Otolaryngol Clin N Am

39 (2006) 943–958

Endoscopic Orbital and Optic Nerve

Decompression
Steven D. Pletcher, MDa,
Raj Sindwani, MD, FACS, FRCSb,
Ralph Metson, MDc,d,*
a
Department of Otolaryngology–Head and Neck Surgery, University of California,
San Francisco, San Francisco, CA, USA
b
Department of Otolaryngology–Head and Neck Surgery, Saint Louis University School
of Medicine, Saint Louis, MO, USA
c
Department of Otology and Laryngology, Harvard Medical School, Boston, MA, USA
d
Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Boston, MA, USA

For more than 100 years, surgical decompression of the orbit has been
used to treat the severe proptosis and optic neuropathy associated with
Graves’ disease. Although decompression techniques involving removal
each of the four walls of the orbit have been described [1–4], the Walsh-
Ogura decompression [5] described in the 1950s was favored by most otolar-
yngologists. This operation uses the familiar Caldwell-Luc approach to
remove the inferior and medial orbital walls, allowing the enlarged orbital
fat and muscles to decompress into the ethmoid and maxillary sinus cavities.
Soon after the introduction of transnasal endoscopic sinus surgery in the
mid 1980s, surgeons began to experiment with endoscopic orbital surgery.
Endoscopic orbital decompression was first described by Kennedy [6] and
Michel [7] in the early 1990s. Enhanced visualization of key anatomic land-
marks allowed for safe and thorough decompression of the entire medial or-
bital wall, as well as the medial portion of the orbital floor. This improved
visualization is most notable in the region of the orbital apex, a critical area
of decompression in patients with optic neuropathy. These advantages have
allowed the endoscopic approach to replace the Walsh-Ogura procedure as
the technique of choice for orbital decompression.
The benefits of endoscopic instrumentation for orbital decompression
can be similarly applied when operating in the vicinity of the optic nerve.
Decompression of the optic nerve involves complete removal of the bone

* Corresponding author: Zero Emerson Place, Suite 2D, Boston, MA 02114.

E-mail address: ralph_metson@meei.harvard.edu (R. Metson).

0030-6665/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.otc.2006.06.003 oto.theclinics.com
944 PLETCHER et al

that forms the medial wall of the optic canal. Although the indications for
and surgical techniques of orbital decompression are fairly well established,
controversy exists regarding both the indications and extent of surgery nec-
essary for optic nerve decompression.

Graves’ orbitopathy (dysthyroid orbitopathy)

Graves’ disease is an autoimmune disorder that affects primarily the thy-
roid and the orbit. Thyroid manifestations are characterized by the produc-
tion of autoantibodies to the TSH receptor with subsequent
hyperstimulation and resultant hyperthyroidism. The thyroid manifesta-
tions of Graves’ disease an be treated with thyroid-suppressive medications,
radiation (I131), or surgery.
The orbital manifestations of Graves’ disease, known as dysthyroid orbit-
opathy, also represent an autoimmune process although the exact antibody
target remains unclear. Inflammation associated with infiltration of T-cells
and deposition of glycosaminoglycan results in enlargement of orbital fat
and extraocular muscles. This increase in volume of contents within the con-
fines of the rigid bony orbit results in increased pressure and resultant prop-
tosis, or compression of the optic nerve. The degree of proptosis does not
correlate with the overall severity of disease, as patients with poor compli-
ance of the orbital septum may not experience significant proptosis but
can have severe compression at the orbital apex and develop optic neurop-
athy. The orbital and thyroid manifestations of Graves’ disease follow dis-
tinct and independent clinical courses.
Clinical manifestations of dysthyroid orbitopathy range from mild find-
ings such as tearing, photophobia, and conjunctival injection to significant
proptosis, diplopia, exposure keratopathy, and visual loss from optic neu-
ropathy. The clinical course of Graves’ orbitopathy can be divided into
the acute phase, characterized by active inflammation, which lasts 6 to 18
months and the chronic phase, characterized by fibrosis with stabilization
of proptosis. It is preferable to perform orbital decompression during the
chronic phase.

