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⚪ Since tissue pH in the inflamed area can fall below 6
(Schade etal.1921; De Jong and Cullen1963) (normal pH is 7.4), there is little free base left for the anesthetic to penetrate the cell membranes (Bieter1936;
de Jong1977).
⚪ Vasodilation in the inflamed area favors rapid elimi-
nation of the anesthetic solution (Kramer and
Mitton1973; Meechan1999).
⚪ Other factors (see Chapter19).
2) Injection can favor the diffusion and spread of the infec-
tion to neighboring tissue if the injection is into deep
tissue and/or under pressure (Kramer and Mitton1973).
Furthermore, injection of epinephrine leads to hypoxia
and reduced blood flow, thus reducing defenses in this
area (Tran etal.1985).
In these cases, an antibiotic is generally administered for
a few days to control the acute phase. The dental procedure
is then performed with anesthesia. In some cases, we can
administer local infiltrative anesthetic gently in areas
affected by abscesses to lance and drain them
(Nordenram 1971). The contraindication is relative in
these cases.
ImpossiblePhysicalAccess
It is sometimes impossible to reach the patient’s mouth to
administer local anesthetic, for example in patients with
severe motor dysfunction caused by cerebral palsy (Hulland
and Sigal2000), advanced Parkinson disease, or with very
severely restricted mouth opening (trismus) (Tyrer1999).
Intraoral local anesthetic techniques are absolutely
contraindicated in these cases.
Summary
● Lack of cooperation on the part of the patient → tech-
niques involving dental local anesthesia are
contraindicated.
● Patients in poor health classified as ASA IV → techniques
involving dental local anesthesia are contraindicated.
● Severe clotting disorders:
⚪ Oral anticoagulants with INR >4 → truncal block and
lingual infiltrations are contraindicated.
⚪ Platelet count <30 000 → truncal block and lingual
infiltrations are contraindicated.
⚪ Hemophiliacs with clotting factor <30–50% → truncal
block and lingual infiltrations contraindicated.
● Infection at the injection site → relative
contraindication.
● Physically impossible access owing to severe motor dys-
function (advanced Parkinson disease, cerebral palsy,
etc.) or very compromised ability to open the mouth
(trismus)
contraindicated.
→ intraoral dental local anesthesia is
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9
Contraindications forLocal Anesthetics
Not all anesthetic drugs have the same characteristics,
therefore in this chapter we address those cases and
circumstances where a specific anesthetic cannot be
administered or where there may theoretically be an interaction. The chapter is divided into two parts: relevant contraindications, which may be absolute or relevant, and
minor contraindications, most of which are not really
contraindications but, on rare occasions, could become
relative contraindications that require the dose of local
anesthetic to be reduced.
Relevant Contraindications
Allergy toLocal Anesthetics
Allergy is an adverse drug reaction triggered by immune
mechanisms. Its duration is unlimited because of immunological memory (Seskin 1978), therefore allergy is an
absolute contraindication for this type of drug and an alternative local anesthetic must be used.
Ester anesthetics undergo hydrolysis in the circulatory
system and form metabolites such as paraacid, which has considerable sensitizing power (Giovannitti
and Bennett1979). Consequently, allergic sensitization in
this group is common, as is cross- sensitization (Adler and
Simon 1949; Aldrete and Johnson1970; Giovannitti and
Bennett1979; Schatz 1984; Adriani et al. 1986). The only
drugs from this group used at present are tetracaine and
benzocaine (very rarely procaine and cocaine), and these
are used mainly as topical anesthetics.
Allergy to modern amide local anesthetics is very rare. At
least 1% of adverse reactions attributed to local anesthetics
are allergic (Verril1975; Giovannitti and Bennett1979) and
rarely cross- reactions. However, cases of allergy to each of
these drugs have been reported (Chapter23).
There are no cases of cross- sensitization between amide
and ester anesthetics since these have very different
aminobenzoic
chemical structures, therefore in the case of multiple
allergy to one group, we can use anesthetics from the other
group (Incaudo etal.1978; Schatz1984).
