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eferences 153
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Contraindications forVasoconstrictors
155
Below, we review the contraindications for sympathomimetic vasoconstrictors (epinephrine, norepinephrine, and
levonordefrin) in three sections: absolute contraindications, relative contraindications, and contraindications of
little relevance. In the last part, we examine the contraindications to felypressin. We also explain that, although there
is potential for further research, including wellstudies on the effects of local anesthetics with vasoconstrictors, most clinical studies on the doses and regimens
used in dentistry have shown that these solutions are very
safe and that relatively few cases of adverse effects have
been reported (Brown and Rhodus2005).
designed
Absolute Contraindications
Below, we analyze some situations in which sympathomimetic vasoconstrictors, especially epinephrine, are absolutely contraindicated and cannot be used (Table10.1).
Uncontrolled Insulin- dependent Diabetes Mellitus
Administration of epinephrine in healthy patients
increases plasma levels of the drug, therefore when levels
of 150–200 pg/ml are reached (as with administration of
two cartridges of a 1:100
16), the blood sugar level increases (Clutter etal.1980) as
glucose is released by the liver as a result of increased neoglycogenesis (Christensen 1979; Hamburg et al. 1980).
Furthermore, when blood epinephrine levels greater than
400
pg/ml are reached (as with administration of five cartridges of a 1:100 000 solution [10 μg/ml]) (Annex 16),
release of insulin is inhibited through the direct action of
epinephrine on the cells of the pancreas (Christensen1979;
Hamburg et al. 1980), thus aggravating the increase in
plasma glucose (Clutter etal.1980).
Studies on intraoral injection of anesthetic solutions
with epinephrine confirm this data (Meechan etal.1991a;
000 solution [10 μg/ml]) (Annex
Meechan1996). In addition, the anxiety felt by the patient
(as is often the case in the dentist’s office) worsens the situation by activating the sympathetic nervous system and
increasing the release of glucose to the bloodstream
(Christensen1979; Hamburg etal.1980; Berk etal.1985).
Increased blood glucose (glycemia) for 20–30
well tolerated by healthy persons (Meechan etal. 1991a;
Meechan1991b,1996).
Such situations are very serious in diabetic patients
(Christensen1979) and are worse for patients with insulindependent diabetes mellitus (Berk etal.1985). Nevertheless,
both types of patients can be treated at the dentist’s office
and receive anesthetic solutions with epinephrine, provided they are carefully monitored (Dos Santosetal.2015). It is important to remember that these patients,
and any patients with uncontrolled systemic disease, are
considered ASA (American Society of Anesthesiologists)
III (Wilson etal.2008). However, most insulin- dependent
diabetic patients are young and need considerable discipline to administer insulin, maintain a balanced diet, and
take regular and wellrequirements are often difficult to meet owing to the fact
that young people participate in sports, group activities,
and activities that do not facilitate the necessary discipline
for appropriate insulin treatment (Munroe1983). In these
circumstances, there is an increased risk of diabetic ketoacidosis or hyperglycemic reaction or worsening of an ongoing one (onset of these reactions is slow, usually hours or
days) (Munroe1983; Perusse etal.1992b).
In conclusion, in patients with poorly controlled or
uncontrolled insulin- dependent diabetes, dental local
anesthetic solutions with epinephrine are absolutely contraindicated (Munroe 1983; Perusse et al. 1992b).
Furthermore, since these patients are considered ASA IV
(Malamed2007; Wilson etal.2008), only emergency dental
treatment (analgesics, antibiotics, etc.) is indicated for control of pain and infection (Munroe1983).
planned physical exercise. These
minutes is
Paul
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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156
Table10.1 Summary ofabsolute contraindications
forsympathomimetic vasoconstrictors.
1) Poorly controlled or uncontrolled insulin- dependent
diabetes mellitus.
2) Intolerance to sulfites.
3) Severe asthma controlled by corticosteroids.
4) Arterial hypertension due to pheochromocytoma.
5) Consumption of cocaine in the previous 24 hours.
6) Consumption of psychostimulants by patients with
cardiovascular disease
7) Allergy to vasoconstrictors.
Intolerance toSulfites
Sulfites (sulfite, bisulfite, sodium/potassium metabisulfite,
and sulfur dioxide) are used as antimicrobial drugs, reducing agents, and antibrowning agents in foods such as fruit,
vegetables, salads, mushrooms, potatoes, shellfish, wine,
beer, and juices; in addition, they are used in foods that do
not contain thiamine, such as red meat (Bush etal.1986;
Simon1986; Seng and Gay1986). Sulfites are also used as
antioxidants in various medicines, including local anesthetic
solutions containing sympathomimetic vasoconstrictors
(Huang and Fraser1984; Schwartz and Sher 1985; Bush
et al. 1986; Simon 1986; Seng and Gay 1986), therefore
alldental local anesthetic solutions with epinephrine, norepinephrine, and levonordefrin contain sulfites (Huang
and Fraser 1984; Schwartz and Sher 1985; Seng and
Gay1986). The United States Food and Drug Administration
(FDA) includes sulfites in the Generally Recognized As
Safe category (Bush et al. 1986; Simon 1986; Seng and
Gay1986).