Medical treatment of dysthyroid orbitopathy

Local measures such as lubrication, eyelid taping, and patching for pa-
tients with dryness and diplopia represent initial conservative treatment ap-
proaches. More aggressive treatments include the use of systemic
corticosteroids and orbital radiation. Both of these treatments appear to
be most effective during the acute phase of the disease. Systemic corticoste-
roid treatment usually results in marked improvement, but the symptoms
generally recur following discontinuation of steroid treatment. Because of
the deleterious side effects of long-term corticosteroid use, steroid treatment
 ENDOSCOPIC ORBITAL AND OPTIC NERVE DECOMPRESSION 945

are often used as a temporizing measure or in conjunction with surgical de-

compression. The use of orbital radiation is controversial, and its efficacy
has been challenged by two recent randomized prospective trials [8,9].

Endoscopic orbital decompression

The endoscopic technique allows for unmatched visualization of critical
anatomic regions including the skull base and orbital apex and avoids exter-
nal or sublabial incisions. The entire medial orbital wall as well as the medial
portion of the orbital floor is removed with endoscopic decompression
(Fig. 1).

Technique
The patient is positioned in the supine position, and topical vasoconstric-
tion is achieved with topical oxymetazoline (0.05%) pledgets. The eyes
are maintained within surgical field, protected with scleral shields. Image-
guidance systems may be used at the surgeons discretion. Local injection
of lidocaine 1% with 1:100,000 epinephrine is administered along the lateral
nasal wall in the region of the maxillary line (a bony eminence that extends
from the anterior attachment of the middle turbinate to the root of the
inferior turbinate).
Surgery begins with an incision just posterior to the maxillary line. The
uncinate process is medialized and removed, exposing the natural ostium
of the maxillary sinus. With orbital decompression it is important to widely
open the maxillary sinus to achieve adequate access to the orbital floor and
prevent blockage of the ostium from orbital fat, which protrudes following
decompression. Enlargement is performed primarily in a posterior direction
as extension of the antrostomy too far anteriorly risks of damage to the

Fig. 1. Bone removed during endoscopic orbital decompression includes the medial orbital wall
and the medial aspect of the orbital floor.
946 PLETCHER et al

nasolacrimal duct. Using a 30 degree endoscope, the wide antrostomy

should allow easy visualization of the infraorbital nerve as it courses along
the floor of the orbit.
An endoscopic sphenoethmoidectomy is performed in standard fashion.
We advocate removal of the middle turbinate during orbital decompression
to optimize exposure of the medial orbital wall and facilitate postoperative
cleaning. An image guidance system may be used at this point to confirm
removal of all ethmoid cells along the medial orbital wall, and to ensure
complete dissection to the sphenoid face and posterior skull base.
The skeletonized medial orbital wall is then carefully penetrated in a con-
trolled fashion with a spoon curette or other blunt instrument. It should be
noted that once the lamina is transgressed, orbital fat should not be visible,
as long as the underlying periorbital fascia is left intact. The thin bone of the
lamina papyracea is elevated while preserving the underlying periorbita.
Bone fragments are removed using Blakesly forceps (Fig. 2). Bone removal
proceeds superiorly toward the ethmoid roof, inferiorly to the orbital floor,
and anteriorly to the maxillary line. Bone in the region of the frontal recess
is left intact; if bone is removed from this region, herniated fat may obstruct
drainage of the frontal sinus.
As dissection proceeds posteriorly, thick bone is encountered in the re-
gion of the orbital apex within 2 mm of the sphenoid face. This bone corre-
sponds to the annulus of Zinn, from which the extraocular muscles originate
and through which the optic nerve passes. This landmark represents the pos-
terior limit of a standard decompression. For patients with optic neuropa-
thy, experienced surgeons may consider continuing the decompression
posteriorly into the sphenoid sinus; however, the benefits of incorporating

Fig. 2. Once the medial orbital wall has been exposed, Blakesly forceps are used to remove frag-
ments of the lamina papyracea.
 ENDOSCOPIC ORBITAL AND OPTIC NERVE DECOMPRESSION 947

