TITLE: Surgery for Exophthalmos
SOURCE: Grand Rounds Presentation, UTMB, Dept. of Otolaryngology
DATE: April 7, 2004
RESIDENT PHYSICIAN: Frederick S. Rosen, MD
FACULTY PHYSICIAN: Matthew W. Ryan, MD
SERIES EDITORS: Francis B. Quinn, Jr., MD and Matthew W. Ryan, MD
"This material was prepared by resident physicians
in partial fulfillment of educational requirements established for the
Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and
Neck Surgery and was not intended for clinical use in its present form. It was
prepared for the purpose of stimulating group discussion in a conference
setting. No warranties, either express or implied, are made with respect to its
accuracy, completeness, or timeliness. The material does not necessarily
reflect the current or past opinions of members of the UTMB faculty and should
not be used for purposes of diagnosis or treatment without consulting
appropriate literature sources and informed professional opinion."
Introduction
Exophthalmos, or proptosis,
occurs when there is a discordant relationship between the soft tissue and bone
of the anterior orbit and the globe. The
adult orbit has a fixed volume of approximately 30 ml. When the soft tissue
contents of the orbit exceed this amount, exophthalmos occurs. As an example, an increase in soft tissue
volume of 5 ml (16%) will result in 4-5 mm of proptosis.
Graves disease represents the most common cause of
bilateral exophthalmos. This condition
is generally referred to as Graves orbitopathy (ophthalmopathy).
Graves orbitopathy typically
affects middle-aged women. It is 5 times
more common in women than men. Peak
incidence occurs in the 3rd and 4th decades of life, and
is 6 times more common in Caucasians.
Severe exophthalmos is more common in elderly men. In addition, there is an increased prevalence
in smokers, and a genetic predisposition has been established.
Though associated with Graves Disease, exophthalmos is
NOT necessarily associated with hyperthyroidism. 20% of patients with Graves
orbitopathy are euthyroid.
Graves orbitopathy likely arises from autoimmune,
primarily T-cell, dysfunction resulting in lymphocytic infiltration and immune
complex deposition with resultant edema and proliferation of extraocular
muscles, intraconal and extraconal fat, and the lacrimal gland. There is some deficit in T-cell function that
results in the production of antibodies that are normally suppressed.
There are both infiltrative and noninfiltrative
ocular changes in Graves. Infiltrative
changes involve mononuclear cells causing activation and proliferation of
fibroblasts resulting in the production of collagen and
glycosaminoglycans. The end result is
edema and fibrosis. Noninfiltrative
changes involve spastic retraction of eyelids, an increase in palpebral fissure
width, and sympathetic hypertonia.
Ultimately, thickening of the external ocular muscles,
orbital fat herniation, proptosis, retraction of both the upper and lower
eyelids, descent of the eyelid-cheek complex, and divergence of gaze
occur. In addition, one may see eyelid
edema, conjunctivitis, photophobia, chemosis, lagophthalmos, headache, gritty
sensation in the eye, retrobulbar pain, and tearing. Thickening of the superior rectus muscle can
result in decreased venous flow via compression of the superior ophthalmic
vein. Hypertrophy of the extraocular muscles can result in ophthalmoplegia and
thus diplopia, most frequently involving the inferior and medial rectus muscles
resulting in limitation of both upward and lateral gaze.
The natural progression of Graves orbitopathy is from
no signs or symptoms to eyelid retraction, lid lag, and edema, followed by soft
tissue signs and symptoms, followed by proptosis, followed by involvement of
extraocular movement, followed by corneal involvement, followed by visual loss
secondary to optic neuropathy. Optic
neuropathy occurs in less than 5% of Graves orbitopathy, but it is the most
common cause of vision loss in this setting; the progression is usually
insidious. This neuropathy usually
occurs in patients with proptosis, but can occur in patients without
significant proptosis. Except for cases
of rapidly progressive exophthalmos (malignant exophthalmos) the eyelids are
capable of closing sufficiently to protect the cornea. Thus, while approximately 50% of Graves
patients experience eye symptoms, only approximately 5% of cases are severe
enough to warrant intervention.
