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Clinical Manifestations
The paralysis affects the side of the face where the anesthetic was injected (ipsilateral), with the following
manifestations:
● Eye: owing to involvement of the temporal branch of the
facial nerve.
○ A strange sensation such as numbness may initially be
noted in the eye (Cooley and Coon1978).
○ Difficulty closing the eye. The most important sign
(Figure22.3).
○ Occasional tearing or, on the contrary, hyposecretion
(Genthon etal.1987).
○ Bell’s sign, when the patient closes eye, the eye globe
turns upwards and there is slight movement of upper
eyelid (García-
○ Rapid, uncontrolled, and repetitive horizontal (side to
Fernández1969; Bernsen1993).
side) or vertical (up and down) movements may rarely
be observed in both eyes (nystagmus). Nystagmus is
caused by a central nervous system effect (ParsonsSmith and Roberts1970).
● Face: owing to involvement of the zygomatic branch of
the facial nerve.
○ A strange sensation such as numbness may initially be
noted on the face (Cooley and Coon1978).
○ Disappearance of the nasolabial fold and flattening of
the face with disappearance of the physiognomic traits
(García-
Fernández1969) (Figure22.3).
○ Deviation of the commissure to the healthy side of the
face owing to the predominance of the muscles on this
side (García-
○ The sign is even more noticeable when the patient
Fernández1969) (Figure22.3).
tries to force a gesture such as laughing, speaking,
or blowing (the paralyzed cheek is inflated).
(Bernsen 1993); when the patient wrinkles his/her
brow, no lines are seen on the affected side.
● Other less common manifestations include the following:
○ Altered sense of taste (Droter 1959; García-
Fernández1969; Genthon etal.1987; Bernsen1993).
○ Altered hearing (Tiwari and Keane 1970; Genthon
etal.1987), noises and ringing (tinnitus) (Droter1959),
and even ear pain (Stoy and Gregg 1951; GarcíaFernández1969; Genthon etal.1987; Bernsen1993).
○ The auriculotemporal nerve may occasionally be anes-
thetized, with the result that the skin around the ear
and temporal region is also anesthetized (Stoy and
Gregg1951; García-
○ Although very rare, vertigo and dizziness resulting
Fernández1969).
from central nervous system involvement have
been reported (Droter 1959; Parsons-Smith and
Roberts 1970).
Facial Palsy Associated withMandibular Block
Facial palsy is generally associated with mandibular block,
and, although uncommon, it is thought to occur in 1in
200mandibular block procedures (Table22.14). There are
two forms of presentation.
Immediate Onset andShort Duration
This is the most common situation by far in clinical
practice. The paralysis is observed immediately or within
minutes following the injection and lasts from minutes to
5
a fewhours (generally 30
minutes to 2 hours, rarely 7 hours)
(Table22.15). The clinical manifestations are partial and
slight, since the facial nerve is for motor supply and local
Inhability
to close eye
Nasolabial
ld disappear
trend
Asymmetry
of mouth
Figure22.3 Inability to close eye and Bell’s sign. Trend to
disappearance of the nasolabial fold, and deviation of the
commissure with asymmetry of mouth.
anesthetics affect motor nerves to a lesser extent than sensory nerves. For the same reason, facial palsy disappears
Table22.14 Occurrence offacial paralysis after mandibular
block.
Sample size
Reference Percentage
Kaufman etal. (2000) 1.1% 1/179
Keetley and Moles (2001) 0.3% 2/580
Nooh and Abdullah (2010) 0.02% 1/5000
0.45% → 1/200
(cases/total)
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Table22.15 Clinical cases withfacial paralysis after mandibular block.
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Facial Palsy 411
Patient
Reference Age Sex Onset Duration
1. Immediate paralysis of short duration
Droter (1959) 24 ♀ Left 2
Haugen (1966) 38 ♀ Left <5
Haugen (1966) 28 ♀ Left <5
Gray (1978) 44 ♀ Left 3
Gray (1978) 29 ♀ Left 3
Gray (1978) 16 ♀ Left 2
Cooley and Coon (1978) 18 ♀ Right 5
Cooley and Coon (1978) 22 ♀ Left 5
Cooley and Coon (1978) 30 ♂ Right <5
2. Late- onset paralysis of long duration
Stoy and Gregg (1951) 45 ♀ Left >Minutes 6
ParsonsTiwari and Keane (1970) ? ♂ Left Hours 5.5
Ling (1985) 22 ♂ Left 13
Shuaib and Lee (1990)
Shuaib and Lee (1990)
Tzermpos etal. (2012) 20 ♀ Left 24
a
The same patient on two different occasions.
