J Oral Maxillofac Surg

70:1123-1130, 2012

Traumatic Optic Neuropathy After

Maxillofacial Trauma: A Review
of 8 Cases
Sarvesh B. Urolagin, MDS,* Sharadindu M. Kotrashetti, MDS,
Tejraj P. Kale, MDS, and Lingaraj J. Balihallimath, MDS

Purpose: To study the incidence and prognostic factors of traumatic optic neuropathy in maxillofacial
trauma cases.
Material And Method: Eight patients diagnosed with traumatic optic neuropathy among 354 cases of
maxillofacial trauma treated from December 2008 through May 2011 were included in this retrospective
study. Factors at the time of trauma, clinical findings, computed tomographic findings, and interventional
modalities were studied for any improvement in vision.
Results: Of 354 maxillofacial trauma cases, 8 cases (2.25%) were diagnosed with traumatic optic
neuropathy. Patients ages ranged from 21 to 60 years. The causes of trauma were road traffic accidents
in 7 patients and surgery for zygomaticomaxillary complex (ZMC) fractures in 1 patient. All patients had
ZMC fracture; 1 patient had Le Fort II, mandible condyle, and ramus fractures and 2 had associated cranial
bone fracture. Six patients were administered steroid therapy; 1 patient showed improvement in visual
acuity. Two patients underwent decompression by a lateral orbital approach; 1 patient showed an
improvement in visual acuity. In 2 other patients, a spontaneous recovery was observed. Four of the 8
patients underwent open reduction and fixation of the maxillofacial fractures. Of the remaining patients,
1 patient had a nondisplaced ZMC fracture that was treated without surgical intervention and the other
3 patients refused any surgical intervention.
Conclusions: The present findings showed the occurrence of traumatic optic neuropathy in association
with ZMC, Le Fort II, and cranial bone fractures. Additional risk factors such as a history of a loss of
consciousness, injury to the superolateral orbital region, fracture of the optic canal, evidence of orbital
hemorrhage, and evidence of blood within the posterior ethmoidal cells should be considered during the
evaluation.
2012 American Association of Oral and Maxillofacial Surgeons
J Oral Maxillofac Surg 70:1123-1130, 2012

The incidence of traumatic optic neuropathy in asso-
ciation with midfacial and craniofacial fractures has
been reported to be 2.5% to 10%.1-4 Common injuries
resulting in traumatic optic neuropathy include a
blow to the ipsilateral brow or forehead, most often
because of a motor vehicle or bicycle accident, a fall,
or an assault.5-8 It is also a potential complication that
should be suspected in fractures involving the edge of
the orbital rim.
Optic nerve damage, which can occur in 5% of cases
after a head injury, is classified as a direct or an indirect
injury.9 Direct injuries, which are caused by a penetrat-
ing injury to the area of the optic nerve, result in poor
visual recovery. Indirect injuries are caused by forces
that are transmitted at different levels after blunt
head trauma.10 The most common site of an indi-
rect optic nerve injury is the optic canal.11
The present report describes a retrospective study
of 8 cases of traumatic optic neuropathy associated
with maxillofacial trauma. The cases were managed
by steroid therapy, surgical intervention, and obser-
vation.

Received from the Department of Oral and Maxillofacial Surgery, Address correspondence and reprint requests to Dr Urolagin:
KLE VK Institute of Dental Sciences, Nehru Nagar, Belgaum, Kar- Department of Oral and Maxillofacial Surgery, KLE VK Institute of
nataka, India. Dental Sciences, Nehru Nagar, Belgaum, Karnataka 590010, India;
*Lecturer. e-mail: drsarveshbu@sify.com
Professor and Head. 2012 American Association of Oral and Maxillofacial Surgeons
Associate Professor. 0278-2391/12/7005-0$36.00/0
Reader. doi:10.1016/j.joms.2011.09.045

1123
1124 OPTIC NEUROPATHY AFTER MAXILLOFACIAL TRAUMA

Table 1. CLINICAL PRESENTATIONS OF PATIENTS WITH TRAUMATIC OPTIC NEUROPATHY

Interval From
Vision Loss to
Age (yr) Cause Treatment Associated Maxillofacial Trauma

30 30 RTA Other 1 Day 1 Day ZMC Fx Le Fort I, II, or III Cranial Bone Fx
Cases 3 5 7 1 4 4 8 1 2
Abbreviations: Fx, fracture; RTA road traffic accident; ZMC, zygomaticomaxillary complex.
Urolagin et al. Optic Neuropathy After Maxillofacial Trauma. J Oral Maxillofac Surg 2012.

