The main long-term sequelae of orbital fractures are ophthalmic functional impairment and aesthetic deformity. Thus, it is important that ophthalmologists be familiar with the evaluation and management of blunt orbital trauma and orbital fractures.^1–3 In cases of more extensive injury to the craniofacial skeleton, the ophthalmologist will likely contribute to the care of the patient as part of a multidisciplinary medical team, including specialists in the area of otolaryngology, oral and maxillofacial surgery, plastic surgery, and neurosurgery.

The past 15 to 20 years have seen remarkable advances in the evaluation and treatment of orbital and craniofacial trauma, largely as a result of the improved ability to diagnosis the extent of craniofacial injury using computed tomography (CT).^1–6 This period has also witnessed the increased use of rigid internal fixation of craniofacial fractures, including many of those that involve the orbit.^6–10 This chapter will detail relevant applied orbital anatomy, classification and patterns of orbital fractures, mechanisms of injury, evaluation and treatment of orbital fractures, and associated complications.

The orbital roof is an extension of the supraorbital rim and can be considered part of the skull. The roof is composed predominantly of frontal bone separating the orbital contents from the anterior cranial fossa and the frontal sinus. The medial wall of the orbit is formed by the thin orbital plate of the ethmoid bone (lamina papyracea), which separates the orbit from the ethmoid sinus. The lacrimal sac fossa, composed of the lacrimal bone and frontal process of the maxilla, is located in the anterior aspect of the medial orbit and contains the lacrimal sac drainage apparatus. The nasolacrimal duct continues inferiorly through the medial portion of the maxilla via the nasolacrimal canal. Inferiorly, the medial portion of the floor is composed of the orbital aspect of the maxilla and overlies the maxillary sinus. The infraorbital groove runs through the orbital aspect of the maxillary bone, extending anteriorly from the inferior orbital fissure. Fractures of the orbit most commonly involve this portion of the orbital floor medial to the infraorbital groove. The more lateral aspect of the orbital floor is composed of somewhat thicker bone of the zygoma. The superior tip of the palatine bone also contributes to a small portion of the orbital floor posteriorly. The lateral wall of the orbit is composed of the zygoma (anteriorly) and the greater wing of the sphenoid (posteriorly), separating the orbit from the temporal fossa and middle cranial fossa, respectively. The superior orbital fissure lies between the roof and lateral wall of the orbit posteriorly and is formed by a gap between the greater and lesser wings of the sphenoid. The majority of the motor and sensory nerves to the eye and ocular adnexa pass through the superior orbital fissure. The zygomatic bone establishes not only the shape and contour of the inferior lateral orbital rim, but also the malar eminence (cheekbone). The zygoma has several important points of articulation with the orbit, including the zygomaticofrontal sutures (superolateral orbital rim), zygomaticomaxillary suture (inferior orbital rim), and a broad posterior attachment with the sphenoid bone. The zygomatic arch also articulates with the temporal bone at the zygomaticotemporal suture.

The bony confines of the orbit determine the potential orbital volume, which is filled by the eye and associated soft tissues. The bony orbit provides a framework for support of the ocular adnexal soft tissues, which include fibroadipose tissue (orbital fat), extraocular muscles, blood vessels, and the cranial nerves serving the eye (II through VI). The orbital fibroadipose tissue contains an elaborate connective-tissue “ligament” system, as described by Koornneef.^12,13 Fibrous tissues extend from the periosteum lining the orbit (periorbita) to the bulbar fascia (Tenon's capsule) and fascial sheaths of the extraocular muscles and their check ligaments. This diffuse connective tissue framework supports orbital structures and maximizes the function of the eye, particularly with regard to ocular motility. Restriction of ocular motility may thus occur if this connective-tissue system is compromised significantly by trauma, including entrapment within a fracture site.

The bony orbit also provides important support and attachments for the eyelids. The orbital septum extends from a condensation of periosteum at the orbital rim (arcus marginalis) to help form the intermediate connective tissue lamellae of the eyelids.¹⁴ The eyelids are further supported medially and laterally by canthal tendons, which have complex, firm attachments to the bony orbital rim.^15,16 The anatomy of the medial canthal tendon is intricately associated with the lacrimal drainage apparatus and attaches via an anterior crus to the anterior lacrimal crest and a posterior crus to the posterior lacrimal crest. The posterior attachment is particularly important for maintaining adequate eyelid-globe apposition.¹⁶ The lateral canthal tendon attaches to the zygoma just inside the lateral orbital rim at the lateral tubercle.¹⁵ Displacement of the orbital rims may thus cause distortion of the eyelids and palpebral aperture. This is particularly true in injuries to the nasoethmoid-orbital complex, which can produce telecanthus (widening of the intercanthal distance), as well as in zygomatico-orbital fractures, which can produce displacement (dystopia) of the lateral canthus.

Additional terms common to fracture nomenclature elsewhere in the body may also be used to describe orbital fractures. These terms include closed if the fracture is not associated with a violation of the integument (i.e., intact soft tissue and skin) versus open (or compound) if the fracture communicates with an overlying skin laceration. Displacement is used to describe the degree to which a segment of bone is spatially dislocated from its normal anatomic position. Comminution is used to describe the degree of fragmentation of the fracture. Displacement and comminution may be graded from nonexistent (nondisplaced, noncomminuted) or mild to severe. Occasionally a circular segment of the orbital wall may fracture and become displaced but remain attached on one side, producing a trap door fracture.

The degree of bony orbital disruption is frequently related to the amount of energy producing the injury. Manson has proposed a classification of facial fractures based on anatomic location and the pattern of comminution and displacement related to energy⁶:

  Low-energy orbital fractures: These demonstrate simple linear or circular blow-out fractures (or, less commonly, blow-in fractures) of one or two walls, typically the floor or medial wall (with no involvement of the orbital rim).
  Middle-energy orbital fractures: These typically involve at least two orbital walls, usually accompanied by fracture of the orbital rim. Usually these fractures do not involve the most posterior portion of the orbit.
  High-energy orbital fractures: These include extreme disruption of multiple segments of the orbital rim and orbital walls. Frequently these injuries are circumferential, with three or four walls of the internal orbit destroyed.

Orbital fractures can be classified further by the pattern of involvement with the contiguous facial skeleton. Fractures confined to the anatomic boundaries of the orbit per se are termed isolated fractures. Orbital fractures with significant involvement of the adjacent areas are named accordingly. Zygomatic fractures (also known as trimalar or tripod fractures) typically involve disruption of the zygoma at the zygomaticofrontal and zygomaticomaxillary sutures at the orbital rims and along the zygomatic arch and have variable orbital floor involvement. Many authors refer to such fractures as zygomatico-orbital (or similarly orbitozygomatic) fractures.²¹ Fractures of the nasoethmoid complex may frequently involve the orbit, these are referred to as nasoethmoid-orbital fractures. Le Fort fractures also deserve special mention. These complex fractures are divided into three categories (Fig. 2):

  Le Fort I: Low, transverse maxillary fractures that do not involve the orbit (in contrast to Le Fort II and III fractures, which may cause complex disruption of the orbit)
  Le Fort II: Fractures involve the nasoethmoid and maxillary bones with disruption of the inferior and medial orbital walls
  Le Fort III: Fractures extend from the nasoethmoid region across the orbit, involving the orbital floor and the medial and lateral walls

When bilateral and complete, Le Fort III fractures result in craniofacial disjunction in which the entire facial skeleton is completely disarticulated from the base of the skull.²²

  Hydraulic mechanism theory: Increased intraorbital hydraulic pressure is primarily responsible for orbital fracture.
  Bone conduction (buckling) theory: Bone conduction through the orbital rim directly to the orbital floor can result in isolated fracture of the orbital floor.

Isolated orbital blow-out fractures tend to occur when the orbit is struck at low velocity by objects that have a slightly greater diameter than that of the orbital aperture (e.g., baseballs, fists), the orbital floor being the location most typically involved. The relatively thin bone of the orbital floor tends to become displaced into the maxillary sinus due to the lack of resistance of the underlying air-filled space and to some extent the effects of gravity.

