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Pathophysiology
Vasoconstriction follows the path of the superior alveolar
arteries (in injections into the superior arch) or of the lower
alveolar arteries (in mandibular block) to the maxillary
artery, from where it will reach the infraorbital artery,
whose branches perfuse the skin (zygoma, infraorbital border, wing of the nose). One variant is from the maxillary
artery to the greater palatine artery (palate).
Injecting directly into the maxillary artery (not from the
alveolar arteries) is also possible (Kronman and Giunta1987;
Heasman and Reid1995). It is important to remember the
anatomical variations of the maxillary artery, which runs
superficially and laterally to the lateral (external) pterygoid
muscle at this level (Pretterklieber etal.1991). The maxillary artery varies widely in diameter (2–6 mm)
(Biermann 1943) and often descends to the mandibular
foramen (Lacouture etal.1983) (Figure3.13, Chapter13).
Another possibility is the retrograde flow of the anesthesia, and especially the vasoconstrictor, from the alveolar
arteries to the maxillary artery. This option is less probable
(Heasman and Reid1995).
Localized Late- onset Skin Lesion
The frequency of this type of lesion, which affects the skin
of the lips, is unknown, although it is thought to be exceptional, given that very few cases have been reported. It is
noteworthy that most occur after mandibular block in children aged 7–10
years (Table22.4).
Clinical Manifestations
The affected skin depends on the region where the anesthesia is injected. Thus, in cases of mandibular block, the
skin of the lower lip is affected above the chin or adjacent
to the commissure; the skin of the upper lip is affected in
maxillary infiltrations.
Clinical manifestations appear during the first hours
minutes to 3 hours) after administration of the anes-
(30
thetic (rarely before 3
days) (Table22.4) and are character-
ized by the appearance of a reddish patch (erythematous
macule), which is usually accompanied by itching (pruritus) or a burning sensation. Occasionally, it first manifests
as a pale patch that progresses to an erythematous macule
within a few hours (Torrente-
Castells etal.2008).
During the following days or weeks, the lesion progresses
to necrosis of the skin with formation of a crust that leaves
a pigmented or hypopigmented area or simply a scar on
healing. Sensory alterations on the chin are a potential
sequela (Krüger and Nehse1991).
Causes andPathophysiology
The causes are not well known, although two possible
mechanisms have been posited (Curley and Baxter1987):
Ischemic Necrosis Dueto Vasospasm
Vasoconstriction results from needle- induced irritation of
the sympathetic fibers surrounding the arterial wall, thus
leading to vasoconstriction along the terminal branches, in
Table22.4 Characteristics ofcases oflocalized delayed skin lesion
Anesthetic
Reference Age/sex Technique Skin affected
Lederman etal. (1980)
Curley and Baxter (1987) 7/♀ InfP left Upper lip 2.2/L- 50- 50 Hours
Krüger and Nehse (1991) 33/♀ MB left + inf mental Lower lip
Torrente- Castells etal. (2008) 10/♀ MB left + inf mental Lower lip
MB, mandibular block; inf mental, infiltration in mental nerve; InfP, buccal infiltration in posterior upper arch (molars); ml, injected milliliters;
LAS, local anesthetic solution: L- 100, lidocaine 2% with epinephrine 1:100 000; A- 100, articaine 4% with epinephrine 1:100 000; L- 50- 50,
lidocaine with epinephrine 1:50 000 and with norepinephrine 1:50 000.
7/♀
8/♀ MB left Lower lip
7/♀ MB left Lower lip near
9/♀ MB left Lower lip near
MB left Lower lip
Chin
Chin
commissure
commissure
Chin
Chin
1.8/L- 100 30 min
<1.8/L-
100 1 h
1.8/L- 100 45 min
−/L- 100 2 h
5.4/A- 100 3 days
1.8/A- 100 3 h
Time to onsetml/LAS
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this case at the level of the skin. It may also be caused by
exogenous epinephrine injected intravascularly that is
transported toward the terminal peripheral branches of the
skin of the face.
In mandibular block, the path covered by the vasoconstrictor effect runs from the inferior alveolar artery (branch
of the maxillary artery) to its mental branch and from here
by anastomosis (Kawai etal.2006) with the submandibular
and inferior labial arteries (both branches of the facial
artery), leading to vasoconstriction of the vessels of the
skin of the chin (Torrente-
Castells et al. 2008). Direct
injection into the area of the mental nerve is an aggravating
factor, leading to vasospasm of the arteries that supply the
skin of the chin and the intraoral mucosa in the region of
the lower canine and first mandibular premolar (Krüger
and Nehse1991; Torrente- Castells etal.2008).
Type III Allergic Reaction
A type III allergic reaction, or immune complex–mediated
reaction (e.g. Arthus reaction or serum sickness), is an
antigen–antibody reaction in the walls of the blood vessels
that leads to acute vasculitis with tissue necrosis. This reaction manifests locally within a few hours. It very rarely
occurs with local anesthetics (Lederman etal.1980).
