Facial Fractures I Upper Two Thirds

FACIAL FRACTURES I: UPPER TWO THIRDS
Larry Hollier MD and James Thornton MD
INTRODUCTION
There has been a gradual evolution in the management of craniofacial trauma over the past three
decades. Early approaches to fractures favored
closed reductions or visualization through minimal
incisions, usually in delayed fashion after swelling
had resolved. It subsequently was appreciated that
results were improved by early definitive treatment,
widely exposing and mobilizing the fracture fragments, and stabilizing them with newly developed
internal fixation devices. More recently efforts have
focused on technological advances that facilitate
accurate diagnosis and refinements in technique to
improve access to the fracture and stability of the
reduction. Persistent problems such as postoperative enophthalmos and soft-tissue deformities are
also being addressed by incorporating evolving
technology, such as radiographic techniques and
advances in fixation, into modern fracture management.
The basic tenets of management of craniofacial
trauma, however, are unchanged and well accepted:
early operative anatomic reduction of all fractures,
followed by rigid internal fixation and primary bone
grafting of significant skeletal defects.1-5
ZYGOMATIC FRACTURES
HISTORY
The following highlights in the history of zygomatic fractures are excerpted from Huffman and
Lierles1 classic review.
Little was written about zygomatic fractures until
1751, when duVerney reported two cases. Before
that time, in fact, fractures of the zygoma were
thought to be an ailment not to be treated (Edwin
Smith Papyrus, ca. 1650 BC), and consequently were
largely ignored. At first, treatment consisted of
reducing the body of the malar bone, which was
approached via the (a) gingivobuccal sulcus; (b)
maxillary antrum; (c) nose; or (d) skin over the

malar prominence.
Keen2 pioneered the intraoral approach to the
malar bone by incising the gingivobuccal sulcus.
His technique was criticized for its high risk of contamination by organisms in the mouth. In 1906
Lothrop3 devised the transantral approach through
the canine fossa, exposed through an upper
gingivobuccal sulcus incision. The technique, currently known as the Caldwell-Luc approach, avoids
external incisions and gives access to the maxillary
sinus for debridement of pulverized bone and
mucosal debris and for drainage. In 1931 Shea4
suggested a nasal approach that entered the antrum
with a urethral sound to engage the antral surface
of the zygoma.
A number of transcutaneous approaches have
been recommended over the years. For example,
Matas6 passed a suture around the medial arch for
traction elevation, and Manwaring7 and Gill8 used
towel clips and cow-horn dental forceps. Roberts9
designed a corkscrew instrument that could be
inserted into the malar bone for elevation; following the reduction, the corkscrew was removed.
Kazanjian10 placed a screw into the malar bone, left
it in place, and attached it to a transcutaneous wire
for headcap traction. To reduce arch fractures,
Gillies11 incised the temporal hair-bearing skin and
passed a bone hook deep to the temporal fascia
down to the body of the zygoma to elevate this
segment.
The discovery of antibiotics opened the door to
more extensive internal approaches, and in 1942
Adams12 first used suspension wires for facial fracture reduction and fixation. Kazanjian and Converse,13 among others, recommended extensive
periosteal elevation for wide exposure of the fractured bone.
In 1950 Fryer14 reported stabilization of zygomatic fractures with transcutaneous Kirschner wires,
and 2 years later Anthony15 proposed using an
inflatable antral balloon for the reduction of zygo-
SRPS Volume 9, Number 26
matic fractures, a technique that was subsequently

refined by Franchebois16 in 1959.
Plate fixation for stabilization of craniofacial fractures resulted from work by the Swiss AO
Group.17,18 Rahn18 points out that this technology
was first applied to the treatment of patients with
mandibular fractures. Some of the early plates used
in the midfacial area were actually designed for
hand fractures.19 The first published report of rigid
fixation for the treatment of fractures of the midface
was in 1973 by Michelet.20
Since that time, plating technology has advanced
greatly.21 Currently most plating systems designed
for use in the craniofacial skeleton are composed
of titanium and use screws 1.0, 1.5, or 2.0 mm in
diameter. As technology has improved, self-drilling
screws have been developed that allow insertion
without the use of drill bits, further simplifying the
process of stabilization. Additionally, resorbable
fixation systems have become commonplace in
craniofacial surgery. Although there is still some
concern regarding their place in fracture management, these systems have found widespread application in pediatric craniofacial surgery.
ANATOMY
The zygoma articulates with the greater wing of
the sphenoid, frontal and temporal bones, and maxilla22 (Fig 1). From a clinical standpoint, the zygoma
has two faces: the lateral or malar surface and the
more medial orbital surface.
The body of the zygoma gives prominence to
the cheek, while the zygomatic arch is formed by
union of the zygomatic bone and the slender
zygomatic process of the temporal bone at the
oblique temporozygomatic suture.23 The zygoma
furnishes attachments for the masseter, temporalis,
zygomaticus, and zygomatic head of the quadratus
labii superioris muscles. The broad attachment of
the masseter produces the major deforming force
on the zygomatic body and arch when fractured.22
The temporal fascia attaches to the sharp superior
border of the arch, while the masseter muscle and
fascia attach to the inferior border of the arch.23
In 1944 Ungley and Suggit24 coined the phrase
zygomatic tripod, yet the zygoma is more properly called a tetrapod because of its attachment to
the sphenoid. According to Knight and North,25 to
speak of fractures of the zygoma is misleading; in
Fig 1. Frontal and lateral views of the zygoma and its articulations. (Reprinted with permission from Cohen SR: Craniofacial
Trauma. In: Ruberg RL, Smith DJ Jr, Plastic SurgeryA Core
Curriculum. St Louis, CV Mosby, 1994. Ch 17.)
fact, the zygomatic bone itself is not fractured, but

rather it is separated from adjacent bones either at
the suture lines or by fractures of those other bones.
Knight and North prefer the term malar fracture
to describe fractures in this area because anatomically these fractures involve more than one bone.25
An important aspect of malar fractures that cannot be overemphasized is the involvement of the
orbit. Malar injuries tend to have a profound impact
on globe position because the zygoma constitutes

the majority of the lateral orbital wall and a significant portion of the orbital floor. Even small degrees
of displacement of the zygoma may greatly increase
the intraorbital volume and produce enophthalmos.
Consequently the orbit must be carefully evaluated
preoperatively in all of these injuries.
DIAGNOSIS
Physical Examination
When seen shortly after the injury, most patients
with malar fractures are noted simply to have swelling in the periorbital region, frequently with anesthesia in the distribution of the infraorbital nerve.
As the swelling resolves, many of the classic findings of zygomatic fractures may be appreciated.
Occasionally one may palpate step deformities at
the level of the infraorbital rim or frontozygomatic
sutures. In particularly severe injuries there may be
a visible depression of the malar eminence. Trismus may be noted secondary to impingement on
the coronoid process by the posterior aspect of
the malar fragment.
Of particular importance are the potential ocular
findings, and complete ophthalmologic exam
should be carried out in all patients with suspected
malar fracture. The globe may be significantly displaced due to involvement of the orbital floor and
lateral orbital wall in these injuries. When the orbital
volume has been expanded, enophthalmos is
apparent. When the malar fragment is inferiorly
displaced, a hypoglobus or inferior displacement
of the globe can be seen. Additionally, disturbances
in visual fields or in visual acuity may be present
due to direct damage to the extraocular muscles
or the globe itself.
Radiographic Findings
The role of plain x-rays in the diagnosis of facial
fractures remains controversial. It is generally
accepted that the Waters view is the single most
helpful plain film, particularly for zygomatic fractures.26-29 The Waters x-ray is taken in 30 degrees
of occipitomental projection and gives a view of
the zygomatic buttresses. In many emergency centers, however, it is traditional to obtain a facial
series of four radiographs to screen for fractures.
This series typically includes a Waters view as well

as a submentovertex view, a lateral view, and a
posteroanterior view.29 When one considers the
cost of taking and interpreting four films, this rapidly approaches the cost of a single CT scan.
Patients suspected of having a facial fracture should
proceed directly to CT scanning.
Axial views taken at 1.5 mm cuts through the
craniofacial skeleton will show all fractures. It may
be helpful, particularly when evaluating the orbit, to
also obtain coronal images of the facial skeleton.
This requires that the neck be placed in hyperextension, and that is not possible in many trauma
patients because of concerns regarding cervical
spine injuries; in these cases coronal reformations
of the axial CT scan data are recommended. These
tend to be more accurate when the axial cuts are
no more than 1.5 mm apart.
A relatively recent development has been the
widespread use of three-dimensional CT reconstructions.30,31 No additional images are required to
obtain these reconstructions; rather, the existing
data are simply reformatted to create a virtual image.
Clearly this is not necessary for the majority of
facial fractures, but in complex injuries, particularly
those involving the nasoorbitoethmoid region, 3-D
reconstructions can help with fracture diagnosis
and localization.31,32
These technologies allow accurate preoperative
characterization of facial injuries, but they are of no
value in fracture reduction. To this end, some centers are evaluating the use of intraoperative CT
scans.33 Stanley33 described 25 patients who underwent open reduction of displaced zygomatic or
orbital floor fractures. All patients were fitted with
a radiolucent graphite head-holder to correctly
position the head for the scan. Although this did
add some time and complexity to the cases, only 7
of 25 patients had to have secondary revisions of
the fracture fragments or bone grafts. As this technology improves, intraoperative localization of the
reduced fracture fragments will become easier and
more precise.
CLASSIFICATION
Many classification schemes have been proposed for malar fractures.25,26,34-39 These were perhaps more important in the past, when their primary aim was to identify and categorize which frac-
tures were likely to be stable following closed reduction. Manson and colleagues38 classification
system was based on the energy required to produce the fracture. Not surprisingly, they found that
high-energy injuries required more frequent operative intervention and wider exposure for anatomic reduction.
MANAGEMENT
Because of how they affect treatment of the
injury, perhaps the two most important characteristics of a malar fracture are its displacement and its
comminution. Undisplaced fractures are most often treated conservatively, while displaced malar
fractures are typically treated surgically. Comminution of the fracture and its buttresses requires wider
exposure to anatomically align the fracture, and
possibly even bone grafting.
Most authors agree that undisplaced zygomatic
fractures require no therapy. Patients should be
followed closely, placed on a soft diet, and the
malar eminence should be protected, particularly
during sleep. This regimen is followed for 6 weeks,
during which time the patient is reevaluated at least
once to rule out occult orbital floor fracture or any
displacement that may necessitate treatment.
When deciding on the appropriate treatment of
a zygomatic fracture, one must distinguish between
a true malar fracture and an isolated zygomatic
Fig 2. Temporal incision for reduction of

