Visual Loss due to Orbital Fracture

The Role of
Early
Reduction
Alan F. Lipkin, MD; Gayle
E. Woodson, MD;
Robert H. Miller, MD
\s=b\Serious injury
to the optic
nerve is an
uncommon, usually permanent, complica-
tion of orbital fractures. Occasionally
it is
due to reversible
changes,
such as ede-
ma, contusion,
or compression
of the
optic
nerve. The
early management
of
visual loss due to orbital fracture is con-
troversial. Some authors advocate emer-
gency optic nerve decompression;
others
recommend steroid
therapy
alone. We
present a case of
nearly complete
unilat-
eral loss of vision after a lateral orbital
fracture with
compression
of the
optic
nerve by bony fragments. Computed
tomographic scanning
of the orbit
helped
us to
pinpoint
the cause of visual
compro-
mise and also served as a guide
in
plan-
ning surgery. Large dosages
of
steroids,
combined with early
reduction of the frac-
ture,
resulted in substantial
recovery
of
vision. This case illustrates the
impor-
tance of
precisely determining
the nature
of the injury and the cause of visual
compromise.
A
protocol
for management
of these injuries
is presented.
(Arch Otolaryngol
Head Neck Surg
1987;113:81-83)
Eye
injury
serious enough
to result
in blindness
has been estimated
to occur in 3% of facial fractures.1
When
blindness
is immediate and
complete,
the prognosis
for even
par
tial
recovery
is
poor.23 Progressive
or
incomplete
visual loss
may
be amelio
rated either
by large dosages
of ste
roids or
by emergency optic
nerve
decompression, depending
on the
mechanism of
injury,
the
degree
of
trauma to
the
optic canal,
and the
period
of time that
elapses
between
injury
and
medical intervention.4
We
recently
treated a
patient
who
sustained severe visual
impairment
after
fracture
of the lateral orbital
wall, optic canal,
and
zygoma.
Com
puted tomography
was used to help
us
localize the site of
presumed optic
nerve
injury. Early
reduction of the
fractures,
combined
with
large
dos
ages
of
steroids,
resulted
in substan
tial
recovery
of vision.
REPORT OF A CASE
A
30-year-old
man was brought
via
ambulance to the Ben Taub General
Hospi
tal
emergency room, Houston,
after sus
taining
facial and head
injuries
in a motor
vehicle accident. His face had struck the
windshield, leading
to a brief loss of con
sciousness and
subsequent disorientation,
confusion,
and combativeness. On initial
examination,
there were multiple
facial
lacerations and
complete
external
ophthal-
moplegia
on the left side. Chemosis and a
small subconjunctival hemorrhage
were
present. The pupil
was 7 mm in diameter
and nonreactive to
light
or accommoda
tion. The
patient
was not
sufficiently coop
erative for visual
acuity testing,
but there
was no apparent response
to confrontation
on the left side. Vision in the
right eye
was
normal.
Computed tomographic (CT)
scans of the
head and facial bones revealed a medially
displaced
fracture of the lateral wall of the
left
orbit,
with the
fragment compressing
to the
optic
nerve (Fig 1). Additionally,
there were two fractures of the
zygomatic
arch, a fracture of the posterolateral
wall
of the sphenoidal sinus,
and a fracture of
the
squamous portion
of the temporal
bone
with no visible brain injury.
The patient's
mental status cleared over a period
of
several hours,
and an ophthalmologic
examination was performed.
The left
eye
could only
differentiate light
and dark;
there was not sufficient
acuity
to differen
tiate fingers or letters. There was no evi
dence of
injury
to the
globe.
The patient
was given an intravenous
bolus of 10
mg
of dexamethasone sodium
Accepted
for publication
March
21,
1986.
From the
Department
of
Otorhinolaryngology
and Communicative
Sciences, Baylor College
of
Medicine,
Houston. Dr
Lipkin
is now in
private
practice,
Denver.
Presented in
part
at the Southern Sectional
Meeting
of the American
Academy
of Facial
Plastic and Reconstructive Surgery, Orlando,
Fla,
Jan
18,
1986.
Reprint requests
to
Department
of Otorhino-
laryngology
and Communicative
Sciences, Baylor
College
of
Medicine,
1
Baylor Plaza, Houston,
TX
77030
(Dr Woodson).
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Fig 1.Preoperative computed tomographic
scan reveals
medially
displaced
fracture of left lateral orbital wall with
bony fragment
compressing optic nerve.
