were 30-gaugeshort; only one case reported long
• Trismus needlebreakage (27-gauge)with the needle remaining in the
• Soft tissue injury tissues.12
• Hematoma Pogrel reported on 16patients whom he evaluated over a
• Pain on injection 25-year period (1983-2008) following needle breakage.1
• Burning on injection Fifteen patients had received IANB, one a PSA. Thirteen
• Infection of the 16 needles were 30-gauge short, 3 were 27-gauge
• Edema short.
• Sloughing of tissues Independent of the cited literature, this author is aware
• Postanesthetic intraoral lesions of 51 cases that progressed to litigation in which broken
It must be emphasizedthat with any complication associ dental needle fragments remained within the soft tissues
ated with the administration of a local anesthetic, a written of the patient receiving the injection.28 Fifty of these
note should be entered onto the patient's dental chart. For eventsinvolved30-gaugeshort needles;a 27-gaugeshort was
complications that become chronic, a note should appear involvedin the other case.Allbut 1 involvedadministration
whenever the patient is re-evaluated. of an IANB.A posterior superior alveolar nerve block was
used in the other case.
Amanufacturer of dental localanestheticneedlesreported
NEEDLE BREAKAGE
that over a 6-year period (1997-2002),27 doctors contacted
Sincethe introduction of non-reusable, stainlesssteel dental the company reporting instances of broken dental needles.
local anesthetic needles, needle breakage has become an All incidents involved30-gaugeshort needles.29
extremelyrare complication of dental local anesthetic injec Longdental needlesmost likelyhavebroken during injec
tions (Fig. 17-1). Pogrel has (roughly) estimated the risk of tion. However,because the long needle is unlikely to have
needle breakage among Northern California dentists at 1 in been inserted to its full length (approximately32 mm) into
14 million inferior alveolar nerve blocks.1 In the United soft tissue, some portion of the needle would remain visible
States, 1.43 million boxes of dental needles (100 needles in the patient's mouth. Retrieval of the fragment with a
per box; 143,000,000 needles) were sold by one needle hemostat is easilyaccomplished.Litigationdoes not occur in
manufacturer in 2004, 1.56million boxes in 2005, and 1.43 such incidents.
million boxes in 2006.2 Reports of broken dental needles in Table 17-1 summarizes the accumulated findings pre
the published literature appear only infrequently,but they sented to this point. Although some reports may have been
292
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CHAPTER17 LocalComplications 293
Figure 17-3. A. Radiograph of a broken dental needle (note bend in needle: arrow). B, Radiograph of a broken dental needle in the ptery
gomanchbular space. (B, From Marks RB, Carlton DM, McDonald S: Management of a broken needle in the pterygomanchbular space: report
of a case, J Am Dent Assoc 109:263-264,1984.Reprinted by permission.)
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294 PARTIV Complications,LegalConsiderations, Questions, and Future
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CHAPTER 17 Local Complications 295
Figure 17-5. Needle fragments can migrate as is shown in the series of panoramic films taken at 3-month intervals. (Courtesy
Dr. Carlos Elias De Freitas. From Malamed SF,Reed KR, Poorsattar S: Needle breakage: incidence and prevention, Dent Clin N Amer
54:745-756, 2010.)
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296 PARTIV Complications,LegalConsiderations, Questions, and Future
with the small needles used in dentistry, trauma to a nerve Hemorrhage into or around the neural sheath is another
produced by contact with the needle is allthat maybe needed cause. Bleeding increases pressure on the nerve, leading to
to produce paresthesia.f-" Insertion of a needle into a paresthesia.31-33,3s
foramen, as in the second division (maxillary) nerve block The local anesthetic solution itself may contribute to the
via the greaterpalatine foramen, alsoincreasesthe likelihood development of paresthesiaafter local anesthetic injection.39
of nerve injury. Haas and Lennon took a retrospective look at paresthesia
after injection oflocal anesthetic in dentistry in the province
of Ontario, Canada, over a 20-year period (1973-1993).31
This report included voluntary submissions by dentists to
their insurance carriers for claims of paresthesia.Only cases
where no surgery was performed were considered. One
hundred forty-three casesof paresthesiaunrelated to surgery
were reported in this period. All reported casesinvolvedthe
inferior alveolaror the lingual nerve or both, with anesthesia
of the tongue reported most often, followedby anesthesiaof
the lip.Pain (hyperesthesia)was reported by 22% of patients.
Paresthesiawas reported more often after administration of
a 4% local anesthetic-prilocaine HCl and articaine HCI.
Observed frequencies of paresthesia after administration of
articaine HCl and prilocaine HCl weregreaterthan expected,
based on the distribution of local anesthetic use in Ontario
in 1993.31 According to Haas, the incidence of paresthe
sia resulting from all local anesthetics is approximately
1:785,000; for 0.5%, 2%, and 3% local anesthetics, it is
approximately 1: 1,250,000,and for 4% local anesthetics, it
is approximately 1:485,000.31
In 2006 Hillerup and Jensen in Denmark, reviewing
insurance claims,suggestedthat articaine should not be used
by inferior alveolar nerve block because it had, in their
opinion, a greater propensity for paresthesia." Yet,of the 54
case reports of paresthesia reviewed,42 (77%) involvednot
the inferior alveolar nerve but the lingual nerve (see later
discussion) (Table 17-2).
In response to Hillerup and Jensen's article, the Pha
rmacovigilanceWorking Committee of the European Union
reviewedreports of paresthesiaassociatedwith articaine and
other local anesthetics in 57 countries, estimating that the
number of patients treated with articaine is approximately
100million annually.41 Their published report (October 30,
2006) states the following:"This investigationis a follow-up
Figure 17·6. Surgical excision of needle fragment (see patient to an inquiry initiated in 2005. This enquiry resulted from
from Fig. 17-5). Courtesy Dr. Carlos Elias De Freitas CVM. suspicions that were raised in Denmark, that a local anes
From Malamed SF,Reed KR, Poorsattar S: Needle breakage: inci thetic, articaine, was responsible for an increased risk of
dence and prevention, Dent Clin N Amer 54:745-756,2010.) nerve injuries compared with the risk associatedwith other
TABLE 17-2
Distribution of Analgesic Solution and Nerve Affected, Including 54 Nerve Injuries in 52 Patients
Inferior Alveolar Nerve Lingual Nerve Sum, N (%)
Articaine 4% 5 24 29 (54)
Prilocaine 3% 4 6 10 (19)
Lldocaine2% 3 7 10 (19)
Mepivacaine3% 0 4 4 (7)
Mepivacaine3% + Articaine 4% 0 1 1 (2)
Number of nerve injuries 12 42 54 (100)
From Hillerup S, Jensen R: Nerve injury caused by mandibular block analgesia, Int J Oral Maxillofac Surg 35:437--443, 2006.
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CHAPTER 17 LocalComplications 297
TABLE 17-3
Number of cases of nerve damage with percentage of U.S. National Sales Figures
Approximate Share of LA
Anesthetic # of Cases(%) Market in United States.% Ratio (1.0 Expected)
Lidocaine HCI 20 (35) 54 0.64
Prilocaine HCI 17 (29.8) 6 4.96
Articaine HCI 17 (29.8) 25 1.19
Articaine HCI + Lidocaine HCI 1 (1.75)
Lidocaine HCI + Prilocaine HCI 1 (1.75)
Bupivacaine HCI 1 (1.75)
Mepivacaine HCI 0 (O) 15
From Pogrel MA:Permanent nerve damage from inferior alveolarnerve blocks--an update to include articaine, J Calif Dent Assoc 35:271-273, 2007
(modified to include ratio).
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298 PARTIV Complications,LegalConsiderations, Questions, and Future
resolution occurred in 34 of the 108cases(31.4%).Of these, a matter of time before such contact does occur. As Pogrel
25 resolvedwithin 2 months, and the remaining 9 resolved opined: "It is reasonableto suggestthat during a career,each
within 240 days," dentist may encounter at least one patient with an inferior
However,the report by Garisto and colleaguesrelied on alveolar nerve block resulting in permanent nerve involve
data from the AERS.The FDA Website for AERSdisplays ment. The mechanisms are unknown and there is no known
the following warning: ''AERS data do have limitations. prevention or treatment."32
First, there is no certainty that the reported event was actu
ally due to the product. FDAdoes not require that a causal Management
relationship between a product and event be proven, and Nichol reported that most paresthesias resolve within
reports do not always contain enough detail to properly approximately 8 weeks without treatment.47 Only when
evaluate an event. Further, FDAdoes not receiveall adverse damage to the nerve is severewill the paresthesiabe perma
event reports that occur with a product. Many factors can nent, and this occurs only rarely.
influence whether or not an event will be reported, such as In most situations, paresthesia is minimal, with the
the time a product has been marketed and publicity about patient retaining most of the sensoryfunction to the affected
an event. Therefore, AERScannot be used to calculate the area. Therefore, the risk of self-inflicted tissue injury is
incidence of an adverseevent in the U.S.population."46 minimal.
So,as of January 2012,"the jury is still out;' as the saying Garisto and coworkers,in reviewing248 reports of par
goes. Proponents of one side of the argument adamantly esthesia,had data on resolution in 108 cases.The period of
believe that 4% local anesthetics do carry a greater risk of resolution ranged from as little as 1 day to as many as 736
paresthesia, be it transient or permanent, but the others days. Confirmed resolution of paresthesia was reported in
believe that other factors are usually involved, primarily 34 of the 108cases (31.4%).Of the 34 casesthat did resolve,
mechanical trauma, especiallywhen the paresthesiainvolves 25 did so within 2 months; the remaining 9 cases resolved
only the lingual nerve, as is the case in 89% of the cases within 240 days."
cited by Garisto and colleages.44 McCarthy48 and Orr49 have recommended the following
So what should the doctor do? As with all procedures sequence in managing the patient with a persistent sensory
under consideration for use by a doctor, as well as with any deficit after local anesthesia:
drugs being considered for administration, the doctor must 1. Be reassuring. The patient usually telephones the office
weighthe benefit to be gained from use of the drug or thera the day after the dental procedure complaining of still
peutic procedure against the risks involvedin its use. Only being a little numb.
when, in the mind of the treating doctor, the benefit to be a. Speakwith the patient personally.Do not relegate
gained clearly outweighs the risk should the drug or the the duty to an auxiliary.Remember that if patients
procedure be used. cannot get through to speak to their doctor, they can
alwaysget the doctor's attention through litigation.
Problem b. Explain that paresthesia is not uncommon after local
Persistent anesthesia, rarely total, in most cases partial, can anesthetic administration. Sisk and associateshave
lead to self-inflictedsoft tissue injury. Biting or thermal or reported that paresthesia may develop in up to 22%
chemicalinsult can occur without a patient's awarenessuntil of patients in very select circumstances,"
the process has progressed to a serious degree. When the c. Arrange an appointment to examine the patient.
lingual nerve is involved,the sense of taste (via the chorda d. Record the incident on the dental chart.
tympani nerve) also may be impaired. 2. Examine the patient in person.
In some instances, loss of sensation (paresthesia) is not a. Determine the degree and extent of paresthesia.
the clinicalmanifestation of nerve injury. Hyperesthesia(an b. Explain to the patient that paresthesia normally
increased sensitivityto noxious stimuli) and dysesthesia (a persists for at least 2 months before resolution
painful sensation occurring to usually nonnoxious stimuli) begins, and that it may last up to a year or longer.
also may be noted. Haas and Lennon reported that pain was c. "Tincture of time" (e.g.,observation) is the
present in 22% of the 143 cases of paresthesia that they recommended treatment, although surgery might be
reviewed.31 considered as an option.
d. Record all findings on the patient's chart using the
Prevention patient's own descriptors, such as "hot," "cold,"
Strict adherence to injection protocol and proper care and "painful,""tingling,""increasing,""decreasing;'and
handling of dental cartridges help minimize the risk of par "stayingthe same."
esthesia.Nevertheless,casesof paresthesiawill still occur in e. Suggestthat simple observation for 1 to 2 months is
spite of care taken during the injection. Whenever a needle recommended, but on that same day,offer to send
is inserted into soft tissues, anywhere in the body, in an the patient for a second opinion to an oral and
attempt to deposit a drug (e.g., local anesthetic) as close to maxillofacialsurgeon (OMS),who will be able to
a nerve as possiblewithout actuallycontacting it, it is simply map out the affectedarea and would be able to
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CHAPTER17 LocalComplications 299
perform the surgical repair, if that is deemed through which terminal portions of the facial nerve extend
necessary. (Fig. 17-7).
f. If surgical repair is suggested by this first consultant, The facialnerve branches and the musclesthey innervate
a second opinion should be sought from another are listed below:
OMS. It generally is deemed appropriate to observe 1. Temporal branches
the situation for minimally 1 to 2 months before a. Frontalis
considering the surgical option. b. Orbicularis oculi
3. Reschedule the patient for examination every 2 months c. Corrugator supercilii
for as long as the sensory deficit persists. 2. Zygomaticbranches
4. Dental treatment may continue, but avoid a. Orbicularis oculi
readministering local anesthetic into the region of the 3. Buccalbranches: supplying the region inferior to the
previously traumatized nerve. Use alternate local eye and around the mouth
anesthetic techniques if possible. a. Procerus
5. It would be prudent to contact your liability insurance b. Zygomaticus
carrier should the paresthesia persist without evident c. Levatorlabii superioris
improvement beyond 1 to 2 months. d. Buccinator
e. Orbicularis oris
4. Mandibular branch: supplying muscles of the lower lip
FACIAL NERVE PARALYSIS and chin
The seventh cranial nerve carries motor impulses to the a. Depressor anguli oris
muscles of facial expression, of the scalp and external ear, b. Depressor labii inferioris
and of other structures. Paralysis of some of its terminal c. Mentalis
branches occurs whenever an infraorbital nerve block is
administered, or when maxillary canines are infiltrated. Cause
Muscle droop is also observed when, occasionally,motor Transient facial nerve paralysis is commonly caused by the
fibers are anesthetized by inadvertent deposition of local introduction of local anesthetic into the capsule of the
anesthetic into their vicinity. This may occur when anes parotid gland, which is located at the posterior border of
thetic is introduced into the deep lobe of the parotid gland, the mandibular ramus, clothed by the medial pterygoid and
Zygomatic branches
nerve
Buccal branches
Mandibularbranch
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300 PARTIV Complications,LegalConsiderations, Questions, and Future
Figure 17-8. Facial nerve paralysis. Inability to close eyelid (A) and drooping of lip on affected side (patient's left) (B).
masseter muscles.35•50-53Directing the needle posteriorly or A needle tip that comes in contact with bone (medial
inadvertently deflecting it in a posterior direction during aspect of the ramus) before depositing local anesthetic solu
an IANB,or overinserting during a Vazirani-Akinosinerve tion essentiallyprecludes the possibility that anesthetic will
block, may place the tip of the needle within the body of the be deposited into the parotid gland during an IANB.If the
parotid gland If local anesthetic is deposited, transient needle deflectsposteriorly during this block and bone is not
paralysiscan result. The duration of the paralysisis equal to contacted, the needle should be withdrawn almost entirely
that of the soft tissue anesthesiausually noted for that drug. from the soft tissues, the barrel of the syringe brought pos
teriorly (thereby directing the needle tip more anteriorly),
and the needle readvanced until it contacts bone.
Problem Becauseno contact ismade with bone during the Vazirani
Loss of motor function to the muscles of facial expression Akinosinerve block,overinsertion of the needle,either abso
produced by local anesthetic deposition is normally transi lute (>25 mm) or relative (25 mm in a smaller patient),
tory. It lasts no longer than severalhours, depending on the should be avoided,if possible.
local anesthetic formulation used, the volume injected, and
proximity to the facialnerve.Usually,minimal or no sensory Management
loss occurs. Within seconds to minutes after deposition of local anes
During this time, the patient has unilateral paralysisand thetic into the parotid gland, the patient senses weakening
is unable to use these muscles (see Fig. 17-8). The primary of the muscleson the affectedside of the face.Sensoryanes
problem associated with transient facial nerve paralysis is thesia is not present in this situation. Management includes
cosmetic: the person's face appears lopsided No treatment the following:
is known, other than waiting until the action of the drug 1. Reassurethe patient. Explain that the situation is
resolves. transient, will last for a few hours, and will resolve
A secondary problem is that the patient is unable to without residual effect.Mention that it is produced by
voluntarily close one eye. The protective lid reflex of the the normal action of local anesthetic drugs on the facial
eye is abolished Winking and blinking become impossible. nerve, which is a motor nerve to the muscles of facial
The cornea, however, does retain its innervation; thus if expression.
it is irritated, the corneal reflexis intact, and tears lubricate 2. Contact lenses should be removed until muscular
the eye. movement returns.
3. An eye patch should be applied to the affectedeye until
muscle tone returns. If resistanceis offered by the
Prevention patient, advise the patient to manually closethe affected
Transient facial nerve paralysis is almost always prevent eyelidperiodicallyto keep the cornea lubricated.
able by adhering to protocol with the inferior alveolar and 4. Record the incident on the patient's chart.
Vazirani-Akinosinerve blocks (as described in Chapter 14), 5. Although no contraindication is known to
although in some situations,branches of the facialnerve may reanesthetizingthe patient to achievemandibular
lie closeto the site of localanesthetic deposition in the IANB anesthesia,it may be prudent to forego further dental
and Vazirani-Akinosinerve blocks. care at this appointment.
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302 PARTIV Complications,LegalConsiderations, Questions, and Future
involved region until symptoms resolve and the patient is lasts significantlylonger than does pulpal anesthesia.Dental
more comfortable. patients receiving local anesthetic during their treatment
If continued dental care in the area is urgent, as with usuallyare dismissedfrom the dental officewith residual soft
an infected painful tooth, it may prove difficult to achieve tissue numbness. (See the discussion in Chapter 20 of the
effectivepain control when trismus is present. The Vazirani local anesthesia reversalagent, phentolamine mesylate.)
Akinosi mandibular nerve block usually provides relief of
the motor dysfunction, permitting the patient to open his Problem
or her mouth, allowing administration of the appropriate Trauma to anesthetized tissues can lead to swellingand sig
injection for clinicalpain control, if needed nificant pain when the anesthetic effects resolve.A young
In virtually all casesof trismus related to intraoral injec child or a handicapped individual may havedifficultycoping
tions that are managed as described,patients report improve with the situation, and this may lead to behavioralproblems.
ment within 48 to 72 hours. Therapy should be continued The possibilitythat infection will develop is remote in most
until the patient is free of symptoms.If pain and dysfunction instances.
continue unabated beyond 48 hours, considerthe possibility
of infection. Antibiotics should be added to the treatment Prevention
regimen described and continued for 7 full days. Complete A localanesthetic of appropriate duration should be selected
recoveryfrom injection-related trismus takes about 6 weeks if dental appointments are brief. {Referto the discussion
(range, 4 to 20 weeks).59 of lip chewing and duration of anesthesia for specific
For severe pain or dysfunction, if no improvement is drugs, p. 281.)
noted within 2 or 3 days without antibiotics or within 5 to A cotton roll can be placed between the lips and the
7 days with antibiotics, or if the ability to open the mouth teeth if they are still anesthetized at the time of discharge.
has become limited, the patient should be referred to an oral The cotton roll is secured with dental flosswrapped around
and maxillofacial surgeon for evaluation. Other therapies, the teeth (to prevent inadvertent aspiration of the roll)
including the use of ultrasound or appliances,are available (Fig. 17-10).
for use in these situations.69•70 Warn the patient and the guardian against eating, drink
Temporomandibularjoint involvementis rare in the first ing hot fluids, and biting on the lips or tongue to test for
4 to 6 weeksafter injection. Surgicalintervention to correct anesthesia.A self-adherent warning sticker may be used on
chronic dysfunction may be indicated in some instances.59•63 children (Fig. 17-11).
Management
SOFT TISSUE INJURY Management of the patient with self-inflicted soft tissue
Self-inflictedtrauma to the lips and tongue is frequently injury secondary to lip or tongue biting or chewing is
caused by the patient inadvertently biting or chewing these symptomatic:
tissues while still anesthetized (see Fig. 17-9). 1. Analgesicsfor pain, as necessary.
2. Antibiotics, as necessary,in the unlikelysituation that
Cause infection results.
Trauma occurs most frequentlyin younger children,in men 3. Lukewarmsaline rinses to aid in decreasingany swelling
tally or physicallydisabled children or adults, and in older that may be present.
old patients; however,it can and does occur in patients of all 4. Petroleum jelly or other lubricant to cover a lip lesion
ages.The primary reason is the factthat soft tissue anesthesia and minimiz.eirritation.
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CHAPTER17 LocalComplications 303
Cause
Because of the density of tissue in the hard palate and its
firm adherence to bone, hematoma rarely develops after a
palatal injection. A rather large hematoma may result from
arterial or venous puncture after a posterior superior alveo
lar or inferior alveolarnerve block. The tissues surrounding
these vesselsmore readily accommodate significantvolumes
of blood. The blood effusesfrom vesselsuntil extravascular
exceeds intravascular pressure, or until clotting occurs.
Hematomas that occur after the inferior alveolarnerve block
usually are only visibleintraorally,whereas PSAhematomas
are visible extraorally.
Problem
A hematoma rarely produces significant problems, aside
from the resulting"bruise:' which may or may not be visible
extraorally. Possible complications of hematoma include
Figure 17-11. Self-adherent warning sticker to help prevent trismus and pain. Swellingand discoloration of the region
accidental trauma to anesthetized tissues in children. usually subside gradually over 7 to 14 days.
A hematoma constitutes an inconvenienceto the patient
and an embarrassment to the person administering the drug
(Fig. 17-12).
HEMATOMA
The effusionof blood into extravascularspacescan be caused Prevention
by inadvertent nicking of a blood vessel (artery or vein) 1. Knowledgeof the normal anatomy involvedin the
during administration of a local anesthetic. A hematoma proposed injection is important. Certain techniques are
that developssubsequent to the nicking of an artery usually associatedwith a greater risk of visiblehematoma. The
increasesrapidly in sizeuntil treatment is instituted because PSAnerve block is the most common, followedby the
of the significantlygreaterpressure of blood within an artery. IANB (a distant second) and the mental/incisivenerve
Nicking of a vein may or may not result in the formation of block (a close third when the foramen is entered, a
a hematoma. Tissue density surrounding the injured vessel distant third if the technique described in Chapter 14 is
is a determining factor. The denser the surrounding tissues adhered to).
(e.g.,palate), the lesslikelya hematoma is to develop,but in 2. Modifythe injection technique as dictated by the
looser tissue (e.g., infratemporal fossa), large volumes of patient's anatomy. For example,the depth of
blood may amassbefore a swellingis evernoted and therapy penetration for a PSAnerve block may be decreasedin
instituted. a patient with smaller facial characteristics.":"
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304 PART IV Complications, Legal Considerations, Questions, and Future
3. Use a short needle for the PSA nerve block to decrease artery, and the pterygoid plexus of veins. They are located
the risk of hematoma. posterior, superior, and medial to the maxillary tuberosity.
4. Minimize the number of needle penetrations into Bleeding normally ceases when external pressure on the
tissue. vessels exceeds internal pressure, or when clotting occurs.
5. Never use a needle as a probe in tissues. Digital pressure can be applied to the soft tissues in the
Hematoma is not always preventable. Whenever a needle mucobuccal fold as far distally as can be tolerated by the
is inserted into tissue, the risk of inadvertent puncturing of patient (without eliciting a gag reflex).Apply pressure in a
a blood vessel is present. medial and superior direction. If available, ice should be
applied (extraorally)to increasepressure on the site and help
Management constrict the punctured vessel.
Immediate. When swelling becomes evident during or
immediatelyafter a localanesthetic injection, direct pressure Subsequent. The patient may be discharged once bleeding
should be applied to the site of bleeding.For most injections, stops. Note the hematoma on the patient's dental chart.
the blood vesselis locatedbetweenthe surfaceof the mucous Advisethe patient about possible sorenessand limitation of
membrane and the bone; localized pressure should be movement (trismus). If either of these develops,begin treat
applied for not lessthan 2 minutes. This effectivelystops the ment as describedfor trismus. Discolorationwilllikelyoccur
bleeding. as a result of extravascular blood elements; it is gradually
Inferior Alveolar Nerve Block. Pressureis applied to the resorbed over 7 to 14 days.
medial aspect of the mandibular ramus. Clinicalmanifesta If sorenessdevelops,advisethe patient to take an analge
tions of the hematoma, which are visibleintraorally,include sic such as aspirin or NSAID.Do not apply heat to the area
possibletissue discoloration and probable tissue swellingon for at least 4 to 6 hours after the incident. Heat produces
the medial (lingual) aspect of the mandibular ramus. vasodilation, which may further increase the size of the
Anterior Superior Alveolar (lnfraorbital) Nerve Block. hematoma if applied too soon. Heat may be applied to the
Pressure is applied to the skin directly over the infraorbital region beginning the next day.It servesas an analgesic,and
foramen. The clinical manifestation is discoloration of the its vasodilating properties may increase the rate at which
skin below the lower eyelid.Hematoma is unlikelyto occur blood elements are resorbed, although the latter benefit is
with anterior superior alveolar (ASA)nerve block because debatable.The patient should apply warm moist heat to the
the technique described requires application of pressure to affectedarea for 20 minutes everyhour.
the injection site throughout drug administration and for a Ice may be applied to the region immediatelyon recogni
period of at least 1 to 2 minutes thereafter. tion of a developinghematoma. It acts as both an analgesic
Incisive (Mental) Nerve Block. Pressureis placeddirectly and a vasoconstrictor,and it may aid in minimizing the size
over the mental foramen, externally on the skin or intra of the hematoma. Time (tincture of time) is the most impor
orally on the mucous membrane. Clinical manifestations tant element in managing a hematoma. With or without
include discoloration of the skin of the chin in the area treatment, a hematoma willbe present for 7 to 14days.Avoid
of the mental foramen and/or swellingin the mucobuccal additional dental therapy in the region until symptoms and
fold in the region of the mental foramen (see Fig. 17-12). signs resolve.
As with the ASA nerve block, pressure applied during
administration of the drug effectivelyminimizes the risk
of hematoma formation during incisive (but not mental)
PAIN ON INJECTION
nerve block. Pain on injection of a local anesthetic can best be prevented
Buccal Nerve Block or Any Palatal Injection. Placepres through careful adherence to the basic protocol of atrau
sure at the site of bleeding. In these injections, the clinical matic injection. (SeeChapter 11.)
manifestations of hematoma usually are visible only within
the mouth. Causes
Posterior Superior Alveolar Nerve Block. The PSA 1. Carelessinjection technique and a callous attitude
nerve block usually produces the largest and most estheti ("Palatalinjections alwayshurt" or "This will hurt a
callyunappealing hematoma. The infratemporal fossa, into little") all too often become self-fulfillingprophecies.
which bleeding occurs, can accommodate a large volume 2. A needle can become dull from multiple injections.
of blood. The hematoma usually is not recognized until 3. Rapid deposition of the local anesthetic solution may
a colorless swellingappears on the side of the face around cause tissue damage.
the temporomandibular joint area (usually a few minutes 4. Needleswith barbs (from impaling bone) may produce
after the injection is completed). It progressesover a period pain as they are withdrawn from tissue.62
of days, extending inferiorly and anteriorly toward the
lower anterior region of the cheek. It is difficult to apply Problem
pressure to the site of bleeding in this situation because of Pain on injection increases patient anxiety and may lead to
the location of the involvedblood vessels.It is also relatively sudden unexpected movement, increasingthe risk of needle
difficult to apply pressure directly to the posterior superior breakage, traumatic soft tissue injury to the patient, or
alveolar artery (the primary source of bleeding), the facial needle-stickinjury to the administrator.
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CHAPTER17 LocalComplications 305
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306 PARTIV Complications,LegalConsiderations, Questions, and Future
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CHAPTER17 LocalComplications 307
Sterlle Abscess
1. Secondaryto prolonged ischemia resulting from the use
POSTANESTHETIC INTRAORAL LESIONS
of a local anesthetic with vasoconstrictor (usually Patients occasionallyreport that approximately 2 days after
norepinephrine) an intraoral injection of local anesthetic, ulcerations devel
2. Usuallydevelopson the hard palate oped in their mouth, primarily around the site(s) of the
injection(s). The primary initial symptom is pain, usuallyof
Problem a relativelyintense nature.
Pain, at times severe, may be a consequence of epithelial
desquamation or a sterileabscess.It is remotelypossiblethat Cause
infection may develop in these areas. Recurrent aphthous stomatitis or herpes simplex can occur
intraorally after a local anesthetic injection or after any
Prevention trauma to the intraoral tissues.
Use topical anesthetics as recommended.Allowthe solution Recurrent aphthous stomatitis (recurrent aphthous ulcer
to contact the mucous membranes for 1 to 2 minutes to ation) is the most common oral mucosa! disease known
maximize its effectivenessand minimize toxicity. to human beings." Recurrent aphthous stomatitis is more
When using vasoconstrictors for hemostasis, do not use frequently observed than herpes simplex,typically develop
overly concentrated solutions. Norepinephrine (Levophed) ing on gingival tissues that are not attached to underlying
1:30,000 is the agent most likely to produce ischemia of bone (e.g., movable tissue), such as the buccal vestibule
sufficient duration to cause tissue damage and a sterile (Fig.17-14).In spite of much continuing research,the causes
abscess (Fig. 17-13).Norepinephrine is not availablein any remain poorly understood, the ulcers are not preventable,
dental local anesthetic solution in North America.Epineph and treatment remains symptomatic.
rine (1:50,000)alsomayproduce this problem, if reinjection Herpes simplex can develop intraorally, although more
of the solution occurs whenever ischemia resolves,over a commonly it is observed extraorally.It is viral and becomes
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308 PARTIV Complications,LegalConsiderations, Questions, and Future
Problem
The patient describesacute sensitivityin the ulcerated area.
Many considerthat the tissue has become infected as a result
of the local anesthetic injection they received;however,the
risk of a secondary infection developing in this situation is
minimal.
Prevention
Unfortunately,there is no means of preventing these intra
oral lesions from developing in susceptible patients. Extra
oral herpes simplex, on occasion, may be prevented or its
clinicalmanifestations minimized if treated in its prodromal
Figure 17-14. Aphthous stomatitis. (From Eisen D, Lynch D: phase. The prodrome consists of a mild burning or itching
The mouth: diagnosis and treatment, St Louis, 1998,Mosby.) sensation at the site where the virus is present (e.g., lip).
Antiviral agents,such as acyclovir,applied qid to the affected
area effectivelyminimize the acute phase of this process.
Management
Primary management is symptomatic. Pain is the major
initial symptom, developing approximately 2 days after
injection.Reassurethe patient that the situation is not caused
by a bacterial infection secondary to the local anesthetic
injection, but in fact is an exacerbationof a processthat was
present, in latent form, in the tissuesbefore injection.Indeed,
most of these patients have experiencedthis response before
and are resigned to it happening again.
No management is necessary if the pain is not severe.
However,if pain causes the patient to complain, treatment
can be instituted, usually with varying degrees of success.
The objective is to keep the ulcerated areas covered or
anesthetized.
Topicalanesthetic solutions (e.g.,viscous lidocaine) may
be applied as needed to the painful areas.A mixture of equal
amounts of diphenhydramine (Benadryl) and milk of mag
nesia rinsed in the mouth effectivelycoats the ulcerations
and provides relief from pain. Orabase, a protective paste,
without Kenalogcan provide a degreeof pain relief.Kenalog,
a corticosteroid, is not recommended because its anti.
inflammatory actions increase the risk of viral or bacterial
involvement. A tannic acid preparation (Zilactin) can be
applied topicallyto the lesions extraorallyor intraorally (dry
the tissues first). Studies from the University of Alabama
have demonstrated that most patients achieve substantial
Figure 17-15. lntraoral lesion (herpes simplex:)on the palate. pain relief for up to 6 hours.81•82
(From Eisen D, Lynch D: The mouth: diagnosis and treatment,
The ulcerations usually last 7 to 10 dayswith or without
St Louis, 1998,Mosby.)
treatment. Maintain records on the patient's chart.
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CHAPTER 17 Local Complications 309
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sence Int 30:461-465, 1999. 45. National Weather Service,Lightning Safety:Odds of becoming
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24. Murray M: A forgotten entity: "broken needle while adminis 46. U.S. Food and Drug Administration Center for Drug Evalua
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27. Baart JA, van Amerongen WE, de Jong KJ, et al: Needle break 48. Personal communication. F.M. McCarthy,1979.
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51. Cooley RL, Coon DE: Transient Bell's palsy following man 69. Carter EF: Therapeutic ultrasound for the relief of restricted
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52. Crean SJ,PowisA: Neurologicalcomplications of local anaes 509, 1986.
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54. Tveter-as K, Kristensen S: The aetiology and pathogenesis of safety: a modified posterior superior alveolar injection tech
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55. Dhanrajani PJ,Jonaidel 0: Trismus:etiology,differentialdiag 50:554--557, 2002.
nosis and treatment, Dent Update 29:88-92, 94, 2002. 72. Harn SD, Durham TM, Callahan BP, et al: The posterior
56. Leonard M: Trismus:what is it, what causesit, and how to treat superior alveolar injection technique: a report on technique
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57. Marien M Jr: Trismus:causes,differentialdiagnosis,and treat 73. Malamed SF, Hersh E, Poorsattar S, Falke! M. Reduction
ment, Gen Dent 45:350-355, 1997. of local anesthetic injection pain using an automated dental
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Systemic Complications
The therapeutic use of drugs is commonplace in dentistry, harm if handled improperly; conversely,any drug may
with the administration of local anesthetics considered be handled safelyif proper precautions are observed.
essential whenever potentially painful procedures are con • Principle 3: The potential toxicity of a drug rests in
templated. It is estimated (conservatively)that dental pro the hands of the user. A second factor in the safeuse
fessionals in the United States administer in excess of 6 of drugs (after the drug itself) is the person to whom
million dental cartridgesper week,or more than 300million the drug is being administered. Individuals react
per year. differentlyto the same stimulus. Therefore,patients
Local anesthetics are extremely safe drugs when used as vary in their reactions to a drug. Beforeadministering
recommended. However,wheneverany drug, including local any drug, the doctor must ask the patient specific
anesthetics,is used, the potential for unwanted and undesir questions about his or her medical and drug history.
able responses exists.In this chapter, systemicadverse reac Physicalevaluation and the ensuing dialogue history
tions to drugs in general,and local anesthetics in particular, related to local anesthetic administration are presented
are reviewed. in Chapters 4 and 10.
Severalgeneral principles of toxicology(the study of the
harmful effectsof chemicalsor drugs on biologicalsystems)
CLASSIFICATION OF ADVERSE
are presented to further an understanding of the material in
DRUG REACTIONS
this chapter.
Harmful effectsof drugs range from those that are incon Classifyingadversedrug reactions, in the past, has been the
sequentialto the patient and entirelyreversibleonce the drug object of much confusion; reactions were labeled as side
is withdrawn, to those that are uncomfortable but not seri effects,adverse experiences,drug-induced disease, diseases
ously harmful, to those that can seriously incapacitate or of medical progress, secondary effects,and intolerance. The
prove fatal to the patient. term adverse drug reaction (ADR) is preferred at this time.
Whenever any drug is administered, two types of actions Box 18-1 outlines the three major methods by which
may be observed: (1) desirable actions, which are clinically drugs produce adversereactions.
sought and usually beneficial;and (2) undesirable actions, Overdose reactions, allergy,and idiosyncrasyare impor
which are additional and are not sought. tant topics in relation to local anesthetics and pain control
• Principle 1:No drug ever exerts a single action. All in dentistry.A brief overviewof each is presented, followed
drugs exert many actions, desirable and undesirable. by an in-depth look at overdoseand allergy.
In ideal circumstances,the right drug in the right dose Overdose reactions are those clinicalsigns and symptoms
is administered via the right route to the right patient that manifest as a result of an absolute or relative over
at the right time for the right reason and does not administration of a drug, which leadsto elevatedblood levels
produce any undesirable effects.1This ideal clinical of the drug in its target organs (places in the body where
situation is rarely,if ever,attained, because no drug is the drug exerts a clinical action). Signs and symptoms of
so specificthat it produces only the desired actions in overdose are related to direct extension of the normal
all patients. pharmacologic actions of the drug in its target organs. Local
• Principle 2: No clinically useful drug is entirely devoid anesthetics are drugs that act to depress excitable mem
of toxicity. The aim of rational drug treatment is to branes (e.g.,the central nervous system [CNS]and myocar
maximize the therapeutic and to minimize the toxic dium are the target organs for local anesthetics). When
effectsof any given drug. No drug is completelysafe or administeredproperly and in therapeutic dosages,they cause
completelyharmful. All drugs are capable of producing little or no clinicalevidenceof CNSor cardiovascularsystem
311
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312 PART IV Complications,LegalConsiderations, Questions, and Future
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CHAPTER 18 Systemic Complications 313
/~- ....•.
I '
1 36 mg ' Figure 18·1. Under normal conditions,
1 local ' . both constant absorption of local anesthetic
\anesthetic 1--------t Blood
from the site of deposition into the cardio
' .•..• - ,,, / I vascular systemand constant removal of the
Anesthetic level
in blood
l-_-;:-.Overdose threshold
drug from the blood by the liveroccur.Local
anestheticlevelsin the blood remain low and
below the threshold for overdose.