Materials and Methods Results

IRB approval was granted by our institutions Re- The patients ages ranged from 21 to 60 years. The
search and Ethical Committee. All patients who were causes of maxillofacial trauma were road traffic acci-
diagnosed with traumatic optic neuropathy associated dents in 7 patients and surgery for zygomaticomaxil-
with maxillofacial trauma from December 2008 through lary complex (ZMC) fractures in 1 patient.
May 2011 were included in the study. Maxillofacial trauma was assessed based on clinical
The diagnosis of traumatic optic neuropathy was and CT findings. All patients in the study had ZMC
made on clinical grounds. The criteria used were fractures; 1 patient had Le Fort II, mandible condyle, and
blurring of vision, decreased visual acuity, an ab- ramus fractures. In 2 patients, there was an associated
sence of light perception, and any relative afferent cranial bone fracture (Table 1). There was clinical evi-
pupillary defect (RAPD). dence of injury to the superolateral orbital region in 7
Of 354 patients treated for maxillofacial trauma patients (Fig 1), and the types of injury ranged from a
closed blunt injury to an open laceration (Table 2).
during this period, 8 patients (2.25%) were diag-
Four patients were treated for vision loss on the day
nosed with traumatic optic neuropathy. Each pa-
of trauma (50%), and the treatment interventions for
tient underwent a baseline neuro-ophthalmologic
the other 4 patients ranged from 2 to 11 days after the
examination.
trauma. Six patients were administered steroid ther-
Cases of traumatic visual loss caused by a direct
injury to the globe (open globe, traumatic cataract,
retinal detachment, choroidal rupture, or vitreous
hemorrhage) were excluded. All patients diagnosed
with traumatic optic neuropathy were admitted to the
hospital and underwent computed tomographic (CT)
scanning to identify fractures of the orbit and to rule
out displaced fracture fragments compressing the op-
tic nerve, hematoma, bleeding in the ethmoid air
spaces, and cerebral injury. Whenever possible, a
visual-evoked potential (VEP) was performed.
Patients who had no contraindication to intrave-
nous methylprednisolone were administered mega-
doses of methylprednisolone according to the proto-
col used in the Third National Acute Spinal Cord
Injury Study (NASCIS III), ie, a 30-mg loading dose per
kilogram of body weight over 1 hour followed by 5.4
mg/kg/hour for the next 23 hours, which is tapered
to 250 mg 4 times per day for the next 2 days and then
to oral steroids 1 mg/kg tapered rapidly over 11 days.
Patients who did not respond to the steroid therapy
and had displaced fracture fragments compressing the
optic nerve underwent optic canal decompression.
Fixation of the maxillofacial fractures was carried out FIGURE 1. Injury to the superolateral orbital region.
at the same time. Visual acuity and pupil response Urolagin et al. Optic Neuropathy After Maxillofacial Trauma.
were assessed postoperatively. J Oral Maxillofac Surg 2012.
UROLAGIN ET AL 1125

Table 2. CLINICAL AND COMPUTED TOMOGRAPHIC CONDITIONS OF PATIENTS WITH TRAUMATIC

OPTIC NEUROPATHY

Injury to Fracture of Evidence of Evidence of Blood Evidence of

Superolateral Optic Orbital Within Posterior Cerebral Lesions History of Loss
Orbital Region Canal Hemorrhage Ethmoidal Cells on Imaging* of Consciousness

Present 7 4 2 6 3 5
Absent 1 4 6 2 5 3
*Epidural hemorrhage and subarachnoid hemorrhage.
Urolagin et al. Optic Neuropathy After Maxillofacial Trauma. J Oral Maxillofac Surg 2012.