In cases of type III allergic reaction, skin allergy tests
usually yield negative results (Lederman etal.1980; Curley
and Baxter1987), although when the same drug is applied
at the same site, the late skin eruption re- occurs. However,
when another solution is used, the reaction does not appear
(Lederman etal.1980).
Facial Hematomas
A hematoma is caused by extravasation of blood from a
vessel to the surrounding tissue as a result of needle injury
(Kuster and Udin1984). If the vessel is an artery, blood
accumulates quickly; if it is a vein, blood accumulates
slowly (Laskin1984). In all cases, bleeding is self- limiting
because of pressure from the surrounding tissue.
Many techniques can lead to hematoma, for example
mandibular block, although given that the vessels are very
deep, the hematoma is not clinically visible (Kuster and
Udin1984). Even so, small hematomas are common on the
oral mucosa as a result of techniques involving maxillary
infiltration into the lateral incisors and first molars: hematoma has been estimated to appear in 1% of cases (Evans
et al. 2008), although with the minimum volume/minimum injection time technique, this frequency is multiplied
since several injections are made at the same site.
In this section, we will examine hematomas that appear
on the skin of the face, but not the smaller yet common
hematomas that appear on the mucosa.
Technical Factors Contributing toHematomas
The techniques that most frequently lead to hematomas on
the face are as follows:
1) Injections into the area of the upper molars in buccal
infiltration, posterior superior alveolar nerve block,
andhigh tuberosity approaches (Bennett1984; Laskin
1984; Roberts and Sowray 1987; Jastak et al. 1995;
Malamed2004). At this level, 0.5% of injections can lead
to facial hematoma (Kuster and Udin1984), especially
when the needle is inserted higher and deeper, since it
is easier to inject into a branch of the pterygoid venous
plexus or the posterior superior alveolar artery (Harn
etal.2002).
2) Block applied at the level of the foramina (infraorbital
and mental) (Laskin1984; Roberts and Sowray1987;
Joyce and Donnelly 1993; Jastak et al. 1995;
Malamed2004; Karkut etal.2010). With some exceptions and specific cases such as those already discussed, these techniques are not recommended in
current practice (Evers and Haegerstam1981; Kleier
et al. 1983; Haglund and Evers 1985; Joyce and
Donnelly1993).
Clinical Manifestations
● Swelling, which appears in the area of the upper molars
(Kuster and Udin 1984) and can appear on the skin of
the malar region or masseter. This swelling is very large
and cosmetically undesirable because a large quantity
of blood can accumulate in the infratemporal space,
thus highlighting the resulting facial asymmetry
(Malamed 2004). Swelling appears rapidly if the lesion
affects an artery, such as a branch of the facial artery or
a buccogingival branch of the posterior superior
alveolar artery, which follows an irregular path along
the maxillary tuberosity (Jastak et al. 1995; Harn et al.
2002; Malamed 2004), or slowly if the lesion affects a
vein of the pterygoid venous plexus (Jastak et al. 1995;
Malamed 2004).
● Skin discoloration, also known as ecchymosis
(Bennett 1984; Kuster and Udin 1984; Roberts and
Sowray 1987; Malamed 2004), progresses downwards
and forwards along the muscle planes of the cheek
until it reabsorbs spontaneously after 10–15 days
(Malamed 2004).
● Other occasional manifestations include the following:
○ Sensation of tightness, but not pain, in the area affected
(Jastak etal.1995).
○ Difficulty opening the mouth (trismus) if the tip of the
needle has irritated the lateral (external) pterygoid
muscle (Malamed2004).
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Management by theDentist
● The patient should be advised that the hematoma reab-
sorbs within 10–15
days (Bennett 1984; Malamed 2004).
Often no interventions are recommended and invasive
measures such as drainage are contraindicated (Bennett
1984; Roberts and Sowray 1987; Jastak et al. 1995;
Malamed 2004).
● If the swelling is detected early, the dentist may attempt
to control it by pressing on the affected area for 15
minutes (Kuster and Udin1984; Laskin1984) and/or applying ice to the skin for its vasoconstrictive effect (Kuster
and Udin1984; Jastak etal.1995; Malamed2004). In the
case of a hematoma affecting the region of the upper
molars, it is difficult to apply direct pressure, therefore a
finger should be inserted directly into the mouth and
pressure applied at the bottom of the vestibular surface
of the upper molars, whereas on the outside pressure can
be applied to the skin of the malar region (Malamed2004).
● As an option, some authors recommend that the patient
apply heat to the affected area 24
hours after the procedure to aid reabsorption of the hematoma (Laskin1984;
Jastak etal.1995; Malamed2004). Heat causes vasodilation, favors withdrawal of the extravasated blood, and
has an analgesic effect.