Time
Patient Factors
Age. Although ADRs,including overdose, can occur in
0.11%......_
persons of any age,individuals at both ends of the age spec
trum experiencea higher incidence of such reactions." The --30' -2er -1 er µ 1er 2er 3er
functions of absorption, metabolism, and excretion may be Figure 18-2. Normal distribution curve (bell curve).
imperfectly developed in very young persons and may be
diminished in older-old persons, thereby increasingthe half
life of the drug, elevating circulating blood levels, and
increasingthe risk of overdose.9 pound of body weight. One of the major factors involvedin
Weight. The greater the (lean) body weight of a patient producing local anesthetic overdose in the past was lack of
(within certain limits), the larger the dose of a drug that can consideration of this extremely important factor. Determi
be tolerated before overdosereactions occur (providing the nation of maximum doses according to milligram per kilo
patient responds "normally" to the drug). Most drugs are gram or milligram per pound of body weightis based on the
distributed evenlythroughout the body. Larger individuals responsesof the "normal-responding"patient, which are cal
have a greater blood volume and consequently a lower level culated from the responses of many thousands of patients.
of the drug per milliliter (mL) of blood. Maximum recom An individual patient's response to drug administration,
mended doses (MRDs)oflocal anestheticsnormally are cal however,may demonstrate significantvariation. The normal
culated on the basis of milligram of drug per kilogram or distribution curve (Fig. 18-2) illustrates this fact. The usual
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314 PARTIV Complications,LegalConsiderations, Questions, and Future
cerebralblood levelof lidocaine necessaryto induce seizure response to various stimuli. The apprehensive patient who
activity is approximately 7.5 µg/mL. However,patients on overreacts to stimulation (experiencing pain when gentle
the hyporesponding sideof this curve may not convulseuntil pressure is applied) is more likelyto receivea larger dose of
a significantlyhigher brain-blood level is reached, whereas local anesthetic, which would seeminglyincrease his or her
others (hyperresponders) may convulse at a brain-blood risk of local anesthetic overdose.However,a recent study in
levelconsiderablylower than 7.5 µg/mL. rats demonstrated that stress-induced changes in arterial
Other Medications. Administration of concomitant carbon dioxide tension (decreased paC02) and in partial
medications may influence local anesthetic drug levels. pressure of oxygenin arterial blood (increasedpa02) signifi
Patients taking meperidine (Demerol), phenytoin (Dilan cantly raised the seizure threshold for both lidocaine and
tin), quinidine (an antidysrhythmic), or desipramine (a tri articaine.19 Stress significantlyincreased the latency period
cyclicantidepressant) have increased local anesthetic blood for the first tonic-clonic seizure induced by toxic doses of
levels and thus may experience toxic actions of the local both lidocaine and articaine.19
anesthetic at lower administered doses because of protein
binding competition. The Hi-histamine blocker cimetidine Drug Factors
slowsthe biotransformation of lidocaine by competing with Vasoactivity. All local anesthetics currently used by
the local anesthetic for hepatic oxidativeenzymes,leading to injection in dentistry are vasodilators. Injection into soft
somewhat elevatedlidocaine blood levels.":" tissuesincreasesperfusion in the area,leadingto an increased
Sex. Studies in animals have shown that sex is a factor rate of drug absorption from the site of injection into the
in drug distribution, response, and metabolism, although cardiovascularsystem.This causestwo undesirable effects:a
it is not of major significancein humans. In humans, the shorter duration of clinical anesthesia and an increased
only instance of sexual differenceaffectinga drug response blood levelof the local anesthetic.
is pregnancy. During pregnancy, renal function may be Concentration. The greater the concentration (percent
disturbed, leading to impaired excretion of certain drugs, solution injected) of the local anesthetic administered, the
their accumulation in the blood, and increased risk of greater the number of milligrams per milliliter of solution
overdose. However, local anesthetic seizure thresholds for and the greater the circulating blood volume of the drug in
the fetus,newborn, and mother are significantlydifferent.":" the patient. For example, 1.8mL of a 4% solution is 72 mg
In the adult woman, the seizure threshold is reported to of the drug, but 1.8mL of a 2% solution represents only
be 5.8 mg/kg, in the newborn 18.4mg/kg, and in the 36 mg. If the drug is clinicallyeffectiveas a 2% concentra
fetus 41.9 mg/kg. This is thought to be a result of the tion, higher concentrations should not be used. The lowest
efficient placental clearance of lidocaine into the mother's concentration of a given drug that is clinically effective
plasma. should be selected for use. For commonly used local anes
Presence of Disease. Diseasemay affectthe abilityof the thetics in dentistry, these "ideal" concentrations have been
body to transform a drug into an inactive by-product. determined and are represented in the commerciallyavail
Hepatic and renal dysfunction impairs the body's ability to able forms of these drugs.
break down and excrete the local anesthetic, leading to an Dose. The larger the volume of a local anesthetic
increased anesthetic blood level, whereas heart failure administered, the greater the number of milligrams injected
decreases liver perfusion (the volume of blood flowing and the higher the resulting circulating blood level. The
through the liver during a specificperiod), thereby increas smallestdose of a givendrug that is clinicallyeffectiveshould
ing the half-livesof amide local anesthetics and increasing be administered. For each of the injection techniques dis
the risk of overdose.P'" cussed in this book, a recommended dose has been pre
Genetics. Genetic deficiencies may alter a patient's sented. Where possible, this dose should not be exceeded.
response to certain drugs.A geneticdeficiencyin the enzyme Although "dental" doses of local anesthetics are relatively
serum pseudocholinesterase (serum cholinesterase,plasma small compared with those used in many nondental nerve
pseudocholinesterase, plasma cholinesterase) is an impor blocks,significantlyhigh blood levelsof the local anesthetic
tant example.This enzyme,produced in the liver,circulates can be achieved in dental situations because of the greater
in the blood and is responsible for biotransformation of vascularity of the intraoral injection site or inadvertent
the ester local anesthetics. A deficiency in this enzyme intravascular injection.
quantitativelyor qualitativelycan prolong the half-lifeof an Route of Administration. Local anesthetics,when used
ester local anesthetic, thereby increasing its blood level. for pain control, exert their clinical effects in the area of
Approximately1in 2820 individuals,or 6% to 7% of patients deposition. Ideally then, a local anesthetic drug should not
in most surgical populations, possesses atypical serum enter into the cardiovascularsystem.Almost all other thera
pseudocholinesterase.18 peutic agents must enter the CVS and achieve a minimum
Mental Attitude and Environment. A patient's psycho therapeutic blood levelbefore their clinical action(s) occur.
logical attitude influences the ultimate effect of a drug. Local anesthetics administered for antidysrhythmic pur
Although of greater importance with regard to anti.anxiety poses must reach such a therapeutic blood levelto be effec
or analgesicdrugs, it is also important with regard to local tive. Indeed, one factor involvedin terminating pain control
anesthetics. Psychological attitude affects the patient's by a local anesthetic consistsof its diffusion out of the nerve
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CHAPTER18 SystemicComplications 315
tissue and its subsequent entry into the CVS and removal
from the site of deposition. Causes
A factor in local anesthetic overdose in dentistry is "inad Elevatedblood levelsof localanestheticsmay result from one
vertent" intravascular injection. Extremely high drug levels or more of the following:
can be obtained in a short time, leading to serious overdose 1. Biotransformation of the drug is unusually slow.
reactions. 2. The unbiotransformed drug is too slowlyeliminated
Absorption of local anesthetics through oral mucous from the body through the kidneys.
membranes is also potentially dangerous because of the rate 3. Too large a total dose is administered.
at which some topically applied anesthetics enter the circula 4. Absorption from the injection site is unusually rapid.
tory system. Lidocaine HCl and tetracaine HCl are absorbed 5. lntravascular administration.
well after topical application to mucous membranes. Benzo
caine, which is not water soluble, is poorly absorbed. Biotransformation and Elimination. Ester local anesthet
Rate of Injection. The rate at which a drug is injected is ics, as a group, undergo more rapid biotransformation in
a very important factor in the causation or prevention of the liver and blood than the amides. Plasma pseudocholin
overdose reactions. (Accordingto the author, rate of injec esteraseis primarily responsiblefor their hydrolysisto para
tion is the single most important factor.) Whereas intravas aminobenzoic acid.
cular injection may or may not produce signsand symptoms Atypicalpseudocholinesteraseoccurs in approximately 1
of overdose (indeed, lidocaine is frequently administered out of every 2820 individuals, or 6% to 7% of patients in a
intravenouslyin dosesof 1.0to 1.5mg/kgto treat ventricular surgicalpopulation.18 Patients with a familialhistory of this
ectopy), the rate at which the drug is injected is a major disorder may be unable to biotransform ester agents at the
factor in determining whether drug administration will usual rate, and subsequently,higher levelsof ester anesthetics
prove clinicallysafe or hazardous. Malagodi and associates may develop in their blood.
demonstrated that the incidence of seizureswith etidocaine Atypical pseudocholinesterase represents a relative con
went up when the rate of intravenous (N) infusion was traindication to the administration of ester local anesthetics.
increased," Amide local anesthetics may be used without increased
Rapid N administration (15seconds or less) of 36 mg of risk of overdose in patients with pseudocholinesterase
lidocaine produces greatly elevated levels and virtually deficiency.
ensures an overdose reaction. Slow (60-second or more) N Amidelocal anestheticsare biotransformed in the liverby
administration produces significantly lower levels in the hepatic microsomal enzymes. A history of liver disease,
blood, with a lesser risk that a severeoverdose reaction will however,does not absolutelycontraindicate their use. In an
develop. ambulatory patient with a history of liverdisease(American
Vascularity of the Injection Site. The greater the vascu Society of Anesthesiologists [ASA]Physical Status classifi
larity of the injection site, the more rapid the absorption of cation system 2 or 3), amide local anesthetics may be used
the drug from that area into the circulation. Unfortunately judiciously (relativecontraindication) (Fig. 18-3).
(as regards local anesthetic overdose) for dentistry, the oral Minimum effectivevolumesof anesthetic should be used.
cavity is one of the most highly vascular areas of the entire Average,even low-average,doses may be capable of produc
body.However,some areaswithin the oral cavityare lesswell ing an overdose if liver function is compromised to a great
perfused (e.g.,the site for the Gow-Gatesnerve block), and enough degree (ASA 4 or 5); however, this situation is
these usually are more highly recommended than other, unlikelyto occur in an ambulatory patient.17
better-perfused, sites (e.g.,those for the inferior alveolaror Renaldysfunction also can delayelimination of the active
posterior superior alveolarnerve block). local anesthetic from the blood. A percentageof all anesthet
Presenceof Vasoconstrictors. The addition of vasocon ics is eliminated unchanged through the kidneys: 2% pro
strictor to a localanestheticproduces a decreasein the perfu caine, 10% lidocaine, 5% to 10% articaine, and 1% to 15%
sion of an area and a decreasedrate of systemicabsorption mepivacaine and prilocaine. Renal dysfunction may lead to
of the drug. This, in turn, decreasesthe clinical toxicity of a gradual increasein the levelof activelocalanesthetic in the
the local anesthetic (see Table3-1). blood.16
.... - .•..
1
1
/' 36 mg',,
local
\ anesthetic /
1-------...a Blood
/
-- __.. Figure 18-3. In patients with significant
liver dysfunction, removal of a local anes
' __
...... ...•. / thetic from the blood may be slowerthan its
absorption into the blood, leading to a slow
tz:--
An~s~~~~~
but steady rise in the blood anesthetic level.
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316 PART IV Complications, Legal Considerations, Questions, and Future
,,..--,
Figure 18-4. Evenin a patient I; ' \
v~:_
\ anesthetic /
be absorbed into the cardiovascu \ I
lar system more rapidly than the
livercan removeit. This produces
' ' ••... _ •.•....... I
Anesth~~c~~~~
a relativelyrapid elevation of the
anesthetic blood level.
Time (5-10 min)
TABLE 18-2
Maximum Recommended Doses of Local Anesthetics
Drug Formulation MRD mg/lb (mg/kg}
Articaine With epinephrine None listed* 3.2 (7.0)
Lidocaine Plain 3oot 2.0 (4.4)t
With epinephrine soot 3.3 (7.0)f
Mepivacaine Plain 4oot 2.6 (5.7)t
With levonordefrin 4oot 2.6 (5.7)t
Prilocaine Plain 600t 4.0 (8.8)t
With epinephrine 600t 4.0 (8.8)t
ExcessiveTotal Dose. Givenin excess,all drugs are capable anesthesiais capableof obtunding the full mouth in an adult
of producing signs and symptoms of overdose (Fig. 18-4). with six cartridges, and with two cartridges in the primary
Precisemilligram dosagesor the blood levelsat which clini dentition. Yetdespitethis abilityto achievewidespreadanes
cal effects are noted are impossible to predict. Biological thesia with minimum volumesof anesthetic,the administra
variability has a great influence on the manner in which tion of excessivevolumes is the most frequently seen cause
persons respond to drugs. of local anesthetic overdose.21•22
The MRD of parenterally administered (injected) drugs
is commonly calculated after consideration of a number of Rapid Absorption Into the Circulation. Vasoconstrictors
factors, including the following: are consideredan integral component of all local anesthetics
1. Patient's age. Individuals at either end of the age whenever depth and duration of anesthesia are important.
spectrum may be unable to tolerate normal doses, There are but fewindications for the use of local anesthetics
which should be decreased accordingly. without a vasoconstrictor in dentistry. Vasoconstrictors
2. Patient's physical status. For medicallycompromised increase both the depth and the duration of anesthesia and
individuals (ASA3, 4, and 5) the calculatedMRD reduce the systemic toxicity of most local anesthetics by
should be decreased. delaying their absorption into the CVS. Vasoconstrictors
3. Patient's weight. The larger the person (within limits), should be included in local anesthetic solutions unless
the greater is the volume of distribution of the drug. specifically contraindicated by the medical status of the
With a usual dose, the blood levelof the drug is lower patient or the duration of the planned treatment. 23 The
in the larger patient, and a larger milligram dose can be American Dental Associationand the American Heart Asso
administered safely.Although this rule is generallyvalid, ciation have summarized this as follows:''Vasoconstrictor
there are alwaysexceptions;care must be exercised agents should be used in local anesthetic solutions during
whenever any drug is administered. dental practice only when it is clear that the procedure will
MRDs of local anesthetics should be determined after be shortened or the analgesia rendered more profound.
consideration of the patient's age, physicalstatus, and body When a vasoconstrictor is indicated, extreme care should be
weight. Table 18-2 provides maximum recommended doses taken to avoid intravascular injection. The minimum pos
based on body weight for lidocaine,mepivacaine,prilocaine, sible amount of vasoconstrictor should be used,"?' Rapid
and articaine. absorption of local anesthetics also may occur after their
It is highly unlikely that the maximum figures indicated application to oral mucous membranes.Absorption of some
in Table 18-2 will be reached in the typical dental practice. topically applied local anesthetics into the circulation is
There is rarely an occasionto administer more than three or rapid, exceeded in rate only by direct intravascular injec
four cartridges during a dental appointment. Regionalblock tion," Local anesthetics designed for topical application are
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CHAPTER18 SystemicComplications 317
used in a higher concentration than formulations suitable lntravascular Injection. Intravascular injection may occur
for parenteral administration. with any type of intraoral injection but is more likelywhen
From the perspective of overdose, amide topical anesthet a nerve block is administered33:
ics, when applied to wide areas of mucous membrane,
increase the risk of serious reactions. Benzocaine, an ester Nerve Block Positive Aspiration Rate, %
anesthetic, which is poorly, if at all, absorbed into the Inferior alveolar 11.7
cardiovascular system, is less likely to produce an overdose Mental or incisive 5.7
reaction than amides, although cases of methemoglobin Posterior superior alveolar 3.1
emia from excessive benzocaine administration have been Anterior superior alveolar 0.7
reported.f" The risk of allergy (more likely with esters than (Long) buccal 0.5
amides) must be addressed before any drug is used. Serious
overdose reactions have been reported after topical applica Both N and intra-arterial (IA) injections are capable of
tion of amide local anesthetics.P'" producing overdose(Fig. 18-6).Aldrete demonstrated that a
The area of application of a topical anesthetic should be rapidly administered IA injection may cause retrograde
limited. There are few indications for applying a topical to blood flow in the artery as the anesthetic drug is deposited
more than a full quadrant (buccal and lingual/palatal) at one (Fig. 18-7).34 Intravascular injections of local anesthetic
time. Application of an amide topical to a wide area requires within the usual practice of dentistry should not occur.With
a large quantity of the agent and increases the likelihood of knowledgeof the anatomy of the site to be anesthetized and
overdose. proper technique of aspiration beforethe anesthetic solution
When a spray topical anesthetic is needed, the use of is deposited,overdoseas a result of intravascularinjection is
metered dosage forms is strongly recommended. Disposable minimized.
nozzles for metered sprays make maintenance of sterility Prevention. To prevent intravascular injection, use an
simpler (Fig. 18-5). Ointments or gels, if used in small aspirating syringe. In an unpublished survey conducted by
amounts (as on the tip of a cotton applicator stick), may be the author, 23% of dentists questioned stated that they rou
applied with minimal risk of overdose. tinely use nonaspirating syringes to administer local anes
thetics.There is no justificationfor the use of a nonaspirating
syringe for any intraoral injection technique, because it is
impossible to determine the precise location of the needle
tip without aspirating.
Use a needle no smaller than 25 gauge when the risk of
aspiration is high. Although aspiration of blood is possible
through smaller-gauge needles, resistance to the return of
blood into the lumen of smaller-gaugeneedles is increased,
leadingto an increasedlikelihood of an unreliable aspiration
test. Therefore,injection techniqueswith a greaterlikelihood
of positive aspiration dictate the use of a 25-gaugeneedle.A
27-gauge needle can be utilized in lieu of 25-gauge as it
provides relatively reliable aspiration; however, 30-gauge
needles should be avoided,if at all possible,when injections
are administered into more vascular areas of the oral cavity.
Aspirate in at least two planes before injection.Figure 18-8
illustrates how an aspiration test may be negative even
though the needle tip lieswithin the lumen of a blood vessel.
The use of multiple aspiration tests before injection of solu
tion, with the needlebevelin differentplanes,overcomesthis
Figure 18·5. Metered spray with disposable nozzle. potential problem. After the initial aspiration, rotate the
,.--
/ ',
I 36mg '--
1 local - - Blood
\ anesthetic ,. •.•.- - - Figure 18-6. Direct rapid intravascular
' __
.••.. ,,,. / administration of one cartridge of local
anesthesiaproduces marked elevationof the
anesthetic blood levelin a very short time.
Anesth~~c~~~~ ~- _
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318 PART IV Complications, Legal Considerations, Questions, and Future
''
A. temporales Rami
profundae occipitales
a. occipitalis
A. sphenopalatina
A. transverse faciei
A. alveolaris A. meningea media
superior posterior
Anastomosis
r. auricularis a.
occipitalis cum
a. auricularis posterior
A. angularis
Ramus mastoideus
Ramus stemocleidomastoideus
A. infraorbitalis Ramus occipltalls aurlcularls posterior
A.labialis
superior
A. palatina
descendens
A. pharyngea
A. buccalis ascendens
A. stemocleldomastoldea
A. palatlna ascendens
A. lablalls Inferior
A. carotis extema
A. mentalis A. carotls lntema
A. thyreoidea superior A. carotis communis
A. faclalls
Figure 18·7. Reversecarotid blood flow.Rapid intra-arterial deposition oflocal anesthetic into the inferior alveolarartery (X) produces
an overdosereaction. Blood flow in the arteries is reversedbecause of the high pressure produced by the rate of injection. Arrows indicate
the path of the solution into the internal carotid artery and cerebral circulation.
A B c
Figure 18-8. Intravascular injection of local anesthetic. A, Needle is inserted into the lumen of the blood vessel.B, Aspiration test is
performed. Negativepressure pulls the vesselwall against the bevd of the needle; therefore no blood enters the syringe (negativeaspiration).
C, Drug is injected. Positivepressure on the plunger of the syringe forces local anesthetic solution out through the needle. The wall of the
vesselis forced awayfrom the bevel,and anesthetic solution is deposited directly into the lumen of the blood vessel.
syringeabout 45 degreesto reorient the needle bevelrelative (seizure). In the event that the level does exceed this
to the wall of the blood vessel,and reaspirate. minimum, onset of the reaction willbe slowerand signsand
Slowly inject the anesthetic. Rapid intravascular injection symptoms will be lessseverethan those observed after more
of 1.8 mL of a 2% localanesthetic solution produces a blood rapid injection. Slow injection is the most important factor
levelin excessof that necessaryfor overdose.Rapid injection in preventing adverse drug reactions-it is even more impor
is defined (by the author) as administration of the entire tant than aspiration. The idealrate of local anesthetic admin
volume of a dental cartridge in 30 seconds or less. The istration is 1.0mL/min. Giventhat many dentists administer
same volume of anesthetic deposited intravascularlyslowly LA more rapidly than this ideal, the recommended rate of
(minimum, 60 seconds) produces slightly elevated blood LAadministration is deposition of a 1.8-mLcartridge in not
levelsthat are still below the minimum for serious overdose less than 60 seconds.Becausethe recommended volumes of
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CHAPTER18 SystemicComplications 319
local anesthetic for most intraoral injection techniques are 2. Choice of local anesthetic: In most instances where
considerably less than 1.8 mL, most injections can be admin serious LAoverdosehas occurred in children, the local
istered safely (and comfortably) in less than 1 minute. anesthetic administered has been a "plain'' drug, either
••• mepivacaineHCl 3% (usually) or prilocaine HCl 4%.
The truth about local anesthetic overdosage in den Both of these are excellentlocal anesthetics--when used
tistry35:Administration of too large an LA dose relative to properly.The rationale behind the clinician'sselection
the weight (and age) of the patient is the most common of a short-acting drug for children includes that
cause of serious local anesthetic overdose reactions in den (1) most pediatric appointments are of short duration,
tistry.Although some serious cases of local anesthetic over and (2) "plain"local anesthetics possessa shorter
dose have occurred in adult patients,5 an overwhelming duration of residual soft tissue anesthesia,minimizing
majority of problems commonly developin the child who is the likelihood of inadvertent soft tissue injury as the
young (2 to 6 years), lightweight (<30 kg [66 lb]), and well child bites or chewshis or her numb lip or tongue.
behaved; requires multiple procedures in four quadrants; As a rule, the pediatric dentist administers a "plain"
and is managed in the office of an inexperienced general local anesthetic only when treatment is limited to one
dentist.3 quadrant. If treatment extends to two or more
Reviewof many of the casesthat resulted in serious mor quadrants in one visit, a vasopressor-containingLAis
bidity or death revealsa number of shared factors, none of selected.Prolonged posttreatment soft tissue anesthesia
which in itselfmight pose a serious problem; however,when leads to the increased possibility of soft tissue damage;
added together, they act to produce clinicalsigns and symp however,this risk is outweighed by benefits accrued
toms of local anesthetic overdose. These factors are pre through delayedabsorption of the local anesthetic into
sented in Box 18-3. the CVS (the risk of overdoseis diminished).
1. Treatment plan: In interviewswith trained pediatric Postoperativesoft tissue injury can be prevented in
dentists, it has been the author's experiencethat when many ways,such as securing a cotton roll in the buccal
presented with the patient described in the preceding fold and advisingthe parent to watch the child. (See
section (young, lightweight,well behaved), the pediatric Chapters 16 and 17.)Availabilityof the local anesthesia
dentist (with few exceptions)will not treat all four reversalagent-phentolamine mesylate----decreases
quadrants at one visit using local anesthetic alone. residual soft tissue anesthesia duration significantly.36•37
Limiting treatment to one or two quadrants per visit Reversalof local anesthesia is discussedfully in
represents a more rational approach to this patient's Chapter 20.
needs, and enhances safety. Table 18-3presents the local anesthetic of choice for
A dentist confronted with a (well-meaning)parent or 117dentists who treat children.38
grandparent who complains of the difficultiesof getting 3. Volume of local anesthetic administered: Pain control for
to the dental officeand the inconvenienceof having to the entire primary dentition can be achievedwith
miss a half-day of work, and wanting to have the child's approximatelytwo cartridges of local anesthetic. In the
dental care accomplishedin one visit (not two or smaller child patient, there is rarely a compelling need
more), might feel pressured into agreeingto this to administer a 1.8-mLvolume oflocal anesthetic in
request, thus increasingthe risk for local anesthetic any one injection.Yetfull cartridges are commonly
overdose.This is more likelyto occur in officesof administered when children receivelocal anesthetic
younger (by which I mean "inexperienced") dentists administered by nonpediatric dentists. In many of the
who are developingtheir practice and wish to keep their instances where a death resulted, a total of five,six, or
patients "happy:' seven cartridges were administered.3
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320 PARTIV Complications,LegalConsiderations, Questions, and Future
In those situations where LAmust be administered to 5. Exceeding the maximum dosage based on patient's body
all four quadrants of a smaller child, pain control can weight: An important factor, especiallywhen younger,
be achievedwith not more than two cartridges, as lighter-weightpatients are managed, is maximum
follows:one fourth of a cartridge each for the right and recommended dose (MRD). Determine the weight of
left incisivenerve blocks (anesthetizing all mandibular the patient (in kilograms [kg] or pounds [lb]) before the
primary teeth); or one half of a cartridge each for right start of treatment. It is preferable to weigh the child on
and left inferior alveolarnerve blocks;one quarter of a a scale,because parents frequently can offer only a
cartridge each for the right and left anterior superior rough estimate of their child's weight (usually
alveolarnerve blocks. In lieu of the anterior superior underestimating it). One must alwaysremember that
alveolarnerve block, maxillary infiltrations may be these figures are not absolutes.Exceedingthe MRD of a
administered with one sixth of a cartridge per injection drug does not guarantee that an overdosewill happen
(Table 18-4). (see Table 18-5 and discussion). On the other hand,
4. Local anesthetic administered to all four quadrants at one administering dosagesbelow the maximum calculated
time: Administration, over 1 or 2 minutes, of four or by body weight is no guarantee that adversereactions
more cartridges of a local anesthetic without a will not be seen. The likelihood of ADRsdevelopingis
vasopressorto all four quadrants makes little dose related. Smaller dosagesminimize (but do not
therapeutic sense and considerablyincreasesthe risk of eliminate) this risk; larger doses increase (but do not
an overdose.Administration of local anesthetic to one guarantee) it.
quadrant, treating that area, then anesthetizing the next Maximum recommended dosagesof commonly
quadrant, and so on, makes considerablymore sense administered local anesthetics are summarized in
from both a therapeutic and a safetyperspective.For Table 18-5.
equal volumes of local anesthetic, administration over a The intrinsic safety of local anesthetics is illustrated in
longer time frame (e.g., 1 to 2 hours) results in a lower Table 18-6, which presents the volume of local anesthetic
blood levelwhen compared with administration of the administered on 65 occasions by a general dentist who
entire dose at one time. removed third molars from college-agedindividuals.
None of these patients experienced an adverse response
to the local anesthetic, although many received dosages
many times the MRD.39 This is one indication that local
TABLE 18-4 anesthetics are extremely safe drugs when administered to
Recommended Volumes of Local Anesthetic for healthy,younger (teenageto mid-20s) adult patients. Unfor
lntraoral Injections tunately,when they are administered in overlylarge dosesto
Adult Pediatric younger,lightweightpatients, overdose is a significant risk.
Technique Volume. ml Volume. ml Virtually all local anesthetic overdose reactions are pre
Infiltration (supraperiosteal) 0.6 0.3 ventable if the clinician adheres to the very basic, simple
Inferior alveolar 1.5 0.9 recommendations presented in the preceding section. In the
Gow-Gates mandibular 1.8 0.9 unlikelysituation that an overdosereaction develops,adher
Mental or incisive 0.6 0.45 ence to the basic steps of emergency management will lead
Posterior superior alveolar 0.9 0.45 to a successfuloutcome in essentiallyall cases.
Anterior superior alveolar 0.9 0.45
(infraorbital) Clinical Manifestations
Greater (anterior) palatine 0.45 0.2
Clinical signs and symptoms of overdose appear whenever
Nasopalatine 0.2 0.2
the blood levelin that drug's target organ(s) becomes overly
Maxillary (second division) 1.8 0.9
high for that individual (Box 18-4). Target organs for local
TABLE 18-5
Maximum Recommended Dosages of Local Anesthetics
Clinical Percent mg/Cartridge Recommended* Absolute
Drug mg I ml (1.8 ml} mg/kg mg/lb Maximum.* mg
Articaine 4 40 72 7.0 3.2 None listed
Lldocaine 2 20 36 4.4 2.0 300
Mepivacaine 2 20 36 4.4 2.0 300
Mepivacaine 3 30 54 4.4 2.0 300
Prilocaine 4 40 72 6.0 2.7 400
Bupivacaine 0.5 5 9 1.3 0.6 90
*Maximum recommended doses of local anesthetics are for local anesthetic solutions containing vasoconstrictors or without vasoconstrictors.
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CHAPTER18 SystemicComplications 321
TABLE 18-6 anesthetics include CNS and the myocardium. The rate of
Local Anesthetic Administration for Removal onset of signs and symptoms and, to an extent,their severity
of Third Molars correspond to this level. Table 18-7 compares the various
modes of local anesthetic overdose.
Procedure
(Number of
Third Molars Number of Number of Number of
Extracted at Patients in Cartridges Cartridges NOTE: It is possiblethat the "excitatory"phaseof the
Visit) Category (Range) (Average) overdosereactionmaybe extremelybriefor maynot
occurat all,inwhichcasethe firstclinicalmanifestation
1 5 4-10 6.2 of overdosemaybe drowsinessprogressingto
2 13 4-23 12.18 unconsciousness and respiratoryarrest.Thisappearsto be
3 8 10-20 15.33 morecommonwith lidocainethan withother local
4 39 6-26 19.24 anesthetics.
40
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322 PART IV Complications, Legal Considerations, Questions, and Future
TABLE 18-7
Comparison of Forms of Local Anesthetic Overdose
Too Large a Slow Bio- Slow
Rapid lntravascular Total Dose Rapid Absorption transformation Elimination
Likelihood of Common Most common Likelywith "high normal" Uncommon Leastcommon
occurrence doses if no vasoconstrictors
are used
Onset of signs Most rapid (seconds); 3-5 min 3-5 min 10-30min 10 min-several hr
and symptoms intra-arterial faster
than intravenous
Intensity of signs Usuallymost intense Gradual onset with increased intensity; may Gradual onset with slow increase in
and symptoms prove quite severe intensity of symptoms
Duration of signs 1-2 min Usually5-30 min; depends on dose and ability to Potentiallylongest duration because
and symptoms metabolize or excrete of inability to metabolize or
excreteagents
Primary Aspirate,slow Administer Use vasoconstrictor;limit Adequate pretreatment physical
prevention injection minimal doses topical anesthetic use evaluation of patient
or use nonabsorped
type (base)
Drug groups Amides and esters Amides;esters Amides;esters only rarely Amides and esters Amides and esters
only rarely
Lldocalne
blood levels
µg/mL
Cardlovascular system Central nervous system
Q]f
0.5
Normal blood level after 1.0 Normal blood level after
intraoral injection 1.5 intraoral injection
No cardiovascular actions 2.0 0.5-4.0
2.5 Anticonvulsant actions
1.8-5.0 3.0
Antidysrhythmic actions 3.5
4.0
4.5
5.0
4.5-7.0
5.5
CNS depression
6.0 manifest as excitation (except lidocaine)
6.5
5.0-10.0
7.0
ECG alterations
Myocardial depression
Peripheral vasodilation 7.5-10.0
CNS depression
manifest as tonic-clonic seizures
10.0+
Massive peripheral vasodilation 10.0+
Intensive myocardial depression Generallzed CNS depression
Cardiac arrest
Figure 18-9. Local anesthetic blood levelsand actions on cardiovascularand central nervous systems.
actions.t':" The mechanism of this action is depression of Tonic-clonic seizures generally occur at levelsgreater than
hyperexcitable neurons found in the amygdala of seizing 7.5 µg/mL. With further increases in the lidocaine blood
patients. level,seizure activity ceasesand a state of generalized CNS
Signsand symptoms of CNStoxicity appear at a cerebral depression develops. Respiratory depression and arrest
blood levelgreaterthan 4.5 µg/mL.Generalizedcortical sen (apnea) are manifestations of this. Chapter 2 describes the
sitivity is noted: agitation, talkativeness, and irritability. method through which a CNS-depressant drug, such as a
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CHAPTER18 SystemicComplications 323
i
maximum is 5 µg/mL-the level at which undesirable Unconscious... assessand provide external cardiac
actions become more likely.44 compression if necessary
Increased blood levels (5 to 10 µg/mL) lead to minor Conscious... assesscirculation
alterations on the electrocardiogram,myocardialdepression, D... DEFINITIVECARE
decreased cardiac output, and peripheral vasodilation. At Diagnosis:
levelsabove 10 µg/mL,these effectsare intensified:primarily Management: Emergencydrugs and/or assistance
massiveperipheral vasodilation, marked reduction in myo (emergencymedical services,dial 9-1-1)
cardial contractility,severebradycardia,and possiblecardiac
arrest.45,46
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324 PART IV Complications, Legal Considerations, Questions, and Future
as to the patient's degree of recovery, do not permit the D (definitive care): In the presence of tonic-clonic
patient to leave the office alone; consider emergency convulsions:
medical assistance (e.g., dial 9-1-1). 1. Protect the patient's arms, legs,and head. Loosen tight
Slower Onset R,f 5 minutes a'fter administration). Pos clothing, such as ties, collars,and belts, and remove the
sible causes of reactions of a sloweronset include abnormal pillow (or "doughnut") from the headrest.
biotransformation and renal dysfunction.Followthis proto 2. Immediately summon emergencymedical assistance
col for dealingwith the sloweronset of signs and symptoms (i.e., 9-1-1).
in a consciouspatient. 3. Continue basic life support. Maintenance of an
P-7A-7B-7C. Position the conscious patient comfort adequate airway and adequate ventilation are of the
ably.A, B, and C are assessed as adequate (patient is con utmost importance during management of local
scious and talking). anesthetic-induced tonic-clonic seizures.Increased
D (definitive care): oxygenutilization and hypermetabolism,with increased
1. Reassurethe patient. production of C02 and lactic acid, occur during the
2. Administer oxygen. seizure,leading to acidosis,which, in turn, lowersthe
3. Monitor vital signs. seizurethreshold (the blood level at which local
4. Administer an anticonvulsant. Overdose reactions anesthetic-induced seizuresbegin), prolonging the
caused by abnormal biotransformation or renal reaction." Cerebral blood flow during such a seizure is
dysfunction usually progress somewhat in intensity and also increased,elevatingstill further local anesthetic
last longer (becausethe drug cannot be eliminated blood levelswithin the CNS.
rapidly). If venipuncture can be performed and if 4. Administer an anticonvulsant. The blood levelof the
equipment is available,titrate 1 mg of midazolam/min local anesthetic declines as the drug undergoes
until the clinical signs and symptoms of overdose redistribution; if acidosisis not present, seizurescease
subside. usually within about 1 to 3 minutes. Anticonvulsant
5. Summon medical assistance.When venipuncture is not therapy is not indicated for most seizures.If the seizure
practical, or when an anticonvulsant drug has been is prolonged (4 to 5 minutes with no indication of
administered, seek emergencymedical assistanceas terminating), consider administering an anticonvulsant,
soon as possible.Postexcitementdepression usually is but only if trained in parenteral drug administration
moderate after a mild excitement phase. Administration (IY,intramuscular [IM], intranasal [IN]) and
of midazolam or any other anticonvulsant will intensify ventilation of a possibly apneic patient. N midazolam,
this depression to varying degrees.Monitoring of the titrated at a rate of 1 mg/min until seizurescease,is the
patient's status and adherence to the steps of basic life preferred treatment.P'" Ifvenipuncture is not feasible,
support are normally more than adequate for this 5 mg/mL midazolam may be administered IM at a dose
situation. of 0.2 mg/kg for adult or pediatric patients.51•52 The
6. After termination of the reaction, be sure that the vastus lateralis is the preferred site for IM injection.
patient is examined by a physician or a hospital staff Intranasal (IN) midazolam can be administered in
member to determine possible causes.The examination patients weighingless than 50 kg at a dose of 0.2 mg/kg
could include blood tests and hepatic and renal (up to 10 mg).53 Seizuresusually stop within 1 to 2
function tests. minutes after IN midazolam. Maintain basic life
7. If the patient is not transported to a hospital by support, and obtain the assistanceof emergencymedical
emergencymedical services(EMS),do not let him or personnel.
her leavethe dental officealone. Arrangements should Postseizure (Postictal) Phase. CNSdepressionis usually
be made for an adult companion if hospitalization is present at an intensity equal that of the excitation phase
deemed unnecessary. (Fig. 18-10). The patient may be drowsy or unconscious;
8. Determine the cause of the reaction before proceeding breathing may be shallowor absent; the airwaymay be par
with therapy requiring additional local anesthetics. tially or totally obstructed; blood pressure and heart rate
may be depressedor absent.A more intense postseizurestate
Severe Overdose Reaction is noted when anticonvulsants have been administered to
Rapid Onset (within 1 minute). Signs and symptoms terminate the seizure.
include loss of consciousnesswith or without convulsions. P-7A-7B-7C. Implementation of the steps of basic life
The probable cause is intravascular injection. support is crucial:airway,breathing, and circulation must be
P-7A-7B-7C. Place the unconscious patient in the provided as needed. In all postictal situations, maintenance
supine position. A, B,and C are assessedand maintained, as of an adequate airway is necessary; in some other cases,
necessary. Remove the syringe from the mouth (if still assisted or controlled ventilation may be indicated; for a
present), and place the patient supine with feet elevated small percentage of the most severe reactions, chest com
slightly.Subsequent management is based on the presence pression must be added to the first two steps of basic life
or absence of convulsions. support.