and optic nerve decompression into standard orbital decompression are un-
clear, and may lead to inadvertent injury to the nerve.
Removal of the orbital floor can be technically challenging, depending on
its thickness. Only that portion of the floor that is medial to the infraorbital
nerve is removed. A spoon curette is used to engage the orbital floor at its
medial extent and down-fracture the bone (Fig. 3). The bone of the orbital
floor is thicker than that of the medial orbital wall, and significant force may
be required for this maneuver. If the spoon curette is not sturdy enough for
this portion of the procedure the heavier mastoid curette may be used. The
bone may fracture in one large piece, typically with a natural cleavage plane
at the canal of the infraorbital nerve, or, more frequently, it fractures into
several small pieces. A 30-degree endoscope and angled forceps may facili-
tate bone removal while preserving the infraorbital canal as the lateral limit
of dissection.
Once the lamina papyracea and medial orbital floor have been removed,
the periorbita is fully exposed. A sickle knife is then used to open this fascial
layer. Care must be taken to avoid ‘‘burying’’ the tip of the sickle knife and
potentially injuring the underlying orbital contents such as the medial rectus
muscle. The periorbital incision should be initiated at the posterior limit of
decompression (just anterior to the sphenoid face) and brought anteriorly so
that prolapsing fat does not obscure visualization. Parallel incisions are per-
formed along the ethmoid roof and orbital floor. To minimize the risk of
postoperative diplopia, a 10 mm-wide sling of fascia overlying the medial
rectus muscle may be preserved while the remainder of the periorbita is re-
moved using angled Blakesley forceps (Fig. 4) [10]. In patients with optic
neuropathy, the fascial sling technique is not used to allow maximal

Fig. 3. A spoon curette is used to down-fracture the medial portion of the orbital floor.
948 PLETCHER et al

Fig. 4. Following bony decompression, a sickle knife is used to incise the periorbita. In patients
without optic neuropathy, a sling of fascia may be preserved overlying the medial rectus muscle
to minimize postoperative diplopia.

decompression. A ball-tipped probe and sickle knife may be used to identify

and incise remaining fibrous bands that often course superficially between
lobules of orbital fat. Upon completion of the procedure, a generous pro-
lapse of fat into the opened ethmoid and maxillary cavities should be ob-
served (Fig. 5). The globe may be blotted to encourage maximal fat
herniation and confirm a decrease in retropulsive resistance.
Depending on the clinical scenario and desired degree of decompression,
a subsequent lateral decompression may be performed through an external
approach. When performed immediately following medial decompression,
the orbital contents are easily retracted in a medial direction, allowing for
excellent exposure of the lateral bony wall. Bilateral decompressions may
be performed concurrently or in a staged procedure.
Nasal packing is avoided to ensure maximal decompression and avoid
compression of exposed orbital contents. The patient is discharged the
morning after surgery with a prescription for oral antistaphylococcal antibi-
otics and instructions to begin twice daily nasal saline irrigations. At the first
postoperative visit 1 week following surgery, crusts and debris are cleaned
from the surgical site under endoscopic guidance.
For patients with severe comorbidities, a strong preference for local an-
esthesia, or in whom surgery is being performed on an only seeing eye, de-
compression may be performed under local anesthesia with sedation [11].
This approach allows the surgeon to monitor the patient’s vision throughout
the procedure. Sedation may be achieved with an intravenous bolus of pro-
pofol (0.4–0.8 mg/kg) before injection of local anesthesia, followed by an in-
fusion of 75 to 95 mg/kg during the procedure. Local anesthesia is
 ENDOSCOPIC ORBITAL AND OPTIC NERVE DECOMPRESSION 949

Fig. 5. Following decompression, orbital fat protrudes into the ethmoid and maxillary spaces
(A). With the ortbital sling technique, a strip of periorbita remains to support the medial rectus
muscle and minimize postoperative diplopia (B).

administered initially with 4% cocaine pledgets followed by injection of

lidocaine 1% with 1:100,000 epinephrine. Patients may report discomfort
during removal of the lamina papyracea. This sensation may be relieved
by infiltration of a small amount of additional anesthetic solution along
the medial orbital wall.

Results
The goals of orbital decompression vary depending upon the indication
for the procedure. In patients with compressive optic neuropathy,
950 PLETCHER et al

restoration of visual deficits is the key outcome, while in patients with cor-
neal exposure or severe proptosis, ocular recession may be the primary end
point. The reported incidence of improvement following endoscopic orbital
decompression for Graves’ orbitopathy ranges from 22% to 89% [6,12,13].
This wide variation in results reflects the diverse patient populations and
definitions of improvement. Postoperative deterioration of visual acuity oc-
curs in less than 5% of patients [7,12,13]. Ocular recession as a result of en-
doscopic decompression alone averages 3.5 mm (range 2–12 mm). The
addition of concurrent lateral decompression to the endoscopic procedure
provides an additional 2 mm of globe recession [13].