● Some authors suggest reassessing the lesion at 48 hours
to determine whether an infection has developed (very
unusual) and prescribe antibiotics (Laskin1984).
axon is split, the nerve stem remains intact thanks to the
supporting connective tissue. Recovery is spontaneous
weeks or 2–6 months).
(6–8
● Neurotmesis. When there is axonal degeneration and
anatomical damage to the nerve and therefore complete
rupture of the nerve stem. The resulting lesion is permanent and a scar neuroma may form as a result of interference in neuronal regeneration.
General Causes
1) Needle injury (physical effect). The tip of the needle,
especially if barbed outwards (typical in mandibular
block after pressing the needle against the bone) (Stacy
et al. 1994), can directly injure the nerve stem and
lead to intraneural hemorrhage (Haas and Lennon
1995; Pogrel and Thamby2000) (Figure22.2), which in
turn could increase pressure on the nerve fibers, thus
altering metabolism and nerve function (Haas and
Lennon1995). The situation is aggravated by the sub
sequent intra- and extraneural fibrosis (Pogrel and
Thamby2000).
Repeating the number of injections, especially in
mandibular block, increases the risk of this type of
-
Nerve Lesions
This section includes nerve lesions caused by injection of
dental local anesthesia. Thus, we can mention the following:
1) Electric shock sensation on insertion of the needle.
2) Long- term paresthesia caused by persistent neuropathy.
3) Alterations of the sense of taste caused by injury to the
chorda tympani.
4) Hoarseness by block of recurrent laryngeal nerve.
Anatomical Lesions
In 1943, Seddon described three basic types of lesion of the
peripheral nerves (Seddon1943):
● Neurapraxia. When there is no axonal degeneration,
although the axons are intact, they do not conduct electrochemical impulses. There is no loss of axonal continuity. In these cases, recovery is spontaneous (10 days
to3 weeks).
● Axonotmesis. When there is axonal degeneration. There
is no anatomical damage to the nerve, and although the
Figure22.2 Nerve injury caused by a needle barbed outward.
Redrawn from Stacy etal. (1994).
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lesion (Pogrel et al. 1995; Pogrel and Thamby 2000;
Hillerup and Jensen 2006). In some series, 35% of
patients report having received more than two injections at the same site (Hillerup and Jensen2006).
Note: It is interesting that, in five cases involving
exploratory surgery, no evidence of needle-
induced
microtrauma was observed, although the area was
slightly pale and there were adhesions around the nerve
(Pogrel and Thamby2000).
2) Neurotoxicity caused by contamination of anesthetic
solution (chemical effect). For some time, professionals
had a bad habit of submerging the local anesthesia cartridges in surface disinfectants, often alcohol, with the
result that the disinfectant entered the cartridge through
the diaphragm or the rubber plunger (made from semipermeable membranes), thus making the injection
more painful and irritating the tissues and, more importantly, the nerve (Shannon and Feller 1972; Shannon
and Wescott1974).
3) Neurotoxicity caused by the individual components of
the local anesthesia solution (chemical effect).
Experiments with animals (Lundy et al. 1933; Tui
et al. 1944; Skou 1954; Fink and Kish 1976; Myers
etal.1986; Kalichman etal.1993) have demonstrated the
neurotoxic effect of local anesthetics, especially when
these are used at high concentrations. Clinical studies
have also demonstrated this adverse effect in medical
practice (Rigler et al. 1991) and in dental practice
(Nickel 1990; Haas and Lennon 1995; Miller and
Haas 2000; Van Eeden and Patel 2002; Hillerup and
Jensen2006; Garisto et al.2010), especially when high
concentrations are administered, as is the case with lidocaine 5% (Rigler et al. 1991), articaine 4% (Haas and
Lennon 1995; Miller and Haas 2000; Van Eeden and
Patel2002; Hillerup and Jensen2006; Hillerup etal.2011;
Garisto et al. 2010), and prilocaine 4% (Haas and
Lennon1995; Miller and Haas2000; Garisto etal.2010).
Immediate Electric Shock Sensation
Immediate electric shock sensation (cramp) is mainly felt
in mandibular block. When the needle is inserted, the
patient experiences a sudden and short electric shock sensation, which is like an intense burning sensation along the
nerve that has been touched by the tip of the needle (lingual nerve or inferior alveolar nerve). The sensation lasts a
second but is very unpleasant for the patient, although it
has the advantage of producing deep and quick anesthesia
with a small amount of anesthetic solution.
The frequency of electric shock sensation in mandibular
block is around 3% (Table22.5), and this is more common
in the lingual nerve than in the inferior alveolar nerve
Table22.5 Percentage ofcases ofelectrical shock sensation
after mandibular block andrecovery.
Sample size
Reference
Harn and
Durham (1990)
Krafft and
Hickel (1994)
Lustig and
Zusman (1999)
Pogrel and
Thamby (2000)
Pogrel and
Thamby (2000)
Nooh and
Abdullah (2010)
Morris etal.
a
(2010)
a
Cadaver, contact the needle with the nerve.