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CHAPTER18 SystemicComplications 325
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326 PART IV Complications, Legal Considerations, Questions, and Future
TABLE 18-8
Dilutions of Vasoconstrictors Used in Dentistry
mg per Cartridge Maximum No. of Cartridges Used for
Dilution Drug Available mg/ml (1.8 ml) Healthy Patient and Cardiac-Impaired Patient
1:1000 Epinephrine (emergencykit) 1.0 Not applicable Not availablein local anesthetic cartridge
1:10,000 Epinephrine (emergencykit) 0.1 Not applicable Not availablein local anesthetic cartridge
1:20,000 Levonordefrin 0.5 0.09 10 (H), 2 (C)
1:30,000 Levarterenol 0.034 0.06 5 (H), 2 (C)
1:50,000 Epinephrine 0.02 0.036 5 (H), 1 (C)
1:100,000 Epinephrine 0.01 0,018 10 (H), 2 (C)
1:200,000 Epinephrine 0.005 0.009 20 (H), 4 (C)
C, Cardiac-impaired patient; H, healthy patient.
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CHAPTER 18 SystemicComplications 327
TABLE 18-9
Classification of Allergic Diseases (After Gell and Coombs)
Principal Antibody Time of
Type Mechanism or Cell Reactions Clinical Examples
Anaphylactic(immediate, IgE Secondsto Anaphylaxis(drugs, insect venom, antisera)
homocytotropic, antigen induced, minutes Atopic bronchial asthma
antibody mediated) Allergicrhinitis
Urticaria
Angioedema
Hay fever
II Cytotoxic (anti.membrane) IgG 'fransfusion reactions
IgM (activate Goodpasture's syndrome
complement) Autoimmune hemolysis
Hemolytic anemia
Certain drug reactions
Membranous glomerulonephrosis
III Immune complex (serum sickness IgG (form complexes 6-8 hr Serum sickness
like) with complement) Lupus nephritis
Occupational allergicalveolitis
Acute viral hepatitis
IV Cell-mediated (delayed)or 48 hr Allergiccontact dermatitis
tuberculin-type response Infectious granulomas (tuberculosis,mycoses)
Tissue graft rejection
Chronic hepatitis
Adapted from Krupp MA, Chatton MJ: Current medical diagnosis and treatment, LosAltos, Calif, 1994,LangeMedical.
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328 PART IV Complications, Legal Considerations, Questions, and Future
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CHAPTER18 SystemicComplications 329
uncommon; those most frequently reported are labeled QUESTION: Did the local anesthetic solution contain a
as allergy.If the patient mentions any unusual reaction to vasoconstrictor?
local anesthetics,the followingprotocol should be observed
before use of the questionable drug is carried out. If the QUESTION: Were you taking any other drugs or medica
patient relates a history of alleged local anesthetic allergy, tions at the time of the incident?
it is imperative that the dentist consider the following
factors: QUESTION: Canyou provide the name, address,and tele
1. Assumethat the patient is truly allergicto the drug in phone number of the doctor (dentist or physician) who
question and then take whatever steps are necessaryto was treating you when the incident occurred?
determine whether the alleged"allergy"is indeed an
allergy.A recent paper on food allergyrevealedthat Answersto these questions provide enough information
30% of Americans have reported (alleged)one or more to permit a doctor to make an informed determination as to
food allergies,but true food allergyin the U.S. whether a true allergic reaction to a drug occurred. This is
population actually occurs at a rate of approximately the initial step in managing alleged local anesthetic allergy.
4% in adults and 5% in children.73 The dialogue history follows.
2. Any drug or closelyrelated drug to which a patient
claims to be allergicmust not be used until the alleged QUESTION: Describe exactly what happened.
allergycan be absolutelydisproved.
3. For almost all drugs commonly implicated in allergic This is probably the most important question because it
reactions, equally effectivealternate drugs exist (e.g., allowsthe patient to describe the actual sequence of events.
antibiotics, analgesics). The "allergy,"in most instances, is explained by the answer
4. The only drug group in which alternativesare not to this question. The symptoms described by the patient
equally effectiveconsists of local anesthetics. should be recorded and evaluated to help in formulating a
••• tentative diagnosis of the adverse reaction. Did the patient
Two major components are useful for determining the lose consciousness?Did convulsions occur? Was there skin
veracity of a claim of allergy: (1) dialogue history, whereby involvement or respiratory distress?The manifestations of
additional information is sought directly from the patient, allergic reactions are discussed in the followingparagraph.
and (2) consultation for a more thorough evaluation if Knowingthem can aid the evaluator in rapidly determining
doubt persists. the nature of the reaction that occurred.
Allergicreactions involveone or more of the following:
Dialogue History. The followingquestions are included in skin (itching, hives, rash, edema), gastrointestinal system
the dialogue history between the dentist and a patient with (cramping, diarrhea, nausea, vomiting), exocrine glands
an allegedallergyto localanesthetics.The firsttwo questions (runny nose, watery eyes), respiratory system (wheezing,
are the most critical, for they immediately establish in the laryngeal edema), and cardiovascular system (angioedema,
evaluator'smind a senseof whether allergydoes or does not vasodilation, hypotension). Most patients describe their
exist.74 local anesthetic "allergy'' as one in which they experienced
palpitations, severe headache, sweating, and mild shaking
QUESTION: Describe exactly what happened. (Describe (tremor). Such reactions are almost alwaysof psychogenic
your "allergic" reaction.) origin or are related to the administration of overly large
doses of vasoconstrictor (e.g., epinephrine). They are not
QUESTION: What treatment was given? allergic in nature. Hyperventilation, an anxiety-induced
reaction in which patients lose control over their breathing
Following these two questions, the evaluator may con (inhaling and exhaling rapidly and deeply), is accompanied
sider others that will help elucidate the actual reaction. by dizziness, lightheadedness, and peripheral paresthesias
(fingers,toes, and lips). Complaints of itching,hives,rash, or
QUESTION: What position were you in during injection edema lead to the presumptive conclusion that an allergic
of the local anesthetic? reaction actually may have occurred.
QUESTION: What was the time sequence of events? QUESTION: What treatment was given?
QUESTION: Were the servicesof emergency medical per When the patient is able to describe his or her manage
sonnel necessary? ment, the evaluator usually can determine its cause. Were
drugs injected? If so, what drugs? Epinephrine, histamine
QUESTION: What drug was used? blockers, corticosteroids, or anticonvulsants?Was aromatic
ammonia used?Oxygen?Knowledgeof the specificmanage
QUESTION: What volume of the drug was administered? ment of these situations can lead to an accurate diagnosis.
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330 PART IV Complications, Legal Considerations, Questions, and Future
Drugs used in the management of allergic reactions A positive response to this usually indicates the occur
include three categories: vasopressors (epinephrine [Adrena rence of a more seriousreaction. Most psychogenicreactions
lin]), histamine blockers {diphenhydramine [Benadryl] or are ruled out by a positive answer,although an overdoseor
chlorpheniramine [Chlor-Trimeton]), and corticosteroids allergicreaction indeed may have occurred.
(hydrocortisone sodium succinate [Solu-Cortef] or dexa
methasone [Decadron]). QUESTION: What local anesthetic was administered?
Mention of the use of one or more of these drugs increases
the likelihood that an allergic response did occur. Anticon A patient who is truly allergic to a drug should be told
vulsants, such as diazepam or midazolam, are administered the exact (generic) name of the substance. Many persons
intravenously to terminate seizures induced by overdose of with documented allergic histories wear a medical alert
local anesthetic. Aromatic ammonia is frequently used in the tag or bracelet (Fig. 18-11)that lists specificitems to which
treatment of syncopal episodes. Oxygen may be adminis they are sensitive.However,some patients respond to this
tered in any or all of these reactions but is not specific for question with, "I'm allergic to local anesthetics" or "I'm
allergy. allergic to Novocain" or "I'm allergic to all 'caine' drugs."
Of 59 patients reporting allergy to local anesthetics, 54
QUESTION: What position were you in when the reaction could name one or more local anestheticsthey believedwere
took place? responsible. Five referred to only caine drugs.76 Novocain
(procaine) and other esters rarely are used today as inject
Injection of a local anesthetic into an upright patient is able local anesthetics in dentistry (although the esters
most likelyto produce a psychogenicreaction (vasodepres (primarily tetracaine) maintain some popularity in medi
sor syncope). This does not exclude the possibility that cine); the amides have replacedthe estersin clinicalpractice.
another type of reaction may occur, but with the patient Yet patients throughout the world frequently call the local
supine during the injection, vasodepressor syncope is a less anesthetics they receive "shots of Novocain."Two reasons
likelycause,eventhough transient loss of consciousnessmay exist for this. First, many older patients at one time received
(on very rare occasions) occur in these circumstances.75 In Novocain as a dental local anesthetic, and its name has
some of the evaluations of allergy to local anesthetics that become synonymous with intraoral dental injections.
the author has carried out, the patient had been given an Second, despite the fact that United States dentists do not
intracapsular injection of corticosteroid in the knee. Seated injectprocaine or procaine-propoxycaine,many stilldescribe
upright on a table in the physician's treatment room, the local anesthetics as Novocain when talking with their
patient was able to watch the entire procedure, which was patients. Thus the usual response of a patient to this question
profoundly disturbing. In an effort to make such injections
more tolerable,lidocaineor another localanestheticis added
to the steroid mixture. In spite of this, however,the intracap
sular injection of corticosteroid and lidocaine is extremely
uncomfortable. Many patients experience their "allergic
reaction" at this time. Therefore, the supine position is rec
ommended as being physiologicallybest tolerated for the
administration of all local anesthetic injections.
QUESTION: Were the services of a physician, emergency Figure 18-11. Medical alert bracelet provides vital medical
medical services, or a hospital necessary? information about the patient.
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CHAPTER18 SystemicComplications 331
remains, "I'm allergic to Novocain:' This response, received person is able to locate patient records and describein detail
from a patient who has been managed properly in the past what transpired. If it is not possible to locate or contact the
after an adverse reaction, indicates that the patient was sensi doctor, the patient's primary care physician should be con
tive to ester local anesthetics but not necessarily to amide sulted. Direct discussionwith the patient and the doctor can
local anesthetics. However, the answers usually are too provide a wealth of information that the knowledgeable
general and vague for any conclusions to be drawn." dentist can use to determine more preciselythe nature of the
previous reaction.
QUESTION:What amount of drug was administered?
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332 PART IV Complications, Legal Considerations, Questions, and Future
responses to the paraben preservative (before 1984, the pro nature. Arrange an appointment for immediate consultation
tocol included testing for parabens) and none to the amide and allergytesting. Do not carry out any dental care requir
local anesthetic itself. Numerous psychogenic responses ing the use of injectable or topical local anesthetics. For
(syncope, hyperventilation, palpitations) have been observed incision and drainage of an abscess, inhalation sedation
during intracutaneous or intraoral testing phases. with nitrous oxide and oxygen might be an acceptable
Such testing may be carried out by any person who is alternative.
knowledgeable about the procedure and is fully prepared to Acute pain may be managed with oral analgesics,infec
manage whatever adverse reactions may develop. It must be tion with oral antibiotics. These constitute only temporary
remembered that skin testing is not without risk. Severe measures.After complete evaluation of the "allergy,"defini
immediate allergic reactions may be precipitated by as little tive dental care may proceed.
as 0.1 mL of drug in a sensitized patient. Emergency drugs, Emergency Protocol No. 2. Use general anesthesia in
equipment, and trained personnel always must be available place of local anesthesia for management of a dental emer
whenever allergy testing is performed. gency.When properly used, general anesthesia is a highly
Intracutaneous allergy testing should be carried out only effectiveand relativelysafealternative.Its lack of availability
after an intensive dialogue history in which the evaluator has is a major problem in most dental practices.
become convinced that the prior reaction to the local anes When general anesthesiais used, be carefulto avoid local
thetic was not allergy. The testing procedure is used to anesthetics in these procedures:
confirm this fact for the patient. The intraoral challenge test 1. Topicalapplication (via spray) to the pharynx and
was added to the protocol when several patients with nega tracheal mucosa immediatelybefore intubation.
tive responses to intracutaneous testing stated, "But the 2. Infiltration of the skin with local anesthetic before
dentist will give me a larger amount in the mouth:' It was venipuncture to decreasediscomfort.
intended to provide the patient with the psychological General anesthesia,administered in the dental officeor in
support needed to receive intraoral local anesthetic injec a hospital operating theater,is a viableshort-term alternative
tions safely. to local anesthetic administration in managing the "allergic"
Informed consent is obtained before allergy testing. This patient, provided adequate facilities and well-trained per
consent includes, among other possible complications, acute sonnel are available.
allergy (anaphylaxis), cardiac arrest, and death. Emergency Protocol No. 3. Histamine blockers used
A continuous intravenous infusion is started before all as local anesthetics should be considered if general anes
allergy testing procedures are performed, and emergency thesia is not available, and if it is deemed necessary to
drugs and equipment are readily available throughout the intervene physicallyin the dental emergency.Most inject
testing. able histamine blockers have local anesthetic properties.
Diphenhydramine hydrochloride in a 1% solution with
Dental Management in the Presence of 1: 100,000epinephrine provides pulpal anesthesia for up to
Alleged Local Anesthetic Allergy 30 minutes." Although the quality of soft and hard tissue
When doubt persists concerning a history of allergyto local anesthesia attained with diphenhydramine, lidocaine, or
anesthetics, do not administer these drugs to the patient. prilocaine is equivalent,an undesirable side effectfrequently
Assume that allergy exists. Do not use local anesthetics, noted during injection of diphenhydramine is a burning or
including topical anesthetics, unless and until allergy has stingingsensation,which limits the use of this agent for most
been absolutelydisproved - to the patient's satisfaction. patients to emergency procedures only.85-87 Nitrous oxide
and oxygen used along with diphenhydramine minimize
Elective Dental Care. Dental treatment requiring local patient discomfort whileincreasingthe pain reaction thresh
anesthesia (topical or injectable) should be postponed until old. Another (possibly positive) side effect of diphenhydr
a thorough evaluation of the patient's "allergy"is completed. amine and many histamine blockers is CNS depression
Dental care not requiring local anesthesiamay be completed (sedation, drowsiness),which may prove somewhat benefi
during this time. cial during treatment but mandates that a responsible
adult guardian be availableto take the patient home after
Emergency Dental care. Pain or oral infection presents a treatment.
more difficult situation in the "I am allergic to Novocain"
patient. Commonly, this patient is new to the dental office, Management of the Patient With Confirmed Allergy.
requiring tooth extraction, pulpal extirpation, or incision Management of the dental patient with a confirmed allergy
and drainage (I&D) of an abscess,with an unremarkable to local anesthetics varies according to the nature of the
medical history exceptfor the alleged"allergyto Novocain." allergy. If the allergy is limited to ester anesthetics, an
If, after dialogue history, the "allergy"appears to have been amide anesthetic may be used (provided it does not con
a psychogenic reaction but some doubt remains, consider tain a paraben preservative, which is closely related to
one of severalcourses of action. the esters). No dental local anesthetic cartridge manufac
Emergency Protocol No. 1. The most practical approach tured in the United States since January 1984 contains
to this patient is to provide no treatment of an invasive methylparaben.
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CHAPTER 18 SystemicComplications 333
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334 PART IV Complications, Legal Considerations, Questions, and Future
Signs and symptoms of generalized anaphylaxis, listed cardiovascular signs and symptoms may be the only ones
according to their typical progression, follow: present. The reaction or any part of it can last from minutes
• Skin reactions to a day or longer.88•90
• Smooth muscle spasm of the gastrointestinal With prompt and appropriate treatment, the entire reac
(cramping) and genitourinary tracts and of respiratory tion may be terminated rapidly. However,hypotension and
smooth muscle (bronchospasm) laryngealedema may persist for hours to days despite inten
• Respiratory distress sivetherapy. Death, which may occur at any time during the
• Cardiovascular collapse reaction, usually is secondary to upper airway obstruction
In fatal anaphylaxis, respiratory and cardiovascular dis produced by laryngeal edema.91
turbances predominate and are evident early in the reaction.
The typical reaction progression is shown in Box 18-7. Management
In rapidly developing reactions, all signs and symptoms Skin Reactions. Management is predicated on the rate at
may occur within a very short time with considerable which the reaction appears after antigenic challenge.
overlap. In particularly severe reactions, respiratory and Delayed Skin Reactions. Signs and symptoms develop
ing 60 minutes or longer after exposureusuallydo not prog
ress and are not considered life threatening. Examples
include a localized mild skin and mucous membrane reac
BOX 18-7 Typical Reaction Progression of tion after application of topical anesthetic.In most instances,
Generalized Anaphylaxis the patient already may have left the dental office and is
calling back later describing these signs and symptoms, or
1. Earlyphase: skin reactions
the patient may still be in the dental officeat the conclusion
a.Patient complains of feelingsick
of his or her treatment.
b.Intense itching (pruritus)
Basic management follows the usual P-+A-+B-+C-+D
c.Flushing (erythema)
algorithm used in management of all medical emergencies.
d.Giant hives (urticaria) over the face and upper
P-+A-+B-+C. Position the conscious patient comfort
chest
ably.A, B, and C are assessedas adequate (patient is con
e. Nausea and possiblyvomiting
scious and talking).
f. Conjunctivitis
D (definitive care):
g. Vasomotor rhinitis (inflammation of mucous
1. Oral histamine blocker: 50 mg diphenhydramine or
membranes in the nose, marked by increased
10 mg chlorpheniramine; a prescription for
mucous secretion)
diphenhydramine, 50 mg capsules,one q6h for 3 to 4
h. Pilomotor erection (feelingof hair standing
days should be given to the patient.
on end)
2. If still in the dental office,the patient should remain in
2. Associatedwith skin responses are various
the officeunder observation for 1 hour before discharge
gastrointestinal or genitourinary disturbances related
to ensure that the reaction does not progress.
to smooth muscle spasm
3. Obtain medical consultation, if necessary,to determine
a. Severeabdominal cramps
the cause of the reaction. A complete list of all drugs
b. Nausea and vomiting
and chemicalsadministered to or taken by the patient
c. Diarrhea
should be compiled for use by the allergyconsultant.
d. Fecaland urinary incontinence
4. If drowsinessoccurs after oral histamine blocker
3. Respiratory symptoms usually develop next
administration, the patient should not be permitted to
a. Substernal tightness or pain in chest
leavethe dental officeunescorted.
b. Cough may develop
Immediate Skin Reactions. Signs and symptoms of
c. Wheezing (bronchospasm)
allergydevelopingwithin 60 minutes require more vigorous
d. Dyspnea
management. Examplesinclude conjunctivitis,rhinitis, urti
e. If the condition is severe,cyanosisof the mucous
caria, pruritus, and erythema.
membranes and nail beds
P-+A-+B-+C. Position the conscious patient comfort
f. Possiblelaryngealedema
ably.A, B, and C are assessedas adequate (patient is con
4. The cardiovascularsystem is next to be involved
scious and talking).
a. Pallor
D (definitive care):
b. Lightheadedness
1. Administer parenteral (IM, N) histamine blocker:
c. Palpitations
50 mg diphenhydramine (25 mg if less than 30 kg
d. Tachycardia
[66 lb]) or 10 mg chlorpheniramine (5 mg ifless than
e. Hypotension
30 kg [66 lb]).
f. Cardiac dysrhythmias
2. Monitor and record vital signs (blood pressure, heart
g. Unconsciousness
rate and rhythm, respiratory rate) every 5 minutes
h. Cardiac arrest
for 1 hour.
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CHAPTER18 SystemicComplications 335
3. Observe the patient a minimwn of 60 minutes for respiratory movements,or when it is impossibleto carry out
evidence of recurrence. Discharge in the custody of a artificial ventilation in the presence of a patent airway
responsible adult if any parenteral drugs have been (tongue not causing obstruction). Partial obstruction of the
given. larynx produces stridor (a characteristic high-pitched
4. Prescribe an oral histamine blocker for 3 days. crowing sound), in contrast to the wheezingassociatedwith
5. Fully evaluate the patient's reaction before further bronchospasm. A partial obstruction may gradually or
dental care is provided. rapidly progress to total obstruction accompanied by the
6. If, at any time during this period, uncertainty exists as ominous "sound" of silence(in the presence of spontaneous
to the condition of the patient, activate EMS {9-1-1). respiratory movements). The patient rapidly loses con
sciousnessfrom lack of oxygen.
Respiratory Reactions P~A~B~C. Position the unconscious patient supine.
Bronchospasm. A, B, and C are assessed.If airway is maintained and the
P~A~B~C. Position the conscious patient comfort victim'schest is making spontaneous respiratory movements
ably.Most persons experiencingrespiratory distressprefer to but no air is being exchanged, immediate and aggressive
be seatedupright to varyingdegrees.A,B,and C are assessed. treatment is mandatory to savethe victim's life.
Airway is patent, although patient is exhibiting respiratory D (definitive care):
distress.C is assessedas adequate. 1. Epinephrine. Administer 0.3 mg (if >30 kg) {0.15mg if
D (definitive care): <30 kg) epinephrine IM in the vastus lateralis muscle.
1. Terminatetreatment (if started). Epinephrine may be administered every 5 to 10 minutes
2. Administer oxygenvia full face mask, nasal hood, or as needed until recovery,or until help (9-1-1) arrives on
nasal cannula at a flow of 5 to 6 liters/min. the scene to take over management.
3. Administer epinephrine IM in the vastus lateralis 2. Followingadministration of epinephrine, activate EMS.
muscle (0.3 mg if>30 kg; 0.15 mg if <30 kg) or another Summon emergencymedical assistanceand administer
appropriate bronchodilator via metered dose inhaler oxygen.
(MDI) (albuterol) (Fig. 18-12).Dose may be repeated 3. Maintain the airway.If only partially obstructed,
every 5 to 10 minutes until recoveryor help (EMS) epinephrine may halt the progress of the edema
arrives on the scene to take over management. through its vasoconstrictiveactions.
4. ActivateEMS(9-1-1).If alone with victim, it is important 4. Additional drug management:histamine blocker IM or
to administer epinephrine before activatingEMS. N (50mg diphenhydramineor 10mg chlorpheniramine),
5. On recovery (bronchospasm resolves),administer corticosteroidIM or N (100mg hydrocortisone sodiwn
histamine blocker to minimize risk of relapse (50 mg succinateto inhibit and decreaseedema and capillary
IM diphenhydramine [25 mg if <30 kg] or 10 mg IM dilation).
chlorpheniramine [5 mg if <30 kg]). 5. Perform cricothyrotomy.If the preceding steps have
6. EMSwill evaluatethe patient's status and will failed to secure a patent airway,an emergencyprocedure
determine whether transport to the hospital emergency to create an airway is critical for survival.Figures 18-13
department for observation or additional treatment is and 18-14both illustrate the anatomy of the region and
warranted. the technique. Once established,the airwaymust be
Laryngeal Edema. Laryngeal edema may be present maintained, oxygenadministered, and artificial
when movement of air through the patient's nose and mouth ventilation used as needed. Monitor the patient's vital
cannot be heard or felt in the presence of spontaneous signs.The patient definitelywill require hospitalization
followingtransfer from the dental officeby paramedical
personnel.
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336 PART IV Complications, Legal Considerations, Questions, and Future
~Base of tongue
' Epiglottis
Eplglottlc
cartilage
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CHAPTER18 SystemicComplications 337
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338 PART IV Complications, Legal Considerations, Questions, and Future
B c
D E
Figure 18-17. Summary of basic life support. A. Airway-head tilt, chin lift. B, Assess breathing. C, 1Wo full ventilations. D, Assess carotid
pulse. E, External chest compression-IS compressions: 2 ventilations.
8. Needlesshould be disposable,sharp, rigid, capable of 11. Injection should be made slowly,over a minimum of
reliable aspiration, and of adequate length for the 60 seconds if 1.8mL of local anesthetic is deposited.
contemplated injection techniques. 12. Observe the patient both during and after local
9. Aspirating syringesmust alwaysbe used for all anesthetic administration for signs and symptoms
injections. of undesirable reaction. Never givean injection
10. Aspiration should be carried out in at least two planes and leavethe patient alone while doing other
before injection. procedures.
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CHAPTER 18 Systemic Complications 339
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340 PARTIV Complications,LegalConsiderations, Questions, and Future
48. RyanCA,Robertson M, CoeJY:Seizuresdue to lidocainetoxic 70. Shojaie AR, Haas DA: Local anesthetic cartridges and latex
ity in a child during cardiac catheterization, Pediatr Cardiol allergy:a literature review,J Can Dent Assoc68:622--626,2002.
14:116-118,1993. 71. Perusse R, Goulet JP, Turcotte JY: Contraindications to
49. Rivera R, Segnini M, Baltodano A, et al: Midazolam in the vasoconstrictors in dentistry. Part II. Hyperthyroidism, dia
treatment of status epilepticus in children, Crit Care Med betes, sulfite sensitivity,cortico-dependent asthma, and pheo
21:991-994, 1993. chromocytoma, Oral Surg Oral Med Oral Pathol 74:687--691,
50. Bertz RJ, Howrie DL: Diazepam by continuous intravenous 1992.
infusion for status epilepticus in anticonvulsant hypersensitiv 72. BruzeM, GruvbergerB,Thulin I: PABA,benzocaine,and other
ity syndrome, Ann Pharmacother 27:298-301, 1993. PABAesters in sunscreens and after-sun products, Photoder
51. Lahat E,AladjemM, Eshel G, et al: Midazolam in treatment of matol Photoimmunol Photomed 7:106-108, 1990.
epileptic seizures,Pediatr Neurol 8:215--216,1992. 73. BoyceJA,Assa'adA, Burks AW,et al: Guidelinesfor the diag
52. Wroblewski BA, Joseph AB: Intramuscular midazolam for nosis and management of food allergy in the United States:
treatment of acute seizures or behavioral episodes in patients report of the NIAID-Sponsored Expert Panel, J Allergy Clin
with brain injuries, J Neurol Neurosurg Psychiatr55:328-329, Immunol 126(Suppl6):Sl-S58, 2010.
1992. 74. Malamed SF: Medical emergencies in the dental office,ed 6,
53. Hanley DF Jr, Pozo M: Treatment of status epilepticus with St Louis,2007,Mosby.
midazolam in the criticalcare setting,Int J Clin Pract 54:30-35, 75. Peter R: Sudden unconsciousness during local anesthesia,
2000. Anesth Pain Control Dent 2:140-142, 1993.
54. Feldman HS,Arthur GR,Pitkanen M, et al:Treatment of acute 76. Chandler MJ,Grammer LC,Patterson R:Provocativechallenge
systemictoxicity after the rapid intravenous injection of ropi with local anesthetics in patients with a prior history of reac
vacaine and bupivacaine in the conscious dog, Anaesth Analg tion, J AllergyClin Immunol 79:883-886,1987.
73:373-384, 1991. 77. Orr DL II: It's not Novocain,it's not an allergy,and it's not an
55. Daublander M: The role of the vasoconstrictor. Paper pre emergency!Nev Dent AssocJ 11:3--6,2009.
sented at: 3M ESPE Expert Conference, Munich, Germany, 78. Riedenburg MM, Lowenthal DT: Adverse nondrug reaction,
April 2011. N Engl J Med 279:678--679,1968.
56. KellamSA,Smith JR,ScheffelSJ:Epinephrine absorption from 79. Hodgson TA, Shirlaw PJ, Challacombe SJ: Skin testing after
commercial gingival retraction cords in clinical patients, anaphylactoid reactions to dental local anesthetics:a compari
J Prosthet Dent 68:761-765, 1992. son with controls, Oral SurgOral Med Oral Pathol 75:706-711,
57. ADA/PDR:Ada guide to dental therapeutics, ed 5, Chicago, 1993.
2009,The American Dental Association. 80. Rozicka T, Gerstmeier M, Przybilla B, et al: Allergy to local
58. Gomes ER, Demoly P: Epidemiologyof hypersensitivitydrug anesthetics:comparison of patch test with prick and intrader
reactions, Curr Opin AllergyClin Immunol 5:309-316,2005. mal test results, J Am Acad Dermatol 16:1202-1208,1987.
59. Brown DT, Beamish D, Wildsmith JA:Allergicreaction to an 81. Eggleston ST, Lush LW: Understanding allergic reactions to
amide local anaesthetic, Br J Anaesth 53:435-437, 1981. local anesthetics,Ann Pharmacother 30:851-857, 1996.
60. Aldrete JA,O'Higgins JW: Evaluation of patients with history 82. Canfield DW,GageTW:A guideline to local anesthetic allergy
of allergyto local anesthetic drugs, South Med J 64:1118-1121, testing, Anesth Prog 34:157-163, 1987.
1971. 83. SwansonJG:An answerfor a questionableallergyto local anes
61. Boren E, Teuber SS,Nguwa SM,et al:A critical reviewoflocal thetics, Ann Emerg Med 17:554,1988.
anesthetic sensitivity,Clin RevAllergy Immunol 32:119-128, 84. Malamed SF:The use of diphenhydramine HCl as a local anes
2007. thetic in dentistry,Anesth Prog 20:76-82, 1973.
62. Jackson D, Chen AH, Bennett CR: Identifying true lidocaine 85. Ernst AA, Anand P, Nick T, et al: Lidocaine versus diphen
allergy,J Am Dent Assoc 125:1362-1366,1994. hydramine for anesthesia in the repair of minor lacerations,
63. Doyle KA, Goepferd SJ: An allergy to local anesthetics? The J Trauma 34:354--357,1993.
consequences of a misdiagnosis,ASDC J Dent Child 56:103- 86. Uckan S, Guler N, Sumer M, et al: Local anesthetic efficacy
106, 1989. for oral surgery: comparison of diphenhydramine and prilo
64. ThyssenJP,Menne T,ElberlingJ,et al:Hypersensitivityto local caine, Oral Surg Oral Med Oral Pathol Oral Radiol Endod
anaesthetics-update and proposal of evaluation algorithm, 86:26-30,1998.
Contact Dermatitis 59:69-78, 2008. 87. Willett J, Reader A, Drum M, et al: The anesthetic efficacyof
65. Harboe T, Guttormsen AB,Aarebrot S, et al: Suspectedallergy diphenhydramine and the combination diphenhydramine/
to local anaesthetics:follow-up in 135cases,ActaAnaesthesiol lidocaine for the inferior alveolar nerve block, J Endod
Scand 54:536-542,2010. 34:1446-1450,2008.
66. Haas DA:An update on local anesthetics in dentistry, J Can 88. Lieberman P, Kemp SF,Oppenheimer J, et al. The Diagnosis
Dent Assoc68:546-551,2002. and Management of Anaphylaxis:An Updated PracticeParam
67. Schwartz HJ, Sher TH: Bisulfite sensitivity manifesting as eter,AllergClin Immunol 115(3):S483-S523,2005
allergy to local dental anesthesia, J Allergy Clin Immunol 89. Oh VM: Treatment of allergic adverse drug reactions, Singa
75:525--527,1985. pore Med J 30:290-293, 1989.
68. Seng GF,Gay BJ:Dangers of sulfites in dental local anesthetic 90. Adkinson NF Jr, Busse WW, Bochner BS, et al: Middleton's
solutions: warnings and recommendations, J Am Dent Assoc allergy:principles and practice, ed 7, St Louis,2009,Mosby.
113:769-770,1986. 91. Stafford CT: Life-threatening allergic reactions: anticipating
69. PerusseR, Goulet JP,TurcotteJY:Sulfites,asthma and vasocon and preparing are the best defenses,Postgrad Med 86:235--242,
strictors, Can Dent AssocJ 55:55-56, 1989. 245, 1989.