apy, and 1 patient showed improvement in visual
acuity. Two patients underwent decompression by a
lateral orbital approach; 1 patient showed an im-
provement in visual acuity. In 2 other patients, a
spontaneous recovery was observed. Four of the 8
patients underwent open reduction and fixation of
the maxillofacial fractures. Of the remaining 4, 1 pa-
tient had a nondisplaced ZMC fracture that was
treated without surgical intervention and 3 patients
refused any surgical intervention (Table 3).
Discussion
Traumatic optic neuropathy is seen most often in
boys in their first or second decade of life, but case
series have included a wide age range in male and
female patients. In 1 series,12 patients older than 40
years were found to have a worse visual outcome
independent of the mechanism of injury, the severity
of visual loss, or the intervention used. In the present
study, the patients ages ranged from 21 to 60 years.
Two patients who were 32 and 35 years old, respec-
tively, had a spontaneous recovery, 1 22-year-old pa-
tient recovered after decompression surgery, and 1
60-year-old patient recovered with steroid therapy
(Tables 1, 3).
Traumatic optic neuropathy has been reported to
occur in 0.5% to 5% of patients with closed head
injuries and in 2.5% of those with midfacial fractures.1
In the present study, the occurrence of traumatic
optic neuropathy in association with maxillofacial
trauma was 2.25%. Data from Germany have indicated
that an impairment or loss of vision from optic nerve
injury occurs in approximately 10% of patients with
craniofacial fractures.2 Kallela et al3 analyzed clinical
and CT findings from 10 patients with optic neurop-
athy after maxillofacial blunt trauma. In their review,
the number of blinded eyes was 14 and all patients
had midfacial fractures. Isolated trauma of the optic
nerve usually is associated with a blunt skull trauma
involving fractures of the skull and optical canal but
may also occur from blunt ocular trauma.13 Fractures
of the medial orbital wall, optic canal, zygoma, or
floor may be present.4 The ZMC fracture was the
common maxillofacial fracture in the present study,
followed by Le Fort II, mandible condyle, and ramus
fractures in 1 patient. In 2 patients, there were asso-
ciated frontal bone and temperoparietal bone frac-
tures (Table 1).
The intraorbital segment of the optic nerve usually
is spared from injury because of the laxity and buff-
ering by the surrounding fat and extraocular muscles.
The intracranial segment is protected by the sur-
rounding brain and bones and because shearing
forces usually are absorbed by the intracanalicular
segment and thus do not reach the intracranial seg-
ment.
In the present study, a superolateral orbital injury
was seen in 7 patients (87.5%; Fig 1, Table 2). The
injuries ranged from a blunt contusion to an open
laceration wound. In 1 patient, there was a frontal
bone fracture associated with a laceration wound.
Some investigational studies have shown that blows
to the malar and frontal areas are transmitted mostly
to the optic foramen.1 These forces may cause com-
pression, shearing, contusion, and stretching injuries
to the optic nerve, even in the absence of a fracture.
Furthermore, the sheath of the optic nerve is firmly

Table 3. RESPONSE TO VARIOUS THERAPEUTIC INTERVENTIONS OF PATIENTS WITH TRAUMATIC

OPTIC NEUROPATHY

Recovery After Start of Recovery After Optic Spontaneous Recovery Surgical Intervention for
Steroid Treatment Nerve Decompression Without Intervention Maxillofacial Trauma