Patient Evaluation
On physical exam, hyperemia over the lateral rectus
muscle is pathognomonic of
A complete ophthalmologic exam is necessary. The amount of globe protrusion is measured
using Hertel exophthalmometry.
Radiographic imaging is an important part of the
evaluation. A CT or MRI of the orbit and
sinuses represents the standard of care.
This helps to rule out other pathologic conditions of the orbit,
especially in a case of unilateral exophthalmos. In addition, imaging will help to establish
the presence or absence of sinusitis, septal deviation, and hypoplastic
maxillary sinuses – all of which will affect the approach to treatment.
MRI measurement of T2 relaxation time can be useful
for detecting external ocular muscle edema.
Proptotic patients with an increased mean T2 relaxation time are more
likely to respond to anti-inflammatory therapy, while those without T2
relaxation time prolongation are more likely to require orbital decompression.
In Graves Disease, T3, Free T4 Index, TSH, TRH, and
TSI (a type of IgG) are all elevated.
These generally return to normal after I-131 ablation of the thyroid.
Differential Diagnosis
Pseudotumor cerebri represents the second most common cause of
bilateral exophthalmos. CT or MRI shows
generalized edema of the orbital soft tissues and occasionally the brain. However, there is no specific enlargement of
the external ocular muscles. The use of
high dose corticosteroids will generally improve the proptosis within 24 to 48
hours.
Meningioma en plaque results
in severe exophthalmos with eyelid edema.
Usually, the lower lid is affected without lid retraction.
Axial myopia is a common cause of unilateral exophthalmos. This is diagnosed by retinoscopy and A-scan
ultrasound.
Inflammatory pseudotumor
mimics a neoplasm with the sudden onset of proptosis, lid edema, pain, ophthalmoplegia,
and visual loss. This typically responds
to steroids.
Lymphoma of the orbit typically causes eccentric
proptosis. CT or MRI typically
demonstrates a mass, or masses, located near the orbital apex. Other orbital masses, generally associated
with unilateral proptosis, include metastasis, vascular anomalies,
neurofibromas, and retinoblastoma.
In addition, congenital shallowness of the orbits,
such as in Apert or Crouzon Syndromes, may be the cause of proptosis. In such cases, surgery is generally cosmetic.
Treatment
With the exception of acute and progressive Graves
orbitopathy (malignant exophthalmos), the disease is self-limited in the
majority of patients. Serial testing of
visual fields allows for early detection of malignant exophthalmos. If left untreated, progression to blindness
from either corneal exposure or optic neuropathy will result.
Medical treatment should be the first step in
addressing Graves orbitopathy. This is
typically managed by the Endocrinologist.
I-131 and levothyroxine are used to achieve euthyroid status. While exophthalmos generally improves with
correction of hyperthyroidism, this is not always the case. Surgical treatment of Graves orbitopathy is
generally delayed until both the status of the orbit and the thyroid have
stabilized for 6 months.
An exception to this rule occurs in the 1-2% of patients
who experience acute deterioration in visual fields or visual acuity secondary
to optic neuropathy. These patients may
be treated initially with prednisone 80-120 mg/day for 2 weeks. If visual dysfunction does not improve, or
prolonged use of steroids is required, then decompression of the orbit is
indicated.
Low dose radiation therapy to the orbits represents
another non-surgical option. This is NOT
appropriate in the acute or subacute setting with associated visual loss
because of the early edema associated with radiation. It is a reasonable alternative for stable
Graves orbitopathy, though results are less dramatic. Usually the treatment course requires 200 cGy
of fractionated photon radiation over 2 weeks.
With this treatment, the condition typically arrests or improves;
resolution is rare. In addition one must
be very confident that the patient will not require surgery, since orbital
decompression and fat manipulation becomes very difficult after the radiation.
Because immune dysregulation is thought to be at the
heart of Graves orbitopathy, immunomodulation would seem a logical treatment
option. Both cyclophosphamide and
cyclosporine have been tried, but long term efficacy has NOT been established.