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Legal Considerations
There existseverallegaltheories by means of which plaintiffs duty occurred,that the health professional'sconduct wasnot
may proceed against defendant health professionals. the cause of damage, or that no damage exists.In addition,
For instance, contract law has provided a basis for suits the elements must be logically linked. For instance, if a
in which a health professional is accused of guaranteeing doctor negligentlyadministers a drug that the patient is his
a result related to treatment such as promising that admin torically allergic to and the patient contemporaneously
istration of local anesthesia and any subsequent procedure developsagoraphobia,the doctor would not be liablefor the
will be pain free. When the result does not meet the agoraphobia.
plaintiff's personal satisfaction, remedy may be sought in
court. Because the contract in this example was based on
the patient's subjectiveopinion, the defendant doctor must
DUTY
prove that the patient never felt pain-an extremelydifficult Briefly,the health professional owes a duty to the patient
assignment. Plaintiff suits based in contract law against if the health professional's conduct created a foreseeable
health providers are relativelyrare. risk to the patient. Generally, a duty is created when a
Recenthistory has seena disturbing and dramatic increase patient and a health professional personally interact for
in the number of suits filed under criminal law theories by health care purposes. Face-to-faceinteraction at the practi
government prosecutors in areas such as allegedfraudulent tioner's place of practice most likelywould fulfillthe require
activityon the part of the health care provider and for plain ment of a created duty; interaction over the telephone,
tiff morbidity or mortality. Historically,prosecutors crimi Internet, etc., may not be as clear-cut regarding establish
nally attacking health providers must be able to prove that a ment of duty.
criminal mind (mens rea) exists and that society has been
injured. The current trend is to rewritethe lawto not require Breach of Duty
proof of mens rea (such as in the Patient Protection and A breach of duty occurs when the health care professional
Affordable Care Act or "Obamacare") to negate any real fails to act as a reasonable health care provider, and this in
analysesof intent. This change bodes ill for health profes medical or dental malpractice casesis proved to the jury by
sionalsand others in that they now have the burden of proof comparison of the defendant's conduct with the reasonable
that requires defendants to prove their innocence, rather conduct of a similarly situated health professional. Testi
than requiring prosecutors to prove guilt. This singularly mony for this aspect of a suit for malpractice is developed
significantchange in criminal law is exacerbatedby the fact by expert witnesses.Exceptionsto the rule requiring experts
that the forum for such controversies may be a regulatory are casesin which damage results after no consent was given
agency,rather than a courtroom with its attendant Consti or obtained for an electiveprocedure, and casesin which the
tutional safeguards. defendant's conduct is obviously erroneous and speaks for
However,the legal theory covering most health profes itself (res ipsa loquitur), such as wrong-sided surgery. In
sional lawsuit activity is that of the tort. A tort is a private addition, some complications are defined as malpractice per
civil wrong not dependent on a contract. The tort may or se by statute, such as unintentionally leaving a foreign body
may not lead to further prosecution under criminal or other in a patient after a procedure.
legal theories, such as trespass to the person. Classically,a
viable suit in tort requires perfection of four essential ele
ments: duty, a breach of that specificduty, proximate cause
STANDARD OF CARE
leadingto damage,and damage related to the specificbreach Experts testifying as to alleged breach of duty are arguing
of duty.A health professionalmay successfullydefend a suit about standard of care issues.It is often mistakenlyassumed
in tort by proving that no duty existed, that no breach of that the standard of the practitioner's community is the one
341
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342 PART IV Complications, Legal Considerations, Questions, and Future
by which he will be judged. Today, the community standard The administration of local anesthesia is a procedure
is the national standard. If specialists are reasonably acces that is not immune to the liabilitycrisis.Although extremely
sible to the patient, the standard will be the national standard safe, given estimates that more than 300,000,000 dental
for specialists, whether or not the practitioner is a specialist. local anesthetic administration procedures are performed
The standard of care may also be illustrated by the profes annually in the United States,at times the administration of
sional literature. Health care professionals are expected to be local anesthesia will result in unintended damage to the
aware of current issues in the literature, such as previously patient. If the elements of duty, breach of duty, and proxi
unreported complications with local anesthetics. Often arti mate cause accompany that damage, malpractice may have
cles will proffer preventative suggestions and will review been committed. However,complications most often occur
treatment options. with no fault on the part of the local anesthetic administra
Simply because an accepted writing recommends conduct tor. In these situations, most complications are still foresee
other than that which the health care provider used is not able, and because they are predictable, the reasonable
necessarily indicative of a breach of duty. For instance, spe practitioner needs to be aware of optimal immediate and
cific drug use other than that recommended by the generic long-term treatment for the complications of local anes
Physicians' Desk Reference (PDR)is commonplaceand legally thetic administration.
acceptableas long as the health care provider can articulate The purpose of this chapter is not to describe in great
a reasonablepurpose for his conduct. Part of this reasoning detail the prevention or treatment of various local anesthetic
may likely include a benefit/risk analysis of various treat complications, but to simply mention foreseeable com
ment options for a specificpatient. plications and comment on the standard of care with regard
In addition, there is no single standard of care treatment to appropriate prevention and treatment. Obviously,some
plan for a givensituation. Severalviabletreatment plans may complications are common and others are rare, and fre
exist and all may be within the standard of care, such as the quency is an issue that would be considered in legalevalua
option of choosing different local anesthetic formulations tion of a case. In any case, the health professional who is
for a procedure. administering potent local anesthetics by definition tells
Finally, ultimately, the standard of care may be deter the public that it can trust in that professional while in his
mined by the jury itself after it weighs expert opinion, the or her care. When pretreatment questions arise, it is the
professional literature, opinions of professional societies or health professional's duty to investigate controversial or
boards, and so forth. unknown areas to minimize risk and maximize the benefits
of his or her therapeutic decisions.When foreseenor unfore
seen complications arise, the health professional must be
PROXIMATE CAUSE ableto act in a reasonablemanner to addressthese untoward
Proximate cause is the summation of actual cause and legal events.
cause.Actual cause exists if a chain of events factuallyflows Adequate legal response to a local anesthetic complica
from the defendant's conduct to the plaintiff's injury. Legal tion or emergencyis often equivalent to adequate dental or
cause is present if actual cause exists, and if the plaintiff's medical response. However,when damage persists, plaintiff
attorney can prove that the harm sustained was foreseeable attorneys will argue that the dental or medical response was
or was not highly extraordinary in hindsight. not an adequate legal response and will seek damages.The
fact that the treatment rendered by the practitioner may be
recognized by most of the profession as optimal may not
DAMAGE convince a jury when the plaintiff can find an expert who
Damage is the element of the cause of action that usually is offers an opposite opinion. However,damage alone will not
most easy to identify because it is most often manifested prove malpractice. The tort can be successfullydefended
physically.Simplybecause damage is present does not mean by showing no duty, no breach of duty, or no proximate
that malpractice has been committed, but damage must be cause. In many cases,no matter what the complication dis
present to fulfill all elements of the tort. cussed in this chapter, these legal defenses are the same in
The nation has seen a dramatic rise not only in tort-based theory and are applicable across the board, although the
malpractice lawsuits over the past severalyears, but also in dental/medical responses are more specific to the specific
regulatory activity (Obamacare alone will result in the cre situation.
ation of at least 159new regulatory agencies),both or which If one is uncomfortable with any of the various situations
result in the predictable sequelae of increased costs and mentioned in this chapter,further individual researchin that
decreasedaccessto doctors for patients. Trauma centershave area may be warranted.
closed, doctors are actively and passively (i.e., by limiting In addition to the civil, or tort, remedies available to
their practice or opting for earlyretirement) leavinglawsuit the plaintiff patient, a health care practitioner may have
friendly communities or states, and patient consumers now to defend conduct in other forums. Depending on the dis
are starting to feel directly the loss of health professional position of the plaintiff and his or her representative, the
availability and other consequences of a litigation system conduct of the health practitioner may be predictablyevalu
that has never been busier. ated not only civilly,but perhaps criminally, or via other
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CHAPTER19 LegalConsiderations 343
governmental agencies such as licensing boards, better busi Consent is essentialbecause many of the procedures that
ness bureaus, and so forth. Although theoretically, the argu doctors perform would be considered illegal in other set
ments presented by competing sides in these varying forums tings, for instance, an incision developedby a doctor during
are the same no matter what the forum, very real differences surgery versus an equivalent traumatic wound placed in a
are involved. In particular, the penalties and the burden of criminal battery.
proof are significantly different. Consent may be verbalor written, but when a controversy
If the case is taken to a state agency, typically the board presents at a later date, a written consent is extremelybenefi
that issued the health professional's license, the rules of evi cial (Fig. 19-1). In fact, because many times consent is
dence are not onerous as far as admission by the plaintiff. required to fulfillthe standard of care for a procedure, lack
Essentially, the regulatory agency can accept any evidence of written consent may reduce the fact finding to a "he said/
it deems relevant, including hearsay, which means the defen she said" scenario. This circumstance may greatly diminish
dant may not have the right of facing an accuser. The burden the plaintiff's burden of proving the allegations and may
of proof, which typically rests with the moving party or even shift the burden of proof to the defendant.
plaintiff, may even be arbitrarily assigned to the defendant When the mentally challenged or children younger than
by the agency. The reason why the rules of evidence are the age of majority are treated, consent from a legalguardian
so liberal in state agency forums is because the issuance of is necessary for elective procedures. Whenever restraint is
an agency professional license may be deemed a privilege planned or anticipated, consent is warranted.
and not a right. The significance of proper representation Consent obtained before one procedure is performed
and preparation if one is called before a regulatory agency may not be assumed for the same procedure at a different
cannot be understated when one considers the very real time, or for a different procedure at the same time. In addi
possibility of loss of a license and subsequent loss of ability tion, consent obtained for one health care provider to treat
to practice. may not be transferableto another health careprovider,such
If one is summoned to a civil forum, the rules of evidence as a partner doctor or an employee dental hygienist or reg
and the burden of proof are more strictly defined. Rules of istered nurse.
evidence are subject to state and federal guidelines, although Consent is not necessary at times. When a patient is
this is an area that is not black and white, and attorneys treated in an emergency setting (e.g., a spontaneously or
frequently are required to argue zealously for or against traumatically unconscious patient), consent is implied.
admission of evidence. In a civil forum, the burden of proof However,when possible, consent may be obtained from a
generally remains with the plaintiff, and the plaintiff is legal guardian. The possibility of obtaining consent from a
required to prove his or her allegations by a preponderance guardian before an emergency procedure is performed is
of evidence. Expressed mathematically, a preponderance is time dependent. In an urgent situation, time may be avail
anything over 50%. This essentially means that anything that able to discusstreatment options with a guardian. However,
even slightly tips the scales in favor of the plaintiff in the during a more emergent situation, taking time to discuss
jury's opinion signifies that the plaintiff has met the burden treatment options may actually compromise the patient.
and thus may prevail. Generally,emergencyaid rendered in nondental or non
In criminal cases, which again may be initiated for exactly medicalsettingsdoes not require consent secondaryto Good
the same conduct that may place the defendant in other Samaritan statutes, which apply to "rescues:' However, a
forums, the burden of proofrests squarely with the prosecu source of liabilityevenwhen one is being a Good Samaritan
tion (i.e., the state or federal government). In addition, the is reckless conduct. Recklessconduct in a rescue situation
burden is met only by proof that is beyond a reasonable often involvesleavingthe victim in a situation that is worse
doubt, not simply a preponderance of evidence. Although than when the rescuer found the victim.An exampleof such
the definition of reasonable doubt is open to argument, rea conduct is seen when a rescuer offers to transport a victim
sonable doubt is a more difficult standard to meet than is to a hospital for necessarytreatment and then abandons the
found in agencyor civilforums. victim farther from a hospital than where the victim was
initially found.
The patient who offers to sign a waiver to convince a
practitioner to provide treatment, for instance,will not likely
CONSENT be held to that waiverif malpractice is suspectedand then is
The consent processis an essentialpart of patient treatment adjudicated to exist;it is a recognizedprinciple that a patient
for health care professionals. Essentially,consent involves may not consent to malpractice because such consent goes
explaining to the patient the advantages and disadvantages against public policy.
of differing treatment options, including the benefits and With regardsto localanestheticadministration, is consent
risks of no treatment at all. Often treatment planning will necessary?
result in severalviableoptions that may be recommended by Consent is required for any procedure that poses a fore
the doctor. The patient makes an informed decision as to seeable risk to the patient. If the administration of local
which option is most preferable to that patient, and treat anesthetic could foreseeablyresult in damage to the patient,
ment can begin. consent should be considered.
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344 PART IV Complications, Legal Considerations, Questions, and Future
INFORMED CONSENT
4. That all treatments including the one proposed have some risks. The
risks of importance involved in my treatment have been explained to me,
and they are: _
Signature of Patient
Date
Signature of Witness
Further, some patients prefer to not be given any local as differential diagnosis or treatment of atypical facial pain
anesthesia, even for significant operative procedures, thus syndromes, thus establishing the administration of local
rendering the administration of localanesthesiafor dentistry anesthesiaas both diagnosticand therapeutic in and of itself.
optional and not necessarilyrequired. It cannot be assumed Finally,local anesthetic administration involvesinjecting
that local anesthesia is automatically part of most dental or otherwise administering potent pharmaceutical agents.
procedures. If a patient is forced to have a local anesthetic These agents or the means used to administer them may
without consent, technicallya battery has occurred. inadvertently damage a patient. Any health professional
At times, local anesthetic administration is all that is nec conduct that may reasonably be expected to predictably
essaryfor certain diagnostic or therapeutic procedures such result in damage requires consent.
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CHAPTER19 LegalConsiderations 345
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346 PART IV Complications, Legal Considerations, Questions, and Future
During the contract period the business associate must observe the following
responsibilitieswith respect to protected health information:
3. Fulfill an individual's rights to access and amend his or her protected health
information contained in a designated record set, including information held by a
business associate, if appropriate, and receive an accounting of disclosures by a
business associate.
4. Mitigate, to the extent practicable, any harmful effect that is known to the
covered entity of an impermissible use or disclosure of protected health
information by its business associate.
5. A business associate cannot use protected health information for his or her
own purposes. This includes, but is not limited to, selling protected health
information to third parties for the third party's own marketing activities, without
authorization.
Figure 19-2. Sample business associate contract for compliance with the privacy rule of the Health Insurance Portability and Account
ability Act.
exposure of PHI. The HIPAAPrivacy Kit provides a copy For a comprehensivediscussion of all terms and require
of the USDHHS "BusinessAssociateContract Terms";this ments, a completelist of HIPAApoliciesand procedures,and
document provides a concrete format for detailingBAinter a full collectionof HIPAAprivacyforms, the ADAshould be
actions (Fig. 19-2). contacted for an HIPAA Privacy Kit. The relevant ADA
The main HIPAAprivacy compliance date, including all Website is www.ada.org/goto/hipaa. Other Websites that
staff training, was April 14, 2003, although many covered may contain useful information about HIPAAinclude the
entities who submitted a request and a compliance plan by following:
October 15, 2002, were granted 1-year extensions. Local • USDHHS Officeof CivilRights:www.hhs.gov/ocr/hipaa
branches of the ADAmay be contacted for details. It is rec • Work Group on Electronic Data Interchange:
ommended that dentists prepare their officesahead of time www.wedi.org/SNIP
for all deadlines, including preparation of privacy policies • Phoenix Health: www.hipaadvisory.com
and forms, business associatecontracts, and employeetrain • USDHHS Officeof the Assistant Secretaryfor Planning
ing sessions (Fig. 19-3). and Evaluation:http://aspe.os.dhhs.gov/admnsimp/
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CHAPTER 19 Legal Considerations 347
I hereby certify that the following employees of the below named dental office
have received the office policy regarding the Health Insurance Portability and
Accountability Act (HIPAA) Privacy Rule.
Dental Office _
Address _
City State _
I understand the office privacy policy and procedures needed to protect the
private health information of patients and will access only information that is
reasonably needed to carry out my duties.
Name Date
Figure 19·3. Sample staff training registry to be signed by all employees to verify receipt of the office policy to comply with the privacy
rule of the Health Insurance Portability and Accountability Act.
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348 PARTIV Complications,LegalConsiderations, Questions, and Future
in milliliters, carpules, cartridges, cc's, and so forth. The An accurate medical history is mandatory in minimizing
most standard limiting factor in the administration of the occurrence of allergy.Patients, in part because doctors
certain doses of local anesthetics to a patient is the patient's do not takethe time to explainthe differencebetween allergy,
weight. Other factors that need to be considered include overdose,and sensitivity,often list any adversedrug reaction
medical history, particularly cardiovascular disease, and as an "allergy."Inaccurate reporting of drug-related allergy
previous demonstration of sensitivity to normal dosing. by patients is not rare. In fact, more than half of patient
The presence of acute or chronic infection and concomi reported allergies are not allergies at all, but some other
tant administration of other oral, parenteral, or inhaled reaction that may not have even been drug related.
agents may alter the textbook recommendations for local The duty of the health professional when administering
anesthetic dosages. The reasonable practitioner needs to local anesthetics includes avoiding known allergenic sub
be able to readily determine the proper dosage levels to stances, including the local anesthetic in particular and any
be administered to patients before the time of admini chemical additions to the local anesthetic solution. If an
stration. At times, one local anesthetic formulation may be allergicreaction occurs, whether fault is present or not, the
significantlymore advantageousthan another. The minimal health care provider must be able to treat the drug-related
amount of local anesthetic, and of vasoconstrictor con allergy in a reasonable manner. Reasonabletreatment may
tained therein if applicable, needed to achieve operative be the difference between resultant transient rhinorrhea
anesthesiashould be used.An inabilityto properly dose most versus death.
patients leads to provision of health care below the standard
of care.
Overdosemay occur without health professionalerror, as INSTRUMENTS
in a previously undiagnosed hypersensitivepatient, or in a
patient who givesan incomplete medical history. Intravas Syringe
cular injection can occur even with judicious negativeaspi A compromised syringe may still be usable in administer
ration through an appropriate needle and following slow ing a local anesthetic. But if, for instance, the syringe
injection and may result in overdose. cannot be controlled in a normal manner (e.g., secondary
Generally,the initial presentation of overdose is physio to an ill-fitting thumb ring), any damage resulting from
logic excitement,which is followedby depression. Depend such lack of control would be foreseeableand a breach of
ing on the timing of the diagnosisof overdose,the treatment duty. A properly prepared and functioning syringe is man
protocol will vary. Rapid accurate evaluation is very benefi datory for safe local anesthetic administration. Factors to
cial as opposed to a delayeddiagnosis,and speaks favorably be aware of in evaluating a syringe include all components
for the responsible health care provider. It is much more of the syringe from the thumb ring, to the slide assembly,
desirable to treat syncope secondary to overdose rather to the harpoon, to the threads that engage the needle, and
than cardiac arrest, which may follow inadequately treated so forth.
syncope and respiratory arrest.
Adding to the diagnostic challenge is the fact that often Local Anesthetic Cartridge
more than one chemicalis present within the localanesthetic Originally,cartridgesweremuch differentthan they are now.
solution that may cause overdose (e.g., lidocaine and epi Problemsthat havebeen identifiedthrough the yearsinclude
nephrine). The operator must be cognizant of the latency the fact that chemicals can leach from or into the solution
and duration of different components of the local anesthetic within the cartridge, and that the contents are subject to
solution. extremes of heat or cold or prolonged shelf life. Cartridges
However, no matter the particular manifestation or are now coatedwith a protectivefilm,thus helpingto prevent
whether fault is or is not included in the origin of any situ any shattered glasseffectfrom cartridge fracture, which can
ation of overdose, the reasonable practitioner needs to be occur even with normal injection pressures.
prepared to effectivelyhandle the overdose.An inability to
reasonably treat complications that are foreseeable,such as Local Anesthetic Needle
overdose,is a breach of duty. Disposableneedleshavebeen the norm for decades;although
If an overdose occurs, results can range from no damage they avoid many problems formerly manifest with reusable
whatsoeverto death, and often depend on the preparedness needles, malfunction can still occur. Needle breakage can
of the health practitioner for this foreseeableemergency. occur with or without fault from the operator.Absentinten
tional bending and hubbing of the needle into loosemucosa,
underlying muscle,and bone, needlesstill occasionallybreak
for other reasons, as when a patient grabs the operator's
ALLERGY hand during an injection.Also,latent manufacturing defects
Relatedto overdose,but not a dose-dependent manifestation will occasionallybe noted during routine inspection of the
oflocal anesthetic administration, allergicreactions are fore needle before local anesthetic administration. In addition
seeable,although relativelyrare, particularly for severealler to needle barbs, the author has discarded preoperatively
gic responses such as anaphylaxis. inspected needles with defects such as those seen in needles
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CHAPTER19 LegalConsiderations 349
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350 PART IV Complications, Legal Considerations, Questions, and Future
soft tissues is indeed a blind procedure. At times, the goal of Permanent lingual nerve injury also occurs in the absence
an injection is intravenous or intra-arterial injection. This is of third molar surgery and secondary to needle penetration
not typically the case with the use of local anesthetics for during inferior alveolar/lingualnerve blocks. Lingual nerve
pain control, and a positive aspiration necessitates that addi injury can result from pressure placed on the nerve during
tional measures be taken for a safe injection. The prepared operative procedures (e.g.,with lingual retractors).
health professional should be able to articulate exactly what A higher incidence of lingual nerve injury has been noted
the goal of administration of a local anesthetic is, and how with certain local anesthetic solution formulations over
that is technically accomplished. For instance, why was a others. The practitioner whose patient developsparesthesia
particular anesthetic and needle chosen? What structures after routine use of,for instance,4% localanesthetic solution
might be encountered by the needle during administration instead of 2% solution must be prepared to explain such
of a block? In addition, what measures are taken if a struc decisions as why solutions that are twice as toxic as others
ture is inadvertently compromised by a needle? Even with and generallyare equallyeffectivemay have been habitually
optimal preparation, vascular compromise can result in used. Obviously,the suggestion here is that no treatment
tumescence, ecchymosis, or overt hemorrhage that may need should be rote; rather, treatment should be planned on a
to be addressed. These conditions can be magnified by bleed patient-by-patient basisafter a thoughtful risk/benefitanaly
ing dyscrasia. The medical history may reveal certain pre sis has been performed.
scriptions that may alter bleeding time; this may indicate the Finally,lingual nerve injury can occur when no health
need for preoperative hematologic consultation. care professional treatment whatsoever is provided. Pares
thesia can occur with mastication, and a presenting chief
complaint of anesthesia can occur spontaneously. Both of
NEURAL PENETRATION these conditions may be rectifiedby dealingwith the pathol
Just as a rich complex of vesselsis present in the head and ogy associated with the change in function, such as by
neck area, so it is with nerves. Neural anatomy can vary removing impacted third molars or freeingthe lingual nerve
considerablyfrom the norm, and penetration of a nerve by from an injury-susceptibleposition within the periosteum.
a needle can occur on rare occasions,evenin the most careful However,no matter what the cause,the prudent operator
and practiced hands. Permanent changesin neural function will be prepared to address neural injury effectivelywhen
can result from a singleneedle-stick;although this complica it occurs.
tion does not necessarilyimply a deviation from the stan
dard of care, the practitioner must be prepared to treat the
complication as optimally as possible.
CHEMICAL NERVE INJURY
Lingual nerve injury is an event that has been zealously It is not surprising that potent chemicalssuch as local anes
contested in the courts in recent years. Typically, rare thetics occasionally will compromise nerve function to a
instances of loss or change in lingual nerve function have greater degree than they are designed to do. Local anesthet
occurred during mandibular third molar surgery. Plaintiff ics, after all, are specificallyformulated in an effort to alter
experts readily opine that but for negligence(i.e., malprac nerve function, albeit reversibly.Just as systemic toxicity
tice), this injury will not occur, period. In these experts' varies from local anesthetic to local anesthetic, so limited
opinions, lingual nerves are damaged only secondary to nerve/local toxicity at times may alter nerve function in a
unintentional manipulation with a surgicalblade, periosteal waythat is not typicallyseen. Deposition of local anesthetic
elevator,burr, and so forth, when the operator is working in solutions directlyon a nerve trunk or too near a nerve trunk
an anatomic area that should have been avoided.In spite of in a susceptible patient may result in long-term or perma
the fact that defenseexperts routinely counter these plaintiff nent paresthesia.Localanesthetic toxicitygenerallyincreases
opinions, occasionallyjuries will rule for the plaintiff, and as potency increases.In addition, nontargeted nerves in the
lingual nerve awardshave exceeded$1,000,000. head and neck may be affected by local anesthetic deposi
Although lingual nerve injury occasionally occurs sec tion, as when transient amaurosis occurs after maxillary or
ondary to unintentional contact with surgical blades, peri mandibular nerve block when the optic nerve is affected.
osteal elevators, burrs, and so forth, when an operator One should not be particularly surprised at the various
unintentionally directlyencounters an unintended anatomic neural manifestations of these potent agents giventhat toxic
structure, it is more likelythat the injury results secondary overdose is actually a compromise of higher neural func
to other means. For instance,lingual nerve anatomy has been tions. Anyone who chooses to utilize agents designed to
shown to be widelyvariant from the averageposition lingual relievepain directlyon or near nerve tissue must be prepared
to the lingual plate in the third molar area. Lingual nerve for even the rare complications seen. Adequate treatment
position has been shown to vary from within unattached may range from reassuring a patient who has transient
mucosa!tissue low on the lingual aspect of the lingual plate, amaurosis to treating or referring for treatment a patient
to firmly adherent within lingual periosteum high on the with permanent anesthesiaresulting from an adversechemi
lingual plate, to within soft tissues over the buccal cusps of cal compromise of the nerve caused by the local anesthetic
impacted third molars. solution or other agents.
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CHAPTER19 LegalConsiderations 351
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352 PART IV Complications, Legal Considerations, Questions, and Future
Although most adverse reactions to local anesthetics employment. However,if the employer asked the employee
occur rapidly, delayed sequelae are possible. Just as patients to perform a task on the way home, responsibility for that
who have been administered agents by intravenous, inhala employeeconduct may attach. An employer generallyis not
tion, oral, or other routes are evaluated post procedure, so responsible for statute violation or criminal conduct by
too should patients who have been administered local anes employees.
thetics. Any question about a less than optimal recovery from An employer may not be responsible for an independent
local anesthesia should be addressed before the patient is contractor.One test usedto evaluatethe relationshipbetween
released from direct care. an employerand another is to discernwhether the employer
For instance, it is widely accepted that patients may drive has the authority to direct how a task is done, as opposed to
after administration of local anesthesia for dental purposes. simply requesting that a task be completed. For instance, a
Occasionally, a postprocedure concern that may arise sec dentist may request that a plumber make repairs, but likely
ondary to local anesthesia and/or other procedures may will not direct how the repairs are to be accomplished,so the
dictate that a patient who was not accompanied may need plumber would likelybe independent. The same dentist will
to obtain assistance before leaving the place of treatment. request that a dental hygienist perform hygiene duties, but
Patients whose employment requires higher than normal the dentist may choose to instruct how the duties will be
mental or physical performance may be cautioned about the performed, thus rendering the hygienistless independent.
potential effects of local anesthetic administration. As an With regard to the administration of local anesthesia,
example, U.S.Air Force and U.S. Navy pilots are restricted dentists and dental hygienistsroutinely accomplishthis task.
from flying for 24 hours status post local anesthetic Generally speaking, and subject ultimately to state statutes,
administration. although a dental hygienistmay be an independent contrac
Somepractitioners routinely calleachpatient after release tor according to many elemental definitions, the dental
and several hours after treatment has been terminated to hygienist generally is not an independent contractor with
ensure that recovery is uneventful. Such calls are usually regard to the provision of health care services.This includes
welcomedby patients as a sign that their health careprovider the administration of local anesthetics. Thus, the employee
is truly concerned about his or her welfare.Occasionally,the dentist may be adjudicated responsible for any negligent
practitioner's call may enable one to address a developing conduct that causes damage to a patient during the course
concern or an objectivecomplication early on. of hygiene treatment.
With regard to the degree of supervision, one must
consult the state statutes. Often verbiage such as "direct" or
RESPONDEAT SUPERIOR
"indirect" supervision is used, and understanding the defini
Respondeat superior ("let the superior reply"), or vicarious tions of these or other terms is paramount for both supervis
liability,is the legal doctrine that holds an employer respon ing and supervised health care providers.
siblefor an employee'sconduct during the course of employ
ment. The common law principle that all have a duty to
STATUTE VIOLATION
conduct themselves so as to not harm another thus also
appliesto employeesassignedtasksby an employer.Respon Violation of a state or federal statute usually leads to an
deat superior is justified in part by the assumption that the assumption of negligence if statute-related damage to a
employer has the right to direct the actions of employees. patient occurs. In other words, the burden of proof now
For the health professional,responsibilitymay be shared by shiftsto the defendant to provethat the statute violation was
clerical staff, surgical or other assistants, dental hygienists, not such that it caused any damage claimed.
laboratory technicians, and so forth. At times vicarious lia Twobasic types of statutes exist:malum in se and malum
bilitywillbe appliedbetweenemployerdoctors and employee prohibitum. Malum in se (bad in fact) statutes restrict
doctors if the employee doctors are agents of the employer behavior that in and of itself is recognized as harmful, such
doctor within a practice. as driving while inebriated. Malum prohibitum (defined as
Respondeat superior does not relieve the employee of bad) conduct in and of itself may not be criminal, reckless,
responsibility for employee conduct; it simply enables a wanton, etc.,but is regulatedsimplyto, for instance,promote
plaintiff to litigate against the employer. social order. Driving at certain speeds is an example of a
An employer is not responsible for employee conduct malum prohibitum statute. The difference between legally
that is not related to employment. What type of employee driving at 15 mph in a school zone and driving at 16 mph
conduct is related to the job is an arguable proposition, as in a school zone is not the result of a criminal mind but is a
are most legal issues.For instance, the question of whether social regulatory decision.
an employer is responsible for employee conduct outside For instance, if one is speeding while driving, several
the normal workplace is open to a case-by-caseevaluation. sequelaemay result when that statute violation is recognized.
Conduct during trips to and from the workplace may or First, the speeder may simply be warned to stop speeding.
may not be relatedto employment.For example,an employer Second, the speeder may be issued a citation and may
probably would not be responsible for employee conduct have to appear in court, argue innocence, pay a fine if
when the employee is driving home from the place of found guilty,attend traffic school,etc.Third, if the speeder's
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CHAPTER19 LegalConsiderations 353
conduct causes damage to others, additional civil or criminal even significant damage, does not fulfill all requirements of
sanctions may apply. Fourth, the situation may be com the tort of malpractice.
pounded civilly or criminally if multiple statute violations If, however, the practitioner determines that a duty
are present, such as speeding and driving recklessly or driving existed, the duty was breached, and breach was the proxi
while intoxicated. mate cause of damage, it is likely that malpractice has
Occasionally, statute violation is commendable. For occurred. In this instance, the health professional is likely
instance, a driver may swerve to the "wrong" side of the ethically,if not yet legally,responsiblefor making the patient
centerline to avoid a child who suddenly runs into the street "whole."If the damage is minimal (e.g.,transient ecchymo
from between parked cars. At times, speeding may be con ses),nominal recompense,perhaps even a judicious apology,
sidered a heroic act, such as when a driver is transporting a may be all that is required. If,however,the damage is signifi
patient to a hospital during an emergency. However, even if cant, significantrecompense may be required.
the speeder has felt that he is contributing to the public Certainly,any significant damage whatsoever from mal
welfare somehow, the statute violation is still subject to practice requires that the health professional contact his
review. liabilitycarrier as soon as possible.The same holds true, even
For health professionals, for instance, administration if damage is not evident, when the health care professional
of local anesthetic without a current health professional receivesnotice of patient dissatisfaction,often in the form
license or Drug Enforcement Agency (DEA) certification is of a request for records. The liability insurance carrier's
likely a violation of statute. If the type of harm sustained by representative will help evaluate the situation and will
the patient is the type that would have been prevented by provide valuable insight from a significant experiencepool.
obeying the statute, additional liability may attach to the In all likelihood,the carrier will be more successfulin nego
defendant. tiating a settlement to any case that is controversialas far as
Conversely, an example of a beneficial statute violation damages. The practitioner should be very cautious about
occurred when a licensee did not fulfill mandatory basic undertaking any such negotiations without his carrier's
CPR (cardiopulmonary resuscitation) certification, but input. Such unauthorized negotiations, or similar conduct,
chose to complete ACLS (advanced cardiac life support) cer such as not informing the carrier about a potential com
tification instead. When admonished by the state board that plaint in a timely fashion, may even cause liability coverage
a violation of statute had occurred, potentially putting the to become the practitioner's sole responsibility.At times, if
public at greater risk, the licensee pointed out to the regula the practitioner and the patient still have a good working
tory board that ACLS certification is actually more beneficial relationship,the carrier will allowthe practitioner to negoti
to the public than CPR The licensing board then changed ate a reasonablesettlement.This course of action is advanta
the statute to allow CPR or ACLS certification as a require geous in that the patient receives immediate financial aid
ment to maintain a license. that may be necessary for additional expenses or time off
Generally, employers are not responsible for statute viola from work. In addition, the plaintiff patient will not be
tions of employees. An exception to this guideline is seen in required to overcome the assumption that the health care
the health professions. When employees engage in the prac provider acted reasonably and to prove malpractice, which
tice of dentistry or medicine, even without the knowledge or may be very difficult.
approval of the employer, both that employee and the No matter whether the damage is secondary to negli
employer may be held liable for damage. Employer sanctions gence, the practitioner must try to treat the patient opti
may be magnified, such as loss of one's professional license, mally.It is hoped that the patient will not independently seek
if an employee practices dentistry or medicine with employer treatment elsewhere because this course of action may
knowledge. simply prolong recovery and aggravatefuture legal consid
Finally, at times some types of specific conduct are defined erations. One near universalfinding in filed and servedmal
statutorily as malpractice per se. For instance, unintention practice actions is criticism, usually unwarranted, by a
ally leaving a foreign body in a patient after a procedure may nontreating health professional.If, on the other hand, refer
be deemed malpractice per se. In these types of cases, theo ral would be beneficial,the practitioner should facilitatethat
retically simply the plaintiff's demonstration of the foreign referral for the patient and not just send the patient out to
body, via radiograph, a secondary procedure to remove the fend alone.After a referral is made, continued care as needed
foreign body, etc., may be all that is required to establish for the patient is advisableif possible.
malpractice. Once legal action has been initiated, it may be wise to
refuse further treatment for the patient because the patient
has now effectivelyexpressedthe opinion that the practitio
IF MALPRACTICE EXISTS ner's conduct was belowthe levelof the standard of care and
Although attorneys and doctors do not alwaysagreeon when has resulted in damage. It is an unfortunate circumstance
all the elements of malpractice are present, occasionallythe when a plaintiff patient realizesthat the perceivedmalprac
health professional may feel that he or she has made a tice did not exist and is unable to continue care with the
mistake that has damaged a patient. As can be easily and health professionalmost familiar with the intricacies of that
successfullyargued,simplythe factthat a patient has damage, patient's individual circumstances.
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354 PART IV Complications,LegalConsiderations, Questions, and Future
Many patients shortsightedly and unintentionally limit Daublander M, Muller R,LippMD: The incidenceof complications
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different legalformulae. past decade or so, but since my doctor started me on Lipitor
However,one thing that never changesis that reasonable (atorvastatin) a few months ago for high cholesterol,I swearit's
and responsiblehealth care practitioners will continue to be been fallingout much faster.Mydoctor discountsthe possibility,
but I looked in the Physicians'Desk Reference(PDR) and alo
informed as to the current standard of care and will attempt
pecia is listed under "adverse reactions."What do you think?
to optimize their decision making and treatment planning
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Future Trends in Pain Control
' I ' I
Although local anesthesia remains the backbone of pain consistentlyreliable clinical results (e.g.,shorter onset time,
control in dentistry,researchcontinues in both medicine and more comfortableinjection). Recentchangesin the formula
dentistry with the goal of improving all areas of the local tion of the buffering solution and in its deliveryhave greatly
anesthetic experience,from that of the administrator to that increased the effectivenessof this technique.
of the patient. Much of this researchhas focusedon improve Residual soft tissue anesthesia-anesthesia of the lips,
ments in the area of local anesthesia-safer needles and tongue, chin, or face--oftentimes lasting 5 hours or longer
syringes;more successfultechniques of regionalnerve block, after injection of a vasopressor-containinglocal anesthetic,
such as the anterior middle superior alveolar (AMSA)and is usually unneeded and may, on occasion, present as a
palatal anterior superior alveolar (P-ASA)(see Chapter 13); potential inconvenienceor problem for the patient. Admin
and newer drugs, such as articaine HCl. These advanceshave istration of a vasodilating drug into the site of previous
been discussed in some depth in previous editions of this local anesthetic administration increasesvascular perfusion,
text and in preceding chapters of this 6th edition: intraosse allowing the local anesthetic drug to be removed from the
ous anesthesia (see Chapter 15); self-aspirating, pressure, site of injection more rapidly, thereby decreasingthe dura
and safetysyringesand computer-controlled localanesthetic tion of residual soft tissue anesthesia.
delivery (C-CLAD) systems (see Chapter 5); and articaine The inability of the traditional (Halsted approach) infe
HCl (see Chapter 4). These drugs, devices,and techniques rior alveolarnerve block (IANB)to provide consistentlyreli
are now a part of the mainstream of pain control in the able pulpal anesthesia has been a vexing problem for all
United States and elsewhere. dentists. The lack of reliable,easyto visualizelandmarks and
Some of the items discussedin previous editions havenot extreme variations in patient anatomy have led to exceed
progressed into the dental mainstream: the local anesthetics ingly high failure rates with this vitally important dental
centbucridine and ropivacaine; the ultra-long-acting local nerve block. Infiltration anesthesia,a mainstay in maxillary
anesthetics tetrodotoxin (TTX) and saxitoxin (STX); the anesthesia, did not demonstrate significant clinical success
topical anesthetic EMLA(eutecticmixture of local anesthet when lidocaine,mepivacaine,and prilocaine were employed
ics);and the technique of electronicdental anesthesia(EDA). by mandibular infiltration in adult patients. However,recent
The reader who is interested in these items is referred to the clinical trials of mandibular infiltration with articaine have
5th edition of this textbook.1 shown promise.
Since publication of the 5th edition in 2004, the dental A current area of clinical research that has demon
profession in the United States has witnessed the introduc strated early promise is the use of intranasally (IN) admin
tion of products and devicesthat enable the doctor to dra istered local anesthesia as a means of providing pulpal
matically decrease the onset time of pulpal anesthesia (the anesthesia to maxillary teeth without the need for injec
local anesthetic "on" switch), and significantly reduce the tion (i.e., no needle). Phase II clinical trials comparing IN
duration of the residual soft tissue anesthesiaassociatedwith local anesthetic versusinjected local anesthetic have demon
intraoral injections of local anestheticscontaining vasopres strated significant clinical successin providing pulpal anes
sors (the local anesthetic "off" switch). In addition, recent thesia bilaterally from the second premolar to the second
research appears to demonstrate the usefulnessof the infil premolar.
tration of articaine HCl in providingpulpal anesthesiain the Computer-controlled local anesthetic delivery(C-CLAD)
adult mandible. has been included in this chapter on future developments
Increasingthe pH of a local anesthetic solution (i.e.,buff since 1997. Today, C-CLAD has moved into mainstream
ering) toward a more physiologicpH, although not new in dentistry. Recent research in this area is reviewed in this
medicine or dentistry, had never been shown to provide chapter.