Smith and Roberts (1970) 25 ♂ Left 1 h 3 weeks
a
a
26 ♂ Left 24 h 2 weeks
26 ♂ Right 24 h 2 weeks
Side of block
Time
min 3.5 h
min 50 min
min 40 min
min 2 h
min 7 h
min 1.5 h
min 25 min
min 1.5 h
min 1 h
weeks
weeks
days 4 weeks
h 8 weeks
before the effect of the anesthesia on the lower lip (Cooley
and Coon1978).
The paralysis is caused by anesthesia of the facial nerve
or any of its main branches because the needle is inserted
too deep or posterior, potentially leading to injection of the
anesthetic into the parotid gland, with the needle trapped
in the capsule, thus numbing the facial nerve on its
path (Figure 3.14, Chapter 3) (Sicher 1950; GarcíaFernández1969; Petersen1971; Cooley and Coon 1978).
Occasionally, the facial nerve follows an anomalous course
and remains in the retromandibular space, thus leaving it
more exposed to the anesthetic solution (Sicher 1950;
García- Fernández1969; Gray1978).
The dentist can manage this situation as follows: (i)
informing the patient, to reassure him/her, that the effect
only lasts as long as the anesthetic; (ii) protecting the eye
from desiccation of the ocular surface (risk of erosion and
ulceration) by closing it with the fingers and placing a
damp gauze for the duration of the paralysis.
Late Onset andLong Duration
This situation is extremely uncommon in clinical practice.
The paralysis appears late (hours or days) after injection
and generally lasts 2–8 weeks (Table 22.15). The causes are
not well known, although the following have been
proposed:
1) Abnormality of the facial nerve resulting from delayed
reflex vasospasm caused by the epinephrine in the local
anesthetic solution or mechanical irritation by the tip of
the needle in the external carotid plexus (Figure 3.14,
Chapter3), which communicates with the stylomastoid
artery to produce vasoconstriction in the vasa nervorum
of the facial nerve, leading to ischemic neuritis (Stoy
and Gregg1951; Tiwari and Keane 1970; Gray 1978;
Ling 1985). The duration of the paralysis depends on
the degree of ischemia and nerve damage (Tiwari and
Keane1970).
2) Paralysis resulting from a latent viral infection (Shuaib
and Lee1990) or a previous neurological disorder triggered and revealed by the mandibular block (ParsonsSmith and Roberts1970).
The dentist can manage these situations as follows: (i)
reassuring the patient because most cases resolve spontaneously, although it may take weeks; (ii) protecting the eye
from desiccation (risk of erosion and ulceration) by closing
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412
it with the fingers and placing a damp gauze over it at night
and wearing dark glasses during the day, and referring the
patient to a opthalmologist; (iii) referring the patient to a
neurologist with a full report so that the patient can receive
an exhaustive neurology work-
up and treatment (Tzermpos
etal.2012). In these cases, the neurologist often administers corticosteroids (Parsons-
Smith and Roberts 1970;
Tiwari and Keane1970; Ling1985; Shuaib and Lee1990).
Facial Palsy Associated withMaxillary Infiltration
The very few case reports of facial palsy associated with
maxillary injection are all of late onset (24–72
hours) and
long duration (one to several weeks) (Genthon etal.1987;
Bernsen 1993). Although the causes are unknown, two
explanations can be postulated:
1) Retrograde injection of the anesthetic solution (with
vasoconstrictor), which runs to the posterior superior
alveolar artery and thereby to the middle meningeal
artery until it reaches the vasa of the facial nerve
through the petrous branches and causes ischemic
neuritis.
2) Immunoallergy (Bernsen 1993), but with poor quality
of evidence.
The dentist can manage these situations in the same way
as for cases of late onset and long duration after mandibular block. Both situations are quite unusual in clinical
practice.
Ocular Complications
Ophthalmological complications are rare after dental local
anesthesia. Some authors estimate that they affect 1 in
1000 patients who receive injections of anesthetic (Steenen
etal. 2012); however, we estimate that this figure is less
frequent, and, as indicated in Table22.16, it could be closer
to one in every 2000 patients.
Many of these situations may go unnoticed because visual disorders affecting a single eye are not very intense and
may even be asymptomatic for the patient since they are
compensated by the healthy eye (Blaxter and Britten1967;
Leopard1971).