Long- acting Anesthetics
Long- acting anesthetics such as bupivacaine, which is
available in 1.8cated in the following cases:
1) Routine short- or medium- duration procedures (Laskin
etal.1977; Jensen etal.1981).
2) Children aged under 12 years, owing to the high risk of
self-
injury of soft tissues (Laskin et al. 1977; Jensen
etal.1981; Moore1984).
3) Patients with developmental disabilities and special
needs (Pricco1977; Jensen etal.1981) or patients with
psychiatric diseases (Jensen et al.1981), for the same
reason as children aged under 12
The main reason for these contraindications is to prevent
discomfort on drinking, eating, and speaking, as well as the
risk of selfcal mucosa) owing to the long duration of anesthesia in
these tissues. Furthermore, the absence of pulpal anesthesia in infiltrations is a major disadvantage in routine procedures (Chapter7).
ml cartridges for dental use, are contraindi-
years.
injury of the soft tissues (tongue, lips, and buc-
Prilocaine, Benzocaine, andMethemoglobinemia
Hemoglobin is an iron transport protein in the red cells
that transports oxygen to tissues. Through their metabolites, prilocaine and benzocaine can alter this protein to
form methemoglobin (MHb), which does not fulfill its
function of transporting oxygen. A review of 242 cases of
local anesthetic- induced toxic MHb collected between
1947 and 2007 revealed that 65% were caused by benzocaine and 30% by prilocaine; both anesthetics were clearly
the most frequently involved (Guay2009).
Local Anesthesia in Dentistry: A Locoregional Approach, First Edition. Jesús Calatayud and Mana Saraghi.
© 2024 John Wiley & Sons Ltd. Published 2024 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Calatayud/local
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Minor Contraindications 149
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Patients with diseases or disorders that hamper transport
of oxygen to tissues are more vulnerable to the toxic methemoglobinemia caused by these local anesthetics. These diseases include the following:
1) Cardiovascular diseases:
● Heart diseases (heart failure, coronary artery insuffi-
ciency, arrhythmia, etc.) because they reduce oxygen
transport (Olson and McEvoy 1981; Duncan and
Kobrinsky1983; Rodriguez et al. 1994) and reduce
the flow of blood to the liver, where the anesthetics
are metabolized (Spoerel et al. 1967; Wilburn-
Goo
and Lloyd1999).
● Anemia and red cell disorders (Spoerel et al.1967;
Olson and McEvoy1981; Duncan and Kobrinsky1983;
Rodriguez etal.1994; Wilburn-
● Insufficient cerebral or peripheral irrigation (Spoerel
Goo and Lloyd1999).
etal.1967).
2) Severe respiratory diseases, since oxygen exchange is
reduced (Anonymous 1994; Wilburn-
Goo and
Lloyd1999).
3) Extreme age groups:
● Newborns and nursing infants have an immature
enzyme system, therefore they have a larger proportion than normal of methemoglobinemia (Künzer
von and Schneider1953; Ross and Desforges1959; Lo
and Agar1986). This situation continues, with some
degree of risk, until the infant is 1
year old
(Severinghaus etal.1991; Kellet and Copeland1983;
Rodriguez etal.1994).
● Elderly people, given that they have diseases that
reduce the oxygen supply to tissues (see points 1 and
2) and take drugs that can produce toxic methemoglobinemia (Wilburn-
Goo and Lloyd1999).
4) Congenital methemoglobinemia. A few hundred
patients throughout the world have these diseases,
which are diagnosed during the first year of life
(Curry1982):
● Hemoglobin M.
● Nicotinamide- adenine- dinucleotide- methemog lobin -
reductase (NADH- MHb- reductase) system deficiency.
● Nicotinamide- adenine- dinucleotide- phosphate- methe-
moglobin- reductase (NADPH- MHb- reductase) system
deficiency.
● Glucose- 6- phosphatedehydrogenase deficiency.
