Phẫu Thuật Tai Mũi Họng Và Phẫu Thuật Đầu Cổ

936
Section 9
Plastic and Reconstructive Surgery
examination has proved otherwise. All Le Fort fractures
also cause some measure of malocclusion.
Application of signifi cant force to the upper
midface area can lead to telescoping nasal fractures and
naso-orbito-ethmoidal fractures. The hallmark of these
injuries is traumatic telecanthus, with the normal inter-
canthal distance being about 35 mm or less. Fracture
lines generally travel posteriorly through the medial
orbital walls. The most urgent issues with these frac-
tures involve possible leakage of cerebrospinal fl uid
with associated meningitis and trauma to the brain, as
well as the possibility of involvement of the optic canals
posteriorly. Careful consideration must be given to the
urgent need for decompression. When repairing these
fractures, it will also be necessary to re-establish the
normal anatomic relationships of the medial canthi.
These injuries are discussed further in Chapter 93.
ZMC fractures involve force directed posteriorly
over the malar eminence or zygomatic arch. They were
formerly referred to as “tripod” fractures, but this term
is not entirely accurate because this bone articulates in
fi ve places, even though two of the fi ve generally do not
require fi xation during reduction. The characteristic
facial deformity of a displaced ZMC fracture is fl atten-
ing of the malar eminence, with or without apparent
enophthalmos, and diffi culty opening the mouth
completely.
The remaining fractures involving the orbit are
referred to as blowout fractures. They were fi rst
described by Smith and Regan in 19571 after observing
Frontal bone
Supraorbital
foramen
Zygomaticotemporal
foramen
Zygomatic bone
Zygomaticofacial
foramen
Maxillary bone
Ethmoid bone
Lacrimal bone
Nasal bone
Infraorbital
foramen
Figure
94-1. Orbital
bones,
frontal view. (From Dutton JJ: Atlas of
Clinical and Surgical Orbital Anatomy.
Philadelphia, WB Saunders, 1994.)
Superior oblique
tendon
Levator palpebrae
superioris muscle
Superior rectus
tendon
Lateral rectus
tendon
Inferior rectus
tendon
Trochlea
Medial rectus
tendon
Figure 94-2. Extraocular muscles,
frontal composite view. (From Dutton
JJ: Atlas of Clinical and Surgical Orbital
Anatomy. Philadelphia, WB Saunders,
1994.)

Chapter 94
Fractures of the Orbit
937
a patient who had been hit in the periorbital area by a
hurling ball. With a Waters view on plain fi lms, the
characteristic opacifi cation of the maxillary sinus was
observed, and the patient complained of diplopia. Sur-
gical exploration via a Caldwell-Luc approach allowed
visualization of the inferiorly displaced orbital fl oor
(maxillary sinus roof) and prolapse of the orbital con-
tents. Repair was undertaken by packing of the maxil-
lary sinus to elevate its roof, and further cadaver
experiments were carried out by the authors.
A classifi cation of orbital fractures was described
in 1967 and consisted of separating the fractures
into “pure” blowout and “impure” blowout fractures.2
Impure blowout fractures referred to those associated
with other orbital rim fractures, mainly those men-
tioned earlier and the occasional unclassifi able rim frac-
ture with a fl oor component. The term was expanded
to include fractures of the orbital roof unassociated
with frontal sinus fractures, which occur almost exclu-
sively in children. The defi nition of a blowout fracture
has come to mean an orbital fl oor, medial wall, or roof
fracture not associated with a rim fracture.
The hydraulic theory suggests that the orbital con-
tents are deformable and that a blow to the soft tissues
causes rapid expansion beyond what the elastic modulus
of the surrounding bone can tolerate. Thus, the weakest
areas of the orbital structures fracture outward, often
lacerating the periorbita and intraorbital tissues, and
allow prolapse into the adjacent sinus. Younger patients
merit special consideration because they often suffer
greenstick-type orbital wall fractures, during which the
orbital contents can herniate and become trapped by
rapid recoil of the partially fractured orbital wall (so-
called trapdoor fractures). A second explanation, the
“buckling” theory, instead explains fracture of the
orbital walls by the application of a load to the thick
orbital rim, which deforms somewhat and causes
the orbital wall posterior to it to bend.3 As the tougher
orbital rim returns to its original position, the thin and
brittle bones of the associated wall have less elasticity
and consequently break. It is likely that some combina-
tion of these mechanisms explains most blowout
fractures.
Determination of Need for Repair
The initial symptoms of the patient will provide the fi rst
clue to the need for and timing of repair. Many patients
with ZMC fractures complain of pain or numbness in
the cheek (or both) and notice deformity of their
cheek. The deformity may be obscured in the early
stages by edema. If the zygomatic arch is involved, the
patient may have symptoms of pain with attempted
opening of the mouth. Because this fracture only rarely
causes signifi cant orbital injury or airway compromise,
the approach to repair is most often elective and based
on the amount of cosmetic deformity or the presence
of symptomatic bony fragments in the temporoman-
dibular joint space. Earlier repair is preferable to obviate
the need for osteotomy. If the fragments are nondis-
placed and stable, surgery is unnecessary.
Patients with blowout fractures of the fl oor may
have the classic triad of enophthalmos, hypoesthesia of
the cheek, and a defi cit of upgaze. Hypoesthesia of the
cheek is common to most patients with blowout frac-
tures of the fl oor because the fracture occurs medial to
the infraorbital canal and often involves it. Young
patients with signifi cant defi ciency of upgaze, particu-
larly if accompanied by nausea and vomiting,4 require
careful evaluation to determine whether a trapped infe-
rior rectus muscle is present. These so-called white-eyed
blowout fractures are the most critical, and repair
should proceed within 24 hours if possible.
Clues to muscle entrapment include age of the
patient, small fracture size, severe pain on attempted
duction, severe limitation of upgaze, and nausea and
vomiting (Figs. 94-3 to 94-5). Traction on the inferior
rectus is thought to activate the oculocardiac refl ex
(bradycardia, hypotension, and vomiting) and could
theoretically be fatal. In addition, the muscle is com-
pressed and quickly becomes ischemic, thereby rapidly
Figure 94-3. Patient 1: 16-year-old with a blowout fracture of the
left orbit.
Figure 94-4. Patient 1: attempted upgaze.

938
Section 9
Plastic and Reconstructive Surgery
leading to irreversible scarring and permanent double
vision.5
Decisions regarding the suitability and timing of
repair of other blowout fractures may be undertaken
with less urgency. Factors affecting such decisions
include the size of the fracture, injury to other adjacent
structures, associated symptoms, and characteristics of
the particular patient.
Symptoms associated with blowout fractures most
commonly include pain, hypoesthesia of the cheek, di -
plopia, and enophthalmos. The former two nearly
always resolve without intervention, and thus only dip-
lopia and enophthalmos remain as possible indications
for repair. Putterman and colleagues6 showed that the
natural history of most uncomplicated blowout frac-
tures (i.e., those without entrapped muscle) is resolu-
tion of the diplopia over a period of days to weeks. Early
enophthalmos (immediate or within the fi rst week)
bodes poorly for cosmetic outcome because this sign
generally portends a large and displaced fracture. With
the advent of CT scanning and more precise measure-
ment of the size and location of these injuries, it became
possible to predict which patients will suffer long-term
consequences, including cosmetic deformity and per-
manent double vision.
It is generally accepted that fractures involving
more than 50% of the orbital fl oor are likely to cause
later enophthalmos. Displaced fractures with an area of
2 cm2 or greater are most signifi cant: approximately
1 cm2 produces about 1 mm of enophthalmos,7 and at
a 2-mm or greater difference in projection of the globes,
an aesthetic defect is noticed. The area of the medial
wall fractured must be accounted for when making this
rough calculation; although the medial wall is repaired
less frequently, it contributes to later enophthalmos
(Figs. 94-6 to 94-8).
The risk of diplopia after repair of a blowout frac-
ture is diffi cult to quantify without a randomized, con-
trolled prospective trial. A small retrospective trial of 54
patients who underwent surgical repair found that
approximately a third of the patients continued to have
diplopia more than 6 months after repair.8 However,
approximately two thirds of these patients had com-
bined fl oor and medial wall fractures, thus making the
risk greater than after fl oor fracture alone, for which it
is about 10% to 12%.
In considering the general health of the patient, it
is best to frankly discuss with the patient that the repair
to be undertaken is for aesthetic reconstruction and
occasionally to prevent double vision, not to treat
abnormal cheek sensation or pain. Nor, in most
instances, is it necessary to undergo surgery to prevent
double vision from persisting. Thus, a patient in her 80s
in a nursing home would be a less likely candidate for
Figure 94-5. Coronal scan of a trapdoor fracture of the left eye;
note the “hanging drop” sign and small, nondisplaced fracture.
Figure 94-6. Patient 2: 4 1/2 months after fracture of the orbital
fl oor and medial wall. Diplopia and 6 mm of enophthalmos are
evident in the right eye.
Figure 94-7. Patient 2: 4 1/2 months after a blowout fracture.

Chapter 94
Fractures of the Orbit
939
intervention than a 22-year-old student with a similar-
appearing fracture.
PREOPERATIVE EVALUATION
Evaluation of Orbital Contents
The most complete evaluation of a patient with an
orbital fracture occurs when the otolaryngologist and
ophthalmologist work together to manage the case.
Ensuring the integrity of the eye is of utmost impor-
tance. Open globe injuries, particularly in the case of
penetrating trauma, are occasionally seen in association
with orbital fractures. A high index of suspicion must
be maintained in patients with decreased vision, obvious
globe deformity, opacifi cation of areas of the cornea,
an irregularly shaped pupil, and areas of hemorrhagic
conjunctival chemosis. Although subconjunctival hem-
orrhage is common in the setting of any orbital frac-
ture, chemosis (signifi cant edema of the conjunctiva)
associated with hemorrhage is quite worrisome for
occult rupture. In such instances, structural integrity of
the eye must be established fi rst, with repair of any sig-
nifi cant orbital fracture undertaken with caution at a
much later time. A retrospective study of open globe
injuries recently found 26% to be associated with orbital
or adnexal trauma (or both), and conversely, a review
of orbital injuries found approximately the same pro-
portion with signifi cant injury to the globe.9,10
The second instance in which orbital fracture repair
ought not be undertaken immediately is in patients
with traumatic optic neuropathy. The sine qua non of
this injury is a relative afferent pupillary defect, except
in those with bilateral neuropathy. A relative afferent
pupillary defect (Marcus Gunn pupil) is observed by
noting a difference in the reactivity of one pupil versus
the other by transferring a bright light rapidly from one
eye to the other. It is important that the patient not
focus on the examiner during the examination because
this will cause constriction of both pupils and render
the examination more diffi cult. The patient should be
asked to focus on a distant object such as a light switch.
The patient will usually note that the light is brighter
in the unaffected eye than in the affected one. Several
caveats attend this examination: a decrease in reactivity
of a pupil can also be caused by third nerve injury,
accompanied by ptosis of the upper eyelid and defi cit
of upgaze, downgaze, and adduction, or by direct pupil-
lary trauma, in which case hyphema will often be
present.
If the patient is thought to have traumatic optic
neuropathy, consideration should be given to surgical
decompression of the optic nerve, particularly when
bony fragments are obviously present in the canal or
posterior orbit on CT scan. Associated fi ndings are
frontal sinus fractures, blood in the posterior ethmoid
air cells and sphenoid sinus, and sphenoid sinus frac-
tures. No established treatment of traumatic optic neu-
ropathy exists. The International Optic Nerve Trauma
Study attempted to determine whether observation,
treatment with corticosteroids, or surgical intervention
made any difference in outcome for patients with indi-
rect (i.e., nonpenetrating) trauma to the optic nerve.11
The trial was changed to an observational one because
of low enrollment, and no clear benefi t was found for
either treatment.
Small case series have suggested that unroofi ng the
bony canal may be of benefi t. Complicating factors in
these reports have been a lack of standardization of
timing or technique of surgery, lack of defi nition of
visual “improvement,” and poor understanding of the
natural history of the disease (a signifi cant number of
patients will improve without treatment). In any case,
repair of orbital fracture in this setting is fraught with
uncertainty and could presumably make the situation
worse.
The third contraindication to early exploration of
orbital fractures is the presence of hyphema (bleeding
into the anterior chamber of the eye). Hyphema is
often visible grossly as a red layer between the cornea
and iris, but more subtle cases may go undetected
without slit-lamp examination. The highest chance of
rebleeding in these patients occurs during the fi rst 5
days after injury, during which the patient must remain
at bed rest and keep the eye shielded. Any further
trauma to the eye (e.g., retraction of the orbital con-
tents during surgery) is to be strictly avoided. If the
hyphema is small and resolves entirely within the 5-day
period, it is probably safe to proceed with repair of the
fracture the following week. If the hyphema is large and
remains unresolved, it is most prudent to defer surgery
on the orbit until a later date.
Examination of ocular motility is easily done by
asking the patient to move the eyes to all extremes of
gaze. Edema of muscle or periorbita or patient discom-
Figure 94-8. Blowout fracture of the fl oor and medial wall of the
orbit.

940
Section 9
Plastic and Reconstructive Surgery
fort is a very common cause of limitation of duction, so
in instances in which there is doubt about the nature
of the limitation, forced ductions should be performed.
This is done by instilling anesthetic drops into the eye
and then holding a cotton-tipped applicator soaked in
these drops over the conjunctiva at the 6-o’clock posi-
tion for at least 90 seconds. Toothed forceps can then
be used to fi rmly grasp the conjunctiva and underlying
connective tissue and rotate the eye in each direction.
Resistance to forced movement suggests either entrap-
ment of tissues in a fracture site or decreased compli-
ance of the extraocular muscle (e.g., by hematoma).
If possible, a dilated fundus examination should be
performed to rule out or document any intraocular
hemorrhage or retinal pathology before exploration of
the fracture.
Associated Soft Tissue Injuries
Any associated soft tissue injuries should be noted at
the time of initial examination. This will guide repair
of any lid or lacrimal injury, and a preexisting lacera-
tion can often be used for good surgical access. If the
repairs are to be performed at the same surgery, the
fractures should be repaired before any eyelid repair to
avoid undoing the reconstruction already performed.
However, during exploration and repair, the tissue
must be kept hydrated and treated as gently as possible
to avoid further damage. A laceration, no matter how
small, between the lacrimal punctum and medial
canthus usually means avulsion of the canalicular system
and should be repaired within 72 hours with a silicon
stent. Most injuries, excluding dog bites and motor
vehicle collisions with sharp laceration, leave the bulk
of the periorbital tissue intact. The blood supply in this
area is excellent, so every attempt should be made to
complete the original repair with the available tissue.
Extreme caution should be exercised during any
attempt at débridement of apparently devitalized soft
tissue in the area. A laceration at the orbital rim is par-
ticularly helpful to the surgeon because it provides
direct access to the ZMC and orbital fl oor.
Imaging
CT scanning with fi ne cuts through the orbit and direct
coronal projections if possible is the best study for eval-
uation of orbital fractures. Most modern coronal recon-
structions are more than adequate for evaluation of the
size of the fracture and the orbital contents. Intrave-
nous contrast material is not necessary, and magnetic
resonance imaging of the orbits is of little use in the
evaluation of bony injury.
When evaluating an orbital fracture, attention must
be paid to the size of the fracture. Tiny trapdoor frac-
tures may be missed on an initial look by radiology, so
if clinically suspected, scrutiny of the fi lm for the posi-
tion and size of the inferior rectus and surrounding
tissue is important. The rough area of the fracture may
be calculated by measuring its width and length on the
scan while keeping in mind that a fracture approxi-
mately 1 cm2 will produce about 1 mm of enophthal-
mos. The normal aesthetics of the orbit allow up to a
2-mm difference in the projection of the eyes.
Access to the scans during surgery, if at all possible,
can be extremely helpful in orientation within the
orbit.
SURGICAL APPROACHES
Zygomaticomaxillary Complex Fractures
By combining the approaches described later with a
buccal sulcus incision, most ZMC fractures can be
reduced and plated. If the arch is involved and dis-
placed medially, a Gillies maneuver may suffi ce for
repair. If, however, the arch is badly comminuted and
displaced outward, it is likely that a coronal incision
will be required. This is described in more detail in
Chapter 93.
When reduction plus fi xation of the zygomatic and
maxillary bones has been accomplished, it is necessary
to examine the state of the orbital fl oor. Most often,
repair of the fl oor will also be required lest a large
defect be left and place the patient at risk for a subop-
timal cosmetic result.
Blowout Fractures of the Orbital Floor
Surgical access for repair of blowout fractures depends
on the patient’s associated injuries. If a laceration is
present along the inferior orbital rim, it is acceptable
to expose the fracture site by way of this laceration.
Most frequently, however, there is no associated lacera-
tion, and blowout fractures of the fl oor should be
approached via a transconjunctival incision. Subciliary,
mideyelid, and rim incisions all provide good exposure
but leave the patient with a risk of eyelid malposition
because of scarring within the delicate lamellae of the
lower eyelid. A transconjunctival incision as described
here is rapid and provides wide access to the fl oor and
very little risk of entropion or ectropion (Fig. 94-9).
This incision can also be combined with a lateral can-
thotomy for access to the zygomaticofrontal suture and
lateral wall and with a transcaruncular incision for
access to the medial wall.
The patient is placed under general anesthesia for
the surgery. An antibiotic such as cephalexin and a
steroid such as dexamethasone should be administered
intravenously during surgery. The opposite eye usually
need not be left exposed in the surgical fi eld unless late
repair of enophthalmos is being performed and com-
parison of projection is necessary.
Before placement of a lubricated corneal protective
lens, forced ductions should be performed with toothed
forceps and any limitation noted (Fig. 94-10). Although
the goal of the surgery is to improve any limitation of
duction, at the end of surgery the excursion of the eye
must be at least as good as at the beginning.
An assistant uses a Desmarres or similar retractor
to refl ect the lower eyelid down anterior to the rim, and
a malleable retractor is used to hold the orbital contents
back, with both retractors compressing the tissue some-
what over the rim (Fig. 94-11). A Colorado needle–

Chapter 94
Fractures of the Orbit
941
medially, care should be taken to stay anterior to the
origin of the inferior oblique muscle and avoid the lac-
rimal system.
A Cottle or similar small sharpened periosteal ele-
vator is then used to cut the periosteum of the rim and
lift the periorbita in one continuous layer back to the
fracture site (Fig. 94-13). The medial shelf of the frac-
ture, the lateral shelf, and later, the posterior shelf must
all be accessible and free of periosteum for proper
implant placement. As the fracture site is exposed,
gentle elevation of the orbital contents from the maxil-
lary sinus should proceed in a hand-over-hand manner
by using the elevator and malleable retractor (Fig.
94-14). The maxillary sinus may be débrided of bone
fragments and clot. Care is taken to disturb the infra-
orbital neurovascular bundle as little as possible. A
small orbital branch of the infraorbital vessels may be
encountered and should be divided with cautery.
When all orbital tissue has been freed and brought
superiorly, the posterior limit of the fracture should be
located. This is done by bringing the elevator around
from the medial or lateral fi xed bone or, in some cases,
by drawing the elevator superiorly along the posterior
wall of the sinus until the upper aspect is reached.
Figure 94-9. Inferior conjunctival fornix 3 weeks after repair of a
blowout fracture via a transconjunctival approach.
Figure 94-10. Forced duction.
tipped Bovie or similar insulated electrocautery device
is used to palpate the rim of the orbit and then cut
down directly on it. This will place the incision roughly
in the inferior conjunctival fornix, well below the lower
extent of the tarsus and well away from the globe (Fig.
94-12). If it is necessary to carry the incision fairly far
Figure 94-11. Retraction of the lower eyelid and orbital contents.
Figure 94-12. Transconjunctival incision with a Colorado needle.