(cases/total)
347/9587 Lingual 3.6% 85%
856/12
40/731 Lingual
1/80 Lingual 1.3% —
1/320 Inferior
2/5000 Lingual 0.04% 100%
2/44 Lingual 4.5%a—
Nerves
affected
104 Lingual 7% 98%
and inferior
alveolar
alveolar
Average 3.2% 95.7%
Rounded
average
Electric
shock
5.5% 100%
0.3% —
3% 95%
Total
recovery
(ratio 4:1). In the case of the lingual nerve, the area affected
by the sensation is the tongue on the side the anesthetic is
injected; in the case of the inferior alveolar nerve, the area
affected is the half of the lower lip on the side which the
anesthetic is injected.
When faced with these situations in the office, we advise
the following:
● Show the patient that you are aware how unpleasant the
sensation is and state that this happens because the anesthetic was injected immediately above the nerve, when
the normal approach is to inject it to the side.
● Tell the patient that the discomfort has the advantage
that the anesthetic effect is quicker and stronger.
● In cases where this accident is repeated in the same
patient, we advise against using mandibular block because
it indicates a possible anatomical abnormality and
repeated injury could carry a risk of long- term paresthesia. As alternatives, we propose the use of another mandibular block technique such as Gow- Gates (Chapter16)
or infiltrative techniques accompanied by intraligamentary or intraosseous approaches (Chapter18).
Electric Shock Sensation After theTranspalatal Approach
An interesting variation of this problem is in the transpalatal (greater palatine canal) approach, which in 1% of cases
can lead to an intense sensation of electric discharge or
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burning in the palate on the side of the injection (Sved
etal.1992). This occurs because the needle is inserted into
the greater palatine canal, which leads to the pterygopalatine fossa, where the maxillary division of the trigeminal
nerve (CN V
No permanent or long-
) is located.
2
term lesions have been reported
at this level, probably because the technique is rarely used.
Long- Term Paresthesia
The frequency of long- term paresthesia or nonsurgical
neuropathy caused by dental local anesthesia is unknown
(Pogrel and Thamby 2000; Hillerup and Jensen 2006);
however, some authors provide estimates, although these
vary widely, ranging from 1:5000injections to 1:14million
injections (Table 22.6). Clinical experience tells us that
cases of long-
term paresthesia are not often seen in clinical
practice, therefore a frequency ranging from 1:5000 to
1:10 000 seems excessive. Furthermore, the study by
Garisto et al. (2010), which reported a frequency of
1:14 million, recognizes that this is improbable and that
the frequency may be even greater. We believe that the true
value lies somewhere between the figures reported
(Table22.6), that is, a median of 1
Table22.6 Frequency oflong- term paresthesia after
mandibular block, asestimated by various authors
Reference Nerves affected
Harn and
Durham (1990)
Krafft and Hickel
(1994)
Pogrel and
Thamby (2000)
Sambrook and
Goss (2011)
Pogrel and
Thamby (2000)
Ehrenfeld etal.
(1992)
Haas and
Lennon (1995)
Garisto etal.
(2010)
Data ordered by estimated frequency.
a
Data from Pogrel and Thamby (2000) (two series of patients).
b
Estimated 30% of mandibular block (data from Annex 1).
Lingual 1:4743 1:5000
Lingual 1:12
Lingual and
a
inferior alveolar
Lingual and
b
inferior alveolar
Lingual and
a
inferior alveolar
Lingual and
inferior alveolar
Lingual and
inferior alveolar
Lingual and
inferior alveolar
: 100 000injections.
Estimated frequency
Estimated
number
104 1:10 000
1:26 762 1:25 000
1:48 956 1:50 000
1:160 571 1:160 000
1:200 000 1:200 000
1:785 000 1:800 000
1:13 800 970 1:14 000 000
Round
number
By far the most frequently involved technique is mandibular block (99%) (Table22.7) and the most frequently
involved nerves are the lingual nerve (70%, tongue involvement), the inferior alveolar nerve (20%, involvement of
half of the lower lip), and both nerves (10%) (Table22.7).
The reason for more frequent involvement of the lingual
nerve seems to be that in 33% of cases it is composed of a
single bunch of nerve fibers (possibly one to eight), whereas
the inferior alveolar nerve is composed of three to 14 bundles, therefore injury is offset by the remaining healthy
bundles (Pogrel etal.2003; Khoury et al.2010). Also, the
inferior alveolar nerve may be partially protected from
oncoming the needles by a crest of thickened bone, which
bulges anteriorly in the sulcus colli, and the protection of
the lingula (Khoury Mihailidis etal.2011). In contrast, the
lingual nerve is quite bare, with no bony protection, exposing it to an increased risk of direct contact during needle
insertion due to its anteromedial position (Khoury
Mihailidis etal.2011) (Figure 3.14, Chapter 3).