Smith and Regan's¹⁷ classic “hurling ball experiment” offered support for the hydraulic mechanism theory. Using a cadaver, they produced isolated internal orbital blow-out fractures by striking a hurling ball placed over the orbit when the soft tissues were intact. When the soft tissues were removed (by exenteration) and the opposite orbit was struck with a similar force, no orbital fractures were produced. When the striking force was sufficiently increased, the orbital floor and orbital rim collapsed simultaneously. Small, blunt objects of a diameter less than that of the bony orbit (e.g., golf balls, racquetballs) are generally believed to have a greater likelihood of rupturing the globe while leaving the orbital walls intact. Using an experimental primate model, however, Green and colleagues²⁴ demonstrated that relatively low energy forces applied to the eye alone can also produce orbital blow-out fractures, offering further support for the hydraulic mechanism theory. Others have shown that direct compression of the orbital rim alone may produce a transient buckling deformation of the walls of the orbit sufficient to produce isolated internal fractures without fracturing the orbital rim, supporting the bone conduction (buckling) theory.²⁵ Proponents of the bone conduction theory also suggest that this mechanism better explains the etiology of less commonly seen blow-in fractures, particularly those involving the orbital roof.

In reviewing these and other reports on the mechanisms of orbital fractures, it appears clear that the hydraulic mechanism and bone conduction theories are not necessarily mutually exclusive explanations of orbital blow-out fracture pathology. Both mechanisms may contribute to the production of orbital wall fractures, depending on the nature of injury. It is also clear that higher energy forces applied to the orbital skeleton are more likely to produce fractures of the orbital rims as well as the internal orbital walls. Higher energy injuries to the orbital and midfacial skeletal region are dissipated in characteristic fashion through a system of buttresses, which contribute the principle structural supports of the facial skeleton. Motor vehicle accidents, falls, sports/play accidents, and assaults compromise the most typical events producing orbital fractures. The pattern of orbital fractures also appears to be affected by growth patterns of the craniofacial skeleton.²⁶ The increased craniofacial ratio and lack of frontal sinus pneumatization of younger children, particularly those younger than 7 years of age may place the cranium at increased risk for injury relative to the proportionally smaller midface, and may in part explain the higher proportion of orbital roof fractures in younger children.^19,20,26 Continued development of the maxilla, with “unfolding” of the face from beneath the overhanging cranium with increasing age, subsequently exposes the face to increased risk of trauma. Intrinsic to this process is the remodeling of the elastic cancellous bone of the infant's face into the adult form of more compact, dense bony buttresses connected by thin and brittle membranous bony plates. Thus, the changing anatomy of the cranial and facial structures surrounding the orbit can contribute to a developmentally specific dissipation of impacting energy and a corresponding pattern of orbital and craniofacial fractures.²⁶

Orbital soft tissue injury and deformation also occurs with orbital trauma and (aside from injury to the globe) is responsible for the main sequelae of orbital blow-out fractures: enophthalmos and diplopia.^{1–3,27–30} Enophthalmos may be caused by multiple mechanisms, the most prominent of which is enlargement of the bony orbit (loss of bony support), particularly when more than 50% of the orbital floor is involved. Disruption of the orbital fibroadipose connective tissue system (musculofibrous ligament system) contributes to formation of posttraumatic enophthalmos due to displacement and change in the shape of orbital soft tissue.^27,28 The loss of bone and ligament support permits posterior displacement and reshaping of orbital soft tissues under the influence of gravity and the remodeling forces of fibrous scar contracture. It is clear that these soft tissue changes are not insignificant and that enophthalmos can worsen within a period of months in some patients.^4,28 Fat atrophy is believed to be a less frequent mechanism of enophthalmos. The soft tissue changes following orbital blow-out fracture are predominantly believed to be responsible for the relatively poor results obtained with late reconstruction versus early reconstruction. Diplopia due to incarceration of the extraocular muscles or surrounding fibroadipose connective tissue may also occur with orbital blow-out fractures. Additionally, direct injury to the muscle or its nerve supply within the orbit can also occur as a result of contusion and ischemia.^29–32

CLINICAL EXAMINATION

Evaluation of the patient with orbital trauma should proceed in a logical, defined manner.^1–3 Initial evaluation includes a determination of the extent of associated systemic and ocular (globe) injuries. Life-threatening injuries take highest priority, and initial management to ensure an adequate airway, ventilation, and circulation are essential. More extensive craniofacial injuries may be associated with neurologic damage of the brain or spine. In most cases, the initial patient assessment will have been completed by emergency room personnel and other specialists. If a high index of suspicion for globe injury is present, then the globe should be protected by a shield or similar device. A complete history should be obtained, including the mechanism of injury as well as whether there was any loss of consciousness or other sensory complaints such as decreased vision or diplopia. Assessment of the orbital injury should include as complete an eye examination as possible to assess the presence of rupture of the globe, traumatic optic neuropathy, or an evolving orbital compartment syndrome (i.e., dramatically increased intraorbital pressure secondary to orbital hemorrhage or edema). These conditions require emergent treatment. Assessment of visual function in the emergency setting includes pupillary reaction, visual acuity, and confrontation visual fields. Ideally, slit-lamp examination and dilated fundus examination are performed to assess the degree of injury to the globe. In many cases this may not be feasible because of the condition of the patient, forcing this portion of the ophthalmic examination to be deferred. In particular, pharmacologic pupil dilation (for examination of the fundus) must not be done if the patient has an unstable neurologic status requiring monitoring of pupil reaction. The presence of an afferent pupillary defect (Marcus Gunn pupil) is highly suggestive of traumatic optic neuropathy. If further clinical examination supports the diagnosis of traumatic optic neuropathy and no other contraindications exist, then treatment with megadoses of corticosteroids or optic canal decompression may be appropriate.² Further orbital evaluation includes an assessment of ocular motility, globe position, eyelid and canthal position, orbital rim palpation, and facial sensation. The face is also inspected and palpated for possible associated facial and nasal deformities. Malocclusion or difficulty opening the jaw may suggest the presence of zygomatic fracture or other more complex facial fracture. Cerebrospinal fluid rhinorrhea may also be noted in cases of injury to the nasoethmoid complex.

Ocular motility examination includes assessment of ocular alignment in primary position and eccentric gaze positions. Any limitation of ocular ductions is suggestive of entrapment (restriction) of the extraocular muscles or associated connective tissue. It is important to remember, however, that diplopia may be caused by any number of ocular motor abnormalities that may be present in the acute trauma setting, such as decompensation of a previous phoria or damage at any level of the central nervous system and peripheral motor unit. Within the orbit, damage to the soft tissues may produce orbital hemorrhage (subperiosteal hematoma or frank intraorbital hemorrhage) and edema. Rarely extraocular muscle laceration/avulsion may also occur. Orbital edema is invariably associated with injury to the orbital soft tissues; when severe, the edema may cause mechanical limitation of ocular movement. Blunt orbital trauma may also cause direct injury to the extraocular muscle or its immediate nerve supply, producing extraocular muscle weakness (paresis).

Some degree of head trauma may also accompany orbital injuries, and the potential for higher level disruption of ocular motility, such as cranial neuropathies or damage to cerebral or brainstem areas serving ocular motor function, should also be considered. The ocular motor examination should therefore be correlated with other clinical and radiologic findings. Forced duction and force-generation testing are certainly helpful in distinguishing ocular muscle restriction from paresis, with the caveat that in the early period after injury, orbital edema or hemorrhage may produce a mild to moderately positive forced duction test. Thus, forced duction testing is most useful when orbital edema has largely subsided. Saccadic velocities can also be helpful in differentiating restrictive from paretic etiologies,³² but such testing is frequently not feasible in the acute setting, and in most cases this determination can be made on the basis of clinical and radiologic findings alone. Patients with limitation of ocular motility subjectively experience binocular diplopia, provided vision is relatively intact in both eyes. In addition to objective measures of ocular motility, the severity (i.e., subjective complaint) of diplopia can be quantitated by determining the range or area of single binocular vision, measured in degrees. Quantitation of the field of single binocular vision can formally be done with a device such as a Goldmann perimeter, which is helpful for calculating the degree of visual impairment or disability. Clinically significant diplopia is usually considered to be diplopia within the central 30° of fixation. Diplopia in downgaze is considered to be more poorly tolerated. Of course, occupational and recreational considerations will determine what is significant for an individual patient.