Surgery
The goal of surgery is to enlarge the confining space
of the orbit via removal of 1 to 4 walls of the bony orbit with incision of the
periosteum to allow for prolapse of the orbital soft tissues into adjacent
spaces. Theoretically, up to 15 mm of
decompression can be achieved by removing all 4 walls (usually, surgery results
in 3-7 mm of decompression). However,
intractable strabismus and hypoglobus can result from excessive decompression.
Patients must be made aware of the risks associated
with decompression of the orbit. The
most common complication is diplopia.
Other potential complications include injury to the optic nerve or
retina from prolonged globe retraction.
Retrobulbar hematoma – a potential cause of blindness – is also a
possibility. Injury to the infraorbital
nerve and epistaxis may also occur.
Indications for orbital decompression vary depending
on time course. In the acute or subacute
phase of the disease, surgery is indicated if steroids fail to improve visual
disturbance OR if steroids are required for long-term maintenance of
vision. Functional indications for
surgery, generally present in the acute or subacute phase, include corneal
exposure with keratitis, usually in patients with significant lid retraction. More commonly, functional indications are
related to optic neuropathy. This may be
manifested by decreased visual acuity, visual field defects, abnormal visual
evoked potentials, and disk edema.
Patients with optic neuropathy are usually older, usually have LESS
proptosis, and usually have a shorter duration of eye disease. Globe prolapse anterior to the eyelids is
another early indication.
In the late phase, decompression is generally
performed for cosmesis, which is a relative indication. Again, this should occur only after orbital
findings have stabilized for approximately 6 months.
In general, the more advanced the exophthalmos, the
more extensive the surgery required to produce even a modest improvement. As a result, very few patients are satisfied
with the initial surgical procedure.
Needless to say, these patients frequently require
more than orbital decompression.
Strabismus surgery for the correction of diplopia and lid lengthening
for eye lid retraction are common adjunctive procedures. Ideally, orbital decompression is performed
first, followed by strabismus surgery and then lid lengthening.
Orbital Decompression
For each of the 4
sides of the orbital aperture a technique has been described for orbital decompression. The name of the surgeon associated with each
technique will be placed in parentheses.
SUPERIOR ORBITAL DECOMPRESSION (Naffziger)
This involves complete unroofing of the orbit via a
frontal craniotomy. The advantage of
this approach is that a very large amount of orbital bone can be removed. Major disadvantages include the need for a
craniotomy and the transmission of pulsations from the brain to the globe
postoperatively. The problem with
pulsations can be overcome by using a titanium shield to support the frontal
lobe.
This approach must be performed in conjunction with
neurosurgery. The optic nerve must be
visualized. The orbital roof is removed
from just anterior to the optic foramen anteriorly to the anterosuperior
orbital rim. Periosteum must be left
intact as bone is removed to prevent injury to the levator muscle. Once the entire superior periosteum has been
uncovered, an H-shaped incision may be made in the periosteum to allow
herniation of orbital fat into the cranial vault. Titanium mesh can then be secured with
self-tapping screws to cover the orbital roof.
The cranial flap is then replaced.
A temporary tarsorrhaphy should be considered if edema associated with
the procedure has caused an immediate worsening of proptosis. Postoperative steroids can be given for 3
days, at which time the tarsorrhaphy can be removed.
This approach is uncommon, but is most frequently used
in the setting of orbital trauma.
MEDIAL DECOMPRESSION (Sewell)
This may be approached via a coronal incision, which
should be considered for cosmesis, or, more commonly, a standard external
ethmoidectomy incision.
After incision, the medial canthal tendon is tagged
and divided. The anterior and posterior
ethmoid arteries are identified and the anterior artery is ligated with a
clip. Beginning at the lacrimal fossa, a
complete ethmoidectomy is performed. One
must take care not to injure the optic nerve.
When using a coronal incision, the medial canthal
tendon is left intact. Ethmoidectomy is
performed from above. There is a greater
risk to the lacrimal sac and insertion of the trochlea because of the need for
wider periosteal undermining for exposure.
Once ethmoidectomy has been
completed, the medial periosteum is incised (various incisions have been
described) and the orbital fat is allowed to herniate or gently teased into the
ethmoidectomy cavity. Great care must be
taken to avoid injury to the medial rectus muscle.