Causes ofLong- term Lesions
1) Needle- tip injury, given that in 40% of cases there is a
history of electric shock sensation, although this data
varies widely between authors (Table22.7).
2) Neurotoxicity of local anesthetic solutions, especially
those administered at high concentrations. Thus, articaine 4% has a 9- fold higher risk than average and a 22fold greater risk than solutions with lidocaine 2%,
which is the standard local anesthetic (Table22.8). The
same is true of prilocaine 4%, which carries a 4- fold
greater risk than average and a 35-
fold greater risk than
lidocaine 2% (Table22.8). Therefore, some authors do
not recommend these two solutions for mandibular
block (Hillerup and Jensen2006; Hillerup etal.2011),
especially since the standard solution of lidocaine 2%
with epinephrine yields similar efficacy for inferior
alveolar nerve (Annex 24), under the usual conditions
of dental work.
Clinical Manifestations
1) Paresthesia and dysesthesia. These are the main mani-
festations; they occur in the area innervated by the
affected nerve (half of the tongue for the lingual nerve
or half of the lower lip and the chin for the inferior alveolar nerve). The sensation is abnormal and generally
unpleasant, and may involve heat, loss of feeling, tingling, numbness, burning sensation, prickling, and
even pain. The most characteristic sensation of paresthesia is tingling or numbness (Girard1979) and dysesthesia (abnormal sense of touch).
There are variations with respect to pain, such as
more increased sensitivity to a stimulus (hyperalgesia),
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Table22.7 Long- term paresthesia: most frequently involved techniques, most affected nerves, andhistory ofelectric shock sensation.
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Basic study data Technique used Nerves affected History of electric shock
Sample
Reference Origin Cases
size
Gerlach etal. (1989) Germany 12 — 1985–1988 100 0
Years of
study
Mandibular
block Other Lingual
N % N % N %
7 58 5 42 0 0
Inferior
alveolar Both Proportion Percentage
— —
Harn and Durham (1990) United States 51 41 1985–1990 100 0 51 100 0 0 0 0 52/52 100
Ehrenfeld etal. (1992) Germany 9
8 1987–1991 100 0 8 89 1 11 0 0 4/9 44
Krafft and Hickel (1994) Germany 18 18 1987–1990 100 0 18 100 0 0 0 0 0/18 0
Haas and Lennon (1995) Canada 143 — 1973–1993 100 0 92 65 42 30 9 6 31/143 22
Pogrel and Thamby (2000) United States 93 83 1983–2000 100 0 57 69 18 22 9 11 47/83 57
Hillerup and Jensen (2006) Denmark 54 52 1997–2004 100 0 40 77 10 19 2 4 20/36 55
Alcaina etal. (2010) Spain 2 2 — 100 0 1 50 0 0 1 50 1/2 50
Garisto etal. (2010) United States 226 —
Hillerup etal. (2011) Denmark 115 —
1997–2008 95
2001–2007 94 6 — — — — — — — —
a
5 170 89 14 7 7 4 18/191 10
Sambrook and Goss (2011) Australia 8 8 2009 100 0 2 25 4 50 2 25 — —
Average 99% 1% 72% 18% 10% 42%
Rounded average 70% 20% 10% 40%
a
Garisto etal. (2010) also report 4% high tuberosity block and 1% mental block (in total 5% other techniques).
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Table22.8 Greater risk oflong- term paresthesia after
mandibular block witharticaine 4% andprilocaine 4%
withrespect tothe general average risk andlidocaine 2%, which
is thestandard anesthetic.
Greater risk
Anesthetic
Articaine 4% General
Prilocaine 4% General
a
Estimated based on data from 1993with consumption of lidocaine
forecast from 1973 and of articaine from 1983 and averaging the total
number of years.
than
risk
Mean 9
Lidocaine 2% 6.3 Hillerup etal.
Mean 22
risk
Mean 4
Lidocaine 2%0 Legarth (2005)
Mean 35
Times
greater Reference
3.6 Garisto etal.
5 Hillerup etal.
5 Miller and Haas
11 Legarth (2005)
20 Hillerup and
a
15
45 Garisto etal.
0 Legarth (2005)
5 Miller and Haas
7.5 Garisto etal.
a
11
90 Garisto etal.
(2010)
(2011)
(2000)
Jensen (2006)
(2011)
Haas and Lennon
(1995)
(2010)
(2000)
(2010)
Haas and Lennon
(1995)
(2010)
Table22.9 Occurrence altered taste inpatients withinjuries
tothe lingual nerve.
Sample size
Reference
Ehrenfeld etal. (1992) 5/8 63%
Haas and Lennon (1995) 22/101 22%
Hillerup and Jensen (2006) 33/42 79%
Garisto etal. (2010) 44/170 26%
Average 48%
(cases/total) Percentage
≈ 50%
chorda tympani nerve (Table22.9). The alterations the
patient perceives are as follows:
● Reduced perception of taste (hypogeusia) and, more
rarely, absence of taste (ageusia) (Haas and
Lennon1995; Hillerup and Jensen2006).
