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440
2) Hyperventilation syndrome. This syndrome does not
always accompany vasovagal syncope, although when it
does, the level of carbon dioxide (CO
) falls, leading to a
2
marked reduction in the concentration of this gas in
blood (hypocapnia) and respiratory alkalosis caused by
the increase in pH resulting from the reduction in carbonic acid. CO
is a key factor in the self- regulation of
2
cerebral blood flow, which is independent of arterial
pressure, therefore the reduction in CO
causes cerebral
2
vasoconstriction, reducing blood flow to this organ
(Harrison1973; Campbell etal.1976; Noble1977; Salins
etal.1992) and peripheral vasodilation (Noble1977).
3) Hypoglycemia. The parasympathetic reaction leads to
increased insulin levels, which in turn reduces the
blood glucose level (hypoglycemia). This also deteriorates because the hyperglycemic effect of epinephrine is
reduced in situations of respiratory alkalosis due to
hyperventilation, as reported elsewhere (Salins
etal.1992). Interestingly, blood sugar levels tend to selfregulate after the vasovagal syncope (Salins etal.1992).
Predisposing Factors
As we have seen, anxiety, fear, and pain are the main triggers of vasovagal syncope, although other factors can favor
its appearance. Here, we classify them as more important
and less important:
● More important, main factors (Table23.5):
○ Patient age. In general, patients aged under 30–35 years
account for 80% of cases. However, in children aged
<14 years, the frequency of this type of reaction is very
low (one per 2000=0.05%) because children react to
emotional tension differently than adults. They do not
repress the fight or flight response, but rather scream,
cry, and kick up a fuss. They resist the injection and
therefore do not experience a vasovagal reaction
(Kuster and Udin1985). It is estimated that around
third of young adults are prone to this type of
onereaction (Yjipaavalniemi and Sane1981).
○ Male sex. This is the main factor in 75% of cases. It is
important to remember that males account for 40% of
visits (Annex 1). The reason is that society teaches
males not to show emotions such as fear or pain,
therefore they repress the fight or flight reaction, thus
leaving themselves open to vasovagal syncope.
○ Previous history. Patients with a history of fainting or
syncope in other dental treatments or injections, blood
donation, and vaccination. This is the case in almost
half of all patients treated.
● Less important, additional factors (Table23.5):
○ Lack of sleep.
○ Receiving dental treatment on an empty stomach.
○ Excess heat and humidity.
Clinical Manifestations
Vasovagal syncope occurs in 75% of cases during administration of the local anesthetic or shortly after during dental
treatment (Table 23.6) and can progress through several phases:
1) Early phase, presyncope, or prodrome. This phase lasts
several minutes and is characterized by the following:
● The patient is ill at ease, dizzy, and weak, with facial
flushing.
● The first typical cutaneous signs appear, especially
on the face, with pallor and cold sweat, sometimes
accompanied by nausea (rarely vomiting)
(McGimpsey1977).
● Occasionally, palpitations resulting from the increase
in heart rate, as well as respiratory abnormalities
Table23.5 Factors predisposing tovasovagal syncope.
Factor
Main factors
Younger age 82 81 83 — 80
Male sex 76 81 70 — 75
Previous history 50 28 48 —
Additional factors
Lack of sleep — — 0, 7 12 5
Empty stomach 28 80 8 19 35
Heat 24 — 23 — 25
Data expressed as percentages for main and additional factors.
Harrington-
Kiff (1969)
(%)
McGimpsey
(1977)
(%)
Edmondson
etal. (1978)
(%)
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Salins
etal. (1992)
(%)
45
Rounded
average
(%)
Table23.6 Time ofonset ofvasovagal syncope.
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441
Sample
Reference
Hannington- Kiff (1969) 50 — — 84
McGimpsey (1977) 100 31 47 78
Edmondson etal. (1978) 139 45 22 67
size
with more frequent, superficial, or deep breathing
(hyperventilation).
● Less frequently, ringing in the ears (tinnitus), blurred
vision, and mouth opening, such as when yawning.
● Examination of cardiovascular parameters at the onset
of this phase reveals increased blood pressure and heart
rate due to anxiety (Campbell etal.1976), although this
all changes radically during the next phase.
2) Late phase or syncope (faint). The main characteristic
of this phase is loss of consciousness (syncope or fainting) due to severe hypotension and bradycardia. It is
important to point out that this does not occur in all
patients who experience vasovagal syncope: if the
patient realizes what is happening and starts treatment
during the first phase, it can be avoided relatively easily.
In older studies on extractions, 30% of patients fainted
(Hannington- Kiff 1969; McGimpsey 1977), although
today, and with the patient lying down, this percentage
is much lower. Thus, we can observe the following:
● Loss of consciousness (fainting or syncope). If timely
measures are taken, as we will see, the fainting episode lasts less than 1 minute and rarely more than
minutes (Hannington- Kiff1969; McGimpsey1977).
2
● The faint may be accompanied by dilation of the
pupils (mydriasis).
● Trembling or shaking is relatively common.
● The cardiovascular examination reveals the biphasic
response. Low blood pressure, which may fall to lower
than 50–60 mmHg (systolic) and at which point the
patient faints (Harrison1973; Campbell etal. 1976;
Kuster and Udin1985), and bradycardia (under 50–60
During
anesthesia (%)
During
extraction (%)
Mean 75
blood can reach the brain and raise the legs 15–30° to
facilitate venous return.