The position of the globe is also assessed (Fig. 3). As detailed previously, outward expansion of the orbital walls (blow-out fractures) can produce enophthalmos. Inward expansion of the orbital walls (blow-in fractures) can reduce orbital volume, potentially producing exophthalmos. In the early period after blunt orbital trauma, orbital edema and hemorrhage can transiently increase the orbital soft tissue volume, producing exophthalmos or “masking” the underlying potential for enophthalmos. As orbital edema subsides, the true globe position becomes evident. Over a more extended period of time (several months), soft tissue changes (cicatrization and, less commonly, fat atrophy) may contribute to the production of late enophthalmos. Globe position can be grossly assessed by direct visual inspection. Viewing the axial projection of the globes from above (“bird's-eye view”) or from below (“worm's-eye view”) facilitates a gross determination of axial globe position.

Quantitative exophthalmometry is performed for formal measurement of the degree of axial globe malposition. A difference of greater than 2 mm is considered abnormal. Typically a difference equal to or greater than 3 mm is required to produce an obvious clinical difference between the two eyes, although preexisting lid and facial morphology (e.g., prominent dermatochalasis or eyebrows) may make the difference clinically less obvious and minimize disfigurement. It is important to note that standard Hertel exophthalmometry may not be accurate if the lateral orbital rim is disrupted. The globe may also be displaced in a nonaxial direction, generally toward the area of least resistance. Hypo-ophthalmos (i.e., downward displacement of the globe) associated with disruption of the orbital floor is the most common nonaxial type of displacement. Globe dystopia can be assessed by the relationship of the globe to the surrounding anatomic landmarks and the contralateral eye (if not involved by the injury). Typically with hypo-ophthalmos, the globe sinks downward and the inferior corneal limbus may drop below the lower eyelid margin, producing a “setting sun” appearance. Globe dystopia can be measured with a ruler, noting the distance and direction of globe displacement in millimeters. In extreme cases of orbital floor disruption, the globe may actually subluxate into the maxillary sinus.³³

Eyelid and canthal appearance may also be affected in numerous ways by blunt orbital trauma. Almost invariably, eyelid edema and ecchymosis is noted, in some cases sufficient to shut the eye completely, making examination difficult. Mechanical ptosis may also occur secondary to edema. Direct or indirect injury to the levator muscle or aponeurosis may also occur after blunt trauma. Eyelid lacerations are also common, varying from superficial to complex, depending on the nature of the injury. All eyelid lacerations should be examined and irrigated with saline, particularly if the wounds are contaminated. In some cases, the lacerations may facilitate approach for repair of orbital or other facial fractures. When eyelid lacerations involve the eyelid margin medial to the lacrimal puncta, injury to the canaliculus should be suspected and evaluated further by diagnostic lacrimal (canalicular) probing or irrigation. Displacement of the medial canthus may occur with soft tissue injury (laceration) or with fractures of the medial nasoethmoid-orbital region, which may result in telecanthus (widening of the distance between the medial canthi). Co-existent damage to the canaliculi, lacrimal sac, or other portions of the lacrimal system may be associated with such injuries. In rare cases of extreme orbital or craniofacial injury, traumatic hypertelorism (increase in the intraorbital distance) may occur as a result of disruption and lateral dislocation of the entire bony orbit or orbits. Lateral canthal displacement may also occur after soft tissue injury or fractures involving the lateral orbital rim. Most typically, inferior lateral canthal dystopia occurs with zygomatico-orbital (i.e., tripod or trimalar) fractures when the fracture segment is displaced and rotated inferiorly.

Examination should also include palpation of the bony orbital rims and periocular soft tissues. Crepitus (a crackling sound) on palpation is a sign of air trapped in the soft tissues (emphysema). Orbital and subcutaneous eyelid emphysema is most typically associated with fractures of the medial orbital walls, although communication with any of the perinasal sinuses may potentially allow air to dissect into the soft tissues. Usually the emphysema produces minimal complications, and the patient is simply instructed not to increase nasopharyngeal pressure (i.e., avoidance of nose blowing, sneezing, Valsalva maneuver). Occasionally the accumulation of air within the orbit can be sufficient to produce some mass effects that can potentially cause central retinal artery occlusion or compressive optic neuropathy and severe visual loss.³⁴ Extreme vision-threatening orbital emphysema may necessitate decompression by direct aspiration of the air pockets.

Palpation of the globe and orbital soft tissues directly can also be used to estimate the degree of resistance to retropulsion as a rough gauge of the intraorbital pressure or tension. This should be performed only if a ruptured globe has been ruled out. Intraorbital pressure can be increased as a result not only of air accumulation, but more typically of edema or hemorrhage, which may be sufficient to produce an orbital compartment syndrome. When the globe or optic nerve is compromised by increased orbital pressure, emergency measures are required to reduce orbital pressure, including lateral canthotomy/cantholysis and other adjunctive medical and surgical treatment.² As alluded to in the Classification section, inward displacement of portions of the orbital wall may also produce compression of vital ocular structures. Although inward displacement of the orbital roof is probably the most common location, inward displacement of the relatively thicker lateral wall of the orbit (zygoma) may potentially create the most serious damage to the globe and orbital soft tissues. In some cases, bony disruption and associated edema may be sufficient to produce optic nerve compression or superior orbital fissure syndrome, manifested by ipsilateral ptosis of the upper eyelid, proptosis, ophthalmoplegia, hypesthesia of the ophthalmic branch of the trigeminal nerve, and dilation/fixation of the pupil. In such cases, prompt reduction of inwardly displaced orbital fractures is indicated. Adjunctive high-dose corticosteroids can also be considered.³⁵

The bony orbital rims should also be palpated to detect the presence of any disruption (step-off). Frequently, point tenderness is noted at the fracture site. Edema can make detection of some smaller step-off fractures more difficult. Areas contiguous with the orbital margins may also be inspected and palpated if these areas are potentially involved by the injury. Zygomatico-orbital fractures may also cause malocclusion or pain with chewing (trismus), and the patient may have tenderness in the temperomandibular joint area. Finally, to assess the presence of facial hypesthesia, it is helpful to ask the patient whether he or she is subjectively aware of any decreased facial sensation or numbness. A gross test of facial sensation by light touch can be done, and the zone of hypesthesia can be mapped out. The zone of hypesthesia can provide clinical clues as to the fracture location.

RADIOLOGIC IMAGING

After the history and physical examination, consideration is given to further assessment of the orbital injury with radiologic imaging. The indications for radiologic imaging area are based on the physician's assessment of the injury and include gross orbital and facial deformity, limitation of ocular motility, and associated neurologic injuries. CT is the imaging modality of choice in the assessment of orbital/craniofacial fractures because it provides excellent detail of the bony injury as well as the orbital soft tissues in most cases (Fig. 4). Ideally, both axial and direct coronal views are preferred. Coronal views are necessary for adequate imaging of the orbital floor and orbital roof. With direct views, 3-mm views (cuts) are usually adequate. In cases in which the patients cannot be positioned for direct coronal imaging, coronal reconstructions can be performed, provided that finer (1.5-mm) axial cuts are used. Reconstructed coronal images lack the resolution of direct coronal images, but they are usually adequate when direct coronal imaging cannot be obtained. Spiral CT, which allows rapid imaging and multiplanar formatting, will likely become useful in the assessment of orbital trauma as this newer technology becomes increasingly available.