● Altered perception of taste with a burning sensation
on the tongue, bitter taste, or bad taste (dysgeusia)
(Haas and Lennon1995; Hillerup and Jensen2006).
Of clinical interest, there are no differences in involvement between the right and left sides (Harn and
Durham 1990; Haas and Lennon 1995; Pogrel and
Thamby2000).
3) These symptoms may very occasionally be accompa-
nied by painful ulceration on the dorsum of the tongue,
which usually resolves after a few weeks when the paresthesia disappears (Martis1969), or late-
onset trismus
(Smyth and Marley2010).
Management by theDentist
The recommendations are as follows:
1) Reassure the patient, given that 60% of cases resolve
without sequelae within 6
2) Prescribe vitamin B
months (Table22.10).
for a few weeks since this helps
12
the nerve to recover (Tamaddonfard et al. 2014;
Horasanli etal.2017; Hasegawa etal.2018).
3) If the patient does not recover within 2–3 weeks, refer to
a neurologist with a full report.
pain with normally painless stimuli (allodynia), or
absence of pain with stimuli that are normally painful
(analgesia).
There are also variations with respect to stimuli in
general, for example loss of sensitivity to stimuli (anesthesia), reduced sensitivity to stimuli (hypoesthesia), or
increased sensitivity to stimuli (hyperesthesia).
2) Altered sense of taste in 50% of cases in which the lingual
nerve is involved, owing to its association with the
Around 60% of cases resolve within 6 months
(Table22.10). This period is generally accepted, although
some authors recommend waiting 2 years (Girard1979).
In some countries, such as Denmark, these complications are not considered malpractice, but rather accidents
or adverse effects of local anesthesia (Hillerup and
Jensen2006). Finally, in cases that do not resolve and cases
of pain and severe dysesthesia, the patient should be
referred to a pain clinic since surgery does not lead to
improvement and may worsen the patient’s condition
(Ehrenfeld etal.1992; Pogrel and Thamby2000).
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Table22.10 Occurrence oflong- term paresthesia that resolved
months.
within 6
Sample
Reference
Harn and
Durham (1990)
Ehrenfeld etal.
(1992)
Krafft and
Hickel (1994)
Pogrel etal.
(1995); Pogrel
and Thamby
(2000)
Hillerup and
Jensen (2006)
Alcaina etal.
(2010)
Garisto etal.
(2010)
Sambrook and
Goss (2011)
size Nerves affected Resolved
51 Lingual 96%
9 Lingual
Alveolar inferior
18 Lingual 95%
12 Lingual
Alveolar inferior
22 Alveolar inferior 23%
2 Alveolar inferior 100%
108 Alveolar inferior 32%
8 Alveolar inferior 75%
23%
33%
60%
Alterations ofthe Sense ofTaste
Ten percent of the fibers of the facial nerve (CN VII) leave
the nerve 15
mm after exiting the stylomastoid foramen.
After a varied course, they join the upper border of the lingual nerve to form the chorda tympani, which also carries
special visceral afferent (taste) fibers from the anterior twothirds of the tongue as well as general visceral efferent
parasympathetic fibers that synapse at the submandibular
ganglion and go on to provide innervation of the sublingual and submandibular glands.
Injury to these fibers leads to reduced sense of taste
(hypogeusia) on the affected side of the tongue or even total
disappearance of the sense of taste (ageusia) for sugarsweet, salty, bitter, and acid- lemon flavors, as assessed using
gustometry (Paxton etal.1994; Hillerup and Jensen2006).
Atrophy of the fungiform papillae on the affected side of the
tongue may also be observed (Cowan1990).
Of note, there have been three cases of involvement of
the sense of taste only, with no other nervous abnormality.
None of the three recovered within a year (Paxton
etal.1994; Pogrel and Thamby2000).
Hoarseness
There have been few reports of hoarseness immediately
after injection in mandibular block. Hoarseness was
accompanied by dysphagia and breathing difficulty, which
lasted 2–3
hours before resolving without sequelae. The
cause is thought to be recurrent laryngeal nerve block
(branch of the vagus nerve, CN X) because of an anatomical variation (Cilasun etal.2012).
Trismus
Trismus is a limitation of mouth opening. The frequency
of trismus caused by local anesthesia is around 1–3%
(Table22.11) and, as we will see, the disorder is associated
mainly with mandibular block (Table22.12), therefore by
weighting the average, with respect to all the other dental
local anesthesia techniques – mandibular block accounts
for 30% of the techniques used (Annex 1)– the frequency
of trismus is around 1%.
Local Anesthetic Techniques Implicated
inthe Development ofTrismus
1) Mandibular block, which irritates the medial (internal)
pterygoid muscle (Stone and Kaban 1979; Stacy
et al. 1994). The technique leads to trismus in 3% of
cases (Table22.11) and accounts for 95% of all cases of
trismus (Table22.12).