Fig 2.Postoperative computed tomographic scan reveals satisfacto
ry
reduction of orbital fractures.
Management
of Orbital Fractures
No
Injury to Vision
Reduction of Fractures
as Indicated
Complete
Blindness
Steroids Only
Orbital
Injury
Initial Stabilization
Head and Neck Evaluation
Ophthalmologic
Evaluation
,
Facial
Roentgenograms.
Visual Loss
4r
Computed Tomographic Scans of Orbits and Face
Nerve Injury
Subtotal or Delayed
Loss
Hematoma or
Fragments Injuring
Nerve
I
Steroids and
Surgery
Ophthalmic Injury
Emergency Ophthalmologic
Care
Later Reduction of Fractures
No Hematoma
or
Fragments Injuring
Nerve
Steroids
No Improvement
^
Improvement
Surgery
4
Fig
3.Our current management
of orbital fractures.
phosphate
and
brought
to
surgery.
The
fractures were reduced
through a brow
incision and
preexisting
facial lacerations.
The main
fragment,
which included the
zygoma
and lateral wall of the
orbit,
was
reduced
only
after the
application
of a
large
amount of rotational force. The CT
images
were used as a guide
for the direc
tion of motion
in
reducing
and
wiring
the
fractures.
Postoperatively,
the
patient
was main
tained on a course of dexamethasone sodi
um
phosphate (10 mg intravenously every
six
hours),
and the dose was
tapered
over a
ten-day
course. His vision and extraocular
motions
gradually improved
over this
peri
od. After three
days,
he was able to count
fingers
with the left
eye,
and after ten
days,
he was able to read
newsprint.
A
postoperative
CT scan
(Fig 2)
revealed
satisfactory
reduction of the orbital frac
tures. One
year later,
the
patient
has 20/70
vision in his left eye,
normal
motility,
and
an
acceptable
cosmetic result.
COMMENT
The
globe
and
optic
nerve are
highly
vulnerable to
permanent injury
after
blunt facial trauma.
Hyphema,
lens or
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retinal
detachment,
scierai
rupture,
and
damage
to the nerve
may
all occur
at the time
of
impact
and lead to
permanent
visual loss.
Injury
to
the
optic
nerve after facial fracture can
occur
anywhere along
the
course
of
the
nerve,
but it is most common
within the
bony optic
canal.3
Shearing
forces after fractures can be
great
enough
to transect the
nerve, leading
to immediate and irreversible
blind
ness. Stretch
injuries
to the nerve are
potentially reversible,
but
they may
be associated with intraneural or
extraneural hematomas that can com
press
the
remaining
viable neurons.
In
fact, injury
to the nutrient vessels
of the nerve with
hemorrhage
into the
sheath, edema,
and contusion
may
be
the most
frequent
mechanism of
visual loss.5 The
central retinal artery
and
ophthalmic artery are
seldom
seriously injured.
Clinically,
the
timing
and
progres
sion of visual loss can be
crucial
in
determining
further treatment.
Blindness
occurring
at the moment of
injury
carries a
poor prognosis,
regardless
of treatment.5
Delayed
or
progressive
loss of vision
implies
that
a viable nerve is
being compressed by
edema or
bleeding;
in such
cases, early
treatment
may improve
the
prospect
for
recovery.
The
injury
can be local
ized
using
a combination of
special
ized
physical
and
radiologie
examina
tions.
Early ophthalmologic
consulta
tion is
essential in all cases of midface
or frontal
injury.1
In addition to docu
mentation of visual
acuity, major
injuries
to
the
globe
and adnexa can
be excluded.
Interpretation
of
plain
roentgenograms may
be difficult
because of
superimposed
soft-tissue
swelling
or bone artifact.
Computed
tomography
allows the
deeper
struc-
tures of the orbit
(including
the
optic
nerve
itself)
and facial bones to be
visualized with
unsurpassed accuracy*
and
may
be used to
pinpoint
the most
likely
areas of severe
injury.
It is
generally agreed
that initial
treatment should focus on the overall
stabilization of the
patient, particu
larly
in
ruling
out head
injury
that
may
need
urgent
attention. Severe
injuries
to the
sclera, lens,
or retina
may require emergency ophthalmic
surgery. Nonoperative
intervention
may
consist of
administration of
pharmacologie
doses of corticoste-
roids
(dexamethasone, up
to 5
mg/
kg/d)
to reduce
microcirculatory
spasm, edema,
and nerve cell necro
sis.1 The best results are achieved
if
steroids are
given immediately
after
injury.