2) Unfasten tight clothing, belts, ties, and shirt collars so
as not to interfere with blood flow.
Note: Some professionals tend to place the patient in a
seated position with the head between the legs at the level
of the heart to help blood reach the head. This posture is
not recommended because it prevents us from monitoring
the patient’s breathing and consciousness and from raising
the patient’s legs to favor venous return (McCarthy1982).
Most patients recover with these measures and
therefore do not reach the next phase:
● When the patient is already unconscious, we apply
the basic PABC or PCAB management protocol.
However, it is important to implement the following:
1) Maintain the posture: patient lying down with the
legs raised.
2) Provide 100% oxygen through a mask (Hannington-
Kiff 1969; Verrill 1975; McCarthy 1982; Milan
etal.1986).
3) Initiate support measures:
■ Inhalation of ammonia salts arousal and con-
sciousness (McCarthy 1982; Kuster and
Udin1985).
■ Placement of cold towels on the patient’s head
and forehead (McCarthy 1982; Kuster and
Udin1985).
■ If the patient is cold, cover him/her with a blan-
ket (McCarthy1982; Kuster and Udin1985).
■ If possible, check blood glucose.
If the patient does not recover within 30–60 seconds of applying these measures, call the emer-
3) Recovery phase, which is characterized by recovery of
consciousness, accompanied by confusion, disorientation, weakness, and, occasionally, headache.
Management by theDentist
When the patient is conscious, it is essential to apply the
initial measures we saw in the section on basic management of complications, as follows:
1) Place the patient lying down (supine decubitus) with
the head at the same height as the heart so that the
gency services: the patient may have a more
severe underlying problem (i.e. myocardial
infarction, cardiac arrhythmia, cerebrovascular
accident, hypoglycemia) (Greenwood 2008;
Sambrook etal.2011).
● When the patient has recovered:
1) Do not allow him/her to stand up until total reso-
lution of symptoms.
2) Provide a sugary drink to raise the low sugar levels
resulting from the vasovagal syncope (Edmondson
Total: anesthesia
and extraction (%)
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442
etal.1978; Salins etal.1992). Hypoglycemia may
also be a contributing factor to the syncopal episode, which often occurs as patients may skip a
meal and come to the dental appointment.
3) Decide whether the patient should continue with
the treatment. We suggest the following:
■ If the loss of consciousness lasts less than
10–15
seconds, the total recovery time takes less
than 15
35
minutes, and the patient is less than
years old, treatment can be continued if the
patient agrees.
■ If the loss of consciousness lasts more than
1
minute, the total recovery time takes more
than 30
40
minutes, and the patient is older than
years of age, suspend treatment, recommend
the patient to see a doctor and not to drive, and
ask a relative or friend to take the patient home.
■ If in doubt, suspend treatment.
Prevention
Although vasovagal syncope is easily controlled in healthy
patients, in ASA III patients with cardiovascular abnormalities, who tolerate anxiety and pain poorly, the situation
may become life-
threatening:
1) Position during treatment
Ever since the contour dental chair was introduced in
the 1960s, we have been working with the patient lying
back, the dentist seated (Golden1959; Anderson1960),
and a high aspiration rate (Thompson1967). Not only
does this form of working improve precision dental
work, but with the patient lying back, cerebral blood
flow is better. In addition, the risk of vasovagal syncope
is higher with the patient seated and the dentist standing (Bourne1957,1970).
Table 23.4 shows that the frequency of vasovagal
syncope in the pre-1980, when patients were seated
while the dentist stood, was higher than when dental
work was carried out with the patient lying down and
the dentist seated (1.5% vs. 0.5%).
2) Control of anxiety
Patients with high levels of anxiety should be offered techniques to reduce anxiety and approaches that are beyond
the scope of this book (conscious sedation, intravenous
sedation). To determine the level of anxiety, we propose
two key questions in the health questionnaire (Chapter8):
1) How frightened/anxious are you about dental
treatment?
Not at all □ A little □ Some □ Quite a lot □
A lot □
If the patient selects the last two options (quite a lot
or a lot), and especially the last, we should obtain
more detailed information.
2) Have you ever had an abnormal reaction, felt dizzy,
or fainted at the dentist’s or doctor’s office when
receiving a local anesthetic or vaccination or giving blood?
Yes □ No □
An answer in the affirmative should lead us to ques-
tion the patient, given that a previous history is a
major predisposing factor (see above) (Table23.5).
Hyperventilation Syndrome
Hyperventilation syndrome or reaction, which is also
known as psychogenic dyspnea (Gardner 2000), was first
described in 1937 (Kerr etal.1937). Its definition should be
refined since many of its components are confusing
(Gardner2000; Malmberg etal.2001). Nevertheless, doctors frequently use it. The signs and symptoms of hyperventilation syndrome are often associated with vasovagal
syncope, with some overlap between both conditions,
although the vasovagal components are usually much
more predominant than the respiratory components.
We can define hyperventilation syndrome as rapid and
continuous respiration caused by anxiety that leads to a
reduction in carbon dioxide (CO
) in blood (hypocapnia) and
2
causes vasoconstriction of the cerebral vessels. This in turn
leads to reduced blood flow in the central nervous system
(CNS) and respiratory alkalosis, which decreases ionized calcium concentration and causes musculoskeletal reactions.