Little is known about the mechanism of sensitization to
sulfites (Schwartz and Sher 1985; Bush et al. 1986;
Simon1986). It is thought to result from the following: (i)
release of histamine via a nonimmune pathway, (ii) action
of the parasympathetic nervous system and gastrin, and
(iii) deficiency of the enzyme sulfite oxidase (responsible
for oxidizing sulfite to inactive sulfate). It is therefore more
appropriate to talk of intolerance or reactions to sulfites
than allergy until we can better determine to what extent
these reactions are immunological.
The prevalence of intolerance to sulfites in the general
population is unknown, although the condition is considered extremely rare (except in the case of asthmatic patients
[see below]) (Bush et al.1986). Furthermore, although it
has been demonstrated that subcutaneous sensitization to
sulfites is very difficult (the oral route and, even more so,
the inhaled route are the most common routes of sensitization) (Goldfarb and Simon1984; Bush et al.1986), there
have been reports of reactions (urticaria, angioedema,
inflammation, dyspnea, etc.) after administration of dental
local anesthesia with epinephrine solutions caused by the
sulfites they contain (Huang and Fraser 1984; Schwartz
and Sher 1985; Schwartz et al. 1989; Dooms-
Goossens
etal.1989; Campbell etal.2001).
In conclusion, anesthetic solutions containing adrenergic vasoconstrictors are absolutely contraindicated in
patients who do not tolerate sulfites, since these solutions
contain sulfites as antioxidants.
Asthma Controlled withCorticosteroids
For reasons that remain unknown, asthmatic patients are
particularly sensitive to sulfites, and it has been estimated
that around 5% of asthmatics could be very sensitive to
these drugs (Seng and Gay 1986; Simon1986). Although
other authors have reported this figure to be excessive
(Bush etal.1986), a more selective study has shown that
not all asthmatics are the same. Thus, 8% of patients with
severe asthma controlled by corticosteroids are sensitized to
sulfites, whereas fewer than 1% of asthmatics who do not
need corticosteroids are sensitized (Bush et al. 1986). In
addition, the literature shows that most asthmatics who
experience bronchospasms and reactions to sulfites are
patients who need corticosteroids (Bush et al. 1986;
Schwartz etal.1989).
In conclusion, in patients with severe asthma whose disease is controlled with corticosteroids, local anesthetic
solutions containing adrenergic vasoconstrictors are absolutely contraindicated, since 8% do not tolerate the sulfites
used as antioxidants in these solutions. Furthermore,
asthma patients whose disease is difficult to control and
have frequent attacks that require admission to hospital
and corticosteroids are classed as ASA IV, therefore only
immediate dental treatment is indicated (analgesics, antibiotics, etc.) for control of pain and infection (Perusse
etal.1992b; Steinbacher and Glick2001; Malamed2007).
Pheochromocytoma- induced Arterial Hypertension
Pheochromocytoma is an unusual tumor of the medulla of
the adrenal gland that is generally benign and produces
epinephrine and norepinephrine (Hickler and Thorn1977;
Cryer 2001; Keiser 2001). The most typical symptom in
most cases is arterial hypertension, and the tumor is
thought to cause fewer than 0.1–0.5% of diagnosed cases of
hypertension (Sutton etal.1981; Plouin etal.1981).
The arterial hypertension produced by this tumor is permanent in 50–60% of cases, although 25–50% of cases
involve paroxysmal hypertension (Hickler and Thorn1977;
Keiser2001), that is, hypertension that takes the form of
crises lasting minutes or even hours that are usually
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spontaneous or caused by physical effort, emotional tension, or abdominal palpation. Attacks of paroxysmal hypertension, which result from release of catecholamines, can
lead to death from myocardial infarction (even in the
absence of heart disease), from arrhythmias, or from brain
hemorrhage (Hickler and Thorn1977; Keiser2001).
In conclusion, sympathomimetic vasoconstrictors are
contraindicated in patients with pheochromocytoma
owing to the risk of fatal heart abnormalities or cerebrovascular accidents (Perusse et al.1992b). In addition, these
patients can be considered ASA III or IV depending on the
degree of severity.