The role of
surgery
after
injuries
to
the nerve is
controversial,
with thera
peutic regimens
in
major
centers
ranging
from routine
exploration
after all cases of traumatic visual loss
to never
performing surgery. Hughes8
found
that,
even in
injuries
that
directly
involve the
optic
canal
(only
6% in his
series), decompression
of
the nerve did
not
change
the
poor
prognosis
for
recovery
of useful
vision. His results are contradicted
by
several
Japanese investigators910
who
have
collectively performed
hundreds
of transethmoidal
optic
nerve decom
pressions
after
trauma. In over 400
operations performed by Pukado,10
some
improvement
occurred in
nearly
every case, including
those in whom
there was no initial
light perception
and those in whom months had
elapsed
since their
injuries.
Anderson
et al7 are more selective in their use of
surgery, reserving
it for
patients
who
either
(1)
sustain
delayed
visual loss
that is
unresponsive
to 12 hours of
corticosteroid
therapy
or
(2) initially
improve
while
receiving
steroid thera
py
but
then
deteriorate,
either while
receiving
steroid
therapy
or when
it
is
being tapered. Although
we
generally
favor this
selective and
pragmatic
approach,
we feel that the results of
high-resolution
CT scans should also
be
considered when
making
the deci
sion about
surgery.
Fractures and
hematomas can be
precisely
located
preoperatively, aiding
the
surgeon
in
approaching
areas of
potentially
reversible
injury.
Our current
management
of orbital
fractures is as follows
(Fig 3):
After
initial
stabilization and routine facial
roentgenograms,
all
patients
are eval
uated
by
both the
otolaryngology
and
ophthalmology
services. If
the
injury
does not threaten
vision,
the
fractures
are reduced as indicated. If vision is at
all
compromised,
a
high-resolution
CT
scan of the orbits and facial bones
with soft-tissue and bone
settings
is
obtained.
Special
effort
is
made to
visualize the
optic
nerves and
canals.
High-dosage
steroids are adminis
tered. If
fragments significantly
impinge
on the
nerve,
CT
images
are
used as a
guide
for
relocation or
removal of
the involved bone. Hema
toma is also a relative indication for
immediate
surgery.
In
cases
where
there is no obvious
impingement
on
the
nerve,
steroids are
given,
and the
patient
is
carefully
observed. If the
patient's
vision
deteriorates
despite
medical
treatment,
the nerve is
explored
and
decompressed. By
treat
ing posttraumatic optic
nerve
injuries
aggressively,
usable vision can be
pre
served in a number of
patients.
References
1. Holt
GR,
Holt JE: Incidence of eye injuries
in facial fractures: An analysis
of 727 cases.
Otolaryngol
Head Neck
Surg 1983;91:276-279.
2. Maniglia AJ, Kronberg FG,
Culbertson W:
Visual loss associated with orbital and sinus
diseases.
Laryngoscope 1984;94:1050-1059.
3. Manfredi
SJ, Raji MR, Sprinkle PM,
et al:
Computerized tomographic
scan
findings
in
facial fractures associated with blindness. Plast
Reconstr Surg 1981;68:479-490.
4. Krausen
AS, Ogura JH,
Burde
RM, et al:
Emergency
orbital
decompression: A
reprieve
from blindness.
Otolaryngol
Head Neck
Surg
1981;89:252-256.
5. Edmund
J,
Gottfriedsen E: Unilateral
optic
atrophy following
head injury. Acta Ophthalmol
1963;41:693-697.
6. Grove AS:
Computed tomography
in the
management
of orbital trauma.
Ophthalmology
1982;89:433-440.
7. Anderson
RL, Panje WR,
Gross CE:
Optic
nerve blindness
following
blunt forehead trau-
ma.
Ophthalmology 1982;89:445-455.
8. Hughes
B: Indirect
injury
of the
optic
nerves and chiasma. Bull Johns
Hopkins
Hosp
1962;111:98-126.
9. Niho
S,
Niho
M,
Niho K:
Decompression
of
the
optic
canal
by
the transethmoidal route and
decompression
of the
superior
orbital fissure.
Can J
Ophthalmol 1970;5:22-40.
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surgical
decompression
of the
optic
nerve. Mod Probl
Ophthalmol 1975;14:474-481.
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