Cases of congenital methemoglobinemia are considered
absolute contraindications (Jastak etal.1995; Coleman and
Coleman 1996; Wilburn-
Goo and Lloyd 1999). The first
three causes are considered relative contraindications,
therefore they can be administered with local anesthetics,
albeit at reduced maximum doses, but the first three causes
are considered absolute contraindications in ASA III
patients. Other anesthetics, such as lidocaine and
tetracaine, have been involved, although the association is
much weaker. Chapter23 contains a review of methemoglobinemia caused by dental local anesthetic.
Cholinesterase Deficiency andEsther Anesthetics
Procaine and tetracaine are ester local anesthetics that are
metabolized by the enzyme cholinesterase or pseudocholinesterase in blood (Kalow1952). It is known that one in
every 3000 people have a deficiency or abnormality of this
enzyme (Kalow and Gunn1959) and that the deficiency is
hereditary (Kalow and Staron 1957; Foldes etal. 1963).
Consequently, affected patients are at risk of intolerance
and toxicity (Foldes etal.1963).
At present, this problem is of little relevance, since procaine is rarely used as an injectable anesthetic (it has been
replaced by more modern amide agents). In any case, the
contraindication is absolute.
Myasthenia Gravis andEsters
Myasthenia gravis is a rare autoimmune disease characterized
by skeletal muscle weakness resulting from antibodies
attacking acetylcholine receptors in the postsynaptic
(motor) membrane. In patients with myasthenia gravis,
injected ester anesthetics (procaine and tetracaine) must be
avoided because they are hydrolyzed by plasma cholinest-
erases and the patients are treated with anticholinesterases
(pyridostigmine, neostigmine), which inhibit the enzymes
that metabolize these anesthetics, therefore there is a risk
of poisoning by ester anesthetics (Patton and Howard1997;
Yarom etal. 2005; Patil et al. 2012). This is not the case,
however, with benzocaine (also an ester anesthetic,
although topical) (Yarom etal.2005).
Minor Contraindications
Procaine andSulfonamides
Procaine, or novocaine, is an ester anesthetic, like tetracaine. It inhibits the bacteriostatic effect of sulfonamides,
which compete with pararesults from the metabolization of ester anesthetics
(Woods1940), which are a substrate of the acid for folic
acid synthesis (De Jong1977).
In conclusion, procaine and sulfonamides are not widely
used today; in addition, this interaction between the doses
and regimens used in dental local anesthetics is considered
of minor relevance (Moore1999).
aminobenzoic acid. This acid
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Lidocaine andCimetidine
Cimetidine is a histamine H2 receptor antagonist that
inhibits secretion of hydrochloric acid in the stomach. It is
therefore used in the treatment of stomach ulcers and in
conditions requiring control of stomach acid secretion.
Clinical studies have shown that cimetidine diminishes
the metabolism of lidocaine by 20–25% (Feely et al.1982;
Wing et al. 1984), thus increasing its plasma levels by
40–50% (Kishikava et al.1990; Feely et al.1982). This is
because it reduces blood flow to the liver, which means
that a smaller amount of lidocaine is metabolized (Feely
et al. 1982) and the drug directly inhibits the oxidative
mechanism for the biotransformation of lidocaine in the
liver (Feely etal.1982; Wing etal.1984).
It is noteworthy that other H
receptor antagonists such
2
as ranitidine (Feely and Guy1983; Robson etal.1985) and
famotidine (Kishikava et al.1990) are not subject to this
interaction.
In conclusion, this interaction is considered to be of
minor relevance in the doses and regimens used in the dental anesthetic lidocaine (Tucker1986; Moore1999).
Lidocaine andPropranolol
Propranolol is a nonselective betablocker (it blocks adren-
and β2 receptors) that is used to treat patients with
ergic β
1
arterial hypertension, arrhythmia, angina pectoris, hyperthyroidism, etc. (Weiner1988).