Hyperventilation syndrome is estimated to account for
8% of general complications (Matsuura1989; Malamed1993)
and rarely appears in children for the same reasons as vasovagal reaction.
Pathophysiology
The main cause of the syndrome is the patient’s emotional
status (anxiety, fear, hysteria, phobia), which increases the
respiratory rate, thus reducing the level of carbon dioxide
in blood and leading to hypocapnia, also known as hypocarbia. CO
is a basic factor in the self- regulation of cerebral
2
blood flow that is independent of arterial blood pressure,
with the result that the constriction of the cerebral vessels
reduces the quantity of blood in the brain (Campbell
etal.1976; Noble1977; Chapman1984; Milan etal.1986;
Salins et al.1992; Gardner 2000) and leads to peripheral
vasodilation (Noble1977).
The reduction in the pressure of CO
in blood reduces
2
carbonic acid levels, therefore blood pH increases (respiratory alkalosis) from 7.4 (normal) to 7.55, leading to two
phenomena:
● The Bohr effect, which describes the effect of changes in
blood pH on the avidity with which hemoglobin binds
oxygen. In acidic conditions, the hemoglobin binds
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oxygen with less affinity and makes it more available to
the tissues. In alkaline conditions, such as with hypocarbia, the hemoglobin binds oxygen with more affinity,
thus making it more difficult to release and worsening
oxygenation of the brain (Chapman1984).
● Reduction in ionized calcium, leading to musculoskele-
tal irritation, which manifests as cramps, shaking, and
tetany (muscle spasms) (Harrison1973; Chapman1984).
Anxiety also leads to increased activity of the sympathetic nervous system and release of epinephrine and norepinephrine, which in turn produces cardiovascular
manifestations in the form of increased arterial pressure
and heart rate (tachycardia) (Harrison1973; Chapman1984;
Milan etal.1986). Finally, a vicious cycle is created: anxiety
leads to hyperventilation, which in turn increases anxiety
(Compernolle etal.1979).
Clinical Manifestations
Clinical manifestations can be classified as follows:
1) Manifestations due to anxiety.
● 80% with dizziness, disorientation, weakness that
rarely progresses to loss of consciousness (syncope/
fainting) (Compernolle etal. 1979; Chapman1984);
in 60% accompanied by anxiety, nervousness, and agitation (Compernolle etal.1979).
● 60% with palpitations owing to the increased heart
rate (Compernolle etal.1979).
● 60% with pallor and excessive sweating (diaphoresis)
(Compernolle etal.1979; Chapman1984).
● Other manifestations are headache, blurred vision,
ringing in the ears (tinnitus), nausea, and, more rarely,
vomiting (Harrison1973; Compernolle etal.1979).
● During the examination, the state of agitation reveals
an increase in heart rate (tachycardia) and arterial
blood pressure.
● Sometimes the patient feels a sensation of chest tight-
ness (distress) that may be made worse by breathing,
although it is neither serious nor irradiated
(Harrison 1973; Chapman 1984). The sensation is
caused by irritation of the intercostal muscles and
diaphragm due to increased respiratory effort
(Chapman1984).
2) Respiratory manifestations.
● Increased respiratory rate (tachypnea) in 75% of cases,
which reaches 25–30 breaths per minute instead of
the normal rate (9–16). The breaths are deep or superficial. This is a basic sign (Harrison1973; Noble1977;
Chapman1984; Milan etal.1986).
● Sensation of asphyxia and difficulty breathing (dysp-
nea), occasionally with a “lump in one’s throat” (globus
sensation) in 50% of cases (Compernolle etal.1979).
● Frequent movements to open the mouth and dry
mouth sensation caused by anxiety and continuous
breathing with the mouth open.
3) Musculoskeletal manifestations (caused by reduced
ionized calcium levels). Typical findings for this manifestation include the following:
● Feeling of numbness, tingling, and dullness (pares-
thesia) in the fingers and hands in 80% of cases, feet
in 50% of cases, and face (tongue and lips) in 40% of
cases, with muscle cramps and pain that can lead to
muscle stiffness.
● Tetany (50% of cases), which is characterized by mus-
cle spasms in the hands and feet (carpopedal spasm)
involving the following:
■ Stiffness of the hands (fingers and wrists) in flexion
or extension, which is often painful (Geffner and
Murgatroyd1980).
■ Feet (less common), with stiffness of the toes and
ankles in flexion.
Differential Diagnosis
● Vasovagal syncope. Hyperventilation syndrome does not
involve loss of consciousness or reduced heart rate/arterial blood pressure; in addition, it does not improve with
the patient lying down.
● Asthma or allergic respiratory manifestations
(Gardner 2000). Hyperventilation syndrome does not
involve breath sounds (wheezing) because there is no
constriction of the bronchioles. In addition, it improves
with treatment.
● Heart attack (angina pectoris or myocardial infarction). The
chest pain is not severe and does not irradiate to the arms or
shoulders. Furthermore, it improves with treatment.
Management by theDentist
We apply the basic measures (initial measures) seen above,
although here we place emphasis on the patient’s position.