isolated zygomatic arch fractures. A & B, The
incision is carried through the temporoparietal and temporalis fascia. C, A Dingman
elevator is placed deep to the temporalis
fascia behind the depressed zygomatic arch.
(Reprinted with permission from Feinstein FR,
Krizek TJ: Fractures of the Zygoma and Zygomatic Arch. In: Fostor CA, Sherman JE (eds),
Surgery of Facial Bone Fractures. New York,
Churchill Livingstone, 1987.)
arch fracture. There are two indications for surgery in zygomatic arch injuries: contour deformity
and trismus. Because of the proximity of the arch
to the coronoid process of the mandible, displaced
arch fractures may cause pain on mouth opening.
In thin patients or significantly displaced fractures,
there may be a visible concavity over the fracture
site. In these situations the fracture is best managed by operative reduction, most often through
Gilliess temporal approach40 (Fig 2). The Gillies
reduction involves an incision in the temporal hairline and dissection down to the level of the
temporalis muscle. The bone elevator is then passed
inferiorly along the surface of the temporalis muscle
behind the zygomatic arch and the fragment is
raised and aligned.40
An alternative approach in patients in whom the
temporal incision is objectionable is to place an
elevator through a gingivobuccal sulcus incision
and pass it cephalically beneath the arch for elevation.
Although most isolated arch fractures remain
stable after reduction,11,40,41 some form of stabilization is desirable while the fracture is healing.42 For
this we prefer to place two deep sutures around
the zygomatic arch, passing them transcutaneously
from one side of the arch to the other. The sutures
are then tied over a metal eye-shield or Aquaplast
splint (PS Thermoplastic, Wycoff NJ).43 The stabiliz-
ing sutures must not be tied too tightly to avoid

pressure necrosis of the skin under the splint.43
In cases of displaced malar fracture, the surgeon
must first decide which incisions are necessary for
exposure (Fig 3). A gingivobuccal sulcus incision is
always used to expose the zygomaticomaxillary
buttress and the face of the maxilla. A lower eyelid
incision is also necessary for exposure of the orbital floor and infraorbital rim. This incision may be
transconjunctival, subciliary, or subtarsal; the decision of which one to use largely depends on the
surgeons experience, and will be discussed further in the section on Orbital Fractures.
Fig 3. Common incisions for exposure of the zygoma. Upper

and lower eyelid incisions. (Reprinted with permission from
Rohrich RJ, Hollier LH, Watumull D: Optimizing the management of orbitozygomatic fractures. Clin Plast Surg 19(1):149,
1992.)
The zygomaticofrontal suture is usually accessed

by a lateral extension of the upper blepharoplasty
incision. The skin in the lateral aspect of the
supratarsal fold is marked and the area is infiltrated
with local anesthetic. Some authors advocate visualization and fixation of the zygomaticofrontal suture through the lower lid incision after superior
cantholysis.44 Incisions in the brow are to be
avoided.
A coronal incision obviates the need for the
upper eyelid incision, but is indicated only when
anatomic reduction of the fracture is impossible
without visualizing the zygomatic arch, such as in
high-energy injuries where comminution of the infraorbital rim and zygomaticomaxillary buttress removes the visual cues for proper orientation of the
fracture fragments. In these situations reconstruction of the zygomatic arch provides a great deal of
information regarding the rest of the malar complex.

The surgical endoscope has been used to assist
with reduction and fixation of malar injuries. Lee
and colleagues45 report a cadaveric and clinical study
in which the endoscope was used to help visualize
and repair the zygomatic arch using a limited preauricular incision, a gingivobuccal sulcus incision, and
an eyelid incision. Once all the articulations of the
zygoma have been checked visually, the fracture
fragments are mobilized for easy repositioning during the reduction. These fractures are often impacted and require a good deal of effort to mobilize. In the most difficult cases, mobilization can be
facilitated by a bone screw introduced through a 3to 4-mm incision in the cheek and placed into the
bone of the zygomatic arch. In addition to facilitating disimpaction of the fracture, the screw can then
be used as a handle to align the buttresses.
The nature and location of the fixation to be
used once the fracture has been reduced is controversial. Numerous authors report their respective experiences and results.39,46,47 We feel that the
zygomaticofrontal region should be plated first using a 1.0-mm plate. This allows the surgeon to
establish the correct vertical position of the zygoma
while moving the fracture fragments and aligning
the infraorbital rim and zygomaticomaxillary buttress. The infraorbital rim is plated with a 1.0- or
1.5-mm plate, ideally placed on the superior aspect
of the infraorbital rim. Anterior placement of the
plate along the rim risks palpability in the postoperative period. Placement of this second plate essentially locks in the position of the fracture fragments, and should only be done once alignment of
the zygomaticomaxillary buttress is ensured. The
zygomaticomaxillary buttress is plated last using a
1.5- or 2.0-mm L plate. A larger plate can be used
with confidence at this site because it will not be
palpable postoperatively.
Clearly not all of these buttresses need to be
plated in every case. Various investigators have
looked into the stability of malar fractures following fixation of varying degrees.39,48-51 Rinehart and
colleagues48 demonstrated that two-point miniplate
fixation at the frontozygomatic suture and zygomaticomaxillary buttress was sufficient to withstand
postoperative stresses. Davidson, Nickerson, and
Nickerson49 found that in some cases one-point
fixation was sufficient, provided it incorporated the
frontozygomatic suture line. In our opinion, if plates

are to be avoided at any site, it should be at the
infraorbital rim due to potential problems with plate
palpability.
At the end of the operation, the soft tissue of the
malar region should be resuspended to the infraorbital rim using suture. This serves not only to anatomically reposition the facial soft tissues, but also
to support the lower lid and theoretically to
decrease the risk of postoperative lower lid retraction.
COMPLICATIONS
Enophthalmos
The incidence of delayed enophthalmos following zygomatic fractures is reported to be as
low as 3% in some series.55 Nevertheless, in no
other facial fracture can the enophthalmos be as
severe as in an untreated or poorly treated malar
fracture. This is due in no small part to the fact
that the zygoma comprises almost the entire lateral orbital wall and a large portion of the floor.
As the entire lateral wall is posterior to the axis of
the globe (Fig 4), any increase in volume produced by lateral rotation of the wall will result in
posterior displacement of the eye and enophthalmos (Fig 5).
Diplopia
Barclay52,53 reviewed the literature of zygomatic
fractures and concluded that approximately 10%
of patients have initial diplopia, and in half of this
patient population the diplopia will become permanent (5% overall). Other authors25,54,55 report
a 3.4% to 8% incidence of diplopia in fractures
of the zygoma. While transient diplopia is present
on either upward or downward gaze on the side
of injury, permanent diplopia is usually evident
only on upward gaze (hypotropia) on either side.
When the orbital floor is involved in the zygomatic fracture, the most common cause of diplopia
is entrapment of orbital tissues in the region of the
inferior rectus muscle.56 Hypotropia is most often
seen in patients with posteriorly located floor fractures.57 Seiff and Good56 hypothesized that the
deficit in downgaze was related to changes in the
effective origin and insertion of the inferior rectus
muscle.
Other possible causes of diplopia are injury to
the nerves or any of the extraocular muscles, or
scar tissue tethering the muscles to the bone fragments. Patients complaining of diplopia in the postoperative period should be followed closely by an
ophthalmologist. If the floor was reconstructed
using an implant, a postoperative CT scan should
be obtained to ensure that the floor implant is not
improperly positioned or causing a mechanical
restriction of globe movement. The majority of
patients will improve over time with conservative
management, but if after 4 to 6 months the symptoms remain, rebalancing of the extraocular muscles
may be necessary.
Fig 4. The transverse axis of the globe extends from the lateral
orbital wall to the lacrimal bone. The entire lateral wall is behind
this axis, whereas the orbital floor lies primarily in front of the
axis. (Reprinted with permission from Pearl RM: Treatment of
enophthalmos. Clin Plast Surg 19(1):99, 1992.)
The treatment of enophthalmos depends on the

patients complaints. Most patients will recognize
and request correction of the orbital asymmetry
secondary to the enophthalmos, yet there is also
retrodisplacement of the malar eminence which
tends to be much less obvious to patients but is still
directly related to the enophthalmos.
Fig 5. Loss of orbital volume below the globe will produce

inferior displacement of the eye, while loss of volume behind the
globe will result in retrodisplacement and enophthalmos. (Reprinted with permission from Pearl RM: Treatment of enophthalmos. Clin Plast Surg 19(1):99, 1992.)
In the most complete correction of the deformity, the zygoma is reduced and repositioned to
reduce the orbital volume and eliminate the enophthalmos. This is done by recreating the fracture
with a saw and moving it superiorly, medially, or
anteriorly (Fig 6).58
An alternative approach, focusing on just the
enophthalmos, addresses the increased orbital volume directly by augmentating the orbital cone with
graft material.59 In delayed cases it is critical to fully
release the periorbita to let the globe move anteriorly following graft augmentation. A 1-mm advancement of globe position is seen for every 1.37-1.5
mL of graft material introduced.59
Regardless of the approach chosen, the AP
position of the eye should appear overcorrected
immediately after surgery and, because of swelling,
the operated eye should appear proptotic compared with the other side. Bilateral symmetry postoperatively predicts enophthalmos once the swelling has resolved.
Traumatic Optic Neuropathy
Optic neuropathy is a rare complication of zygomatic fractures, reported in only 1.3% to 2.1% of
some series.54,60 It is likely, however, that many
patients with very slight neuropathy go undetected
on cursory exams, as the mildest symptom is diminished color perception. The diagnosis and management of optic neuropathy will be discussed
Fig 6. Correction of enophthalmos following malar fracture. A,