We assessed this problem by reviewing 110 cases published in the international literature between 1936 and
2019 (Annex 36). Ages ranged from 4 to 73 years, with a
mean of 33 years (Peñarrocha- Diago and SanchisBielsa 2000; Rishiraj et al.2005). Females accounted for
70% of cases and males 30% (Annex 36), which is consistent with the fact that more women than men attend clinics
(Annex 1). In addition, children aged 4–16 years account
Table22.16 Frequency ofocular complications after injection
oflocal dental anesthesia.
Sample
Reference
Bartlett (1972) 3727 1 1:3727
Hidding and Khoury (1991) 1518 2 1:759
Peñarrocha-
SanchisKaufman etal. (2000) 179 3 1:60
Malamed etal. (2001) 1325 1 1:1325
Nooh and Abdullah (2010) 5000 2 1:2500
Diago and
Bielsa (2000)
size Cases Proportion
000 14 1:3571
50
Average 1:1990
Rounded average 1:2000
for over 10% of patients, and in this case the proportion of
males and females is similar (50%) (Annex 36). It must
benoted that the data obtained from these series may be
biased as only the most dramatic cases are published.
Anesthetic Techniques Involved
Although ocular complications can occur with any dental
local anesthetic (Marinho 1995), they have a higher incidence in the following cases (Annex 36):
● Injections into the maxillary arch (this accounts for close
to half of all cases), both through buccal infiltration
(most through infiltrations in posterior teeth, mainly
molars) and through transpalatal techniques, high tuberosity techniques, and techniques involving infraorbital
nerve block. Ocular complications are even more frequent with the latter three techniques (Chapter14).
● Mandibular block accounts more than 50% of cases, and
not only with the conventional or direct technique, but
also with the Gow- Gates technique (Norris 1982; Fish
etal.1989; Dryden1993).
Clinical Manifestations
Most clinical manifestations affect the eye on the side of
the injection (ipsilateral), although the contralateral eye
may be involved in some cases. This indicates a poor prognosis and will be commented on below. Thus, we can
describe the following complications (Annex 36):
● Visual disorders in over 80% of patients:
○ Double vision (diplopia) in approximately 60%.
○ Impairment of vision, with blurred vision or loss of
visual acuity in 20%.
○ Blindness (amaurosis) in 20%.
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Ocular Complications 413
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● Pupillary disorders in 30% of cases, with dilation of the
pupil (mydriasis) in more than two-
thirds (Figure22.4)
and, much less frequently, with contraction of the pupil
(miosis).
● Eye disorders:
○ Drooping of the upper eyelid (ptosis) in 30%.
○ Periorbital and/or orbital sensation ranging from
numbness to burning sensation or even pain in 15%.
○ Orbital and/or periorbital blanching in 10%.
○ Other much less frequent disorders include the
following:
■ Rapid, uncontrolled, and repetitive horizontal (side
to side) or vertical (up and down) movements
observed in both eyes (nystagmus).
■ Posterior displacement of the eyeball within the
orbit (enophthalmos).
● Eye examination:
○ Partial paralysis due to inability to move the eye in a
particular direction or complete paralysis (ophthalmoplegia) in around 40%:
■ Inability to move the affected eye outward (away
from the nose), that is, loss of abduction, affecting
30% (Figure22.4).
■ Other movements, without taking into account loss
of abduction or complete paralysis in 10%.
○ Deviation in the alignment of the eye in relation to the
other eye (strabismus) in 10% (both convergent and
divergent).
○ Absence of contraction when the pupil is exposed to
light in 10%.
● Extraocular manifestations in 30%:
○ Dizziness or sensation of vertigo in 10%, rarely accom-
panied by nausea (Cooley and Cottingham1979).
○ Facial blanching in 10%. This may occasionally affect
the hard palate (Dryden1993; Wilkie2000). Reddening
of the face (flushing) is much rarer.
○ Facial sensation in 10% of cases, ranging from numb-
ness to burning sensation to pain.
○ Other less common extraocular manifestations include
the following:
■ Headache (cephalea).
■ Speech disorders (dysarthria), hoarse voice
(Campbell et al. 1979), ranging from partial loss
(dyslalia) to total loss (aphasia).
■ Other much less common manifestations such as
fever, headache, nausea, and vomiting usually
appear in infections of the cavernous sinus, generally one to several days after the injection (Okamoto
etal.2012; Simsek etal.2013).
Other Clinical Aspects ofInterest
Other clinical manifestations and aspects are not frequent,
although they are of particular interest (Annex 36):
● There are five case reports in which clinical manifesta-
tions appeared only when the patient went to bed
(Kronman and Kabani1984) or got up (Goldenberg1990;
Magliocca et al. 2006; Yoon and Chussid2012; Verma
etal.2013). The reasons for this are unknown, although
the manifestations were thought to be due to arteriovenous anastomosis or bone disorders.