Complications
Diplopia is not an uncommon occurrence following orbital decompres-
sion with 15% to 63% of postoperative patients reporting new-onset diplo-
pia or worsening of preexisting symptoms [7,11,13–16]. This complication is
believed to be a result of a change in the vector of pull of the extraocular
muscles. Decompressive surgery rarely alleviates preexisting diplopia. Pa-
tients who have diplopia following decompressive surgery often require stra-
bismus surgery for correction. All patients should be informed of the
possibility of postoperative double vision, as well as the potential need for
further surgical intervention if this persists.
Several methods to decrease postoperative diplopia have been reported.
Multiple authors have described the preservation of a strut of inferomedial
bone between the decompressed floor and medial wall [12,17]. When this
strut is maintained, however, it is technically difficult to remove the orbital
floor through a purely endoscopic technique. The maintenance of a facial
sling in the region of the medial rectus has also been demonstrated to de-
crease the incidence of postoperative diplopia [10]. This technique provides
similar support as the medial strut technique, but allows for endoscopic
access to decompress the medial orbital floor. The concept of a balanced de-
compression (concurrent medial and lateral decompression) has also been
suggested as a means to decrease postoperative diplopia [14,18,19]. When
operating for compressive optic neuropathy, techniques designed to limit
diplopia may also limit the extent of decompression, and postoperative dip-
lopia is often accepted as a concession to improved visual acuity.
Postoperative bleeding following decompression is best managed through
endoscopic identification and direct cauterization of the bleeding site. Nasal
packing is generally not used to avoid pressure on the exposed orbital apex
and optic nerve. Postoperative infection is minimized through the use of
postoperative antibiotics with staphylococcal coverage. A large maxillary
antrostomy and limited bone removal in the frontal recess region minimize
the risk of developing postoperative sinusitis. Epiphora may develop if the
maxillary antrostomy is extended too far anteriorly with transection of
the nasolacrimal duct. This complication is treated with an endoscopic
 ENDOSCOPIC ORBITAL AND OPTIC NERVE DECOMPRESSION 951

dacryocystorhinostomy. Leakage of cerebrospinal fluid and blindness are

very rare complications that have been reported following nonendoscopic
decompression techniques.

Optic nerve decompression

Historically the most common, and perhaps most controversial, indica-
tion for optic nerve decompression has been traumatic optic neuropathy
(TON). The efficacy of decompression in this setting remains unclear. Endo-
scopic and nonendoscopic techniques of optic nerve decompression have
also been used for a variety of nontraumatic causes of compressive optic
neuropathy such as benign tumors and inflammatory or fibroosseus lesions
[20]. It is in these patients with nontraumatic, compressive optic neuropathy
that endoscopic optic nerve decompression appears to be most successful.
Controversy regarding the treatment of TON exists because the two
mainstays of therapy, corticosteroids and surgical decompression, have
not shown definitive clinical benefit when compared with observation alone
[14,21]. To address this issue the International Optic Nerve Trauma Study
(IONTS) was undertaken. The initial goal of a randomized, controlled trial
was abandoned when patient recruitment was insufficient to support this
study design. Thus, a comparative nonrandomized interventional study
with concurrent treatment groups was performed with 127 patients [14].
No clear benefit was found for either corticosteroid therapy or surgical optic
canal decompression. The authors discussed numerous published uncon-
trolled studies, and their overall recommendation based on the IONTS
and their literature review was that treatment should be determined on an
individual patient basis.
Several retrospective studies subsequent to the IONTS have suggested
improvement in visual acuity with optic nerve decompression following fail-
ure of visual improvement with steroids [22–24]. The uncontrolled nature of
these studies, however, must be taken into account when considering surgi-
cal decompression for traumatic optic neuropathy.

Surgical anatomy
The optic nerve may be divided into three segments: the intraorbital, the
intracanalicular, and the intracranial segment. Optic nerve decompression
aims to relieve compressive forces within the intracanalicular portion of
the nerve. The canal of the optic nerve is formed by the two struts of the
lesser wing of the sphenoid and carries both the optic nerve and the ophthal-
mic artery. At the orbital apex is the fibrous annulus of Zinn.