942
Section 9
Plastic and Reconstructive Surgery
At intervals of several minutes during the surgery,
it is wise to withdraw the retractors from the orbit and
allow the tissues to reperfuse.
A suitable implant is now cut to size, dipped in
antibiotic solution, and placed in the orbit to support
the tissue (Fig. 94-15). It is critical that the implant rest
fi rmly on the posterior edge of the fi xed bone around
the fracture or the fracture will remain incompletely
reduced. A small unrepaired area at the anterior exten-
sion of the fracture is acceptable if necessary. When the
implant is properly placed, it will remain in position
when the retractors are gently removed. It must be
placed several millimeters posterior to the rim or it will
be palpable postoperatively. Inspection of the tissue
surrounding the implant ensures that no orbital con-
tents are trapped beneath the plate, and forced duc-
tions are again performed to confi rm the absence of
trapping.
A small pilot hole is drilled in the anteromedial
corner of the implant, and the plate is fi xed with a tita-
nium microscrew (Fig. 94-16). It is not necessary that
the screw be perpendicular to the implant because it is
not providing structural support (placement of the
Figure 94-13. Anterior extent of the fracture with herniation of
orbital fat into the sinus.
Figure 94-14. Exposure of the fl oor fracture.
implant fi rmly on the medial, lateral, and posterior
shelves ensures support), but it does prevent rotation
or migration of the material. If insuffi cient bone is
present medially, the plate may be fi xed with hardware
placed laterally, but great care must be taken to not
place the screw through the infraorbital canal. Usually,
one point of fi xation is suffi cient.
A Penrose or similar drain may be placed in the
wound to emerge at its lateral extreme. The drain is
placed superior to the implant and sutured to the lid
with a 5-0 nylon loose drain stitch. The end is cut to
approximately 5 mm beyond the lid margin. A 5-0 nylon
modifi ed Frost stitch is then placed through the skin
and orbicularis in the center of the lid just inferior to
the lashes. It is taped to the brow under tension and
serves to extend the conjunctival edges and obviate the
need for closure of the wound (Fig. 94-17). The stitch
Figure 94-15. Measurement of a nylon implant.
Figure 94-16. Fixation of the nylon implant with a titanium
screw.

Chapter 94
Fractures of the Orbit
943
and drain are removed the following morning before
the patient is discharged home. Before closure of the
lid, ophthalmic antibiotic-steroid ointment is placed on
the eye. A light absorbent dressing is placed so that
perception of light may be checked by the nursing staff
through the patch.
Blowout Fractures of the Medial Wall
of the Orbit
Repair of medial blowout fractures is similar in princi-
ple, but the incision used is either a Lynch incision or
a conjunctival incision placed between the plica semi-
lunaris and the caruncle.12 A Desmarres retractor is
used to retract the caruncle medially, and a Colorado
needle again makes the incision through the conjunc-
tiva, with the eye protected by a narrow malleable
retractor and corneal shield. Tissue is then gently
divided with blunt Stevens scissors in a posteromedial
direction to avoid the lacrimal system. The periosteum
is again incised and elevated posteriorly to expose the
fracture site. It is likely that at least the anterior and,
possibly, the posterior ethmoid arteries will require
cautery and division. If the posterior ethmoid artery is
reached, dissection must proceed with great care
because the optic foramen will be found 3 to 8 mm
posterior to this artery. Frequently, a less robust allograft
is needed, such as 0.4-mm nylon. Caution is required
to avoid driving the fi xation screw above the frontoeth-
moidal suture.
The incisions may be joined to provide wide expo-
sure of the fl oor and medial wall.
Fractures of the Roof of the Orbit
Fractures of the roof of the orbit associated with intra-
cranial injury may be approached via a coronal incision
to provide wide access for examination and repair of
possible dural injury. Other fractures without intracra-
nial involvement may be exposed endoscopically by way
of the frontal sinus. The bony fragment may be reduced
and, if necessary, fi xated. If associated outer table frac-
tures are to be repaired, they may then be plated
through the same sub-brow incision while taking care
to preserve the supraorbital neurovascular bundle.
Most commonly, however, roof fractures that need to
be repaired require neurosurgical consultation and a
combined approach.
Choice of Implant Material
In the current era, alloplastic materials have advanced
enough that surgeons can often avoid the use of
autografts, thereby precluding donor site morbidity
and resorption. Titanium mesh has been a common
choice for reconstruction of the orbit because it is
readily shaped and cut. However, tissue adheres strongly
to this mesh, thus making it less desirable in such
situations.
A variety of plastic materials have been designed for
reconstructive use. Silicon is an older implant that
causes no adhesions but is quite soft. Porous polyethy-
lene is a popular choice for fl oor and medial wall frac-
tures and is particularly useful when barrier coated on
the side facing the orbit. It is available in numerous sizes
and shapes and is easily shaped with scissors or scalpel.
Although no fi xation is theoretically required, the peri-
osteum over the implant must be closed with inter-
rupted sutures.
Our group uses nylon foil implants. This material
is easily shaped, has some memory, and rarely becomes
infected. The 0.6-mm thickness is malleable enough to
bend for insertion but stiff enough to support the
orbital contents. A 0.4-mm thickness is useful for repair
of medial wall fractures, where less strength is necessary
and the ability to temporarily deform the plate is desir-
able. No tissue adhesion occurs, and because the
implant is fi xed to bone, closure of periosteum is
unnecessary.
A relatively new alloplastic material has also been
found to be well suited to repair of these fractures: a
titanium mesh–reinforced thin porous polyethylene
sheet. It has the advantages of tissue ingrowth and
excellent memory with easy intraoperative shaping, and
the barrier coating on the side placed toward the orbit
prevents adherence of tissue.
POSTOPERATIVE MANAGEMENT
Our group admits patients overnight for observation
and pain control after fracture repair. If orbital hemor-
rhage occurs, the most serious complication of the
surgery, it will be noted quickly and may be drained as
soon as possible. Placement of a drain and lack of con-
junctival closure are intended to help prevent buildup
of signifi cant orbital pressure in the event of bleeding,
but occasionally, opening of the wound, evacuation of
hematoma, and possibly removal of hardware may be
necessary. Oral narcotic/acetaminophen combinations
generally suffi ce for control of pain. The patient rests
with the head of the bed elevated and is instructed to
not bend below the waist, lift greater than 5 lb, or strain
for 3 days. Nose blowing is not allowed for the following
Figure 94-17. Postoperative view of a patient with a drain and trac-
tion stitch in place.

944
Section 9
Plastic and Reconstructive Surgery
4 weeks. Nausea is treated with an antiemetic because
vomiting might cause a severe increase in orbital pres-
sure. An antibiotic such as cephalexin and a steroid are
administered intravenously while in the hospital. Anti-
biotics are taken orally for 7 days postoperatively to
prevent infection of the allograft, along with rapidly
tapering doses of oral steroid.
The patient is seen in the offi ce 1 week and 1
month postoperatively and as needed after that. In the
event of entrapped muscle, it is wise to prepare the
patient and family for the probable subsequent tempo-
rary paresis of the involved muscle and to reassure them
that when the patch is removed, the abnormal eye posi-
tion is expected and almost certainly temporary (Figs.
94-18 to 94-21).
Figure 94-18. Trapdoor fracture of the left eye 24 hours after
repair.
Figure 94-19. Upgaze.
Figure 94-20. Patient 2, 1 week postoperatively—the diplopia has
resolved.
Figure 94-21. Patient 2, 1 week postoperatively.
PEARLS
• Documentation of the condition of the eye before
and after surgery is critical.
• Young patients with small fl oor fractures,
particularly when experiencing severe pain or
nausea, must be suspected of having an entrapped
inferior rectus muscle.
• Muscle entrapment does not occur in large
fractures, but muscle herniation (not an emergency)
does.
• Floor implants should be placed far enough
posterior to the orbital rim that they are not
palpable.
• Approximately 1 cm2 of fracture will allow the eye to
move posteriorly about 1 mm.

Chapter 94
Fractures of the Orbit
945
4. Bansagi ZC, Meyer DR: Internal orbital fractures in the pediatric
age group: Characterization and management. Ophthalmology
107:829-836, 2000.
5. Smith B, Lisman RD, Simonton J, et al: Volkmann’s contracture
of the extraocular muscles following blowout fracture. Plast
Reconstr Surg 74:200-216, 1984.
6. Putterman AM, Stevens T, Urist MJ: Nonsurgical management of
blow-out fractures of the orbital fl oor. Am J Ophthalmol 77:232-
239, 1974.
7. Fan X, Li J, Zhu J, et al: Computer-assisted orbital volume mea-
surement in the surgical correction of late enophthalmos caused
by blowout fractures. Ophthal Plast Reconstr Surg 19:207-211,
2003.
8. Biesman BS, Hornblass A, Lisman R, et al: Diplopia after surgical
repair of orbital fl oor fractures. Ophthal Plast Reconstr Surg
12:9-16, discussion 17, 1996.
9. Hatton MP, Thakker MM, Ray S: Orbital and adnexal trauma
associated with open-globe injuries. Ophthal Plast Reconstr Surg
18:458-461, 2002.
10. Ioannides C, Treffers W, Rutten M, et al: Ocular injuries associ-
ated with fractures involving the orbit. J Craniomaxillofac Surg
16:157-159, 1988.
11. Levin LA, Beck RW, Joseph MP, et al: The treatment of traumatic
optic neuropathy: The International Optic Nerve Trauma Study.
Ophthalmology 106:1268-1277, 1999.
12. Graham SM, Thomas RD, Carter KD, et al: The transcaruncular
approach to the medial orbital wall. Laryngoscope 112:986-989,
2002.
PITFALLS
• Failure of the implant to rest on the posterior shelf
of bone may cause continued enophthalmos.
• Manipulation of the orbit in the presence of
signifi cant globe injury or traumatic optic
neuropathy must be avoided.
• Failure to check and document that forced ductions
at the conclusion of the procedure are as free as or
better than those at the beginning may allow orbital
tissue trapped under the implant to go unnoticed.
References
1. Smith B, Regan WF Jr: Blow-out fracture of the orbit; mechanism
and correction of internal orbital fracture. Am J Ophthalmol
44:733-739, 1957.
2. Converse JM, Smith B, Obear MF, et al: Orbital blowout fractures:
A ten-year survey. Plast Reconstr Surg 39:20-36, 1967.
3. Fujino T, Makino K: Entrapment mechanism and ocular injury
in orbital blowout fracture. Plast Reconstr Surg 65:571-576,
1980.

section 10
Orbital Surgery
Chapter 95
Orbital Decompression
S. Tonya Stefko and Carl H. Snyderman
Decompression of the orbit may be considered for the
treatment of space-occupying lesions causing compro-
mise of function as a result of expansion of the orbital
contents or a decrease in the rigid orbital confi nes. The
volume of the orbit averages about 30 mL, and only
anteriorly is it not bound by bone. By far the most
common indication for decompression is Graves orbi-
topathy, but similar surgical techniques are applied to
infectious, traumatic, neoplastic, and iatrogenic compli-
cations (e.g., orbital hematoma after sinus surgery)
(Figs. 95-1 and 95-2).
The incidence of Graves disease in the general
population is about 1% to 3%. Females are affected
about fi ve times as often as men, but older men who
experience orbitopathy often have a more fulminant
course. About a third of patients with Graves disease will
have orbitopathy, often asymmetrical and usually mild
or moderate. Approximately 85% of patients evaluated
primarily for orbitopathy will be found to have a dysthy-
roid state. In adults, Graves disease is the most common
cause of unilateral and bilateral proptosis. The fi rst
report of decompression for this condition occurred in
1911.1
The pathogenesis of Graves orbitopathy remains
only partially understood. Serum levels of antibodies to
the thyroid-stimulating hormone (TSH) receptor and
collagen XIII seem to correlate with orbital disease
activity.2 TSH receptors are found on orbital fi broblasts,
which may differentiate into adipocytes, and are more
sensitive to TSH receptor antibodies than dermal fi bro-
cytes are. The proptosis is due to an increase in retro-
bulbar glycosaminoglycan deposition and edema, as
well as to a later increase in retrobulbar fat. Smoking is
thought to affect this either by creating increased
oxygen-reactive species or by causing local tissue
hypoxia, both of which lead to increased chemokines
recruiting T cells from the bloodstream. TH2 cells are
the predominant type involved in the orbital disease.3
The acute phase of the disease, which consists of
orbital congestion, infl ammatory cell infi ltrate, and
forward movement of the globe, generally lasts between
6 and 24 months. After this phase, the disease is char-
acterized pathologically by increased fi brosis of the
tissues. A second acute phase may occasionally affect
the patient later in life. Asymmetrical involvement of
the orbits is frequent.
The only external factor proved to affect Graves
orbitopathy is cigarette smoking. Current smoking out-
weighs previous smoking as a predictor of disease sever-
ity. Patients in whom orbital disease develops are four
times as likely to smoke, and discontinuation of smoking
appears to lessen the severity, as well as protect patients
from the development of further symptoms.4 Pretibial
myxedema, acropachy, and female sex are also associ-
ated with more severe orbital disease.5
Symptoms of Graves orbitopathy include eyelid
retraction, proptosis, diplopia, dryness of the eyes, a
sensation of pressure behind one or both eyes, and
947

948
Section 10
Orbital Surgery
swelling of the lids and conjunctiva (chemosis). Signs
consists of eyelid retraction more than 1 mm from the
limbus, eyelid lag on downward gaze (failure of the
upper eyelid to descend properly when the patient
looks down), unilateral or bilateral proptosis, restric-
tion of extraocular movements (particularly upward
gaze and abduction), hyperemia over the insertions of
the horizontal rectus muscles, and corneal staining with
fl uorescein observed with a cobalt fi lter (Figs. 95-3 and
95-4).
The course of the orbital disease and the course of
any associated thyroid disease in Graves disease are
independent. Euthyroid patients may have severe orbi-
topathy causing optic neuropathy or corneal perfora-
tion, whereas severely hyperthyroid patients may have
no signs or symptoms. Treating the thyroid abnormali-
ties is essential to the patient’s general health, but it is
unlikely to help the eye disease. Exceptions are removal
of a large goiter, which may lessen the orbital symp-
toms, and treatment with radioactive iodine, which
sometimes acutely worsens the condition of the orbits
(ameliorated by concurrent treatment with oral
steroid).6
Orbital decompression is sometimes undertaken
for other causes of proptosis: infection with abscess,
tumor, trauma to the optic nerve, or hematoma (such
as might occur after endoscopic sinus surgery). Absces-
ses located along the lamina papyracea in the orbit or
medially along the roof or fl oor are most amenable to
endoscopic drainage. In the setting of head trauma and
a new optic neuropathy, traumatic optic neuropathy is
assumed. If the optic canal is fractured, the fragments
may be removed endoscopically, but authors disagree
about the benefi ts of this procedure.7-9 Occasionally, an
orbital apex tumor causing compressive optic neuropa-
thy may be successfully treated by decompression when
resection of the tumor is inadvisable.10
ANATOMY
The orbit is bounded by four walls: superior, medial,
inferior, and lateral. The medial wall of the orbit extends
Figure 95-1. Patient with Graves orbitopathy preoperatively.
Figure 95-2. Patient with Graves orbitopathy 6 days after balanced
decompression of both eyes.
Figure 95-3. Patient with Graves orbitopathy, optic neuropathy in
the right eye, visual acuity of 20/50 in the right eye, and Ishihara
color vision of 1.5 of 11 plates. Note the apical crowding.
Figure 95-4. Coronal view of the patient from Figure 95-3.

Chapter 95
Orbital Decompression
949
from the ethmoidal roof superiorly to its junction with
the inferior wall inferiorly. Posteriorly, it is continuous
with the medial surface of the optic canal. Anteriorly,
it is bounded by the thicker bone of the lacrimal fossa
and ascending process of the maxilla. The inferior wall
of the orbit is thicker than the medial wall and is divided
by the infraorbital neurovascular bundle. The bulge of
the canal is often visible, and the vessels can be visual-
ized through the thinned bone. The lateral wall of the
orbit is bounded laterally by the temporalis muscle
(Figs. 95-5 and 95-6).
PATIENT SELECTION
By the time that a patient with Graves disease has
reached the otolaryngologist for consultation, the
patient will most likely have been evaluated by an oph-
thalmologist. A frank conversation between the two
physicians will establish the urgency with which surgery
should proceed: a patient with severe exposure keratitis
may require decompression within the week, whereas
another patient with inactive disease and strictly cos-
metic concerns may be scheduled when convenient for
Frontal bone
Supraorbital
foramen
Zygomaticotemporal
foramen
Zygomatic bone
Zygomaticofacial
foramen
Maxillary bone
Ethmoid bone
Lacrimal bone
Nasal bone
Infraorbital
foramen
Figure
95-5. Orbital
bones,
frontal view. (From Dutton JJ: Atlas of
Clinical and Surgical Orbital Anatomy.
Philadelphia, WB Saunders, 1994.)
Superior oblique
tendon
Levator palpebrae
superioris muscle
Superior rectus
tendon
Lateral rectus
tendon
Inferior rectus
tendon
Trochlea
Medial rectus
tendon
Figure 95-6. Extraocular muscles,
frontal composite view. (From Dutton
JJ: Atlas of Clinical and Surgical Orbital
Anatomy. Philadelphia, WB Saunders,
1994.)