Through an intraoral incision, osteotomies are made with a
reciprocating saw and the zygoma is mobilized. B, Three-point
fixation of the repositioned zygoma with a wire loop at the
frontozygomatic suture, a microplate inside the orbital rim/
floor, and a miniplate across the zygomaticomaxillary buttress.
(Reprinted with permission from Longaker MT, Kawamoto HK:
Enophthalmos revisited. Clin Plast Surg 24(3):531, 1997.)
more thoroughly under Orbital Fractures, but clearly

it is not necessary to have a true orbital fracture to
exhibit this complication; any trauma to the head
can result in optic neuropathy. In a retrospective
study of 61 patients with facial trauma and optic
neuropathy, Wang and colleagues61 found 27
(44%) had no orbital fracture. Regardless of treatment, the improvement in visual acuity of this subset of patients was far better overall than if an orbital
fracture was present (83% vs 38%).
Typically when a diagnosis of optic neuropathy

is made after a facial injury, surgery for fracture
fixation is delayed pending the administration of
steroids and stabilization or improvement of the
visual deficit.
Persistent Infraorbital Nerve Anesthesia
The course of the infraorbital nerve near the
malar eminence weakens this area, and fracture
lines through the nerve foramen are common (Fig
7). Neurapraxia of the infraorbital nerve manifests
as diminished sensation in the cheek and upper lip.
In Zinggs39 large series, almost 24% of patients
with malar injuries suffered some form of infraorbital nerve dysfunction, though the changes were
typically transient. Some investigators report lower
rates of permanent hypesthesia after zygomatic fractures when plate fixation is used, compared with
wire fixation.46,62-64
and stomach.65 A patient who is noted to have

bradycardia intraoperatively should be suspected
of having incarceration of intraorbital fat or muscle
in the fracture line, even if the fracture is undisplaced.
Prompt release of the entrapped soft tissue should
protect against life-threatening cardiac arrhythmia
and ischemic muscle necrosis.
Soft Tissue Descent
Phillips and colleagues 66 noted downward
migration of the skin, fat, and muscle overlying the
malar prominence after open reduction of complex orbitozygomatic fractures. To prevent this
complication, they recommend periosteal suspension of the soft tissues of the malar region to the
orbital rim through the subciliary incision. In addition to restoring contour, periosteal suspension
helps to support the lower eyelid and reduces the
risk of postoperative ectropion.
Through a lower eyelid incision, the previously
dissected zygomatic periosteum is pulled upward
and sutured to the orbital rim with heavy sutures
passed through two or three drill holes in the bone
or a preexisting plate (Fig 8). The thicker skin,
subcutaneous tissue, and muscle of the cheek are
resuspended in their anatomic position over the
malar eminence, while the thinner eyelid tissue overlies the orbital septum. No deep sutures are placed
in the eyelid itself to avert postoperative shortening.
Fig 7. Sensory deficits in the cheek and upper lip area indicate
nerve involvement in orbitozygomatic fractures. (Reprinted
with permission from Rohrich RJ, Hollier LH, Watumull D:
Optimizing the management of orbitozygomatic fractures. Clin
Plast Surg 19(1):149, 1992.)
ORBITAL FRACTURES
ANATOMY
Bradycardia
Bradycardia before or during the operative
reduction of an orbitozygomatic fracture is felt to
be part of the oculocardiac reflex, a triad of symptoms that also includes nausea and syncope. The
oculocardiac reflex is mediated by the ophthalmic
division of the trigeminal nerve (the afferent limb)
passing through the reticular formation to the vagus
nerves visceral motor nuclei. The efferent limb
message is carried by the vagus nerve to the heart
Seven bones make up the orbit: the frontal

bone, maxilla, zygoma, ethmoid, lacrimal bone,
greater and lesser wings of the sphenoid, and
palatine bone. The first four constitute the strong
outer rim of the orbit and protect the more delicate bones forming the walls of the interior orbit.
The orbital cavity is bound by superior, lateral, inferior, and medial walls.
The superior wall is arched and quite thin. This
thinness notwithstanding, isolated roof fractures are
development of the face out from the relative

protection of the cranium, and to pneumatization of the maxillary sinus, which directs forces
applied to the midface along the inferior orbital
rim.
The lateral orbital wall is formed by the strong
zygomatic and frontal bones. Consequently, isolated fractures of the lateral wall are the least common of all orbital fractures. The lateral wall, however, is always involved in fractures of the malar
complex, as it forms the articulation of the zygoma
with the greater wing of the sphenoid.
Fig 8. Above, The ptotic soft tissue is elevated and suspended

to the orbital rim with suture. Below, The previously stripped
periosteum of the orbital rim is resuspended to prevent recurrence of ptosis. (Reprinted with permission from Phillips JH,
Gruss JS, Wells MD, Chollet A: Periosteal suspension of the lower
eyelid and cheek following subciliary exposure of facial fractures.
Plast Reconstr Surg 88:145, 1991.)
rare in adults because of the protection afforded

the superior wall by the thick supraorbital rim, frontal bone, and frontal sinus.67 In children, roof fractures are the most common orbital fracture, presumably because the cranium is proportionately
larger than that of adults and the frontal sinus is not
completely pneumatized.68
Koltai and colleagues68 reviewed a series of
40 children 1 to 16 years old who were admitted
to their institution with orbital fractures. The fracture distribution by sites was as follows: 14 orbital
roof, 10 orbital floor, 14 mixed, and 2 medial
wall. The age at which the probability of orbital
floor fracture exceeded the probability of orbital
roof fracture was approximately 7 years. The
authors postulate this is due both to forward
The inferior orbital wall is most vulnerable to

injury because of a combination of factors, including thinness of the maxillary roof, presence of the
infraorbital canal, and curvature of the floor. Jones
and Evans69 correlated thickness of the bone in the
orbital floor and medial wall with incidence of blowout fracture. Immediately behind the orbital rim
the floor is concave, while farther back it becomes
convex. The anterior depression in the floor and
the thin nature of the bone account for the frequency of orbital fractures here.69 Oluwole and
White70 report a case of orbital floor fracture in a
70-year-old as a result of vigorous blowing of the
nose.
The medial wall of the orbit is almost vertical
with a slight lateral inclination. The two thin bones
of the wall, the lacrimal bone and the lamina
papyracea of the ethmoid, make it susceptible to
fracture. Several important soft-tissue structures
near the medial wall are also easily injured. The
lacrimal sac is protected anteriorly by the frontal
process of the maxilla, which makes up the anterior lacrimal crest, and posteriorly by the lacrimal
bone, which forms the posterior crest. The medial
canthal tendon attaches to the medial wall and is
subject to disruption with injuries to this area.
Manson71 gives an excellent description of the
anatomy of the ligamentous support of the globe,
which comprises the medial and lateral check ligaments, the medial and lateral canthal ligaments, an
inferior sling, and a superior sling. The inferior
sling includes not only Lockwoods ligament and
extensions, but also the fascial condensations
around the inferior rectus muscle and Tenons cap-
sule. The superior sling is composed of Whitnalls

ligament, condensations of the levator and superior rectus fascia, and Tenons capsule.
Lockwoods suspensory ligament72 is a fascial
hammock that extends from the medial to the lateral wall of the orbit, cradling the eyeball and helping maintain the vertical level of the globe (Fig 9).
This fascial web is a direct extension of the fascia
bulbi described by Tenon73 in 1806.
described as the hydraulic theory, in which pressure generated within the orbit blows out the floor
of the socket (Fig 10A). This is in direct contradistinction to the theory of bone conduction or buckling, which maintains that the force delivered to the
rim is transmitted along the bone to the floor,
thereby causing the fracture (Fig 10B). Fujino78-80
experimentally demonstrated this to be a potential
pathogenic mechanism of blowout fracture.
Fig 9. Suspensory apparatus of the eye.
PATHOMECHANICS OF INJURY
There has been a great deal of controversy over
the years regarding the pathomechanics of orbital
fractures. This is particularly true with respect to
fractures of the orbital floor and medial wall. While
fractures of the orbital roof are rare and lateral
orbital wall fractures are due primarily to malar injuries, floor and medial wall fractures are caused by
one of two primary mechanisms: 1) an indirect
transmission of force blows to the orbital rim, or 2)
direct transmission of pressure from the globe or
intraorbital contents to the floor. Erling and colleagues74 provide an excellent review of the history of this controversy, along with experimental
data to support the latter hypothesis.
Erling et al74 point out that it was Raymond Pfeiffer
who, in 1943, proposed that blowout fractures were
due to the force of the injury delivered to the globe,
which was then transmitted to the walls of the orbit
to produce the fracture.75 A similar theory was
espoused by Smith and Regan76 and Converse and
Smith.77 These authors proposed what can best be
10
Fig 10. Mechanism of injury of orbital blowout fractures. A,

Hydraulic theory. B, Bone conduction theory. (Reprinted with
permission from Waterhouse N, Lyne J, Urdang M, Garey L: An
investigation into the mechanism of orbital blowout fractures. Br
J Plast Surg 52:607, 1999.)
Erling and colleagues74 reviewed multiple CT

scans of fractures of the medial and inferomedial
orbital walls, and could see the footprint of the
globe transferred directly to the fracture sitethat
is, the shape of the defect coincided very closely
with the shape of the globe, implicating direct globewall contact as the source of the fracture. In reality,
as the authors readily admit, both hydraulic forces
and a bone conduction mechanism are likely at

play in producing orbital blowout fractures.
BLOWOUT FRACTURES
Clinical Findings
The main findings of orbital blowout fractures
are diplopia and enophthalmos. Converse et al81
correlated these clinical findings with the underlying pathology.
Diplopia
Diplopia is caused by restricted ocular movement. In blowout fractures this is most common in
upward gaze, and can be primaryin the central
visual fieldor secondaryonly on extreme peripheral gaze. As the eyes seldom deviate more than
20 degrees from the central axis, primary diplopia
is very troublesome to patients.
Diplopia may be due to mechanical or nonmechanical causes. Mechanical globe restriction
is due to alteration of the intraorbital contents by
the fracture line. The intraorbital structuresthe
inferior oblique or inferior rectus muscles,
Lockwoods ligament, Tenons capsule, intermuscular membrane, or periorbital fat may be incarcerated by the fracture, with resultant physical
limitation of globe movements82 (Fig 11). The
restriction is confirmed clinically by the forced
duction or traction test (Fig 12).
Fig 11. Mechanism of entrapment of intraorbital fat and fascia

producing diplopia after a blowout fracture. (Reprinted with
permission from Manson P: Facial Fractures. In: Aston SJ, Beasley
RW, Thorne CHM (eds), Grabb and Smiths Plastic Surgery, 5th
ed. Philadelphia, Lippincott-Raven, 1997.)
Fig 12. Forced duction or traction test. (Reprinted with

permission from Converse JM: Kazanjian and Converses Surgical Treatment of Facial Injuries, 3rd Ed. Baltimore, Williams &
Wilkins, 1974.)
Mechanical globe restriction may also be due