Craniofacial fractures can also be imaged with the use of three-dimensional (or, more accurately, pseudo-three-dimensional) reconstructions. Although three-dimensional reconstructions can provide a perspective that may help conceptualize the extent of the injury, they are not essential for treatment. Three-dimensional imaging has some disadvantages: besides entailing additional cost, time, and radiation, it obscures the intricate details of fracture anatomy in the middle orbit by summing individual images. This technique also provides no information regarding the relationship between bone and soft tissues, which is particularly important in the assessment of orbital injuries. Standard two-dimensional CT scans, however, adequately show the degree of orbital bony disruption as well as the associated orbital soft tissue changes, particularly the relationship of the extraocular muscles (and orbital connective tissues) with the fracture site.¹

Before CT scanning was readily available, facial x-ray series were used in the radiologic assessment of orbital fractures. Typical views included Caldwell's (anteroposterior) view, Waters' view, lateral view, and submental vertex view (particularly good for viewing the zygomatic arches). Waters' view, which is obtained with the chin slightly elevated, is considered the most useful x-ray view for imaging the orbital floor, inferior rim, and maxillary sinus. Because CT scans are superior to x-rays in terms of sensitivity and reliability, in most situations today plain orbital/facial x-rays are obtained only when a CT scan is unavailable or when only very minimal injury is suspected. Magnetic resonance imaging (MRI), although able to image orbital soft tissue exquisitely well with a small surface coil, is generally of limited usefulness in the initial assessment of orbital/craniofacial injuries because of its limited ability to image bone. It is contraindicated in cases of suspected retained ferromagnetic foreign bodies. MRI may have a secondary role in the management of orbital trauma in cases where CT scanning suggests the presence of soft tissue injury, such as intramuscular hemorrhage or sub-dural optic nerve sheath hemorrhage. In such cases, the better soft tissue resolution potentially available with MRI may allow more specific diagnostic interpretation.²

In summary, the goal of clinical and radiologic evaluation is to determine the location and severity of orbital fractures as well as associated fractures of other anatomic areas of the craniofacial skeleton. Considering the patient's risk of permanent aesthetic and functional impairment, this initial assessment constitutes the crucial basis upon which to formulate treatment recommendations.

Controversy has surrounded the management of orbital blow-out fractures. Throughout the past 50 years, opinions have ranged from suggestions that all orbital blow-out fractures should be repaired to the suggestion that none should be repaired primarily. The historical perspective on the management of blow-out fractures has been concisely summarized in a recent review.¹ With the improved assessment of orbital injuries afforded by CT scanning, greater consensus has developed regarding the indications for early surgery (i.e., surgery performed within the first 2 weeks after injury).^1,2 There is widespread agreement that early repair of blow-out fractures is indicated for the following:

Symptomatic, clinically significant diplopia with positive forced duction test and/or CT evidence of muscle entrapment showing no improvement over 1 to 2 weeks

  Early enophthalmos of at least 3 mm or significant hypo-ophthalmos
  A large (greater than 50%) orbital wall defect likely to produce late enophthalmos
  Associated displaced orbital rim or facial fractures

Observation (conservative treatment) is indicated for patients demonstrating the following:

  Minimal diplopia with good motility that shows evidence of clinical improvement over several weeks and no CT evidence of muscle entrapment
  Absence of significant clinical enophthalmos or hypo-ophthalmos and small orbital wall fractures that are not likely to produce late enophthalmos

Even with this general consensus, it is obvious that gray areas invariably occur. In such situations, informed discussion with the patient is particularly important regarding the relative merits and risks of primary surgical intervention versus a more protracted period of observation.

It is clear that as soon as appropriate indications for surgery are confirmed, it is appropriate to proceed. Early surgery is technically easier before soft tissue scarring and bony malunion progress. In cases with obvious clinical and CT evidence of frank muscle entrapment, expeditious repair is advised (within 48 hours if possible) to minimize ischemic muscle injury and fibrosis, which may otherwise limit final outcome. Similarly, in cases where early enophthalmos is clinically obvious, a large (greater than 50%) orbital blow-out fracture is noted on CT scan (which is likely to result in late enophthalmos), or displaced orbital rim fractures or more complex orbital/craniofacial fractures are present, surgery can be scheduled within several days after the injury if the patient is otherwise stable. Nonophthalmic indications for repair of orbital fractures involving other parts of the craniofacial skeleton include facial deformity, malocclusion or trismus due to bony impingement on the muscles of mastication, or an unstable facial skeleton (which can be seen with panfacial fractures). In such cases, the internal orbital fractures can be explored in the same operative setting when necessary. In cases of small or isolated blow-out fractures causing diplopia, but without frank extraocular muscle entrapment on CT scan, a period of observation (1 to 2 weeks) is appropriate, during which time serial examination and quantitation of diplopia and extraocular muscle limitation is performed. Forced duction and force-generation testing may be performed during this time to assess the etiology and severity of strabismus. However, the previously mentioned caveat holds: forced duction testing may be positive after the initial injury as a result of edema or hemorrhage, thus limiting the utility of this test early on. In this subset of patients, ocular motility is assessed more reliably after the orbital edema subsides.

Some authors have recommended a short course of corticosteroids to speed resolution of edema,³⁷ but this practice is not widely followed. A course of oral antibiotics (e.g., amoxicillin/clavulanate [Augmentin] or cefaclor) and nasal decongestants (e.g., pseudoephedrine) is recommended by some to minimize the risk of sinusitis. This is certainly most useful for those cases in which the maxillary sinus is completely opacified or when the patient is immunocompromised. During this period, all patients are instructed to refrain from strenuous activities and sports and to avoid nose-blowing, which may cause orbital emphysema. If restrictive strabismus causing diplopia or clinically significant enophthalmos or hypo-ophthalmos is noted after orbital edema subsides, it is preferable to proceed with surgery while one still has an early “window of opportunity.” The decision to perform surgery will obviously be based on the patient's functional and occupational needs and aesthetic concerns. Based on review of the literature, it is reasonable to tell the patient that diplopia will typically stay the same or improve with time, whereas enophthalmos will stay the same or worsen with time (i.e., 3 to 6 months). Although secondary orbital, eyelid, or strabismus surgery can be performed many months after the initial injury, there is widespread agreement that the results of such surgery are not as successful as primary orbital fracture repair.

SURGICAL REPAIR: OVERVIEW

The surgical approach to orbital fracture repair is dictated by anatomic location and severity of the orbital fractures and associated injuries. Most orbital fracture repairs are performed under general anesthesia. Isolated fractures of the internal orbit may be directly repaired, whereas fractures of the orbital rims should be repaired before those involving the internal orbit in order to establish proper spatial relations and provide anterior support. Orbital fractures are usually repaired in conjunction with other associated fractures of the craniofacial skeleton. Subperiosteal exposure is required for all fractures requiring repair.³⁸ The inferior and lower medial orbit can be approached via an eyelid incision (infraciliary or transconjunctival approach). In cases where additional exposure of the more superior medial orbit is required, this can be facilitated by extension of the conjunctival incision through the caruncle (taking care to avoid injury to the lacrimal apparatus and inferior oblique muscle) or through a skin incision (Lynch's incision) in the medial canthus. Exposure of the medial orbit may also be accomplished via a coronal approach. The lateral orbit can be exposed by extension of the lower eyelid incision (either transcutaneous or transconjunctival) into the lateral canthus. This incision is usually angled slightly inferiorly along a “crow's foot” pattern. Lateral cantholysis, which consists of lysis of the inferior crus (and occasionally also the superior crus) of the lateral canthal tendon, is helpful to improve exposure. Isolated exposure of a fracture at the zygomatico-frontal suture can also be performed via an upper eyelid crease incision or small incision paralleling the orbital rim. The superior orbit can be approached extracranially via an extended upper eyelid crease incision, an incision just below the eyebrow cilia or via a coronal approach. When necessary, the orbital roof may also be exposed intracranially (via craniotomy) with the assistance of a neurosurgeon. In complex orbital fractures involving the maxilla or zygoma, a buccal sulcus incision can be used to expose fractures involving the maxillary buttresses and lower nasoethmoid-orbital region, if necessary.

Internal Orbital Fractures

Internal orbital fractures may involve any wall of the orbit, but most typically they involve the orbital floor (79%) and medial wall (30%).³⁹ Repair of internal orbital fractures necessitates that they be completely exposed and that all herniated or entrapped orbital soft tissues be liberated. Reduction of displaced segments of the orbital walls is occasionally possible; however, because the walls of the internal orbit are thin and frequently comminuted, it is usually necessary to reconstruct the internal orbital defect with an orbital implant to prevent orbital volume deficiencies and recurrent herniation of the orbital soft tissues. The options for orbital implants include autogenous grafts (e.g., bone, cartilage, fascia) and alloplastic materials (either permanent or absorbable). The relative merits of these materials are widely debated.⁴⁰ Among autogenous implants, bone grafts are most typically used. These offer the advantage of excellent biocompatibility but require a second procedure to harvest the graft, with attendant donor-site morbidity and increased operating time. Variable resorption (or conversely graft take) may produce late undercorrection of enophthalmos/hypo-ophthalmos. The typical sites for harvesting bone grafts include the cranium, rib, and iliac crest. Cranial bone is favored by many because it is membranous bone and undergoes relatively less resorption than endochondral bone (e.g., rib, iliac crest). The anterior wall of the maxillary antrum is also a source of membranous bone, but the amount of bone available for grafting is limited to only about 1 × 1.5 cm in adults.