As the patient experiences difficulty breathing, he/she
should be seated, not lying horizontally (in contrast with
the approach to a vasovagal syncope) (Harrison 1973;
Chapman1984). Furthermore, specific measures for these
cases are presented in increasing order of importance,
asfollows:
1) Explain to the patient what is happening to reassure
him/her and ask him/her to breathe more slowly (six to
eight breaths per minute) and thus reduce the respiratory rate (Harrison1973; Chapman1984). This measure
is usually successful.
2) Breathe into a paper or plastic bag. This approach
should only be applied when the previous measure has
failed. The patient is asked to place a paper bag over his/
her nose and mouth and breathe into the bag (a plastic
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bag is also suitable, although as it is softer, it collapses
easily over the nose and mouth). Thus, by breathing
his/her own air, CO
re- enters the patient’s lungs and
2
the signs and symptoms tend to improve (Harrison
1973; Compernolle et al. 1979; McCarthy 1982;
Chapman1984).
Today, paper bag rebreathing should never recommended unless myocardial ischemia can be ruled out
and the patient’s oxygenation has been directly measured by arterial blood gases or pulse oximetry: since
these conditions are impossible to achieve outside
the hospital this method is not recommended
(Callaham1989).
3) Medication. If the previous measure fails because the
patient is very nervous, then this last alternative must
be applied. This situation is very unusual because the
previous measures are usually successful. In this case,
intramuscular midazolam 5 ml (5 mg) is injected, and in
5–15
minutes the patient relaxes and recovers.
Midazolam can also be given orally, although its effect
takes more than 30 minutes.
A classic alternative is to inject diazepam (Valium
2
ml (10 mg) intramuscularly, although as it is not water-
®
soluble, this is more painful (Chapman1984).
Patients who experience hyperventilation syndrome generally recover very well, do not lose consciousness, and can
continue with their dental treatment.
Toxicity Induced by Sympathomimetic
Vasoconstrictors
Approximately 3% of the general adverse reactions that occur
during administration of local anesthetic are to epinephrine (Fast etal.1986; Matsuura1989). Interestingly, these
reactions are usually confused with vasovagal syncope.
Pathophysiology
Initially, it was thought that the signs and symptoms were
caused by the action of catecholamines (epinephrine and
norepinephrine) in the brain. However, it has been shown
that this is not the case because the low lipid solubility of
these substances makes it difficult for the drugs to penetrate the CNS and intraventricular or intracisternal injections (direct administration to the brain) lead to sedation
(Marley and Stephenson1972).
The real cause of these actions is via the cardiovascular
system, metabolic action, and neuromuscular transmission
caused by these same adrenergic amines (Jastak etal.1995).
)
The reactions appear immediately as a result of an inadvertent intravascular injection, overdose, or severe interactions
with other drugs (Pogrel etal.2014). In any case, the effect
is usually short, since catecholamines are inactivated after a
few minutes (less than 5) (Lund1951).
Allergic- like Reactions
These are also known as anaphylactoid reactions (Baldo
etal.2008) or allergic-
like reactions because they are nonimmune reactions caused by emotional tension that can
lead to release of compounds such as histamine (Ring1985)
and reactions such as the following:
● Urticaria associated with anxiety (Milan et al. 1983;
Tauberg etal.1983).
● Angioedema associated with anxiety (Barclay and
Edwards1971; Chue1976).
Note: The clinical description of these conditions is provided in this chapter (see below) in the section on allergy,
where such conditions are typical.
Fortunately, this type of reaction is very rare and, logically, is confused with allergic reactions, since it is characterized by similar manifestations, but can be distinguished
from allergic reactions by the negative result in allergy
tests. Patients who experience reactions can be treated at
the dentist’s office with anxiolytics and sedation (Milan
etal.1983; Tauberg etal.1983).
Symptoms ofReaction toEpinephrine
As we have seen, onset is rapid, occurring shortly after
injection or even during injection. The reaction lasts only a
few minutes and is characterized by the symptoms set out
below (Dick1953; Holroyd etal.1960; Jastak etal.1995;
Malamed2004):
● Patient- reported symptoms:
○ Sensation of anxiety, nervousness, fear, and
apprehension.
○ Palpitations (tachycardia) resulting from the force and
speed at which the heart contracts. This is the main
symptom.
○ Dizziness, vertigo, and weakness.
○ Occasionally, nausea, which rarely progresses to vom-
iting, difficulty breathing (dyspnea) caused by anxiety
and, more rarely, headache, which is sometimes throbbing owing to the force with which the heart pumps
blood, thus increasing pressure in the head.
● The signs are as follows:
○ Pale and cold skin, mainly on the face, and sweating
(diaphoresis).
○ Occasionally, trembling in the lips and hands.
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● The cardiovascular examination reveals increased heart
rate, with frequent premature ventricular contraction,
increased systolic arterial pressure and increased blood
pressure.
Symptoms ofReaction toNorepinephrine
As seen above, onset of the reaction is rapid, shortly after
the injection or even during the injection, generally at high
concentrations, such as 1:25
(33
μg/ml) (Boakes etal. 1972; New Zealand Committee
000 (40 μg/ml) or 1:30 000
onAdverse Drug Reactions1974), and the reaction lasts a
few minutes. The symptoms are set out below (Boakes
etal.1972; Meyer1986; Van der Bijl and Victor1992):
● Patient- reported symptoms:
○ Headache is the main symptom and the most frequent.