Clinical studies have shown how propranolol can reduce
the metabolism of lidocaine by 20–40% (Svendsen
etal. 1982; Bax et al.1985) and thus increase its plasma
levels by 20–30% (Ochs etal.1980; Svendsen etal.1982).
This is because propranolol reduces blood flow in the liver
by 20–30% (Price et al. 1967; Trap-
Jensen et al. 1976;
Westaby etal.1984)– with the result that lower quantities
of lidocaine are metabolized – and because of the direct
action when enzyme activity against lidocaine is reduced
in the liver (Bax etal.1983,1985).
Of note, other nonselective betablockers such as pindolol
(Svendsen etal.1982) do not present this interaction.
In conclusion, this interaction is considered to be of
minor relevance in the doses and regimens used with lidocaine in dentistry (Tucker1986; Moore1999). However, it
may prove important in medical practice during infusions
for the treatment of arrhythmia (Moore1999).
Lidocaine andSuccinylcholine
Succinylcholine is a potent muscle relaxant with rapid and
short action (minutes). It is used for induction of general
anesthesia to relax the muscles and thus facilitate
intubation.
Clinical studies have shown that intravenous high- dose
lidocaine prolongs the muscle block induced by succinylcholine (Usubiaga etal.1967; Winkinski etal.1970; Telivuo
and Katz1970). This effect has also been found, albeit less
intensely, with other local anesthetics (mepivacaine, prilocaine, bupivacaine, etidocaine, procaine, and cocaine)
(Telivuo and Katz1970; Matsuo etal.1978).
In conclusion, this interaction is considered to be of
minor relevance in the doses and regimens used with lidocaine in dentistry.
Bupivacaine andCardiotoxicity
All local anesthetics are toxic for the central nervous system (CNS) and for the heart. However, bupivacaine is particularly toxic for the heart and can cause severe arrhythmia
with tachycardia and ventricular fibrillation (Albright1979;
Reiz and Nath 1986; Maxwell et al. 1994; Mather and
Chang2001). Thus, when these conditions develop, resuscitation is more problematic and it may take 45
minutes to
restore a normal heart rate (Albright1979). Mortality has
reached 40% (Reiz and Nath 1986). The toxic effect is
caused directly through action on the myocardium (Moller
and Covino1988; Graf etal.2002; Bozkurt etal.2003) and
indirectly via the CNS (Heavner1986; Thomas etal.1986).
Toxicity is disproportionately more pronounced with intravenous injection than with other routes of administration,
for example intraoral administration (Albright1979), owing
to the high lipid solubility of this drug and marked binding to
plasma proteins. In other words, after intraoral injection, the
drug gradually enters the bloodstream and its free fraction
(the truly toxic component) is low, although after intravenous injection a large amount enters the general circulation.
The free fraction increases since increased concentrations of
an anesthetic in blood are associated with lower levels of the
fraction bound to plasma proteins (Shnider and Way1968;
Tucker etal.1970; Mather etal.1971).
The patients most predisposed to this type of adverse effect
are as follows: (i) adults who receive high doses, above
50–360 mg (Reiz and Nath 1986) or above 90 mg (Moore
et al.1977; Albright1979), which are generally associated
with intravascular injections (Moore et al. 1977), and
(ii)small children (aged under 12 months) owing their immature metabolism, which is unable to produce plasma proteins
and transport high levels of bupivacaine as a free fraction
(Mazoit et al. 1988; Luz et al.1996; Knudsen et al. 1997;
Meunier etal.2001), and the immaturity of the liver, which
prevents metabolism of the drug (Meunier etal.2001). The
risk is low in dentistry for the following reasons:
1) The maximum dose in dentistry is 90 mg (American
Dental Association2003).
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2) Bupivacaine is contraindicated in children aged under
12
years (see above) to prevent the risk of self- injury of
the soft tissues (tongue, lips, and buccal mucosa) owing
to the long action of the anesthetic in these tissues
(Pricco1977; Jensen etal.1981; Moore1984).