2) In the upper arch, posterior superior alveolar nerve
block or the high tuberosity approach. When applied in
the area of the maxillary molars, these techniques can
irritate the lateral (external) pterygoid muscle (Stone
and Kaban1979; Shaner etal.2007) and account for 5%
of all cases (Table22.12) as compared to trismus following mandibular block.
Table22.11 Occurrence oftrismus after mandibular block.
Sample size
Reference
Krafft and Hickel (1994) 49/12 104 0.4%
Kaufman etal. (2000) 3/179 1.6%
Ridenour etal. (2001) 1/30 3%
Mikesell etal. (2005) 10/114 9%
Moore etal. (2006) 2/187 1.1%
Lenka etal. (2014) 1/40 2.5%
Mohajerani etal. (2014) 2/80 2.5%
Dubey etal. (2017) 3/50 6%
Kiran etal. (2018) 0/70 0%
(cases/total) Percentage
Average 3%
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408
Table22.12 Cases oftrismus caused by mandibular block
andtechniques involving theupper molars
Mandibular
Reference
Campbell (1954) 1 0
Brown (1976a) 19 1
Brooke (1979) 16 0
Stone and Kaban (1979) 3 1
Adam etal. (1995) 1 0
Shaner etal. (2007) 0 1
Rounded percentage 95% 5%
block
40 3
Maxillary techniques
involving upper molars
Causes ofTrismus
1) Mechanical injury or irritation of the pterygoid muscles
(medial and lateral) by the tip of the needle, especially if
it is barbed outwards (Stacy etal.1994).
2) Mechanical irritation of the muscles mentioned above
by residue of silicone or aluminum, which can enter the
lumen of the needle when this is inserted through the
membrane of the cartridge. It is important to remember
that such residue has been found in around 10% of needles (Kelly and Cohen1984) (see Chapter13).
3) The toxic- chemical effect of local anesthetics and vaso-
constrictors on the muscles. In vivo experimental studies
in animals demonstrate this effect (Brun1959; Libelius
etal. 1970; Benoit and Belt1972; Dolwick etal. 1977;
Benoit1978; Fort et al. 1979; Foster and Carlson1980;
Tal1982). The effect is one of muscular alteration and
degeneration that, fortunately, is reversible within
15–30 days (Libelius etal.1970; Dolwick etal.1977; Fort
etal.1979; Foster and Carlson1980; Tal1982). Increased
concentrations worsen the situation (Bennett etal.1971).
Clinical Types ofTrismus
Acute Early- onset Trismus
Acute early- onset trismus appears immediately or almost
immediately after the effect of the anesthetic wears off. Acuteonset trismus is the most frequent type by far and is characterized by pain when trying to force the mouth open, and pain or
painful sensitivity during palpation and exploration of the
pterygoid muscles with the fingers at the injection site.
Table22.13 Day ofonset oflate chronic trismus dueto
thepresence ofa fibrous band
Brown (1976a)
Day
1 4 5
2 7 3 70%
3 2 4
4 2 0
5 1 1
6 1 3
7 1 0
9 1 0
14 1 0
n=20
Brooke (1979)
n=16
adjacent to the pterygoid muscles (Campbell1954; Killey
and Kay 1967; Brown 1976a; Brooke 1979; Stone and
Kaban1979; Adam etal.1995).
Its symptoms are characterized (Killey and Kay 1967;
Brown1976a; Brooke1979) by late onset (during the first
days in 70% of cases, although it can take up to 14 days)
3
(Table22.13) and absence of pain when forcing or palpating the injection site (only a mechanical limitation to the
range of motion in mouth opening). Very rarely, it may be
accompanied by longMarley2010) (see section “Long
Chronic Late- onset Trismus Dueto Infection
term paresthesia (Smyth and
-Term Paresthesia”).
This type of trismus is due to infection caused by microorganisms injected via the needle (e.g. contamination by
saliva, food remains, contact between the needle and skin)
into the tissue adjacent to the pterygoid muscles. Both
thepterygomandibular space and the lateral pharynx are
infected (Brown 1976a; Brooke 1979; Cohen and
Quinn1988; Kitay etal.1991).
Clinically, onset is late, 2–3 days after administration of
the anesthetic (Cohen and Quinn1988; Kitay etal.1991),
with pain while trying to close the mouth, pain on palpation of the injection site, and, in more advanced cases,
complications in the form of sublingual inflammation,
inflammation of the soft palate, inflammation of cervical
lymph nodes (adenopathy), or fever (Cohen and
Quinn1988; Kitay etal.1991). Acute trismus can occasionally become chronic (Adam etal.1995).