Numerous types of alloplastic implants are available for orbital reconstruction and can be categorized as nonporous, porous, and absorbable. Nonporous implants include metallic implants (usually composed of titanium or vitallium) such as miniplates, microplates, and grids or mesh. Additional nonporous orbital implants include silicone, Supramid, and Teflon, among many others. Recent interest has increased in the use of porous implants that allow fibrous ingrowth. Fibrovascular ingrowth has at least two potential advantages: (1) it anchors the implant to the surrounding orbital tissues, rendering the implant less likely to migrate or extrude; and (2) it is able to resist late infection. Commercially available porous orbital implants include hydroxyapatite and high-density porous polyethylene. Hydroxyapatite is hard and brittle, limiting its usefulness as an orbital floor implant. High-density polyethylene (Medpor) can be fabricated to be thin and malleable enough to be fitted into the orbit while still providing good structural support. Absorbable implants, such as Gelfilm and polygalactin (Vicryl) as well as newer compounds are also available for orbital fractures, but they are generally limited to smaller fractures that do not require a great deal of rigid support.

The advantages of alloplastic orbital implants include decreased operating time, lack of donor-site morbidity, absence of early resorption, and increased ease of handling and contouring. Complications associated with alloplastic implants have recently been reviewed and include infection and complications related to migration or extrusion. The exact incidence of such complications is difficult to determine, but overall it is believed to be low.⁴¹ Complications associated with orbital implants depend not just on the type of implant, but also on the surgical technique employed. Proper positioning and stable fixation of alloplastic orbital implants can be expected to decrease complications markedly.^41,42 Ultimately the choice of implant material is determined by the experience of the surgeon.

ORBITAL BLOW-OUT FRACTURE. Repair of the typical orbital blow-out fracture involving the orbital floor (with or without involvement of the lower medial wall) proceeds as follows. Forced-duction testing is performed immediately before the start of surgery to assess the degree of restriction. The inferior orbital rim can be approached via a transcutaneous eyelid incision placed just below the eyelashes (infraciliary), the lower eyelid crease, or the orbital margin. In these cases, dissection proceeds in a submuscular plane, just anterior to the orbital septum down to the inferior orbital rim. Alternatively, a transconjunctival approach may be used. This approach is believed to reduce the risk of postoperative eyelid retraction or ectropion.^43,44 If a transconjunctival approach is used, it is helpful to perform a lateral canthotomy and cantholysis to improve exposure. The incision through the conjunctiva and lower lid retractors can be made through the deeper fornix, going through the orbital fat to the inferior orbital rim. Alternatively, an incision can be made through the conjunctiva and lower lid retractors approximately 3 to 4 mm below the inferior tarsal border, continuing the dissection in a plane anterior to the orbital septum down to the orbital rim. This latter approach has the advantage of minimizing fat prolapse into the field.

Once the inferior orbital rim is reached, an incision is made in the periosteum with a scalpel or sharp edge of a periosteal elevator. It is important that this periosteal incision remain at the edge of the orbital rim rather than deviating posteriorly, particularly near the medial aspect of the inferior orbital rim where the inferior oblique muscle is located. Once the periosteum is incised, it can then be bluntly elevated with the periosteal elevator extending the dissection in a sweeping fashion more posteriorly to expose the anterior edge of the fracture. It is helpful to expose as much of the more anterior portion of the fracture as possible before attempting to extract the orbital soft tissues from within the fracture itself. The orbital soft tissues should be handled with blunt dissection and gently removed from within the fracture using blunt periosteal elevators and malleable retractors in a hand-over-hand technique (Fig. 5). In some cases, fibrosis (occurring even within 1 to 2 weeks after injury) can make release of the entrapped orbital soft tissues difficult. The temptation to use sharp dissection should be avoided, however. In some cases, it is helpful to remove a small amount of the more anterior orbital floor using rongeurs to allow better leverage to get beneath and elevate the prolapsed tissues.

The location of the infraorbital neurovascular bundle should be determined during the course of dissection. The typical blow-out fracture is usually medial to the course of the infraorbital neurovascular bundle. The neurovascular bundle can be seen as a faint shadow extending beneath the thin bone of the orbital floor, or it may be directly visible within the fracture. A small blood vessel is frequently seen extending superiorly from the infraorbital artery into the orbit. It is frequently necessary to lyse this small branch during dissection. The infraorbital neurovascular bundle itself should be preserved. In some cases, the orbital soft tissues are adherent to the infraorbital neurovascular bundle, and they must be gently teased off in order to reposit the tissues and allow placement of an orbital implant. The entire 360° perimeter of the fracture should be exposed and all prolapsed tissue replaced back into the orbit. It is particularly important that the posterior extent of the fracture be established. Usually the more posterior bone of the orbital floor remains intact. This posterior ledge can be used to support the orbital implant.

Once all entrapped tissues are released and the fracture site has been completely isolated, a decision is made regarding placement of an orbital implant. If the fracture is relatively small, no orbital implant may be needed once the entrapped tissues are released. Alternatively, a thin, absorbable implant (e.g., Gelfilm) may be placed over the small fracture site as an added precaution against recurrent entrapment. For larger defects, an autogenous graft or alloplastic implant is necessary. The implant must be sufficiently sized to bridge the entire defect on all sides, and it must be able to support the orbital soft tissues. If the implant is sufficiently malleable, it can be contoured for optimal coverage of the defect and reconstitution of the orbital shape. After the orbital implant is placed, forced-duction testing should be repeated to ensure that all entrapment has been released.

The implant should be well supported and stable to prevent migration or slippage, which can result in undercorrection of enophthalmos or other sequelae related to orbital implant malposition. Fixation of the orbital implant to an intact orbital rim by various means can reduce the potential for implant migration and takes little additional operating time. Methods to secure the implant include gluing, placing a “tab” at the anterior edge (for thin, synthetic implants), or direct fixation to the rim with a suture, wire, screws, or miniplates. Direct fixation is probably the most reliable technique. To fixate the implant with a suture or wire, two holes are drilled through the inferior orbital rim, and then the suture or wire is passed in a mattress fashion through two corresponding holes placed in the implant and tied. The knot should be placed in a location where it will not be palpable or irritate the globe. Usually the knot can be buried near the junction between the implant and the orbital floor. The orbital implant may also be secured relatively easily with metallic screws (from a miniplate or microplate set; see Orbital Rim Fractures section), placed through the implant just inside the orbital rim (see Fig. 5). It is important that the implant not project anteriorly past the orbital rim so that it will not be palpable. Synthetic implants and bone grafts of sufficient thickness and tensile strength can also be secured with a miniplate cantilevered over the orbital rim and into the internal orbit. This technique of fixation can be particularly helpful for large internal fractures, where the miniplate provides additional support and rigid fixation.

When more extensive disruption of two or more walls is present within the internal orbit, rigid fixation is essential. Metallic grids or mesh implants are available, which can be custom shaped to span a large portion or the entire defect and then fixed to the orbital rim (Fig. 6). This type of implant can then be used as a platform for additional alloplastic implants or bone grafts to augment the internal orbital reconstruction and volume. Many surgeons routinely place a bone graft or other implant over these metallic grid or mesh implants, whereas others report that placement of the metallic orbital implant alone can be successful. After the orbital implant is secured, the periosteum is closed. After this, the eyelid incisions (either conjunctival or transcutaneous) are closed, usually in a single layer. It is important to avoid catching the orbital septum in the closure because this places the patient at risk of postoperative lower eyelid malposition. If a lateral canthotomy and cantholysis has been performed, the lateral canthus should be reconstituted by aligning the natural eyelid margin landmarks (lash line). The lateral canthal tendon may be reapproximated with absorbable suture (e.g., 5-0 Vicryl) just inside the lateral rim to the periosteum. Care should be taken to avoid overtightening this lateral canthal suture or placing the suture too anteriorly, which can result in an unnatural, acutely angled appearance.