Onset is immediate or within a few minutes. It is usually severe (often so intense that patients press their
hands to their head). It generally affects the temporal
or occipital area (nape of the neck), although there
have been reports of frontal headache. The headache
may be throbbing, although not always, and rarely
may persist for hours or days, albeit with less intensity.
This is due to involvement of the CNS.
○ Other symptoms include anxiety, nervousness, appre-
hension, nausea (although rarely vomiting), and difficulty breathing (dyspnea) caused by anxiety.
● The signs are as follows:
○ Pale and cold skin, mainly on the face, and sweating
(diaphoresis).
○ In contrast, the skin of the face is sometimes flushed.
● The cardiovascular examination reveals reduced heart
rate (bradycardia), which is a very characteristic sign,
and increased arterial pressure (both systolic and
diastolic).
The general cause of reaction to norepinephrine is the
encephalopathy caused by the hypertensive crisis.
2) Monitor the patient every 5 minutes, recording heart
rate and blood pressure.
3) If the situation persists:
■ Administer oxygen through a mask. However, it is
important not to confuse this situation with hyperventilation, in which case oxygen worsens the situation.
■ Administer a sedative (diazepam or midazolam)
parenterally (intramuscular); however, when these
drugs take effect, the reaction has generally resolved.
4) Wait until the patient has completely recovered,
seated in the dental chair, from the fatigue resulting
from the adrenergic excitation and only allow him/
her to leave when fully recovered. When in doubt of
any resolution of symptoms, activate emergency
medical response services.
● Exceptionally, in predisposed patients, these situations
(owing to the increased heart rate and/or increased blood
pressure) can cause a heart attack (angina pectoris or
myocardial infarction) or cerebrovascular accident. In
these cases, and although beyond the scope of this book,
the support measures set out at the beginning of this
chapter should be followed and the emergency services
called (911in the United States, 112 in the European
Union, and 999in the UK).
Systemic Toxicity Induced by
Local Anesthetics
Approximately 1.5% of all general complications occurring
during administration of local anesthetics are caused by
toxicity (Malamed1993). It is important to remember that
many such complications are mistaken for allergy and vasovagal syncope, when allergic reactions are usually very
different from local anesthetic- induced toxicity (see below).
Pathophysiology
Management by theDentist
● The usual approach is as follows:
1) Interrupt the dental procedure in progress.
2) Wait and see if the reaction resolves itself, given that
it is usually mild or moderate and disappears after
a few minutes (less than 5), and continue with
treatment.
● If the reaction does not resolve within a few minutes:
1) Place the patient in a comfortable position, generally
erect or seated/semiseated (never lying down). This
position minimizes the effect of hypertension on
brain tissue.
Local anesthetics block sodium channels indiscriminately
in excitable membranes (Covino1987; Lai etal.2004), the
main targets being the nervous system and the muscles,
especially the heart and cardiovascular system. In the case
of toxicity, it is important to take into account the plasma
level of the local anesthetic: venous concentrations are
20–50% lower than arterial levels (Eriksson et al. 1966;
Moore etal.1977; Knudsen etal.1997), but physicians use
the venous plasma values (expressed as micrograms per
milliliter, μg/ml) (Annex 13).
Despite marked individual variability, toxic manifestations begin to appear when the local anesthetic exceeds a
specific concentration (Annex 13). In addition, toxicity
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increases with the greater relative potency of the anesthetic and therefore is observed at lower plasma levels
(Covino1987; Garfield and Gugino1987).
Local anesthetics first attack the CNS, which is more vulnerable, therefore lower plasma concentrations should be
sought. Thus, as local anesthetic concentrations in blood
increase, the drug can easily cross the blood–brain barrier
owing to its high lipid solubility (Garfield and Gugino1987)
and low molecular weight (Covino 1987), affecting the
CNS and leading to seizures. Subsequently, as plasma levels gradually increase, the cardiovascular system, which is
more resistant, becomes involved, thus initiating the collapse that leads to death (Covino 1987; Garfield and
Gugino1987). The areas affected are as follows:
● CNS. In the delicate balance between inhibition and
excitation, initial excitation is the predominant initial
characteristic. The inhibitory neurons are blocked and
the patient may have shaking, tremors, diplopia, tinnitus, and seizures. As toxicity advances, both inhibition
and excitation are depressed, resulting in loss of consciousness (Garfield and Gugino1987).
● Heart. Contractility is reduced, as is heart rate (bradycar-
dia) (Covino1987).
● Vessels. The direct action of the anesthetic leads to vaso-
dilation as a result of relaxation of the vascular muscle
tissue, and blood pressure falls (hypotension). In addition, as the sympathetic preganglionic nerve fibers are
anesthetized, thus blocking the vasoconstrictor effect,
both the vasodilator effect and hypotension become
more pronounced.
During the convulsion phase, breathlessness is accompanied by a marked increase in oxygen consumption owing to
the effort of muscular contractions. We therefore observe
the following:
● The amount of oxygen reaching the tissues decreases
(hypoxia), thus aggravating cerebral depression.
● CO
levels increase (hypercarbia), with two effects:
2
is a basic feature of self- regulation of cerebral
1) CO
2
blood flow. Increased CO
levels lead to increased
2
blood flow, with the result that the amount of local
anesthetic reaching the brain also increases
(Covino1987).