to a relative change in the effective origin and
insertion of the inferior rectus muscle. 56 The
authors found that the inferior rectus looped
inferiorly and then rose to contact the globe at a
steep angle, which placed the inferior rectus at
a mechanical disadvantage and impaired eye
movement.
Nonmechanical causes of diplopia are less common and include injury to one or more of the
extraocular muscles, damage to one of the nerves
to an extraocular muscle, hematoma, and edema.
The forced duction test is unreliable during the
first week after injury because nonmechanical
causes of restriction often give spurious results.
Riley and Mazow83 remind us that orbital trauma
is seldom if ever restricted to the inferior rectus
muscle. Their four-step test effectively differentiates paresis from entrapment as the etiology of
diplopia.
More sophisticated methods of assessing diplopia, such as the Hess screen test and the diplopia
test, have also been described.84 Testing must be
done in all cardinal directions of gaze while the
patient faces forward with the head held straight.
Emery and associates85 trace the progress of
diplopia in untreated, isolated orbital blowout fractures. When diplopia was present at the time of
the initial examination, it resolved within 15 days in
55% of the patients. Over time, an additional 18%
of patients had resolution of their diplopia, for a
total of 73% of the original group. However, diplopia became permanent in 27%.
11
Enophthalmos
Enophthalmos is a measure of the difference
between the anterior corneal surface and the lateral orbital rim. Clinically this manifests as an exaggerated superior sulcus above the upper lid and
pseudoptosis. Pseudoptosis is distinguished from
true ptosis by the fact that there is no change in the
distance between the inferior lid margin and the
pupil; rather, more of the upper lid is visible due to
the retropositioning of the eye.
The degree of enophthalmos is most accurately
determined by Hertel exophthalmometer, which
uses the lateral orbital rim as a reference point. As
such, it cannot be used when the rim is displaced,
as in a displaced zygomatic fracture. A discrepancy
between the eyes of 3 mm or greater is considered significant.82 Edema often hinders accurate
assessment of the degree of enophthalmos on initial presentation.
The anterior-posterior level of the globe depends
on numerous factors, including the amount of periorbital fat, the status of the check ligaments arising
from the sheath of the lateral and medial rectus
muscles, and the tone of the rectus muscles, which
exert slightly more pull posteriorly than the oblique
muscles do anteriorly.
Posttraumatic enophthalmos results from inferior and posterior displacement of the globe and
intraorbital soft tissues (Fig 13).71 Displacement is
possible only if there has been both an increase in
volume of the bony orbit and a disruption of the
ligaments that supported the globe. The etiology
of enophthalmos may be enlargement of the bony
orbital cavity, escape of orbital fat or orbital fat
necrosis, muscle entrapment, or soft tissue scarring and contracture of the periorbita.82
Mustarde86 showed that even when the orbital
floor is completely absent, Lockwoods ligament
will support the eye as long as its anchoring points
to Whitnalls tubercle of the zygoma laterally and
to the lacrimal crest mediallyare preserved.
Manson71 confirms that even with most of the bony
floor gone, the globe will maintain its position provided there is no disruption of the periosteum or
supporting structures.
By using axial and coronal CT scans and MRI
studies of cadaveric orbits, Pearl87 showed that volumetric expansion of the orbit leading to posterior
12
Fig 13. Schematic of posttraumatic, enophthalmic orbital

shape. (Reprinted with permission from Manson PN et al:
Mechanisms of global support and posttraumatic enophthalmos: I. The anatomy of the ligament sling and its relation to
intramuscular cone orbital fat. Plast Reconstr Surg 77:193, 1986.)
displacement of the globe is possible only with

volume changes posterior to the vertical axis of
the globe. Increases in volume anterior to the
vertical axis have no effect on anteroposterior globe
position despite increase in intraorbital volume. The
axis of the orbit tends to lie at approximately the
level of the lateral orbital rim.
A number of studies have correlated changes in
orbital volume with subsequent severity of enophthalmos.88 Schuknecht and associates89 used CT
scans to quantify orbital volume in patients with
enophthalmos after zygomatic fracture. Enophthalmos of 2.5 to 3 mm correlated with a mean increase in orbital volume of 3.4 mL, while enophthalmos of 3.5 to 5 mm correlated with increase in
orbital volume of 7.1 mL.
Raskin and colleagues90 analyzed the orbital volumes of 30 patients with blowout fractures and
found that an increase of orbital volume of more
than 13% 1 month after injury or surgery was highly
predictive of enophthalmos. Fractures with enophthalmos on initial examination tended to involve
the medial wall as well as the orbital floor.
Orbital Emphysema
Orbital emphysema is commonly seen after floor
fractures with involvement of the medial walls. The
emphysema is usually an isolated radiographic finding with no clinical symptoms.91-93 Although orbital
emphysema is usually benign and self-limiting, the
intraorbital air mass can cause central retinal artery

occlusion. Hunts and colleagues93 reviewed eight
cases of orbital emphysema associated with orbital
fractures. Seven of the eight patients had needle
aspiration of the air mass after localization by CT
scan because of visual deterioration, rising intraocular pressure, severe pain, or motility disturbances.
There was resolution of symptoms and recovery
of visual acuity in all cases.
Ophthalmologic Evaluation and Management
The overall incidence of ocular injuries in association with facial fractures ranges from 7% to
40%.55,81,94-104 The most common problems are
hyphema and retinal hemorrhage,103 but corneal
laceration, choroidal rupture, retrobulbar and vitreous hemorrhage, retinal detachment, glaucoma,
angle recession, retinal tear, traumatic cataract, subluxation or rupture of the globe, and Marcus Gunn
pupil are occasional findings.85,100 Progressive retrobulbar pressure that goes undetected may lead
to visual loss. The classic symptoms of retrobulbar
blindness are pain, proptosis, and third nerve palsy
with gradual decrease in visual acuity.105
Clinical evaluation of the patient with an acute
orbital injury should include documentation of the
visual acuity as well as the status of the cornea,
conjunctiva, and sclera; the anterior chamber, iris,
and lens; and the posterior chamber, vitreous humor, and retina106,107 (Fig 14).
Gossman, Roberts, and Barr108 discuss the ophthalmic aspects of orbital trauma. In a prospective
review of 283 cases of facial fracture seen at their
facility, serious ocular injuries were noted in 12.5%
of orbital blowout fractures and 37.5% of
orbitozygomatic fractures. The authors evaluation of a patient with fracture of the orbit for the
possibility of ocular or optic nerve injury consists
of five points, and may be performed by nonophthalmologists without specialized equipment in
under 5 minutes. The assessment should take into
consideration visual acuity, pupillary reaction, anterior segment (conjunctiva, cornea, and anterior
chamber), posterior segment (iris, lens and capsule, vitreous, retina, and optic nerve), and ocular
motility. Urgent ophthalmic consultation is indi-
Fig 14. Checklist for evaluating the injured eye. (Reprinted with
permission from Barton FE Jr, Berry WL: Evaluation of the acutely
injured orbit. In: Aston SJ et al (eds), Third International
Symposium of Plastic and Reconstructive Surgery of the Eye
and Adnexa. Baltimore, Williams & Wilkins, 1982.)
cated in the event of decreased vision or other

abnormality except ocular motility disturbance. Subconjunctival hemorrhage, hyphema, and an oblong
pupil suggest ocular perforation, and globe rupture must be ruled out before undertaking repair
of orbital fractures.
Traumatic Optic Neuropathy
Traumatic optic neuropathy is a relatively
uncommon finding in facial trauma. When rupture
of the globe is excluded, the incidence of blindness associated with orbital fractures is reported to
be 2% to 2.4%.98,100,103 The cause of impaired
vision is thought to be either direct trauma to the
optic nerve itself109 or ischemia of the nerve from
increased pressure secondary to edema or hemorrhage.108,110 In addition, the operative reduction
itself may cause damage to the vision as a result of
the same mechanism.110-113
In patients with impaired vision, McCartney and
Char,114 Lipkin et al,115 and Rohrich and colleagues51
stress the importance of high-resolution CT scans
in identifying the cause of blindness. According to
Kallela and associates,116 the most common CT
finding in posttraumatic blindness is swelling of the
optic nerve, followed by fracture within the optic
canal. High-resolution CT scans should help to
identify these problems.
13
Once the diagnosis of traumatic optic neuropathy has been made, treatment is controversial. Most
authors agree that patients who lose their sight at
the moment of injury are not likely to recover it.
Those whose vision is progressively compromised
in the postinjury period stand the best chance of a
complete visual recovery. Wang and colleagues61
provide an excellent review of this subject as well
as their own clinical data. They point out that the
most definitive data would be provided by a prospective randomized trial; however, the only one
such designed, the International Optic Nerve
Trauma Study, was discontinued because of the
relatively small numbers involved.
Wang and colleagues61 evaluated a group of 61
consecutive patients presenting with visual loss following a facial trauma. They compared the three
commonly used treatment options: high-dose steroids, surgical intervention, and observation alone.
They found that patients who sustained penetrating facial trauma had poorer outcomes than patients
who had blunt trauma. Only 27% of patients who
had no light perception on initial presentation had
improved visual acuity after treatment, compared
with 100% of patients who had light perception or
better on admission. In addition, only 38% of
patients with orbital fractures had improvement,
while 83% of patients without orbital fractures
improved. These authors provide an algorithm for
management of traumatic optic neuropathy based
upon the degree of visual loss61 (Fig 15).
Fig 15. Algorithm for the management of traumatic optic

neuropathy. NLP, no light perception. LP, light perception.
(Reprinted with permission from Wang BH, Robertson BC,
Girotto JA, et al: Traumatic optic neuropathy: a review of 61
patients. Plast Reconstr Surg 107:1655, 2001.)
14
In all cases of traumatic optic neuropathy, these

authors recommend the use of megadose steroids.
Other authors117 have recommended that the steroid regimen consist of an initial intravenous loading dose of 30 mg/kg of methylprednisolone, followed in 2 hrs by 15 mg/kg every 6 hours.
In a separate study, Mine and associates118 evaluated 34 patients with traumatic optic neuropathy
and found that in patients who initially could perceive hand movements or better, vision improved
significantly more with surgery to decompress the
optic canal than without surgery. In patients whose
initial visual acuity was only light perception or
worse, surgery was less helpful.
Radiographic Evaluation
Plain radiographs are used by some practitioners as a screening test for orbital fractures. The
Waters view is probably the most useful among
the plain films. The most common radiographic
finding in patients with orbital floor fractures is opacification of the maxillary sinus, although many
patients with orbital fractures will not have this on
x-ray. Crikelair and colleagues119 evaluated 32
patients whose plain x-rays were read as blowout
fracture. Tomography confirmed the fracture in
only 17, and of these only four patients had significant pathology at the time of surgery. For this
reason, most surgeons feel that CT scanning is the
standard of care for diagnosis of all craniomaxillofacial
injuries. Its high degree of accuracy and its ability to
precisely characterize the fractures make it particularly desirable in orbital fractures.85,120-122
When evaluating the orbit specifically, it is preferable to obtain a CT scan with 1.5 mm cuts in both
the axial and coronal planes. The coronal sections
are best for accurately characterizing fractures of
the floor, roof, and medial wall;123 they also provide invaluable information regarding the status of
the extraocular muscles. Even in subtle, minimally
displaced orbital floor fractures, coronal CT scans
may reveal a rounding of the inferior rectus muscle
in cross-section that is indicative of an injury to the
floor secondary to edema and damage within the
muscle itself.124,125
Wachler and Holds126 describe two patients in
whom small blowout fractures were associated on
the CT scan with absence of the inferior rectus
muscle in multiple sections on the scan. At the
time of surgery the inferior rectus muscle was found

to be severely entrapped within the fracture site.
The standard CT scan can also be reformatted to
give oblique sagittal cuts. These are particularly useful
for gauging the proximity of the injury to the orbital
apex.127 They also may help the surgeon in better
determining the level of inclination of the floor, which
may facilitate dissection of the defect and placement
of the material to reconstruct the floor.
Yet another benefit of CT scanning for orbital
fractures may be in the determination of orbital
volume. As previously discussed, some investigators have found that increases in orbital volume as
determined by the CT scan may directly correlate
with the severity of a subsequent enophthalmos
that ensues.90 It is conceivable that a more widespread use of these volumetric measurements in
the future could provide a much more objective
approach to the decision to operate in those situations in which there is no visual disturbance, but
merely a floor defect. Currently many surgeons
will operate on floor defects 1 cm2 in diameter
although there is no objective evidence to support
this practice.
subtarsal, subciliary, and transconjunctival incisions.