356
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CHAPTER20 Future Trends in Pain Control 357
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358 PART IV Complications, Legal Considerations, Questions, and Future
TABLE 20-1
Percentage of RN Ions Present in LA Solution at
Various pH Values
pH Lldocaine Articaine Mepivacaine Bupivacaine
pKa7.9 pKa7.8 pKa7.6 pKa8.1 Onpharma-
7.4 (body 24.03 28.47 38.69 16.63
pH)
6.5 (plain) 3.83 4.77 7.36 2.45
3.5 (with 0.004 0.005 0.008 0.003 Sodium Bicarbonale-lnj.,8.4%,USP
Neutralizing Additii••e Solution
epi)
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CHAPTER 20 Future Trends in Pain Control 359
and 1 minute 51 seconds for buffered LA (P <.05). Eighty In the mandible, where anesthesia in the adult is usually
percent of buffered subjects obtained pulpal anesthesia limited to nerve blocks (inferior alveolar,Gow-Gates),large
within 2 minutes.8 areas of soft tissue anesthesiadevelop along with the desired
At this time (January 2012), clinical trials are under pulpal anesthesia.The anterior two thirds of the tongue, the
wayto determine whether buffered local anesthetic solution lower lip, and the cheek are left without sensation for many
provides a more profound level of pulpal anesthesia, as hours followingcompletion of dental treatment.
seems likely given that approximately 6000 times the RN Techniquessuch as periodontal ligament (PDL)injection
ionic form of local anesthetic is availableto penetrate the (also known as intraligamentary injection [ILI]12and intra
nerve membrane. osseous [IO] injection)13 provide localized areas of pulpal
Developments Since the 5th Edition. Previous editions anesthesia with a minimum of associated soft tissue anes
of this book referenced studies in both medicine and den thesia. Anesthesia of the tongue or lip is essentially non
tistry in which NaHC03 or hyaluronidase was added to existent followingthese injections.
local anesthetic cartridges with extremely variable results.9
The introduction of a stabilized form of NaHC03 along Residual Soft Tissue Anesthesia
with use of a delivery device makes addition of NaHC03 Although a long duration of residual STAmay be desirable
to the dental cartridge with removal of a like volume of followingsome dental procedures such as surgery (oral sur
LA from the cartridge an easy to accomplish chairside gical, periodontal, and endodontic), most operative dental
procedure. care requires profound anesthesia (pulpal) during the rela
tivelybrief treatment period whilethe patient is in the dental
chair.Once the traumatic part of the treatment is completed,
PHENTOLAMINE MESYLATE continued anesthesiaof the tissues,hard or soft,is no longer
{THE LOCAL ANESTHETIC "OFF" SWITCH) needed. However,the need for effectiveintraoperative pain
The local anesthetic armamentarium today consistsof drugs control normally mandates the use of a vasoconstrictor
that provide a range of durations of pain control, from containing local anesthetic.14 Patients commonly are dis
short-acting drugs (=30 minutes of pulpal anesthesia) to charged from the dental office with residual numbness to
long-acting drugs that provide pulpal anesthesia up to 7 their lips and tongue, which typically persists for an addi
hours and soft tissue anesthesia up to 12 hours." Short tional 3 to 5 hours.15
duration drugs provide pulpal anesthesia for approximately ResidualSTApresents as an inconvenienceor embarrass
30 minutes and include mepivacaineHCl 3% and prilocaine ment to the patient, who is unable to function normally
HCl 4%. The long-duration categoryconsistsofbupivacaine for many hours after leaving the dental appointment. In a
HCl 0.5% with epinephrine 1:200,000, providing pulpal surveyby Rafiqueand associates16of patients receivingintra
anesthesia for up to 7 hours (commonly from 90 to 180 oral local anesthesia,the authors stated that several aspects
minutes) with soft tissue anesthesiafor up to 12 hours. It is of the post-local anesthetic experience were disliked by
interesting to note that bupivacaine HCl is a long-acting patients, including three major areas-functional, sensory,
anesthetic onlywhen administered by nerve block (e.g.,infe and perceptual.
rior alveolarnerveblock). It is not nearlyas long actingwhen Functionally,patients dislikedtheir diminished ability to
administered by supraperiosteal (infiltration) injection. speak (lisping), to smile (asymmetric), or to drink (liquid
Becausethe usual length of dental treatment is approxi runs from the mouth), and their inabilityto control drooling
mately 44 minutes, the short-duration anesthetics fail to while still numb. Sensorially,lack of sensation was described
meet the pain control needs of many patients.11 The as quite discomforting, and the perception that their body
intermediate-duration category is used most often. With was distorted (e.g.,swollenlips) was equallyunpleasant. For
inclusion of a vasopressor (epinephrine or levonordefrin many patients,these sequelaebecome a significantdetriment
[in North America]), the drugs in this group provide to their quality of life,making it difficultfor them to return
pulpal anesthesia of approximately 60 minutes' duration. to their usual activitiesfor hours after treatment. When the
Intermediate-duration drugs include articaine HCl 4% with dental appointment concludes at a time approaching a
epinephrine 1: 100,000 and 1 :200,000; lidocaine HCl 2% meal-either lunch or dinner-the patient must consider
with epinephrine 1:50,000 and 1: 100,000; mepivacaineHCl whether to eat while numb or postpone dining until residual
2% with levonordefrin 1:20,000; and prilocaine HCl 4% STAresolves.
with epinephrine 1 :200,000. Although not normally a significant problem, residual
It is pulpal anesthesia that allows a tooth to be treated STA occasionally may lead to self-inflicted injury in any
painlessly.Anesthesiaof associatedsoft tissues (STA)occurs patient. Self-inflictedinjury to soft tissues, most commonly
hand-in-hand with pulpal anesthesia. Although necessary the lip or tongue, is more apt to be noted in younger children
for many treatments such as curettage, periodontal surgery, and in mentally disabled adult and pediatric patients17•18
extractions, implants, and subgingivaltooth preparation, to (Fig. 20-3).
be completed painlessly,the duration of STAis considerably A study of pediatric patients by Collegeand colleagues17
longer than that of pulpal anesthesia,averaging3 to 5 hours revealed that a significant percentage of inferior alveolar
in the intermediate-duration group of LAs. nerve blocks were associatedwith inadvertent biting of the
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360 PARTIV Complications,LegalConsiderations, Questions, and Future
HOW LOCALANESTHETICSWORK
AN OVERVIEW
When a local anesthetic is deposited closeto a nerve, it dif
fusesinto the nerve.When the dental drill stimulates a tooth
distal to this site (the area that is "numb"), a nerve impulse
is propagated. However,this impulse travels only so far as
the area of the nerve where the LAhas been deposited. The
nerve impulse then dies out, never reaching the patient's
brain. As long as enough LA stays in the nerve, the painful
nerve impulse does not reach the brain. This defines the
duration of anesthesiaproduced by the LAdrug.
Localanesthetics"stop working'' when the volume of LA
within the nerve is greater than the volume of LA outside
the nerve. The process of diffusion reverses, and the drug
begins to leavethe nerve and move into the soft tissues sur
rounding it. Individual nerve fibersare graduallyunblocked,
causing the patient to tell the doctor that he or she is "start
ing to feel it again."
As the drug exits the nerve, it is absorbed into capillaries
that carry LA molecules away from the injection site via
the venous circulation. The greater the volume of blood
flowing through the area where the LA was deposited, the
more rapidly this diffusion out of the nerve occurs. This
Figure 20-3. Self-inflicted soft tissue injury of lips.
explainswhy"plain" LAshave a shorter duration of both soft
tissue and pulpal anesthesia than those containing a vaso
pressor. Local anesthetics inherently are vasodilators. Injec
TABLE 20-2 tion of a plain LAincreasesvascularperfusion at the injection
Percentage of Patients, by Age, With Self-Inflicted Soft site, allowing entry of a lesser volume of LAinto the nerve
Tissue Injury Following IANB and more rapid diffusion of the drug back out of the nerve.
As a group, plain LAsprovide a shorter duration with less
%
profound anesthesiathan is provided by anestheticscontain
Age, yr With Soft Tissue Trauma
ing a vasopressor.
<4 18 The addition of epinephrine or levonordefrin to LA
4-7 16
diminishes blood flow into the site of LA deposition. This
8-11 13
permits a greatervolume of LAto diffuseinto the nerve and,
12+ 7
because less blood flows through the region, allows LA to
Data from CollegeC, FeigalR, Wandera A, et al: Bilateralversus unilateral remain within the nerve in a higher concentration for a
mandibular block anesthesiain a pediatric population, Pediatr Dent
longer time, thus providing a longer duration of more pro
22:453-457, 2000.
IANB, Inferior alveolarnerve block. found anesthesia.
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CHAPTER 20 Future Trends in Pain Control 361
low-frequency electrical current is delivered to the area (Fig. administered IV or IM but can be injected subcutaneously
20-4). Application of this low-frequency (2.5 Hz) electrical to prevent local tissue necrosis when vasoconstrictor drugs
current to an area that has been recently injured is beneficial extravasate.23 The pharmacokinetics of phentolamine is
for the patient in two ways: (1) it acts to increase tissue largely unknown; 10% of a parenteral dose is excreted in the
perfusion produced by capillary and arteriolar dilation, and urine unchanged.
(2) it simultaneously stimulates the contraction of skeletal
muscle. The net effect of these two processes is a pumping Availability. Phentolamine is available as a 5 mg/mL solu
action in the area of application of the current. Therapeuti tion for parenteral administration.
cally, a 1hour treatment given at a low frequency helps to
decrease edema (skeletal muscle-stimulating effect), and Phentolamine Mesylate for Reversal of Residual STA
increased perfusion and skeletal muscle stimulation act to Clinical Trials-Adu/ts and Adolescents. An injectable
"cleanse" the area of tissue injury breakdown products.19 form of phentolamine mesylate (PM) has been formulated
With electrodes placed intraorally around the site where to terminate the numbing sensation associated with local
local anesthetic is injected, it was possible to shorten the anesthesia when it is no longer required. The product, which
duration of STA. This technique was short-lived because it is available under the proprietary name Ora Verse (Septodont
was difficult to position the electrodes intraorally and to Inc. Lancaster, Pa), contains 0.4 mg PM (0.235 mg/mL)
have them adhere firmly to the moist intraoral mucous packaged in a 1.7 mL dental cartridge22 (Fig. 20-6). In May
membranes. 2008, the FDA approved phentolamine mesylate, which was
Another approach to the question of how to minimize
residual STA consists of injection of a vasodilating drug into
the area of prior local anesthetic administration. In theory,
this should hasten the redistribution of LA from the nerve
into the cardiovascular system (CVS), thereby decreasing the
duration of residual STA.
Phentolamine Mesylate
Phentolamine is an a-adrenergic receptor antagonist
approved for use by the U.S. Food and Drug Administration
(FDA) in 1952 (Fig. 20-5). Approved uses of phentolamine
currently include (1) diagnosis of pheochromocytoma, (2)
treatment of hypertension in pheochromocytoma.P'" and
(3) prevention of tissue necrosis after norepinephrine extra
vasation. 22.i3 An early use of injectable phentolamine involved
the management of impotence (erectile dysfunction}."
Phentolamine is a short-acting, competitive antagonist at
peripheral a-adrenergic receptors. It antagonizes both a1
and <Xi receptors, thus blocking the actions of the circulating
catecholamines epinephrine and norepinephrine. Phentol
amine also stimulates ~-adrenergic receptors in the heart
and lungs.
The clinical effects of phentolamine include peripheral
vasodilation and tachycardia. Vasodilation results from both
direct relaxation of vascular smooth muscle and a blockade.
The drug produces positive inotropic and chronotropic
effects, leading to an increase in cardiac output. In smaller
doses, the positive inotropic effect can predominate and raise
blood pressure; in larger doses, peripheral vasodilation can
mask the inotropic effect and lower blood pressure. These
actions make phentolamine useful in treating hypertension
caused by increased circulating levels of epinephrine and
norepinephrine, as occurs in pheochromocytoma.
The effects of phentolamine in treating impotence are
mediated by a-adrenergic blockade in penile blood vessels.
Actions of the drug cause relaxation of the trabecular cav
ernous smooth muscles and dilation of the penile arteries; Figure 20-4. A and B, Electronic dental anesthesia (EDA) unit,
this increases arterial blood flow into the corpus cavernosa circa 1980.
and subsequently causes an erection.24 Phentolamine is Continued
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362 PARTIV Complications,LegalConsiderations, Questions, and Future
Figure 20-4, conrd. C and D, Intraoral use of transcutaneous electrical nerve stimulation (TENS) for comfortable administration of
local anesthesia and (E and F) for treatment without the need for local anesthesia.
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CHAPTER 20 Future Trends in Pain Control 363
STAR QUESTIONNAIRE
assessedby both the patient and an observer blinded to the protocol werealsotrained to tap their tongue. The procedure
treatment.P" To determine the impact of functional defi involvedlight tapping of these soft tissues with the index or
cits, a patient-reported outcomes questionnaire (SoftTissue middle finger. Research assistants instructed patients that
Anesthesia Recovery[STAR])was developed (Fig.20-7). In during the study,they would rate the injected side as feeling
the mandibular study,the time to recoveryof tongue sensa normal, tingling, or numb, and that they may tap the non
tion was also a secondary endpoint. The dental procedure injected side as a comparison. Assessmentswere made every
had to be completed within 60 minutes of the LAinjection, 5 minutes.
and the patient's lip had to still be numb at that time, or he STAR Questionnaire. The STARquestionnaire measures
or shewas excludedfrom the study.All244patients random quality of life (seeFig.20-7). It was developedspecificallyfor
ized in the mandibular study reported lip anesthesia at 1 these studies to quantify a patient's perceivedclinicalbenefit
hour; only 194reported that their tongue was still numb at derived from reversingsoft tissue anesthesia.
this time. The maxillary study enrolled 240 patients. FunctionalAssessmentBattery (FAB). The FABincluded
Patients were randomized to receive one of four local measurements of smiling, speaking, and drooling, and
anesthetics: 2% lidocaine + epinephrine 1: 100,000; 2% drinking 3 ounces of water at various time points during the
mepivacaine + levonordefrin 1:20,000; 4% articaine + study.28 Each functional assessmentwas rated as normal or
epinephrine 1: 100,000; or 4% prilocaine + epinephrine abnormal by a research assistant and by the patient.
1:200,000. Drugs were randomized using a 6 : 1:1: 1 ratio Heft-Parker Visual Analog Scale (H-P VAS). The H-P
based on usage patterns in the United States. VASis a 170mm visual analog scale that contains the fol
At the conclusionof treatment, the patient receivedeither lowingverbal descriptors:none, faint, weak,mild, moderate,
PM or a control injection. The patient and all investigators strong, intense, and maximum possible.29 Patients were
were blinded to the treatment assigned.The study drug was asked to place a mark on the line that corresponded to their
administered at the same site, and in the case of PM, the current assessment of pain at the injection site and at the
same number of cartridges (one or two) was used as in the procedural site.
previous LA injection(s). The control was a sham injection
in which the plastic needle cap attached to the dental syringe Efficacy of Phentolamine Mesylate: Adolescents and
containing an empty cartridge was pushed against, but did Adults.26 In the maxillarytrial, the median time to recovery
not penetrate, intraoral soft tissue at the site of the previous of normal sensation in the upper lip was 50 minutes for PM
LA injection. This sham allowed for a blinded comparison patients and 132.5minutes for sham patients, for a reduction
of injection site pain. After receivingPM or the sham injec in upper lip anesthesia of 82.5 minutes (P <.0001).
tion, all patients were observed for 5 hours for collection of In the mandibular trial, the median time to recovery of
efficacyand safety data, and were monitored for up to 48 normal sensation in the lower lip was 70 minutes for PM
hours. patients and 155minutes for sham patients, for a reduction
The 5 hour observation and testing period was a primary in lower lip anesthesia of 85 minutes (P <.0001).
determinant of the lower age limit (4 years) for patients. It Within 30 minutes of PM administration, 26.7% of
was believed (correctly,it turned out) that younger patients maxillary patients reported return of normal lip sensation
would be unable to cooperate fullywith the assessments(see as compared with 1.7% in the control group. At 1 hour,
later) required over the 5 hour period of observation. 59.2% had normal upper lip sensation versus 11.7% for
Lip and Tongue Palpation. All patients were trained in sham. At 90 minutes, these figures were 75% and 25%,
assessingthe numbness of their lip. Those in the mandibular respectively.Upper lip anesthesia persisted beyond 2 hours
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364 PARTIV Complications,LegalConsiderations, Questions, and Future
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CHAPTER20 Future Trends in Pain Control 365
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366 PARTIV Complications,LegalConsiderations, Questions, and Future
the nerve bundle supply the molar teeth, and nerves on the Recent Findings-Mandibular Infiltration With Articaine
inside (core fibers) supply the incisor teeth. Therefore the HCl. Since the introduction of articaine HCl 4% with epi
local anesthetic solution deposited near the inferior alveolar nephrine 1: 100,000 in the United States in June 2000,
nerve may diffuse and block the outermost fibers but not numerous anecdotalreports havebeen receivedfrom doctors
those located more centrally, leading to incomplete man claimingthat they no longer needed to administer the IANB
dibular anesthesia. to work in the adult mandible painlessly.They claimed that
The difficulty in achieving mandibular anesthesia has, mandibular infiltration with articaine HCl was uniformly
over the years, led to the development of alternative tech successful.These claims were initially met with skepticism.
niques to the traditional (Halstedapproach) inferior alveolar Over the past 5 years, four well-designedclinicaltrials have
nerveblock.Thesehaveincluded the Gow-Gatesmandibular compared infiltration in the adult mandible of articaine HCl
nerve block," the Akinosi-Vazirani closed-mouth nerve 4% with epinephrine 1: 100,000 versus lidocaine 2% with
block,49the PDL (intraligamentary) injection," intraosseous epinephrine 1: 100,000 or 1:80,000.
anesthesia,51 and, most recently,buffered local anesthetics.52 Kanaa MD, Whitworth JM, Corbett IP, et al: Articaine
Although all maintain some advantagesover the traditional and lidocaine mandibular buccal infiltration anesthesia:
Halsted approach, none is without its own faults and a prospective randomized double-blind cross-over study,
contraindications. J Endod 32:296-298, 2006.59
The ability to provide localized areas of anesthesia by Robertson D, Nusstein J, Reader A, et al: The anesthetic
infiltration injection without the need for nerve block injec efficacy of articaine in buccal infiltration of mandibular
tions has a number of benefits. Meechan53 has enumerated posterior teeth, J Am Dent Assoc 138:1104--1112, 2007.60
them as follows:(1) technicallysimple, (2) more comfortable These first two papers assessedthe effectivenessof artic
for patients, (3) can provide hemostasiswhen needed, (4) in aine buccal infiltration administered in lieu of an IANB.
many cases obviates the presence of collateral innervation, Haase A, Reader A, Nusstein J, et al: Comparing anes
(5) avoids the risk of potential damage to nerve trunks, (6) thetic efficacyof articaine versuslidocaine as a supplemental
lesserrisk of intravascularinjection, (7) saferin patients with buccal infiltration of the mandibular first molar after an
clotting disorders,(8) reducesrisk of needle-stickinjury,and inferior alveolar nerve block, J Am Dent Assoc 139:1228--
(9) preinjection application of topical anesthetic masks 1235, 2008.61
needle penetration discomfort. Kanaa MD, Whitworth JM, Corbett IP, et al: Articaine
buccal infiltration enhances the effectivenessof lidocaine
inferior alveolar nerve block, Int Endod J 42:238-246,
Mandibular Infiltration 2009.41
Attempts at mandibular infiltration have been made in These two papers studied the effectivenessof an articaine
the past. In a 1976 study of 331 subjects receiving IANB buccal infiltration as a supplement to the IANB.
with lidocaine HCl 2% with epinephrine 1: 80,000, 23.7% These clinicallyimportant clinicaltrials are summarized
had unsuccessful anesthesia." Supplemental infiltration of in the followingsection.
1.0 mL of the same drug on the buccal aspect of the man
dible proved successful in 70 of the 79 subjects. Of the Kanaa MD, Whitworth JM, Corbett IP, et al: Articaine
remaining 9, 7 were successfully anesthetized following and lidocaine mandibular buccal infiltration anesthesia:
additional infiltration of 1.0 mL on the lingual aspect of the a prospective randomized double-blind cross-over study,
mandible. J Endod 32:296-298, 2006. 59
Yonchakand associatesinvestigatedinfiltration on inci
sors and reported 45% success following labial infiltration Design. Infiltrations were administered to 31 subjects
(lidocaine 2% with 1: 100,000 epinephrine) and 50% with in the buccal fold adjacent to the mandibular first molar. A
lingual infiltrations of the same solution for lateral incisors, dose of 1.8 mL was administered at a rate of 0.9 mL per 15
and 63% and 47% for central incisors on labial and lingual seconds.The order of drug administration was randomized,
infiltration.55 with the second injection administered at least 1 week after
Meechanand Ledvinkafound similar successrates (50%) the first. The same investigator administered all injections.
on central incisor teeth followinglabialor lingualinfiltration Electricalpulp testing (EPT) was used to determine pulpal
of 1.0 mL of lidocaine 2% with 1: 80,000 epinephrine.56 sensitivity.Baseline readings were obtained, and EPT was
In 1990 Haas and colleagues compared mandibular repeated once every2 minutes after injection for 30 minutes.
buccal infiltrations for canines with prilocaine HCl versus If no response (to maximal EPT stimulation of 80 µA)
articaine HCl and found no significantdifferences.57Success occurred, the number of episodesof no response at maximal
rates were 50% for prilocaine and 65% for articaine (both stimulation was recorded. The criterion for successfulanes
4% with epinephrine 1:200,000). A second study noted a thesia was no volunteer response to maximal stimulation on
63% successrate on mandibular second molars with arti two or more consecutiveepisodes of testing. (This had been
caine, and 53% with prilocaine (both 4% with epinephrine established as the criterion for success in many previous
1:200,000).58 clinicaltrials.)
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CHAPTER 20 Future Trends in Pain Control 367
Results. The total number of episodes of no sensation on At 2 minutes, the premolars were tested. At 3 minutes, the
maximal stimulation in first molars over the period of the control canine (contralateral side) was tested. This testing
trial (32 minutes) was greater for articaine (236 episodes) cycle was repeated every 3 minutes for 60 minutes. Complete
than for lidocaine (129) (P <.001). Twenty (64.5%) subjects absence of sensation to maximal EPT stimulation on two or
experienced anesthetic success following articaine, whereas more consecutive readings was the criterion for successful
12 (38.7%) did so with lidocaine (P<.08). The design of the anesthesia. The onset of anesthesia was defined as the time
trial allowed for a maximal possible duration of anesthesia at which the first of two consecutive no responses to EPT of
of 28 minutes. Six subjects receiving articaine achieved 28 80 occurred.
minutes of anesthesia compared with 2 given lidocaine. Results. Articaine was significantly better than lidocaine
Discussion. The difference between articaine and lido in achieving pulpal anesthesia in each of the four teeth
caine was most obvious toward the end of the study period. (P <.0001 for all four teeth). Table 20-3 summarizes these
The percentage of patients showing no response at maximal findings.
stimulation was reduced at all reference points after 22 The onset of successful anesthesia was significantly
minutes with lidocaine. With articaine, however, the greatest faster for articaine than for lidocaine for all four teeth tested
percentage of nonresponders was noted at the end of the trial (Table 20-4).
(32 minutes). Discussion. The exact mechanism of the increased effi
Conclusion. Overall, 4% articaine with epinephrine was cacy of articaine is not known. One theory relates to the
more effective than 2% lidocaine with epinephrine in pro 4% concentration of articaine versus the 2% lidocaine
ducing pulpal anesthesia in lower molars following buccal solution. However, Potocnik and coworkers found that 4%
infiltration. and 2% articaine formulations were superior to 2% lido
caine in blocking nerve conduction.62 A second theory is
Robertson D, Nusstein J, Reader A, et al: The anesthetic that the thiophene ring of articaine enables it to diffuse
efficacy of articaine in buccal infiltration of mandibular more effectively than the benzene ring found in other local
posterior teeth, J Am Dent Assoc 138:1104-1112,2007."° anesthetics.
Regarding onset of anesthesia, previous studies of lido
Design. A total of 60 blinded subjects randomly received caine following IANB found onset times ranging from 8
buccal infiltration injections of 1.8 mL of 2% lidocaine with
epinephrine 1 : 100,000 and 4% articaine with epinephrine
1: 100,000 in two separate appointments at least 1 week
apart. Each subject served as his/her own control. Sixty infil TABLE 20-3
trations were administered on the right side, and 60 on the SuccessRate in Achieving Pulpal Anesthesia-Articaine
left side. For the second infiltration in each subject, the inves versus Lidocaine
tigator used the same side randomly chosen for the first Articaine. Lidocaine.
infiltration. The teeth chosen for evaluation were the first Tooth % Success* % Success*
and second molars and the first and second premolars. The
Second molar 75 45
same investigator administered all injections. Before injec First molar 87 57
tions were administered, baseline values were determined on Second premolar 92 67
the experimental teeth with EPT. A single infiltration was First premolar 86 61
administered buccal to the first mandibular molar, bisecting
Modified from Robertson D, Nusstein J, ReaderA, et al: The anesthetic
the approximate location of the mesial and distal roots. The
efficacyof articaine in buccal infiltration of mandibular posterior teeth,
1.8 mL was deposited over a period of 1 minute. One minute J Am Dent Assoc 138:1104-1112,2007.
after injection, the first and second molars were pulp tested. *P <.0001for all four teeth.
TABLE 20-4
Onset Time (Minutes) of Pulpal Anesthesia-Articaine versus Lidocaine
Articaine Onset (Min} ± Lidocaine Onset (Min} ±
Tooth Standard Deviation Standard Deviation PValue
Second molar 4.6±4.0 11.1±9.5 .0001
First molar 4.2 ± 3.1 7.7±4.3 .0002
Secondpremolar 4.3 ± 2.3 6.9±6.6 .0014
First premolar 4.7 ± 2.4 6.3 ± 3.1 .0137
Modified from Robertson D, Nusstein J, ReaderA, et al: The anesthetic efficacyof articaine in buccal infiltration of mandibular posterior teeth, J Am Dent
Assoc 138:1104-1112,2007.
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368 PART IV Complications, Legal Considerations, Questions, and Future
to 11 minutes for the first molar, and from 8 to 12 minutes a gradual increasein pulpal anesthesia.This is likelya result
for the first premolarf':" Articaine provided a more rapid of the effect of the infiltrations' overcoming failure or the
onset of pulpal anesthesia for all tested teeth than for slow onset of anesthesia following IANB. Therefore, for a
IANB. However, pulpal anesthesia declined steadily over maximum effectwith the 4% articaine infiltration, a waiting
the 60 minute test period. Therefore, if profound pulpal time is required before onset of pulpal anesthesiais achieved.
anesthesia is required for 60 minutes, buccal infiltration It may be prudent to wait for signs of lip numbness before
of 4% articaine with epinephrine 1: 100,000 will not administering the infiltration. Without an effectiveIANB,
provide the duration needed because of declining pulpal buccal infiltration of articaine alone has a relatively short
anesthesia. duration (see previous two citations). A fairlyhigh percent
Condusion. Buccal infiltration of the first mandibular ageof patients receivingthe articaine infiltration maintained
molar with 1.8mL of 4% articaine with epinephrine pulpal anesthesia through the SOthminute. Articaine infil
1: 100,000is significantlybetter than a similar infiltration of tration demonstrated a decline in the incidence of pulpal
2% lidocaine with epinephrine 1: 100,000 in achieving anesthesia after the 52nd minute. Becausemost dental pro
pulpal anesthesia in mandibular posterior teeth. Clinicians cedures require less than 50 minutes for completion, this
should keep in mind that pulpal anesthesiawilllikelydecline injection protocol should prove successfulfor most dental
slowlyover 60 minutes. treatments. The 2% lidocaine demonstrated a decline after
the 60th minute.
Haase A, ReaderA, Nusstein ], et al: Comparing anesthetic Condusion. Buccalinfiltration of the first molar with a
efficacy of articaine versus lidocaine as a supplemental cartridge of 4% articaine with epinephrine 1: 100,000
buccal infiltration of the mandibular first molar after an resulted in a significantlyhigher successrate (88%) than was
inferior alveolar nerve block, J Am Dent Assoc 139:1228- attained with buccal infiltration of a cartridge of 2% lido
1235,2008.61 caine with epinephrine 1: 100,000 {71o/o) after IANB with
4% articaine with epinephrine 1: 100,000.
Design. Seventy-threesubjectsparticipated in a prospec
tive, randomized, double-blind, crossover study comparing Kanaa MD, Whitworth JM, Corbett IP, et al: Articaine
the degree of pulpal anesthesia achievedby means of man buccal infiltration enhances the effectiveness of lido
dibular buccal infiltration of two anesthetic solutions: 4% caine inferior alveolarnerve block,Int EndodJ 42:238-246,
articaine with epinephrine 1: 100,000and 2% lidocainewith 2009.41
epinephrine 1: 100,000,following an IANB with 4% artic
aine with epinephrine 1: 100,000.Subjects served as their Design. The goal of this study was to compare man
own controls. The side chosen for the first infiltration was dibular tooth anesthesia following lidocaine IANB with
used againfor the secondinfiltration. Injectionswereadmin and without supplementary articaine buccal infiltration.
istered at least 1weekapart. The same investigatoradminis In this prospective, randomized, double-blind, crossover
tered all injections.An EPT was used to test the first molar study,36 subjectsreceivedtwo IANBinjections with 2.2 mL
for anesthesia in 3 minute cyclesfor 60 minutes. The IANB lidocaine 2% with epinephrine 1:80,000 over two visits.At
was administered over 60 seconds. Fifteen minutes after one visit, infiltration of 2.2 mL of articaine 4% with epi
completion of the IANB,the infiltration was administered nephrine 1: 100,000 was administered in the mucobuccal
buccal to the first mandibular molar, bisecting the approxi fold opposite the mandibular first molar. At the other visit,
mate location of the mesial and distal roots. The 1.8 mL was a dummy injection was performed. At least 1weekseparated
deposited over a period of 1 minute. Sixteen minutes after the two visits. Pulpal anesthesia of the first molar, the first
completion of the IANB (1 minute following the infiltra premolar, and the lateral incisor teeth was assessedwith an
tion), EPT testing of the first molar was performed. At 3 EPT every 2 minutes for the first 10 minutes, and then at 5
minutes, the contralateral canine was tested. This cyclewas minute intervals for 45 minutes post injection. Successful
repeated every 3 minutes for 60 minutes. Anesthesia was anesthesia was the absence of sensation on two or more
consideredsuccessfulwhen two consecutiveEPTreadings of consecutivemaximal EPT stimulations. The number of epi
80 were obtained within 10 minutes of the IANB and infil sodes of no response to maximal EPT stimulation was
tration injection, and the 80 reading was maintained con recorded. The onset of pulpal anesthesiawas considered the
tinuously through the 60th minute. first episode of no response to maximal stimulation (two
Results. The articaine formulation was significantly consecutive readings), whereas the duration of anesthesia
better than the lidocaine formulation with regard to anes was taken as the time from the first of at least two consecu
thetic success:88% versus 71o/o for lidocaine (P <.01), with tive maximal readings with no response until the onset of
anesthesia developing within 10 minutes after IANB and more than two responses at less than maximal stimulation,
buccal infiltration, sustaining the 80 reading on the EPT or the end of the 45 minute test period, whichever was
continuously for the 60 minute testing period. sooner.
Discussion. Anesthetic success was significantly better Results. IANB with supplemental articaine infiltration
with the 4% articaine formulation than with the 2% lido produced greater successthan IANBalone in first molars {33
caineformulation.Bothanestheticformulationsdemonstrated vs. 20 subjects, respectively;P <.001), premolars (32 vs. 24;
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CHAPTER 20 Future Trends in Pain Control 369
TABLE 20-5
Articaine Buccal Infiltration Enhancesthe Effectiveness of Lidocaine Inferior Alveolar Nerve Block
First Molar First Premolar Lateral Incisor
SuccessIANB+ dummy 55.6% 66.7% 19.4%
SuccessIANB+ infiltration 91.7% (P <.001) 88.9% (P =.021) 77.8% (P <.001)
Onset (mean) IANB+ dummy (minutes) 6.8 8.9 10.9
Onset (mean) IANB+ infiltration (minutes) 4.5 (P<.06) 4.2 (P <.002) 6.9 (P=.40)
Duration ofpulpal anesthesia (mean) IANB+dummy (minutes) 29.0 31.3 29.1
Duration of pulpal anesthesia (mean) IANB+ infiltration (minutes) 38.8 (P <.001) 37.8 (P =.013) 30.0 (P =.90)
Modified from Kanaa MD,Whitworth JM, Corbett IP,et al: Articaine buccal infiltration enhances the effectivenessof lidocaine inferior alveolarnerve
block, Int Endod J 42:238-246,2009.
P =.021),and lateral incisors (28vs. 7; P <.001).Additionally, split (0.5 mL per site)betweenbuccal and lingual,the success
IANB with articaine supplemental infiltration produced rate increased to a statisticallysignificant 92%.
significantlymore episodesof no response than IANBalone Jaber and colleaguesused a split dose {0.9mL per site)
for first molars (339 cases vs. 162, respectively; P <.001), of 2% lidocaine with 1: 100,000 epinephrine to confirm
premolars {333cases vs. 197; P <.001), and lateral incisors this finding.69 For buccal infiltration of 1.8 mL alone, suc
(227 casesvs. 63; P <.001) (Table20-5). cessful anesthesia of the central incisor was 77%, and it
Discussion. Onset of pulpal anesthesia In this study,the was 97% for the split buccal/lingual dose. Investigators
anesthetic effect for mandibular first molars peaked 25 also compared articaine 4% with epinephrine 1: 100,000
minutes post injection with the dummy injection versus 6 versuslidocaine 2% with epinephrine 1: 100,000as an anes
minutes followingarticaine infiltration. For first premolars, thetic for infiltration in the anterior mandible and found
peak anesthetic effect occurred at 30 minutes post injection that articaine was superior to lidocaine in obtaining pulpal
versus 8 minutes following articaine infiltration, and for anesthesiaof the central incisor when infiltrated adjacent to
lateral incisors,peak anesthetic effectoccurred at 40 minutes the tooth buccally alone {94%) or in split buccal/lingual
post injection versus 20 minutes followingarticaine infiltra injections (97%).
tion in the first molar region. The increased success rate for infiltration in the adult
Duration of pulpal anesthesia The maximum duration mandibular incisor region is thought to be due to the fact
of anesthesiapossible in this trial was 43 minutes. Duration that the cortical plate of bone, both buccal and lingual, is
of pulpal anesthesiawas significantlylonger for first molars thin and might provide little resistanceto infiltration.
and first premolars, but not for lateral incisors. Developments Since the 5th Edition. Although anec
Conclusions. IANB injection supplemented with artic dotal reports and several studies had hinted at the efficacy
aine buccal infiltration was more successfulthan IANBalone of articaine in providing pulpal anesthesiafollowingadmin
for pulpal anesthesiain mandibular teeth. Articaine infiltra istration via mandibular infiltration in adults, it had not
tion increasedthe duration of pulpal anesthesiain premolar receivedserious consideration at the time the 5th edition of
and molar teeth when givenin combination with a lidocaine this textbook was published in 2004.
IANBand produced more rapid onset for premolars.
These four clinical trials clearly demonstrate that artic
aine by mandibular buccal infiltration in the mucobuccal Summary and Conclusions
foldby the firstmandibular molar can provide more success Failurerates for profound pulpal anesthesiafollowingtradi
ful anesthesia of longer duration to mandibular teeth when tional IANB on non-pulpally involvedteeth are quite high.
administered alone or as a supplement to IANB. This has led to the development of severalalternative tech
One thing to consider is that in each of these trials, buccal niques, including the Gow-Gates mandibular nerve block,
infiltration of articaine was administered adjacent to the first the Akinosi-Vaziraniclosed-mouth mandibular nerve block,
mandibular molar. The trials demonstrated the effectiveness periodontal ligament injection, and intraosseous anesthesia.
of articaine in improving pulpal anesthesia successrates in The introduction of the articaine HCl has spurred interest
molars and premolars. However,successrates and duration in the use of this local anesthetic by infiltration in the
of anesthesia were not improved as significantlyin lateral adult mandible.
incisors (i.e., teeth at a distance from the site of local anes Initial studies in which articaine was infiltrated in the
thetic deposition). buccal fold adjacent to the first mandibular molar showed
In 2002, Meechan and Ledvinka studied the effects of significantlygreater success rates compared with lidocaine
infiltrating 1.0 mL of 2% lidocaine with 1:80,000epineph 2% infiltration (all with epinephrine). Additional studies
rine buccallyor linguallyto the mandibular central incisor.56 using articaine mandibular infiltration (by the first molar)
A successrate of 50% was achievedwith the buccal or the as a supplement to IANB (with lidocaine or articaine)
lingual injection site. However,when the injection dose was revealed the same significant increases. In each of these
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370 PART IV Complications, Legal Considerations, Questions, and Future
studies, a full cartridge oflocal anesthetic (1.8 mL or 2.2 mL) nervous system (CNS)-depressant drug midazolam in the
was administered. Future studies are called for to determine management of status epilepticus in young children.":"
the minimal volume of LA solution needed to produce the Lahat and associatescompared IN midazolam (0.2 mg/kg)
best clinical result. At this time, the recommendation is to versusintravenous (IV) diazepam (0.3 mg/kg) in 47 children
administer a full cartridge of articaine 4% with epinephrine aged 6 months to 5 years.72 Twenty-threeof 26 seizureswere
1: 100,000 (or 1:200,000) in the mucobuccal fold adjacent terminated with IN midazolam-24 of 26 with IV diazepam.
to the mandibular first molar when treating molars or pre The speed at which seizureswere terminated was consider
molars in the adult mandible. ably faster with IN midazolam (5.5 minutes) than with IV
When mandibular incisors are treated, the recommenda diazepam (8.0 minutes).
tion is to administer a split dose of articaine, 0.9 mL in the Pediatric dentistry has utilized IN sedation dating as far
buccal fold adjacent to the tooth being treated and 0.9 mL back as the early 1990s.75-78The dosage of midazolam most
on the lingual aspect of the same tooth. Splitting of the LA often cited as most effectiveand safeis 0.2 mg/kg-the same
dose is not effectivein the mandibular molar region. dose employed in critical care medicine for termination of
The articaine mandibular infiltration injection can be seizures.
repeated later in the dental procedure if pulpal anesthesia Intranasal instillation of local anesthetics has been
begins to wane and the patient starts to become sensitive. employedin medicine primarily in the realm of ear nose and
An EPT can be used effectivelyto assesspulpal anesthesia throat (ENT) procedures.Y" Tetracaine,an ester-type local
before invasive dental treatment is started," Studies have anesthetic, is commonly used to provide a numbing effect
demonstrated that absence of patient response to an 80 before surgical manipulations in the nose. Many patients
readingwasan assuranceof pulpal anesthesiain vital asymp receivingIN tetracaine have commented on how their upper
tomatic teeth.70•71 TwoconsecutiveEPT readings at maximal teeth felt numb, sparking interest in a possible dental appli
output (80 µA) 2 or 3 minutes apart is almost alwaysindica cation of IN local anesthetic. For dental application, the
tive of profound anesthesia.Certosimo and Archer reported vasoconstrictor oxymetazolinewas added to the tetracaine
that patients who had EPT readings of less than 80 experi to enhance effectiveness.Oxymetazolineis the active ingre
enced pain during operative procedures in asymptomatic dient in the nasal decongestant spray,Afrin.
teeth." In a Phase II double-blind, randomized clinical trial,
Ciancio and colleaguescompared IN tetracaine with oxym
etazolineversus injectablelidocaine 2% with 1: 100,000epi
INTRANASAL LOCAL ANESTHESIA nephrine in providing pulpal anesthesia bilaterally in the
Absorption of drugs through the nasal mucosa to achievea maxilla from first molar to first molar (teeth #3 through
systemiceffect has a long and varied history. The nares are #14)81 (Fig. 20-11). Success was defined as the ability to
extremelyvascular,so most drugs instilled into them will be accomplishthe dental procedure without the need for rescue
absorbed rapidly and distributed systemically(Fig. 20-10). medication (injectable local anesthetic) (Fig. 20-12). The
"Snorting a line" of cocaine is an example of illicit use of tetracaine nasal spray group had a successrate of 88% (22
this route of drug administration. Critical care medicine has of25) versus93% (14of15) in the lidocaineinjection group.
used intranasal (IN) drug administration of the central In the IN group, all failuresto achieveadequate pulpal anes
thesia occurred on first molars (#3 or #14). Teeth#4 through
#13 had 100%success.81
Phase III clinicaltrials havejust begun as this text is being
written (October 2011).