Pathophysiology
Compression on the optic nerve may result from neoplastic, inflamma-
tory, or traumatic processes. Initial theories of vascular compromise from
952 PLETCHER et al

external compression with resultant injury to the optic nerve have been
largely discarded. Manual compression resulting in conduction block and
focal demyelination from compression are the favored pathophysiologic ex-
planations for compressive optic neuropathy. Rapid recovery following de-
compression results from relief of the manual compression block while
a delayed recovery may occur over a period of weeks to months as a result
of remyelination [25].
Traumatic optic neuropathy may be divided into two categories: indirect
and direct. Direct TON results from a penetrating injury with projectiles or
other sharp objects. In these cases the intraorbital portion of the optic nerve
is generally injured and decompression is not recommended. Indirect TON
results from blunt trauma to the head. This injury can occur with or without
associated fractures of the orbital canal. The pathophysiology of visual loss
in these cases is frequently unclear, and may include intraneural edema, he-
matoma, shearing injury to the microvasculature or axons, altered cerebro-
spinal fluid circulation, and interruption of direct axonal transport. If there
is evidence of complete disruption of the optic nerve, decompression is not
indicated, as the optic nerve will not recover from such injury. In cases
where edema, hematoma, or moderate bony compression is suggested, how-
ever, decompression may be considered.

Evaluation and treatment

Compressive optic neuropathy may have an insidious onset resulting in
delayed diagnosis. Patients’ initial symptoms are often vague including
mild blurry or ‘‘fuzzy’’ vision without significant loss of visual acuity and
with normal fundoscopic examination. More rigorous examination often re-
veals variable, limited visual field defects, a decrease in color vision, and an
afferent papillary defect on the affected side. Unfortunately, these symptoms
may go unnoticed until the more advanced stages of compression result in
decreased visual acuity. Thus, careful ophthalmologic examination is essen-
tial in discovering early signs of compression and, if abnormal, should be
evaluated with an MRI scan. Once a compressive optic neuropathy is diag-
nosed, surgical decompression is considered based upon the pathology and
extent of the compressive lesion. Systemic corticosteroids frequently provide
temporary improvement and may be considered while awaiting definitive
treatment.
Patients with suspected TON generally have sustained significant blunt
force trauma and should be evaluated by a trauma team for evidence of mul-
tisystem injury. As soon as TON is suspected, examination by an ophthal-
mologist is mandatory. Visual acuity should be determined as soon as
possible and closely monitored. Patients should be tested for an afferent pu-
pillary defect, which may be the only sign of TON in unconscious patients.
If possible, formal visual field testing and color vision testing should be per-
formed as abnormalities of color and peripheral vision typically precede
 ENDOSCOPIC ORBITAL AND OPTIC NERVE DECOMPRESSION 953

decreased visual acuity in the progression of optic neuropathy. Evaluation

of ocular pressure and fundoscopic exam may also yield important informa-
tion. A fine cut CT scan through the orbit and optic canal should be ob-
tained to look for fractures and bone displacement in the orbital apex.
Observation and treatment with corticosteroids are both reasonable med-
ical approaches to traumatic optic neuropathy. Steroid dosing is controver-
sial, and in the IONTS steroid dosing did not correlate with clinical
outcome. Frequently a loading dose of methylprednisone (30 mg/kg bolus)
followed by a continuous infusion of 5.4 mg/kg/h is given for 48 hours. This
regimen is based upon studies of spinal cord injury.

Endoscopic optic nerve decompression

Traditional surgical approaches for optic nerve decompression include
transorbital, extranasal transethmoid, transantral, intranasal microscopic,
and craniotomy approaches. Endonasal endoscopic decompression of the
optic nerve offers many advantages over these approaches, including excel-
lent visualization, preservation of olfaction, rapid recovery time, a lack of
external scars, and less operative stress in patients who may be suffering
from multisystem trauma.

Technique
Patients are prepared for surgery in a similar manner to those undergoing
orbital decompression. A standard sphenoethmoidectomy is performed. The
sphenoid face is widely opened and the bulge of the optic canal is identified
along the lateral wall of the sphenoid sinus, superior to the carotid artery. In
some patients, the optic canal may be initially identified in a posterior eth-
moid or Onodi cell, which can be seen on preoperative CT scan [26]. Iden-
tification and opening of the Onodi cell is important to provide adequate
surgical exposure and allow full access to the optic canal.
Following exposure of the medial orbital wall, a spoon curette is used to
fracture the lamina papyracea approximately 1 cm anterior to the optic ca-
nal. The lamina is then carefully removed in a posterior direction to expose
the annulus of Zinn and the optic canal. Care must be taken to avoid pen-
etration of the periorbita, as subsequent herniation of orbital fat will ob-
scure the surgical field. As the optic canal is approached, the thin lamina
will be replaced with the thick bone of the lesser wing of the sphenoid.
This bone must be thinned before removal. A long-handled drill with a dia-
mond burr is used to methodically thin the medial wall of the optic canal
(Fig. 6). While drilling, care must be taken to prevent contact of the drill
bit with the prominence of the carotid artery, which is located just inferior
and posterior to the optic nerve. Care should also be taken to avoid excess
generation of heat while drilling this bone as thermal damage to the optic
nerve may result. After the bone is appropriately thinned, a microcurette
954 PLETCHER et al

