Evaluation of the patient with orbital trauma should proceed in a logical, defined manner.1, 2 and 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 is 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, some would advocate treatment with megadoses of corticosteroids, although this has not been shown to be more effective than observation alone.49 In two specific instances of traumatic optic neuropathy, surgery may be indicated. Optic nerve sheath fenestration may be indicated if an intradural sheath hematoma is the cause of the traumatic optic neuropathy. Optic canal decompression may rarely be indicated if bony fragments from the sphenoid wall are clearly impinging on the optic nerve within the bony optic canal. Further orbital evaluation includes an assessment of ocular motility, globe position, eyelid and canthal position, orbital rim palpation, and facial sensation and movement. 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.50 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,48 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. Quantization 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. When an involved eye without muscle entrapment or strong mechanical restrictions moves more than 10° or 20° on each Hess chart, natural recovery can be expected.51

The position of the globe is also assessed (Fig. 48.4). 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. Indeed displacement of intraconal fat with disruption of ligamentous support has been shown to cause enophthalmos. The shape of the retrobulbar orbital contents changes from a modified cone to a sphere, and the globe sinks backward and downward.42 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 >2 mm is considered abnormal. Typically a difference ≥3 mm is required to produce an obvious clinical difference between the two eyes, although pre-existing 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. In such cases, the Naugle exophthalmometer may be useful in that it measures the position of the globe relative to the maxilla and frontal bone. Early (<4 weeks after injury) exophthalmometry has been shown to correlate poorly with predictions of enophthalmos, whereas late exophthalmometry readings (>4 weeks) were more predictive of late enophthalmos.52 CT imaging with volumetric analysis can detect 1-mL volume changes in the bony orbit, which correlate with 1 mm of enophthalmos. Therefore, a 2-mL change in orbital volume detected on CT could be expected to be clinically significant with 2 mm of enophthalmos as measured by exophthalmometry.53 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.54

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). Coexistent 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.55 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 earlier (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, hypoesthesia 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.56