2) The increase in CO
also increases carbonic acid lev-
2
els and therefore decreases pH (respiratory acidosis).
The free fraction of the local anesthetic increases as
the fraction bound to plasma proteins decreases. The
free fraction exerts the pharmacologic and toxic
effect, and thus increases toxicity (Tucker and
Mather1979; Scott1975a; Covino1987; Garfield and
Gugino1987; Knudsen etal.1997).
Causes ofLocal Anesthetic- induced Toxicity
Inadvertent Intravascular Injection
Inadvertent intravascular injection is the most common
cause of local anesthetic-
induced toxicity (Covino 1978;
Scott1986). It acts through two pathways:
1) Passage to the bloodstream. In this case, the intravascu-
lar injection sends the local anesthetic into the bloodstream. However, passage is not slow and gradual, as is
the case with subcutaneous injection. Consequently,
the high concentration of drug can reach the target
organs, and lower doses can reach toxic levels in the
CNS and cardiovascular system.
It has been estimated that rapid intravascular injection of a 1.82%), which is equivalent to 36
same concentration in blood as a 1080-
ml cartridge of 2% anesthetic (e.g. lidocaine
mg of drug, reaches the
mg dose
injected subcutaneously (equivalent to 30 cartridges)
(Scott1986).
Slow injection, even if it is intravascular, partially
reduces this risk since passage of the drug into the
bloodstream is slightly slower, thus enabling it to dilute
(Campbell and Adriani1958; Forrest1959). In addition,
slow injection enables the lungs to retain the drug –
albeit for a short period – thus attenuating its toxic
effect (Tucker and Mather1979; Scott1986).
2) Direct passage to the brain. Retrograde arterial flow has
been demonstrated in experiments (Aldrete et al.
1977,1978) and enables intraorally injected anesthetic
to reach branches of the superior alveolar artery (maxillary) or inferior alveolar artery (mandibular) and reverse
the flow of blood with the force of the injection, to the
extent that it reaches the maxillary artery and, from
there, the external carotid artery and even the internal
carotid artery, where normal flow returns and the drug is
transported to the brain (Figure22.6, Chapter22). Thus,
mg of injected anesthetic can reach the cerebral blood-
2
stream at a concentration of 20 μg/ml (Aldrete
etal.1977,1978), although, fortunately, for a short time.
Intravascular injection therefore has a series of specific
characteristics that can be summarized as follows:
1) The toxic reaction occurs within a few minutes (if the
drug passes into the bloodstream) or even immediately
(if the drug passes directly to the brain), with rapid
onset of symptoms and even convulsions (Scott1986).
2) The toxic reaction is short- lived, fortunately, because, as
the blood in the CNS passes into the bloodstream, its
toxic concentration in the brain decreases rapidly.
Furthermore, not all techniques for administering local
anesthetics are equally likely to inject the drug into the
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bloodstream. Table13.2 (Chapter13) summarizes the percentages of positive aspirations in the different techniques
for administering dental local anesthesia. It is very important to aspirate before injection and to inject the drug slowly.
Overdose
Administration of excess local anesthetic is a less common
cause of toxicity, although it is more frequent in the following situations:
1) Children, especially preschool children and those aged
under 6–8
years (Goodson and Moore 1983; Hersh
etal.1991; Virts1999).
2) Low- weight adults and adults with low body mass. This
is very often the case with elderly people.
3) Administration of topical anesthetics (Weisel and
Tella1951; Adriani and Campbell1956; Wehner and
Hamilton1984; Mehra etal.1998). It is important to
remember that topical anesthetics contain much
higher concentrations of anesthetic and their quantity
must be added to the quantity of anesthetic already
injected.
Toxicity by overdose is characterized by a series of spe-
cific factors, as follows:
1) The toxic reaction appears much later, generally
5–20
minutes after the injection, although rarely more
than 30
minutes later (Weisel and Tella 1951; Adriani
and Campbell 1956; Wehner Hamilton 1984; Mehra
etal.1998; Goodson and Moore1983; Hersh etal.1991;
Virts1999).
2) The reaction is much more severe and long- lasting than
that caused by intravascular injection. In a case series of
pediatric sedation and local anesthetic overdoses by
Goodson etal., a distinct separation of fatal and nonfatal overdoses was demonstrated when the maximum
recommended dose (MRD) was exceeded by threefold.
This meant that any combination of adding the relative
MRDs of the sedatives and the MRD of the local anesthetic administered was highly likely to lead to death or
significant morbidity (irreversible brain damage). This
study demonstrated that any combination of the following would be very likely to result in serious morbidity or
mortality: (1) an overdose of local anesthetic by three
times its MRD, (2) an overdose of a sedative agent by
three times its MRD, or (3) a combination of dosing of
the local anesthetic and the sedative that exceeds the
sum of their respective MRDs by threefold (Goodson
and Moore1983; Hersh etal.1991).
To avoid this complication, every attempt should be
made not to exceed the MRDs of dental anesthetic
according to body weight (Annex 10). It must also be
remembered that the dose of topical anesthetic administered should be added to the injected dose (Cannell1996;
Meechan1998).
Rapid Absorption
Rapid absorption may result from injection into very vascularized tissue (Scott1986), for example inflamed areas,
as is the case with patients receiving dental treatment. This
situation is very rare in dentistry because of the low doses
and local anesthetic solutions we apply.