Fig. 6. Endoscopic view of the right posterior nasal cavity following wide sphenoidotomy. The
lamina papyracea has been removed to reveal periobita near the orbital apex. A diamond burr is
used to thin the bone of the optic canal.

is used to fracture the thinned bone in a medial direction, away from the op-
tic nerve (Fig. 7). Bone fragments are then removed from the decompressed
nerve using blakesly forceps (Fig. 8), with resultant medial decompression of
the optic nerve (Fig. 9).
Controversy exists regarding the length of optic canal that should be de-
compressed as well as the necessity for decompression of the optic sheath.
With compressive optic neuropathy secondary to neoplasms, the extent of
decompression is dictated by the size and location of the neoplasm. For

Fig. 7. A microcurette is used to elevate thinned bone of the optic canal.

 ENDOSCOPIC ORBITAL AND OPTIC NERVE DECOMPRESSION 955

Fig. 8. Blakesly forceps are used to remove bone fragments and expose the underlying optic
nerve.

cases of TON and dysthyroid orbitopathy, removal of bone for a distance of

1 cm posterior to the face of the sphenoid sinus is generally thought to be
sufficient [27].
Incision of the sheath has been advocated by some authors to further de-
compress the nerve itself; however, this maneuver may be unnecessary and
risks damage to the underlying nerve fibers and ophthalmic artery as well as
cerebral spinal fluid (CSF) leak, with resultant risk of meningitis. With clear

Fig. 9. The decompressed optic nerve is visible along the lateral wall of the sphenoid sinus.
956 PLETCHER et al

risks and an absence of data to suggest benefit for sheath decompression, we

do not advocate this maneuver for most patients undergoing optic nerve
decompression.

Results
Most patients who undergo optic nerve decompression for compressive
nontraumatic optic neuropathy will have significant improvement in visual
acuity. An immediate improvement in visual acuity is frequently observed,
probably from relief of a mechanical conduction block. Further improve-
ment may occur over a period of weeks to months as remyelination of the
nerve leads to more efficient conduction [25].
The efficacy of optic nerve decompression in traumatic optic neuropathy
is unclear. Much of the difficulty in determining the success of surgical inter-
vention arises from the relatively high rate of spontaneous recovery from
TON. Thus, well-controlled studies with significant power are required to
delineate the efficacy of surgical intervention. Unfortunately, such studies
have not been possible due to the rarity of this condition.
In cases of nontraumatic, compressive optic neuropathy, however, the
natural course of disease is not one of spontaneous resolution. Thus, it is
reasonable to conclude that visual improvement following surgical decom-
pression is a direct result of the procedure. In our recent experience of endo-
scopic optic nerve decompressions for nontraumatic optic neuropathy,
improved visual acuity was noted following 8 of 10 decompressions. One pa-
tient required multiple decompressions due to progression of her fibrous
dysplasia with recurrent impingement upon the optic nerve [20].

Complications
The risk of CSF leak, meningitis, and visual loss with optic nerve decom-
pression appears to be higher than with standard endoscopic sinus surgery
or orbital decompression. Although several studies with 20 to 45 patients re-
port no complications, the IONTS and another recent study reported sev-
eral cases of CSF leak, some with associated meningitis and visual
decompensation [14,23]. In the IONTS, it is unclear whether the complica-
tions occurred in patients who underwent endoscopic decompression repre-
senting less than 40% of patients in their series, or an external approach.

Summary
With excellent visualization of the orbital apex and optic canal, the endo-
scopic transnasal approach is well suited for both orbital and optic nerve
decompression. This operation is an advanced endoscopic technique, and
should be performed only by surgeons experienced in endoscopic nasal
surgery. Although the indications and expected results for orbital
 ENDOSCOPIC ORBITAL AND OPTIC NERVE DECOMPRESSION 957

decompression are well established, those for optic nerve decompression

continue to evolve.

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