Recent Consumption ofCocaine
Cocaine was addressed in Chapter1, since it was the first
local anesthetic, and in Chapter 12, since it is a topical
anesthetic that is still in use. Illegal consumption of and
addiction to cocaine in developed countries cause serious
medical and social problems (Friedlander and
Gorelick1988; Goulet etal.1992).
Cocaine taken intranasally is quickly inactivated on
entering the bloodstream by plasma pseudocholinesterase.
However, it remains in blood for more than 6
peak at 60
minutes and a half- life of 1.5 hours (Annex 11).
hours, with a
This is because the drug remains in the mucosa for more
than 3 hours owing to its vasoconstrictive effect (Van Dyke
et al. 1976). Consumption stimulates the central nervous
system (CNS) and peripheral sympathetic nervous system
(Benchimol etal.1978; Pasternack etal.1985) with general-
ized sensitization of the body to the action of catecholamines
(Tainter etal.1949; Tye etal.1967; Benchimol etal.1978;
Kossowosky and Lyon 1984; Nanji and Filipenko 1984;
Howard etal. 1985; Goulet et al. 1992). Therefore, high
doses can produce a direct toxic effect on the heart, with
possible coronary spasm (Benchimol etal.1978; Kossowosky
and Lyon 1984; Schachne et al. 1984; Friedlander and
Gorelick1988). Ingestion results in increased arterial blood
pressure and heart rate, with increased oxygen consumption by the heart that can in turn lead to the following:
● Hypertensive crises with a risk of cerebrovascular acci-
dents (Friedlander and Gorelick1988).
● Arrhythmias (Benchimol et al. 1978; Nanji and
Filipenko1984; Friedlander and Gorelick1988).
● Angina pectoris (Pasternack etal.1985) or acute myocar-
dial infarction, even in young patients with no previous
history of heart disease (Kossowosky and Lyon 1984;
Schachne et al.1984; Cregler and Mark1985; Howard
etal.1985; Pasternack etal.1985; Weiss1986).
The dentist should try to identify recent consumption of
cocaine based on suspicious behavior (mania, restlessness,
irritability, or depression, dilated pupils, red eyes, runny, or
bloody nose, frequent intakes of breath through the nose
without allergy or having a cold, etc.), careless appearance
(Friedlander and Gorelick 1988), or as part of taking a
medical history and asking about recreational drug use
(Goulet etal. 1992), although patients may not disclose
their consumption.
In conclusion, anesthetic solutions containing sympathomimetic vasoconstrictors, especially epinephrine, are
contraindicated in patients who have consumed cocaine
during the previous 24 hours (Goulet etal.1992), given that
plasma levels of the drug are maintained for more than
6
hours (Van Dyke etal.1976).
Patients withCardiovascular Diseases Who Take
Amphetamines andPsychostimulants
Children with psychological disorders, such as attentiondeficit hyperactivity disorder, are generally treated with
amphetamine and other psychostimulants (atomoxetine,
dexamfetamine, modafinil, etc.) (Table10.2) (Moore and
Hersh 2006). If these patients also have cardiovascular
problems such as arrhythmia or arterial hypertension, then
local anesthetic solutions with sympathomimetic vasoconstrictors (mainly epinephrine and levonordefrin) are
contraindicated (Moore and Hersh 2006; Hersh and
Moore2008).
Note: For some authors, selegiline, an antiparkinson and
antidepressant monoamine oxidase inhibitor (MAOI), is
absolutely contraindicated in patients receiving sympathomimetic amines such as epinephrine. Selegiline can cause
increases in arterial pressure since it produces amphetamine compounds (- metamfetamine and - amfetamine)
during metabolism in the liver (Friedlander etal.2009).
Allergy toVasoconstrictors
We generally think of vasoconstrictors as epinephrine and
norepinephrine. Given that these drugs are natural neurotransmitters and hormones, there are no cases of allergy to
their base forms, as this would not be compatible with
human life. However, exogenous forms administered in
local anesthetics include bitartrates and hydrochlorides,
Table10.2 Amphetamines andpsychostimulants.
Amphetamine Atomoxetine
Dexamphetamine Dexmethylphenidate
Methamphetamine Methylphenidate
Modafinil Pemoline
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158
and two cases of allergy to epinephrine have been reported
(Kohase and Umino2004).
Felypressin (Octapressin®), which is used in many countries in the European Union, and levonordefrin (synthetic
vasoconstrictor), which is used in the United States, are
artificial drugs, therefore they can cause allergic sensitization. In fact, one case of allergy to levonordefrin has been
reported (Germishuys and Anderson 1982). Allergy is an
absolute contraindication for these drugs.
Of note, these situations are exceptional since, despite
years of experience with these drugs, only three cases of
allergy have been reported.