Postoperative care includes light (or no) dressings and ice, as tolerated, for 12 to 24 hours after surgery. If a synthetic orbital implant is used, prophylactic antibiotics (e.g., IV cefazolin [Ancef]) are given perioperatively and a course of oral antibiotics (e.g., Augmentin, cefaclor) can be continued for 7 to 10 days after surgery. Pressure patching of the operative eye is avoided during the immediate postoperative period so that any change in the orbital status can be detected (e.g., visual loss, orbital hemorrhage). The patient should be instructed to contact the physician should they notice any such signs. A transient increase in orbital edema as a result of surgery can be expected in the immediate postoperative period. Some generalized limitation of ocular motility can be expected when orbital edema is prominent. In the absence of any contraindications, some surgeons advocate the use of parenteral or oral corticosteroids perioperatively in order to minimize postoperative edema. The postoperative result is appreciated after resolution of edema (Fig. 7).

Orbital Rim Fractures

Orbital rim fractures occur with various degrees of displacement and comminution, typically proportional to the direction and energy of the impact. Extensive orbital rim fractures almost invariably include damage to the internal walls of the orbit. Reduction and fixation of unstable orbital rim fractures should precede repair of the internal orbit. The aim of orbital reconstruction is to restore normal orbital anatomy by accurately repositioning the displaced fracture segments followed by stable fixation.^1–3,38,39 The orbital rims determine the circumference of the orbital aperture and provide a supportive anterior framework for the walls of the orbit as well as the attachment of the canthal tendons. Although repair of isolated nondisplaced rim fractures is not required, open reduction with fixation is indicated for rim fractures with significant displacement, comminution, or bone loss. Orbital rim fractures may be a component of a more complex craniofacial fracture pattern, including nasoethmoid orbital fractures,^45–47 zygomatico-orbital (tripod or trimalar fractures),^48–54 cra-nio-fron-tal fractures and maxillary fractures including Le Fort II and III fractures (see Classification section).^38,39 When multiple orbital rims are disrupted, the order of reconstruction depends on the nature of associated craniofacial fractures. When severe panfacial fractures are present, the order of repair in the orbital region (after reduction and fixation of the lower face and mandible) generally begins superiorly with the cranial base/frontal region (which includes the superior orbital rim and orbital roof), followed by reconstruction of the medial nasoethmoid-orbital region and the lateral orbit/zygoma, followed by repair of the inferior orbital rim and maxillary buttresses. Because these repairs frequently involve a multidisciplinary team, it is essential that a clear surgical plan be established beforehand, including the order in which repair of the involved anatomic regions will proceed.

Methods of stabilization include interosseous wiring and miniplate fixation. Interosseous wiring is generally sufficient for repair of isolated orbital fractures resulting from low-energy injuries. Higher energy injuries, which result in multiple orbital rim fractures and comminution, benefit from rigid miniplate fixation to maintain a stable three-dimensional reconstruction and improve osteosynthesis (Figs. 8, 9, and 10). Miniplate fixation allows bridging of areas of extensive comminution. Miniplates come in various sizes (i.e., plate thickness [“profile”] and screw size) and shape. Miniplates generally have a profile of at least 1 mm and utilize screws equal to or greater than 1.5 mm, whereas microplates have profiles on the order of 0.5 mm and screw sizes of approximately 1 mm. Plates and screws of intermediate size are also available, and these appear to be ideal for orbital reconstruction. Most miniplates (and screws) are composed of corrosion-resistant metals, such as titanium or vitallium (an alloy of cobalt, chromium, and molybdenum). Because these metals are nonmagnetic, postoperative MRI is not contraindicated after reconstruction with these materials. These materials do produce some artifact on CT scan; however, this artifact is less than that noted with stainless steel, with titanium having the least artifact.

The general application of these devices is relatively straightforward. Reduction and alignment of the displaced bone fragments is performed first. In some cases, particularly when multiple fracture sites are present within a given anatomic region, initial alignment using interosseous wiring may be helpful to link the segments together before the miniplates are applied. A miniplate is then sized and contoured to span the fracture. Using special instruments provided in the set, the miniplate can be customized to fit. The miniplate should be placed in such a manner that will be virtually impalpable while still affording stable alignment and fixation. With the typical straight or curved miniplate, at least two screws are placed on either side of the fracture line to prevent late rotation of the fracture segments. Low-speed drills with continuous cooling are used to minimize bony necrosis. Most sets now supply self-taping screws. Emergency screws, which have a slightly larger diameter shaft, are available if stripping occurs during placement of the standard screw. Miniplates have revolutionized the management of orbital/craniofacial fractures, but it is important to remember that they are alloplastic devices and may be associated with complications such as infection, soft tissue irritation, and exposure. Fortunately these complications appear to be relatively uncommon in the orbital region. The following sections include special considerations that apply to the management of specific regional orbital rim fractures.

SUPERIOR ORBITAL RIM. The superior orbital rim is contiguous with the frontal bone and cranium. This portion of the cranium is divided into a central (frontal sinus) area and two lateral (frontotemporal orbital) areas. Most fractures involving the superior orbital rim and frontal skull are linear fractures with little displacement.^{18–20,38,39} Extensive frontal bone injuries usually produce stellate fracture patterns extending within one or two areas of the frontal portion of the skull frequently involving the superior orbit. Open reduction and stabilization is required for these displaced fractures. Rigid fixation of the supraorbital regions (“frontal bar”) stabilizes forehead projection. The temporal bones and anterior cranial base can be used to confirm anatomic alignment in cases of more extensive fractures. Usually a single curved miniplate can be used to repair a fracture of the superior orbital rim itself. Bony defects are repaired with placement of carefully contoured bone grafts.

Fractures in this region may involve the frontal sinus, including the anterior or posterior wall, or both. Simple fractures of the anterior wall can be managed by direct reduction and fixation with preservation of the sinus. Fractures involving the posterior wall and nasofrontal duct require a more complex repair. The potential for dural laceration in displaced posterior wall fractures necessitates either obliteration or cranialization of the frontal sinus, usually with the assistance of a neurosurgeon or otolaryngologist.

Severe disruption of the orbital roof requires stabilization with bone grafts or alloplastic implants with rigid intracranial fixation to the frontal bar. Reconstruction of the superorbital rim (frontal bar) establishes the proper width of the orbit as well as a stable reference point for realignment of the nasal ethmoid and lateral orbit in the case of more extensive upper midfacial and panfacial fractures. When exposing the superior orbital rim and orbital roof, caution should be observed medially to avoid injury to the trochlea and the supraorbital neurovascular bundle.

MEDIAL ORBITAL RIM (NASOETHMOID-ORBITAL REGION). The bones of the medial orbital rim represent the lateral aspect of the nasoethmoid complex, and fractures of the medial orbital rim are most typically the component of a more generalized nasoethmoid orbital injury. Nasoethmoid orbital fractures may be isolated or associated with other more extensive craniofacial fractures (e.g., Le Fort II and III). Successful management of nasoethmoid orbital injury requires consideration of both the bony and soft tissue injury.^{38,39,45–47} The most important soft tissue structure in the nasoethmoid-orbital region is the medial canthal tendon. The medial canthal tendon has medial and posterior insertions to the anterior and posterior lacrimal crest in the anterior portion of the medial orbit.¹⁶ Disruption of the medial canthal tendon or the bony segment containing the insertion of the medial canthal tendon can result in telecanthus. Because the lacrimal drainage system is closely tied with this area, it is at risk for injury from the original trauma as well as during surgical repair.