950
Section 10
Orbital Surgery
surgeon and patient. If the patient has not undergone
a complete ophthalmologic examination, including
evaluation of optic nerve function, extraocular move-
ment, and ocular surface, one must be conducted
before planning surgery. Documentation of preopera-
tive visual function is critical.
Occasionally, other disease processes will necessi-
tate surgical decompression of the orbits, including
infection, tumor, hemorrhage, and trauma. Usually,
these cases will develop more rapidly than dysthyroid
orbitopathy, and the decision regarding timing and the
approach for surgery will be more urgent. Surgical
approaches are the same; however, each of these cases
will have its attendant challenges. In all these situations,
the anatomy will be obscured and great care must be
taken to avoid harm to vital structures that the surgeon
seeks to protect.
In the case of an orbital abscess causing proptosis,
particularly in children younger than 9 years, it is often
prudent to wait 24 to 48 hours for a response to intra-
venous antibiotics. In adults, particularly when the
abscess is associated with concurrent sinus disease, the
decision to proceed with endoscopic drainage of the
cavity (when located medially) or external drainage
(when located superiorly or laterally) should be made
earlier (Fig. 95-7). In the case of optic neuropathy,
surgery should proceed as soon as safely possible.
Orbital hematoma, whether traumatic, iatrogenic,
or rarely, spontaneous, should also be approached with
urgency. If optic neuropathy is present and lateral can-
thotomy/cantholysis has failed, decompression of the
orbit is necessary. Endoscopic decompression of the
medial wall is particularly helpful because a fairly pos-
terior decompression of the optic nerve is possible.
Frequently in cases of trauma with fracture of the
orbit, the orbit will have decompressed itself. In some
instances, however, bone fragments may impinge on
orbital structures and require urgent removal or reduc-
tion. This occurs again in the presence of optic neu-
ropathy or with an intractable increase in intraocular
pressure (Fig. 95-8).
In cases of Graves orbitopathy, communication
between the ophthalmologist, otolaryngologist, and
patient will determine how best to serve the patient.
Patients may be divided into two groups: those who
require urgent surgery during an active phase of disease
and those who seek cosmetic and functional improve-
ment later in the course of the disease. Whenever pos-
sible, it is best to defer patients from the fi rst group into
the second. If the patient has active orbitopathy char-
acterized by infl ammatory signs and evolution and can
be treated by nonsurgical means, this should be pursued
fi rst. Temporization may often be accomplished with
the use of oral (1 mg/kg/day) or intravenous pulse
prednisone or by radiation treatment of the orbits (up
to 2000 cGy, below the threshold for causing optic neu-
ropathy). Retinopathy rarely occurs late after radiation
treatment, but nearly always in diabetic patients, and
cataract formation appears only as frequently as it does
when patients are treated with steroids.11 Surgery is
both more technically challenging and more likely to
be complicated by excessive bleeding in the setting of
active infl ammation. However, some patients will
require immediate surgery, particularly when an
impending corneal perforation or severe optic neurop-
athy is present.
Patients who have passed the active stage and
entered the cicatricial phase are good candidates for
decompression, either for improvement in appearance
or for maximization of residual function. Endoscopic
decompression of the medial wall combined with
removal of the medial fl oor and lateral wall offers the
most signifi cant decrease in proptosis, up to 6 to 10 mm.
The degree of improvement depends partly on the
increase in volume, but also on the rigidity of the tissues
(periorbital tissues that are more densely fi brotic relax
poorly into the newly created space). Decompression of
Figure 95-7. Twelve-year-old patient with a superior subperiosteal
orbital abscess that improved after endoscopic ethmoidectomy and
percutaneous drainage of the abscess.
Figure 95-8. Patient with bone fragments in the optic canal and
right optic neuropathy after closed head injury.

Chapter 95
Orbital Decompression
951
the orbital roof is seldom performed. Unilateral or
bilateral orbital decompression may be performed at
the same time.
PREOPERATIVE EVALUATION
All patients undergoing orbital decompression require
a comprehensive preoperative ophthalmologic exami-
nation. A computed tomography (CT) scan of the orbit
is helpful to identify any anatomic abnormalities before
surgery.
It is helpful for the otolaryngologist to see the
patient preoperatively to obtain a history of sinonasal
problems and evaluate the anatomy of the nasal cavity.
The CT scan should be reviewed to assess for occult
disease and anatomic variations that may pose prob-
lems: low cribriform plate, Onodi cells, Haller cells, or
nonpneumatization of sinuses. Active sinusitis should
be treated and completely resolved before proceeding
with elective orbital decompression. Severe deviations
of the nasal septum can interfere with surgical access
and may need to be corrected at the same time. Coex-
istent sinus problems such as chronic sinus obstruction
or nasal polyposis can also be addressed. Informed
consent includes the usual discussion of risks from
endoscopic sinus surgery: visual loss, diplopia, cerebro-
spinal fl uid (CSF) leak, hemorrhage, sinusitis, loss of
olfaction, and intranasal synechiae.
PREOPERATIVE PLANNING
Preoperative counseling is particularly important so
that the patient understands that this procedure, when
performed for Graves disease, is likely to be the fi rst in
a series of surgeries. New-onset or worsened postopera-
tive diplopia will occur in about a third of patients
undergoing decompression of three walls,12 but it has
been observed in retrospective series that a “balanced
decompression” consisting of only the medial and
lateral walls is associated with only about a 10% inci-
dence of new-onset diplopia.13 Strabismus surgery may
be performed for unresolved diplopia, and eyelid
surgery (either correction of retraction or blepharo-
plasty) may be required after that.
SURGICAL APPROACHES
Over the years a number of different operations have
been described for decompression of the orbit, which
may include anywhere from one to four walls. The
amount of decompression that can be achieved increases
with the number of walls removed. Removal of the supe-
rior wall is not usually performed because of its minimal
additional benefi t and the added morbidity. The medial
wall may be decompressed from an external ethmoid-
ectomy approach, a transantral approach, or a transna-
sal approach. The inferior wall may be decompressed
from a transconjunctival approach, a transantral
approach, or a transnasal approach. With the advent of
endoscopic sinus surgery techniques, most surgeons
prefer a transnasal endoscopic approach for decom-
pression of the medial and inferior orbital walls.
Removal of bone lateral to the infraorbital nerve pro-
vides minimal additional decompression and risks
injury to the infraorbital nerve. The lateral orbital wall
is decompressed from an external approach.
Medial Wall
The nose is decongested with pledgets soaked in 0.5%
oxymetazoline. If a septoplasty is necessary for access, it
is performed fi rst. The inferior aspect of the middle
turbinate is resected to provide greater access and room
for the orbital tissues to expand. The uncinate process
is removed and the antrostomy is maximally enlarged
posteriorly and superiorly. The bulla ethmoidalis is
opened for removal of ethmoid air cells in an anterior-
to-posterior direction. The sphenoid sinus is opened
and the sphenoidotomy is maximally enlarged with Ker-
rison rongeurs. Residual septations are then removed
in a posterior-to-anterior direction along the skull base.
The nasofrontal recess is exposed, but further dissec-
tion of the frontal sinus is unnecessary.
The medial wall of the orbit is palpated and the
thin bone of the lamina papyracea is fractured anteri-
orly. Bone fragments are carefully elevated from the
underlying periorbita with a Cottle elevator or ball-
tipped probe. Removal of bone continues posteriorly to
the anterior face of the sphenoid sinus. Superiorly,
bone is removed to within 2 mm of the skull base while
being careful to not fracture the skull base. Removal of
bone continues inferiorly to the junction of the medial
and inferior orbital walls. Examination of the maxillary
sinus with an angled endoscope usually reveals the neu-
rovascular bundle of the infraorbital nerve running
across the roof of the maxilla. The fl oor of the orbit is
then removed with angled Kerrison rongeurs to the
medial aspect of the neurovascular bundle. Removal of
additional bone does not contribute to decompression
and risks injury to the nerve.
If the decompression is being done for proptosis,
decompression of the orbital apex beyond the anterior
wall of the sphenoid sinus is not necessary.14 If the
patient is undergoing decompression for visual loss,
additional bone is removed posteriorly. Landmarks
within the sphenoid sinus are fi rst identifi ed: the carotid
canal, optic canal, and optic-carotid recess.15 The bone
is carefully thinned with a diamond drill over the optic
canal until it can be fractured and elevated with a small
elevator. Drilling of bone should be along the axis of
the optic canal to avoid injury to the carotid artery.
A sickle blade is then used to incise the periorbita
of the medial orbit, starting posteriorly and superiorly
and proceeding anteriorly. Multiple parallel incisions
are made from the ethmoid roof to the fl oor of the
orbit. The medial rectus muscle is often infi ltrated and
enlarged and is susceptible to injury if the incisions are
too deep. Intervening strands of periorbita are tran-
sected to allow complete herniation of the orbital con-
tents. Gentle external pressure on the orbit with the
hand facilitates herniation of orbital fat into the ethmoid
defect (see Video 95-1).

952
Section 10
Orbital Surgery
Silastic nasal splints are placed to prevent intranasal
synechiae. Nasal packing is not used.
Lateral Wall
The lateral wall of the orbit is approached via a lateral
canthotomy incision. The incision created is approxi-
mately 2 cm in length and extends posteriorly from the
lateral canthal angle in a crow’s foot crease. Stevens or
similar scissors are used to cut the lateral canthal liga-
ment and deepen the incision to bone. Bleeding is
controlled with electrocautery. The periosteum is
incised vertically along the apex of the rim with a scalpel
or needle-tipped electrocautery. A Cottle elevator is
then used to clear the periosteum from the lateral
orbital wall while keeping the periorbita intact as much
as possible. The periosteum must be elevated from both
the interior and exterior surfaces of the lateral wall of
the orbit. The bone should be identifi ed as far superi-
orly as the fossa of the lacrimal sac and inferiorly to just
above the level of the zygomatic arch. Careful elevation
along the exterior surface proceeds in a posterior direc-
tion and then turns medially in the temporal fossa.
Once the periosteum has been elevated from the
bone, a wide ribbon retractor is inserted between the
periorbita and bone by an assistant. A Desmarres vein
retractor is placed over the cut surface of the skin. An
oscillating bone saw is used to cut through the lateral
wall, perpendicular to the bone. Frequent pauses to
assess position and adequacy of protection of the orbital
contents are essential. It is only necessary to make an
osteotomy posteriorly through the vertical zygomatico-
frontal buttress. A parallel osteotomy is made inferiorly
above the zygomatic arch, again through the triangular
thick bone of the rim.
A rongeur is now used to grasp the vertical strut,
which is rocked medially and laterally until the bone
breaks free posteriorly. It will be necessary to elevate
the remainder of the temporalis muscle from the pos-
terolateral surface of the bone with electrocautery.
Bone wax is applied as needed, and any remaining
small fragments of bone are removed with the same
instrument. The sharp surfaces of the remaining zygo-
matic and frontal bones are smoothed with a burr or
rongeur.
A short-bladed knife, such as a sickle knife, is now
applied to the periorbita in a very superfi cial manner,
directed posteriorly to anteriorly, to slit the fi brous
septa and allow the orbital contents to prolapse into the
temporal fossa. Care is taken to place no traction on
the orbital fat and to remain superfi cial so that the lac-
rimal gland and lateral rectus muscle are not damaged.
Bipolar cautery is used to obtain hemostasis.
Careful closure of the wound is accomplished by
precise realignment of the upper and lower gray lines
of the eyelid with a single horizontal stitch of 6-0 absorb-
able material, such as polyglactin, buried laterally. The
deep tissues are reapproximated with inverted 6-0
suture and the skin closed carefully with running 7-0
nylon or interrupted chromic gut suture. Before com-
plete closure, a longitudinal strip of 0.25-inch Penrose
drain is placed into the wound to emerge between
suture bites. A patch is placed loosely over the eye to
absorb drainage. The patient is admitted for observa-
tion overnight, both for pain control and to monitor
for any hemorrhage (Figs. 95-9 and 95-10).
POSTOPERATIVE CARE
Patients are administered a steroid pulse intravenously
while undergoing surgery and observation (8 to 12 mg
of dexamethasone during the procedure, and 4 to 8 mg
every 8 hours thereafter while in the hospital). A rapid
taper of oral steroid medication is adequate for most
patients; those decompressed in an acute setting require
a much more aggressive regimen and longer taper.
Figure 95-9. Postoperative axial view of the patient from Figure
95-3 with right optic neuropathy secondary to Graves orbitopathy.
One week after balanced decompression, visual acuity in the right eye
was 20/25 and Ishihara color vision was normal (17/18 plates). Note
the herniation of the enlarged medial rectus into the bony defect.
Figure 95-10. Postoperative coronal view of the patient from
Figure 95-3. Note the bony defects with herniation of the orbital
contents.

Chapter 95
Orbital Decompression
953
Patients are instructed to not blow their nose for 1
month after the procedure, and a steroid/antibiotic
ointment is applied to the sutures twice a day for a week.
Nonabsorbable sutures are removed in 5 to 7 days.
Intranasal splints are removed at 1 week, and a saline
spray is used as necessary to minimize crusting. Muco-
salization of the orbital tissues is usually complete by 2
months. Patients are counseled to expect some initial
diplopia and that the fi nal appearance is often not
reached for at least 3 months.
Patients are observed for at least 6 months after
surgery before consideration of extraocular muscle or
eyelid surgery.
COMPLICATIONS
The risks associated with endoscopic medial and infe-
rior orbital decompression are similar to those after
any endoscopic sinus surgery. Excessive or aggressive
removal of bone superiorly can fracture the skull base
and cause a CSF leak. Injury to the ethmoidal arteries
can occur and result in a retro-orbital hematoma. Pos-
teriorly, the optic nerve and carotid artery are at risk
for injury. The medial rectus muscle is often enlarged
and is susceptible to injury when the periorbita is
incised. Postoperatively, the exposed orbital fat is at
greater risk for infection, but this is a rare occurrence.
Positive pressure ventilation after extubation or nose
blowing by the patient postoperatively can force air into
the orbital tissues and result in subcutaneous emphy-
sema. Injury to the infraorbital nerve can lead to loss of
sensation of the midface.
The lateral rectus muscle is susceptible to injury
during decompression of the lateral orbital wall. Ecchy-
mosis of the periorbital tissues is common but may be
associated with a hematoma.
As discussed previously, unbalanced decompres-
sion of the orbit can result in signifi cant diplopia. The
diplopia is often transient but may require corrective
surgery if it persists beyond 6 months.
SUMMARY
Decompression of the orbit is considered for the treat-
ment of Graves ophthalmopathy and other mass lesions
of the orbit (abscess, hematoma, and neoplasm).
Maximal decompression can be achieved with endo-
scopic decompression of the medial and inferior orbital
walls and external decompression of the lateral wall.
Balanced decompression minimizes the risk for postop-
erative diplopia.
References
1. Dollinger J: Die Druckenlastung der Augenhöhle durch Entfer-
nung der äusseren Orbitalwand bei hochgradigem Exophthal-
mus (Morbus basedowii) und konsekutive Hornhauterkrankung.
Dtsch Med Wochenschr 37:1888-1890, 1911.
2. El-Kaissi S, Frauman AG, Wall JR: Thyroid-associated ophthal-
mopathy: A practical guide to classifi cation, natural history and
management. Intern Med J 34:482-491, 2004.
3. Ludgate M, Baker G: Unlocking the immunological mechanisms
of orbital infl ammation in thyroid eye disease. Clin Exp Immunol
127:193-198, 2002.
4. Cawood T, Moriarty P, O’Shea D: Recent developments in thyroid
eye disease. BMJ 329:385-390, 2004.
5. Fatourechi V, Bartley GB, Eghbali-Fatourechi GZ, et al: Graves
dermopathy and acropachy are markers of severe Graves ophthal-
mopathy. Thyroid 13:1141-1144, 2003.
6. Bartalena L, Marcocci C, Bogazzi F, et al: Relation between
therapy for hyperthyroidism and the course of Graves ophthal-
mopathy. N Engl J Med 338:73-78, 1998.
7. Goldenberg-Cohen N, Miller NR, Repka MX: Traumatic optic
neuropathy in children and adolescents. J AAPOS 8:20-27,
2004.
8. Kountakis SE, Maillard AA, El-Harazi SM, et al: Endoscopic optic
nerve decompression for traumatic blindness. Otolaryngol Head
Neck Surg 123:34-37, 2000.
9. Levin LA, Beck RW, Joseph MP, et al: The treatment of traumatic
optic neuropathy: The International Optic Nerve Trauma Study.
Ophthalmology 106:1268-1277, 1999.
• In patients with compressive optic neuropathy, it is
vital to perform posterior medial wall
decompression to relieve pressure on the optic nerve
in the orbital apex.
• When decompressing the optic canal, the optic
nerve sheath should be opened cautiously in the
superonasal quadrant to minimize the risk of injury
to the ophthalmic artery.
• Any removal of intraconal fat must be done with a
minimum of traction and from the inferotemporal
quadrant (between the lateral and inferior rectus
muscles) to decrease the risk of retrobulbar
hematoma and injury to orbital structures.
PITFALLS
• The medial and lateral rectus muscles are often
enlarged and just deep to the periorbita and may be
injured by aggressive sharp dissection.
• Bony decompression without adequate division of
the periorbital septa is ineffective.
• Aggressive endoscopic removal of bone superiorly
may be associated with fractures of the skull base
and CSF leak.
• Unrecognized injury to the ethmoid arteries may
cause retro-orbital hematoma, a risk that is
increased when the patient coughs or struggles when
emerging from anesthesia.
• Monopolar cautery should be avoided near the apex
of the orbit.
PEARLS
• Balanced decompression (medial and lateral orbital
walls) minimizes the likelihood of postoperative
diplopia.
• Careful realignment of the lateral commissure of the
eyelids is necessary for an optimal cosmetic result.

954
Section 10
Orbital Surgery
10. Kloek CE, Bilyk JR, Pribitkin EA, Rubin PA: Orbital decompres-
sion as an alternative management strategy for patients with
benign tumors located at the orbital apex. Ophthalmology
113:1214-1219, 2006.
11. Wakelkamp IM, Tan H, Saeed P, et al: Orbital irradiation for
Graves ophthalmopathy: Is it safe? A long-term follow-up study.
Ophthalmology 111:1557-1562, 2004.
12. Russo V, Querques G, Primavera V, Delle Noci N: Incidence and
treatment of diplopia after three-wall orbital decompression in
Graves ophthalmopathy. J Pediatr Ophthalmol Strabismus 41:219-
225, 2004.
13. Graham SM, Brown CL, Carter KD, et al: Medial and lateral
orbital wall surgery for balanced decompression in thyroid eye
disease. Laryngoscope 113:1206-1209, 2003.
14. Snyderman C, Hobson S: Endoscopic orbital decompression.
In Myers E (ed): Operative Otolaryngology. Philadelphia, WB
Saunders, 1997, pp 796-806.
15. Snyderman C, Hobson S: Endoscopic orbital decompression for
endocrine ophthalmopathy. In Myers E, Bluestone C, Brackmann
D, Krause C (eds): Advances in Otolaryngology–Head and Neck
Surgery. St Louis, CV Mosby, 1996, pp 205-215.