INFERIOR DECOMPRESSION (Hisch and
Urbanek)
This involves creation of an orbital floor blowout
fracture while sparing the infraorbital nerve.
The approach involves either a transconjunctival or a subciliary
incision plus a Caldwell-Luc maxillary antrostomy. This allows for visualization of the floor
while removing bone via the antrostomy.
The bone becomes thicker and denser as the surgeon reaches the posterior
extent of the orbit. A total of 3 cm of
bone removal from anterior to posterior is usually adequate and safe. Medially, the floor can be removed up to the
lacrimal fossa, and laterally to the zygoma.
After incision of the periorbita and decompression of
orbital fat, forced duction testing should be performed to ensure that the
extraocular muscles are not hindered.
LATERAL DECOMPRESSION (Kronlein)
This was the first technique for orbital decompression
described in the literature (Dollinger, 1911).
The approach options for this technique include a coronal incision, a
direct rim incision (or lateral extension of a subciliary incision), an
extended lateral canthotomy, or an upper lid crease incision with extension
along a laugh line over the rim. When
performed in combination with medial decompression or endoscopic decompression,
it is best performed AFTER these techniques.
The orbital contents can be gently retracted medially
and protected allowing excellent exposure.
Following incision, the periosteum over the lateral
orbital rim is exposed from the reflection of the zygomatic arch to the
zygomaticofrontal suture. An incision in
the periosteum is made along the length of the lateral rim. The periosteum is then elevated on both the
infratemporal fossa side and the orbital side of the lateral rim form 3-3.5 cm
posteriorly. The roof and floor of the
orbit are also exposed. The lateral
canthus is left intact. Leaving the
lateral rim intact, as much orbital bone as possible is removed using a cutting
burr to excavate the lateral orbital wall while the malleable protects orbital
contents. Bone is removed to the level
of the lateral periosteum, fascia of the temporalis muscle, and to the dura
superiorly until the thick bone of the skull base is encountered posteriorly (a
2.5-3.5 cm diameter circle of bone should be removed). The periorbita is then incised and the
orbital fat teased out. Alternatively,
the lateral rim can be cut and mobilized on a hinge of periosteum before bone
removal, then fixated with a microplate or wire at the conclusion of the
procedure.
Of note, CSF leak was the most common complication in
one series examining this technique (Graham).
This occurred while burring down bone of the greater sphenoid wing with
inadvertent penetration of the inner bony cortex and dura. Reportedly, these leaks were easily repaired
intraoperatively without recurrence.
COMBINED MEDIAL AND INFERIOR DECOMPRESSION (Walsh-Ogura)
Like the inferior approach mentioned above, this
involves a Caldwell-Luc/transantral approach. This was the surgical technique of choice for
orbital decompression until the 1990’s, at which time endoscopic techniques
became more popular.
ENDOSCOPIC DECOMPRESSION
Non-minimally invasive techniques are falling out of
favor as the endoscopic approach becomes more prevalent. An endoscopic approach avoids an external
incision, benefits from limited morbidity, allows for excellent access to the
optic nerve at the orbital apex when needed, and can be performed under local anesthestic.
The eyes must be included in the surgical field, and
are best protected with corneal shields.
The procedure begins with a standard uncinectomy. A very large middle meatal antrostomy is
created and the 30 degree endoscope should be used to identify the position of
the infraorbital nerve in the roof of the maxillary sinus. A total ethmoidectomy is performed, and the
sphenoid ostium is identified and enlarged.
The lamina papyracea is then
skeletonized, and the position of the anterior and posterior ethmoid arteries
is noted. Classically, the middle
turbinate is resected to improve exposure for post-operative cleaning (though
some authors retain the middle turbinate because it prevents the prolapse of
orbital fat from obstructing the sphenoid ostium). Similarly, a small piece of lamina should be
retained in the frontal recess area to prevent prolapsing fat from obstructing
the frontal sinus. A spoon curette or
Freer elevator is then used to crack the lamina papyracea in its thin
midportion and a Cottle is used to bluntly elevate bone away from the
periorbita taking care to leave the periorbita intact so fat does not herniate
into the field of view. Bone should be
removed up to the roof of the ethmoid superiorly, the face of the sphenoid
posteriorly, the maxillary line (nasolacrimal duct) anteriorly, and the
maxillary antrostomy inferiorly.