Now primarily of historical interest, the CaldwellLuc approach was used extensively in the past. It
involved an incision in the upper gingivobuccal sulcus and a maxillary antrotomy. The floor was
approached from below, with the sinus frequently
packed with gauze or a balloon to elevate the floor.
This technique is not in general use today.
Of the most commonly used incisions, the
subtarsal approach gives the most direct access to
the orbital rim and floor (Fig 16). An incision is
made in a natural fold in the lower lid below the
tarsus, and dissection is carried through the orbicularis down to the level of the septum orbitale. This
is then dissected down to the level of the orbital
floor.
Treatment
The indications for operative management of
orbital fractures is the source of some controversy.
A survey of the American Society of Oculoplastic
and Reconstructive Surgery members128 revealed
that most of these surgeons favored exploration of
radiographically confirmed orbital floor fractures
when enophthalmos was >2 mm at any time during the first 6 weeks of injury, or if diplopia in the
primary fields of gaze did not clear within 2 weeks.
Diplopia that persisted beyond 2 weeks is most
likely the result of entrapment that can only be
resolved surgically. This can frequently be confirmed based upon the CT scan data or upon a
positive forced duction test.
Other indications for operative intervention include a large orbital floor defect (>1 cm2) or significant hypoglobus (an abnormally low vertical position of the globe).
Incisions
Numerous approaches to the orbit have been
suggested. Currently the most common are the
Fig 16. Subtarsal incision to reach the floor of the orbit.

(Reprinted with permission from Converse JM, Cole G, Smith B:
Late treatment of blow-out fracture of the floor of the orbit. A
case report. Plast Reconstr Surg 28:183, 1961.)
Bruising and ecchymosis to the surrounding tissues tend to be less with the subtarsal incision than
with some of the other techniques which require
more extensive dissection, and the scar is usually
quite acceptable.129
The subciliary incision was originally described
by Converse in 1944.130 The incision is placed in
the lower lid just below the lash line (Fig 17). The
skin and orbicularis are incised and the dissection
carried in the plane superficial to the septum orbitale
down to the orbital rim.
Manson and colleagues131 modified the subciliary
incision by extending it laterally below the lateral
canthal ligament. The lateral canthal complex is
mobilized to allow access to the lateral orbital wall
15
Fig 17. Extended subciliary incision with creation of a skinmuscle flap for access to the orbital floor and zygoma. (Reprinted with permission from Manson PN et al: Single eyelid
incision for exposure of the zygomatic bone and orbital reconstruction. Plast Reconstr Surg 79:120, 1987.)
and zygomaticofrontal suture, obviating the need

for an upper lid incision.
The transconjunctival approach begins by incising the conjunctiva below the tarsus of the lower
lid. The incision is carried through the lower lid
retractors and then into the plane between the
septum orbitale and the orbicularis oculi muscles
(Fig 18). The dissection is then carried in this plane
to the level of the orbital floor. A lateral canthotomy
improves the exposure.
Fig 18. Transconjunctival approach to the orbital floor. (Reprinted with permission from Appling WD, Patrinely JR, Salzer TA:
Transconjunctival approach vs subciliary skin-muscle flap approach for orbital fracture repair. Arch Otolaryngol Head Neck
Surg 119:1000, 1993.)
16
The transconjunctival incision has the advantage

that it does not create an external scar. The primary disadvantage of the transconjunctival
approach is the need for a lateral canthoplasty in
patients who have had a lateral canthotomy. Great
care must be taken to reaffix the lateral canthal
tendon to the inner aspect of the orbital rim periosteum at the same level as the contralateral lower
eyelid.
Perhaps the most important difference between
these incisions is the frequency of ectropion after
surgery they are associated with. Appling and
coworkers132 compared the results in 63 patients
undergoing orbital explorations through either a
subciliary incision or a transconjunctival incision.
The patients with transcutaneous incisions demonstrated a 12% rate of transient ectropion and a
28% rate of permanent scleral show. In contrast,
the transconjunctival approach resulted in no transient ectropion and a 3% rate of permanent scleral
show.
Grafts to the Orbit
Orbital floor fractures are unique in that, unlike
other facial fractures, they are not managed by
reduction and fixation of the fractured floor. Rather,
the general approach is to reconstruct the orbital
floor defect with bone or alloplast. Selection of
the appropriate material for each patient is discussed
more extensively below.
The success or failure of the reconstruction
hinges on anatomic placement of the implants
that is, the entire defect must be defined and the
implant placed to completely cover it. In defining
these defects, one must take into account the shape
of the orbital floor as it rises posteriorly. A common mistake is to dissect straight back into the
floor rather than up to the stable posterior ledge of
the defect. The elevator is inserted straight back
into the defect to the posterior wall or maxillary
sinus and moved superiorly until it reaches the
undersurface of the posterior, stable ledge of the
floor. The elevator is then moved anteriorly until
the edge of the defect is appreciated.
There are many proponents for the use of autogenous graft materials in reconstruction of the
orbital floor. Nguyen and Sullivan133 review the
indications for the various types of grafts. Advocates of autogenous grafts cite the increased risk
of infection associated with prosthetic materials.
On the other hand, the use of autogenous tissues
implies a donor site, which results in a longer
operative time, potential donor site morbidity, and
possible graft resorption.
The most popular graft material used in the floor
is autologous membranous bone,134 particularly split
cranium, due to its low rate of infection and resorption. Antonyshyn and colleagues135 report on the
superior results obtained with bone grafts in their
series. Other autogenous graft materials for the
orbital floor include cartilage,136-138 iliac bone,139,140
split rib,141 and fascia lata.142
If an alloplastic implant is chosen, it should provide good structural support, be nonreactive, well
tolerated by the surrounding tissue, and have a low
rate of infection. A large number of such implants
have been tried, including teflon,143,144 Supramyd,145
Silastic,146 Gelfilm,147 and numerous others. But
perhaps the most commonly used materials today
are titanium mesh and MedPor.
Metallic meshes have the advantage of strength
and ease of contouring, allowing the implant to be
customized to the shape of the floor and defect.
Sargent and Fulks148 examined the fate of 57 orbital
reconstructions with vitallium mesh. The authors
report no infection around the mesh and no cause
for removal of the implant after an average of 9
months. Glassman and associates149 report the
Johns Hopkins experience with titanium implants.
These authors utilize the implant as a support for
the bone graft or alloplastic material used to cover
the defect. Of 38 reconstructions, there were two
infections requiring removal of the implants and
drainage.
When evaluating these two series, the critical
difference is that Sargent and Fulks148 used metallic
mesh alone without bone graft material. Glassman
and colleagues149 used the mesh as a support for
bone graft material. Clearly metallic mesh alone is
safe and effective in reconstructing the orbital floor.
A bone graft would add little to a floor reconstruction, and may increase the risk of infection.
An alternative material for reconstruction of the
orbital floor is high density porous polyethylene
(MedPorPorX Surgical, College Park GA). These

implants are in common use for augmentation of
the facial skeleton and have now been designed
for placement in the floor. Choi et al150 report a
series of 25 orbital reconstructions with these
implants. Over a 31-month follow-up period there
were no cases of orbital infection, implant exposure, or loss of structural support. MedPor implants
are now even designed with channels through the
implant for placement of miniplates to stabilize the
reconstruction.
Complications
Associated with Alloplastic Implants
The chief concern regarding infection of
alloplastic implants for floor reconstruction stems
from their proximity to the maxillary antrum. A
review of the literature discloses that implants made
of teflon or silicone are at greatest risk of infection.151-153 Frequently there is some antecedent
event such as dental surgery or upper respiratory
infection that leads to bacteremia.154 Because
smooth-walled implants such as silicone and teflon
are surrounded by a pseudocapsule that prevents
vascular ingrowth, bacterial colonization of the
implant could be disastrous. Implants of high-density
porous polyethylene or coralline hydroxyapatite,
which allow vascular ingrowth, may be less susceptible to microbial invasion.
Implant extrusion may occur quite late: Brown
and Banks155 report three patients who had extrusion of silicone or teflon implants between 10 and
17 years after their initial surgery.
Persistent Diplopia
Diplopia occurring immediately after an orbital
fracture may be due to A, soft tissue entrapment by
the bone fragments; B, orbital hemorrhage or edema,
with increased intraorbital pressure; C, mechanical
restriction or contusion of one of the extraocular
muscles; or D, cranial nerve palsy. Diplopia following surgical repair may be secondary to inadequate
release of the original incarceration, reincarceration,
or adhesions to the reconstruction.
17
Biesman156 examined 54 patients who underwent repair of orbital floor fractures. Clinically significant diplopia, defined as double vision impairing
normal daily activities, was present preoperatively
in 86% and persisted for at least 6 months after
surgery in 37%. Diplopia that manifested only on
extreme up or down gaze was not included. The
majority of patients with persistent visual disturbances had combined medial wall and orbital floor
fractures. Of these, 86% had persistent postoperative diplopia.
A forced duction test should always be done
at the end of surgery for orbital floor reconstruction. When a patient presents with postoperative
diplopia, and a normal forced duction test is documented, the residual diplopia is probably not due
to a mechanical restriction and management
should generally be conservative. Diplopia due
to neurapraxia may take up to 6 months to
resolve.157 These patients should be followed in
conjunction with an ophthalmologist throughout
this period. If after this interval symptoms persist, corrective muscle surgery should be considered.
Persistent Enophthalmos
As discussed in the section on Malar Fractures,
enophthalmos following reconstruction for facial
trauma is usually the result of increased orbital
volume. Contributing factors may be fat atrophy, scar contracture, or loss of the supporting
ligaments.
Another factor contributing to postoperative
enophthalmos is the interval between the injury
and surgical correction. Dulley and Fells158 found
a 72% incidence of postoperative enophthalmos
when patients were treated 6 months or more
following the orbital trauma, compared with a
20% rate of enophthalmos when repair was performed within 14 days. In the late surgery group,
40% of patients needed additional eye muscle
or orbital surgery. The mechanism is thought to
be fibrosis or extraocular muscle contraction limiting correction of the anteroposterior position
of the eye. In these late cases, a preoperative
forward traction test should be performed81 (Fig
19).
18
Fig 19. Forward traction test. (Reprinted with permission from