Present 1 1 2 4
Absent 5 1 6 4
Urolagin et al. Optic Neuropathy After Maxillofacial Trauma. J Oral Maxillofac Surg 2012.
1126
FIGURE 2. Computed tomographic scan showing a fracture of the optic canal.
Urolagin et al. Optic Neuropathy After Maxillofacial Trauma. J Oral Maxillofac Surg 2012.
attached to the optic canal, and the canal itself is a
closed space that is inflexible to any edema or hem-
orrhage.1,14
The incidence of optic canal fracture in traumatic
blindness has been reported as 6% to 92%.15 In the
present study, 4 of the 8 patients (50%) had evidence
of an optic canal fracture (Fig 2) on CT scan (Table 2).
Rajiniganth et al16 reported an optic canal fracture in
34% of cases, and their results indicated total blind-
ness, canalicular fracture, and late presentation as
poor prognostic factors.
The present patients displayed a decrease in visual
acuity, blurring of vision, an absent perception of
light, and RAPD. Visual acuity was assessed at bedside
in the emergency department by the Snellen chart
and was confirmed by manual kinetic or automated
static perimetry. A RAPD was detected by performing
a swinging light-pupil test.
The briskness of pupillary constriction to light re-
flects the degree of optic nerve dysfunction. When
checking for RAPD, it is important to use a very bright
light in a dark room to assess the full amplitude of
pupillary response. A RAPD can be estimated subjec-
tively by asking the patient about the difference in the
brightness of light presented in front of each eye.
Patients with optic neuropathy often have red-color
desaturation and a red-capped bottle can be pre-
sented to each eye and the patient can be asked about
the difference in the brightness of the red color. A
positive response would be that the red color looks
faded, pink, or washed out.
The identification and diagnosis of optic neuropa-
thy can be challenging, especially in uncooperative,
inebriated, or unresponsive patients with a neuro-
OPTIC NEUROPATHY AFTER MAXILLOFACIAL TRAUMA
logic deficit and with periorbital swelling. The diag-
nosis was delayed in 3 cases in the present study.
The VEP to flash stimulation and an electroretino-
gram might be supportive in unresponsive patients in
the immediate aftermath of the traumatic event.2,17
Although VEP is not necessary in the diagnosis of
optic neuropathy, it can be useful in patients with
early or subclinical optic neuropathy who may have
normal pupillary responses and no discernible optic
disk changes on clinical examination.18 VEP testing
was performed in 2 patients in the present study. It
was performed to evaluate the response to steroid
therapy. One of these patients underwent surgical
decompression because there was no improvement
noted in the VEP test.
CT scanning was performed in all patients in this
study to screen for cerebral injury and assess the
orbital and optic nerve injuries in the emergency
department. It has been reported that there is no
consistent correlation among the finding of an optic
canal fracture, the severity of visual loss, and the
prognosis for visual recovery.19 CT scans were helpful
in the management of maxillofacial injuries and to
plan for the decompression procedure.
Ultrasonography recently has been advocated to
screen and detect abnormalities in the optic nerve
diameter in patients with head trauma that could
involve the optic nerve,20,21 including its use in bed-
side emergency department conditions.22
It has been reported that 20% and 38% of patients
with traumatic optic neuropathy will have a sponta-
neous recovery of vision.23,24 In the present study, 2
patients (25%) had a spontaneous improvement of
visual acuity (Table 3). Corticosteroids were used
UROLAGIN ET AL
initially to decrease edema and vasospasm in an effort
to limit ischemic nerve cell death. The rationale for
intravenous corticosteroids for the treatment of trau-
matic optic neuropathy was derived from the results
of the NASCIS II.25 The NASCIS I, II, and III showed
benefits to patients with spinal cord injuries who
received high-dose corticosteroids within 8 hours of
injury.26-28 Although widely accepted, whether the
corticosteroids are of similar benefit in the treatment
of traumatic optic neuropathy is unproved. In the
present study, 6 of 8 patients (75%) received steroid
therapy and 1 patient had an improvement in visual
acuity (Table 3).
The benefit of any kind of intervention is not clearly
established.29 The International Optic Nerve Trauma
Study, with data from 127 enrolled patients, failed to
show a clear benefit from corticosteroid therapy or
optic nerve decompression. The investigators con-
cluded that neither corticosteroid therapy nor optic
canal decompression should be considered the stan-
dard of care for patients with traumatic optic neurop-
athy and that therapeutic decisions should be based
on the individual patient.30
Some investigators have recommended surgical inter-
vention alone or in conjunction with corticosteroids for
certain presentations of traumatic optic neuropathy.
Several criteria for surgical intervention have been put
forward for different procedures and different clinical
circumstances.31-34 Most reports have shown a measur-
able improvement in vision in 31% to 82% of patients
undergoing surgical intervention with or without corti-
costeroid therapy.32,35 One study advised caution in the
repair of Le Fort III fractures in patients with concomi-
tant orbital apex or optic canal fractures because of
possible secondary optic nerve damage.36 Some investi-
gators have noted no relation between the timing of
trauma and surgery, whereas others have found a ben-
efit from surgery within a specified time frame.16,37 One
patient in the present study developed traumatic optic
neuropathy after surgery for a ZMC fracture, which
improved with steroid therapy (Table 1).
In the present study, all patients presented with a
ZMC fracture, and 3 patients had associated frontal
bone fracture, temperoparietal bone fracture, and Le
Fort II with bilateral mandibular condyle and ramus
fractures (Tables 1, 2). Of 6 patients who were ad-
ministered steroid therapy, 1 patient showed an im-
provement in visual acuity. Two patients underwent
decompression by a lateral orbital approach (Fig 3); 1
patient showed an improvement in visual acuity. In 2
other patients, a spontaneous recovery was observed.
Four of 8 patients underwent open reduction and
fixation of maxillofacial fractures. Of the remaining 4,
1 patient had a nondisplaced ZMC fracture that was
treated without surgical intervention and 3 patients
refused any surgical intervention (Table 3).
1127
FIGURE 3. Endoscopically assisted decompression of the optic
nerve.
Urolagin et al. Optic Neuropathy After Maxillofacial Trauma.
J Oral Maxillofac Surg 2012.
In a retrospective study of 35 patients, 4 different
variables were suggested to indicate a poor outcome
in patients with traumatic optic neuropathy: blood in
the posterior ethmoid cells, loss of consciousness, age
older than 40 years, and an absence of improvement
after 2 days of steroid treatment.38 In addition to these
variables, the presence of an orbital hemorrhage
(Fig 4) and evidence of cerebral lesions (Fig 5) were
included in the present study (Table 2).
Previous laser interferometric studies have shown
that forces applied to the frontal bone are transferred
and concentrated in the optic canal region.39 Bleed-
ing within the posterior ethmoidal cells presumably
reflects a greater amount of energy applied to this
region; therefore, it makes make sense that this sign
is associated with a worse visual prognosis. Simi-
larly, it could also account for the fact that loss of
consciousness is associated with a lower likelihood
of visual recovery.38 When these factors were as-
sessed in the present study, 6 patients presented
blood in the posterior ethmoid cells (Fig 6) and 5
patients had a history of a loss consciousness (Table
2). Two patients had neither posterior ethmoid
bleeding nor a loss of consciousness, but this find-
ing did not correlate with an improvement in vi-
sion.
Age was another variable associated with a poor
outcome. It has been speculated that the recovery of
vision in such patients may be impaired by an age-
related axonal lipid peroxidation and membrane hy-
drolysis occurring after the trauma. This hypothesis
has been supported by recent studies in mammals in
which brain aging was associated with a gene expres-
sion profile indicative of oxidative stress and de-
creased neurotrophic support in the neocortex.40,41
The authors cannot draw any conclusion because the
1128 OPTIC NEUROPATHY AFTER MAXILLOFACIAL TRAUMA