● There are two case reports where ophthalmological com-
plications occurred in the same patient at different times
(Goldberg1978; Williams etal.2011) and one case where
the complication occurred on three occasions (Petrelli
and Steller1980). The causes involved were bone or anatomical disorders and a history of myositis in the external muscles of the eye.
● In children younger than 16 years, more than 90% of
cases are caused by mandibular block, appear after a few
minutes (rarely before 2 hours), and last minutes to a few
hours. There have been no reports of sequelae, except for
one case that lasted 4 days (Hales1970) and was due to
maxillary infiltration in the molars.
Onset andDuration
Figure22.4 Affected eye (arrow) with a dilated pupil
(mydriasis) that does not move outward to accompany the
healthy eye (loss of abduction).
The onset and duration of complications can be summarized as follows (Annex 36):
● Onset
○ Around 90% appear between the first few minutes and
1 hour after the injection.
○ A small percentage appear after 24 hours.
● Duration
○ More than 80–90% resolve in a few minutes, although
they may take up to 6 hours.
○ A small percentage take several days or weeks to resolve.
○ Long- term sequelae may occur in a small percentage
of patients.
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414
Predictors ofSequelae
Analysis of the cases in Annex 36 revealed a series of indicators that serve to guide us with respect to the outcome of
ocular complications.
● Factors indicative of a favorable outcome:
○ If the complications appear within an hour of the
injection, nearly all patients recovered.
○ If the complications affect children or adolescents
younger than 16
● Factors indicative of a poor outcome:
○ If complications appear after 24 hours, then long- term
years, all patients recovered.
involvement or sequelae are observed in 100% of cases.
○ If ophthalmological complications appear after an
hour, then sequelae or long-
term complications are
observed in 65% of cases.
○ If the contralateral eye is the affected eye then seque-
lae or long-
term complications are observed in 60% of
cases. Involvement of the contralateral eye is unusual.
○ If the complication lasts more than 6 hours, irrespec-
tive of when it started, then sequelae are observed in
50% of cases.
Blindness (amaurosis) is the most common sequela,
affecting 50% of cases with poor outcome. Other sequelae
include mild paralysis (ophthalmoplegia) or mild drooping
of the upper eyelid (ptosis).
Management by theDentist
When faced with such a case, the dentist should act asfollows:
1) Stop treatment and reassure the patient that the event is
usually temporary and resolves without sequelae after a
few minutes or hours in most cases.
2) Examine the affected eye.
3) Cover the affected eye for as long as the disorder persists
to protect it and ensure correct vision with the contralateral healthy eye, as this compensates for the visual defect.
4) Advise the patient not to drive or use dangerous machin-
ery. The patient should be accompanied home.
5) Call the patient the same day/night in order to deter-
mine his/her status.
6) Refer the patient to an ophthalmologist for an evaluation
of the eye and supervision of the recovery process. The
patient should always be given a full report of the event.
This is particularly important in cases indicative of a
poor outcome.
Pathophysiology ofComplications
mechanisms and causes of these alterations after injection
of the anesthetic are not completely clear (Walker etal.2004;
Dogan and Dora2005; Rishiraj etal.2005; Huang etal.2013).
A more detailed explanation is found in Annex 36. In any
case, we propose the following explanations.
Retrograde Arterial Flow
The concept of retrograde arterial flow seems counterintuitive owing to arterial pressure; however, it seems valid if we
consider that the anesthetic solution is injected under pressure and that arterial pressure falls during the diastolic
phase (Williams et al. 2011). This route of intra-
arterial
injection with retrograde flow was demonstrated in invivo
experiments with monkeys (Aldrete etal.1977,1978).
Figures 22.5 and 22.6 show the pathway followed by
anesthetic from the mouth to the eye. The flow of the anesthetic solution runs backwards under pressure to the maxillary artery, which, via retrograde flow, enables the
anesthetic to reach the orbit along two routes:
● The short route, via the middle meningeal artery, which
enters the cranium through the spinous foramen. From
here it joins the ophthalmic artery (by anastomosis)
(Hayreh and Dass1962), which enters the orbit to supply
various structures through its branches. These include
the central retinal artery or the lacrimal artery, which
supplies the lateral rectus muscle and the levator muscle,
or the ciliary artery, which supplies the ciliary ganglion.
● The long route, via the external carotid artery up to the
carotid bifurcation, at which point the anesthetic solu-
tion ascends via the internal carotid. From here, it
reaches the ophthalmic artery.