From Converse JM et al: Orbital blow-out fractures: A 10-year
survey. Plast Reconstr Surg 39:20, 1967.)
Orbital implants may not bring about the desired

forward movement of the eye. Manson159 advocates complete dissection of the orbit with mobilization of the intraorbital soft tissues and reconstruction of the orbital volume with bone grafts.
Ectropion
Ectropion or retraction of the lower lid is typically due to a scar adhesion tethering the lid down
to the orbital rim. This frequently happens when
transcutaneous approaches to the orbital floor are
used, particularly the subciliary incision.132 A Frost
suture in the lid for 24 to 48 hours postoperatively
can help prevent this problem. This suture should
be placed far enough laterally to allow checks of
the vision in the affected eye without removing or
releasing the suture. The suture may be either
taped to the forehead or sutured to the skin posterior to the hairline.
Once ectropion is first noticed postoperatively,
the surgeon should engage the patient in a vigorous program of lower lid massage. The majority of
cases will resolve with this conservative management. If, however, after 4 to 6 months the problem
persists, a release of the scar, usually through a
transconjunctival approach, should be considered.
Earlier intervention should only be considered if
there is a risk of corneal exposure that is problematic and unresponsive to lubrication.
Superior Orbital Fissure and Orbital Apex

Syndrome
Rowe and Killey35 credit Hirschfeld with the first
description of the superior orbital fissure syndrome
(SOFS). The SOFS results from extension of the
fracture line into the superior orbital fissure, injuring cranial nerves III, IV, V1, and VI. This produces
ophthalmoplegia, upper lid ptosis, proptosis, a fixed
and dilated pupil, and a sensory disturbance over
the distribution of the ophthalmic division of the
trigeminal nerve, including loss of the corneal reflex.
The pupil is unresponsive to either direct or indirect light stimulation;160-163 there is, however, a consensual pupillary response in the unaffected eye,
indicating that the ipsilateral afferent arc is intact.
Conservative treatment is generally indicated unless
there is radiographic evidence of nerve compression.
The orbital apex syndrome (OAS) was first
described in 1945 by Kjoer.35 The OAS is essentially the same as the SOFS but without optic
nerve involvement (blindness). Most cases are
the result of ischemic optic neuropathy secondary to retrobulbar hemorrhage or direct trauma
to the optic nerve from extension of the fracture
into the optic foramen.84,164 When presenting
after the injury, these patients should be handled
as discussed in the section on traumatic optic
neuropathy.
Postoperative blindness may be due to multiple
causes, including impingement on the nerve by the
implant reconstruction, hematoma, or damage to
the optic nerve from fracture reduction. These
patients should be managed by urgent CT scanning and returned to the operating room.
Trapdoor Fractures
Orbital blowout fractures may occur in trapdoor
fashion, that is, the fracture pattern is incomplete
and at the time of impact results in an opening of
the floor that subsequently hinges closed again. In
the process, the periorbital soft tissues, including
the inferior rectus muscle, may become entrapped
in the fracture. This is more common in the pediatric population due to the higher incidence of greenstick fractures seen. Because of the soft tissue
incarceration, patients may exhibit bradycardia, nau-
sea, and syncopein other words, oculocardiac

reflex.65
These cases should be considered relative surgical emergencies due to the potential for
ischemic compromise of the inferior rectus. In
their series, Bansagi and Meyer165 found that early
surgical intervention resulted in more complete
return of ocular motility than if operation was
delayed for 2 weeks or longer from the time of
presentation.
BLOW-IN FRACTURES
Orbital blow-in fractures with decreased intraorbital volume and exophthalmos are much rarer than
fractures of the blowout type.166 Pure blow-in
fractures involve the roof, walls, or floor of the
orbit but not the orbital rim, whereas impure blowin fractures include the rim itself.167-172 Distinguishing clinical features are universal proptosis, diplopia (32%), upward displacement of the globe (28%),
restricted ocular motility (24%), rupture of the globe
(12%), superior orbital fissure syndrome (10%),
and occasional optic nerve injury.171
Because of the high risk of injury to the intraorbital contents, early recognition of blow-in fractures
and orbital decompression with reconstruction are
essential to prevent serious permanent complications.
ORBITAL ROOF FRACTURES

Fractures of the orbital roof are rare in all age
groups.172 In adults they are almost always seen
as a component of multiple facial trauma, commonly associated with fractures of the frontal sinus.
These patients present with supraorbital rim fractures, inferior dystopia, limitation of supraduction,
upper eyelid ptosis, and diplopia.172 Depending
on the degree of involvement of the extraocular
muscles and structures in the superior orbital fissure, paralysis of cranial nerves III, IV, and VI may
occur.173 All patients should have a CT scan as
well as ophthalmologic and neurosurgical consultation to rule out associated ocular and intracranial injuries.172
19
Early reduction of large, inferiorly displaced fractures through a combined intracranial and extracranial approach is recommended to prevent progressive herniation of the intracranial contents into the
orbit. This may lead to a pulsatile exophthalmos in
adults and a progressive inferior displacement of
the orbit in the growing child. In small children,
fractures of the orbital roof may occur as an isolated injury because the frontal sinus are not pneumatized until age 7 and cannot disperse the force
of a blow to the superior orbital rim.
NASAL FRACTURES
Nasal structural support can be divided into three
vaults. The upper vault consists of the nasal bones,
ethmoid, superior edge of the septum, and the
vomer. The middle vault comprises the upper lateral cartilages, the majority of the septum, and the
ascending process of the maxilla. The lower vault
contains the lower lateral cartilages and the inferior
edge of the septum.
A diagnostic classification proposed by Stranc
and Robertson174 distinguishes between nasal fractures resulting from a lateral blow and those resulting from a frontal impact. Frontal impact injuries
are further categorized according to the anteroposterior plane of injury. Frontal impact injuries
are more likely to result in significant injuries to the
septum which must be adjusted operatively. In
severe frontal injuries, the entire nasoorbitoethmoid
complex may be involved.
Although nasal x-rays are frequently ordered,
they are largely unnecessary. Nasal fractures should
be detected on physical exam, to include careful
intranasal exploration after shrinking the mucosa
with topical agents. This is particularly important
when examining the septum. Septal hematomas
contained beneath the mucoperichondrium should
be drained immediately due to the risk of long
term cartilage resorption and subsequent loss of
nasal support and saddle deformity.
While it has been reported that open reduction
of nasal fractures can improve the postoperative
results,175-178 most surgeons still approach the acute
nasal fracture in closed fashion, performing open
reduction only when external lacerations make it
possible. Ideally, nasal fractures are reduced in the
first 2 hours after trauma, before nasal swelling
20
becomes severe, but reduction can be successfully

performed anytime within the first 2 weeks of injury,
once swelling has subsided enough to allow visualization of the position of the nose. Local anesthetic alone may suffice, but some degree of intravenous sedation is helpful. The nose is packed
with pledgets containing 4% cocaine, both for
hemostasis and for anesthetic effect. Regional
blocks using lidocaine may also be indicated. A
blunt tipped elevator is be placed intranasally to
elevate any depressed fragments and to reposition
the septum. A headlight and nasal speculum are
useful to visualize the septum.
Rowe and Williams84 believe that the key to good
results in the treatment of a broken nose lies not in
the technique used, but in maintaining stability of
the fragments postreduction. If the elevated nasal
skeleton demonstrates a propensity for collapse
postreduction, packing the nose for several days
with antibiotic-impregnated gauze should be considered. An external nasal splint should always be
placed to help protect the nose from further trauma
for approximately 1 week, and intranasal splints
should also be considered if extensive septal
manipulation has been performed.
Patients undergoing closed reduction for nasal
injuries should always be counseled that subsequent open rhinoplasty may be necessary. In one
series of 107 fractured noses treated by closed
reduction,176 only 50% achieved normal breathing
and 70% looked grossly deviated.
NASOORBITOETHMOID
FRACTURES
Anatomy
The nasoorbitoethmoid complex is defined
anteriorly by the frontal process of the maxilla, the
nasal processes, and the spine of the frontal bone.
Laterally it consists of the lamina papyraceae and
lacrimal fossae, and inferiorly it is bound by the
lower border of the ethmoidal labyrinths (Fig 20).
The anterior and posterior ethmoidal foramina are
located along the upper portion of the lamina
papyraceae at their junction with the frontoethmoidal suture, and carry the vessels so often
torn during nasoorbitoethmoid (NOE) fractures.
Fig 21. Resistance of various parts of the facial skeleton to

fracture-producing forces. (Reprinted with permission from
Luce EA, Tubb TD, Moore AM: Review of 1,000 major facial
fractures and associated injuries. Plast Reconstr Surg 63:26, 1979.)
Fig 20. Anatomy of the nasoorbitoethmoid complex.
Anteriorly the medial orbital wall is formed by

the lamina papyraceae posterior to the lacrimal fossae. The thin bone in this region is in contrast with
the thick, heavy abutments of the nasal bone, frontal processes of the maxilla, and nasal processes of
the frontal bone. Posteriorly the medial orbital wall
is formed by the body of the sphenoid immediately
in front of the optic foramen.
Fractures of the nasoorbitoethmoid complex are
the result of a blow to the upper bridge of the
nose, such as occurs when the face hits the dashboard or steering wheel in an automobile accident.179 A traumatic force sufficient to fracture the
nasal bones usually also fractures the nasoethmoid
complex. The intraorbital area is particularly vulnerable to injury because the fragile framework
beneath179 can only resist a maximum compressive
force of 30 G180 (Fig 21).
Diagnosis
Patients with NOE fracture typically show a flat
nose and a swollen medial canthal region. Palpation of the dorsum of the nose may indicate significant loss of nasal support. Although telecanthus is
a prominent feature in many fractures, it may be
masked by the degree of swelling. Involvement of