Greater Palatalsoft
palatine I I I~ I!! tissue
foramen andbone
Figure 20·10. Intranasal instillation of local anesthesia. Figure 20·11. Diagram of extent of intranasal local anesthesia.
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CHAPTER 20 Future Trends in Pain Control 371
A
Figure 20-12. Intranasal local anesthesia device. (Photos courtesy St. Renatus, LLC, Ft Collins, Colo.)
Developments Since the 5th Edition. Intranasal local plunger. Remarkably, the basic design, mechanics, and
anesthetic administration was not yet a consideration when manual operation of the Pravazsyringe,invented more than
the 5th edition of this textbook was published in 2004. 150 years ago, were virtually identical to those of medical
and dental syringesin current use.
What have we learned over the past century about local
COMPUTER-CONTROLLED LOCAL ANESTHETIC anesthetic delivery systems?What do clinical data reveal
DELIVERY (C-CLAD) about their common use today? Aside from the noted
During the late 1880s, physicians Sigmund Freud, Carl obvious benefit in providing a convenient means of delivery
Koller,and William Halsted were pursuing a common area of a liquid drug, we know (numerous dental studies and
of clinical research: the development of the drug benzoyl consumer surveys have documented this) that the dental
methyl ecognine, more commonly known today as cocaine, syringe predictably invokes fear and anxiety in our
for medicinal use and for application as the first local patients,":" The term trypanophobia (needle phobia) is the
anesthetic.82 extremeand irrational fear of medicaland dental procedures
Although Freud and Koller were the first to notice the involving injection. It is estimated that nearly one in five
anesthetic effectsof cocaine,it was Halsted who introduced adults are dental phobics who will avoid, cancel, or fail to
cocaine as a local anesthetic in dentistry.83 Using a hypoder appear for required dental treatment because of their fear of
mic syringe,Halsted demonstrated that interstitial injection the dental lnjection.":"
of aqueous cocaineresulted in an effectivenerve block of the In 1997,a new local anesthetic deliverysystemwas intro
inferior alveolarnerve,and that a smallamount of anesthetic duced," Originally called The Wand (later renamed The
solution injected into the trunk of a sensoryand motor nerve CompuDent/Wand; Milestone Scientific, Inc., Livingston,
resulted in blockageof sensory and motor function from the NJ), it represented the first computer-controlled local anes
terminal nerve branches. This discovery represented the thetic delivery (C-CLAD)system (Fig.20-13).Within but a
starting point for local pain control in both dentistry and few years, C-CLADtechnology had helped to redefine our
medicine as we know it today. perception and, even more important, the perception of our
This pioneering event relied on the required knowledge patients, as to how local anesthesia can and could be
of bringing together three separate elements: a drug, a drug achieved.91
delivery instrument, and an anatomic technique. Each of C-CLAD devices provide clinicians with the ability to
these components had the potential to influencethe success preciselycontrol the rate of delivery of the local anesthetic
or failure of achievingthe desired result. The drug delivery solution.92 In addition, C-CLADintroduced the concept of
instrument commonly known as the hypodermic syringe using a disposablehandpiece weighinglessthan 10 g, allow
as used by Halsted was a simple hand-driven mechanical ing the clinician to hold it in a pen-like fashion, greatly
instrument developedin 1853by the French generalsurgeon increasing tactile control and improving dexterity during
CharlesGabrielPravas.84 It consistedof a hollow-boreneedle injection" (Fig.20-14). C-CLADdevicesrepresent a signifi
connected to a fluid-containing chamber with a sealed cant advancement for subcutaneous injections and have
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372 PARTIV Complications,LegalConsiderations, Questions, and Future
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CHAPTER20 Future Trends in Pain Control 373
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374 PART IV Complications,LegalConsiderations, Questions, and Future
and coworkers,128 Gibson and associates,129 and Allen and C-CLADdevice over IANBinjection performed with a tra
colleagues.P" ditional syringe.
Versloot, Veerkamp, and Hoogstraten compared the Jalevikand Klingbergevaluated20 adolescentsin need of
behavioral reactions of 125children, aged 4 to 11years,who bilateral surgical exposure of canines and/or extractions for
received dental local anesthesia with a traditional syringe orthodontic reasons in the maxilla.!" Conventional infiltra
compared with a C-CLADinstrument.125 The occurrence of tion anesthesia using a traditional syringe was compared
muscle tension, crying,verbal protest, movement, and resis with a palatal injection performed using the C-CLADdevice
tance was scored on the Venham DistressScaleby two inde on the same patient. A randomized study designwas used to
pendent observersat 15 second intervals.Parents completed determine the order of injection, and scoring of patient pain
the Dental Subscaleof the children's Fear Survey Schedule. perceptions was recorded using a visual analog scale imme
Results demonstrated a measurable reduction in overall diatelypost treatment. Resultsindicate that the sensation of
behavior reactions and patient anxietywhen C-CLADinjec pain was significantly lower (P <.01) when the C-CLAD
tions were used as compared with the standard syringe.The devicewas used than when the traditional syringewas used;
C-CLAD system demonstrated its greatest effect on low patients who reported fear of injection experienced much
anxiety children by producing the most positive reaction, less pain when receiving a C-CLAD injection (P <.001).
making the C-CLADsystemuseful in treatment of the pedi Investigators concluded that the C-CLAD device and the
atric patient. palatal injection technique weresuperior compared with the
Ram and Kassirercompared the reactions of 138children, conventional syringe and injection technique, especially
24 to 38 months old, who receiveddental local anesthesiaof among those who reported fear of injections.
the maxillaryincisors by comparing a C-CLADsystemwith Gibson and associatespublished results from 62 patients
a conventional syringe.126 PDL and P-ASAinjection tech between the agesof 5 and 13yearswho required dental local
niques using a C-CLAD instrument were compared with anesthesia.129 Patients were randomly assigned a C-CLAD
conventional supraperiosteal buccal infiltration performed device or a traditional syringe injection. Pain ratings were
with a traditional syringe. Behavior reactions related to recorded, and subjects rated their satisfaction with treat
crying, facial expression, and eye squeeze were indepen ment. Investigatorsfound that C-CLADinjections resulted
dently scored for each injection. Results demonstrated that in significantly fewer disruptive behaviors during initial
children receiving the C-CLAD instrument injection dis moments of the injection. Nearly twice as many children
playedbetter overallbehavior than those given supraperios receivinga traditional palatal injection were disruptive com
tealbuccal infiltration injection performed with a traditional pared with those receivinga C-CLADdevice injection. Dis
syringe. The authors concluded that the C-CLAD instru ruptive behaviors included significantlyincreased intervals
ment provided a benefit in treatment of the pediatric patient of crying and disruptive body movements. In addition, five
and recommended its use in this population. times more patients receivinga traditional palatal injection
Palm, Kirkegaard,and Poulsen studied the perception of required restraint compared with patients anesthetizedwith
pain and the onset of anesthesia following IANB adminis the C-CLAD device. Gibson and colleagues concluded by
tered with a C-CLADdevice and a traditional dental anes stating, "the C-CLADinstrument injection offers a valuable
thesia syringe.127 A split-mouth design was used, with each means of reducingthe disruptivebehavior of children during
patient serving as his or her own control. Thirty-three injections."129
patients between the ages of 7 and 18 years were included. Allen and coworkers studied 40 preschool patients
Allpatients wereblindfolded,and a sound from the C-CLAD between 2 and 5 yearsof age.!" The purpose of the investiga
instrument was heard during each injection. Pain ratings tion was to evaluate the efficacyof a C-CLADinjection in
were scored on a 10 point Visual Analog Pain-Perception reducing pain behavior in the preschool-aged child when
Scale. Results showed that the C-CLAD instrument pro compared with a traditional syringe. A C-CLAD palatal
duced significantlylower pain ratings than were produced injection technique was compared with traditional syringe
by the traditional syringe. Time to onset of anesthesia was infiltration. Results demonstrated the largest difference
similar in this study. Researchers concluded that using a related to the need for patient restraint, with only 3% of
C-CLADinstrument is more effectivein reducing subjective C-CLADpatients requiring restraint compared with 34% of
pain perception compared with a traditional syringe when the intervals for traditional syringe injections. Allen and
IANBis performed. associatesconcluded that preschool-aged children anesthe
Oztas,Tezer,Bodur, and Dogan studied 25 children, aged tized with the C-CLAD device demonstrated significantly
6 to 10 years, with each child serving as his or her own fewerdisruptive behaviorswhen compared with those given
control.128 Contralateral primary mandibular molars were a traditional injection regimen. Additionally, even with
treated in two separatevisitswith random use of the C-CLAD control applied for the increased duration of the injection,
deviceor traditional syringeinjection. Pain perception levels the slower rate of anesthetic delivery of the C-CLAD did
for each injection were assessedwith the Eland Color Scale. appear to reliably reduce pain-related behavior in children.
Resultsof this study show that an overwhelmingnumber of These young children were significantlyless likelyto cry or
patients preferred the PDL injection performed with the to move in a disruptive manner. The authors stated, "most
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CHAPTER20 Future Trends in Pain Control 375
impressively the results showed that none of the preschool the PDL injection with the STAdevice reported subjective
aged children exposed to the C-CLAD instrument required pain responses of "minimal or no pain:' In contrast,
restraint during the initial interval, while nearly half of the those receivinginjections with one of the other two instru
children receiving a traditional injection required some type ments (high-pressure mechanical syringe or conventional
of immediate restraint. These results are important because syringe) were found to have generally higher pain scores
they demonstrate that the C-CLAD instrument can signifi throughout the testing period and required repeated
cantly reduce disruptive behavior in a population of young attempts to achieve a successfuloutcome. Researcherscon
children who are traditionally more difficult to manage. cluded that the STA-Systemdeviceresulted in more predict
Reducing disruptive behavior in preschool-aged children is able, more reliable, and more comfortable anesthesia than
important not only because it creates a more positive experi the high-pressure mechanical syringe and/or the conven
ence for the child, but it also creates a more positive experi tional dental syringe.P?
ence for the practitioner"!" The STA-Systemdeviceand its predecessors-The Wand,
Asarch and associates conducted a study of 57 patients CompuDent, and the Midwest Comfort Control Syringe
between 5 and 13 years of age to evaluate pain-disruptive (DentsplyProfessional901West Oakton Street, Des Plaines,
behavior and each subject's subjective pain perception when IL 60018) represent a material improvement over the tradi
a traditional syringe injection was compared with the tional (antiquated) 150-year-oldhand-driven manual dental
C-CLAD system injection.'!' IANB injection and palatal and syringe. C-CLAD devices have been shown to enable the
buccal infiltration were the only injections administered, dental practitioner to administer a more comfortable and
with each subject receiving a single injection. Authors stated less anxiety-provoking injection. The STA-Systeminstru
the method of use for the C-CLAD device as follows: "A slow ment adds to those previous advances by introducing
rate of administration was used prior to needle insertion. dynamic pressure-sensing (DPS) technology that provides
Upon evidence of negative aspiration, the fast-rate of admin continuous real-time injection feedback and identification
istration was used." Pain perceptions were rated using a 10 of specificpatient tissuesand has been shown to enhance the
point visual analog scale; pain behavior was evaluated by an predictability of the PDL injection130•131 (Fig. 20-16). This is
external examiner, and subjects rated their overall satisfac accomplishedwhile adversetissue reactions are minimized,
tion. Results of this study show no significant differences resulting in a safer,more positivepatient and operator expe
between the C-CLAD device and the traditional syringe. rience during administration of dental local anesthetics.123
However, two subsequent studies published by three of Dental local anesthesia delivery has been changed with
Asarch's coauthors'<'" found that Asarch's study design and the introduction of C-CLAD devices. It can be expected
methods were suspect and called into question whether that current and future C-CLAD devices will continue
injection methods and failure to identify specific injection to permit clinicians to perform dental injections more
sites were shortcomings in that study. Subsequently, two
published studies were consistent with the findings of other
research groups presenting on this topic (i.e., a reduction in
pain-disruptive behavior and the ability to reduce fear
during a dental injection).116'129
Consistent findings in the dental literature support the
use of a C-CLADdevice,reporting a significantreduction in
general pain perception; a measurable reduction in disrup
tive pain behavior; and a substantial reduction in the need
for restraint in the management of pediatric patients requir
ing dental local anesthesia.
Most recently,Ferrari and coworkerspublished data from
60 adult patients receiving a PDL injection and compared
the STA-Systemdevice versus two other manual syringes:
a high-pressure PDL syringe (Ligmaject, IMA Associates,
Bloomington, Ind) and a traditional dental syringe.P?EPT
was performed on all tested teeth at regular intervals to
determine successor failure, and the different instruments
and techniques used were compared. In addition to pulp
testing, patient subjective pain responses were recorded
after treatment. Ferrari reported that the STA-Systemhad Figure 20-16. Dynamicpressure-sensing (DPS)technologythat
100% success in achieving pulpal anesthesia; in addition, providescontinuousreal-timeinjectionfeedbackandidentification
rapid onset of anesthesia was observed. The PDL injection of specificpatienttissueshasbeenshownto enhancethe predict
was used as the primary injection for restorative dental abilityof the periodontalligament(PDL)injection.(Photocour
care in mandibular teeth in this study.All patients receiving tesyMilestoneScientific,Livingstone,
NJ.)
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376 PART IV Complications, Legal Considerations, Questions, and Future
successfully and painlessly than in the past. No longer are 14. Yagiela JA: Local anesthetics. In Yagiela JA, Dowd FJ,
primary advances in dental local anesthesia concentrated in Neidle EA, editors: Pharmacology and therapeutics for den
the areas of pharmacology and pharmacokinetics. Instead, tistry, ed 5, St Louis,2004,CV Mosby,pp 251-270.
dentistry has entered an era in which advances in local anes 15. Hersh EV,Hermann DG, Lamp CJ,et al: Assessingthe dura
tion of mandibular soft tissue anesthesia, J Am Dent Assoc
thesia are being made by altering the fluid dynamics and
126:1531-1536,1995.
physical means by which these drugs are administered to
16. RafiqueS,FiskeJ,BanerjeeA;Clinicaltrial of an air-abrasion/
patients. Fifteen years has passed since the first C-CLAD chemomechanical operative procedure for restorative treat
device was introduced into dentistry (The Wand, 1997). It is ment of dental patients, Caries Res 37:360-364,2003.
understood by many in this field that future advances in 17. CollegeC, FeigalR,Wandera A, et al: Bilateralversus unilat
dental pain control will be derived by improving the drug eral mandibular block anesthesia in a pediatric population,
delivery system, in addition to the drugs used for dental local Pediatr Dent 22:453-457,2000.
anesthesia. 18. TavaresM, Goodson JM, Studen-PavlovichD, et al: Reversal
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2008. Pediatr Dent 22:458-462,2000.
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CHAPTER20 FutureTrendsin PainControl 379
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I
Questions
' / 'I
LOCAL ANESTHETICS
achievea therapeutic blood levelin the myocardium.
QUESTION: Why is it said that intravascular administra The accepted therapeutic blood levelis 1.8to
tion of local anesthetics is dangerous when physicians 5 µg/mL. To achievethis, lidocaine is administered
frequently administer intravenous (IV) lidocaine to correct N slowlyand is titrated until ventricular
serious cardiac dysrhythmias? dysrhythmias on the electrocardiogram (ECG) are
eliminated-typically, a total dose of between 1.0 and
Intravenous administration oflocal anestheticsis potentially 1.5mg/kg. In the typical dental practice, a 1.8 mL
hazardous at all times and in all patients. However, N cartridge of lidocaine (36 mg) is deposited in 15
local anesthetics, such as lidocaine and procainamide, do seconds or less.The rate at which the drug is
have an important place in the management of pre-fatal administered intravenously has a significantbearing
ventricular dysrhythmias, such as premature ventricular on its peak blood level.Overlyrapid N administration
contractions and ventricular tachycardia. Several factors, results in lidocaine blood levelsthat quicklyenter
including weighingthe risk versus the benefit, must be con into the overdoserange, whereas a more slowly
sidered whenever local anesthetics are to be administered administered dose results in blood levelswell within
"safely"intravenously. the therapeutic range for terminating
1. The patient's physical status. Patients receivingN dysrhythmias.!"
lidocaine or other antidysrhythmic drugs have 4. Risk versus benefit. An overdosereaction is alwaysa
potentially life-threatening cardiac dysrhythmias.The possibilitywhenever N lidocaine is administered. Even
myocardium is highly irritable (usuallysecondary to under controlled conditions in a hospital, adverse
ischemia),which is often the primary cause of the reactions related to overlyhigh blood levelsdo
dysrhythmia. Localanesthetics are myocardial develop.!"The risk of administering local anesthetics
depressants.By depressingthe myocardium, lidocaine intravenously alwaysmust be weighed against the
decreasesthe incidence of dysrhythmias.However, potential benefit to be gained from their use. For
patients with normal cardiac rhythms receiving N local high-risk patients with a specificlife-threatening
anesthetics will also have their myocardium depressed; dysrhythmia,the benefit clearlyoutweighsthe risk. For
their cardiac function may be impaired by the local dental patients seekingrelief from intraoral pain, N
anesthetic in this circumstance. local anesthetic administration confers no benefit yet
2. The form of lidocaine used. Lidocainefor N use in the adds many risks.
management of ventricular dysrhythmias,so-called
cardiac lidocaine, is prepared in single-useampules or QUESTION: What should I do when a patient claims to
prefilled syringes.These ampules and syringes contain be allergic to a local anesthetic?
only lidocaine and sodium chloride. The typical dental
cartridge of lidocaine contains lidocaine, distilledwater, Believethe patient! Do not use any form of local anesthetic
vasopressor,sodium bisulfite,and sodium chloride. (especiallytopical anesthetic preparations) on this patient
N injection of these ingredients, in and of itself,might until you are able to definitivelydetermine whether a true,
precipitate unwanted cardiovascularresponses rather documented, reproducible allergy exists.Seekto determine
than terminate them. what actually happened to the patient to prompt such a
3. The rate of injection. Lidocainefor antidysrhythmic use claimand how his or her "reaction"wasmanaged. (Adetailed
is titrated slowlyinto the cardiovascularsystemto discussion of this problem is found in Chapter 18.)
380
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CHAPTER21 Questions 381
QUESTION: Are any local anesthetics safer than others? summary of product characteristics.t" The Committee
Someappear to be implicated more than others in adverse further reported, ''All local anaesthetics may cause nerve
reactions. damage (they are neurotoxic in nature). Nerve injuries may
result from several incidents: mechanical trauma due to
No. When used properly, all currently availablelocal anes needle insertion, direct toxicity from the drug, and neural
thetic formulations are extremely safe and effective."Used ischaemia." Their concluding statement read as follows:
properly" is the key phrase. Aspiration before injection (to "There is no need for new experimental studies or clinical
minimize the risk of intravascular administration) and slow trials:'
administration of the drug are vital. A medical history and Another possible"etiology"of these reports, especiallyas
physical evaluation, to determine potential contraindica related to articaine HCl, is a phenomenon in epidemiology
tions to specificlocal anesthetics or additives,must be com known as the Weber effect, after Dr.J.C.P.Weber.11The Weber
pleted before their use. Maximum dosage of a drug should effect states that the number of reported adverse reactions
be determined for a given patient and not exceeded.Charts to a drug rises until about the middle to the end of the
for the most commonly used local anesthetics are found in secondyear of marketing;it peaks and then steadilydeclines,
Chapters 4 and 18.The figures cited are maximum recom despite steadilyincreasing prescribing rates. The validity of
mended doses (MRDs).The stated MRDshould be decreased the Weber effecthas been demonstrated in many studies of
in patients with certain medical complications and in older adversedrug reactions.12·13
individuals. Most systemicreactions to local anesthetics are In 2007,Pogrelreported on 57 nonsurgicaldental patients
entirely preventable. Overdose reactions that have led to whom he evaluated for post-dental care paresthesia over a
death or significant morbidity frequently result from the 3-year period.14He commented in the introduction to the
administration of too large a dose to a younger, lighter paper, "Wewere aware of the discussion in dental circlesas
weight, well-behaved patient requiring multiple quadrants to the use of articaine for inferior alveolarnerve blocks,and
of dental care, or, less commonly, after "accidental" N are awareof recommendations suggestingthat it not be used
administration. Psychogenic reactions, by far the most for IANBs.This was the predominant reason for submitting
common adverse response to the administration of a local this paper at this time." Lidocainewas responsible for 35%
anesthetic, may be virtually eliminated through enhanced of the cases of paresthesia, articaine and prilocaine each
rapport with the patient, use of an atraumatic injection tech 29.8%.However,at the time the paper waspublished (2007),
nique (seeChapter 11),placement of the patient in a supine lidocaine had approximately a 54% share of the U.S. local
position during injection, and ample doses of empathy. anesthetic market, giving it a risk of paresthesia below that
which would be calculated if all drugs were equally neuro
QUESTION: Do some local anesthetics have a greater risk toxic. The lidocaine ratio was 0.64. Prilocaine, with a 6%
of producing nerve damage (e.g., paresthesia)? market share, had a ratio of 4.96--the highest of any of the
local anestheticsin use in the United States,and articaine, at
Discussion in dental circles continues regarding 4% local the time possessinga 25% market share,had a ratio of 1.19.14
anesthetic formulations and the reported incidence of Pogrel concluded, "Therefore, using our previous assump
paresthesia. Such concern started in 1995with the publica tion that approximatelyhalf of all local anesthetic used is for
tion of a paper by Haas and Lennon,7which stated the inci inferior alveolar nerve blocks, then on the figures we have
dence of paresthesia followingall local anesthetic solutions generated from our clinic we do not see disproportionate
with 1:785,000. For 0.5%, 2%, and 3% local anesthetic, nerve involvementfrom articaine."14
the calculated risk was 1: 1,125,000,and for 4% local anes In 2010,Garisto and associatespublished a report on the
thetics, it was 1:485,000.A subsequent retrospective study occurrence of paresthesia in the United States.15Although
from Denmark provided similarresults,"Neither publication againdemonstrating that 4% solutions had a higher reported
presents scientificdocumentation that 4% solutions are the rate of paresthesia, their reported incidences for all local
cause of the paresthesia. Hillerup reported that 79% of anesthetics were quite astounding: the overall incidence of
the casesof paresthesia involvedthe lingual nerve, and 21% reported paresthesia was 1 in 13,800,970 injections. For
the inferior alveolar,"Malamed, responding to Hillerup's mepivacaine,the incidencewas 1:623,112,900,and for lido
paper,suggestedthat the likelycauseoflingual nerve damage caine, 1: 181,076,673.For articaine and prilocaine,investiga
associatedwith inferior alveolarnerve block administration tors reported 1:4,159,848and 1:2,070,678,respectively.This
is direct needle trauma to the lingual nerve, which lies author might report, for the sakeof comparison,that the risk
directly in the path of needle insertion.9 In response to the of being struck by lightning in the United States on an
Hillerup paper, the Pharmacovigilance Committee of the annual basis is 1:750,000.16
European Union initiated an inquiry into these allegations. A meta-analysis comparing articaine HCl with lidocaine
Its report, releasedon October 20,2006,concluded,"Regard (lignocaine) HCl reported that articaine is more likelythan
ing articaine, the conclusion is that the safety profile of the lidocaine to achieveanesthetic successin the posterior first
drug has not significantly evolved since its initial launch molar area, and that there is no difference in postinjection
(1998).Thus, no medical evidenceexiststo prohibit the use adverse events.17A 2011 review of the articaine literature
of articaine according to the current guidelineslisted in the (116 papers reviewed) concluded, "although there may be
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382 PART IV Complications, Legal Considerations, Questions, and Future
controversy regarding its safety and advantages in compari anesthetic preparations are used. Because of the rapid
son to other local anaesthetics, there is no conclusive evi absorption of some topically applied local anesthetics such
dence demonstrating neurotoxicity or significantly superior as lidocaine, it is recommended that their use be restricted
anaesthetic properties of articaine for dental procedures."18 to the followingsituations:
1. Locally,at the site of needle puncture before injection.
QUESTION: How do I select an appropriate local anes 2. For scalingor curettage, over not more than one
thetic for a given patient and procedure? quadrant at a time.
Pressurized sprays of topical anesthetics cannot be rec
Twofactors are particularly important: ommended unless they release a metered dose of the drug,
1. The duration of pain control necessaryto complete the not a steady uncontrolled dose. Sterilization of the spray
procedure and the possible need for posttreatment pain nozzle must be possible if a spray is used. Many pressurized
control (e.g.,after surgical procedures). Box4-1 lists topical anesthetic sprays are availablein metered form with
currently availablelocal anesthetic formulations by their disposable spray nozzles.
approximate duration of action-both soft tissue and EMLA(eutecticmixture oflocal anesthetics),a combina
pulpal anesthesia. tion of lidocaine and prilocaine, designedto provide cutane
2. The patient's physicalstatus (e.g.,American Societyof ous anesthesia before venipuncture, has been employed in
Anesthesiologists[ASA]classification),hypersensitivity, dentistry with some degree of success.22.z3
methemoglobinemia, or sulfur allergy,which may
preclude the use of some drugs.
For most patients, the duration of desired pain control is
VASOCONSTRICTORS
the ultimate deciding factor in local anesthetic selection, QUESTION: Are there any contraindications to the use of
because usuallythere are no contraindications to the admin vasopressors in dental patients?
istration of any particular agent.
Yes.Use of local anesthetics with vasopressors should be
QUESTION: What local anesthetics should be available in avoided or kept to an absolute minimum in the following
my office? cases24-26:
1. Patients with blood pressure in excessof 200 mm Hg
It is suggestedthat a number of local anestheticsbe available systolicor 115 mm Hg diastolic.
at all times. The nature of the dental practice will dictate the 2. Patients with uncontrolled hyperthyroidism.
number and types of local anesthetics needed. In a typical 3. Patients with severecardiovasculardisease.
dental practice, selectionof a local anesthetic formulation is a. Lessthan 6 months after myocardial infarction
based on the desired duration of pulpal anesthesia, for b. Lessthan 6 months after cerebrovascularaccident
example,lessthan 30 minutes, approximately60 minutes, in c. Daily episodes of angina pectoris or unstable
excessof 90 minutes. One local anesthetic preparation from (preinfarction) angina
each group, as necessitated by the nature of the doctor's d. Cardiac dysrhythmias despite appropriate therapy
practice, should be available. For example, the pediatric e. Post coronary artery bypass surgery,less than 6
dentist has little need or desirefor long-actinglocalanesthet months
ics such as bupivacaine, whereas the oral and maxillofacial 4. Patients who are undergoing general anesthesiawith
surgeon may have little need for shorter-acting drugs such halogenated agents.
as mepivacaine plain, but a greater need for bupivacaine. 5. Patients receivingnonspecific ~-blockers,monoamine
Remember that not all patients have similar local anesthetic oxidaseinhibitors, or tricyclicantidepressants.
requirements, and the same patient may require a different Patients in categories 1 to 3a through 3d are classifiedas
local anesthetic for a dental procedure of a different dura ASA4 risks and normally are not considered candidates for
tion. Amide local anesthetics are preferred to esters because electiveor emergency dental treatment in the office.(Refer
of their decreasedincidence of allergy. to Chapter 3 for a more detailed discussion;also seethe next
question.)
QUESTION: Do topical anesthetics really work?
QUESTION: Often medical consultants recommend
Absolutely,if the topical anesthetic preparation is applied to against inclusion of a vasopressor in a local anesthetic for
mucous membrane for an adequate length of time.19 The a cardiovascular risk patient. Why? And what can I do to
AmericanDentalAssociationrecommends a 1minute appli achieve effective pain control?
cation.20 The Food and Drug Administration recommends
application for a minimum of 1minute. Gilland Orr recom Asindicated,there are severalinstancesin which it is prudent
mend application for 2 to 3 minutes.21 Topical anesthetics to avoid the use of vasopressorsin local anesthetics.Most of
containing benzocaine are not absorbed from their site of these situations (e.g.,severelyelevated,untreated high blood
application into the cardiovascularsystem.Therefore risk of pressure; severecardiovasculardisease) also represent abso
overdose is minimal when benzocaine-containing topical lute contraindications to elective dental care because of
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CHAPTER21 Questions 383
greater potential risk to the patient. If a dental patient with block with an intravenous antianxiety agent (diazepam or
cardiovascular disease is deemed treatable (ASA 2 or 3), then midazolam) for sedation in place of general anesthesia.The
local anesthetics for pain control are indicated. The patient's local anesthetic usually contains a vasopressor such as epi
physician often states that, although local anesthetics can be nephrine in a 1: 100,000or 1:200,000concentration, added
used, epinephrine should be avoided. primarily to decreasethe rate at which the local anesthetic is
absorbed into the cardiovascular system, but also to mini
QUESTION: When should epinephrine be avoided? mize bleeding and prolong the duration of clinicalaction.
One of the fewvalid reasons for avoiding epinephrine is the QUESTION: Why is the use of vasopressorsin local anes
patient with cardiac rhythm abnormalities that are unre thetics recommended for cardiac risk patients?
sponsive to medical therapy. The presence of dysrhythmias
(especiallyventricular) usually indicates an irritable or isch Pain is stressfulto the body. During stress, endogenous cat
emic myocardium. Epinephrine, exogenousor endogenous, echolamines(e.g.,epinephrine, norepinephrine) are released
further increases myocardial sensitivity,thereby predispos from their storage sites into the cardiovascular system at a
ing this patient to a greater frequency of dysrhythmias or to level approximately 40 times greater than the resting level.
more significant types of dysrhythmias, such as ventricular (Referto Chapter 3 for a reviewof the pharmacology of this
tachycardia or ventricular fibrillation. In these patients, group of drugs.)
epinephrine-containing local anesthetics should be avoided, Releaseof epinephrine and norepinephrine into the blood
if at all possible.However,many cardiologiststoday do not increases the cardiovascularworkload; thus the myocardial
even consider the ischemic myocardium a valid reason for oxygenrequirement increases.In patients with compromised
excludingvasoconstrictors from local anesthetics, provided (partially occluded) coronary arteries, this greater myocar
the dose of epinephrine administered is minimal and intra dial oxygen requirement may not be met; ischemia may
vascular administration is avoided. developsubsequentlyand may lead to dysrhythmias,angina!
It is my recommendation that with a patient who is pain (if ischemia is transient), or myocardial infarction (if
deemed able to tolerate the stressesinvolvedin the planned prolonged). Increased cardiac workload may also lead to
dental treatment, a vasoconstrictor should be included in the acute exacerbation of heart failure (acute pulmonary
local anesthetic if there is a reason for its inclusion (e.g., edema). Elevated catecholamine levels can produce a dra
depth or duration of anesthesia, need for hemostasis). As matic increasein blood pressure;this can precipitate another
Bennett has stated,"the greater the medical risk of a patient, life-threatening situation (e.g., a hemorrhagic stroke [cere
the more important effective control of pain and anxiety brovascular accident {CVA},"brain attack"]).
becomes."27 Therefore the goal is to minimize endogenous catechol
amine release during dental therapy. The stress reduction
QUESTION: Why do many physicians still recommend protocol is designed to accomplish this. A local anesthetic
against the use of epinephrine (and other vasopressors) without vasopressor provides pulpal anesthesia of shorter
in cardiovascular risk patients? duration than the same drug with a vasopressor.Profound
pain control of adequate duration is lesslikelyto be achieved
Most physicians never, or at best rarely,use epinephrine in when a vasopressoris excludedfrom a local anesthetic solu
their practice. The only physicians who do so on a regular tion. If the patient experiences pain during treatment, an
basis are anesthesiologists,emergency medicine specialists, exaggeratedstress response is observed.
and surgeons. As used in medicine, epinephrine is almost With proper use (aspiration and slowinjection) of a local
alwaysused in emergencysituations.At those times, the dose anestheticwith minimum concentration of exogenousvaso
is considerably higher than that used in dentistry. The pressor (e.g., 1: 100,000,1:200,000),pain control oflonger
average emergency dose of intramuscular (IM) or N epi duration is virtually guaranteed, and the exaggeratedstress
nephrine (used in a 1: 1000or1:10,000 concentration) for response is avoided.Levelsof catecholaminein the blood are
anaphylaxis or cardiac arrest is 0.3 to 1 mg, whereas one elevated when exogenous epinephrine is administered, but
dental cartridge with 1: 100,000epinephrine contains only these levelsusually are not clinicallysignificant.
0.018 mg. An often repeated and essentiallytrue statement is that
Therefore it is understandable that many physicians, the cardiovascularlyimpaired patient is more at risk from
lacking an intimate knowledge of the practice of dentistry, endogenouslyreleasedcatecholaminesthan from exogenous
think of epinephrine in terms of the dosesused in emergency epinephrine administered in a proper manner.
medicine and not in the much more dilute forms used for
anesthesia in dentistry. QUESTION: Can I administer a local anesthetic with a
An examplefollows.In a hospital situation, a patient with vasopressor even if a physician has advised against it?
a serious cardiovascular problem (ASA4) who requires a
surgical procedure (e.g., emergencyappendectomy) may be Yes.A medical consultation is a request for advicefrom you
consideredtoo great a risk for generalanesthesia.Manyanes to a person with more knowledge of the matter being dis
thesiologists opt to use a regional local anesthetic (spinal) cussed.You are not obligated to heed this advice if you feel
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384 PART IV Complications, Legal Considerations, Questions, and Future
it may be inaccurate. If doubt persists in your mind concern that it should not be used for anypatient. Gingivalretraction
ing the proper treatment protocol following this initial con cord contains 8% racemic epinephrine. Half of this is the
sultation, additional opinions should be sought, preferably levorotatory form, which provides a concentration of active
from a specialist in the "area" of concern, such as a cardiolo epinephrine of 4% (or 40 mg/mL). This is 40 times the con
gist, an anesthesiologist, or a dental expert in local anesthe centration used in the management of anaphylaxisor cardiac
sia. Of course, for some patients, exogenous catecholamines arrest. Absorption of epinephrine through mucous mem
may prove too great a risk; in these cases, "plain" local anes brane into the cardiovascular system normally is rapid but
thetic solutions should be administered. is even more so with activebleeding, such as that occurring
It must always be remembered that the primary respon after subgingivaltooth preparation. Levelsof epinephrine in
sibility for the care and well-being of a patient rests solely in the blood rise rapidly, leading to cardiovascular manifesta
the hands of the person who performs the treatment, not the tions of epinephrine overdose {p.325).
one who gives advice. This increase in cardiovascular activity may prove to be
An incident concerning a medical consultation is worth lifethreatening in patients with preexistingclinicallyevident
relating. A periodontal graduate student was planning four or subclinicalcardiovasculardisease.
quadrants of osseous surgery on a patient whose medical
history was within normal limits, except for a torticollis for QUESTION: If Ielect not to use a vasopressor for a patient,
which she was receiving imipramine, a tricyclic antidepres which local anesthetics are clinicallyuseful?
sant. A written consultation was sent to the patient's physi
cian requesting that the patient be taken off the imipramine The clinicallyavailable local anesthetics are listed by their
before the surgical procedure was performed. The response duration of action in Box 4-1. Mepivacaine 3% (via nerve
was that the patient could not be taken off the drug, because block) can provide up to 40 minutes of pulpal anesthesiafor
it had taken longer than a year to get her medical condition the averagepatient, whereasprilocaine 4% (via nerve block)
stabilized. Moreover, it was recommended that epinephrine can provide up to 60 minutes.
be avoided during this patient's surgery. It was decided to
contact the physician directly to discuss the matter and to
attempt to explain the importance of epinephrine during the
SYRINGES
surgical procedure. In the ensuing conversation, it was agreed QUESTION: What type of syringe is recommended?
that epinephrine could be used, but in a limited dose, and that
the patient was to be monitored (vital signs) throughout the Although a wide variety of syringesare available,two factors
procedure. The surgery was carried off without incident. have primary importance in their selection:
The lesson to be learned from this episode is that the 1. A syringe must be capable of aspiration. Never use a
wording of the original consult was too constricting, or syringe that does not permit aspiration.
indeed might have been construed as threatening, to the 2. A syringe must be sterilizable,unless it is disposable.
physician. Whenever possible, direct contact and discussion In addition, with the introduction of so-called safety
with both parties explaining their needs should be obtained, syringes,it is my recommendation that every consideration
because this is more likely to lead to a satisfactory compro be givento the use of a syringethat is designedto minimize
mise and to better and safer patient management. the risk of accidental needle-stick after injection is com
pleted.Although the unit costof the disposablesafetysyringe
QUESTION: If epinephrine is used in cardiac risk patients, increasesofficeexpenses,the decreasedliability facedby the
is there a maximum dose? doctor in needle-stick injuries should more than cover this
consideration. Although in theory, safety syringes are man
Yes.Bennett recommends, and others agree, that the maxi datory, the lack of effectivedevices in the American dental
mum dose of epinephrine in a cardiac risk patient should be market has severelylimited implementation in clinicalprac
0.04 mg.27 This equates to roughly the following: tice. Traditional dental syringes continue to represent the
• One cartridge of 1:50,000epinephrine standard of care.