Furthermore, the maxillary artery gives off branches to
the infraorbital artery, thus accounting for facial blanching, and the descending palatine artery, which, after crossing the greater palatine foramen, becomes the major
palatine artery, thus accounting for blanching of the palate
(Wilkie2000).
In addition to retrograde arterial flow of local anesthetic,
other variants affecting the arteries have been suggested, as
follows:
● The anesthetic solution reaches the orbit via a vascular
abnormality of the alveolar arteries or the middle menin-
geal artery (Blaxter and Britten1967; Goldenberg 1990;
Koumoura and Papageorgiou2001; Uckan etal.2006).
● On entering the artery, the needle causes a thrombus
that, by retrograde arterial flow, reaches the orbit and
retina and leads to permanent blindness (Tomazzoli-
Gerosa etal.1988).
Table 22.17 summarizes the main complications and the
structures of the eye involved and mechanisms proposed
(Von Arx et al. 2014). It should be noted that the exact
Retrograde Venous Flow
The case of retrograde venous flow is more obvious, given
that there is no arterial pressure and the veins of the head
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Table22.17 Main ocular complications andthe structures ofthe affected eye, aswell aspathophysiology andmechanism
ofproduction.
Ophthalmic complications Anatomical structure involved Mechanism and pathophysiology
Diplopia (double vision) External muscles of the eye (especially the
Amaurosis (blindness) Optic nerve (CN II)
Accommodation disorder
(blurred vision)
Mydriasis (dilated pupil) Pupillary sphincter muscle
Miosis (constricted pupila) Pupillary dilator muscle
Ptosis (drooping upper eyelid) Elevator muscle of the upper eyelid
Periorbital ischemia (ischemic
blanching around the eye)
Ophthalmoplegia (paralysis of
the eye)
Nystagmus Vestibulocochlear nerve (VIII cranial nerve)
Enophthalmos (posterior
displacement)
lateral rectus)
Oculomotor nerve (CN III)
Trochlear nerve (CN IV)
Abducens nerve (CN VI)
Retina
Lens
Ciliary muscle
Parasympathetic fibers of the ciliary ganglion
and of the oculomotor nerve (CN III)
Parasympathetic fibers of the stellate
ganglion and oculomotor nerve (CN III)
Parasympathetic fibers of the stellate and
ciliary ganglion
Oculomotor nerve (CN III)
Superior tarsal muscle
Sympathetic fibers of the ciliar ganglion and
stellate ganglion
Infraorbital artery
Zygomaticofacial artery
Superior labial artery
Posterior superior alveolar artery
Greater palatine artery
Sympathetic fibers
All muscles involved in eye movement
Oculomotor nerve (CN III)
Trochlear nerve (CN IV)
Abducens nerve (CN VI)
External muscles of the eye
Orbital muscle
Sympathetic fibers of the stellate and ciliary
ganglion
1) Block of the motor nerves of the eye
(oculomotor, trochlear, abducens)
2) Block or ischemia of the muscles of the
eye
1) Block of the optic nerve or the retina
2) Vasospasm of the ophthalmic artery or
the central retinal artery
1) Block of the parasympathetic fibers of the
oculomotor nerve and ciliary ganglion
2) Block or ischemia of the ciliary muscle
1) Block of the parasympathetic fibers of the
oculomotor nerve and stellate ganglion
2) Block or ischemia of the papillary
sphincter muscle
Block of the parasympathetic fibers
(Horner-
Oculomotor nerve block
Elevator muscle of the eyelid block or
ischemia
Sympathetic fiber block
Superior tarsal muscle block or ischemia
Stimulation of sympathetic fibers
Oculomotor, trochlear, and abducens nerve
block
Eye muscle block or ischemia
Vestibulocochlear nerve block
Sympathetic fiber block (Hornersyndrome)
like syndrome)
like
Source: Table modified from Von Arx etal. (2014).
and neck lack valves, therefore there is no mechanism to
prevent the retrograde flow of blood. Furthermore, the
veins are more numerous and anatomically more variable
than the arteries and their walls are easily penetrated by
the needle. Figure 22.7 shows the path followed by the
anesthetic solution from the mouth to the eye.