Relative Contraindications
Below, we present those situations (mainly drug interactions) where sympathomimetic vasoconstrictors such as
norepinephrine and levonordefrin are absolutely contraindicated, but where epinephrine can be administered, albeit
with important restrictions. In such situations, we have two
alternatives:
1) Solutions with epinephrine where limitations are
applied, as follows:
● The maximum concentration is 1:100 000 (10 μg/ml),
therefore higher concentrations are contraindicated
(1:80 000 [12.5 μg/ml] and 1:50 000 [20 μg/ml]), but
not lower concentrations (1:200
(McCarthy1982; American Dental Association2003;
Malamed2004).
● The current maximum dose of epinephrine is no
longer 200
μg, although much lower doses of 27–50 μg
can be administered depending on the case.
A suitable alternative in these cases is articaine 4%
with epinephrine 1:200
thetic parameter of 92%-
000 (5 μg/ml) and an anes-
45′/190′- 260′.
2) Solutions that do not contain epinephrine or any other
sympathomimetic vasoconstrictor, such as the following (see Chapter7):
● Solutions that do not contain a vasoconstrictor, such
as mepivacaine 3% with an anesthetic parameter of
91%- 15′/100′- 190′ or prilocaine 4% with an anesthetic
parameter of 87%- 10′/75′- 180′.
● Prilocaine 3% with felypressin 0.03 IU (0.54 μg/ml)
and an anesthetic parameter of 88%- 25′/180′- 220′.
The problem with an epinephrine- free alternative is that
the anesthetic parameter is not very potent (see Chapter7),
and we must remember that onset of pain owing to deficient anesthesia leads to a more marked reaction of the
sympathetic nervous system, with an increased risk for the
patient (Annex 17).
000 [5 μg/ml])
The maximum number of 1.8-
ml cartridges that can be
administered with epinephrine in these circumstances is
summarized in Table10.3.
Nonselective Beta- blockers
Beta- blockers, also known as beta- adrenergic antagonists
and betatwo types (Table 10.4): (i) cardioselective betawhich only act on β
(ii)nonselective betacardioselective β
adrenergic receptor blockers, are classified into
blockers,
receptors, mainly in the heart, and
1
blockers, which act by blocking both
receptors and β2 vasodilators in the arte-
1
rioles of skeletal muscle and via many other actions
(Table6.7, Chapter6). These drugs are used in patients
with disease such as arterial hypertension, angina pectoris
or myocardial infarction, arrhythmias, vascular headaches
(migraine), hyperthyroidism, pheochromocytoma, etc.
(Foster and Aston1983; Goulet etal.1992; Yagiela1999).
Clinical trials in hypertensive patients (Houben
etal.1982) and with healthy volunteers (Hjemdahl et al.
1983; Reeves etal.1984; Dzubow1986; Rehling etal.1986;
Sugimura etal.1995; Niwa etal.1996) have demonstrated
the following:
● Administration of epinephrine in patients who take car-
dioselective beta-
blockers produces very moderate
hemodynamic effects (Houben et al. 1982; Hjemdahl
etal.1983; Rehling etal.1986); the same can be said of
norepinephrine (Hjemdahl et al. 1983). The selective
beta blockers block β
effects, namely vasoconstriction and vasodilata-
and β
2
effects, leaving the alpha effects
1
tion, respectively, and therefore there is less of a hypertensive response to epinephrine.
● Administration of epinephrine in patients taking nonse-
lective beta-
blockers produces severe hemodynamic
effects, with increased arterial pressure and a reflex
decrease in heart rate (bradycardia) (Houben etal.1982;
Hjemdahl etal.1983; Reeves etal.1984; Dzubow1986;
Rehling et al. 1986; Sugimura et al. 1995; Niwa
et al. 1996). The same is true of norepinephrine
(Hjemdahl etal.1983; Reeves etal.1984), although with
lesser intensity, given that the vasodilatory β
effect of
2
norepinephrine is much less pronounced than that of
epinephrine (Reeves etal.1984). The same is true of levonordefrin (Mito and Yagiela 1988). The nonselective
beta blockers block all β
and β2 effects, leaving the alpha
1
effects, namely vasoconstriction, unopposed, and therefore there is a risk for a hypertensive response to
epinephrine.
The mechanism underlying the interaction between sym-
pathomimetic vasoconstrictors (epinephrine and norepinephrine) and nonselective beta- blockers is based on
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Table10.3 Summary ofthe maximum doses ofepinephrine andmaximum number ofcartridges insituations ofrelative
contraindication.