• Twocartridges of 1: 100,000epinephrine
QUESTION: Do computer-controlled local anesthetic
• Four cartridges of 1:200,000epinephrine
delivery systems (C-CLADs)work well enough to justify
I do not recommend the use of 1:50,000epinephrine for
their purchase?
pain control purposes. (Further information on dental man
agement of the cardiovascularrisk patient is available.P:") Yes.In most instances,C-CLADsenablethe patient to receive
effective local anesthesia in an entirely pain-free manner.
QUESTION: What about epinephrine-containing gingival Response from dentists using C-CLADsvaries from those
retraction cord? who are extremelyecstaticto those who do not feelthey are
worth the expense.Most responsesare favorable.In my expe
Racemic epinephrine gingival retraction cord should never rience, C-CLADsmake it easierto more comfortably deliver
be used for cardiovascularrisk patients, and it is my opinion those injections that are "difficult"to administer painlessly.
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CHAPTER21 Questions 385
These include all palatal injections and periodontal ligament QUESTION: Should local anesthetic cartridges be stored
(PDL) techniques. in alcohol or cold sterilizing solution?
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386 PART IV Complications, Legal Considerations, Questions, and Future
QUESTION: What causes cartridges to break during is one in which the patient's chest (heart) and head are paral
injection? lel to the floor with the feet slightly elevated. Presyncopal
episodesmay still occur (pallor,lightheadedness),but actual
1. Damage during shipping.Visuallycheck cartridges loss of consciousnessis extremely unlikely to develop with
before use. the patient in this position.
2. Using excessiveforce to engagethe aspirating harpoon After completion of severalmandibular injections (infe
in the rubber stopper. Proper preparation of the needle, rior alveolar,Gow-Gates mandibular, and Vazirani-Akinosi
cartridge, and syringe (see previous question) precludes mandibular nerve blocks), it is suggested that the patient
breakage caused by excessiveforce.When the needle is be returned to a comfortable,more upright position during
placed onto the syringe before the cartridge, it is the ensuing 5 to 10 minutes. This changein patient position
necessaryto "hit" the plunger to embed the harpoon appears to help speed the onset of mandibular block
into the rubber stopper. This may cause a cartridge to anesthesia.
shatter.
3. Attempting to force a cartridge with an extruded QUESTION: Whydo you {the author) recommend regional
plunger into the syringe. block anesthesia in the maxilla instead of infiltration
4. Using a syringewith a bent aspirating harpoon. {supraperiosteal) anesthesia?
5. Bent needle with an occluded lumen. Alwaysexpel a
small volume of anesthetic from the syringebefore Regionalblock anesthesiain the maxilla is preferred to infil
inserting the needle into the patient's tissues to ensure tration whenever more than two teeth are to be treated. Its
patency of the needle. advantagesinclude the following:
1. Fewerpenetrations of tissue, thus less likelihood of
postinjection problems.
2. Smallervolume of local anesthetic (e.g.,than for
TECHNIQUES OF REGIONAL ANESTHESIA multiple infiltrations of the same area), thereby
IN DENTISTRY decreasingthe risk of systemicreactions such as
QUESTION: What should always be done before local overdose.
anesthetic administration in a patient? 3. Clinicallyadequate anesthesia more likelywhen
infiltration is ineffectivebecause of the presence of
Reviewof the patient's medical history questionnaire (visu infection.
ally or verbally) and a physicalexamination, including vital
signsand visualinspection,are recommended when a patient QUESTION: Do palatal injections always hurt?
is seen for the first time or after a long absence from the
office.This identifiespossiblecontraindications to the use of No. Careful adherence to the protocol for atraumatic injec
local anesthetics or vasopressors and in general determines tions can do much to minimize any discomfort associated
a patient's ability to tolerate physicallyand psychologically with palatal anesthesia. In addition, the following are
the stressesof dental care without undue risk. important:
1. Topicalanesthesia.
QUESTION: What are medical contraindications to the 2. Pressure anesthesia.
use of local anesthetics and vasopressors? 3. Control of the needle.
4. Slowdeposition of solution.
These are discussed in Chapter 4 and in excellent review 5. Positiveattitude of the administrator.
articlesby Perusse,Goulet, and Turcotte.24-26 An area of considerable interest among practicing
dentists is palatal anesthesia and how to increase patient
QUESTION: Should a patient be advised that a local anes comfort. Over the years, I have received many devices
thetic injection will hurt before the injection is started? designedby dentists in an attempt to minimize or eliminate
pain during palatal injections, and I have been told of many
No. Local anesthetic injections need not hurt. Careful techniques. These include using vibrating wands, letting the
adherence to the atraumatic injection protocol described needle trace along the palate for a second or two so patients
in Chapter 11 can make virtually all injections, including know it is coming and it is not a "shock"to them, and avoid
palatal, painless. ing the use of palatal injections unless they are absolutely
necessary.
QUESTION: Is any specific chair position best for admin The clinicalintroduction of C-CLADs(seethe preceding
istration of local anesthetics? and Chapter 5) permits the deliveryof localanesthetic injec
tions in any area of the oral cavity in a pain-free manner in
Yes, absolutely! Because the most commonly observed most situations.
adverse reactions to local anesthetics are psychogenic (e.g., Research into the use of intranasally administered local
syncope), the position of choice during intraoral injections anesthetics has shown promising results. Pulpal anesthesia
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CHAPTER21 Questions 387
bilaterally from second premolar to second premolar was and other factors may be responsiblefor an increasedfailure
achieved in a Phase II clinical trial.31 rate on one side. The solution to this problem is to critically
evaluate one's technique on the less successfulside and to
QUESTION: Why do I miss inferior alveolar nerve blocks seek to correct it without interfering with success on the
more often than any other injection? opposite side. Patience is often necessary.
Of all nerve blocks in dentistry and, with few exceptions, QUESTION: How can I achieve adequate pain control
in medicine too, the inferior alveolar is the most elusive when gaining accessin pulpally involved teeth?
of consistent success. A success rate, bilaterally, of 85%
or greater indicates that one's technique is basicallycorrect. The recommended sequence of injection techniques for
However, many factors can, and do, affect this rate of pulpally involvedteeth follows:
success: 1. Local infiltration, if possible and not contraindicated.
1. Anatomic variation. It is well known that if any one 2. Regionalnerve block.
aspect of human anatomy is consistent, it is its 3. PDL injection, if not contraindicated by the presence of
inconsistency.Strict adherence to injection technique infection.
does not alwaysproduce adequate inferior alveolar 4. lntraosseous injection.
anesthesia. 5. Intraseptal injection.
2. Technical error. The most common technical error 6. lntrapulpal injection.
observed with the inferior alveolarnerve block is 7. Psychosedation,if pain control techniques have proved
insertion of the needle too low on the medial side of unsuccessfulin completelyblocking pain impulses from
the ramus (belowthe mandibular foramen, where the reaching brain.
inferior alveolarnerve enters onto the mandibular 8. Prayer... when nothing elseworks! However,with the
canal). A second common technical error is insertion of introduction of intraosseous anesthesia,this step is
the needle too far anteriorly (laterally)on the medial rarely,if ever,needed.
side of the ramus (thus contacting bone quite soon after The recent (2011) introduction of a method by which
penetration). local anesthetic cartridges can be consistentlybuffered to a
3. Accessory innervation. When isolated regions of pH of between 7.35 and 7.5 brings with it the expectation
mandibular teeth remain sensitivewhen all other areas that, along with increased comfort during injection and
are insensitive,the possibility of accessoryinnervation more rapid onset of anesthesia,the depth of anesthesiawill
should be considered.The technique used in be greater because more of the lipid-soluble RN ionic form
eliminating this problem (which usually is produced by of the localanestheticmoleculeis availableto diffusethrough
the mylohyoidnerve) is described in Chapter 14. the lipid-rich nerve membrane.36 Research projects in this
In September 2011, a supplement to the Journal of the area have been undertaken. Buffered local anesthetics are
American Dental Association, titled Is the Mandibular Block discussed in Chapter 20.
Passe?waspublished.32-35 It concludedthat although the time For all teeth in the mouth, with the probable exception
had not yet arrived to bid farewellto the traditional inferior of mandibular molars, clinicallyadequate pain control for
alveolar nerve block, sufficient alternative techniques are pulpal extirpation can be obtained with local infiltration or
available to enable the doctor to provide successful pain nerve block injection. Difficulties arise most often in the
control in the mandible in virtually all treatment situations: mandibular molars. A working knowledge of alternative
Gow-Gates,Akinosi-Vazirani,and incisive (mental) nerve mandibular anesthesia techniques, such as the Gow-Gates
blocks; intraosseous and periodontal ligament injections; mandibular block or the Vazirani-Akinosi mandibular
and the use of mandibular infiltration anesthesia in adults. block,33 increases the likelihood of obtaining anesthesia. In
These techniques are discussedin Chapters 14, 15,and 20. addition, the use of intraosseous anesthesiagreatlyincreases
successrates in mandibular molars,"
QUESTION: Why do I have a much higher failure rate Mandibular premolars and anterior teeth can be anesthe
with inferior alveolar nerve block on one side than on tized adequately for pulpal extirpation with the incisive
the other? nerve block.
Becauseof significantlydifferent operator positions during QUESTION: What special concerns are involved with local
administration of the inferior alveolarnerve block on con anesthesia in pediatric dentistry?
tralateral sides of the mouth, it is not uncommon for some
doctors to encounter significant differencesin their success Pain control generally is easier to achieve in pediatric den
rates. The inferior alveolaris the only intraoral nerve block tistry. However,two concerns should alwaysbe considered:
for which significantdifferencesin successrates are noted on 1. Increased potential for overdose existsbecause (most)
opposite sides of the mouth. Although basic protocols are children are smaller and weigh less than adults. Use
the same on the right and left sides, the view of the target milligram-per-weightformulas to minimize doses in
area as seen by the administrator, the angle of needle entry, children.
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388 PART IV Complications, Legal Considerations, Questions, and Future
2. Prolonged anesthesia can lead to traumatization of the 11. Weber JCP:Epidemiologyof adversereactions to nonsteroidal
lips and tongue, unless shorter-duration drugs are used, anti-inflammatory drugs. In Rainsford KD, Velo GP, editors:
and both patient and parent are warned of this possible Advances in inflammatory research, vol 6, New York, 1984,
complication. RavenPress,pp 1-7.
12. Hartnell NR, Wilson JP: Replication of the Weber effect using
A third concern relates to injection technique and the
postmarketing adverse event reports voluntarily submitted to
appropriate needle to be used in specifictechniques.A long
the United States Food and Drug Administration, Pharmaco
dental needle is recommended for the injections described therapy 24:743-749, 2004.
in this book for which a considerablethickness of soft tissue 13. WallensteimEJ,FifeD: Temporalpatterns of NSAIDspontane
is to be penetrated. The rationale for this is the rule of thumb ous adverseevent reports: the Weber effectrevisited,Drug Saf
that "a needle should not be inserted into tissue all the way 24:233-237, 2001.
to its hub, unless it is absolutelynecessaryfor the successof 14. Pogrel MA: Permanent nerve damage from inferior alveolar
that injection:' If it is possible for an injection technique to nerve blocks-an update to include articaine, J Calif Dent
be administered in a child with a short (=20 mm length) Assoc 35:271-273, 2007.
needle within the parameters of this rule, then use of this 15. Garisto GA,GaffenAS,LawrenceHP,et al: Occurrence of par
needle is warranted. Psychologically,however,the sight of a esthesia after dental local anesthetic administration in the
United States,J Am Dent Assoc 141:836-844, 2010.
long needle is more traumatic than the sight of a short
16. Availableat: www.lightningsafety.noaa.gov.AccessedOctober
needle (in point of fact, needles and syringes should always
2011.
be kept out of a patient's line of sight, if possible). 17. KatyalV:The efficacyand safetyof articaine versus lignocaine
in dental treatments: a meta-analysis, J Dent 38:307-317,
QUESTION: What is the recommended method of achiev 2010.
ing hemostasis in surgical areas? 18. YappKE,Hopcraft MS, Parashos P: Articaine: a review of the
literature, Br Dent J 210:323-329, 2011.
The recommended technique is local infiltration of a 19. Meechan JG: Intra-oral topical anaesthetics: a review,J Dent
vasopressor-containing anesthetic into the region of the 28:1-14, 2000.
surgery.Only small volumes are necessaryfor this purpose. 20. American Dental AssociationCouncil on Dental Therapeutics:
Epinephrine in a concentration of I : 100,000 is recom Accepted dental therapeutics, Chicago, 1984, The American
Dental Association.
mended (although I: 50,000also may be used).
21. Gill CJ, Orr DL: A double blind crossover comparison of
topical anesthetics,J Am Dent Assoc 98:213, 1979.
References 22. Gunter JB:Benefitsand risks oflocal anestheticsin infants and
1. Radowicka A, Kochmanski M, Zochowski RJ: Rare case of children, Paediatr Drugs 4:649-672, 2002.
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Kardiol Pol 24:237-242, 1981. mixture of lidocaine and prilocaine (EMLA) on the oral
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1986. 24. Perusse R, Goulet JP, Turcotte JY: Contraindications to
3. Mishima S, KasaiK,YamamotoM, et al: Cardiac arrest due to vasoconstrictors in dentistry: Part I. Cardiovascular diseases,
lidocaine, Masui 38:1365--1368, 1989. Oral Surg 74:692--697, 1992.
4. Gilbert TB: Cardiac arrest from inadvertent overdose of lido 25. Perusse R, Goulet JP,Turcotte JY:Contraindications to vaso
caine hydrochloride through an arterial pressure line flush constrictors in dentistry: Part II. Hyperthyroidism, diabetes,
apparatus, Anesth Analg 93:1534--1536, 2001. sulfite sensitivity, cortico-dependent asthma, and pheochro
5. Doumiri M, Moussaoui A, Maazouzi W: Cardiac arrest after mocytoma, Oral Surg 74:587--691, 1992.
gargling and oral ingestion of 5% lidocaine, Can J Anaesth 26. Perusse R, Goulet JP,Turcotte JY:Contraindications to vaso
55:882--883, 2008. constrictors in dentistry: Part III. Pharmacologic interactions,
6. YangJJ,Shen J, Xu J: Cardiac asystoleafter nasal infiltration of Oral Surg 74:592--697, 1992.
lidocaine with epinephrine in a transsphenoidal hypophysec 27. Bennett CR: Monheim's local anesthesia and pain control in
tomy patient with hypertrophic cardiomyopathy,J Neurosurg dental practice, ed 7, St Louis, 1984, Mosby.
Anesthesiol 22:81-82, 2010. 28. Anonymous: Cardiovascular effects of epinephrine in hyper
7. Haas DA,Lennon D: A 21 year retrospective study of reports tensive dental patients, Evidence Report: TechnologyAssess
of paresthesia followinglocal anesthetic administration, J Can ment (Summary) 48:1-3, 2002.
Dent Assoc 61:319-320, 343-326, 329-330, 1995. 29. SilvestreFJ,Verdu MJ, Sanchis JM, et al: Effects of vasocon
8. Hillerup S,JensenR:Nerve injury caused by mandibular block strictors in dentistry on systolicand diastolic arterial pressure,
analgesia,Int J Oral MaxillofacSurg 35:437-443, 2006. Med Oral 6:17--63, 2001.
9. Malamed SF: Nerve injury caused by mandibular block anal 30. YagielaJA:Adversedrug interactions in dental practice: inter
gesia.Letter to the Editor, Int J Oral MaxillofacSurg 35:876- actions associated with vasoconstrictors. Part V of a series,
877, 2006. J Am Dent Assoc 130:701-709, 1999.
10. PharmacovigilanceCommittee of the EuropeanUnion:Adverse 31. Ciancio S,Ayoub F,Pantera E, et al: Nasal spray for anesthesia
effectsfrom local anaestheticsused in relation with dental care of maxillaryteeth. Posterpresentation at International Associa
with a specialfocus on anaesthetics containing articaine, Case tion for Dental Research(IADR) General Session,July 14--17,
number 3200-1367, October 20, 2006. 2010, Barcelona,Spain.
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CHAPTER 21 Questions 389
32. Malamed SP.II the mandibular blodr. puaB 1Am Dent Alloc: 35. Mm:ban JG: Manclibular infiltration aaatbaia in ad1Jhl.
142(Suppl9):35-75, 2011. 1Am Dent Alloc: 142(Suppl9):1~ 2011.
33. Haaa D: Altanatiw: mandibular blodr.teclmiquea:a nvif:w of 36. Malamed SP: Bufrering local anathetic:a in ~ DSA
the Gow-Gata mandibular Dcrft block ami Akinos-Vazinni Pulle 44(1):3, 8-9, 2011.
clmed-mom:hmandibular Dcrft blodr.tedmiqua, 1 Am Dent
Alloc: 142(Suppl9):88-128, 2011.
34. Moon PA, Cuddy MA, Cooke MR. et al: lntraolleoua met
thelia teclmiquea: altmiatifts 1Dmandibular Dcrft b1oc:b,
1Am Dent Alloc: 142(Suppl9):13S-18S,2011.
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Index I
Note: Pagenumbers followedby "f" refer to illustrations; page numbers followedby "t" refer to tables; page numbers followedby "b" refer to boxes.
390
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allergic reactions/sensitivity (Continued) anatomy (Continued) areas anesthetized.See under specific technique
versus overdose,312t cutaneous nerves of face, 175f arthritis, 137
patient's claims of, 380 facialnerve distribution, 299f articaine HCl, 12t, 13f, 16t,2lt, 26b, 52, 53t,
predisposing factors, 326-328 hard palate, 185f 66t, 67f
prevention,328--332 mandible, 185--187,186f 2% with epinephrine, 66t
procaine, 57 mandibular nerve 4% with epinephrine, 72t
questions for evaluation of history of, branches of, 180f anesthetic half-life,65
328--332 pathway of, 181f by buccal infiltration in adult mandible,
signs/symptoms,327, 333-334 maxilla, 183-185 365-370
by classification,327t infratemporal aspect of, 185f mandibular infiltration, 366-369
dermatologic reactions, 333 maxillary nerve, 179f recent study findings, 366-370
generalizedanaphylaxis,333--334 nasal wall and pterygopalatine canal, 177f buccal infiltration versus lidocaine IANB,
respiratory, 336f neural, 350 369t
respiratory reactions, 333 orbit, 176f calculation of milligrams per dental cartridge,
skin responses,333 skull, 174f, 184f 58t
sodium bisulfite,328 trigeminal nerve, 169--183 chemicalformula, 65
testing for, 331-332 mandibular division (V3), 180--183 classificationof, 65
time of onset of symptoms of, 333 maxillary division (V2), 175--179 duration of anesthesia,48t, 65--67
topical anesthetics, 328 motor root, 169 effectivedental concentration, 65
allergies,history of, 136-137. See also allergic pathway of, 170f excretion of, 65
reactions/sensitivity sensory root, 169--183 FDAapproval of, 65
alpha (a) adrenergic receptors, 40, 43 variations in, 54, 56, 387 introduction of, 65
in epinephrine, 49 anemia, 137 versus lidocaine, 367
AlternativeStabident System,265f anesthetic half-life.See specific agents mandibular infiltration in adults (studies)
alternativesto techniques. See under specific angina pectoris, 145 with, 366-369
technique anterior middle superior alveolar (AMSA)nerve maximum recommended dose, 55t, 56b, 65,
American Dental Association (ADA) block 280t, 316t
Accepted Dental Therapeutics, 325--326 advantages,213--214 metabolism of, 65
color coding of cartridges, 101, 102t alternatives,214 onset of action, 65, 272t, 367t
HIPAAPrivacyKit, 345 anatomy of, 213f paresthesiawith use of, 296-297
syringe criteria, 78 area anesthetized,213, 213f pH of plain solution, 65
American Societyof Anesthesiologists(ASA) common names, 213 pH of vasoconstrictor-containing solution,
ASAPS {PhysicalStatus Classification complications,215 65
System),44-45, 60, 147t contraindications, 213 pl(..,65
(See also evaluation of patients) disadvantages,214 potency of, 65
PhysicalStatus ClassificationSystem(ASA failures of anesthesia,215 pregnancy classificationof, 65
PS), 44-45, 60, 133, 145-147, 146f,147t, indications, 213 prepared by, 65
382 injection site, 212f proprietary names, 73t
(See also evaluation of patients) nerves anesthetized,213 risk of nerve damage with, 381
ASA1, 146 positive aspiration rate, 214 safety during lactation, 65
ASA2, 146 precautions, 215 successof lidocaine versus, 272t, 367t
ASA3, 146-147 prepuncture technique, 214f topical anesthetic action, 65
ASA4, 147,382 safetyfeatures,215 toxicity of, 65
ASA5, 147 signs/symptoms,215 vasodilatingproperties of, 65
amide-type local anesthetics, 14, 14f,2lt, 26b syringe angulation, 215f artificialjoints, 139
biotransformation of, 28--29,315 technique, 214--215 ASA(American Societyof Anesthesiologists).
development of, 29t Wand/STAsystem,262b See American Societyof Anesthesiologists
duration of, 58--69 anterior superior alveolar (ASA)nerve block, (ASA)
(See also specific agents) 97, 178, 180f,197 ASA(anterior superior alveolar)nerve block.
hypersensitivityto, 327 for management of hematoma, 304 See anterior superior alveolarnerve block
interactions with inhibitors of metabolism, positive aspiration rate, 317-320 ASAPS. See PhysicalStatus Classification
147-148 antianxiety medications, 152b System(ASAPS)
malignant hyperthermia with, 36, 150--151 antibiotics, prophylactic, 135t ascorbic acid, 153
overdoseof topical, 317 anticonvulsant properties, 30--31,3lt aspirating syringes,83f
preference for, 73 antidepressant medications, 149b active, 119--121,119f
relativevasodilatingvalues,26t antidepressants,vasoconstrictors interaction harpoon devices,78
amines, sympathomimetic, 40b with tricyclic (SignificanceRating= 1), UltraSafe, 118-121
AMSA.See anterior middle superior alveolar 148 aspiration, 164.See also positive aspiration rate
(AMSA)nerve block antioxidants, 104 under specific techniques
analgesia,mechanism of, 33 antipsychoticsor adrenoceptor blockers, disengagementof harpoon from plunger
anatomy interaction with vasoconstrictors during, 90
anterior superior alveolar (ASA)nerve, 180f (SignificanceRating = 4), 149 gauge size and, 93
bifid mandibular canals, 183f antiseptics,topical, 110 harpoon-aspirating syringes, 165
blood and nerve supply to hard and soft antiviral agents, 308 importance of, 381
palate, 178f anxiety-relievingmedications, 152b percentage of dentists who aspirate before
cerebral circulation, 318f aphthous stomatitis, 307, 308f injection, 79t
cranial fossa, 173f apnea, 36 assessment.See evaluation of patients
cranial nerves, 170t, 171f-172f applicator sticks, 111, lllf asthma history, 136
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care and handling of syringes, 89 cellbody, 3-4 COLD (chronic obstructive lung disease),
after use, 120f cell-mediated allergicresponses,327t 136
bent harpoons, 89, 90f centbucridine, 26b, 29 combination products
bent needles, 90f central core theory, 365 articaine HCl with
broken cartridges, 89 central nervous system (CNS) 4% with epinephrine, 72t
disengagement of harpoon during aspiration, actions of local anesthetics on, 29-34 lidocaine with
90 blood levelsand actions of local anesthetics 2% with epinephrine, 60--61
inserting the cartridge, 114f on, 322f 2% without vasoconstrictor (Lidocaine
leakage during injection, 89, 90f depression of, 33f Plain), 59
retracting the piston, 114f effectsof local anesthetics on, 325f epinephrine, 59f,60, 60t
surface deposits, 90 excitation of, 32 mepivacaine HCl with
Carpules, 385. See also cartridges lidocaine toxicity and, 61 2% with levonordefrin, 72t
carticaine. See articaine HCl signs/symptomsof toxicity,3lb, 48, 2% with vasoconstrictor,62, 63t
cartridges, 80f, 101, l 14f.See also injections/ 322-323 3% without vasoconstrictor,61--62,62t
injection techniques; needles;syringes systemicactions on ( See under specific prilocaine HCl with
autoclaving, 104,385 agent) 4% with epinephrine, 72t
blister packs, 104, 105f uses/effectsof local anesthetics on 4% without vasoconstrictor,65t
broken,89, 108,386 (See specific agents; specificagents) procaine/propoxycaine,57-58
bubbles in, 105, 106f Centruroides scorpion venom, 13f procaine/propoxycaine,52
burning sensation on injection, 107 cerebral circulation, 318f procaine/procaine, 57-58
calculatingmilligrams of local anesthetic per, cerebral cortex, 33f complete conduction blockades, 19
58t, 103t channel entry, 13f complications.See also complications under
care and handling of, 104-105, 108f channel protocols, 9f specific type of anesthesia
color-coding of, per ADA, 102t channel specificity,9 aphthousstomatitis,308f
components of, 101-102, 102f charts. See documentation/records/charts burning on injection, 305
composition of solutions, 103t cheeks,retraction of, 111 causes of, 305
contamination of, 305 chemical configuration of local anesthetics, 12t, management of, 305
contents of, 103-104, 327t 15f,21t prevention of, 305
corroded caps, 106f-107f, 107 chemical formulas. See specific agents problems of, 305
cracked, 108f chemical nerve injuries, 350 edema,306-307
currently available,52 chemical structure. See specific agents causes of, 306
extruded stoppers, 105--107 chemotherapy,history of, 138 management of, 306-307
inserting, 114f chest pain (angina), 131-134 prevention of, 306
labels/labeling,102, 103f children. See pediatric dentistry problems of, 306
articaine, 67 chloride, 8 eye injuries, 197
changes in, 56 chloroprocaine, 16t,2lt, 26b, 28 facialnerve paralysis,299-300, 299f-300f
leakageduring injection, 107-108 chronic obstructive lung disease (COLD), cause of, 299-300
perforation of diaphragm, 385 136 management of, 300
plastic, 101 chronotropic effectsof local anesthetics,42 problem of, 300
plungers (stoppers, bungs), 102f circulatory system hematomas,200,283,303-304,303f
cautions for handling, 115f cerebral circulation, 318f causes,303
extruded, 108 transport of anesthesiathrough, 25 home care, 304
latex, 328 uptake rates into, 30 management of, 304
preparation of, 105f Class 1-6 ASAphysicalstatus classification prevention of, 303--304
problem of buffering in prefilled,358 system, 145-147 problems of, 303
product identification packageinserts, 105, ASA1, 146 risks for, 194f
106f ASA2, 146 herpes simplex lesion, 308f
removing used, 117f ASA3, 146-147 injecting into area of infection, 305
retracting the piston, 114f ASA4, 147 malignant hyperthermia (MH), 150--151
rust on caps, 107 ASA5, 147 malpractice per se, 341
sizesof, 102f classificationof local anesthetics needle breakage, 93, 96-99, 111-112,
sticky stoppers, 101, 107 biological, 11-12 292-294, 293f-296f, 293t
storage of, 305, 385 ClassA-D, 12t management of, 294
warmers, 104, 107 cause of effectsof ClassD, 11-12 prevention of, 294
catecholamines esters/arnides/quinoline,26b problem of, 293--294
endogenous, 383 by mode of action, 12t reports of, 292-293
releaseof, 40 by reaction with receptor sites, 11 needle-stick injuries, 113
synthetic, 39 by site of action, 12t nerve damage, 297t
catechol-0-methyltransferase (COMT), 43 clinicalactions of local anesthetics.See under pain on injection, 304--305
catechols,39 specific agents causes of, 304
cations (positivelycharged molecules), 16 clinicalapplications. See under specific agents management of, 305
C-CLAD.See computer-controlled local closed-mouth mandibular block. See Vazirani prevention of, 305
anesthetic deliverysystems;computer Akinosi closed-mouth mandibular block problems of, 304
controlled local anesthetic deliverysystems cocaine (benzoylmethyl ecgonine), 16t,25, 26b, paresthesia,297t
(C-CLAD) 34,69-70,370 with alveolarnerve block, 66
CCS (Comfort Control Syringe)System,88-89, drug interactions with, 149 with articaine, 66
88f--89f,89b habituation dangers, 33 risks of, 381-382
Celebrex (celecoxib),287t overdoses,70 studies on, 381
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complications (Continued) convulsive dose (CD100) and acid-base status, 32t diabetes, 138
postanesthetic intraoral lesions, 307-308 convulsive phase, 32 family history of, 137
causes of, 307-308 convulsive stage of action, 3 lf polydipsia in, 133
management of, 308 convulsive threshold (CD 100), 32t diarrhea, 132
prevention of, 308 core bundles, 19 dibucaine, 26b
problems of, 308 coronary arteries, systemic actions on. See under diclofenac potassium, 287t
postinjection infections, 110, 305-306 specific agent diffusibility, 17
causes of, 305 cotton gauze, 111, 112f diffusion of solution, 18--19
management of, 306 coughing, 132 rate of, 19
prevention of, 306 CPR certification, 353 dilution ratios. See specific agents
problems of, 305 cranial fossa, 173f diplopia, 133
prolonged anesthesia or paresthesia, 294-299 cranial nerves, 170t, 171f-172 f direct-acting sympathomimetic amines, 40,
causes of, 294-298 CN I (olfactory nerve), 170t 40b
management of, 298--299 CN II (optic nerve), 170t disadvantages of techniques. See under specific
prevention of, 298 CN III (oculomotor nerve), 170t technique
problem of, 298 CN IV (trochlear nerve), 170t discomfort of injections, studies on, 84--85
sloughing of tissues, 307, 307f CN IX (glossopharyngeal nerve), 170t disposable syringes, 82-83, 83b
causes of, 307 CN V (trigeminal nerve), 170t, 176f computer-controlled local anesthetic delivery
management of, 307 motor root, 169 systems (C-CLAD), 83-89, 85f, 212,
prevention of, 307 pathway of posterior trunk of mandibular 215-216,253,279,384-385
problems of, 307 nerve, 181f Comfort Control Syringe (CCS) System,
soft tissue injuries, 285 sensory root, 169--183 88--89, 88f--89f, 89b
causes of, 285-287 V1 (ophthalmic division), 169--175 STA-Single Tooth Anesthesia System
lips, 281, 282f, 302f V2 (maxillary division), 175-179, 176f (Wand/STA System), 84f, 88b, 96
management of, 280 V3 (mandibular division), 180--183 Wand/STA System (STA-Single Tooth
prevention of, 287-288, 303f CN VI (abducens nerve), 170t Anesthesia System), 84f, 85--88
problem of, 286-287 CN VII (facial nerve) plastic, 83f
self-inflicted, 68--69, 281 facial nerve distribution, 299f non--<:artridge-containing, 83
systemic (See systemic complications) paralysis of, 299, 300f safety syringes, 83, 83b, 113, 118--119, 384
trismus,240--241,301-302 CN VIII (vestibulocochlear (or auditory) dissociation constants, 16t, 20
causes of, 301 nerve), 170t distilled water, 104
management of, 301-302 CN X (vagus nerve), 170t distress, definition, 145
prevention of, 301 CN XI (spinal accessory nerve), 170t distribution patterns after absorption oflocal
problem of, 301 CN XII (hypoglossal nerve), 170t anesthetics, 27f
Compudent, 371 offace, 175f dizziness, 133
CompuFlo, 372-373 organs innervated by, 171f-172f documentation/records/charts
computer-controlled local anesthetic delivery type and function, 170t allergic reactions, 327-328
systems (C-CLAD), 83-89, 85f, 212, cranium, 176 recording injections, 167
215-216,253,279,356,372-373, criminal cases, 343. See also legal considerations doses
384-385 criteria for ideal local anesthetics, 2 maximum (See maximum dose under specific
Comfort Control Syringe (CCS) System, cross-sensitization, 70 agents; maximum recommended dose
88--89, 88f--89f, 89b crown preparation, 285 (MRD))
future trends, 356, 371-376 cutaneous nerves of face, 175f metered, 111
early devices, 372f CVS. See cardiovascular system (CVS) presentation of, 55
handpiece for, 372f cytoplasm, 4 DPS (dynamic pressure-sensing) technology, 85
STA-Single Tooth Anesthesia, 373f cytotoxic reactions, 327t drilling (for intraosseous anesthesia), 267f
handpiece for, 372f drowsiness, 32
pain-disruptive behavior trials, 373-374 drug allergies. See allergic reactions/sensitivity
Wand/STA System (STA-Single Tooth
D drug interactions, 351. See also adverse drug
Anesthesia System), 84f, 85-88, 88b, 96 damage,342-343 reactions (ADRs); systemic complications
COMT (catechol-0-methyltransferase), 43 if malpractice exists, 353-354 amide local anesthetics with inhibitors of
conduction velocity, St, 10 dendritic zone (peripheral process), 3-4 metabolism, 147-148
conscious sedation, 313f dental cartridges. See cartridges dental drugs with local anesthetics and
consent/informed consent, 332, 343-344, 344f Dental Furniture, Instruments, and Materials vasopressors, 139t
consultations, 130f, 384 (Obtunder), 253 local anesthetic-induced methemoglobinemia
contact lenses, 140 dental hygiene (Significance Rating= 4), 148
contraindications for local anesthetics. See also anesthesia for, 287-288 opioid sedatives with local anesthetics
side effects and overdose under specific local anesthesia map, 288f (Significance Rating= 1), 148
agents dental plexus, 178 overdose reactions due to, 314
articaine with epinephrine, 67 Dental Practice Act, 287 reduction of doses with known, 150
bupivacaine, 68--69 DentalVibe, 163f significance ratings for, l 48b
EMLA, 71 depolarization, !Of sulfonamides and esters (Significance Rating
local anesthetics and vasopressors, 386 phases of, 6-7 = 5), 148
malignant hyperthermia (MH), 150--151 wave of, 10 summation interactions (Significance Rating
medical problem and alternatives, 53t depressant action on myocardium, 34 = 1), 148
prilocaine, 49 desirable actions of local anesthetics, 311 vasoconstrictors, 49
relative/absolute, 28, 73 desirable properties of local anesthetics, 2 with adrenergic neuronal blockers
convulsant actions, mechanism of, 32 detoxification, 27-29 (Significance Rating = 4), 149-150
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Health Insurance Portability and Accountability history taking (Continued) history taking (Continued)
Act (HIPAA), 345-346 bleeding problems/bruising, 132 tobacco use, 140--141
administrative requirements, 345-346 blood transfusions, 139 tumors/cancer
"Business Associate Contract 'Ierms", blurred or double vision, 133 familyhistory, 137
345-346 cancer history, 138 patient history of, 137
Notice of Privacy Practices, 345-346 cardiac problems, 134-138 treatment history, 138
patients' rights, 345 heart attacks/heart defects, 134 radiation, 138
Privacy Rule, 345 heart disease, 134-138 VD/syphilis/gonorrhea, 137
privacy standards, 345, 346f heart murmur, 134 women
staff training registry form sample, 347f pacemakers, 140 birth control use, 141
heart rate prosthetic heart valves,138 pregnant/nursing, 141
assessing rate and rhythm, 143-144 chest pain (angina), 131-134 HN/AIDS, history of, 137
with local anesthetics contact lenses, 140 Hochman #2, 86f
(See specific agents) coughing, 132 Hochman #3, 87f
normal, 143t current pain, 131 Hochman #4, 87f
systemicactions on (See under specific agent) current treatment by physician, 131 Hochman #5, 88f
Heft-ParkerVisualAnalog Scale (H-P VAS), diabetes, 138 Hochman technique, 212
363 diarrhea/constipation/blood in stools, 132 hospitalizations,history of, 131, 139, 151
hematomas, 200, 283, 303-304, 303f.See also difficultyurinating/blood in urine, 133 H-P VAS(Heft-ParkerVisualAnalog Scale),