The cavernous sinus warrants a separate comment. This
large group of fine- walled veins is located in the middle
cranial fossa, on both sides of the sella turcica of the
sphenoid. The anesthetic solution that reaches it can affect
the eye through various pathways:
● Within the cavernous sinus, along the central part, lie
the internal carotid artery and the abducens nerve (CN
VI), which at this level are very vulnerable to the action
of the anesthetic owing to the fine walls that separate
them (Walker et al.2004; Magliocca et al.2006). This
area is also home to the oculomotor nerve (CN III), the
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MOUTH
ORBIT
ry
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meningeal ar
ORBIT
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416
Central retinal artery
Ciliary artery
Lacrimal artery
Ophthalmic artery
Superior orbital fissure
Superior ophthalmic vein
Ophthalmic vein
Internal carotid artery
Middle meningeal artery
External carotid artery
Maxillary artery
Maxillary artery
Superior alveolar artery
(descending loop)
Inferior alveolar artery
Figure22.5 Schematic representation of the arterial
retrograde pathway from the mouth to the eye.
Inferior orbital fissureCavernous sinus
Foramen ovale
Foramen lacerum
Foramen venosum
Pterygoid venous plexus
MOUTH
Lower branches of the
pterygoid venous plexus
Superior alveolar veins
Inferior alveolar veins
Figure22.7 Schematic representation of the venous retrograde
pathway from the mouth to the eye.
Ophthalmic
artery
Middle
tery
Maxillary artery
Internal
carotid artery
External carotid artery
Ciliary artery
Anastomosis
Superior
alveolar arte
Inferior
alveolar arte
Figure22.6 Arterial retrograde pathway of the local anesthetic solution from the mouth to the eye. Redrawn from
Rood (1972).
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Ocular Complications 417
)
Abducens ner
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trochlear nerve (CN IV), and the ophthalmic and maxil-
lary nerves (CN V
and CN V2, respectively), although
1
the latter are in contact with the external wall of the cav-
ernous sinus (dura mater), which is thicker and more
difficult for the anesthetic solution to cross (Figure22.8).
● In addition, the superior ophthalmic vein drains into the
cavernous sinus via the superior orbital fissure. The
anesthetic solution can flow along this pathway by reflux
to the orbit.
In addition to filling with anesthetic and vasoconstrictor,
the cavernous sinus may also become infected by bacteria
from the mouth that enter via a contaminated needle
(Okamoto etal.2012) and then inflamed (thrombophlebitis), thus leading to Tolosaetal.2013), which usually appears after 24
Hunt syndrome (Simsek
hours or several
days and is accompanied by periorbital pain, greater or
lesser eye paralysis (ophthalmoplegia), and general
involvement with headache, fever, nausea, and vomiting.
This complication may take weeks or months to resolve
after medical treatment.
Passive Diffusion tothe Orbit
It is difficult for the anesthetic solution to reach the orbit
by diffusion (Steenen et al. 2012); however, maxillary
buccal infiltrations in the area of the molars, the technique for blocking the posterior superior alveolar nerve
(Holmgreen etal.1979; Peñarrocha- Diago and SanchisBielsa 2000; Koumoura and Papageorgiou 2001;
Horowitz etal. 2005; Magliocca et al.2006), the high
tuberosity technique (Collon1946; Forloine etal.2010),
and the transpalatal technique (Dickson and Coates1945;
Saborido 1977; Mercuri1979) may enable diffusion to
the orbit via two pathways:
● In the posterior part of the maxilla, in the area of the
tuberosity, the solution can spread to the pterygopalatine
fossa and, at its highest part, may enter the orbit via the
inferior orbital fissure. This is the most frequent pathway.
● Via anatomical abnormalities or defects (Magliocca
etal.2006; Williams etal.2011) such as an altered wall in
the maxillary sinus (Petrelli and Steller1980) or by vascular or lymphatic defects or defects of the connective tissue
(Boynes etal.2010). This pathway is extremely unusual.
Once the solution enters the orbit, it is distributed via
intraorbital fat and various fascia, thus leaving some of the
organs at the apex of the orbit more vulnerable, as is the
case of the abducens nerve (CN VI) and the lateral rectus
muscle (Peñarrocha-
Diago and Sanchis- Bielsa 2000;
Steenen et al.2012), and favoring onset of double vision
(diplopia) and abduction deficit.
Irritation ofthe Sympathetic System
Irritation of the sympathetic system occurs because the tip
of the needle can injure the superior or inferior alveolar
artery and irritate the sympathetic plexus that surrounds
them. This irritation spreads throughout the vascular wall
to the maxillary artery until it reaches the sympathetic
plexus of the internal carotid artery, from where it reaches
the peripheral branches (Kronman and Kabani1984). It
then reaches the orbit by the ophthalmic artery, causing
ischemia by vasospasm in some of the tissues and organs it
supplies (Horowitz etal. 2005), which generally leads to
Sella turcica
Cavernous sinus
Internal carotid
Sphenoid sinus
Nasal cavity
Figure22.8 Schematic representation of a cross- section (coronal plane) of the cavernous sinus, in the middle cranial fossa, and its
association with the cranial nerves and the internal carotid artery. Redrawn with modifications from Koumoura and
Papageorgiou (2001) and Pragasm and Managutti (2011).
artery
ve (VI)
Oculomotor nerve (III)
Trochlear nerve (IV)
Ophthalmic nerve (V
Maxillary nerve (V2)
Dura mater
Greater wing of
sphenoid
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blanching (Uckan et al. 2006) and other complications
(Steenen etal.2012). In one case of mandibular block, the
needle did not touch the bone and led to an electric shock
sensation in the lower lip, on touching the nerve stem of
the inferior alveolar nerve (Wilkie2000).