Chapter 96
Optic Nerve Decompression
Allan D. Vescan, Ricardo L. Carrau, Carl H. Snyderman, and Amin B. Kassam
Optic nerve injury with loss of vision is a devastating
event.1-10 Optic nerve injury can be classifi ed in various
ways, including but not limited to the anatomic region
and pathophysiologic mechanisms. Anatomic classifi ca-
tion includes intraorbital, intracanalicular, and intra-
cranial sites of injury. Pathophysiologic classifi cation
includes traumatic and nontraumatic mechanisms of
injury. Traumatic optic nerve injury can be further sub-
classifi ed as either direct or indirect injury. Direct injury
includes penetrating injury to the orbit or optic nerve
canal as a result of a foreign body or fracture of the
lesser wing of the sphenoid. Indirect injury is generally
the result of blunt head trauma. The exact mechanism
of injury is not well understood, however, but may
include hematoma, neural edema, and disruption of
the microvascular circulation and axonal transport.
Nontraumatic causes of optic nerve injury include com-
pressive effects from benign or malignant tumors,
infl ammatory conditions such as Graves’ disease, and
fi bro-osseous lesions. The most effective treatment of
traumatic optic neuropathy (TON) remains controver-
sial. Options for treatment include observation, intrave-
nous corticosteroids, and surgical decompression. In
1999 the International Optic Nerve Trauma Study
(IONTS) attempted to answer the question of which
therapeutic modality was most effi cacious in treating
indirect TON. It attempted to randomize patients to
“megadose” steroids alone or in conjunction with extra-
cranial optic nerve decompression. Because of patient
recruitment factors, however, this was abandoned and
the investigators proceeded to a comparative nonran-
domized interventional study with concurrent treat-
ment groups. They concluded that there was no clear
benefi t of corticosteroid therapy over optic canal
decompression and that treatment should be tailored
to the individual patient. Subsequent to IONTS, several
retrospective series have been published that both
support and refute the use of optic nerve decompres-
sion in addition to corticosteroid use for the treatment
of indirect optic neuropathy.
Despite the controversy regarding TON, optic nerve
decompression to alleviate compressive effects is widely
accepted. Its technique, indications, and complications
are the focus of this chapter, although the concepts
apply to most situations.
PATIENT SELECTION
Patient selection is dictated by the cause of the visual
loss.6,11-14 In the scenario of TON, a diagnosis must fi rst
be secured. The diagnosis of TON is a clinical diagnosis
supported by a history of direct or indirect injury to the
head or face. The level of consciousness of the patient
can make the situation fairly straightforward or make it
a challenge. Features of TON include an afferent pupil-
lary defect, monocular or binocular involvement,
impairment of color vision, visual fi eld defects, loss of
visual acuity (ranging from mild to no light percep-
tion), and delayed development of optic atrophy in the
weeks after the injury. In the setting of compressive
optic neuropathy secondary to benign or malignant
tumors, chronic infl ammatory processes, or fi bro-osseus
lesions, many of the same features will be present;
however, their onset will be much more insidious, and
careful and detailed ophthalmologic assessment will be
required to quantify the visual deterioration. Once
compressive neuropathy is ascertained, the underlying
pathology and degree of compression will dictate the
need for surgical decompression.
PREOPERATIVE PLANNING
Before embarking on endoscopic decompression of the
optic nerve, imaging studies of the paranasal sinuses
and skull base are critical (Figs. 96-1 to 96-4). Under-
standing the close relationship of the optic nerve to the
paracavernous internal carotid artery is fundamental
before proceeding to surgery (Figs. 96-5 and 96-6). In
the setting of benign tumors and fi bro-osseus lesions
leading to compressive neuropathy, the sphenoid sinus
955

956
Section 10
Orbital Surgery
Figure 96-1. Axial computed tomography scan demonstrating a
fracture of the right optic nerve canal (arrow) in a patient involved in
a motor vehicle accident.
Figure 96-2. Coronal computed tomography scan demonstrating
severe fi brous dysplasia with bilateral compression of the optic nerves
(arrows).
Figure 96-3. Axial magnetic resonance image demonstrating peri-
neural extension of adenoid cystic carcinoma (arrow) along the left
optic nerve.
Figure 96-4. Axial magnetic resonance image demonstrating a
recurrent meningioma (arrow) compressing the optic nerve within its
canal and intracranially.

Chapter 96
Optic Nerve Decompression
957
Figs. 96-3 and 96-4) can be added and fused with the
CT scan to give further assistance in preoperative plan-
ning and navigation. Thorough ophthalmologic assess-
ment, including all the issues mentioned in the previous
section, is a prerequisite.
INDICATIONS
There are numerous indications for optic nerve decom-
pression, including but not limited to optic neuropathy
secondary to a compressive effect from either benign
or malignant tumors, infl ammatory processes such as
Graves’ disease, or fi bro-osseous lesions such as fi brous
dysplasia. Direct or indirect TON that has not responded
to conservative or medical management is likewise an
indication.
SURGICAL TECHNIQUE
The patient is positioned supine on the operating table
and an orotracheal airway is secured. We insert cotto-
noids soaked in 0.05% oxymetazoline as a topical
decongestant. Image guidance or intraoperative naviga-
tion systems are useful, if not critical for the surgery. If
an optical tracking navigation system is available, we fi x
the head in a slight turn toward the surgeon’s side with
a three-pin head holder. We then obtain appropriate
image guidance registration via surface fi ducial markers
(placed before imaging), a light-emitting diode–based
face mask, or a laser surface registration device. For
electromagnetic navigation systems, the helmet is placed
and a straight probe is used for registration. Once this
has been completed, the middle turbinate, lateral nasal
wall, and posterior nasal septum are then sequentially
infi ltrated, in a posterior-to-anterior direction, with
0.5% lidocaine (Xylocaine) with 1:100,000 epineph-
rine. Resection of the right middle turbinate may be
necessary, albeit rarely, to improve visualization and
widen the space for instrumentation. In addition, out-
fracturing of the inferior turbinates widens the nasal
corridor.
We use a 0-degree rod-lens endoscope to provide
visualization throughout most of the procedure and
reserve the use of an angled endoscope for visualization
of the superior ethmoid sinuses or skull base. An unci-
nectomy is completed with back-biting rongeurs and a
straight-blade microdébrider. Its superior aspect is
spared because the frontonasal recess does not need to
be exposed. We then complete anterior and posterior
ethmoidectomies with a microdébrider or Tru-cut ron-
geurs (Fig. 96-7). This exposes the skull base (fovea
ethmoidalis) and lamina papyracea. In patients who
suffer trauma to the optic canal and orbit, the surgeon
should be attentive to the possibility of exposed perior-
bita or orbital fat, or both. Via a transmeatal approach
we remove the inferior aspect of the superior turbinate.
The superior turbinate forms the medial aspect of the
posterior ethmoids, and removal of it exposes the
natural ostium of the sphenoid sinus. The ostium is
enlarged in an inferior and medial direction until the
endoscope can be inserted inside the sphenoid sinus
Frontal sinus
Ethmoid sinuses
Optic-carotid
recess
Sphenoid sinus
Optic nerve canal
Optic-carotid
recess
Internal carotid
artery canal
Figure 96-5. Diagrammatic representation in an axial plane dem-
onstrating the lateral-to-medial direction of the optic nerve as it is
followed in an anteroposterior direction and the relationship of the
optic canal and internal carotid artery.
Figure 96-6. Digitally enhanced (highlighted structures) endo-
scopic view of the right sphenoid demonstrating the relationship of
the optic nerve canal and the internal carotid artery. In this patient,
pneumatization of the optic strut resulted in a deep optic carotid
recess. Pneumatization of the anterior clinoid forms the recess supe-
rior to the optic canal.
and nasal anatomy may be distorted and almost impos-
sible to predict (see Fig. 96-2). Image guidance becomes
a valuable tool to assist the endoscopic surgeon in safely
approaching the optic nerve and skull base. We prefer
a fi ne-cut computed tomography (CT) scan of the
sinuses and skull base with contrast enhancement
before proceeding to optic nerve decompression. In
situations in which there may be a soft tissue mass
causing compression, magnetic resonance imaging (see

958
Section 10
Orbital Surgery
for close visual inspection. Herniation of intracranial
structures or an exposed internal carotid artery may be
associated with trauma to the skull base. After these
possibilities are discarded, the rest of the rostrum of the
sphenoid is removed with up- and down-biting 2-mm
Kerrison rongeurs. The rostrum must be removed until
the roof and lateral wall of the sphenoid sinus are in
plane with the roof of the posterior ethmoid sinuses
and the lamina papyracea, respectively. Inferiorly, the
posterolateral septal artery runs 1 cm above the poste-
rior choana, and it is best to avoid injury to it. It can
easily be controlled with bipolar or suction electrocau-
tery. Use of suction electrocautery posterior to the
rostrum or over the lamina papyracea is best avoided.
Next, the posterior aspect of the lamina papyracea is
removed to expose the periorbita covering the orbital
apex (Fig. 96-8). Any injury to the periorbita will result
in herniation of orbital fat, thereby impeding visualiza-
tion. Cauterizing the fat with bipolar electrocautery may
control limited herniation of this fat. The position of
the optic nerve is at the top of the orbital apex, and it
follows a lateral-to-medial and caudal-to-cephalad direc-
tion. The posterior ethmoidal artery is 4 to 6 mm ante-
rior to the nerve.
If the foramen and optic canal are fractured, they
can often be removed with a small Cottle elevator or 1-
to 2-mm bone curette to displace the fractured frag-
ments medially. Otherwise, the medial aspect of the
foramen and canal has to be thinned with a 3-mm burr
mounted on a high-speed drill (Fig. 96-9). It is critical
to provide continuous irrigation to avoid thermal injury
to the nerve or ophthalmic artery. The canal is decom-
pressed back to the optic carotid recess because this
marks the optic strut and the point where the nerve is
intradural (Figs. 96-10 and 96-11). The decompression
Frontal sinus
Ethmoid sinuses
Optic-carotid
recess
Sphenoid sinus
Figure 96-7. Diagrammatic representation in an axial plane dem-
onstrating complete ethmoidectomy and sphenoidotomy to expose
the lamina papyracea and skull base.
Lamina papyracea
Optic foramen
Optic canal
Frontal sinus
Ethmoid sinuses
Optic-carotid
recess
Sphenoid sinus
Figure 96-8. Diagrammatic representation in an axial plane dem-
onstrating removal of the posterior aspect of the lamina papyracea.
The periorbita is preserved to avoid herniation of orbital fat.
Frontal sinus
Ethmoid sinuses
Optic-carotid
recess
Sphenoid sinus
Intact periorbita
Optic foramen
Optic canal
Figure 96-9. Diagrammatic representation in an axial plane dem-
onstrating drilling of the optic foramen (pterygoid process).
should include the medial 120 degrees. More extensive
decompression may be achieved if the optic strut (below
the nerve) and anterior clinoid (above the nerve) are
pneumatized (see Fig. 96-6). The optic nerve sheath is
not opened because this does not contribute to the

Chapter 96
Optic Nerve Decompression
959
decompression. Furthermore, opening the sheath may
cause leakage of cerebrospinal fl uid (CSF) by opening
the meningeal sleeve that often accompanies the optic
nerve extracranially.
Subsequent to the decompression, copious irriga-
tion is performed and Silastic splints are sutured to the
nasal septum to prevent synechia formation. A small
amount of packing can be used if hemostasis is an issue;
however, one must be cautious because of the exposed
optic nerve.
POSTOPERATIVE MANAGEMENT
Typically, patients are kept in the hospital overnight
after optic nerve decompression. We routinely admin-
ister systemic steroids before, during, and after endo-
scopic decompression. Nasal saline sprays are started
before discharge home. We routinely use silicone splints
to prevent the formation of synechiae between the nasal
septum and turbinate. Generally, they remain in place
for 10 to 14 days. Nasal débridement is usually carried
out biweekly for the fi rst few postoperative visits, fol-
lowed by monthly intervals. We recommend switching
to a nasal saline douche after the fi rst week to assist in
remucosalization. We do not perform routine postop-
erative imaging after optic nerve decompression.
Patients are monitored with serial visual examinations
postoperatively, in addition to formal visual fi eld testing
in the fi rst 24 hours.
COMPLICATIONS
Cerebrospinal Fluid Leak
In a patient with postoperative rhinorrhea, testing of
the fl uid for β2-transferrin or β-trace protein is prudent
to confi rm a CSF leak. Accumulation of irrigation fl uid
in the sinonasal tract, with subsequent drainage, can
mimic a CSF leak in the immediate postoperative
period.15,16
A postoperative CSF leak is best managed by imme-
diate re-exploration and surgical repair.
Postoperative Sinonasal Bleeding
Signifi cant postoperative nasal bleeding most com-
monly arises from a branch of the internal maxillary or
anterior ethmoidal arteries, which are amenable to
endoscopic control. Angiography with embolization is
reserved for patients who are not surgical candidates.
Care must be taken with this complication because
blind nasal packing in the setting of a dehiscent, decom-
pressed optic nerve may lead to a decrease in vision.
Subcutaneous Emphysema
Because of a dehiscence in the medial orbital wall and
optic canal, vigorous nose blowing or sneezing can
result in signifi cant subcutaneous air collection and
facial swelling. Patients should be forewarned about
appropriate nasal precautions. Observation and poten-
tial use of antibiotics if any signs of infection are present
are all that is required.
Visual Deterioration
Vision can worsen after optic nerve decompression.
Such deterioration can be related to heat injury to
the optic nerve as a result of inadequate irrigation
during thinning of the optic canal or a vascular
Frontal sinus
Ethmoid sinuses
Optic-carotid
recess
Sphenoid sinus
Intact periorbita
Optic foramen
Optic canal
Internal carotid artery
Figure 96-10. Diagrammatic representation in an axial plane dem-
onstrating complete decompression of the optic canal.
Optic nerve
Internal carotid artery
Figure 96-11. Digitally enhanced (highlighted structures) endo-
scopic view of a decompressed left optic nerve.

960
Section 10
Orbital Surgery
References
1. Kountakis SE, Maillard AA, El-Harazi SM, et al: Endoscopic optic
nerve decompression for traumatic blindness. Otolaryngol Head
Neck Surg 123:34-37, 2000.
2. Cook MW, Levin LA, Joseph MP, et al: Traumatic optic neuropa-
thy: A meta-analysis. Arch Otolaryngol Head Neck Surg 122:389-
392, 1996.
3. Levin LA: Mechanisms of optic neuropathy. Curr Opin Ophthal-
mol 8:9-15, 1997.
4. Luxenberger W, Stammberger H, Jebeles JA, Walch C: Endo-
scopic optic nerve decompression: The Graz experience. Laryn-
goscope 108:873-882, 1998.
5. Levin LA, Joseph MP, Rizzo JF III, Lessell S: Optic canal decom-
pression in indirect optic nerve trauma. Ophthalmology 101:566-
569, 1994.
6. Levin LA, Beck RW, Joseph MP, et al: The treatment of traumatic
optic neuropathy: The International Optic Nerve Trauma Study.
Ophthalmology 106:1268-1277, 1999.
7. Jiang RS, Hsu CY, Shen BH: Endoscopic optic nerve decompres-
sion for the treatment of traumatic optic neuropathy. Rhinology
39(2):71-74, 2001.
8. Rajiniganth MG, Gupta AK, Gupta A, Bapuraj JR: Traumatic optic
neuropathy: Visual outcome following combined therapy proto-
col. Arch Otolaryngol Head Neck Surg 129:1203-1206, 2003.
9. Yang WG, Chen CT, Tsay PK, et al: Outcome of traumatic optic
neuropathy—surgical versus nonsurgical treatment. Ann Plast
Surg 52:36-42, 2004.
10. Anderson RL, Panje WR, Gross CE: Optic-nerve blindness
following blunt forehead trauma. Ophthalmology 89:445-455,
1982.
11. Acheson JF: Optic nerve disorders: Role of canal and nerve
sheath decompression surgery. Eye 18:1169-1174, 2004.
12. Chen C, Selva D, Floreani S, Wormald PJ: Endoscopic optic nerve
decompression for traumatic optic neuropathy: An alternative.
Otolaryngol Head Neck Surg 135:155-157, 2006.
13. Thakar A, Mahapatra AK, Tandon DA: Delayed optic nerve
decompression for indirect optic nerve injury. Laryngoscope
113:112-119, 2003.
14. Lubben B, Stoll W, Grenzebach U: Optic nerve decompression
in the comatose and conscious patients after trauma. Laryngo-
scope 111:320-328, 2001.
15. Pletcher SD, Sindwani R, Metson R: Endoscopic orbital and optic
nerve decompression. Otolaryngol Clin North Am 39:943-958,
2006.
16. Metson R, Pletcher SD: Endoscopic orbital and optic nerve
decompression. Otolaryngol Clin North Am 39:551-561, 2006.
PEARLS
• Thorough review of preoperative imaging is
necessary to account for variations in anatomy such
as Onodi cells.
• Image guidance is an extremely valuable tool in
cases in which normal anatomy is distorted, such as
by fi brous dysplasia and skull base neoplasms.
• Removal of the posterior 1 cm of the lamina
papyracea facilitates identifi cation of the optic
foramen and optic canal decompression.
• Copious irrigation must be used during drilling over
the optic canal to prevent thermal injury.
• One hundred twenty–degree medial decompression
can be achieved to alleviate compressive symptoms.
PITFALLS
• Failure to bring all septations and air cells in plane
with the lateral orbital wall will make decompression
more diffi cult.
• Breach of the periorbita will lead to herniation of fat
and poor visualization.
• Incision of the nerve sheath is contraindicated
because it may produce a CSF leak.
• Care must be taken with postoperative packing to
not cause iatrogenic compression of the exposed
optic nerve.
• A high-speed drill shaft can cause alar burns if left in
the same position for a prolonged period.
event affecting the ophthalmic artery. In addition, small
bony fragments can lead to impingement of the optic
nerve during outfracture of the optic canal with a
curette.