complications under specific nerve block dizziness,133 363
after bilateral mental nerve blocks, 303f dry mouth, 133 hubbing the needle, 292-293
causes,303 excessivethirst (polydipsia), 133 hydrocarbon inhalation anesthetics, 149
home care, 304 eye diseases,137 hydrolysis
management of, 304 fainting (vasodepressorsyncope), 133 enzymatic, 19
prevention of, 303-304 family history, 137 of esters,28, 28t
problems of, 303 frequent urination (polyuria), 133 metabolic, 28f
risks for, 194f frequent vomiting/nausea, 132-133 hydroxyl (OH) substitutions, 39-40
hemodialysis,patient letter for, 138b general health, 131 hygiene,dental, 287-288
hemoglobin, ferrous state of, 143 headaches, 133 hypercarbia, 32
hemorrhages health changes, 131 hyperesthesia,298
as cause of trismus, 301 herpes, 137 hyperresponders, 52-54
into/around neural sheaths, 296 high blood pressure (hypertension), 135 hypertension (high blood pressure), 135
soft tissue, 284 HN/AIDS, 137 hypertensivepatients, 44
hemostasis hospitalizations, 139, 151 hypoglossalnerve (CN XII), 170t
failure of, 212 jaundice, 133 hyporesponders, 52-54
needle gauge for depositing anesthetic for, joint pain/stiffness, 134 hypotension, 33
284 kidney or bladder diseases,137 hypotensiveeffects,33. See also specific agents
preferred solutions, 62 liver diseases,136
recommended solutions, 61 lung diseases,136
techniques for achieving,388 medical history questionnaire, 125-141
uses/effectsof local anesthetics allergicreactions, 328--331,331b IANB.See inferior alveolarnerve block (IANB)
(See specific agents) computer-generated, 125 ibuprofen, 286-287, 287t
hemostats (forceps), 111-112, 112f goals of, 124-125 IDDM (insulin-dependent diabetes mellitus),
Henderson-Hasselbalchequation, 16 importance of, 386 138
hepatic first-pass effect,26f. See also liver long form, 125 IM (intramuscular) administration, time to
function/dysfunction non-English versions, 131 achievepeak blood level,26t
hepatitis, 136 samples, 126f-129f immune complex reactions, 327t
herbal remedies, history of/current, 140 medications/over-the-counter medications/ impulses, 6
Herman Ostrow School of Dentistry (USC), natural remedies, 140 balance between inhibitory and facilitory,
145, 146f,157 other diseases/medicalproblems not listed, 3lf
herpes viruses 141-142 propagation of, 9-10, 1Of
herpes simplex lesion of palate, 307-308, prior problems with dental treatment, 131 impulse spread, 10--11
308f psychiatric care, 138--140 myelinated nerves, 10--11
history of, 137 recent hospitalizations, 131 unmyelinated nerves, 10
heterogeneous lipoprotein membranes, Sf recent weight loss/fever/nightsweats, 132 IN. See intranasal (IN) administration
hexylcaine,26b recreational drug use, 140--141 inactivation (extinction), 8
high blood pressure (hypertension), 135 rheumatic fever,134 inadequate anesthesia
high tuberosity approach, 220f ringing in ears (tinnitus), 133 acidification of tissue, 15
Hillerup paper, 381 seizures, 133 inflamed/infectedtissue, 17-18
HIPAA.See Health Insurance Portability and shortness of breath, 132 incisive (mental) nerve block, 247-251, 387
AccountabilityAct (HIPAA) sinus problems, 132 advantages,248
history taking. See also evaluation of patients skin diseases,137 alternatives,249
alcohol use, 141 stomach problems, 134 areas anesthetized,248, 249f
allergies,136-137 stroke/hardening of the arteries, 134-135 common names, 248-251
(See also allergicreactions/sensitivity) surgeries, 139-140, 151 complications,251
anemia, 137 swallowingproblems (dysphagia), 132 contraindications, 248
arthritis/rheumatism, 137 swollenankles, 132 disadvantages,249
artificialjoints, 139 thyroid or adrenal diseases,138 failures of anesthesia,251
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398 Index
incisive (mental) nerve block (Continued) infiltration techniques injections/injection techniques (Continued)
indications, 248 alternativesto, 225, 270, 365 maxillary anesthesia (See maxillary anesthesia
lingual anesthesia,248f articaine techniques)
lip retraction, 250f by buccal infiltration in adult mandible, multiple injections, 119
for management of hematoma, 304 365--370 multiple insertions, 98
nerves anesthetized,248 buccal nerve block, 274-275, 369t new techniques, 372
positive aspiration rate, 249, 317-320 mandibular infiltration, 366-369 painless technique for, 386
precautions, 251 recent study findings, 366-370 palatal injections, 386-387
safetyfeatures,250 benefits of, 271, 366 physiologicposition of patient, l 58f
signs/symptoms,250 buccal infiltration of mandibular posterior rate of injection, 380
technique, 249-250 teeth, 367 reaspiration, 165f
tongueretraction,248f lANBwith supplemental articaine recapping needle after use, 167f
incisors, 250t infiltration, 35 recommended needles for, 99t
indications for techniques. See under specific lingual infiltration injections, 88 resistance,98--99
technique mandibular (See mandibular infiltration in slow rate of injection, 318--319
indirect-acting sympathomimetic amines, 40, adults (studies)) speed of injection, 166
40b palate (See local infiltration of the palate) steps for
induction process studies on, 271, 274 Step 1:using sterilizedsharp needle,
concentration gradient during, l 9f studies on mandibular infiltration in, 157-158
methods,2 270--274 Step 2: checkingflow of anesthetic
induction time, 20 supraperiosteal (See supraperiosteal solution, 158
infections injections (local infiltration)) Step 3: deciding whether to warm syringe
edema produced by, 306 inflammation, effectson anesthesia of, 277 or cartridge, 158
effectson anesthesia of, 277 informed consent, 332, 343-344, 344f Step 4: positioning the patient, 158
injecting solution into area of, 305 infraorbital canal, 178-179 Step 5: drying the tissue, 158
postinjection, 110,305--306 infraorbital nerve block Step 6: applying topical antiseptic, 158--159
causes of, 305 advantages, 197 Step 7A: applying topical anesthetic, 159,
management of, 306 alternatives,197 159f
prevention of, 306 area anesthetized, 197, l 97f Step 7B:communicating with patient, 159
problems of, 305 common names, 197 Step 8: establishingfirm hand rest,
inferior alveolarnerve block (IANB),19,23, complications,200 159-162, 16lf
80--81,97, 182-183,226-233 contraindications, 197 Step 9: making tissue taut, 159f,162-163,
advantages,227 disadvantages,197 162f
alternatives,227-228 failures of anesthesia,200 Step 10:keeping syringe out of patient's
approaches to nerve, 225 indications, 197 line of sight, 163, 163f
areas anesthetized,227, 227f lifting lip, l 99f Step 1lA: inserting needle into mucosa,
biting injuries with, 359-360 for management of hematoma, 304 163
common names, 227-233 needle advancement, 199f Step 1lB: watching and communicating
complications,233 needle insertion, l 99f with patient, 163-164
contraindications, 227 needle position, 200f Step 12:injecting severaldrops of solution,
depth of penetration, 230f nerves anesthetized, 197 164
disadvantages,227 palpation of infraorbital notch, l 98f Step 13:advancing needle toward target,
facial nerve paralysiswith, 299-300 position of administrator, 198f 164
failure rates with, 232-233, 271, 387 positive aspiration rate, 197 Step 14:depositing drops of anesthetic
indications, 227 precautions, 200 before touching periosteum, 164
for management of hematoma, 304 safetyfeatures,200 Step 15:aspiration, 164-165, 165f
needle and syringeplacement, 230f signs/symptoms,200 Step 16A:depositing solution, 166
needle breakage during, 98 technique, 197-200 Step 16B:communicating with patient,
needle location, 230f inhaled non-volatile general anesthetics,for risk 166
nerves anesthetized,227 of malignant hyperthermia, 152b Step 17:withdrawing syringe, 166
osseous landmarks for, 228f inhibitory impulses, 3lf, 32, 33f Step 18:observing the patient, 164f,
overinsertion of needle, 23lf injections/injection techniques, 162f-163f.See 166-167
pediatric, 283 also cartridges; needles;syringes Step 19:recording injection on chart, 167
position of administrator, 229f appropriate needle use, 388 summary of, 168b
positive aspiration rate, 227, 317-320 broken cartridges, 108 supplemental (See supplemental injection
precautions, 231 burning sensation on injection, 107,385 techniques)
problems of, 356, 365 chair position, 386 technical errors, 387
pterygomandibular raphe, 228f changing direction of needle, 98 tissue preparation, 159f
reasons for missing, 387 contact with osseous tissue, 187 use as topical, 69
safetyfeatures,231 DentalVibe, 163f using multiple cartridges, 121
signs/symptoms,231 effectiveconcentrations for, 69t VibraJect,163f
successwith/without supplemental articaine, hand positions injection sites. See under specific technique
274t incorrect, 162f injuries/trauma
with supplemental articaine infiltration, 35 palm up/palm down, 160f biting/thermal/chemical,298
syringebarrel placement, 229f improper preparation, 385 eye injuries, 197,300
technique, 228-231 injecting into area of infection, 305 needle-stick injuries, 99, 304, 308
tongueretraction,232f leakageduring injection, 89, 90f to nerve sheaths, 294-296
trismus following,301 leakageof solution, 107-108 paresthesia due to, 294
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Index 399
injuries/trauma (Continued) intraosseous (IO) anesthesia (Continued) IO. See intraosseous (IO) anesthesia
self-inflicted,to lips, 68--69,281, 282f,302f, X-Tip,278f ion (sodium) channels, 8, lOf,35--36
349, 359, 360f,360t components, 265f transition stages,9f
soft tissue injuries, 285, 356 intraosseous injections, 264--268,278 ion-conducting stage,9f
causes of, 285--287 advantages,265 ionic forms of local anesthetics, 7t, 16,357
management of, 280 alternatives,266 ischemia,205f
prevention of, 287-288, 303f areas anesthetized, 265 of gingivaltissues, 307
problem of, 286-287 common names, 265 of palatal tissues,201f
innervations complications,268
of cranial nerves, 171f-l 72f contraindications, 265
(See also cranial nerves; specificnerves) disadvantages,266
of individual teeth, 178-179 duration of anesthesia,268 jaundice, 133
instrument-related, 348-349 failures of anesthesia,268 jet injectors, 80-81, 82b
alternative deliverysystems/techniques,349 indications, 265 MadaJet,82f
cartridges, 348 nerves anesthetized,265 SyriJetneedlelessinjector, 82f
needles, 348-349 periodontal ligament injections, 255f joint pain/stiffness, 134
syringes,348 positive aspiration rate, 266 Journal of the American Dental Association, 254
insulin-dependent diabetes mellitus (IDDM), precautions,267-268
138 safetyfeatures,267 K
interdental (perforating) branches, 179 signs/symptoms,267 ketorolac, 287t
intermediate duration local anesthetics, 52, 53b technique, 266-267
kidney function/dysfunction, 137,315
intracellular ionic concentrations, 7t intrapulpal anesthesia,279--280 elimination of local anesthetics by patients
intracutaneous allergytesting, 331-332 intrapulpal injections, 269--270,279--280 with, 29
IntraFlow HTP AnesthesiaDeliverySystem, advantages,269 patient letter for hemodialysis,138b
265, 266f,268b alternatives,269
kinetics of onset of action, 18-23
intraligamentary injections, 254f areas anesthetized, 269 diffusion of solution, 18
syringesfor, 254f canal access,270f induction, 19-20
intramuscular (IM) administration, 26t complications,270
intranasal (IN) administration, 356, 371f, contraindications, 269
386-387 disadvantages,269
L
devicefor, 371f duration of anesthesia,270 lacrimal nerve, 175
extent of, 370f failures of anesthesia,270 lactation, safety of local anesthetics during
future trends, 370-371, 370f-371f instrument, 269 articaine HCl, 65
intraoral challengetest, 331 needle insertion, 269f bupivacaine HCl, 68
intraoral lesions,postanesthetic, 307-308 nerves anesthetized,269 lidocaine HCl, 58
causesof, 307-308 perforation of lingual plate, 268f mepivacaine HCl, 61
management of, 308 positive aspiration rate, 269 prilocaine HCl, 63
prevention of, 308 precautions, 270 laryngeal edema, 335
problems of, 308 safetyfeatures,270 latex allergies,136-137
intraosseous (IO) anesthesia,253-268 signs/symptoms,270 legal considerations. See also legal
advantages,256 technique,269-270 considerations
alternatives,256 intraseptal injections, 262-264, 278-279 actual cause, 342
AlternativeStabident System,265f advantages,263 allergicreactions, 348
areas anesthetized,256 alternatives,263 chemicalnerve injuries, 350
common names, 256 areas anesthetized, 262, 263f consent/informed consent, 332, 343-344,
complications,258 common names, 262 344f
contraindications, 256 complications,264 criminal cases,343
disadvantages,256 contraindications, 263 damage, 342-343
drilling the hole, 267f disadvantages,263 drug interactions, 351
drill withdrawal, 267f duration of anesthesia,264 duty, 341
duration of, 258 failures of anesthesia,264 duty/breach of duty, 341
failures of anesthesia,258 indications, 263 emergencies,343
indications, 256 insertion site, 263f Health Insurance Portability and
IntraFlow HTP AnesthesiaDeliverySystem, needle orientation, 263f,279f AccountabilityAct (HIPAA),345-346
265, 266f,268b nerves anesthetized,262 administrative requirements, 345-346
needle insertion, 267f positive aspiration rate, 263 "BusinessAssociateContract Terms",
nerves anesthetized,256 precautions, 264 345--346
perforation site, 266f safetyfeatures,264 Notice of PrivacyPractices,345--346
periodontal ligament injection, 253-258 signs/symptoms,264 patients' rights, 345
positive aspiration rate, 256 technique,263-264 PrivacyRule, 345
precautions, 257 intravenous (N) administration, 26, 78-79, 317f privacy standards, 345, 346f
safetyfeatures,257 dose required for convulsiveactivity and staff training registry form sample, 347f
signs/symptoms,257 irreversiblecardiovascularcollapse instrument-related, 348-349
Stabident, 278f (dogs), 34t alternative deliverysystems/techniques,
components, 264f hazards of, 78-79 349
dosages/injectionsites,268t prevention of, 317 cartridges, 348
Stabident System,264 risk factors of, 380 needles,348-349
technique, 256-257 time to achievepeak blood level,26t syringes,348
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400 Index
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Index 401
mandibular teeth, 269 medical history questionnaire (Continued) metabolic effectsof agents, 41t. See also specific
average length, 19lt non-English versions, 131 agents
incisors, 274-275 samples, 126f-129f metabolic hydrolysis,28f. See also specific agents
mantle bundles, 19 medical status of patients, 49-50. See also metabolic pathways,29, 30f-31f
mantle fibers, 19 evaluation of patients metabolism of local anesthetics, 52-54. See
maxilla, 183-185, 185f medications, history of/current, 140 under specific agent; specificagents
anatomy, 183-185 membrane channels, 8-9, 9f-10f methemoglobinemia, 48, 153-154, 351
infratemporal aspect of, 185f membrane excitation, 8 acquired, 153
maxillary anesthesia techniques, 97, 188--189, depolarization, 8 causesof, 153
218-223 repolarization, 8 local anesthetic-induced (SignificanceRating
advantages, 219 membrane expansion theory, 12f = 4), 148
alternatives, 219 membranes signs/symptoms and management, 153-154
anterior superior alveolar nerve block, action oflocal anesthetics on, 13f methemoglobin levels,29
197-200 configuration of biological,Sf methylparaben, 104
area anesthetized, 219, 219f nerve cell,4-5 MetLifeDental, 125
branches of maxillary nerve, 179f organization of biological,4 MH. See malignant hyperthermia (MH)
common names, 219 mental (incisive)nerve block, 245 MHAUS(Malignant Hyperthermia Association
complications, 222 advantages,245 of the United States),36
contraindications, 219 alternatives,245 middle superior alveolar (MSA)nerve block,
disadvantages, 219 areas anesthetized, 245, 245f 195-197
failures of anesthesia, 222 complications,247 advantages, 195
field blocks, 188, 189f contraindications, 245 alternatives, 195
greater palatine canal approach, 220-222, disadvantages,245 area anesthetized, 195, 195f
220f-221f failures of anesthesia,247 branches, 178
high tuberosity approach, 219-220, 220f indications, 245 complications, 197
indications, 219 locating the mental foramen, 246f-247f contraindications, 195
local infiltration, 188, 189f for management of hematoma, 304 disadvantages,195
middle superior alveolar (MSA) nerve block, needle penetration site, 247f failures of anesthesia, 196
195-197 nerves anesthetized,245 indications, 195
nerve block, 188, 189f position of administrator, 246f needle penetration, 196f
nerves anesthetized, 219 positive aspiration rate, 245, 317-320 needle position, 195f
palatal anesthesia (See palatal anesthesia) precautions, 247 nerves anesthetized, 195
pediatric, 283 safetyfeatures,247 position of administrator, 196f
posterior superior alveolar (PSA)nerve signs/symptoms,246 positive aspiration rate, 195
block, 191-195 technique,245-246 precautions, 196
precautions, 222 mepivacaineHCl, 12t, 13f,16t,21t,26b, 30-31, safety features, 196
recommended volumes for, 223t 52, 53t, 61t, 62f signs/symptoms, 196
safetyfeatures,222 2% with levonordefrin, 72t technique, 195-196
signs/symptoms,222 2% with vasoconstrictor,62, 63t mixed-acting sympathomimetic amines, 40b
Stabident dosages,268t 3% without vasoconstrictor,61--62,62t mixing pens, 358f
supraperiosteal injections, 189-191 anesthetic half-life,61 modes of action, 14.See also specific agents
maxillary nerve, 179f calculation of milligrams per dental cartridge, classificationof local anesthetics by, 12t
maxillary teeth, 269 58t theories of, 3
availablelocal anesthetic techniques, 223t chemicalformula, 61 vasoconstrictors,40
averagelength, 19lt classificationof, 61 molars
problems of anesthesia on, 270 duration of anesthesia,48t, 54t, 61--62,72t availabletechniques, 250t
maxillofacialand oral surgery,284-285 effectiveconcentrations for, 61, 69t removal of third, 321t
maximum recommended dose (MRD), 55-57, excretion of, 61 molecular weights of local anesthetics, 21t
55t, 280t. See also maximum dose under FDAapproval of, 61 monoamine oxidase (MAO) inhibitors
specific agents withlevonordefrin,280t generic and proprietary names, 150b
calculating,56, 56b maximum recommended dose, 55t, 56b, 61, vasoconstrictors interaction with
drug formulations, 316t 316t (SignificanceRating= 5), 150
factors for calculating onset of action, 61 mood elevation,33-34
age of patient, 316 overdoses,62 motor neurons, 4
physicalstatus of patient, 316 pH of plain solution, 61 Motrin, 287t
weight of patient, 316 pH of vasoconstrictor-containing solution, 61 MRD.See maximum recommended dose (MRD)
mechanisms of action pK.., 61 MSA.See middle superior alveolar (MSA)
anticonvulsant properties, 31 potency of, 61 nerve; middle superior alveolar (MSA)
convulsivephase, 32 pregnancy classificationof, 61 nerve block
local anesthetic molecules, 17f prepared by, 61 mucous membranes
sequence of, 14 proprietary names, 73t absorption of local anesthetics through, 315
medical consultation request form, 130f safetyduring lactation, 61 buffering capacity of, 18
medical history questionnaire, 125-141. See also topical anesthetic action, 61 multiple needle penetration, nasopalatine nerve
history taking toxicity of, 61 block
computer-generated, 125 vasodilating properties of, 61 advantages,210
goals of, 124-125 mepivacaineplain, maximum recommended complications,210
importance of, 386 dose, 280t disadvantages,210
long form, 125 Merthiolate (thimerosal), 110 failures of anesthesia,210
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402 Index
multiple needle penetration, nasopalatine nerve needles (Continued) nerves. See also specific nerve OT nerve block
block (Continued) bent, 90f impulses, 6
precautions, 210 breakage of, 93, 96-99, 111-112, 292-294, normal functioning, 16
safetyfeatures,21O 293f-296f, 293t, 349 peripheral, 5t
signs/symptoms,210 management of, 294 nerves anesthetized. See under specific agent OT
technique, 208-210 prevention of, 294 technique
muscle paralysis,36 problem of, 293-294 nerve sheaths, 18
muscle relaxants, 152b reports of, 292-293 diffusion of local anesthetic through, 16-17
muscle spasms. See trismus care and handling of, 97-98, 166 trauma to, 294-296
myelinated axons, lOf recapping, 113, 116f,167f nerve supply to hard and soft palate, 178f
myelinated nerve fibers,5--6,6f contamination of, 305 neural anatomy, 350
mylohyoidnerve branches, 182 deflection of, 93f, 95-96 neural penetration, 350
myocardium, effectsof local anesthetics on, 34. bi-rotational insertion technique (BRIT), neuron pathways,32
See also under specific agent; specific 95-96,96f neurons, 3--4
agents BRIT (bi-rotational insertion technique), axonal process of, 4
95-96 inhibitatory/excitatory activity,32
in hydrocolloidtubes, 94t motor,4
N disposable,93f, 157-158, 293f multipolar motor/sensory neurons, 4f
NaHC03 (sodium bicarbonate), 357-358 disposal of, 97, 97f, 118f,167f unipolar sensory neurons, 4f
Naprosyn (naproxen sodium), 287t fishhook barbs on, 157 NH2 amine groups, 39--40
narcotics, 152b gauges of, 80, 92-96 NIDDM (non-insulin-dependent diabetes
nasal wall color-coding by,92, 94f mellitus), 138
anatomy, 177f determination of, 158 nodes of Ranvier,5-6, 6f, 10-11, 13
and pterygopalatine canal, 177f larger versus smaller,94b nondepolarizing nerve block, 14
nasociliarynerve, 175 specificationsfor, 95t nondisposable syringes,78--82
nasopalatine nerve block, 205--210 hubbing the needle, 292-293 breech-loading
advantages,206 injection techniques, 99t metallic
alternatives,206 injuries to patients or administrators, 99 cartridge-type aspirating, 78, 79f
application of topical anesthesia,207f,209f insertion of, 96-97 cartridge-type self-aspirating,78-80,
area anesthetized,206, 206f, 21Of lengths of, 96-97, 96t, 97f,294, 385, 388 79b,81b
common names, 206 nondeflecting, 94f,95 plastic, cartridge-type, aspirating, 78, 79b
contraindications, 206 pain harpoon-type aspirating, 79f
disadvantages,206 on insertion of, 98 jet injectors, 80-81, 82b
hand stabilization,2lOf on withdrawal of, 99 MadaJet, 82f
indications, 206 palm-thumb grasp, 95f SyriJetneedlelessinjector, 82f
multiple needle penetration preparation of, 385 pressure syringes,80-81, 8lf, 82b
advantages,21O recommendations for using, 99, 99t, 385 non-insulin-dependent diabetes mellitus
complications,210 reusable, 92 (NIDDM), 138
disadvantages,210 safetyneedles, 92 nonmyelinated axons, lOf
failures of anesthesia,210 screwingonto syringe, 116f nonnervous tissue, diffusibilityof, 23t
precautions, 210 studies, 93 nonselectivebeta-adrenoceptor antagonists,
safetyfeatures, 210 trauma caused by, 308 vasoconstrictors interaction with
signs/symptoms,210 types of, 92 (SignificanceRating= 1), 148--149
technique, 208--210 U.S.dentistry purchases of, 94t nonsteroidal antiinflammatory drugs (NSAIDs),
needle penetration, 207f use of EMLAfor patients with phobias, 71 286, 287t
nerves anesthetized,206 needle-stickinjuries, 113 Noradrenalin. See norepinephrine
patient position, 207f negativeaspiration, 165f (Levarterenol)
position of administrator, 207f negligence,341 norepinephrine (Levarterenol)
positive aspiration rate, 206 Neo-Cobefrin. See levonordefrin availabilityin dentistry, 46
single needle penetration, 208--210 (Neo-Cobefrin) chemical structure, 45, 45f
complications,208 Neo-Synephrine.See phenylephrine HCl maximum doses,46
failures of anesthesia,208 (Neo-Synephrine) mode of action, 45
precautions, 208 nerve blocks. See specific nerve block proprietary names, 45
safetyfeatures, 208 nerve branches, mylohyoid, 182 risks of using, 42
signs/symptoms,208 nerve cell membranes, 4-5 source, 45
technique, 206-208 nerve conduction, 6-7 systemicactions, 45--46
target area, 206f nerve damage, 297t, 381-382 blood pressure, 45
nausea, 132-133 nerve fibers, 19t cardiovasculardynamics,45
needle adapters, 118f classes,5t central nervous system (CNS), 46
needle cap holders, 116f myelinated, 5-6, 6f coronary arteries, 45
needles. See also cartridges; injections/injection unmyelinated, 6f heart rate, 45
techniques; syringes nerve injuries/damage,294-296, 297t metabolism of, 46
anatomy of, 92, 93f facialnerve paralysis,299--300,299f-300f myocardium, 45
bevel, 92, 95--96 cause of, 299-300 pacemaker cells,45
cartridge-penetrating end, 92 management of, 300 respiratory system,46
hub,92 problem of, 300 side effectsand overdose,46
shaft, 92 lingual nerve, 350 termination of action and elimination, 46
attachment of, 82 risk of, 381-382 vasculature,45
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404 Index
parotid gland injuries, 300 peripheral process (dendritic zone), 3-4 physicalevaluation, 12S-131, 142-14S,382. See
patient charts. See documentation/records/ pH also evaluation of patients; history taking
charts alkalinization (devating), 15--16 for atypical plasma cholinesterase,1Sl-1S2
patient evaluation. See evaluation of patients burning sensations on injection, 107 determination of risk, l 4S
patient refusal of local anesthesia,344 clinicalapplications of, 18 dialogue history, l 4S
pattern of distribution after absorption, 27f of convulsant doses, 32t drug-drug interactions (See drug
pCO,,effectsof, 32t of dental cartridgeswith vasopressor,103-104 interactions)
PDL. See periodontal ligament (PDL) injections effectof decreasedtissue pH, l 7f for IIlalignanthyperthermia (MH), lSO-lSl
PDR (Physician's Desk Reference), 342 elevating (alkalinization), 15--16 for methemoglobinemia, 1S3--1S4
peak blood level,time to achieve,26t importance to atraumatic injections of, 1S7 for specificmedical disorders, l4S
peak plasma levels,with and without increasing, 3S6-3S7 vital signs, 142-14S
vasopressor,3St local anesthetics without vasoconstrictors, 18 PhysicalStatus ClassificationSystem(ASAPS),
pediatric dentistry, 280--284 of plain solution 44-4S, 60, 133, 14S-147, 146f,147t,382.
biting injuries with IANB,3S9-360 (See specific agents) See also evaluation of patients
bone density,282-283 for pulpal anesthesia,277-278 ASA 1, 146
bupivacaine use, 68--69 of vasoconstrictor-containing solution ASA2, 146
choice of anesthetics, 281t, 319 (See specific agents) ASA3, 146-147
clinicaltrials for reversalof soft tissue pharlllacokinetics,2S-29 ASA4, 147,382
anesthesia,361-363 distribution, 27 ASAS, 147
complications,281-282 excretion,29 physicochemicalproperties of local anesthetics,
dentition of 4-year-old child, 282f metabolism, 27-29 20, 2lt
factors in risk of overdose,3l 9b uptake, 25--26 physiologiceffectsof local anesthetics, SS
fatalities,280 pharmacologic properties of local anesthetics, physiology
health history questionnaires, 127f 2lt dectrophysiology (See dectrophysiology)
lip trauma, 282f,360t PharmacovigilanceCommittee of the European nerve conduction, 6-7
local anesthetics of choice, 3l 9t Union, 296-297, 381 peripheral nerves, St, 6
local anesthetic usage survey,28lt Hillerup paper, 381 piroxicam, 287t
maximum recommended doses, 280 phentolamine mesylate (OraVerse),3S9-36S pK., l 6t, 23t
normal height and weight, 144 availabilityof, 361 local anesthetics with high/low, 17
NSAIDdosagesfor adolescents,287 candidates for use of, 36Sb values, 14
overdoses,280--281,319 chemicalformula, 362f pK.. See specific agents
pain-disruptive behavior trials, 373-374 clinicaleffectsof, 361 placenta, 27
prevention of lip trauma, 303f clinicaltrials for reversalof residual soft plain solutions, 103t
risk factors, 281b tissue anesthesia (STA),3S9-363 plasma cholinesterase,atypical, 1Sl-1S2
special concerns for, 387-388 clinicalindications for use of, 364 plasma concentrations in target organs, 27
techniques, 282-284 clinicaluse in dentistry of, 36S plungers (stoppers, bungs)
mandibular anesthesia,283-284 efficacyof, 363-364 cautions for handling, 1lSf
maxillary anesthesia,283 Functional AssessmentBattery (FAB),363 extruded, 108
volume of solution administered, 319 Heft-ParkerVisualAnalog Scale(H-P latex, 328
penetration depth. See specific nerve block VAS),363 polydipsia (excessivethirst), 133
technique; specificnerve block technique lip and tongue palpation, 363 polyuria (frequent urination), 133
perforating (interdental) branches, 179 safety of, 364 position of administrator of local anesthetics
peridental injections, 2S3,2S4£ See also STARquestionnaire, 363 buccal nerve block, 23Sf
periodontal ligament (PDL) injections mandibular, 364t greater palatine nerve block, 203f
perilernma, l 9t maxillary,364t inferior alveolarnerve block (IANB),
perineurium, 19t medical uses of, 361 229f
periodontal ligament (PDL) injections, 80--81, OraVersecartridge, 362f infraorbital nerve block, 198f
86--88,97-98, 179,2SSf,279 residual soft tissue anesthesia (STA),3S6 mental (incisive)nerve block, 246f
areas anesthetized,2S6f phenylephrine HCI (Neo-Synephrine),47 middle superior alveolar (MSA)nerve block,
complications,2SS availabilityin dentistry, 47 196f
dynamic pressure-sensing (DPS) technology, chemical structure, 47, 47f nasopalatine nerve block, 207f
37Sf clinicalapplications,47 posterior superior alveolar (PSA)nerve
injection sites,2S7f maximum doses, 47 block, 193f
needle breakage during, 98 mode of action, 47 position of patient. See under specific
new perspectiveson, 373 rebound effects,49 technique
safetyof, 2S4 risks of using, 42 positive aspiration rate, 16Sf.See under specific
STA-intraligamentary,2S3--268 systemicactions technique
studies on, 87 blood pressure, 47 postanesthetic intraoral lesions,307-308
syringes,8lf cardiovasculardynamics,47 causesof, 307-308
speciallydesigned for, 2S4f,2SS central nervous system (CNS),47 management of, 308
use of conventional,2SS-2S6 coronary arteries, 47 prevention of, 308
periodontics, 284 heart rate, 47 problems of, 308
peripheral circulation, 41t metabolism of, 47 posterior superior alveolar (PSA)nerve block,
peripheral nerves myocardium, 47 177-178, 191-19S
classificationof, St pacemaker cdls, 47 advancement of needle, 193f
composition of nerve fibers and bundles in, respiratory system,47 advantages, 192
19f side effectsand overdose,47 alternatives, 192
organization of, 19t termination of action and dimination, 47 area anesthetized, 192, 192f
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Index 405
posterior superior alveolar (PSA) nerve block prevention. See complications (main entry) and prolonged anesthesia or paresthesia (Continued)
(Continued) complications under specific type of prevention of, 298
common names, 192 anesthesia problem of, 298
complications, 191-192, 195 prilocaine HCl, 12t, 13f,16t, 21t, 26b, 52, 53t, prophylaxis.See also risk factors
contraindications, 192 64f,64t antibiotics, 135t, 138--139
disadvantages,192 4% with epinephrine, 72t for cardiac conditions, 135b
failures of anesthesia, 194 4% without vasoconstrictor,65t orthopedic, 140t
indications, 192 anesthetic half-life,63 propitocaine. See prilocaine HCl
length of needle, 194f calculation of milligrams per dental cartridge, propoxycaine HCl, combined with, with
for management of hematorna, 304 58t procaine HCl, 57-58
needle placement, 192f chemicalformula, 63 propoxycaine HCl, 16t, 26b, 57. See also specific
nerves anesthetized, 192 classificationof, 63 agents
position of administrator, 193f clinicalactions of, 48 anesthetic half-life,57
positive aspiration rate, 192,317-320 duration of anesthesia,48t, 54t, 72t chemicalformula, 57
precautions, 194 effectivedental concentration, 63 classificationof, 57
safetyfeatures, 194 with epinephrine, 280t effectivedental concentration, 57
signs/symptoms, 194 excretion of, 63 excretion,57
technique, 192-194 FDAapproval of, 63 metabolism of, 57
tissue retraction and needle orientation, maxim.urnrecommended dose, 55t, 63, 316t onset of action, 57
193f metabolic pathways,3lf pH of plain solution, 57
postinjection infections, 110,305-306 metabolism of, 63 potency of, 57
causesof, 305 onset of action, 63 prepared by, 57
management of, 306 pH of plain solution, 63 topical anesthetic action, 57
prevention of, 306 pH of vasoconstrictor-containing solution, 63 vasodilatingproperties, 57
problems of, 305 pl(..,63 propranolol, 351
postoperative pain management, 287b potency of, 63 proprietary names of agents. See specific agents
postprocedural evaluations,351-352 pregnancy classificationof, 63 prosthetic heart valves,138
postseizure (postictal) phase (overdoses), prepared by, 63 prosthodontics, fixed,285
324-325 proprietary names, 73t protein binding, 20, 21t, 23t
postsurgical pain management, 285-287 safetyduring lactation, 63 proteins, classificationof, 4-5
protocol for perioperative and postoperative signs/symptomsof toxicity,48 proximate cause, 342
pain control, 286-287 topical anesthetic action, 63 PSA See posterior superior alveolar (PSA)
regimens for, 68 toxicity of, 63 nerve block
potency of local anesthetics. See specific agents vasodilating properties of, 63 pseudocholinesterase,28
povidone-iodine (Betadine), 110 prilocaine plain, 280t psychogenicreactions, 351
practice management privacy rule (HIPAA),346f eroticism, 351
avoidanceof private treatment of patients, procainamide, 14, 16t psychologicalissues.See also evaluation of
351 sedation/drowsiness,31-32 patients
business associatecontract sample, 346f uses of, 34 adversedrug reactions due to, 314
business associates,345-346 procaine HCl, 14, 16t, 21t,26b, 30 antianxiety medications, 152b
Dental PracticeAct, 287 anesthetic half-life,57 antidepressant medications, 149b
local anesthetics to have in office,382 chemicalformula, 57 goals of evaluation of, 124-125
postsurgery follow-up,287b classificationof, 57 psychiatric care history, 138--140
post-treatment follow-up,352 combined with, with propoxycaineHCl, psychogenicreactions to local anesthetics,
staff training registry form sample, 347f 57-58 124
precautions. See under specific technique duration of anesthesia,57 temperature of metal syringes, 158
preconvulsivesigns/symptoms,31-32, 31b anesthetic half-life,57 pterygopalatine canal, 177f
preconvulsivestage of action, 33f effectiveconcentrations for, 69t pterygopalatine fossa, 176-178, 177f
pregnant patients, 141 effectivedental concentration, 57 branches, 176f
adversedrug reactions in, 314 excretion,57 pterygopalatine nerves, 177
fetal effectsof drugs, 14lt hypotensiveeffects,33 branches, 177-178
pregnancy classificationsand safety metabolic hydrolysisof, 28f pulpal (hard tissue) anesthesia,62, 223. See also
articaine HCl, 65 metabolism of, 57 infiltration techniques; intraosseous
bupivacaine HCl, 68 onset of action, 57 anesthesia;intrapulpal injections;
FDArisk categories, 141b pH of plain solution, 57 periodontal ligament (PDL) injections;
lidocaine HCl, 58 pH of vasoconstrictor-containing solution, 57 regional block anesthesia in maxilla
mepivacaineHCl, 61 pl(.., 57 achieving adequate pain control, 387
prilocaine HCl, 63 potency of, 57 associatedsoft tissue anesthesia,359
premature ventricular contractions (PVCs),34, topical anesthetic action, 57 duration of, 48, 52, 53b, 54t, 72t, 282t
42-43, 144 toxicity,57 vasoconstrictors,48t
prernaxilla, 184-185 uses of, 25 failure rates, 274
premolars, availabletechniques, 250t vasodilating properties, 57 mandibular teeth, 250t
preparation of agents. See under specific product identification packageinserts, using posterior superior alveolar (PSA)nerve
agents cartridges, 105, 106f block, 191
preparation of syringes, 119f-120f,385 prolonged anesthesia,388 pulpal extirpation, 277-278, 387
pressors. See vasoconstrictors (vasopressors) prolonged anesthesia or paresthesia,294-299 pulse, 143-144,338f
pressure devices,81, 254f causesof, 294-298 PVCs(premature ventricular contractions), 34,
pressure syringes,80-81, 81f, 82b management of, 298-299 42-43, 144
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406 Index
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Index 407
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408 Index
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Index 409
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