Finally, bone from the orbital floor is removed medial
to V2 with downward pressure using a spoon curette on the remaining bony rim of
the maxillary antrostomy. The bone
typically fractures along the cleavage plane of the infraorbital canal.
The periorbita is then
incised with a sickle knife starting posteriorly, keeping the blade superficial
to avoid injury to the extraocular muscles.
In fact, a method of placing a “guard” on the sickle knife using a steri-strip to leave 2-3 mm of blade tip has been
described. Multiple cuts in the
periorbita or complete removal of periorbita should be performed to allow for
herniation of orbital fat.
Gentle orbital pressure during this technique
encourages the extrusion of orbital fat.
The advantages of this technique are a lack of
external incisions and a decreased incidence of oral-antral fistula as compared
to the Walsh Ogura technique. However,
laterally, decompression of the orbital floor is limited by the infraorbital
nerve.
On average, 3.5 mm of exophthalmos can be corrected
with the endoscope alone; an average of 5.4 mm can be corrected if this is
combined with an open lateral decompression.
Postoperatively, visual acuity and extraocular
movement must be checked. Nasal packing
must be avoided to prevent compression of the optic nerve. The patient can be discharged to home in less
than 24 hours on oral antibiotics and nasal saline irrigation. Post-operative endoscopic cleaning is
performed per routine for endoscopic sinus surgery. Nose blowing should be avoided for 2 weeks
postoperatively.
Bilateral orbital decompressions, when required, can
be done at an interval of 1 week.
ORBITAL FAT REMOVAL
This represents an alternative to traditional orbital
decompressive procedures. With this procedure, the preoperative CT scan is
helpful in demonstrating the location of orbital fat pockets. These fat pockets can then be approached via
an upper lid crease and subciliary or transconjunctival incisions. The orbital septum in both upper and lower
eyelids must be opened longitudinally and the fat compartments debulked. Excellent hemostasis must be obtained with
the bipolar, and injury to the lacrimal gland in the superolateral quadrant is
best avoided. Trauma to the inferior
oblique muscle must also be avoided.
As much as 6 mm of proptosis can be corrected with
this technique, which correlates with the removal of 5 to 6 ml of fat.
This may be a more useful technique when orbital fat
involvement is the major underlying problem as opposed to extraocular muscle
involvement or optic neuropathy.
Choosing the Appropriate Technique
For mild (2-3 mm) exophthalmos, any one of the
decompression approaches may be used.
For moderate exophthalmos (3-5 mm), inferior decompression alone may be
sufficient. Alternatively, a combination
of medial and lateral decompression may be used. For severe exophthalmos (5-7 mm), 3 wall
decompression can be performed.
Again, these external approaches have been largely
supplanted by the endoscopic technique with or without lateral decompression.
After healing and stabilization, one may need
additional surgery for eyelid retraction.
Resection of Muller’s muscle may be adequate for slight upper eyelid
retraction. For greater retraction,
transection of the eyelid retractors with the insertion of cartilage or
Gore-Tex grafts to lengthen the eyelids may help.
Results and Complications
The function and cosmesis of approximately 75% of
patients stabilize or improve after surgical decompression.
A corneal abrasion is a real possibility during
orbital decompression. Most believe the
cornea is best protected using a corneal shield. However, some advocate that it is better to
leave the cornea exposed with frequent irrigation because a dilating pupil is
an important early sign of excessive traction on the globe or optic nerve. (It
is important to take frequent breaks while retracting on the globe.)
Retrobulbar hematomas are best avoided by achieving excellent
hemostasis with bipolar cautery and placement of a Penrose drain. If it occurs, it is considered an
emergency. The skin incision should be
opened, the hematoma evacuated, the orbit irrigated, bipolar cautery used for
hemostasis, and a drain placed.
Temporary neuropraxia of the
infraorbital nerve is common, and may be difficult to avoid in inferior
decompression.