the medial canthal tendon is demonstrated by grasping the lower eyelid with a forceps and displacing it
laterally: Inability to pull the lower lid taut indicates
the likely presence of medial canthal tendon disruption. If there is continuing doubt regarding the
stability of the medial canthal tendon, at the time of
operative intervention a large clamp may be inserted
intranasally to the region of the medial canthus and
the medial canthal region palpated externally while
pushing out with the clamp.
Intranasally, fractures of the septum are common, and a septal hematoma should be ruled out.
Any clear nasal drainage is suspected of being cerebrospinal fluid from a dural tear in the region of the
cribriform plate. A glucose test on the fluid can
determine its origin: A glucose level >30 mg is
indicative of cerebrospinal fluid. If confirmation is
needed, a drop of the fluid placed on a clear cloth
will produce a halo sign if it is CSF.
Classification
Gruss181,182 identified five types of NOE fracture,
ranging from isolated bony injuries of the
nasoorbitoethmoid area with little or no displacement, to extensively displaced NOE fractures with
bone loss. Perhaps the most useful classification of
NOE fractures was described by Markowitz and
colleagues.183 They classify NOE injuries into three
21
Fig 22. Classification of NOE fractures. A, Type I. B, Type II. C, Type III. See accompanying text for description. (Reprinted with
permission from Markowitz BL et al: Management of the medial canthal tendon in nasoethmoid orbital fractures: The importance of
the central fragment in classification and treatment. Plast Reconstr Surg 87:843, 1991.)
fracture patterns according to whether the central

segment is single (type I) or comminuted (type II)
and whether the attachment of the medial canthal
tendon is avulsed (type III) (Fig 22).
This classification is particularly useful to the surgeon because it helps guide the treatment. In type
I injuries, stabilization of the bone fragments suffices to correct the position of the medial canthus.
In some type II injuries and all type III injuries,
transnasal canthopexy is necessary.
Markowitz and others 184 review the UCLA
Medical Center experience with nasoorbitoethmoid fractures during a 4-year period in the
mid-1980s. Of 342 patients seen for acute fractures of the midface, 105 had NOE fractures, and
of these only 5 (4.8%) were classified as highenergy injuries. Typically there were fractures of
both orbits, zygomas, and nasoethmoid regions,
with lateral divergence of the orbitsthat is, traumatic teleorbitism. Three of these patients were
blind in both eyes.
Treatment
Surgical correction of NOE fractures should
be undertaken as soon as the patients general
condition permits. Open reduction and internal
fixation using a coronal incision is mandatory.181189
Visualization of the nasal radix and nasoorbitoethmoid complex is helped by releasing the soft
22
tissues of the coronal flap in the periorbital

region. Scoring the periosteum overlying the
nasal radix further releases the soft tissue envelope and improves access. Thorough dissection
of this area is necessary to accurately visualize
all the bone fragments for anatomic reduction.
Exposure using a transverse incision across the
root of the nose (Converse and Hogans open
sky approach) is no longer recommended.
Several landmarks help guide the dissection in
the NOE region. The frontonasal suture essentially indicates the level of the cribriform plate in
the majority of patients. One may follow this
suture posteriorly to help in identification of the
lacrimal fossa, which lies just below the suture
along the anteriormost aspect of the medial orbital
wall 190 (Fig 23). The medial canthal tendon
attaches on either side of the lacrimal fossa. During transnasal canthopexy, the canthal tendon
should be pulled to a point just behind the apex
of the lacrimal fossa.
Other useful landmarks in this region are the
anterior and posterior ethmoidal vessels located
along the frontoethmoidal suture 190 (Fig 24).
Transnasal procedures must be kept below the level
of these vessels, as they essentially mark the inferior limit of the cranial cavity. The posterior ethmoidal foramen lies in close proximity to the optic
canal, and dissection should end before reaching
this point.
Fig 23. Anatomical landmarks of the nasoorbital-ethmoid region. The frontonasal suture can be followed posteriorly to the lacrimal
fossa and ethmoid bone; the medial canthal tendon attaches on either side of the lacrimal fossa. During medial canthopexy, the tendon
should be reattached just behind the apex of the lacrimal fossa. (Reprinted with permission from Brady SM, McMann MA, Mazzoli
RA, et al: The diagnosis and management of orbital blowout fractures: update 2001. Am J Emerg Med 19:147, 2001.)
Fig 24. Anatomical landmarks of the nasoorbital-ethmoid region. The ethmoidal vessels emerge through the anterior and posterior
ethmoidal foramens along the frontoethmoidal suture. Dissection should be kept below the level of the vessels and away from the
optic nerveie, should go no farther than the posterior foramen. (Reprinted with permission from Brady SM, McMann MA, Mazzoli
RA, et al: The diagnosis and management of orbital blowout fractures: update 2001. Am J Emerg Med 19:147, 2001.)
23
Complications
Telecanthus
Residual telecanthus is secondary to inadequate
or delayed primary treatment of the NOE fracture. Posttraumatic telecanthus is characterized
by an increased intercanthal distance, flattening
of the nasal root, and frequently dysfunction of
the lacrimal system. The medial canthi are
rounded, with narrowing of the palpebral opening and epiphora. An epicanthal fold may also
be present. Although the normative values for
intercanthal distance have been well established
(approx. 33 to 34 mm in white males and 32 to
33 mm in white females191), lateralization of the
medial canthal tendon is perhaps best confirmed
by comparing it to the contralateral, uninjured
side. Secondary correction of telecanthus is
much less successful than accurate immediate
treatment.
Disruption of the Lacrimal System
Nasoorbitoethmoid fractures can disrupt the lacrimal apparatus either through avulsion of the
medial canthal tendon-orbicularis oculi muscle
pump or by direct obstruction of the lacrimal collecting ducts. Routine exploration of the canaliculi is not justified because the incidence of injury
to the lacrimal apparatus in NOE fractures is less
than 20%.192 In the event of persistent dacryocystitis or obstruction, a dacryocystorhinostomy or
conjunctivodacryocystorhinostomy can be performed. 188,193
FRONTAL SINUS FRACTURES

The frontal sinuses are prominently situated
above the root of the nose and are prone to fracture during high-velocity impact. If the sinuses are
large, the posterior wall usually remains intact
because the force is dispersed over a wide, pneumatized surface. In this case the dura is not exposed
even though the anterior wall can be severely comminuted. If the sinuses are small, however, the
posterior table absorbs much of the force of the
blow and usually fractures,194 in which case intracranial extension of the injury is reasonably certain.
24
Diagnosis
Signs of frontal sinus fracture may include a
depressed frontal region, CSF rhinorrhea, and
supraorbital nerve anesthesia. There are frequently
lacerations overlying the forehead. On CT exam
an air fluid level may be demonstrated within the
sinus. The proximity of the injury to the nasofrontal
drainage system should also be ascertained.
Treatment
Most nondisplaced linear fractures of the anterior table of the frontal sinus can be managed conservatively.193 Operative treatment is indicated in
cases of 1) displaced fractures of the anterior table
with contour depression;195-197 2) injury or obstruction of the nasofrontal duct;195-201 or 3) significantly
displaced fractures of the posterior table of the
skull201,202 (Fig 25).
Displaced anterior table fractures should be
reduced and stabilized with miniplates. As much
bone as possible should be saved to preserve forehead contour. If necessary, bone defects are
repaired with onlay grafts of the outer table of the
calvarium.203,204
In the event that involvement of the nasofrontal
duct is suspected, it should be carefully evaluated
at the time of surgery. This may involve more
widely opening the fracture defects in the anterior
table. Schmits and associates205 use a bayonet forceps to mark the perimeter of the sinus. One
prong of the forceps is placed inside the sinus at its
very edge, while the other prong lies outside on
the surface of the bone. Drill holes or other markings are made 2-3 mm proximal to the tip of the
forceps to outline the proposed osteotomy. This
is then cut with either a saw or a narrow sidecutting burr.
An alternative is to place an endoscopic light
source within the fracture site. With the room
lights turned down, the sinus will be more brightly
illluminated than the surrounding cranium and the
extent of the fracture and duct involvement clearly
seen.
The ostium of the nasofrontal duct is located
medially in the sinus floor. If duct patency is questionable, fluorescein or other dye should be instilled:
Passage of dye into the nose is verified by staining
of a sponge or cottonoid placed at the level of the
Fig 25. Algorithm for the management of frontal sinus fractures. (Reprinted with permission from Rohrich RJ, Hollier LH: Management
of frontal sinus fractures. Changing concepts. Clin Plast Surg 19(1):219, 1992.)
medial meatus. If no dye is noted, the nasofrontal

duct is considered to be disrupted or occluded,
and an indication that the sinus should be obliterated.
To properly obliterate the frontal sinus, all of the
mucosa within the sinus must be removed, otherwise it will continue to secrete and may produce a
mucocele. It is important to meticulously burr the
inside of the sinus to ensure that all small invaginations of mucosa are removed. The ostium of the
nasofrontal duct is then plugged with a section of
temporalis fascia obtained from the same field or
with an anteriorly based pericranial flap.
The material used to fill the sinus following plugging of the nasofrontal duct is highly controversial. Traditional methods include autologous
fat, 195,198,206-211 temporalis muscle, 202,212,213 or
bone.214-216 The sinus cavity may also be left empty

to fill via a process of spontaneous osteoneogenesis.217-220 Macbeth219 in 1954 first suggested relying on osteoneogenesis for the treatment of chronic frontal sinusitis. The frontal sinus
was opened through an osteoplastic flap,221,222 the
sinus mucosa extirpated, and the nasofrontal ducts
and sinuses allowed to occlude by new bone formation. Bosley220 later published the outcome of
this operation in 100 of Macbeths patients and
reported complete bony obliteration of the frontal
sinus in 93 patients.
In an experimental study on cats, Mickel, Rohrich,
and Robinson223 compared four techniques for frontal sinus obliteration: autogenous fat, muscle, bone,
and spontaneous osteoneogenesis. Although all
four methods produced adequate sinus oblitera-
25
tion, the authors believe that spontaneous

osteoneogenesis offers the additional benefit of
new bone formation without the morbidity of the
donor site.223-225
Although good results have been reported using
195,198,206-211
fat
or muscle202,212,213 for sinus obliteration, the viability of these graft materials in the long
term must be questioned. Keerl and associates226
studied the fat that was implanted into the frontal
sinus of 11 patients for obliteration of the cavity.
Postoperative MRI evaluation showed viable fat in
only 6 of the 11 patients 4 to 24 months later. In
the other 5 patients the fat had necrosed and had
been replaced by granulation tissue or connective
tissue. All patients were symptom-free without evidence of infection. (It should be remembered that
complications from frontal sinus fracture such as
mucocele or mucopyocele tend to occur years
after the initial trauma and surgery, and may not be
known to the primary surgeon.)
Sinus obliteration with hydroxyapatite227 or the
various calcium phosphate bone cements228 has
been reported. Mitigating against the widespread
use of synthetics are the risk of infection when
these materials are placed in communication with
the nasal cavity via the nasofrontal duct and the
relatively high cost.
Sinus obliteration is the standard treatment when
the patency of the nasofrontal duct is in question.
Nevertheless, the modern otolaryngologic literature reflects multiple attempts at sinus preservation
using stenting of the nasofrontal duct with tubing,
although primarily in treatment of chronic inflammatory sinusitis, not frontal sinus fractures.229,230
Amble and colleagues230 used silicone rubber sheeting to stent the nasofrontal duct at the time of
operation for chronic inflammatory frontal sinus
disease. Intranasal anterior ethmoidectomy is also
performed in these patients. No major complications were experienced. Over a period of 6-8
weeks the stents were removed. After an average
follow-up of 4 years, 96% of the patients were
asymptomatic.
There has been increasing interest lately in
endoscopic resection of the intranasal frontal sinus
floor to reestablish drainage of the frontal sinus.231,232
In Close and associates231 series of seven patients,
frontal sinusitis developed in only one after at least
3 months of follow-up; the other six patients
26
remained symptom-free after surgery. One CSF