Sympathetic System Block (Horner- like Syndrome)
Sympathetic system block is the opposite of the previous
situation: instead of irritation of the sympathetic system,
the anesthetic solution induces selective block of the sympathetic fibers.
The most typical manifestations in these cases are
Horner-
like syndrome with contraction of the pupil (miosis), vasodilation of the vessels of the face (flushing), and
posterior displacement of the eyeball in the orbit (enophthalmos). Other typical manifestations of this syndrome,
although not exclusive to sympathetic block and that can
be caused by other factors (see above), include drooping of
the upper eyelid (ptosis), tearing, and, more rarely, dizziness or alterations of the voice.
The mechanisms proposed to explain this selective block
of the sympathetic fibers are as follows:
1) Stellate ganglion block. In mandibular block, the solu-
tion descends via the neck to the pterygomandibular
space by the lateral wall of the pharynx (parapharyngeal space) before passing the paravertebral space and
reaching the stellate ganglion via the alar fascia
(Campbell etal.1979). Some authors consider this possibility highly unlikely because of the distance between
the injection site and the stellate ganglion (PeñarrochaDiago and Sanchis- Bielsa2000).
2) The anesthetic solution reaches the sympathetic plexus
of the internal carotid artery (Dodds 1956). This is at
some distance and thus less likely.
3) The sympathetic fibers that accompany the internal
carotid artery are blocked selectively when this is inside
the cavernous sinus (Walker et al. 2004; Dogan and
Dora2005).
4) The sympathetic fibers are only blocked in the ciliary
ganglion within the orbit (Peñarrocha- Diago and
Sanchis- Bielsa2000).
5) Compression and/or traction of the sympathetic fibers
due to the prolonged position of the neck and head of
the dental chair (Ostergaard and Faix2001). However,
this explanation seems somewhat unlikely.
Other Proposed Causes
Other causes have been proposed to explain special situations. Although some are very unlikely, others are interesting,
for example, hysteria in a 10- year- old girl (Clarke and Clarke
1987), immune response to mepivacaine (Goldberg1978),
vasospasm at the level of the vertebrobasilar vessels leading to contralateral involvement (Machado etal.1999),
or revelation of underlying multiple sclerosis that manifests with alterations in the contralateral eye (Kocer
etal.2009).
Needle- induced Infection
The needle of the syringe can introduce bacteria into deep
tissues and thus cause infection. Infections are now very
rare thanks to modern disposable needle systems and sterile cartridges that are ready for use. Infection can arise
from several sources (Connor and Edelson1988):
1) Contamination by the injection equipment itself (nee-
dle, cartridge, syringe). This possibility is remote, since
the material is sterile before use.
2) Contamination of the tip of the needle through acciden-
tal contact with microorganisms on the skin or hair
before injection.
3) Contamination through the patient’s own flora. This risk
is real, since it is impossible to maintain the oral cavity
sterile, although it can be reduced by applying topical
antiseptic before injecting the needle. Most published
studies on post- anesthesia infections confirm infection of
the oral cavity by saprophytes (Popowich and Brooke
1979; Connor and Edelson1988; Kitay etal.1991).
Clinical Manifestations
The first manifestations appear after 8–10 hours (Popowich
and Brooke1979; Connor and Edelson1988) or during the
first 2–3 days (Cohen and Quinn 1988; Kitay et al.1991),
with localized pain and inflammation.
Fever appears in more advanced phases and may worsen
with general malaise, chills, and vomiting (Popowich and
Brooke 1979; Cohen and Quinn 1988; Connor and
Edelson 1988), local inflamed lymph nodes (adenopathy)
(Popowich and Brooke1979; Cohen and Quinn 1988), and
difficulty swallowing (dysphagia) if the infection reaches the
pterygomandibular space after mandibular block.
Examination of the area may reveal a fluctuant abscess at
the injection site. If the infection is not addressed, advances,
or if complications arise, then the following may be observed:
● Trismus, with pain on forced opening (Cohen and
Quinn1988; Kitay etal.1991).