Chapter 97
Orbital Exenteration
S. Tonya Stefko
PATIENT SELECTION
The radical surgery of orbital exenteration is occasion-
ally necessary in the management of head and neck
cancer. Most frequently for the otolaryngologist, it will
be due to spread of malignant tumor from adjacent
paranasal sinuses or the skull base. Some cancers arising
in the skin will also require total or subtotal removal
of the orbital contents. Invasive fungal infections are
indications for aggressive débridement, sometimes
including orbital exenteration. Rarely, a benign but
locally aggressive tumor or intractable pain will be an
indication.
The most clear-cut indications for orbital exentera-
tion are those involving malignant tumors with no hope
of salvaging vision in the affected eye (Fig. 97-1). These
situations most often include squamous cell carcinoma
and other epithelial malignancies. In the largest
reported series of orbital exenteration, squamous cell
carcinoma (originating in the sinus, skin, or conjunc-
tiva) accounted for one third of exenterations.1 A more
recent series found basal cell carcinoma to be the most
frequent diagnosis, followed by melanoma and seba-
ceous cell carcinoma.2 Conversely, a review of 70 con-
secutive cases of maxillectomy found that 40% of these
patients required concurrent orbital exenteration.3
Imaging is likely to underestimate the extent of tumor
invasion into the orbit, and the decision to proceed may
need to be made in the operating room. The recent
trend, particularly with squamous cell carcinoma, has
been preservation of the orbit except in instances of
proven invasion of the periorbita (by frozen section at
the time of surgery). In several retrospective series there
has been no difference in disease-free survival between
patients treated with orbit-sparing procedures and those
whose surgery included orbital exenteration.4
Malignant tumor of the orbit or eyelids, although
not strictly invading the eye or periorbita itself, may
require removal of the orbital contents because of insuf-
fi ciency of the remaining tissue for protection of the
globe (Figs. 97-2 and 97-3).
Surgical decision making in the setting of aggres-
sive infection is diffi cult. Most fungal infections of
the orbit spread from adjacent sinuses, and two main
types occur. Aspergillus affects both immunocompro-
mised and immunocompetent hosts. In the former
patients, the prognosis is extremely poor if immune
status cannot be improved and if intracranial involve-
ment is present.5 In the latter setting, exenteration
is likely to be necessary in cases of apical involvement,
but not when the infection is confi ned to the anterior,
inferomedial orbit,6 where limited débridement may
suffi ce.
Rhino-orbital-cerebral mucormycosis is a rare but
serious infection caused by Rhizopus species (occasion-
ally Mucor or Absidia). It affects immunocompromised
patients, most often those with a concurrent metabolic
acidosis. These patients require aggressive surgical
débridement to the level of bleeding tissue. This has
frequently included orbital exenteration in the pres-
ence of orbital signs, but one series showed no dif-
ference in survival between patients with orbital
involvement who underwent exenteration and those
who did not.7 However, the overall mortality in patients
with orbital involvement was higher (33% versus 14%).
The operation may be followed by hyperbaric oxygen
therapy, which improves survival.8
Three percent to 17% of patients requiring exen-
teration have benign orbital disease.1,9-12 The various
associated diagnoses include infl ammatory disease,
Stevens-Johnson syndrome, lymphangioma, meningi-
oma, and others. These diseases are either painful,
961

962
Section 10
Orbital Surgery
inadequately controlled medically, and “grossly disfi g-
uring” or, although histologically benign, tend to invade
adjacent tissue.13 The pain associated with the disease
most often resolves immediately after surgery.
PREOPERATIVE EVALUATION
Patients who may be candidates for orbital exenteration
should, at the very least, be evaluated by computed
tomography or magnetic resonance imaging (or both)
of the orbits, sinuses, and brain. In the majority of cases
that involve malignancy, positron emission tomography
is also indicated. When neck dissection is anticipated,
preoperative imaging of the neck and scintigraphy may
be considered. The choice of imaging will be guided by
the patient’s diagnosis. In patients with malignancies
contiguous with the orbit, it is likely that imaging will
underestimate the extent of disease and intraoperative
histopathologic monitoring will be necessary.
Before the operation, coagulation studies, a com-
plete blood count with platelets, and typing and cross-
matching of two units of packed red blood cells should
be performed.
In many instances, given the radical nature of the
surgery, pathology of the lesion should be indepen-
dently confi rmed by pathologists experienced in the
fi eld of head and neck or orbital disease.
Before scheduling surgery, a complete ophthalmo-
logic examination of the remaining eye is indicated
both to guide surgical decision making and to maxi-
mize the remaining vision.
In most otolaryngologists’ practices, exenteration
will be undertaken in conjunction with maxillectomy or
during aggressive sinus débridement (e.g., for invasive
fungal infection). During the informed consent process,
if the decision whether to exenterate the orbit will be
made at surgery, it must be made very clear to the
patient and family that although every effort will be
made to preserve the orbit and eye, this goal will not
preclude complete eradication of disease.
SURGICAL APPROACHES
Total or subtotal exenteration should be planned. Sub-
total exenteration most often means a partially lid-
sparing technique (Fig. 97-4A), which is appropriate in
most cases of benign disease and with tumors that pri-
marily affect the posterior or deep portions of the orbit.
It is inappropriate in any tumors affecting the skin,
conjunctiva, or lacrimal gland. Lid-sparing exentera-
tion gives an excellent color match to surrounding skin
and heals relatively quickly. Globe-sparing exenteration
has been described, with purported advantages of easier
prosthetic fi tting later.14
Figure 97-1. Patient with malignant melanoma destroying the
globe, adnexa, and orbital contents.
Figure 97-2. Advanced cutaneous melanoma of the eyelid with
orbital extension.
Figure 97-3. Patient from Figure 97-2, 12 days after exenteration
with a split-thickness skin graft in the orbit.

Chapter 97
Orbital Exenteration
963
Primary Reconstructive Options
Reconstructive options should be considered before
surgery. The simplest option is healing by secondary
intention, or granulation. The advantages of such
healing are shorter operating time, good color match
to surrounding tissue, excellent visibility for monitoring
of possible recurrence of disease, and a tendency to
produce a shallow socket (easier for eventual patient
care).15 Disadvantages include a long healing time and
the necessity for several painful dressing changes.
Split-thickness skin grafts, most commonly from the
thigh, are frequently used to line the orbital cavity when
total exenteration with removal of periosteum is per-
formed (see Fig. 97-3). Although this leads to shorter
recovery time and excellent visual monitoring for recur-
rence, a deeper cavity is formed, for which care and
prosthetic fi tting are somewhat more diffi cult. The pain
encountered after this reconstructive option is gener-
ally from the donor site.
Local or free tissue fl aps are most commonly per-
formed at our institution, particularly for defects result-
ing from concurrent partial or complete maxillectomy.
Temporalis fl aps,16 with or without cervicofacial,17 radial
forearm,18 and rectus abdominis fl aps, are most fre-
quently mentioned. These fl aps have the advantage of
ample tissue and good vascularity, which is desirable in
a fi eld likely to require radiation therapy. Disadvantages
of longer operating time, donor site morbidity/disfi g-
urement, and a requirement for highly specialized
microsurgical techniques (in the case of free fl aps) dis-
courage their use in very sick patients. These options
also render monitoring for local recurrence of disease
more diffi cult.
It has been reported that most patients are likely to
wear an occlusive eye patch regardless of attempts at
reconstruction.19 Prostheses may be fashioned by a
prosthodontist and may be affi xed by topical adhesive.
Alternatively, prostheses may be fi xed magnetically to
osseointegrated dental implants.20,21
Surgical Procedure
The patient is placed under general anesthesia, and the
surgical margins are marked (see Fig. 97-4A); in the
case of concurrent maxillectomy, that procedure is per-
formed fi rst. A suture tarsorrhaphy is usually helpful. If
the exenteration is to be a lid-sparing technique, an
incision line several millimeters proximal to the eyelid
margins and parallel to them is marked. A knife is used
to cut through skin and orbicularis, and blunt dissec-
tion in the pretarsal/preseptal plane is then carried out
to the level of the orbital rim. Periosteum is incised, and
the surgery proceeds as described in the following
text.
If the skin is to be included in the resection, the
excision margins are drawn at the orbital rim and at
least 1 to 2 cm from the cutaneous lesion. The marked
areas may be infi ltrated with local anesthetic with epi-
nephrine to help with hemostasis. A no. 15 scalpel is
used to cut through skin to the periosteum. Bleeding
should be expected at the supraorbital vessels. The peri-
osteum is elevated with a Cottle or Freer elevator, begin-
ning at the superotemporal portion of the orbit where
the bone is thickest. Dissection in this plane continues
circumferentially and posteriorly, with cautery of the
zygomaticofacial
and
zygomaticotemporal
vessels
encountered in the lateral wall. Resistance will occur in
the area of the trochlea (superomedially) and at the
canthal ligaments and may require sharp dissection in
these areas. The posterior limb of the medial canthal
tendon should be elevated from bone, and the lacrimal
sac should be divided at its junction with the nasolacri-
mal canal. The inferior oblique muscle originates just
A
B
C
D
Figure 97-4. A, Patient with mucoepidermoid cancer of the maxillary antrum who underwent orbital exenteration and radical maxillectomy.
A lid-sparing incision is outlined. B, Postoperative appearance with the lids sewn together, thus eliminating view of the open orbit. C, Oblique
view. D, Patient wearing special glasses that obscure view of the orbit.

964
Section 10
Orbital Surgery
lateral to the sac and should be elevated with the
periosteum.
Dissection proceeds posteriorly toward the orbital
apex, with special care directed to the following areas:
fi rst, elevation of the periosteum over the lamina papy-
racea must be carried out very gently to not create
dehiscences in the bone. The ethmoidal vessels must be
divided and bleeding controlled with bipolar cautery
and bone wax if needed. Second, areas of the roof,
particularly posteromedially, are often quite thin or
contain frank dehiscences. It is here that an iatrogenic
cerebrospinal fl uid leak may be created, either by direct
trauma or by the use of monopolar cautery, which may
travel through emissary foramina or dehiscences.22
Monopolar cautery should be avoided except in the
anterior-most portion of the orbit.
The contents of the superior and inferior orbital
fi ssures and the apical stump must now be divided,
which may be accomplished with a curved knife, curved
enucleation scissors, or a snare. The latter is tightened
to a soft stop and tightened sequentially over a period
of several minutes to assist with hemostasis. The snare
may then be tightened completely to transect the apical
stump, or curved scissors may be used to cut just ante-
rior to it. The orbit should immediately be packed with
gauze and pressure applied for 5 to 10 minutes. The
apex should then be explored cautiously with suction
and bipolar cautery to localize and control any
bleeding.
If the orbit is to heal by granulation, it should now
be lined with a nonadherent dressing such as Telfa fol-
lowed by Xeroform gauze, packed with fl uffed gauze,
and bandaged tightly. A small pledget of cellulose (Sur-
gicel) or other hemostatic agent may be placed over the
apical stump.
It may be possible in some patients to preserve the
eyelids. After a skin graft has been placed in the orbit,
the margins of the eyelid are sewn together to provide
a good appearance or at least a better appearance than
if the orbit were open to view (see Fig. 97-4B to D).
If the lid skin has been spared, it is draped over the
rim and spread posteriorly as far as possible. The
remainder of the orbit may be left to granulate or may
be covered with a split-thickness skin graft. If a split-
thickness graft is used, it is harvested from a non–hair-
bearing area of the inner surface of the thigh or the
abdomen and the donor site covered with an adherent
dressing. Dimensions of the graft are approximately 5
× 10 cm before meshing. The graft is carefully draped
into the orbital cavity, with care taken to ensure that
the epithelial side remains exterior. The graft is sutured
in place at the rim with interrupted 7-0 chromic gut or
silk suture. The wound is then dressed as discussed
earlier.
A
B
C
D
Figure 97-5. A, Patient with a sarcoma of the maxilla treated by maxillectomy. Recurrence in the orbit was treated with radiation therapy.
The tumor recurred once again and destroyed the orbital contents. B, Computed tomography scan demonstrating invasion of the orbit and
destruction of the bony orbital wall. C, Defect after orbital exenteration. D, Reconstruction with a rectus abdominis free tissue transfer.

Chapter 97
Orbital Exenteration
965
If a local or free fl ap is to be used for reconstruc-
tion, it is prepared and placed as dictated by the specifi c
procedure. The patient in Figure 97-5A underwent
maxillectomy for sarcoma of the maxilla. A recurrence
was treated with radiation therapy. The tumor recurred
once again and destroyed the orbital contents and the
orbital wall (see Fig. 97-5B). The orbital defect (see Fig.
97-5C) was reconstructed with a rectus abdominis free
tissue transfer (see Fig. 97-5D).
When fl ap reconstruction is not used, the pressure
dressing remains undisturbed for 3 to 5 days. During
this time the patient should have antibiotic coverage.
After this time, the pressure dressing is gently removed,
and the area is soaked with saline. After 5 to 10 minutes,
the lining layer (nonadherent dressing such as Telfa or
Xeroform) may be gently loosened from the underlying
tissue. Minimal débridement should occur at this stage
because areas of skin that appear devitalized may heal
surprisingly well. The area is coated lightly with antibi-
otic ointment, and the patient and family are instructed
to repeat the application of ointment twice daily. Oint-
ment should also be applied to the light dressing placed
over the orbit to prevent adherence. Vigorous cleaning
of the area should be avoided.
The patient is examined in the offi ce 1 week post-
operatively and then at regular intervals afterward as
dictated by disease process. Weekly or biweekly visits are
appropriate in the fi rst 4 to 6 weeks for cleaning of the
socket and monitoring for infection. In most cases in
which radiation therapy is not necessary, the patient is
ready for prosthesis fi tting in 3 months (Fig. 97-6).
COMPLICATIONS
Possible complications of the operation include intra-
operative bleeding, postoperative hematoma, postop-
erative infection, and dehiscence of the surgical wound.
Intraoperative bleeding is treated by packing and pres-
sure, prothrombotic agents applied to the orbital apex,
and transfusion of packed red blood cells if necessary.
Postoperative hematoma requires therapy if it occurs
under a skin graft or in a free fl ap. The former may be
drained by making a small incision in the graft, gently
evacuating the hematoma, and then replacing the pres-
sure dressing for 2 to 5 days. Free fl aps must be moni-
tored carefully by Doppler ultrasound to ensure patency
of the artery and vein, and a pressure dressing is con-
traindicated. Postoperative infection must be vigorously
treated with intravenous and then oral antibiotics, with
judicious surgical débridement of devitalized tissue or
drainage of purulent collections as needed. Dehiscence
of the surgical wound should raise suspicion of infec-
tion, which must be treated aggressively before consid-
ering secondary repair.
Fistulas resulting from orbital exenteration may
communicate with either the sinuses or dura. If a bone
or dural defect is noted intraoperatively, it should be
repaired. If the orbit is to heal by granulation or a skin
graft is used, a small fl ap of extraocular muscle and fat
may be spared and used to cover either the bone window
or the dural repair.23
A
B
C
Figure 97-6. A, Patient with recurrent basal cell carcinoma in a
previously exenterated orbit. B, Postoperative defect. C, Postopera-
tive appearance with a prosthesis and glasses.
PEARLS
• Orbital exenteration is appropriate for patients with
tumor invasion of periorbita proved by frozen
section examination.
• Patients with invasion of orbital bone only will
probably have comparable survival if the orbital
contents are spared.
• In patients with malignant tumors of the lacrimal
gland, exenteration is the procedure of choice.
• Aggressive débridement of skin grafts early in the
postoperative period is to be avoided.
• Postoperative infection must be treated early and
completely.

966
Section 10
Orbital Surgery
References
1. Levin PS, Dutton JJ: A 20-year series of orbital exenteration. Am
J Ophthalmol 112:496-501, 1991.
2. Rahman I, Cook AE, Leatherbarrow B: Orbital exenteration: A
13 year Manchester experience. Br J Ophthalmol 89:1335-1340,
2005.
3. Yucel A, Cinar C, Aydin Y, et al: Malignant tumors requiring
maxillectomy. J Craniofac Surg 11:418-429, 2000.
4. Carrau RL, Segas J, Nuss DW, et al: Squamous cell carcinoma of
the sinonasal tract invading the orbit. Laryngoscope 109:230-235,
1999.
5. Kraus D, Bullock J: Orbital infections. In Pepose J, Holland G,
Wilhelmus K (eds): Ocular Infection & Immunity. St Louis,
Mosby–Year Book, 1996, pp 1321-1340.
6. Dhiwakar M, Thakar A, Bahadur S: Invasive sino-orbital aspergil-
losis: Surgical decisions and dilemmas. J Laryngol Otol 117:280-
285, 2003.
7. Peterson KL, Wang M, Canalis RF, Abemayor E: Rhinocerebral
mucormycosis: Evolution of the disease and treatment options.
Laryngoscope 107:855-862, 1997.
8. Yohai RA, Bullock JD, Aziz AA, Markert RJ: Survival factors in
rhino-orbital-cerebral mucormycosis. Surv Ophthalmol 39:3-22,
1994.
9. Naquin HA: Exenteration of the orbit. AMA Arch Ophthalmol
51:850-862, 1954.
10. Bartley GB, Garrity JA, Waller RR, et al: Orbital exenteration at
the Mayo Clinic. 1967-1986. Ophthalmology 96:468-473, 1989.
11. Mohr C, Esser J: Orbital exenteration: Surgical and reconstruc-
tive strategies. Graefes Arch Clin Exp Ophthalmol 235:288-295,
1997.
12. Rathbun JE, Beard C, Quickert MH: Evaluation of 48 cases of
orbital exenteration. Am J Ophthalmol 72:191-199, 1971.
13. Rose GE, Wright JE: Exenteration for benign orbital disease. Br
J Ophthalmol 78:14-18, 1994.
14. Catalano PJ, Laidlaw D, Sen C: Globe sparing orbital exentera-
tion. Otolaryngol Head Neck Surg 125:379-384, 2001.
15. Putterman AM: Orbital exenteration with spontaneous granula-
tion. Arch Ophthalmol 104:139-140, 1986.
16. Menon NG, Girotto JA, Goldberg NH, Silverman RP: Orbital
reconstruction after exenteration: Use of a transorbital temporal
muscle fl ap. Ann Plast Surg 50:38-42, 2003.
17. Cuesta-Gil M, Concejo C, Acero J, et al: Repair of large orbito-
cutaneous defects by combining two classical fl aps. J Craniomaxil-
lofac Surg 32:21-27, 2004.
18. Tahara S, Susuki T: Eye socket reconstruction with free radial
forearm fl ap. Ann Plast Surg 23:112-116, 1989.
19. Ben Simon GJ, Schwarcz RM, Douglas R, et al: Orbital exentera-
tion: One size does not fi t all. Am J Ophthalmol 139:11-17,
2005.
20. Nerad JA, Carter KD, LaVelle WE, et al: The osseointegration
technique for the rehabilitation of the exenterated orbit. Arch
Ophthalmol 109:1032-1038, 1991.
21. Konstantinidis L, Scolozzi P, Hamedani M: Rehabilitation of
orbital cavity after total orbital exenteration using oculofacial
prostheses anchored by osseointegrated dental implants posed as
a one-step surgical procedure. Klin Monatsbl Augenheilkd
223:400-404, 2006.
22. Wulc AE, Adams JL, Dryden RM: Cerebrospinal fl uid leakage
complicating orbital exenteration. Arch Ophthalmol 107:827-
830, 1989.
23. Bartley GB, Kasperbauer JL: Use of a fl ap of extraocular muscle
and fat during subtotal exenteration to repair bony orbital
defects. Am J Ophthalmol 134:787-788, 2002.
24. Stern SJ, Goepfert H, Clayman G, et al: Orbital preservation in
maxillectomy. Otolaryngol Head Neck Surg 109:111-115, 1993.
PITFALLS
• Sino-orbital fi stulas are most easily created over the
lamina papyracea and result in chronic discharge.
• Use of monopolar cautery in the deep or superior
aspect of the orbit is to be avoided because
cerebrospinal fl uid leak may result.
• Resection of most of the orbital fl oor frequently
leads to loss of integrity of the eye because of
dystopia, diplopia, or ocular surface problems. This
may be compounded by postoperative radiation
effects on the eye.24