Number of 1.8- ml cartridges
Maximum doses of
epinephrine 1:100
27 μg 1.5 3 Nonselective beta- blockers
μg 2.2 4.5 ASA III cardiovascular
40
50
μg 2.7 5.5 Amphetamines and
Example LAS
Anesthetic parameter 95%Example LAS Articaine 4%
Anesthetic parameter 98%-
a
000 (10 μg/ml) 1:200 000 (5 μg/ml) Clinical situations
Antiparkinson COMTi
Digoxin
psychostimulants
Tricyclic antidepressants
Older antihypertensive
Halothane and thiopental
Lidocaine 2% + epinephrine
1:100 000
45′/190′- 200´ 92%- 45′/190′- 260´
+ epinephrine
000
1:100
60′/190′- 260′ 80%- 35′/410′- 490′
Articaine 4% + epinephrine
1:200 000
Bupivacaine 0.5%
000
1:200
+ epinephrine
Epinephrine can be used, albeit at lower doses (lower number of cartridges). Articaine 4% with epinephrine 1:200 000 (5 μg/ml) is very useful in
these cases since, as it contains half the amount of epinephrine as the 1:100 000 solution (10 μg/ml), we can administer double the amount of
solution with similar potency and efficacy, although this is somewhat lower than the standard solution of lidocaine 2% with epinephrine
1:100 000, as indicated in its anesthetic parameter.
a
LAS, local anesthetic solution.
Table10.4 Beta- blockers.
of the cardioselective β
receptors, thus increasing the risk
1
of cardiac arrest (Foster and Aston1983). Furthermore, this
Cardioselective Nonselective
effect is more intense, given that nonselective beta- blockers
reduce clearance of epinephrine and, to a lesser extent, nor-
Atenolol Carteolol
Bisoprolol Carvedilol
Celiprolol Labetalol
Esmolol Nadolol
Metoprolol Oxprenolol
Nebivolol Pindolol
Propranolol
Sotalol
Timolol
The most common drugs are shown in bold.
epinephrine, thus extending the duration of action of the
exogenous catecholamines (Hjemdahl et al. 1983). It is
interesting that, even though these reactions are thought to
be dose- dependent, there may be idiopathic cases in which
specific sensitivity to these adrenergic receptors aggravates
the reaction (Dzubow 1986). A curious effect is that by
blocking the vasodilatory β
effect, nonselective beta-
2
blockers indirectly increase the vasoconstrictor α affect,
thus increasing the anesthetic potency of local anesthetic
solutions with epinephrine and the duration of soft tissue
and pulpal anesthesia (Zhang etal.1999).
A review of the literature reveals case reports of patients
treated with propranolol (nonselective beta- blocker) who
blockade of the vasodilatory β2 receptors of the arterioles of
skeletal muscle by the beta- blocker, which increases arterial
pressure (systolic and diastolic). Given that only the vasoconstrictor α effect remains, there is a risk of cerebrovascular accidents (Hansbrough and Near 1980) and a reflex
decrease in heart rate (bradycardia) resulting from blockade
were given epinephrine at 40–320 μg (Kram et al. 1974;
Hansbrough and Near1980; Foster and Aston1983) or lev-
onordefrin at 75 μg (Mito and Yagiela 1988). After a few
minutes, the patients experienced an episode of arterial
hypertension accompanied by bradycardia lasting
10–15 minutes, which, in some cases, was complicated by a
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160
cerebrovascular accident (Hansbrough and Near1980) or
cardiac arrest (Foster and Aston1983).
The measure proposed in these cases was not to use local
anesthetic solutions containing epinephrine (Goulet
et al. 1992) or if they did contain epinephrine, then the
dose had to be very low (Dzubow1986), namely, the equivalent of 1.5 cartridges of epinephrine 1:100
which represents 27
μg (Yagiela 1999; Naftalin and
000 (10 μg/ml),
Yagiela2002). In addition, arterial pressure and heart rate
had to be monitored after 5
minutes (Yagiela1999; Naftalin
and Yagiela2002; Malamed2004).
In conclusion, in these patients, local anesthetic solutions containing epinephrine can be used, although at a
maximum concentration of 1:100 000 (10 μg/ml) and an
absolute maximum dose of 27
μg (1.5 × 1.8- ml cartridges).
Heart rate and arterial pressure should be monitored before
administration of local anesthetic containing vasopressor
as well as 5
minutes following administration.
COMT Inhibitor- type Antiparkinson Drugs
The new antiparkinson medicines tolcapone (Tasmar®)
and entacapone produce reversible blockade of catecholO- methyltransferase (COMT), an enzyme that inactivates
peripheral levodopa, therefore these drugs are dopaminergics since they increase dopamine levels. However, they
also inhibit inactivation of exogenously administered catecholamines (e.g., epinephrine, norepinephrine, and levonordefrin) by COMT, leading to increased arterial
pressure, increased heart rate, and risk of arrhythmias (Illi
etal.1995; Ganzberg2003; Friedlander etal.2009). There
have been no reports of this interaction to date, probably
because the drugs are new and little experience is available.