Clinical Manifestations
Much has been learned about the clinical manifestations
of toxicity by local anesthetics from clinical trials with
volunteers who received intravascular infusions (Foldes
etal.1960,1965; Eriksson etal.1966; Usubiaga etal.1966;
de Jong and Bonin1966; Jorfeldt etal.1968; Scott1975a,b;
Friedman etal. 1982; Knudsen et al.1997), from published cases of toxicity (Weisel and Tella1951; Adriani
and Campbell 1956; Goodson and Moore1983; Wehner
and Hamilton1984; Mehra etal.1998; Hersh etal.1991;
Virts 1999), and from updated reviews (Gitman
etal.2019).
We divided clinical manifestations into four phases, from
lesser to greater severity, although there may be numerous
overlaps and presentation may vary widely from one
patient to another (Eriksson etal.1966).
First Phase: Initial
The initial phase is characterized by symptoms that may go
unnoticed by the physician if the patient does not report
them. The manifestations include the following:
● Dizziness, vertigo, somnolence, disorientation, and con-
fusion. Patients sometimes complain of feeling drunk or,
much more rarely, excited and euphoric.
● Sensation of heat that spreads throughout the body.
Patients may also feel cold, although this is much rarer.
● Sensation of numbness or paresthesia in the area of the
mouth (lips, tongue) and face that can spread to the
extremities and throughout the body. The effect is
thought to occur when the local anesthetic leaves the
vessels and blocks the sensory nerve endings (Scott1986).
It is important to note that in a local anesthetic systemic
toxicity or overdose, the patient will note perioral numb-
ness and tingling, and not just numbness on the side
anesthetized.
● Other less common manifestations include a metallic
taste and headache (cephalea) resulting from cerebral
vasodilation.
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Second Phase: Advanced
The advanced phase is characterized, in addition to new
symptoms, by objective signs of toxicity that are observed
by the physician and can be considered very typical.
● Ocular abnormalities, which may be subjective (symp-
toms) or objective (signs):
○ Subjective. Visual abnormalities such as blurred
vision, double vision (diplopia), color blindness, and
seeing lights or flashes and moving objects.
○ Objective. Involuntary eye movements up and down
or side to side (nystagmus), which may first be slow in
one direction and then rapid in the opposite direction.
Dilation of the pupils (mydriasis) in the more advanced
phases. Subtle movements of the eyelashes and eyelids, with occasional difficulty opening the eyes.
● Hearing abnormalities, such as sounds or metallic ech-
oes (tinnitus) or, on the contrary, loss of auditory acuity.
● Difficulty speaking, saying unrecognizable words (slurred
speech). In some cases, this sign must be differentiated
from those observed in neurotic or hysterical patients
(Scott1986).
● Involuntary muscle activity, such as shaking, spasms,
muscle twitch, and trembling affecting the muscles of
the face, fingers, hands, and extremities. This type of
muscle activity must be distinguished from trembling
caused by cold or nervousness (Scott1986).
● Other, less frequent manifestations include difficulty
swallowing and the feeling of “a lump in one’s throat,”
anxiety with a sensation of chest tightness (distress),
nausea (rarer), and vomiting (very rare).
Third Phase: Convulsions
The third phase is characterized only by objective signs of
toxicity. Symptoms are no longer present. The signs are as
follows:
● Loss of consciousness (almost always).
● Convulsions, which usually appear after loss of con-
sciousness, although this is not always the case (Usubiaga
etal.1966).
○ Convulsions take the form of tonic and clonic contrac-
tions. In tonic (static) convulsions, the whole body is
rigid, with the arms stretched or flexed but stiff and
the legs stretched and stiff. Clonic (dynamic) convulsions are characterized by movements of the head and
flexion, stretching, and violent shaking of the limbs.
○ Tonic and clonic contractions frequently alternate for
several seconds, then stop for a few seconds before
entering a new cycle.
○ Foaming at the mouth as a result of air entering and
mixing with saliva and blood (from biting the edge of
the tongue or lips).
○ Convulsions are violent movements that can be dif-
ferentiated from the trembling (which is much
softer) that often occurs during vasovagal syncope
(Scott1986).
● Respiratory difficulty or inability to breath (apnea), espe-
cially during the convulsion. Hyperventilation is rare.
● The end of the convulsion may be accompanied by invol-
untary urination owing to relaxation of the sphincters
(de Jong and Bonin1966).
Note: In the early phases, cardiovascular examination
reveals moderate involvement with increased and
decreased arterial blood pressure and heart rate, although
moderate increases are more common. The acute phase is
characterized by increased arterial blood pressure (Rutten
etal.1989).
Fourth Phase: Final
The final phase is characterized by two possibilities: (i) toxicity is not controlled and the patient develops cardiovascular depression, and (ii) the patient recovers.
1) Cardiovascular depression. The patient always loses
consciousness and toxicity affects the cardiovascular
system, with a marked reduction in heart rate (bradycardia) and arterial blood pressure (hypotension), and
peripheral vasodilation (red and hot skin). If the condition is not controlled the patient dies of cardiorespiratory failure.
2) Recovery. Clinical trials with volunteers show that
recovery time after the patient presents signs and symptoms of toxicity (without reaching the final phase) and
the intravenous infusion of local anesthetic has ceased
is somewhat less than 20 minutes (Table23.7). However,
Table23.7 Average recovery time among clinical trial
volunteers who received local intravenous anesthetics.