Chapter 98
Dacryocystorhinostomy
S. Tonya Stefko and Carl H. Snyderman
External dacryocystorhinostomy (DCR) was fi rst
described by Toti in the early 20th century.1 The tech-
nique is applicable to patients complaining of tearing
and demonstrating obstruction of the lacrimal outfl ow
system. The procedure consists of creating a fi stula for
egress of tears directly from the lacrimal sac into the
nose and bypassing the nasolacrimal duct (Figs. 98-1
and 98-2). Description of endonasal DCR took place
even before report of external DCR.2
PATIENT SELECTION
Patients may complain of tearing for one of three
reasons: hypersecretion of tears, impaired drainage of
tears, or a combination of both. Primary hypersecretion
of tears is uncommon, but secondary hypersecretion is
a frequent cause of tearing. It may be due to a variety
of ocular surface disorders, some as benign in nature
as seasonal allergy. Associated symptoms and signs will
help in making these diagnoses, and their proper treat-
ment should proceed before surgical repair. For
example, a patient with itching may have hypersecre-
tion because of seasonal allergy and may be treated with
antihistamine drops. Refl ex hypersecretion in patients
with ocular surface dryness (as in those with Graves’
disease) must be addressed by referral to an ophthal-
mologist. Abnormal eyelid position can cause refl ex
tearing by rubbing of lashes against the cornea or by
desiccation of the cornea as a result of inadequate
blinking or closure. Patients’ complaints will assist in
making the diagnosis inasmuch as those with surface
disorders causing refl ex hypersecretion will complain
of burning and a foreign body sensation. Fluorescein
drops instilled into the conjunctival cul-de-sac will high-
light defects in the corneal epithelium when viewed
with a cobalt blue fi lter on a penlight in patients with
dry eye.
Impaired drainage of tears can occur at any level of
the lacrimal outfl ow system. In newborns and infants,
the most common site of obstruction is distally at the
valve of Hasner, where canalization is often incomplete
at the time of birth. In most patients, congenital naso-
lacrimal duct obstruction will resolve by the age of 6 to
12 months, so probing of the lacrimal system should be
delayed until the end of the fi rst year of life. Probing
of the lacrimal system is most often curative at this
age.3
In adults, tearing secondary to insuffi cient lacrimal
drainage is common and may be due to functional or
physical obstruction. Functional obstruction includes
poor function of the medial canthal lacrimal pump,
usually secondary to eyelid malposition or aberrant
anatomy. Physical obstruction may occur at the level of
the punctum, canaliculus, common canaliculus, lacri-
mal sac, or nasolacrimal duct. The latter two account
for about 74% of lacrimal outfl ow obstructions4 and are
treated with greater than 90% success by external DCR
surgery.5
Patients may have acute dacryocystitis and complain
of tearing, discharge, swelling, and pain over the lacri-
mal sac. Some cases proceed to periorbital cellulitis
before diagnosis, so a high index of suspicion in this
setting must be maintained. Pressure over the sac pro-
duces purulent refl ux from the punctum, which is often
quite painful for the patient. Probing or irrigation at
this time is useless and may complicate the situation.
About two thirds of acute infections grow gram-positive
organisms in culture, and about 7% are anaerobic.6
Treatment of acute infection consists of at least 3 weeks
of oral antibiotic, antibiotic-steroid drops, and warm
compresses. An abscess in the area necessitates prompt
percutaneous drainage, often possible in the offi ce
under local anesthesia. The sac may then be irrigated
with antibiotic solution. Occasionally, poor response to
oral therapy will necessitate intravenous antibiotic treat-
ment and prompt surgery.
Endonasal DCR has enjoyed renewed interest since
the 1980s but is less preferred because of lagging success
967

968
Section 10
Orbital Surgery
rates and expense. Recent reports suggest that the tech-
nique is becoming more successful.7
Successful DCR requires a functional upper outfl ow
system. Treatment of upper system (punctum, canalicu-
lus, and common canaliculus) obstruction must be
undertaken either separately or in the setting of surgi-
cal DCR. Punctal stenosis may be treated by various
punctoplasty techniques. Canalicular stenosis may be
treated with silicon intubation, generally only in the
setting of incomplete obstruction. Common canalicular
stenosis may sometimes be treated in the setting of DCR
by silicon intubation. If intractable upper system
obstruction is present, primary conjunctivodacryo-
cystorhinostomy with placement of a Jones tube is
necessary.
In 8% to 14% of DCR surgeries, dacryoliths com-
posed of precipitated organic material will be found.8,9
Affected patients may complain of intermittent tearing
and pain and demonstrate distended, tender lacrimal
sacs but minimal or no infl ammation. Alternatively, the
dacryolith may mimic complete obstruction and occa-
sionally cause acute dacryocystitis.
In the presence of any suspicion of a mass in the
lacrimal system, external DCR with biopsy is mandatory.
The symptom of bloody tears is particularly worrisome
for tumor. If intraoperative frozen sections are available,
it may be possible to complete the DCR if the sections
are benign. If malignancy is found, however, dacryocys-
tectomy with appropriate margins should be performed
and creation of an ostium into the nose avoided.
Frontal bone
Supraorbital
foramen
Zygomaticotemporal
foramen
Zygomatic bone
Zygomaticofacial
foramen
Maxillary bone
Ethmoid bone
Lacrimal bone
Nasal bone
Infraorbital
foramen
Figure
98-1. Orbital
bones,
frontal view. (From Dutton JJ: Atlas of
Clinical and Surgical Orbital Anatomy.
Philadelphia, WB Saunders, 1994.)
Horner’s muscle
Superior muscle of
Riolan
Deep head of inferior
pretarsal orbicularis
muscle
Common canaliculus
Anterior arm of medial
canthal tendon (cut)
Lacrimal sac
Figure 98-2. Lacrimal drainage system, superfi cial anatomy. (From Dutton JJ: Atlas of Clinical and Surgical Orbital Anatomy. Philadelphia, WB
Saunders, 1994.)

Chapter 98
Dacryocystorhinostomy
969
PREOPERATIVE EVALUATION
Most patients referred to an otolaryngologist with com-
plaints of tearing will already have been evaluated by an
ophthalmologist and treated for ocular surface disor-
ders causing hypersecretion. If not, ophthalmologic
workup should proceed before any consideration of
lacrimal surgery for correction of tearing.
Complete endonasal examination, with particular
attention paid to the distal end of the nasolacrimal duct
beneath the inferior turbinate, should be performed in
the offi ce. Occasionally, physical obstruction of the
ostium is visible and readily treated. Signifi cant rhinitis
should also be treated before surgical correction
because it also rarely causes functional obstruction.
Note of any septal defects or deviation is important,
particularly if an endonasal approach is selected.
Dilatation and irrigation of the lacrimal system in
the offi ce can be used to localize the outfl ow blockage.
Probing of the lacrimal system, however, has no place
in adult patients. This procedure is rarely if ever cura-
tive and will cause signifi cant patient discomfort. In
addition, there is a risk of trauma to the delicate mucosa-
lined canalicular system, which is a considerably more
diffi cult problem to treat than nasolacrimal duct
obstruction. Quick, easy passage of saline into the naso-
pharynx after topical anesthesia and gentle injection
into the canaliculus may call into question the diagnosis
of lacrimal obstruction. However, this will often occur
in the setting of a dacryolith because the liquid will
drain around the object. It is also sometimes possible
to open the nasolacrimal duct with forceful injection,
but resistance will be palpable and indicates that the
system is probably functionally obstructed. The physi-
cian should note the speed and volume of fl ow, in addi-
tion to the presence of resistance or frank refl ux of
fl uid. Refl ux in the presence of resistance to fl ow indi-
cates obstruction. If refl ux occurs from the canaliculus
being injected or if resistance to easy passage of a 22-
gauge or smaller cannula is felt, canalicular obstruction
is present. Refl ux of fl uid from the opposite lid suggests
obstruction distal to the common canaliculus, and DCR
is likely to be curative.
Computed tomography of the orbits and sinuses
may be ordered in some situations to evaluate sinus and
nasal anatomy and whenever a mass is suspected. It is
particularly helpful in the setting of previous facial
trauma.
A complete medical history is necessary, with par-
ticular attention directed to bleeding/clotting disor-
ders and hypertension-related pathology. If the patient
will be under general anesthesia, evaluation by the
primary physician is frequently necessary.
SURGICAL APPROACHES
External DCR is performed under local anesthesia with
sedation or under general anesthesia. Our preference
is general anesthesia because control of the airway in
the presence of nasopharyngeal blood is desirable.
Before sterile preparation and draping, a local anes-
thetic with epinephrine is injected transcutaneously
over the anterior lacrimal crest and intranasally just
anterior to the middle turbinate. The patient may be
administered nasal decongestant before anesthesia, or
cottonoids soaked in decongestant may be placed.
A no. 15 scalpel blade is used to create an approxi-
mately 1.5-cm skin incision over the anterior lacrimal
crest by cutting in one stroke down to periosteum (Fig.
98-3). A Cottle or similar instrument is used to elevate
the periosteum over the maxillary bone. Elevation pro-
ceeds posteriorly and superiorly and includes the lacri-
mal sac fused to the periosteum (Fig. 98-4).
A small dehiscence of bone is often encountered at
the junction of the maxillary and lacrimal bones and is
useful for insertion of a Kerrison punch to begin bone
Figure 98-3. Anterior lacrimal crest. The incision will be hidden in
the lower eyelid crease.
Figure 98-4. Lacrimal sac elevated from the fossa (medial).

970
Section 10
Orbital Surgery
removal. If this dehiscence is not present, the bone may
often be cut with a small osteotome. Only rarely is it
necessary to drill to gain access to the nose, although
drilling is more frequent in patients with duct obstruc-
tion in the setting of infl ammatory diseases such as
sarcoid or Wegener’s granulomatosis. If the anterior
lacrimal crest obstructs visualization, it may be partially
resected with the bone punch.
A wide area of bone removal facilitates working in
the nose (Fig. 98-5). The patient’s upper punctum is
gently dilated, and a 0 or 00 Bowman or similar probe
is inserted. The probe is immediately turned medially,
and gentle lateral traction is placed on the lid to
straighten the canaliculus. When the probe is in the sac,
it is rotated up over the medial aspect of the brow and
visualized through the wound to be distending the sac.
The sac is opened over the probe, and the incision is
extended as completely superiorly and inferiorly as pos-
sible (Fig. 98-6). The sac may be incised with an angled
crescent blade, an angled needle-tipped cautery, or a
radiofrequency dissector. Extension of the incision in
the sac anteriorly at its upper and lower limits is helpful
for inspection of the interior of the sac. Any foreign
bodies should be removed, and a low threshold for
biopsy should be maintained. The probe is removed
from the lacrimal punctum.
The nasal packing is now removed. An oval or
round opening into the nasal mucosa is created with a
needle-tipped cutting/cautery device. One probe of a
silicon intubation system (such as a Guibor tube) is
passed through the upper canaliculus, into the sac, and
through the fi stula and retrieved in the nose with the
appropriate device (such as a grooved director). The
second probe is passed through the lower canaliculus
and retrieved in the same manner. Both tubes are then
elevated from the lacrimal sac with a small blunt hook,
and 6-0 silk suture is tied around both at about the level
of the skin incision (Fig. 98-7). It should be tied in a
single square knot to facilitate later removal via the
punctum. The hook should then be used to check
tension of the tubes at the medial canthal angle: the
loop should prolapse no farther than the medial limbus
(Fig. 98-8). The ends of the suture are trimmed to
3 mm.
Approximately 4 cm of a 12F red rubber straight
catheter is cut. One end may be beveled with drape
scissors if desired. It is passed, beveled end fi rst, over
both wire probes, into the naris, and up into the wound.
The catheter is retrieved in the wound with sturdy
forceps, such as Adson’s. Double-armed 4-0 chromic
gut suture is passed across the lumen of the tube
approximately 4 mm from its end while taking care to
not cut the silicone stents with the needle (Fig. 98-9).
The tube is retracted into the nose, and both ends of
the suture are passed through the anterior wall of the
lacrimal sac. The tube is pulled up into the sac, the
sutures are tied in a series of six to eight overhand
knots, and the ends are cut (Fig. 98-10).
The lacrimal sac area is now irrigated with an anti-
biotic solution. The three tubes are cut approximately
1 cm proximal to the naris, and a 5-0 nylon loose stitch
Figure 98-5. Lacrimal sac refl ected and bone partially removed
from the fossa.
Figure 98-6. Probe in the lacrimal punctum emerging in the
wound from the opened lacrimal sac.
Figure 98-7. Silicon stents emerging from wound are tied together
with suture (to rest in the area of the sac).

Chapter 98
Dacryocystorhinostomy
971
is fashioned to secure the catheter to the nasal mucosa.
The ends are cut short and rotated into the lumen of
the tube so that they do not irritate the patient. Skin is
closed with running 8-0 nylon suture or interrupted 7-0
chromic suture, and antibiotic-steroid ointment is
applied (Fig. 98-11). This may be followed by a pressure
bandage if signifi cant hematoma is expected.
POSTOPERATIVE MANAGEMENT
Patients are discharged from surgery on a regimen of
oral antibiotic, topical antibiotic-steroid drops, and
nasal steroid spray. Topical antibiotic-steroid ointment
is applied to the stitches until they are removed in 5 to
7 days. Patients are instructed to not blow or pick their
noses for 3 weeks. The fi rst three medications are main-
tained until removal of the red rubber catheter 3 weeks
postoperatively, at which time the drops are tapered
Figure 98-8. Silicon stents should be loose enough to prolapse only
as far as the medial limbus.
Figure 98-9. Rubber catheter around the silicone stents and gut
suture passed across the lumen (for fi xation into the sac remnant).
Figure 98-10. Rubber catheter sewn into the anterior of the sac
remnant and tied to rest in a fi stula.
Figure 98-11. The closed incision will be hidden in the lower
eyelid crease.

972
Section 10
Orbital Surgery
from four times a day to twice a day and then discon-
tinued 1 week later, and the oral antibiotic is discontin-
ued. The nasal steroid is continued until removal of the
silicon stents, 2 months postoperatively.
The patient is seen in the offi ce 1 week postopera-
tively for removal of the skin sutures. Two weeks after
this visit (3 weeks after surgery) the nylon stitch in the
naris is cut and the catheter is withdrawn from the
nostril in the offi ce. The chromic gut suture holding
the proximal end will have dissolved by this time. Two
months postoperatively, the silicon tubes are removed
either from the naris after cutting at the medial canthal
angle or from the punctum by rotating the tube until
the silk suture emerges from one punctum, cutting
between them, and pulling the end with three lengths
of tubing from the punctum (Table 98-1).
References
1. Toti A: Nuovo metodo conservatore di cura radicale delle sup-
purazioni croniche del sacco lacrimale (dacriocistorinostomia).
Clin Mod Firenze 10:385, 1904.
2. Caldwell G: Two new operations for obstruction of the nasal duct
with preservation of the canaliculi. Am J Ophthalmol 10:189,
1893.
3. Kashkouli MB, Kassaee A, Tabatabaee Z: Initial nasolacrimal duct
probing in children under age 5: Cure rate and factors affecting
success. J AAPOS 6:360-363, 2002.
4. Mullner K, Bodner E, Mannor GE: Endoscopy of the lacrimal
system. Br J Ophthalmol 83:949-952, 1999.
5. Kashkouli M, Parvaresh M, Modarreszadeh M, et al: Factors affect-
ing the success of external dacryocystorhinostomy. Orbit 22:247-
255, 2003.
6. Coden DJ, Hornblass A, Haas BD: Clinical bacteriology of dacryo-
cystitis in adults. Ophthal Plast Reconstr Surg 9:125-131, 1993.
7. Ben Simon GJ, Joseph J, Lee S, et al: External versus endoscopic
dacryocystorhinostomy for acquired nasolacrimal duct obstruction
in a tertiary referral center. Ophthalmology 112:1463-1468, 2005.
8. Hawes MJ: The dacryolithiasis syndrome. Ophthal Plast Reconstr
Surg 4:87-90, 1988.
9. Iliadelis E, Karabatakis V, Sofoniou M: Dacryoliths in chronic dac-
ryocystitis and their composition (spectrophotometric analysis).
Eur J Ophthalmol 9:266-268, 1999.
PEARLS
• A functional upper lacrimal drainage system must
be present for dacryocystorhinostomy to be
effective.
• The rubber catheter stent must be sewn securely up
into the body of the lacrimal sac.
• Gentle handling of the puncta and canaliculi is
essential to avoid injury.
• Any suspicion of a mass in the lacrimal sac area
must be approached externally.
PITFALLS
• Too much tension on the silicone stent (placing the
silk suture too deep) will cause erosion of the
lacrimal puncta.
• Failure to put lateral traction on the eyelid (i.e.,
straightening the canaliculus) while passing a
lacrimal probe will cause damage to the canalicular
mucosa.
• Using an unfamiliar absorbable suture (i.e., one that
will not predictably break down at 2 to 3 weeks)
may cause diffi culty in removal of the rubber stent.
Table 98-1
POSTOPERATIVE MANAGEMENT
SCHEDULE AFTER
DACRYOCYSTORHINOSTOMY
One week
postoperatively
Remove skin
sutures
Discontinue
ointment
Three weeks
postoperatively
Remove
rubber
catheter
Discontinue oral
antibiotic
Taper antibiotic-
steroid drops
Two months
postoperatively
Remove
silicone
stent