In conclusion, epinephrine should be reduced to 1.5–3
cartridges of epinephrine 1:100 000 (10 μg/ml), that is, an
absolute maximum dose of 27–50
μg (Hersh and Moore2008;
Friedlander etal.2009).
to difficulty breathing (dyspnea) with exercise or
tension, but not at rest (Malamed2007).
○ Implanted pacemaker (ASA 2019).
○ Conditions occurring more than 3 months after the
following:
■ Cerebrovascular accident that has left neurological
sequelae (McCarthy and Malamed1979; Malamed
2007; Wilson etal.2008).
■ Heart attack (angina pectoris or acute myocar-
dial infarction) (McCarthy and Malamed 1979;
Abraham-
Inpijn etal.1988; Malamed2007; Wilson
etal.2008).
■ Coronary bypass surgery (Perusse etal.1992a).
■ Stents in coronary artery disease (ASA 2019).
○ Heart transplant. Surgical denervation: the transplanted
heart has been denervated, meaning that the vagus nerve
has been transected, losing parasympathetic input and
leaving the heart hypersensitive to the action of catecholamines (Carleton etal.1969; Roca etal.1993; Meechan
etal.2002).
Special attention should be given to the good tolerance of
hypertensive patients (controlled and uncontrolled) to
dental local anesthetic solutions with epinephrine
reported in a systematic review (Bader etal.2002) and of
patients with cardiovascular disease in general, albeit
within certain limits (Annex 17). Of note, it is important
to control pain in these patients, and, as epinephrine in
local anesthetic solutions plays a key role in pain control
(Annex 17), patients should receive local anesthetic
solutions with epinephrine, although not exceeding
maximum concentration of 1:100 000 (10 μg/ml) and
the
not exceeding the absolute maximum dose of 40
(McCarthy 1982; Campbell et al. 1996; Rahn and
Ball2001; American Dental Association2003; Malamed
2004,2007; Herman and Ferguson2010; Anderson and
Bosack2014), that is, 2.2–2.5 cartridges of epinephrine
1:100 000.
Note: See ASA classification in Chapter8.
nervous
μg
ASA III Patients with Cardiovascular Conditions
ASA III patients have severe systemic disease that limits
activity but is not disabling (no symptoms at rest or with
standard exercise). They have reduced tolerance to physical
stress (pain) and psychological stress (anxiety).
Cardiovascular disorders affecting this group include the
following:
○ Uncontrolled arterial hypertension with moderate blood
pressure (95–115/160–200 mmHg) (McCarthy 1982;
Abraham- Inpijn etal.1988; Malamed2007).
○ Congestive heart failure (caused by myocardial infarc-
tion, vascular disease, rheumatic disease, etc.) that leads
Digitalis Glycosides (Digoxin)
Digoxin and digitoxin are digitalis glycosides used as cardiotonic agents for heart failure and arrhythmias. These
drugs have a low therapeutic index, that is, the difference
between therapeutic and toxic levels is small. Small
dose modifications can easily lead to toxic levels (Hersh
and Moore2008).
Intravenous infusion of epinephrine (Fellows etal.1985)
and intraoral injection (Meechan and Rawlins1987,1988;
Meechan et al.1991a) reduce plasma potassium levels on
entering the cells (Fellows et al. 1985). Infusion reaches
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maximum levels at 10–20 minutes and then tends to
normalize (Meechan and Rawlins 1987, 1988; Meechan
et al. 1991a). This is of no relevance in healthy persons.
However, in patients with cardiovascular disease who take
digitalis glycosides, epinephrine can cause arrhythmias
(Kunin et al. 1962; Meechan et al. 1991a; Naftalin and
Yagiela2002; Hersh and Moore 2008), since reduction of
plasma potassium levels worsens these situations (Meechan
and Rawlins1988).
Although there is no recommended regimen in these
cases, some authors recommend an absolute maximum
dose of 40
μg of epinephrine until more information
becomes available (Hersh and Moore 2008). The dose is
equivalent to 2.2 cartridges of epinephrine 1:
00 000.
Amphetamines andPsychostimulants
Amphetamines and psychostimulant derivatives
(Table10.2) are used in children with attention-
deficit and
hyperactivity disorder (see above) (Nissen2006; Moore and
Hersh2006; Hersh and Moore2008). These diseases can
persist into adolescence and even into adulthood (Hersh
and Moore2008).