Local
anesthetic
Procaine 26 Usubiaga etal. (1966)
Lidocaine 18 Foldes etal. (1960), (1965)
Mepivacaine 29 Foldes etal. (1965)
Prilocaine 10–15 Eriksson etal. (1966)
Bupivacaine 20 Knudsen etal. (1997)
Ropivacaine 13 Knudsen etal. (1997)
Mean 17.6≈ 20
Recovery
time (min) Reference
10 De Jong and Walts (1966)
10–15 Eriksson etal. (1966)
38 Usubiaga etal. (1966)
5–20 Knudsen etal. (1997)
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recovery may take 40 minutes in some cases. Short periods of toxicity leave no permanent neurological abnormalities or sequelae (Garfield and Gugino1987).
Clinical Variations
Some local anesthetics present specific characteristics in
the clinical manifestations of toxicity.
1) Tetracaine and toxicity without convulsions.
Tetracaine is a local ester-
type anesthetic that is currently used as a topical anesthetic. Toxicity is characterized by the following: (i) greater frequency than with
other local anesthetics, (ii) rapid and sudden onset with
no initial signs, and (iii) no convulsions in 70–80%
of cases (Weisel and Tella 1951; Adriani and
Campbell1956). Tetracaine-
induced toxicity progresses
rapidly to cardiovascular depression, with loss of consciousness, which can prove fatal (Weisel and Tella1951;
Carabelli 1952; Adriani and Campbell 1956; Adriani
et al. 1959); furthermore, owing to its high degree of
vasodilation, tetracaine is the only topical anesthetic
that enters the bloodstream quicker than by subcutaneous injection (Adriani and Campbell1956).
2) Bupivacaine and cardiotoxicity.
All local anesthetics are toxic for the central nervous
and cardiovascular systems, and bupivacaine is no
exception. However, this local anesthetic is characterized by being the most cardiotoxic (Covino 1987).
Cardiotoxicity has already been addressed (Chapter9),
therefore the maximum dose in dentistry is 90 mg.
Management by theDentist
Onset of the signs and symptoms of local anestheticinduced toxicity should be addressed using the basic initial
measures seen above (e.g. suspend treatment, placing the
patient in the supine position). However, a series of more
specific measures should also be taken, as follows:
1) Remove the anesthetic and/or stop the injection
If the manifestations of toxicity appear during the
injection (immediate manifestations), then the reaction has resulted from intravascular passage directly to
the brain and the injection should be stopped immediately. If topical anesthetic has been applied and the
manifestations of toxicity appear after a few minutes,
then the dose is excessive and the remaining anesthetic
should be removed from the mouth (Wehner and
Hamilton1984).
2) Administer oxygen (O
It has been shown that O
)
2
(Daos etal.1962; Englesson
2
and Matousek 1975) and hyperventilation (Englesson
and Matousek1975) protect against the toxicity of local
anesthetics, since higher doses were needed to kill
experimental animals. Therefore, when necessary, oxygen 100% should be administered through a facemask
and the patient should be asked to breathe more quickly
(hyperventilation) to reduce CO
levels.
2
3) Prevention of lesions caused by convulsions
If the patient begins to experience convulsions, we
should remove the dental unit to prevent the patient
from knocking against it. One member of the dental
team should support the upper part of the body (head,
arms, and trunk), while the other holds the patient’s legs
to avoid contact with the cuspidor or falling from the
chair. The support should not be rigid, but rather should
leave the patient with some freedom while preventing
extreme movements (hyperextension), which can lead
to dislocations and fractures.
Never place anything into the patient’s mouth. Many
dentists and nurses have been trained to prevent
intraoral lesions by introducing handkerchiefs, towels,
or napkins into the patient’s mouth. This maneuver is
dangerous during convulsions owing to the strong contractions of the mouth. In addition, forcing the mouth
open could lead to injury of the soft tissue, dental fractures, or injury to the fingers of the person involved
(never insert your fingers into the mouth of a patient
experiencing convulsions). Clinical studies report mild
oral lesions in around half of cases. These almost all
affect the border of the tongue, and only 2% require surgery (Roberge and Maceira-Rodriguez1985).
If the patient has fallen to the floor, the approach set
out above is followed, although in this case, it is useful
to remove chairs and objects that the patient might come
into contact with. The patient’s head should be protected
by placing a pillow, blanket, towel, or jacket underneath
to prevent violent contact with the floor.
In the absence of intense overdose, these measures
are generally sufficient and the convulsions resolve
within 10
minutes (Scott1986). However, if the convulsions last more than 2–5 minutes, we should move on to
the next stage and administer an anticonvulsant.
4) Injection of an anticonvulsant (midazolam)
The currently used medication is midazolam hydrochloride, a benzodiazepine that is three to four times stronger
than diazepam. As it is water soluble (diazepam is not),
it can be injected intramuscularly, sublingually, or submentally. It is less irritant than other drugs and has 90%
bioavailability and absorption (Blumer 1998). In addition, its half- life is short (2 hours), its plasma peak is
rapid, and its metabolites are not active, thus making it
faster acting, safer, and more efficacious than diazepam
(de Jong and Bonin1981).
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