Chapter 99
Eye Reanimation in Patients with Facial
Paralysis
Barry M. Schaitkin
One of the most important aspects in caring for patients
with facial paralysis is eye care. Inattention to this detail
can lead to corneal exposure, ulceration, and perma-
nent scarring with loss of vision. Patients who have a
concomitant fi fth cranial nerve defi cit are at particu-
larly high risk and should be managed in conjunction
with a corneal specialist. For patients without a sensory
defi cit, primary treatment is the use of topical drops
and lubricants. A wide variety of products are available,
and the otolaryngologist should work closely with an
ophthalmologist if uncomfortable with this fi eld to
ensure optimal care of the patient.
Topical preparations in the form of drops and oint-
ments are available in a wide range of viscosity, depend-
ing on the scope of the exposure problem. Attention
should also be paid to the presence or absence of a
preservative because some patients are intolerant of
these chemicals.1
Other extremely important nonsurgical therapies
include the use of clear moisture chambers, taping the
eyelids closed at night, manual blinking, and external
lid loading. The use of an opaque patch over the eye
should be discouraged because it can lead to corneal
irritation if the eye opens beneath it.
PATIENT SELECTION
Abnormal eyelid position and disorders of the lacrimal
apparatus are the usual ocular symptoms in patients
with paralysis of the eyelids. The surgeon must evaluate
the entire effect of the facial nerve paralysis on the eye,
including brow position, lagophthalmos, lid laxity, lid
position, and epiphora. Most patients can be managed
without surgery indefi nitely, and the decision to operate
is therefore generally elective. Careful assessment of
the lid preoperatively will lead to more satisfactory
outcomes.
The patient’s history, including the cause of the
paralysis and the patient’s likelihood of spontaneous
nerve recovery or recovery after neural reanimation
procedures, is vitally important in surgical planning.
The age of the patient plays a role, and the contralateral
eye should be observed for age-related changes in the
eyelids and brow.
Detailed physical examination of these patients
includes evaluation of visual fi elds and acuity. The con-
junctiva is examined for signs of infl ammation with
topical fl uorescein and ideally with a slit lamp. The level
of the brows, eyelid approximation with involuntary
blink and voluntary effort, tear production, extraocular
muscle function, and pupillary size and response should
be noted.
A systematic evaluation of the eyelids before reani-
mation surgery as suggested by Moe is very useful. Moe’s
Ectropion Grading Scale ranks the lower eyelid on a I
to V scale with predominantly medial and lateral deter-
minations. Likewise, upper eyelid function can be
objectively compared with the normal side by using
medial and lateral measurements of the distance
between the eyelids in the closed position.2
Factors favoring successful medical management of
paralyzed eyelids include an expectation of early recov-
ery, residual facial function, preservation of static lid
tone, normal tear function, normal Bell’s phenome-
non, intact corneal sensation, young age, and the ability
to have close follow-up appointments.
973

974
Section 10
Orbital Surgery
SURGICAL TECHNIQUE
Interested readers will fi nd much more extensive writ-
ings on this subject, including in May and Schaitkin’s
The Facial Nerve,
1 where 100 pages are devoted to eye
reanimation. This chapter will therefore consider only
the most common procedures used in eyelid reanima-
tion. Partial tarsorrhaphy is mentioned only to be
condemned, except in very rare situations, because
of its limitations: restriction of vision, cosmetic dis-
fi gurement, and in some cases, failure to provide
protection.
BROW-LIFT
Patients with brow ptosis have asymmetry as a cosmetic
problem. They will often have visual fi eld defi cits supe-
riorly as a result of redundant skin from the upper
brow. Symmetry can be improved by injection of a small
dose of botulinum toxin (Botox) into the normal side.
A brow-lift can provide more defi nitive resting symme-
try but should never be undertaken at the expense of
corneal protection. Manual distraction of the brow with
the patient sitting upright can indicate the effect of a
brow-lift on lid closure. A direct brow-lift allows the
surgeon to better control the shape and position of the
brow but unfortunately leaves a visible scar.
A
B
C
Skin removal is usually necessary in an older patient.
The procedure is easily accomplished under local anes-
thesia with mild sedation. The ellipse of skin taken
should be larger laterally to mimic the shape of the
normal brow. Removal of only the skin and subcutane-
ous tissue protects the supraorbital neurovascular
bundle. Once the excision is accomplished, the inferior
aspect is sutured with two or three permanent 4-0 clear
monofi lament sutures. If necessary, a portion of the
orbicularis muscle and soft tissue can be included in
this suture to improve drooping of the supratarsal fold.
In general, a man’s brow lies close to the orbital rim
and a woman’s above the rim, although the normal side
should be used for comparison. Beveling the incision
to parallel the hair follicles can reduce scar visibility.
The incision should be kept central for maximal con-
cealment, and meticulous wound closure is necessary.
An endoscopic brow-lift, which has been introduced
more recently, is also an alternative technique.3
Upper Eyelid Procedures
A number of methods can be used to improve upper
eyelid closure, but lid loading with gold is the method
most commonly performed (Fig. 99-1). Jobe, in 1974,
was the fi rst American to place a gold weight and is
responsible for popularizing the procedure.4 This tech-
Figure 99-1. Insertion of a gold weight. A, Gold weights are tried as external lid loads preoperatively. B, Minimal local anesthesia is required.
C, A corneal protector is always used. The incision is made along the tarsal-supratarsal fold with an ophthalmic knife. (Reprinted from May M, Levine
RE, Patel BCK, Anderson RL: Eye reanimation technique. In May M, Schaitkin BM [eds]: The Facial Nerve. New York, Thieme Medical, 2000, p 708.)

Chapter 99
Eye Reanimation in Patients with Facial Paralysis
975
nique remains appealing because of its high success,
simplicity, low complication rate, and cosmetic
acceptability.
Several aspects, emphasized by Jobe, must be
adhered to:
1. Preoperative fi tting of the prosthesis involves fi nding
a weight that closes the eye, with the lower lid in
neutral position, without causing signifi cant ptosis at
rest. One millimeter of ptosis is considered accept-
able. Ideally, the patient wears the prosthesis for 24
hours to evaluate its function during fatigue and in
different head positions. Less expensive sizing pros-
theses are available for this purpose.
2. The prosthesis works best when it is placed medial
to the midpupillary line. Such placement overcomes
the wider area of exposure between the eyelids
medially.
3. The prosthesis should be placed in a pocket just
lateral to the tarsal plate to minimize visibility of the
plate through the soft tissues and decrease the risk
of exposure.
4. The weight is fi xed with three 8-0 monofi lament
permanent sutures 3 mm above the lash line. This
area is easily appreciated surgically inasmuch as a
vascular arcade is noticed below this level in the
tissue pocket.
5. The soft tissues are closed with 7-0 chromic suture
and the skin with absorbable plain gut.
6. Patients with gold sensitivity can have platinum
weights or chains inserted.
The procedure can be performed under local anes-
thesia with or without sedation and combined with
other reanimation procedures. The patient’s midpupil-
lary line is marked before applying topical anesthesia
to the eyelid and placing a corneal protector. Under
loop magnifi cation, an incision is made through the
skin along the tarsal-supratarsal fold. With gentle
forceps traction, Westcott scissors are used to divide the
soft tissues overlying the orbicularis muscle and levator
aponeurosis and expose and identify the tarsal plate as
a dense white structure (Fig. 99-2). The dissection con-
tinues above the tarsal plate inferiorly to within 3 mm
of the lash line (Fig. 99-3).
Two sutures are used for fi xation inferiorly.
Although some authors prefer to suture to the levator
aponeurosis,1 suturing to the soft tissues overlying the
tarsus is also acceptable.5 Kao and Moe have described
a retrograde implantation technique that has certain
advantages but may produce a more apparent surgical
scar5 (see Video 99-1).
Lower Eyelid Procedures
Many procedures have been described for lower eyelid
reanimation, including the Bick procedure (Fig. 99-4),
lateral tarsal strip, medial and lateral canthopexy, car-
tilage grafting, precaruncular medial canthopexy, and
transorbital canthopexy.
The surgeon should have intimate knowledge of
the anatomy of the eyelids before performing lower
eyelid reanimation, including the orbicularis oculi
muscle, the medial and lateral canthal tendons and
A
B
C
Figure 99-2. Surgical dissection and fi xation for the gold weight procedure. A, Double-action scissors are used to sharply dissect a pocket to
the tarsal plate noted as a white plane. B, Further dissection divides the orbicularis muscle and levator aponeurosis. The lowest point of dissec-
tion is 3 mm from the lash line, often noted surgically as the position of the vascular arcade. C, The gold weight is centered at the medial and
central third of the lid to improve coverage medially. Three-point fi xation is necessary to avoid extrusion, and the levator and orbicularis are
closed with 6-0 absorbable suture. (Reprinted from May M, Levine RE, Patel BCK, Anderson RL: Eye reanimation technique. In May M, Schaitkin BM
[eds]: The Facial Nerve. New York, Thieme Medical, 2000, p 709.)

976
Section 10
Orbital Surgery
Figure 99-3. Superfi cial placement of the weight or dissection too
close to the lash line will produce cosmetic disfi gurement and increase
the risk of extrusion. (Reprinted from May M, Levine RE, Patel BCK,
Anderson RL: Eye reanimation technique. In May M, Schaitkin BM [eds]:
The Facial Nerve. New York, Thieme Medical, 2000, p 710.)
their attachment sites, the tarsal plate, and the lacrimal
system.6 Preoperative assessment, in addition to upper
eyelid and brow recommendations, should include
notation of eyelid position relative to the limbus, posi-
tion of the punctum, results of a snap test, and medial
and lateral distances between the upper and lower
eyelids.
The Bick procedure or any of its modifi cations
allow tightening of the lower lid and suspension at a
higher position to the lateral orbital rim. Patient who
do not require skin excision to achieve this result may
best be served with a lateral transorbital canthopexy.7
The procedure begins with a 1.5-cm lateral canthotomy
and cantholysis to expose the periosteum of the lateral
orbital rim. The lid is tightened to achieve the desired
snap without signifi cant displacement of the punctum
of the lower lid. A full-thickness wedge resection is then
designed and executed with fi ne scissors. This creates a
free edge of tarsal tissue that can be resuspended with
5-0 nonabsorbable suture to the lateral orbital perios-
teum. The soft tissues require minimal absorbable
sutures for reapproximation.
Figure 99-4. Lower lid tightening procedure (modifi ed Bick). A, The procedure is performed under local anesthesia with a corneal protec-
tor. The lateral canthal incision follows the relaxed skin tension lines. B, The anatomy of the lateral canthal tendon is key to understanding
the procedure. C, Scissors complete the lateral canthotomy and inferior cantholysis. D, The lower eyelid is pulled laterally to achieve shortening
without distorting placement of the punctum, which would lead to epiphora.
B
C
A
D

Chapter 99
Eye Reanimation in Patients with Facial Paralysis
977
Figure 99-4, cont’d. E, The excess skin is resected. F, Absorbable 4-0 suture is used to reattach the new lateral margin of the tarsus to the
orbital rim. (Reprinted from May M, Levine RE, Patel BCK, Anderson RL: Eye reanimation technique. In May M, Schaitkin BM [eds]: The Facial Nerve.
New York, Thieme Medical, 2000, p 739.)
PEARLS
• The otolaryngologist must acquire familiarity with
this anatomy.
• Preoperative weight selection is important to avoid
ptosis or incomplete closure.
• Gold weights must be sutured in place.
• Neglect of the position and function of the lower
eyelid will lead to imperfect results.
References
1. May M, Levine RF, Patel BCK, Anderson R: Eye reanimation tech-
niques. In May M, Schaitkin BM (eds): The Facial Nerve. New
York, Thieme Medical, 2000, pp 676-774.
2. Moe KS, Linder T: The lateral transorbital canthopexy for correc-
tion and prevention of ectropion. Arch Facial Plast Surg 2:9-15,
2000.
3. Ducic Y, Adelson R: Use of the endoscopic forehead-lift to improve
brow position in persistent facial paralysis. Arch Facial Plast Surg
7:51-54, 2005.
4. Jobe RP: A technique for lid loading in the management of the
lagophthalmos of facial palsy. Plast Reconstr Surg 53:29-31, 1974.
5. Kao C, Moe KS: Retrograde weight implantation for correction of
lagophthalmos. Laryngoscope 114:1570-1575, 2004.
6. Fedok F: Restoration of lower eyelid support in facial paralysis. In
Schaitkin BM (ed): Facial Plastic Surgery: Facial Paralysis. New
York, Thieme Medical, 2000, pp 337-343.
7. Moe KS, Kao C: Precaruncular medial canthopexy. Arch Facial
Plast Surg 7:1-6, 2005.
PITFALLS
• Surgically corrected brow position can make eye
closure diffi cult.
• Patients without eventual neural recovery will
undergo atrophy over time, which can make upper
lid loads more apparent.
• Patients who are allergic to gold can be transitioned
to platinum.
• If the lower eyelid is tightened too much, it will ride
underneath the equator of the globe and provide a
poor cosmetic and functional result.
E
F

section 11
Cranial Base Surgery
Chapter 100
Surgery of the Anterior Cranial Base
Ricardo L. Carrau, Carl H. Snyderman, Allan D. Vescan, and Amin B. Kassam
Anterior cranial base surgery has been the most con-
spicuous arena for cooperation between otolaryngolo-
gists and neurologic surgeons. From an otolaryngologist’s
perspective, the anterior cranial base is the region most
commonly involved by extracranial neoplasms.1-6 Most
frequently they consist of neoplasms arising from the
nasal cavity or paranasal sinuses. A wide variety of
benign and malignant neoplasms may involve the ante-
rior cranial base, as demonstrated in Table 100-1.2
Although some of these neoplasms have been asso-
ciated with exposure to environmental carcinogens, the
cause of the majority of neoplasms involving the ante-
rior cranial base is unknown. Squamous cell carcinomas
arising in the nasal cavity or paranasal sinuses, unlike
those arising in other areas of the upper aerodigestive
tract, are not associated with the use of alcohol
or tobacco products. Squamous cell carcinoma of
the paranasal sinuses, however, has been associated
with exposure to nickel refi ning, softwood dust,
leather tanning processing, chromium, soldering
and welding, radium dial painting, and isopropyl oils.
Hardwood workers have an increased incidence of
adenocarcinoma.4,6
The symptoms and signs of neoplasms involving the
anterior cranial base are nonspecifi c and are not useful
in predicting a histologic diagnosis. These symptoms
and signs do, however, refl ect the location of the tumor
and may be predictive of the extent of involvement of
adjacent anatomic structures. Nonetheless, the clinical
manifestations of the tumor may be identical to those
of infl ammatory sinus disease. Common symptoms
include unilateral or bilateral nasal obstruction, recur-
rent epistaxis, rhinorrhea, and anosmia. Diplopia may
be associated with invasion of orbital structures. Intra-
cranial extension with signifi cant involvement of the
frontal lobes may occur without the production of any
particular symptoms (Fig. 100-1). Because of this “silent”
area of the brain, the fi rst indication of invasion of the
brain may be symptoms associated with elevated intra-
cranial pressure, such as headache. On further ques-
tioning, patients and family members may relate subtle
alterations in personality with disinhibition of emotions
and inappropriate responses.
As a result of the location of these tumors there may
be no external manifestations until the tumor reaches
a large size. With slow-growing benign and malignant
neoplasms, remodeling of bone with widening of the
nasal dorsum may be seen (Fig. 100-2). Extension later-
ally into the orbit may result in periorbital swelling,
proptosis, or restriction of extraocular movement and
diplopia.7 Visual loss is a late occurrence and is seen
more often with tumors that originate close to the optic
chiasm or orbital apex. Intracranial extension may be
associated with signs of elevated intracranial pressure,
such as papilledema. Evidence of frontal lobe involve-
ment may be suggested by detecting abnormal refl ex
responses associated with frontal lobe release (glabella
blink response, palmar-mental refl ex).
979
CR
Sella

980
Section 11
Cranial Base Surgery
A
B
Figure 100-1. A and B, Mag-
netic resonance images demon-
strating extensive neoplasm with
erosion of the skull base and inva-
sion of the right frontal lobe.
Table 100-1
TUMOR DIAGNOSIS AND PATIENT STATUS
Tumor
Total
Disease Status (Follow-up: Months)
NED
AWD
DOD
DOC
Benign Lesions
Meningioma
4
2 (48)
1 (31)
—
1 (36)
Ossifying fi broma
2
2 (27)
—
—
—
Cranial defect
2
1 (30)
—
—
1 (1)
Chondroblastoma
1
1 (45)
—
—
—
Fibrous dysplasia
1
—
1 (18)
—
—
Inverted papilloma
1
1 (22)
—
—
—
Pituitary adenoma
3
1 (44)
2 (26)
—
—
Subtotal
14
8
4
0
2
Low-Grade Malignancies
Chordoma
7
4 (32)
2 (13)
1 (29)
—
Esthesioneuroblastoma
6
4 (27)
1 (13)
—
1 (22)
Adenoid cystic carcinoma
4
3 (31)
—
—
1 (24)
Chondrosarcoma
2
2 (27)
—
—
—
Subtotal
19
13
3
1
2
High-Grade Malignancies
Squamous cell carcinoma
7
3 (33)
1 (23)
3 (7)
—
Undifferentiated carcinoma
2
—
1 (24)
1 (36)
—
Adenocarcinoma
2
1 (33)
—
1 (12)
—
Osteogenic sarcoma
2
2 (36)
—
—
—
Melanoma
1
—
1 (43)
—
—
Rhabdomyosarcoma
1
—
—
1 (10)
—
Malignant fi brous histiocytoma
1
1 (16)
—
—
—
Subtotal
16
7
3
6
—
Grand total
49
28
10
7
4
AWD, alive with disease; DOC, dead of other causes; DOD, dead of disease; NED, no evidence of disease.