Retinal hemorrhage is a rare complication, and almost
always seems to occur in diabetic patients.
This complication necessitates ophthalmologic consultation.
Orbital cellulitis is also
rare. It may be a good idea to treat
those patients with purulent rhinorrhea or other evidence of sinusitis with
prophylactic antibiotics preoperatively.
Retinal vascular occlusion (heralded by pain in the
eye and/or decreased vision), corneal ulcer, and retrobulbar hematoma represent
the 3 major eye emergencies that may occur as a complication of decompressive
surgery. At least the first 2
necessitate prompt ophthalmologic consultation.
Furthermore, the patient should be instructed at discharge to seek
immediate care for increased pain in the eye or decreased vision.
Diplopia
As many as 50% of patients experience some degree of
diplopia postoperatively. In fact, some
authors contend that virtually all patients undergoing orbital decompression
will experience some degree of diplopia at some time during their postoperative
course. Preoperative diplopia is often worsened by decompression. Many patients will experience spontaneous
resolution of their diplopia once inflammation subsides. Other patients may have diplopia present only
on peripheral gaze and do not require any further treatment. But, if significant diplopia is still present
6 to 8 months after decompression, then correction must be performed by
ophthalmology. Several modifications
have been proposed to avoid diplopia.
One is complete removal of the inferior periorbita
when performing inferior decompression.
This is thought to prevent fibrosis of the periorbita to the inferior
rectus.
Another is orbital lipectomy rather than orbital
decompression. Small series have shown
that lipectomy alone is unlikely to worsen diplopia, and likely to make it
better.
Preservation of a bony orbital strut in the lamina
papyracea, though technically difficult, has for several years been thought to
play an important role in diplopia prevention.
Decompression confined to the lateral wall rarely
causes diplopia.
A “balanced” decompression involving both the medial
and lateral orbit is also far less likely to result in diplopia. Along those lines, avoidance of any
involvement of the orbital floor is far less likely to result in diplopia.
More recently, Metson has
described the orbital sling technique during endoscopic orbital
decompression. In this technique, 2
horizontal incisions are made in the medial periorbita that approximate the
superior and inferior margins of the medial rectus muscle. These incisions sit approximately 10 mm apart
beginning just anterior to the face of the sphenoid and extending all the way
to the maxillary line. The remaining
periorbita above and below the above mentioned incisions can then be removed to
allow for prolapse of orbital fat. Thus,
a medial sling of periorbita is left in place to protect the medial rectus
muscle. Forced duction with lateral
rotation of the globe can be used intraoperatively to confirm the location of
the medial rectus before the periorbital incisions are made. In Metson’s series,
no patients who underwent the orbital sling technique experienced worsened
diplopia. Those patients who had a
lateral decompression in addition to the orbital sling were even more likely to
experience improvement in diplopia postoperatively.
Another more recently described option is orbital rim
advancement, which involves the use of onlay grafts to the bony orbit, rather
than decompression of orbital contents, to change the globe-rim
relationship. Goldberg reported a series
in which onlay grafts (porous polyethylene) were used either in isolation or in
combination with orbital decompression.
The onlay is typically placed via an inferior transconjunctival approach
with suspension of the suborbital orbicularis oculi fat (SOOF) from the implant
(a SOOF lift). Using this onlay
technique, proptosis decreased an average of 4.65 mm. This technique is most useful in fibrotic,
“woody” orbits or when the bony orbits are shallow (e.g., congenitally
hypoplastic maxilla).
Conclusion
The most common cause of bilateral exophthalmos is
Preoperative imaging is vital and should include both
the orbits and the sinuses.
The current surgical treatment of choice is endoscopic
orbital decompression or lateral decompression or both. Every effort should be made to protect the
inferior and medial rectus muscles and to minimize the extent of postoperative
diplopia, which remains common following orbital decompression.
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McCann JD. Treatment of Prominent Eyes with Orbital Rim Onlay Implants:
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Dale H. Rice, Steven D. Schaefer edd. Lippincott Williams & Wilkins. C. 2002. pp. 319-324.
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