The drugs act by releasing norepinephrine and other catecholamines or by blocking their uptake (Hersh and
Moore2008), with the result that they increase heart rate
and blood pressure (Nissen2006; Moore and Hersh2006).
There have been reports of children with acute myocardial
infarction and cerebrovascular accidents after receiving
these drugs (Nissen2006; Hersh and Moore2008). In these
conditions, exogenous administration of catecholamines
in local anesthetic solutions can increase the risks (Hersh
and Moore2008).
While no definitive criterion has been established, some
authors recommend reducing the maximum doses of epinephrine in line with the recommendations for tricyclic
antidepressants, that is, an absolute maximum dose of 50
μg
of epinephrine (Hersh and Moore2008), which is equivalent to 2.7 cartridges of epinephrine 1:100 000 (10 μg/ml).
Tricyclic Antidepressants
Antidepressive drugs are grouped into four major categories (Table 10.5) according to their mechanism of action
and chemical structure. For our purposes, the most important are tricyclic and tetracyclic or heterocyclic antidepressants, since these inhibit uptake of norepinephrine in
adrenergic nerve endings, thus increasing their
concentration at receptor sites (Boakes et al. 1973;
Hollister 1978; Yagiela et al.1983; Yagiela 1999; Naftalin
and Yagiela 2002), including heart muscle (Fowler
et al. 1976; Yagiela 1999), and boosting the effect of
Table10.5 Different types ofantidepressants andtheir
mechanism ofaction.
Tricyclic: Norepinephrine and serotonin uptake inhibitors
Amitriptyline Clomipramine
Desipramine Doxepin
Imipramine Nortriptyline
Protriptyline Venlafaxine
Duloxetine
Tetracyclic: Norepinephrine uptake inhibitors
Amoxapine Lofepramine
Maprotiline Mianserin
Mirtazapine Reboxetine
MAOIs: Monoamine oxidase (MAO) inhibitors
Phenelzine Isocarboxazid
Moclobemide Nialamide
Tranylcypromine Selegiline
SSRIs: Selective serotonin reuptake inhibitors
Citalopram Escitalopram
Fluoxetine Fluvoxamine
Paroxetine Sertraline
Trazodone
Table adapted from Rodríguez and Reneses (2002).
Inhibit the reuptake of norepinephrine and serotonin.
a
Venlafaxine and duloxetine are not tricyclics but inhibit the
reuptake of norepinephrine and serotonin.
b
Reboxetine is not a tetracyclic but inhibits the reuptake of
norepinephrine.
a
a
b
sympathomimetic vasoconstrictors. Tricyclic antidepressants are used to treat depression, neuropathic pain
(atypical
orofacial pain, chronic pain, etc.), severe abnormalities
caused by anxiety, nocturnal enuresis in children etc.
(Goulet etal.1992; Yagiela1999; Naftalin and Yagiela2002).
Experimental animal studies (Goldman1971a; Goldman
etal.1971b; Yagiela etal.1983,1985) and clinical trials in
healthy volunteers (Svedmyr1968; Boakes etal.1973) and
in patients with depression (Persson and Siwers1975) have
shown that administration of catecholamines such as epinephrine, norepinephrine, and levonordefrin in patients
taking tricyclic or tetracyclic antidepressants produces
hypertensive reactions and alterations of heart rhythm
(arrhythmias) by boosting the effect of epinephrine two-
to
fourfold and that of norepinephrine and levonordefrin
four- to ninefold (Svedmyr1968; Boakes etal.1973; Yagiela
et al.1985). It is interesting to point out that long- term
administration of this type of antidepressant (more than
2–3 weeks) can lead to desensitization to sympathomimetic
vasoconstrictors and therefore a reduced effect of the interaction (Moyer et al. 1979; Weiss et al. 1980; Brown and
Rhodus2005).
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162
MAOI (Monoamine Oxidase Inhibitors) antidepressants
are still associates with this
interaction in many books
on dental local anesthesia (Bennett 1984; Roberts and
Sowray1987; Gaudi and Arreto2005). However, experimental animal studies (Yagiela etal.1983,1985) and clinical trials (Elis etal.1967; Boakes etal.1973) have been unable to
demonstrate this type of interaction. This is logical, given
that the main enzyme responsible for inactivation of adrenergic vasoconstrictors (epinephrine, norepinephrine, and
levonordefrin) is COMT and not the monoamine oxidase
(MAO) inhibited by MAOI drugs (Boakes etal.1973; Yagiela
et al. 1985). Phenylephrine, a vasoconstrictor that is no
longer in use, is the only drug that is metabolized by MAO
and can be boosted by MAOIs (Yagiela etal.1985).