FIGURE 4. Computed tomographic scan showing evidence of an orbital hemorrhage.

Urolagin et al. Optic Neuropathy After Maxillofacial Trauma. J Oral Maxillofac Surg 2012.

study group was small and recovery was seen in
patients 22 and 60 years old regardless of the inter-
vention (Tables 1, 3).
Various surgical approaches, such as transfrontal cra-
niotomy,42 extranasal transethmoidal,43 transantral eth-
moidal,44 lateral facial,45 and endoscopic procedures,
were developed to access the optic nerve.32,46,47 Endo-
scopic optic nerve decompression using an intranasal
and transethmoidal or trans-sphenoidal approach re-
cently has gained popular support.30,48-50 Decompres-
sion in the present cases consisted of a combination of
lateral orbital and endoscopic intranasal transethmoidal
approaches.
Kountakis et al32 reported that 32% of patients
showed an improvement in vision using a protocol
that allowed megadose steroids with a bolus intrave-
nous delivery of methylprednisolone 30 mg per kilo-
gram of body weight over 1 hour, followed by a
5.4-mg/kg/hour infusion for 47 hours. The patients
without improvement after 48 hours underwent en-
doscopic optic nerve decompression; using this ap-
proach, they found improvement in 82% of patients.
In another study of 44 patients, 10 showed an
improvement after steroid therapy and 11 showed
an improvement after endoscopic optic nerve de-
compression, with an overall improvement of
48%.16 Lateral orbitotomy has been reported to
have some benefit when used as salvage therapy in
patients who are not completely blind after a failure
of steroid therapy.51
Yu-Wai Man and Griffiths49 recently assessed the
effects and safety of surgical interventions in the man-

FIGURE 5. Computed tomographic scan showing evidence of cerebral lesions.

Urolagin et al. Optic Neuropathy After Maxillofacial Trauma. J Oral Maxillofac Surg 2012.
UROLAGIN ET AL
FIGURE 6. Computed tomographic scans showing evidence of blood within the posterior ethmoidal cells.
Urolagin et al. Optic Neuropathy After Maxillofacial Trauma. J Oral Maxillofac Surg 2012.
agement of traumatic optic neuropathy. Given the
relatively high rate of spontaneous visual recovery,
they concluded that there is no evidence that surgical
decompression of the optic nerve provides any addi-
tional benefit.49 However, in selected cases in which
orbital bone fragments or foreign bodies impinge on,
but do not transect, the optic nerve, surgical interven-
tion may be indicated. In any case, one should be
aware of the fact that surgical intervention carries a
definite risk of complications. Similar to corticosteroids,
the use of surgery in traumatic optic neuropathy
remains controversial and each case needs to be
assessed individually.
The most widely accepted contemporary treat-
ments for traumatic optic neuropathy have included
observation, steroids, and surgical decompression,
but concerns about the use of steroids in patients
with acute brain trauma has led to recent recommen-
dations not to treat traumatic optic neuropathy with
steroids.49,52,53
Previous reports have advised caution in the repair
of Le Fort III fractures. Conversely, the present study
found the occurrence of traumatic optic neuropathy
in association with ZMC, Le Fort II, and cranial bone
1129
fractures. Additional risk factors, such as a history of a
loss of consciousness, injury to the superolateral or-
bital region, fracture of the optic canal, evidence of
orbital hemorrhage, and evidence of blood within the
posterior ethmoidal cells, should be considered dur-
ing the evaluation. These factors become more impor-
tant especially in uncooperative, inebriated, or unre-
sponsive patients with a neurologic deficit and with
periorbital swelling.
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