leak was treated successfully by endoscopic means.
In the event of a CSF leak or when the posterior
wall is significantly displaced, the sinus should be
cranialized.233 In 1978 Donald and Bernstein234
described the cranialization procedure in which the
posterior sinus table is removed and the brain
allowed to expand anteriorly to fill the original sinus
space (Fig 26).
Fig 26. Cranialization of a frontal sinus fracture with comminution of the posterior wall. The posterior table is excised, the
nasofrontal duct is plugged with temporalis muscle, and the
anterior wall is reduced and stabilized with rigid fixation,
supplemented by bone grafting as necessary. (Reprinted with
permission from Luce EA: Frontal sinus fractures: Guidelines to
management. Plast Reconstr Surg 80:500, 1987.)
Cranialization is best accomplished through a

bifrontal craniotomy in conjunction with the neurosurgeon. All remnants of bone are removed from
the posterior wall and the mucosal lining is thoroughly excised by burring. As in obliteration, the
nasofrontal duct is plugged and a pericranial flap or
galea frontalis flap is used to separate the dura
from the sinus floor (Fig 27).
Pericranial or galeal flaps can also be used to
seal the nasofrontal duct and even to completely
obliterate the sinus cavity.235 Thaller and Donald236
describe harvesting pericranial flaps up to 10 x 14
cm by extending the posterior dissection. The flap
is folded upon itself like an accordion to seal off
the nasal cavity and obliterate the sinus.
Fig 27. A flap of pericranium is preserved and used to cover the

exposed dura in posterior table frontal sinus fractures. (Reprinted with permission from Rohrich RJ, Hollier LH: Management of frontal sinus fractures. Changing concepts. Clin Plast Surg
19(1):219, 1992.)
Complications
Complications of frontal sinus surgery can be
early or late.237 Early complications are defined as
those occurring within the first 6 months of surgery, and the most common is frontal sinusitis. The
presenting complaint is frontal headaches with or
without frontal sinus opacification on x-ray examination. Initially these patients should be treated
medically with decongestants and antibiotics,
reserving more aggressive intervention for persistent cases.
Another potential early complication is meningitis, which is fortunately rare after frontal sinus surgery. Freihofer203 reports only two cases of meningitis in 71 patients operated on for fractures of the
frontal sinus. Both patients were successfully
treated with antibiotics.
Late complications consist primarily of mucocele
and mucopyocele resulting from impaired drainage of the frontal sinus and residual mucosa that
continues to secrete. When infection occurs, it
tends to do so years after the initial injury.203
Untreated, the infectious process can extend
through the posterior table of the frontal sinus and
lead to brain abscess. Aggressive management by
sinus obliteration is mandatory in these cases.
Hardy and Montgomerys238 experience with
frontal sinus fractures consists of 250 cases. Most
patients had chronic frontal sinusitis that failed to
respond to conservative measures, and were
treated by the osteoplastic procedure with fat obliteration of the sinus. Four percent required sec-
ondary revision and 2.7% developed fat necrosis

and infection.
In Freihofers203 experience with 71 fractures of
the frontal sinus, early postoperative meningitis
developed in two patients. One mucopyocele of
the sinus with osteomyelitis of the frontal bone
was diagnosed 1 years after surgery. On surgical exploration, mucosal remnants were found to
be attached to the wall. The cavity was extensively
debrided, the affected bone was removed, and the
sinus was obliterated with cancellous grafts from
the iliac crest. Two-and-a-half years later, the patient
remained asymptomatic.
In Donalds233 series of 21 patients with frontal
sinus fractures who had cranialization, there were
five deaths, although none was directly related to
the frontal repair. The operative complication rate
was less than 5% and consisted primarily of transient CSF leak.
Manson, Crawley, and Hoopes239 reviewed the
postoperative results of 42 frontal cranioplasties
using wire mesh-methyl methacrylate (n=25) or
autogenous bone (n=17). Despite published
reports of high infection rates associated with acrylic
cranioplasties, the authors found that the choice of
reconstructive material did not affect the outcome.
Risk factors identified were timing of the procedure and cranial vault reconstruction in communication with previously infected ethmoid sinuses and
the nose. A history of previous bone infection
(62% of their series) and absence of the frontal
sinus were thought to increase the risk of
postcranioplasty infection, but statistical analysis of
the data could not confirm this suspicion.
THE FUTURE OF
FACIAL FRACTURE TREATMENT
Recent advances in hardware technology have
facilitated the management of facial fractures and
contributed to improved results of treatment.
Notable among them has been the development
of biodegradable plate fixation.240-251 Most of the
current biodegradable systems utilize a mixture of
polyglycolic acid (PGA) and polylactic acid (PLA).240
The PLA component is stronger and more resistant to degradation, while the PGA is absorbed
more rapidly.249-251 By altering the relative percent-
27
ages of these two components, plates of various

strengths and degradation characteristics can be
manufactured.
Despite multiple successful reports of absorbable plates and screws in fracture fixation,245-247,252,253
their acceptance is far from universal. The relative
benefits of biodegradability may be outweighed by
the ease of use of standard titanium systems. The
advantage of plate degradation is more obvious in
the pediatric population, particularly for cranial vault
remodeling procedures, but most drill holes for
resorbable systems still need to be tapped, increasing the surgical time.
A recent advance has been the development of
titanium screws that do not require predrilling.254
In addition to introducing an additional step, drilling
can cause thermal damage to the bone or the hole
may be overdrilled, resulting in a loose screw.254
Drill-free screws have a modified screw shaft and a
cutting flute that moves the bone fragments out of
the screw hole and away from the leading edge of
the screw.254 Despite the obvious advantages, these
screws are only useful in stable bone fragments.
Sufficient pressure must still be applied to the screw
to engage the bone cortex for drilling.
Yet another technologic breakthrough has been
the development of numerous bone substitutes.
Porous hydroxyapatite granules have been used
for years in the treatment of bone defects and to

correct problems with soft tissue contour.255 More
recently calcium phosphate-based pastes have been
developed that harden within 10 minutes of application.256 These bone cements provide a fast and
effective method for resurfacing bony contour
deformities or for filling small skeletal defects. Still
controversial is the degree to which these substances are incorporated into or replaced by the
native surrounding bone. More work will be necessary before the long term results achieved with
this material in the craniofacial skeleton can be
known for certain.
Perhaps the most exciting news in the management of facial trauma has been the development of
intraoperative CT scanning.257 The results of facial
fracture surgery depend on accurate anatomic
reduction of the bone fragments, which is currently
limited by the bulk of contrast CT scanners and
difficulty registering the CT findings to the patients
anatomy.258 The ability to radiographically image
the bone fragments at the time of surgery would
clearly facilitate fracture reduction. Another promising technology is the development of threedimensional intraoperative navigational systems that
use 3-D computer assisted imaging to locate anatomical points on the patients face and reference
them to preoperative CT scan data. 259 These
devices are currently undergoing clinical trials.
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34

Facial Fractures I Upper Two Thirds

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FACIAL FRACTURES I: UPPER TWO THIRDS

Larry Hollier MD and James Thornton MD

maxillary antrum; (c) nose; or (d) skin over the

SRPS Volume 9, Number 26

matic fractures, a technique that was subsequently

fact, the zygomatic bone itself is not fractured, but

SRPS Volume 9, Number 26

on globe position because the zygoma constitutes

This series typically includes a Waters view as well

SRPS Volume 9, Number 26

Fig 2. Temporal incision for reduction of

SRPS Volume 9, Number 26

ing sutures must not be tied too tightly to avoid

Fig 3. Common incisions for exposure of the zygoma. Upper

The zygomaticofrontal suture is usually accessed

information regarding the rest of the malar complex.

SRPS Volume 9, Number 26

frontozygomatic suture line. In our opinion, if plates

The treatment of enophthalmos depends on the

SRPS Volume 9, Number 26

Fig 5. Loss of orbital volume below the globe will produce

Fig 6. Correction of enophthalmos following malar fracture. A,

more thoroughly under Orbital Fractures, but clearly

SRPS Volume 9, Number 26

Typically when a diagnosis of optic neuropathy

and stomach.65 A patient who is noted to have

Seven bones make up the orbit: the frontal

SRPS Volume 9, Number 26

development of the face out from the relative

Fig 8. Above, The ptotic soft tissue is elevated and suspended

rare in adults because of the protection afforded

The inferior orbital wall is most vulnerable to

SRPS Volume 9, Number 26

sule. The superior sling is composed of Whitnalls

Fig 9. Suspensory apparatus of the eye.

Fig 10. Mechanism of injury of orbital blowout fractures. A,

Erling and colleagues74 reviewed multiple CT

SRPS Volume 9, Number 26

and a bone conduction mechanism are likely at

Fig 11. Mechanism of entrapment of intraorbital fat and fascia

Fig 12. Forced duction or traction test. (Reprinted with

Mechanical globe restriction may also be due

SRPS Volume 9, Number 26

Fig 13. Schematic of posttraumatic, enophthalmic orbital

displacement of the globe is possible only with

SRPS Volume 9, Number 26

intraorbital air mass can cause central retinal artery

cated in the event of decreased vision or other

SRPS Volume 9, Number 26

Fig 15. Algorithm for the management of traumatic optic

In all cases of traumatic optic neuropathy, these

SRPS Volume 9, Number 26

time of surgery the inferior rectus muscle was found

subtarsal, subciliary, and transconjunctival incisions.

Fig 16. Subtarsal incision to reach the floor of the orbit.

SRPS Volume 9, Number 26

and zygomaticofrontal suture, obviating the need

The transconjunctival incision has the advantage

SRPS Volume 9, Number 26

(MedPorPorX Surgical, College Park GA). These

SRPS Volume 9, Number 26

Fig 19. Forward traction test. (Reprinted with permission from

Orbital implants may not bring about the desired