Chronic Late- onset Trismus Dueto Fibrous Band Formation
Chronic late- onset trismus is much less common and is
caused by an injury to a small artery that causes a hematoma that fibroses to form a fibrous band within or
Treatment ofTrismus
Conservative Treatment (Mechanical Therapy)
This is the treatment of choice owing to its success both in
acute trismus and in chronic trismus (Campbell 1954;
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Brown1976b; Berry1976; Nicholls1976). The key component of treatment involves exercises to open and close the
mouth (physical therapy) that prevent a clot from forming
and subsequent fibrosis and ankylosis (Stone and
Kaban1979). The main recommendations are as follows:
● Vigorous exercises to open and close the mouth accompa-
nied by lateral movements (Campbell 1954; Nicholls
1976; Brooke1979) for 5–10
minutes two or three times
per day. The patient can help by using his/her fingers to
force the mouth to open or by using devices such as
clothes pegs. The devices designed by Kaban may prove
useful in uncooperative children (Kaban etal.1977). The
condition improves in 5–7
● Exercise may initially be quite painful, and adjunctive
measures include analgesics and/or anti-
days.
inflammatory
drugs (Stone and Kaban1979), muscle relaxants such as
®
diazepam (Valium
) (Stone and Kaban 1979), and heat,
because of its relaxing effect on muscles, which makes
exercise easier. The heat may be dry or wet and should be
applied to the face and the angle of the mandible several
times per day or accompanied by shortwave or ultrasound therapy in 10- minute sessions three times weekly
(Campbell1954; Stone and Kaban 1979; Brooke1979).
Sugar- free chewing gum may also be used.
● Antibiotics may be administered in cases of suspected
infection, provided that no major improvement is observed
after 2–3 days of exercise (Stone and Kaban1979).
Treatment should be maintained until the patient recov-
ers and may take several days. It generally takes less than a
week (Nicholls1976).
Brown1976a). A sensation of mechanical limitation and
resistance to opening is observed (Killey and Kay1967),
followed by a sudden opening in the mouth as if a fibrous
band was breaking and overcoming the resistance (Killey
and Kay1967; Brown1976a).
● The mouth is opened 3.5–6 cm (the opening is measured
from the incisal edge of the upper and lower central incisors) (Stone and Kaban1979), the mandible is moved so
that it opens and closes and is moved in to lateral excursive
movements for 10–15
Finally, a dental jaw-
minutes (Stone and Kaban 1979).
opening device is placed on one side
to maintain the gained opening until the patient emerges
from anesthesia (Stone and Kaban1979). It is ideal if the
opener is in place during the first post-
● Complications (Brown1976a): (i) Pain is relatively fre-
operative night.
quent in the affected temporomandibular joint owing to
traumatic arthritis of the condyle and glenoid fossa
(treated with analgesics). (ii) The intervention is followed
by some loss of the gained opening because the forced
opening is inherently traumatic and induces a degree of
muscle spasm. (iii) Trismus recurs in 10% of cases, with
the result that the procedure has to be repeated.
● Post- operative measures. During the following days, con-
servative, physical therapy exercises should be continued, with opening and closing exercises and analgesics
(Stone and Kaban1979).
● Findings of interest. There is no association between the
duration of trismus and the efficacy of the intervention
with forced opening under general anesthesia
(Brown1976a). Prognosis is more favorable for patients
with good lateral mobility immediately after surgery
(Stone and Kaban1979).
Forced Opening Under General Anesthesia
Forced opening under general anesthesia is indicated when
conservative measures such as physical therapy fail
(Brown1976b; Berry1976; Brooke1979; Adam etal.1995),
as occurs in 20% of cases in some series (Brooke1979),
although the consensus is that it only affects a minority of
patients (Brown 1976b). Treatment can be considered to
have failed when no improvement has been observed after
3 weeks or the improvement is negligible (Brooke 1979).
These findings are important because if trismus is prolonged over time, it can lead to ankylosis of the bones of
the temporomandibular joint (Stone and Kaban1979). The
available options are as follows:
● Surgery (by an oral and maxillofacial surgeon). An instru-
ment is placed over the occlusal surface of the molars on
both sides in order to slowly force the mouth open
(Brown 1976a; Stone and Kaban 1979) while trying to
avoid damaging the dentition or displacement of the second premolar to the maxillary sinus (Killey and Kay1967;
Surgical Drainage
In patients with severe antibiotic- resistant infection with
pus, surgery should be performed to drain the pus
(Brown1976a; Cohen and Quinn1988; Kitay etal.1991),
therefore the patient must be referred to an oral and maxil-
lofacial surgeon. In these cases, the abscess should be identified using magnetic resonance imaging and computed
tomography, high doses of antibiotics should be administered, and physical therapy should be continued after surgery (opening/closing exercises, analgesics).
Facial Palsy
Facial palsy is caused by involvement of the facial nerve
(CN VII) and is known as Bell’s palsy after the Scottish surgeon Charles Bell, who first described it in 1830 (Van
Gijn2011).
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