3) It is important to remember that in dentistry, aspiration
is mandatory to prevent intravascular injections.
In conclusion, cardiotoxicity is considered an extremely
rare adverse effect with the doses and regimens of bupivacaine used in dentistry.
Amide Anesthetics andMalignant Hyperthermia
Malignant hyperthermia (MH) or malignant hyperpyrexia
is a rare and severe familial disease (Britt and Kalow1970)
that is triggered after administration of general anesthesia
and with concomitant drugs, especially halothane and succinylcholine (Britt and Kalow 1970; Kalow et al. 1970;
Adriani and Sundin1984). The pathophysiology of MH
is still not fully understood. During acute episode of
MH, intracellular calcium increases in skeletal muscle,
causing uncontrolled muscle contractions (Fukami and
Ganzberg2005). It appears that there may be a defect in the
RYR1 gene for a calcium channel receptor in the sarcoplasmic reticulum. It is autosomally dominant with variable
penetrance, but some patients without the genetic defect
still can develop MH (Fukami and Ganzberg2005).
Symptoms generally appear within 2
anesthesia, with increased exhaled carbon dioxide (hypercapnia), increased heart rate (tachycardia, which may progress to various types of arrhythmia), and increased body
temperature (pyrexia) accompanied by sweating and muscle rigidity (including all muscles but notable masseter
muscle rigidity and trimus is a presentation of MH), even if
the patient has received a potent muscle relaxant such as
succinylcholine (Britt and Kalow 1970; Kolb et al. 1982;
Fukami and Ganzberg 2005). The condition is potentially
fatal (Kolb etal.1982; Ording1985).
The problem arose when it was suggested that amide
local anesthetics could trigger this clinical picture, given
that sporadic cases had been described with lidocaine and
bupivacaine (Britt1972; Klimanek etal.1976; Gibbs1984).
Furthermore, it has been suggested that stress (Gronert
et al. 1980; Kolb etal. 1982) and infection (Adriani and
hours of onset of
Sundin1984)– both of which circumstances arise in the
dentist’s office– could trigger MH. This concern was further reinforced with the publication of an important book
on dental local anesthesia, where it was stated that these
agents could act as triggers (Malamed1986). Note: This
point was corrected in subsequent editions.
Current data call into doubt this contraindication to the
use of amide anesthetics in patients with MH, for various
reasons:
1) Clinical cases of MH associated with amide anesthetics
resolved spontaneously with no specific treatment
(dantrolene and cooling) and did not present the mortality usually associated with these conditions
(Britt1972; Klimanek etal.1976; Gibbs1984). It is possible to think that some of these reactions were caused
more by stress than by the anesthetics themselves
(Minasian and Yagiela1988; Dershwitz etal.1989).
2) The disease has been reproduced in experimental por-
cine models with halothane and succinylcholine,
although never with local anesthetics (only poisoning
due to the excess dose administered) (Hall etal.1972;
Kerr etal.1975; Wingard and Bobko1979; Harrison and
Morell 1980). The current body of evidence indicates
that the triggering agents are succinylcholine and volatile inhalational anesthetics (sevoflurane, enflurane,
isoflurane, desflurane, and halothane) (Morgan
etal.2013).
3) Patients diagnosed with MH who have received amide
local anesthetics for muscle biopsy or dental treatment
or epidural anesthesia during labor, etc. did not develop
MH (Willatts 1979; Berkowitz and Rosenberg 1985;
Adriani and Sundin1984; Gielen and Viering1986).
4) Similarly, no cases of MH were reported in the main
reviews on adverse effects of local anesthetics: Danish
Malignant Hyperthermia (Ording 1985), Malignant
Hyperthermia Association of the United States
(MHAUS) (Minasian and Yagiela1988), and the reviews
of the Massachusetts Society of Oral Maxillofacial
Surgeons (MSOMS) (D’Eramo 1999; D’Eramo
etal.2003).
In conclusion, current data indicate that use of amide
local anesthetics is not contraindicated in patients diagnosed with MH.
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