● Paresthesia of the mental nerve (Barnard1976).
● Cellulitis of the neighboring skin due to extension to
thesoft tissue (Popowich and Brooke1979).
● Osteomyelitis due to extension to bone tissue
(Barnard1976).
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Management by theDentist
● Initial management includes the following (Popowich
and Brooke 1979; Connor and Edelson 1988; Kitay
etal.1991):
○ Antibiotics, which act mainly against anaerobic flora,
such as amoxicillin, tetracyclines, clindamycin, or
metronidazole.
○ Incision and drainage of the fluctuant abscess.
● Where the clinical course is not clear, the patient should
be sent to an oral and maxillofacial surgeon for a more
depth examination, including blood culture, com-
inputed tomography, magnetic resonance, biopsy (cancer
screening) (Barnard 1976; Popowich and Brooke1979;
Cohen and Quinn1988; Connor and Edelson1988; Kitay
etal.1991), and treatment.
Post- injection Mucosal Ulceration
Although rare, necrosis of the mucosa may be observed at
the injection site. It usually occurs in the palatal mucosa,
where there is less tissue elasticity (Hartenian and
Stenger1976) and more rarely in the buccal attached gingiva (Carroll1980). Curiously, a case of mucosal ulceration
was reported in the pterygotemporal depression after mandibular block (Giunta etal.1975).
Clinical Manifestations
Symptoms appear at 1–4 days after injection and usually
last 1–2
characterized by the following:
Proposed Causes
1) Ischemia caused by the vasoconstrictor in the anes-
2) Trophic alteration of the mucosa caused by needle injury
weeks (Allen 1979; Jastak etal. 1995). They are
● Loss of mass on the mucosal surface, leading to ulcera-
tion that may be accompanied by a grayish surface
(Giunta etal.1975; Hartenian and Stenger1976), which
rarely affects the bone and causes a sequestrum that
appears on the ulcer some weeks later (Carroll1980).
● Pain on palpation and frequent reddening of the borders
of the ulcer (Hartenian and Stenger1976; Carroll1980).
thetic solution or by excessive pressure when the injection is too fast and/or the volume injected too great
(Giunta et al. 1975; Hartenian and Stenger 1976;
Carroll1980).
or ischemia caused by the factors mentioned above,
leading to lack of irrigation and irreparable necrosis
(Hartenian and Stenger1976; Jastak etal.1995). In such
cases, the ulcer may last for more than a month
(Hartenian and Stenger1976; Carroll1980).
3) Inadvertent injection of anesthetic solution contami-
nated with disinfectant (Hartenian and Stenger 1976;
Jastak etal.1995). This is now unlikely since the cartridges come in blister packs and no longer have to be
placed in disinfectant solutions.
Management by theDentist
● Management is essentially based on monitoring to
ensure that a scar forms within 1–2
weeks. In cases of
discomfort, symptomatic treatment can be administered.
The patient should try to avoid brushing the area by
applying rinses with a disinfectant such as chlorhexidine
and administering analgesics if the procedure is painful.
● If the lesion has not healed within a month, the patient
may have a trophic ulcer, in which case a biopsy is necessary to screen for cancer and stimulate scarring, as is
habitual in trophic ulcers (Giunta etal.1975; Hartenian
and Stenger1976).
Breakage ofthe Needle
At the beginning of the twentieth century, dental needles
broke easily. Theodor Blum, from NewYork, published 120
cases collected between 1914 and 1931 (Blum1932) showing that 90% of breakages were in what was considered to
be at the time a fine- gauge needle (23G and 25G) and that
there were no differences between the left and right
sides. Fortunately, the frequency of needle breakage has
decreased for several reasons:
1) New stainless- steel alloys introduced after the Second
World War (Harrison 1948) made needles much more
resistant than those that had previously been made of
steel, platinum, or platinum-iridium at the start of the
twentieth century (Blum1932; Bump and Roche1973).
2) The introduction of disposable needles in 1959 (Dobbs
1965) and the early 1960s (Bedrock et al. 1999; Pogrel
2009). These needles removed the need for reuse and
resterilization, processes that weaken the metal (Blum
1932; Fraser-
3) Disuse of the Fischer mandibular block method, or
1- 2- 3 method, by which the needle changes direction
within the tissue, thus increasing the risk of breakage
(Blum1924). Consequently, 80% of breakages occurred
during mandibular block (Blum1932).
The frequency of needle breakage is currently extremely
low, and although no exact figures are available, one author
Moodie 1958; Bump and Roche 1973).
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