Nasoethmoid orbital injuries may also be associated with fracture extension into the anterior cranial fossa (adjacent to the cribriform plate), which may result in cerebrospinal fluid rhinorrhea, pneumocephalus, olfactory nerve disruption, and potential frontal lobe injury. Markowitz and colleagues⁴⁵ have proposed a classification scheme for nasoethmoid orbital fractures that is related to the condition and position of what they term the central fragment (the portion of the frontal process of the maxilla providing the bony insertion of the medial canthal tendon). Three types of fractures are outlined:

  Type 1: A nasoethmoid orbital fracture that results in the central fragment's being fractured as a single segment (either nondisplaced or displaced)
  Type 2: A fracture involving comminution of the bony central fragment, but not involving insertion of the medial canthal tendon
  Type 3: A fracture involving comminution of the central fragment extending through the insertion of the medial canthal tendon

Reconstruction is based on the degree of disruption of the central fragment of the medial orbital rim. Displaced type 1 injuries can be repaired by direct reduction and fixation of the central fragment using microplates or miniplates, with superior fixation to the frontal bone, and inferior fixation to the adjacent inferior orbital rim/maxillary buttress. It is important that the medial canthal tendon be left attached to the central fragment; thus, subperiosteal dissection underlying the medial canthal tendon insertion is avoided.

Type 2 fractures, because of bony comminution, generally require transnasal wiring to stabilize the central fracture segment containing the medial canthal tendon and to minimize the risk of postoperative telecanthus. The canthal tendon-bearing portion of the central fragment is isolated by subperiosteal dissection, except for the area of medial canthal tendon insertion, which is not detached. Transnasal (28-gauge) wires are passed through drill holes placed superior and posterior to the lacrimal fossa (and medial canthal tendon) and on the central fragment. These wires are then passed across the nose in a trans-septal fashion. If a bilateral nasoethmoid fracture is present, the two central fragments can be linked together. With unilateral fractures, the transnasal wire extends to the intact contralateral nasal dorsal bone. All other nasal and orbital bone segments are first linked by wires and then fixed to the frontal bone and inferior orbital rim/maxillary buttress with junctional plate and screw fixation. Tightening of the transnasal wires produces central fragment reduction and creates proper intercanthal dimensions. The intercanthal soft tissue distance is rarely overcorrected, and it is more frequently undercorrected. Therefore, transnasal reduction should deliberately minimize the bony interorbital distance between the medial orbital rims to obtain a satisfactory result.

Type 3 comminuted fractures rarely avulse the medial canthal tendon; however, the central fragment is frequently too small in such fractures to utilize in reconstruction. In such cases, the medial canthal tendon is detached and transnasal reduction of the medial orbital rim segments is performed, followed by direct transnasal wiring of the medial canthal tendon itself. The medial canthal tendon may be attached to the transnasal wire with a smaller permanent monofilament or braided suture. It is important to pass the transnasal wire posterior and slightly superior to the lacrimal sac fossa in order to achieve proper eyelid-globe apposition and impart a natural appearance to the medial canthus. Care should be taken to preserve the lacrimal system during transnasal wiring; this can be facilitated by placement of lacrimal probes within the canaliculi.

Other techniques for securing the medial canthal tendon in the setting of nasoethmoid orbital fractures have been described. Shore and associates⁴⁷ described repair of telecanthus using a miniplate cantilevered from the lateral aspect of the nose and directed posteriorly into the orbit to provide a stable fixation point for the medial canthal tendon. This technique is probably most applicable for cases of unilateral traumatic telecanthus, in which poor bony support for transnasal wires is suggested on preoperative CT. After fracture reduction with transnasal wiring or medial canthal tendon fixation, soft padded nasal bolsters may be placed to help minimize edema and hematoma as well as to adapt the skin to the nasal bones. Although these external bolsters play no role in the reduction or stabilization of the medial orbital rims, some authors believe they may help mold the bones of the nose and may minimize the scarring and thickening of the medial canthal tissues. These bolsters are secured with an additional transnasal wire, which is removed 7 to 10 days after surgery. Adequate aesthetic repair of extensive fractures in this region can be challenging.

LATERAL ORBITAL RIM (ZYGOMATICO-ORBITAL). The lateral orbital rim is composed primary of zygomatic bone. The large zygomatic bone (zygoma) also establishes the malar projection and midfacial width, thus playing a prominent role in facial aesthetics. The zygoma has articulations with the temporal, frontal, maxillary, and sphenoid bones oriented in three different planes. Isolated lateral rim fractures are uncommon, more typically occurring with disruption of the zygoma as a unit.^48–54 As previously noted, various names have been used to describe zygomatic bone fracture, including “tripod” and “trimalar” fracture. More recently there has been a trend to refer to such fractures as zygomatico-orbital fractures (or conversely “orbitozygomatic” fractures), which more accurately reflects the prominent orbital component of such fractures.⁴⁸ Indeed, the main sequelae of zygomatico-orbital fractures are ophthalmic in nature and include enophthalmos, diplopia, infraorbital nerve dysfunction, and lateral canthal dystopia.

In the pathogenesis of a zygomatico-orbital fracture, disruption occurs with various degrees of displacement at each of the articulations of the zygomatic bone. Unlike other portions of the orbit, significant dynamic forces act on the zygoma, primarily due to the masseter and to a lesser extent the temporalis muscle. Significant displacement of the zygomatic segment of the orbit can occur. The zygoma may be rotated inwardly toward the orbit, causing direct damage or functional impairment of the globe, extraocular muscles, or optic nerve. More typically, however, it rotates outward, creating orbital volume expansion and the potential for enophthalmos.

Classification schemes focusing on the different possible anatomic positions (rotations) of the displaced zygoma have been described, but these have not proved particularly helpful for guiding fracture management.⁵¹ A classification scheme based on the degree of comminution and displacement is more useful for guiding the intensity of treatment. The classification scheme of Manson and co-workers⁶ (see the Classification section) is particularly applicable to zygomatic fractures. Low-energy zygomatico-orbital fractures demonstrate little or no displacement. Frequently the fracture is incomplete through at least one articulation with stability provided at this point (typically the zygomaticofrontal suture). Zygomatico-orbital fractures with minimal degrees of displacement do not require reduction. Conservative treatment consists of a soft diet and protection of the malar eminence for several weeks. These patients should nevertheless be followed closely in the initial weeks after injury in order to detect any early zygomatic displacement due to dynamic traction. Zygomatico-orbital fractures with significant displacement are best managed with open reduction and internal fixation (see Figs. 8, 9, and 10). The number of fracture sites requiring fixation varies with the severity of the injury. For middle-energy zygomatico-orbital fractures, which constitute the vast majority of such injuries, mild to moderate displacement is seen, with a range of comminution.

For simple, displaced zygomatico-orbital fractures with no major comminution, a diversity of opinion exists as to the ideal approach and number and location of points requiring direct visual alignment and fixation. In the era in which interosseous wires were the primary means of fixation, experimental and clinical studies suggested that two-point interfragmentary wiring of the lateral and inferior orbital rims, while the most common method of internal fixation, still permitted rotational displacement of the zygoma about an axis between these two fixation points caused by the continuous traction and force of the masseter muscle. Three-point wire fixation was subsequently advocated by many surgeons, even for simple displaced, noncomminuted zygomatico-orbital fractures. The application of osteosynthesis technology (i.e., rigid miniplates and screws) has led to an evolution in the management of zygomatico-orbital fractures. Miniplates provide greater stability and are more resistant to rotational forces. Most authorities now agree that two-point miniplate application (at two of the following locations: zygomatico frontal suture, inferior orbital rim, or zygomaticomaxillary buttress) provides stable fixation of most noncomminuted displaced zygomatico-orbital fractures.^48,49 Indeed, some surgeons have even suggested that one-point miniplate fixation of zygomatic fractures may be sufficient, provided that appropriate measures be taken to ensure three-point alignment.^51,52 Advocates of one-point fixation caution that such techniques are appropriate only for simple, noncomminuted zygomatico-orbital fractures as assessed by preoperative CT.

For middle-energy zygomatico-orbital fractures with comminution, however, at least a two-point fixation is clearly recommended. The surgical approach to middle-energy zygomatico-orbital fractures is dictated by the degree of exposure and number of fixation points required. The inferior orbital rim fracture site and lateral orbital rim (i.e., zygomaticofrontal suture) fracture sites can be approached quite practically by a single eyelid incision (either transcutaneous or transconjunctival/lateral cantholysis), by extending the incision laterally from the lateral canthal angle. This approach also allows exploration of the orbital floor and confirmation of an adequate reduction by direct inspection of the articulation of the zygomatic bone with the more posterior sphenoid bone, which helps ensure adequate anatomic alignment. Further exposure of the zygomaticomaxillary buttress, if desired, can be obtained via a gingivobuccal sulcus incision. Reduction of the zygoma can be accomplished with an elevator or towel clip. A Girard screw, placed in the malar eminence, may also facilitate reduction. After reduction is performed, the articulation sites at the lateral and inferior orbital rims (and lateral and inferior orbital walls) should be checked to ensure that no soft tissue entrapment is present. Miniplate fixation is performed; after this, any additional repair of the internal orbit can be accomplished.