Chapter 100
Surgery of the Anterior Cranial Base
981
Intranasal examination may be hindered because
of deviations of the nasal septum, mucosal edema, or
obstructing nasal polyps. Examination is greatly facili-
tated with the use of fl exible or rigid fi beroptic endo-
scopes. The appearance and location of the tumor may
suggest a histologic diagnosis. Origin of a tumor from
the nasal vault, medial to the attachment of the middle
turbinate, suggests an esthesioneuroblastoma (Fig.
100-3). Extension of a neoplasm from the maxillary
sinus to the anterior cranial base may be evident. Pos-
teriorly, involvement of the eustachian tube may be
detected. This is important in explaining an associated
middle ear effusion, as well as being a potential route
of spread of tumor to the infratemporal skull base or
carotid canal.
PATIENT SELECTION
Some aspects of the physical examination have already
been addressed. Endoscopic visualization of the nasal
cavity and nasopharynx is considered a routine part of
the examination that may provide useful information
regarding the origin, extent, and vascularity of the
tumor. Additional preoperative testing may include
assessment of olfactory function with “scratch-and-sniff”
panels and neuro-ophthalmologic examination, includ-
ing visual acuity and visual fi eld testing. Biopsy samples
are not usually obtained in the offi ce setting because of
concern for bleeding and possible communication with
cerebrospinal fl uid (CSF) (Fig. 100-4). Additionally,
biopsy may alter the magnetic resonance imaging (MRI)
characteristics of the tumor. However, large fungating
tumors that are easily visualized in the nasal cavity may
undergo biopsy with minor risk in the offi ce setting.
Radiologic imaging is an essential part of the evalu-
ation of these patients. Involvement of the orbit and
intracranial extension may not be clinically apparent.
Computed tomography (CT) of the paranasal sinus
with contrast enhancement is the preferred initial
examination. Images through the skull base are obtained
at 1-mm intervals to achieve maximal resolution. CT
provides excellent bone detail and is superior to MRI
in detecting bony erosion of the anterior cranial base
and paranasal sinuses. A contrast agent provides assess-
ment of the overall vascularity of the tumor (Fig. 100-5).
Coronal images of the anterior cranial base are superior
to axial images in demonstrating intracranial extension.
MRI provides much greater detail of soft tissue
Figure 100-2. Widening of the nasal dorsum is evident with this
neoplasm extending to and involving skin (arrows).
Middle turbinate
Figure 100-3. A mass is noted arising medial to the attachment of
the middle turbinate in the left nasal cavity (arrow). Biopsy confi rmed
an esthesioneuroblastoma.
M
Figure 100-4. This patient had a history of unilateral nasal obstruc-
tion. Endoscopic examination revealed a meningocele (M) in the
region of the cribriform plate.

982
Section 11
Cranial Base Surgery
structures and is complementary to CT scanning in
most patients. Bone detail is poorly visualized, however.
MRI is particularly valuable for demonstrating dural
involvement and invasion of the brain. MRI is also supe-
rior for demonstrating perineural extension of tumor
(Fig. 100-6). Highly vascular tumors may be associated
with fl ow voids within the tumor. When a sinus is opaci-
fi ed, a CT scan may not be able to differentiate tumor
from retained secretions. In this case, the use of MRI
with T1- and T2-weighted images allows differentiation
of tumor and secretions (Fig. 100-7). When the sinus
contains fungus, however, a signal void indistinguish-
able from air may give a false impression of a normal
examination on T2-weighted images (Fig. 100-8).
Angiography is not necessary for neoplasms involv-
ing the anterior cranial base unless there is neoplastic
involvement of the cavernous sinus or extensive extra-
cranial involvement with extension of tumor to the
infratemporal skull base. CT or MR angiography is
usually adequate to establish the status of the vascula-
ture in these areas. If the neoplasm is suspected to be
highly vascular based on CT or MRI characteristics,
angiography with preoperative embolization may be
considered. Nevertheless, preoperative embolization is
rarely necessary because the vascular supply to these
tumors is usually accessible at the time of surgery.
The choice of therapy is dependent on the histol-
ogy of the tumor and its expected biologic behavior,
the tumor site, and involvement of critical anatomic
structures. Surgical excision is the preferred treatment
modality for the majority of benign and malignant
tumors involving the anterior cranial base (Table
100-2). Complete removal of the tumor can be achieved
in the majority of cases with contemporary surgical
techniques. Because regional or distant metastases are
unusual at the time of initial evaluation, the critical
problem is that of local control. Rhabdomyosarcomas,
melanomas, and adenoid cystic carcinomas, which are
known to disseminate hematogenously, are an impor-
tant exception to this concept. Sarcomas are not con-
sidered operable until the absence of distant metastases
is confi rmed by CT scanning of the lungs and liver and
a bone scan.8-10 We prefer the use of a fused positron
emission tomography (PET)/CT study to evaluate for
metastasis.
Cytologic examination of the spinal fl uid is recom-
mended for some tumors with intracranial extension,
such as sarcomas or other high-grade malignancies.
Positive cytology may indicate the need for combined
therapy to prevent intracranial dissemination. The role
of preoperative chemotherapy in the treatment of high-
grade malignancies with intracranial extension has not
been adequately addressed in the adult population.
Strong consideration should be given, however, to the
use of chemotherapy postoperatively in these patients.
Figure 100-5. Computed tomography scan demonstrating bone
erosion of the anterior cranial base resulting from rhabdomyosar-
coma of the left orbit.
Figure 100-6. In this patient with a malignant neoplasm, magnetic
resonance imaging demonstrates tumor involvement of the left cav-
ernous sinus and perineural extension along the route of the trigemi-
nal nerve (arrow).
Table 100-2
CHOICE OF TREATMENT OF
TUMORS OF THE ANTERIOR
CRANIAL BASE
Neoplasm
Treatment
Benign
Surgery
Low-grade malignancy
Surgery ± radiotherapy
High-grade malignancy
Surgery + radiotherapy ±
chemotherapy
Radiotherapy + chemotherapy
± salvage surgery

Chapter 100
Surgery of the Anterior Cranial Base
983
Orbital involvement by a malignant neoplasm may
require orbital exenteration to achieve complete tumor
removal. Orbital exenteration is recommended when
there is soft tissue involvement of the orbit by malignant
neoplasms.7 Surgical therapy may be contraindicated in
patients with malignant neoplasms invading the soft
tissue of the orbit who adamantly refuse orbital exen-
teration. The orbit can usually be spared when there is
involvement by benign neoplasms.
Intracranial extension of malignant neoplasms is
not necessarily a contraindication to surgery. If it
appears that the neoplasm is extradural, the dura may
be excised as the margin (Fig. 100-9). Adequate surgical
margins may also be obtained if there is minimal involve-
ment of the frontal lobes (Fig. 100-10). However, when
dealing with aggressive neoplasms such as squamous
cell carcinoma or adenoid cystic carcinoma, which have
a predilection for extending great distances beyond the
observable margin of the tumor, the likelihood of
achieving local control with surgery is slim. Signifi cant
palliation, however, may be achieved with the addition
of postoperative chemoradiotherapy. Additionally,
A
B
A
B
Figure 100-7. A, A T1-weighted
magnetic resonance image dem-
onstrates a sphenoid sinus mass
(arrows) that is consistent with
either a tumor or secretions. B, A
T2-weighted image, however, dem-
onstrates high signal intensity con-
sistent
with
secretions
from
obstruction of the ostium of the
sinus.
Figure 100-8. A, A T1-weighted
magnetic resonance image dem-
onstrates an extensive lesion of the
sphenoid sinus with remodeling of
bone and erosion of the cranial
base. The variable-density pattern
is consistent with fungal sinus
disease. B, A T2-weighted image
gives a false impression of a clear
sinus. This patient was treated
endoscopically for allergic fungal
sinusitis.
Figure 100-9. This patient has
an extensive neoplasm involving
the nasal cavity and paranasal
sinuses.
Magnetic
resonance
imaging demonstrates protrusion
of tumor into the inferior portion
of the frontal sinus. There is evi-
dence of tumor extension through
the bone of the anterior cranial
base with possible involvement of
the dura.

984
Section 11
Cranial Base Surgery
given the insidious natural history of adenoid cystic
carcinoma, tumor recurrence may not become evident
for 5 to 10 years despite incomplete tumor excision.
Adequate exposure of the anterior cranial base for
excision of neoplasms traditionally requires a combined
intracranial and extracranial approach. The choice of
an extracranial approach depends on the site and
extent of the tumor and aesthetic considerations, as
well as the experience of the surgeon with particular
approaches. For most neoplasms arising from the nasal
cavity or paranasal sinuses, lateral rhinotomy provides
excellent exposure when combined with an intracranial
approach (Fig. 100-11). This approach allows complete
resection of the medial wall of the maxilla and the orbit
and nasal septum. Excellent exposure of the ipsilateral
nasopharynx is also possible. Access to lesions that
extend bilaterally, however, is limited. In addition,
patients object to the facial scars. A midfacial degloving
approach avoids external scarring and provides
improved access to bilateral lesions (Fig. 100-12). It is
also possible to resect some tumors limited to the crib-
riform plate and superior ethmoid air cells through an
intracranial approach exclusively. Most tumors that
were previously managed by lateral rhinotomy com-
bined with a transcranial approach or by a degloving
approach may be removed by endoscopic or endo-
scopic-assisted resection. Endoscopic or endoscopic-
assisted approaches will obviate the need for facial scars
and have been our favored approaches for the past 10
years.
Preoperative informed consent includes discussion
of the various treatment options, as well as the sequelae
and potential risks associated with the surgery. For
patients undergoing anterior craniofacial resection,
standard discussion of risks includes possible brain
injury, hemorrhage, infection, CSF leak, stroke, and
visual loss. Patients are informed that anosmia is a
sequela of the operation.
PREOPERATIVE PLANNING
Special consideration must be given to perioperative
and intraoperative management of these patients. As a
result of the prolonged nature of the surgery, these
patients are at risk for the development of deep venous
thrombosis (DVT). Since anticoagulation is contraindi-
cated in these patients because of the risk of intracra-
nial hemorrhage, DVT prophylaxis is best achieved with
sequential pneumatic compression stockings intraop-
eratively and in the postoperative period until ambula-
tion is possible.
Anterior craniofacial surgery necessarily results in
contamination of the intracranial space by bacterial
fl ora of the upper aerodigestive tract. These are consid-
ered clean-contaminated cases, and perioperative
Figure 100-10. In this patient, squamous cell carcinoma devel-
oped in an inverting papilloma. Magnetic resonance imaging dem-
onstrates minimal tumor invasion of the right frontal lobe.
Figure 100-11. Lateral rhinotomy affords excellent exposure of
the ipsilateral nasal cavity and paranasal sinuses.
Figure 100-12. A midfacial degloving approach is useful for tumors
involving the sinonasal cavity bilaterally.

Chapter 100
Surgery of the Anterior Cranial Base
985
antibiotic prophylaxis is indicated. Broad-spectrum
antibiotics are recommended to provide adequate cov-
erage of the fl ora of the sinuses (Streptococcus pneumoniae,
Haemophilus infl uenzae, Branhamella catarrhalis) and skin
(Staphylococcus aureus). Previous studies have demon-
strated that the use of a single agent such as a broad-
spectrum
cephalosporin
may
provide
adequate
protection. Antibiotic prophylaxis is instituted at least
2 hours before the skin incision and is continued
through the second postoperative day. Antibiotic pro-
phylaxis for 24 hours or less is associated with a signifi -
cant increase in local infections.11,12 Such infections may
be due to transient CSF leaks postoperatively with
potential contamination of the intracranial cavity. Anti-
biotic prophylaxis for more than 48 hours may be asso-
ciated with an increased risk for infection by resistant
organisms.
To minimize the need for retraction of the brain,
which may lead to contusion and the development of
encephalomalacia, it is desirable to minimize intracra-
nial pressure with various anesthetic techniques, includ-
ing removal of CSF by lumbar puncture, as well as using
a balanced anesthetic technique to maintain adequate
cerebral perfusion while minimizing intracranial pres-
sure. Hyperventilation to produce hypocapnia usually
provides adequate relaxation of the frontal lobes. If
signifi cant frontal lobe retraction is necessary, a lumbar
spinal drain is placed preoperatively and approximately
50 mL of spinal fl uid is removed. Because these drains
tend to malfunction intraoperatively, it is best to remove
additional CSF at the time of catheter placement. Addi-
tional CSF may be removed intraoperatively or postop-
eratively to minimize intracranial pressure and decrease
the risk for a postoperative CSF leak. In most cases, the
spinal drain can be removed in the recovery room after
surgery. Relaxation of the brain may be enhanced intra-
operatively with the use of osmotic diuretics such as
mannitol. The surgical approach is designed to mini-
mize frontal lobe retraction through the use of a sub-
frontal approach.
The patient is positioned on a Mayfi eld horseshoe
head holder to improve access to the face and scalp
areas. Because frequent repositioning of the face and
head is necessary with a combined intracranial and
extracranial approach, head tongs or pins are not gen-
erally used. Since access to the airway is limited intra-
operatively, the endotracheal tube is additionally
secured by placement of a wire around a mandibular
or maxillary molar. Wiring of the tube to the maxilla is
preferred, when feasible, because such wiring provides
greater stability. If the patient is edentulous, a circum-
mandibular wire is placed for anchoring of the endo-
tracheal tube.
An additional concern for the anesthesiologist is
the development of an air embolus intraoperatively.
This risk is minimized by operating with the patient in
a supine position. A precordial Doppler probe is used
to detect signifi cant air embolism. A central line is also
placed preoperatively to allow advancement into the
right atrium for aspiration of an air embolus should it
occur.
Most approaches to the anterior cranial base require
exposure of the intracranial structures via frontal crani-
otomy. Before proceeding with the skin preparation,
the eyes are protected by suturing the lids closed with
6-0 silk suture. This allows inclusion of the eyes within
the surgical fi eld and decreases the risk of corneal abra-
sion. The tarsorrhaphy suture may be placed through
the lids at the tarsal line. Pledgets soaked in 0.05%
oxymetazoline nasal solution are placed intranasally
with the strings attached. To allow adequate time for
the vasoconstrictive effects of a local anesthetic, the
proposed incision line is infi ltrated with 0.5% lidocaine
(Xylocaine) with 1 : 200,000 epinephrine at this time.
On average, approximately 20 mL of local anesthetic is
infi ltrated. The skin is then prepared with a povidone-
iodine solution. It may be used around the eyes,
although it is advisable to rinse the eyes with balanced
saline solution to prevent chemical irritation. The povi-
done-iodine solution should be allowed to dry for it to
be most effective.
SURGICAL TECHNIQUES
Open Technique
To provide access to the right and left frontal areas, a
bicoronal scalp incision is made over the vertex of the
scalp. Laterally, the incision extends to the superior
attachment of the auricle. When additional lateral
exposure is necessary, the incision is extended into a
preauricular crease. The incision may be extended as
necessary with a parotidectomy incision (Fig. 100-13).
If lateral exposure is not necessary, small anterior
Figure 100-13. The coronal scalp incision may be extended in a
preauricular skin crease to provide additional lateral exposure.

986
Section 11
Cranial Base Surgery
backcuts are made at the ends of the incision in the
temporal hair-bearing scalp (Fig. 100-14). This increases
the arc of rotation of the scalp fl ap without the need
for extending the incision inferiorly. The incision is
made over the vertex of the scalp to maximize the
length of any potential scalp fl aps used for reconstruc-
tion. For this reason, incisions that follow the hairline
or that have a V-shaped peak projecting anteriorly in
the midline are to be avoided. Because of placement of
the incision high over the vertex of the scalp, an accept-
able cosmetic result is achieved even in bald persons. If
there is any loss of hair along the incision line, it is well
hidden.
Superiorly, the incision extends through all layers
of the scalp, including the pericranium. Laterally, the
incision extends to the level of the deep temporalis
fascia. The lateral dissection is more meticulous to
avoid injury to the superfi cial temporal artery. The
branching pattern of this artery is variable, but in 85%
of patients it divides into major anterior and posterior
branches. By placing the scalp incision in line with the
ear, the posterior branches are divided with preserva-
tion of the anterior branch. Preservation of the super-
fi cial temporal artery is not essential for viability of the
scalp in most patients, but it may be important in
patients who previously have undergone surgery or who
have received radiation therapy. Additionally, if a galeal-
pericranial scalp fl ap is used for reconstruction, collat-
erals from the superfi cial temporal artery are important
to provide adequate circulation to the overlying skin.
The edges of the scalp are elevated with a broad
periosteal elevator, and Raney clips are placed along
the skin margins of the incision to provide hemostasis.
The pericranium is not separated from other layers of
the scalp at this time to prevent desiccation of the fl ap
during a prolonged procedure. The scalp is then ele-
vated, deep to the pericranium, with a periosteal eleva-
tor and blunt dissection with gauze. Laterally, this
requires separation of the pericranium from the deep
temporalis fascia at the origin of the temporalis muscle.
The thin fascial layers overlying the deep temporalis
fascia are easily elevated with a wide periosteal elevator.
Bleeding from perforating veins of the frontal bone is
controlled with bone wax or electrocautery.
As the scalp is elevated and refl ected inferiorly, care
is taken to avoid injury to the supraorbital and supra-
trochlear vessels. The supraorbital vessels and nerve are
usually found in a notch along the medial half of the
superior orbital rim (Fig. 100-15). With a sharp elevator
such as a Cottle instrument, the vessels and nerve can
usually be elevated from the bony notch without injury.
Occasionally, however, the nerve and vessels may be
completely encompassed by a bony foramen. In such
cases, the inferior portion of the foramen can be mobi-
lized with a 2- to 3-mm osteotome (Fig. 100-16). If the
neurovascular bundle is found to exit through a
foramen more than 1 cm from the orbital rim, it may
be sacrifi ced. If a bifrontal craniotomy is performed
without a subfrontal approach, it is not necessary to
elevate the periorbita. A basal subfrontal approach is
generally preferred, however, to provide additional
exposure of the anterior cranial base posteriorly and to
minimize retraction of the frontal lobes.
The periorbita is then elevated from the medial,
superior, and lateral walls of the orbit with an Adson,
Freer, or Penfi eld elevator. The supraorbital nerve runs
along the surface of the orbital tissues. The globe is
retracted with a malleable ribbon retractor to provide
adequate visualization. Pressure on the globe may result
in an ocular refl ex, with resultant bradycardia and
hypotension. This usually recovers quickly once pres-
sure is released. Violation of the periorbita frequently
occurs and results in herniation of orbital fat. Though
a nuisance for visualization, it is not necessary to repair
Figure 100-14. As an alternative to extending the incision inferi-
orly, a short angulation of the incision anteriorly increases the arc of
rotation of the scalp fl ap and provides adequate frontal exposure.
This patient has also been marked for a lateral rhinotomy.
Figure 100-15. Subperiosteal elevation of the frontal scalp reveals
the supraorbital nerve exiting from a completely enclosed bony
foramen (arrows).