Modern selective serotonin reuptake inhibitors (SSRIs),
such as those derived from fluoxetine (Prozac®), are not
subject to this type of interaction because they do not
inhibit the reuptake of norepinephrine, only serotonin (De
Jonghe and Swinkles1992). These antidepressants are rapidly replacing tricyclic antidepressants.
In conclusion, in the case of patients who take tricyclic
and tetracyclic antidepressants, many authors have agreed
that local anesthetic solutions with epinephrine can be
used, although at a maximum concentration of 1:100 000
(10
μg/ml) and an absolute maximum dose of 50 μg (Yagiela
etal.1985; Goulet etal.1992; Naftalin and Yagiela2002;
Malamed2004), which is equivalent to 2.7 cartridges.
Interactions Involving Drugs that are No Longer inUse
Below, we analyze potential drug interactions involving
drugs that are no longer or very rarely in use; however, the
provider should be aware of the interactions.
Older Antihypertensive Agents (Anti- adrenergic Drugs)
Guanethidine and reserpine (alkaloid of rauwolfia) are
neuro- adrenergic blockers that are used in the treatment of
arterial hypertension (Jastak and Yagiela 1983; Jastak
et al. 1995; Yagiela 1999). The drugs have almost been
replaced by new antihypertensive agents, which are much
more efficacious and safer.
Guanethidine and reserpine act by impairing the release
of neurotransmitters (norepinephrine) in the sympathetic
nerve endings and leading to depletion of catecholamines in
many organs (Boura and Green 1965; Mitchell and
Oates1970), therefore prolonged use causes hypersensitivity
of the adrenergic receptors to the direct action of sympathomimetic vasoconstrictors (Emmelin and Engström 1961;
Fleming 1962; Boura and Green 1965; Katz and
Epstein1968), thus generating a risk of exaggerated response
to exogenous catecholamines and increased arterial pressure and arrhythmias (Fleming1962; Katz and Epstein1968;
Jastak et al. 1995). The effect is more pronounced with
norepinephrine (Fleming1962; Boura and Green1965).
In conclusion, patients treated with older antihypertensive agents can receive local anesthetic solutions with epinephrine, although at a maximum concentration of
1:100 000 (10 μg/ml) and an absolute maximum concentra-
tion of 50
General Anesthesia (Halothane andThiopental)
μg, that is, equivalent to 2.7 cartridges.
Halothane is a potent inhaled general anesthetic that sensitizes the heart to the action of epinephrine (Joas and
Stevens 1971; Munson and Tucker 1975; Johnston
etal.1976; Hayashi etal.1993) and, probably, levonordefrin
(Yagiela 1999). Sodium thiopental is an ultrashort-
acting
barbiturate that is administered intravenously for induction
of general anesthesia. It also sensitizes the heart to the
action of epinephrine (Hayashi et al. 1993; Christensen
et al.1993). However, in the presence of exogenous epinephrine, both halothane and thiopental can alter heart
rhythm, thus leading to severe arrhythmia (Hilley
etal.1984). Of note, the action of norepinephrine is more
intense than that of epinephrine when altering heart rate in
these cases (Deterling etal.1954; Katz and Katz1966).
In the case of general anesthesia in patients undergoing
oral surgery, sympathomimetic vasoconstrictors can be
used as hemostatic agents to reduce bleeding and thus
make it easier for the surgeon to visualize the field. In these
circumstances – general anesthesia with halothane and
complementary local anesthesia– a paradoxical finding
is that the likelihood of arrhythmias is reduced
(Kaufman1965; Plowman etal.1974; Johnston etal.1976).
In addition, concomitant administration of local anesthesia and general anesthesia reduce post-
operative pain and
is safer than general anesthesia alone (Kaufman etal.2005).
This observation seems to result from the fact that local
anesthetic interrupts the painful stimulus reaching the
brain and prevents the adrenal sympathetic response
(Alexander etal.1972; Plowman etal.1974). The new general anesthetics (isoflurane, desflurane, and sevoflurane)
are not subject to these interactions. Consequently, halothane has fallen into disuse.
In conclusion, patients placed under general anesthesia
can receive local anesthetic solutions with epinephrine,
albeit at a maximum concentration of 1:100 000 (10 μg/ml)
and an absolute maximum dose of 100 μg (Katz etal.1962;
Katz and Epstein 1968; Buhrow and Bastron 1981).
Similarly, patients receiving sodium thiopental can receive
the same solutions of local anesthetic with epinephrine at
the same concentrations with an absolute maximum dose of
1 μg/kg if used in combination with halothane and 2 μg/kg if
used with another general anesthetic gas (Christensen
etal.1993; Yagiela1999).
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