High-energy zygomatico-orbital fractures are characterized by associated comminution of the greater wing of the sphenoid (in the lateral orbit) and by lateral displacement and posterior segmentation of the zygomatic arch. The external angular process of the frontal bone is also frequently comminuted. These more severe types of zygomatico-orbital fractures are infrequently observed as isolated injuries, being associated more typically with Le Fort and panfacial fractures. The extensive lateral and posterior displacement of the arch results in loss of support for the malar eminence, causing the cheek to be depressed posteriorly and inferiorly. Midfacial width and orbital volume are significantly increased. These high-energy zygomatico-orbital fractures require (1) coronal exposure with reduction and fixation of the zygomatic arch in order to correct facial width and to align and stabilize the forward projection of the malar eminence^6,38,53,54; and (2) rigid fixation of at least two other points of zygomatic articulation, as previously discussed.

INFERIOR ORBITAL RIM. Isolated fractures of the inferior orbital rim are relatively uncommon. Forces sufficient to fracture the inferior orbital rim usually result in internal orbital fractures as well. An inferior orbital rim fracture may be a component of a zygomatico-orbital fracture or a nasoethmoid orbital fracture. With high-energy injuries, extensive comminution of the inferior orbital rim with bone loss may occur, typically as a component of a panfacial fracture. In this setting, inferior orbital rim fracture repair is facilitated by initial reconstruction of the superior, medial, and lateral orbital rims to establish the vertical and horizontal dimensions of the orbital aperture and to allow stabilization of the inferior orbital rim segment(s) by rigid fixation to the zygoma laterally and the nasomaxillary buttress medially. If bone loss (greater than 5 mm) has occurred, bone grafts can be used to fill the defect and are secured by rigid fixation. Inferior orbital rim fractures may extend farther inferiorly through the maxilla. In such cases, attention is directed toward stabilization and rigid fixation of the maxillary buttresses. The thinner bone of the anterior maxillary antrum may be comminuted; in most cases, however, primary repair of this portion of the maxilla is not necessary.

Postoperative Complications

Complications after orbital fracture repair can of course be minimized by good surgical technique. However, because of the severity of such injuries, including the associated soft tissue damage, postoperative complications certainly occur, and the physician should be familiar with their management. Some complications are common to all types of orbital surgery, some are specific to malposition of the orbital rims, and others are related to disruption of the internal orbital walls.³⁶ The most serious complication of orbital surgery is visual loss, which fortunately is rare. Visual loss may be caused by intraoperative manipulation of the globe or optic nerve or by a postoperative orbital hemorrhage that produces central retinal artery occlusion or compressive optic neuropathy. Early detection of visual loss is essential, which is why occlusive dressings are avoided and the patient is followed closely after surgery. Pupil examination to check for an afferent pupillary defect is a reliable, simple way to detect optic neuropathy. Orbital hemorrhage in such cases is usually obvious; when it is found to be causing impairment, it is treated as previously discussed with lateral canthotomy, cantholysis, and other adjunctive medical and surgical treatment.² Repeat orbital CT scanning is appropriate, provided that treatment is not significantly delayed.

The following are among the complications related to malposition of the orbital rims: persistent step-off fracture, bony malunion or resorption creating contour deformity, and frank dislocation of a portion of the orbital rim in the early postoperative period, which is caused by improper alignment or fixation and in late cases by tractional forces acting on an inadequately fixated segment. These complications are more common with fractures of the inferior lateral orbital rims (i.e., zygomatico-orbital fractures) because of the tractional forces of the masseter muscle. If early dislocation is noted, prompt repositioning and stabilization (fixation) should be performed. In cases where this complication is noted later, treatment may consist of onlay bone grafts or synthetic implants (e.g., malar eminence). In more severe cases, however, osteotomy with repositioning and fixation of the dislocated segment is necessary.

Soft tissue disruption associated with orbital rim fractures may also produce late postoperative sequelae, primarily consisting of displacement of the lateral canthus (inferior dystopia) and medial canthus (typically producing telecanthus). Mild lateral canthal dystopia may be managed by lateral canthoplasty with repositioning of the lateral canthus using a tarsal strip procedure, provided that the bony rim/malar position is not significantly displaced. More severe forms of dystopia usually necessitate osteotomy and repositioning of the displaced lateral orbital rim/zygoma. Persistent telecanthus unfortunately is a frequent complication of nasoethmoid orbital fractures (Fig. 11). Treatment is usually performed with medial canthopexy using transnasal wiring or other medial canthal fixation techniques (Fig. 12). Excess scar tissue and displaced bone fragments should be removed from the medial canthal region in order to achieve a satisfactory result. Damage to the nasolacrimal drainage system may also be a sequela of a nasoethmoid orbital or midfacial fracture. If injury to the nasolacrimal drainage system is obvious at the patient's initial presentation, primary repair can be performed. In most cases, the nasolacrimal injury is not noted until later, typically manifesting as nasolacrimal duct obstruction producing epiphora, with or without dacryocystitis. Treatment is accomplished with dacryocystorhinostomy.

Complications related to repair of internal orbital wall fractures include predominantly persistent enophthalmos/hypo-ophthalmos and diplopia, as well as those related to synthetic orbital implants or bone grafts per se. Several of the potential postoperative complications related to alloplastic implants and bone grafts (see Internal Orbital Fractures section) include migration, extrusion, and infection. Such complications are possible with alloplastic implants or bone grafts, but are more common with alloplastic implants. Bone grafts have the potential complication of variable degrees of resorption, which is believed to be greater with endochondral bone compared with membranous bone grafts. Infection or extrusion generally requires removal of the implant or bone graft if prompt improvement with antibiotic therapy is not seen. In the setting of infection, the implant should not be replaced. In many cases, fibrous tissue forms around alloplastic implants after several weeks or months, which may allow enough orbital soft tissue support so that a replacement implant is not required. In other cases, secondary repair with a suitable alloplastic implant or graft must be performed after the infection is adequately controlled. Migration of an alloplastic implant or bone graft, if minor and not causing significant sequelae, may be observed. More marked implant migration causing functional impairment necessitates removal of the alloplastic implant or bone graft.

Globe malpositions after blow-out fracture repair usually are caused by failure of surgery to reconstruct the normal anatomic boundaries (walls) of the orbit. Soft tissue scarring (and perhaps in a small number of cases, fat atrophy) may also contribute to late enophthalmos. Enophthalmos may be corrected by repositioning the implant or by adding additional alloplastic implant or bone graft to augment the volume deficiency. Camouflage techniques such as blepharoplasty of the contralateral upper eyelid or ptosis repair of the ipsilateral eyelid may also be considered. Diplopia after blow-out fracture repair may be due to persistent orbital soft tissue entrapment, but it may also be due to coincident extraocular muscle injury or neurologic injury. Postoperative orbital edema may also be associated with generalized limitation of ocular motility; therefore, ocular motility is most appropriately reassessed after the edema resolves (usually in 2 to 3 weeks). Repeat CT scanning may also be helpful. If the clinical examination and CT findings are suggestive of persistent extraocular muscle entrapment in a patient with functionally significant diplopia, then early orbital re-exploration is indicated.

Persistent ocular motility deficits that are not amenable to orbital surgery generally require strabismus surgery. Usually a period of 6 months or more is allowed for spontaneous improvement, during which time serial orthoptic measurements are taken. Within this waiting period, diplopia may be symptomatically treated with Fresnel prisms, fogging (partial occlusion), or patching (complete occlusion) of one eye. Young children at risk for amblyopia require closer follow-up and appropriate treatment should amblyopia develop. Most authorities consider blow-out fracture repair successful if diplopia is relieved within the functional (30°) fields of gaze. Reoperation is usually not indicated for diplopia occurring in more eccentric fields of gaze, although each case must be individualized.

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